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Sample records for csf total tau

  1. Total-tau and neurofilament light in CSF reflect spinal cord ischaemia after endovascular aortic repair.

    Science.gov (United States)

    Merisson, Edyta; Mattsson, Niklas; Zetterberg, Henrik; Blennow, Kaj; Pikwer, Andreas; Mehmedagic, Irma; Acosta, Stefan; Åkeson, Jonas

    2016-02-01

    Repair of extensive aortic disease may be associated with spinal cord ischaemia (SCI). Here we test if levels of cerebrospinal fluid (CSF) biomarkers for neuronal injury are altered in patients with SCI after advanced endovascular repair in extensive aortic disease. CSF was sampled for up to 48 h in ten patients undergoing endovascular aortic repair and analyzed for the axonal damage markers total-tau (T-tau) and neurofilament light (NFL). Six of ten patients developed SCI (clinically present within 3-6 h). CSF levels of NFL increased up to 37-fold in patients with, but were stable in patients without, SCI. CSF levels of T-tau also increased in patients with SCI, but with some overlap with patients without SCI. Levels of NFL and T-tau did not increase until after the appearance of clinical signs of neurological dysfunction (12-48 h after aortic repair). The CSF biomarkers NFL and T-tau both reflect development of SCI after endovascular aortic repair, but do not rise until after clinical signs of SCI appear. Future studies are desirable to further evaluate potential use of these biomarkers for assessment of the severity of SCI, and also to identify earlier biomarkers of SCI. Copyright © 2015. Published by Elsevier Ltd.

  2. CSF total protein

    Science.gov (United States)

    CSF total protein is a test to determine the amount of protein in your spinal fluid, also called cerebrospinal fluid (CSF). ... The normal protein range varies from lab to lab, but is typically about 15 to 60 milligrams per deciliter (mg/dL) ...

  3. (18)F-AV-1451 and CSF T-tau and P-tau as biomarkers in Alzheimer's disease.

    Science.gov (United States)

    Mattsson, Niklas; Schöll, Michael; Strandberg, Olof; Smith, Ruben; Palmqvist, Sebastian; Insel, Philip S; Hägerström, Douglas; Ohlsson, Tomas; Zetterberg, Henrik; Jögi, Jonas; Blennow, Kaj; Hansson, Oskar

    2017-09-01

    To elucidate the relationship between cerebrospinal fluid (CSF) total-tau (T-tau) and phosphorylated tau (P-tau) with the tau PET ligand (18)F-AV-1451 in Alzheimer's disease (AD), we examined 30 cognitively healthy elderly (15 with preclinical AD), 14 prodromal AD, and 39 AD dementia patients. CSF T-tau and P-tau were highly correlated (R = 0.92, P AV-1451, and mainly in demented AD patients. (18)F-AV-1451, but not CSF T-tau or P-tau, was strongly associated with atrophy and cognitive impairment. CSF tau was increased in preclinical AD, despite normal (18)F-AV-1451 retention. However, not all dementia AD patients exhibited increased CSF tau, even though (18)F-AV-1451 retention was always increased at this disease stage. We conclude that CSF T-tau and P-tau mainly behave as biomarkers of "disease state", since they appear to be increased in many cases of AD at all disease stages, already before the emergence of tau aggregates. In contrast, (18)F-AV-1451 is a biomarker of "disease stage", since it is increased in clinical stages of the disease, and is associated with brain atrophy and cognitive decline. © 2017 The Authors. Published under the terms of the CC BY 4.0 license.

  4. CSF α-synuclein improves diagnostic and prognostic performance of CSF tau and Aβ in Alzheimer's disease.

    Science.gov (United States)

    Toledo, Jon B; Korff, Ane; Shaw, Leslie M; Trojanowski, John Q; Zhang, Jing

    2013-11-01

    Alzheimer's disease (AD) and Lewy body diseases (LBD), e.g., Parkinson's disease (PD) dementia and dementia with Lewy bodies (DLB), are common causes of geriatric cognitive impairments. In addition, AD and LBD are often found in the same patients at autopsy; therefore, biomarkers that can detect the presence of both pathologies in living subjects are needed. In this investigation, we report the assessment of α-synuclein (α-syn) in cerebrospinal fluid (CSF) and its association with CSF total tau (t-tau), phosphorylated tau181 (p-tau181), and amyloid beta1-42 (Aβ1-42) in subjects of the Alzheimer's Disease Neuroimaging Initiative (ADNI; n = 389), with longitudinal clinical assessments. A strong correlation was noted between α-syn and t-tau in controls, as well as in patients with AD and mild cognitive impairment (MCI). However, the correlation is not specific to subjects in the ADNI cohort, as it was also seen in PD patients and controls enrolled in the Parkinson's Progression Markers Initiative (PPMI; n = 102). A bimodal distribution of CSF α-syn levels was observed in the ADNI cohort, with high levels of α-syn in the subjects with abnormally increased t-tau values. Although a correlation was also noted between α-syn and p-tau181, there was a mismatch (α-syn-p-tau181-Mis), i.e., higher p-tau181 levels accompanied by lower α-syn levels in a subset of ADNI patients. We hypothesize that this α-syn-p-tau181-Mis is a CSF signature of concomitant LBD pathology in AD patients. Hence, we suggest that inclusion of measures of CSF α-syn and calculation of α-syn-p-tau181-Mis improves the diagnostic sensitivity/specificity of classic CSF AD biomarkers and better predicts longitudinal cognitive changes.

  5. Neprilysin-Like Activity Correlates with CSF-Tau and Phospho-Tau in Patients with Alzheimer's Disease

    DEFF Research Database (Denmark)

    Sorensen, Katrine Christa Nordskov; Simonsen, Anja Hviid; Holmetoft, Ulla Bachmann

    2013-01-01

    the level and enzyme activity of NEP in serum and CSF, using a sandwich enzyme-linked immunosorbent assay and a fluorescence resonance energy transfer assay, respectively, in patients with AD, frontotemporal dementia (FTD), Creutzfeldt-Jakob disease (CJD), and depression. Results were correlated...... with the levels of CSF AD biomarkers Aβ42, hyperphosphorylated tau (p-tau), and total tau (t-tau). In serum, we found no differences in NEP-like activity or concentration between the groups and there were no correlations between NEP and AD biomarkers. In CSF, no influence of age or gender on NEP levels or enzyme...... activity was seen. However, NEP concentration was lower and the specific activity was higher in FTD compared to AD. Aβ42 levels in CSF did not correlate with NEP concentration or activity in the AD, CJD, or depression groups, but NEP-like activity and Aβ42 levels correlated significantly in the FTD group...

  6. Increased total-Tau levels in cerebrospinal fluid of pediatric hydrocephalus and brain tumor patients

    NARCIS (Netherlands)

    de Bont, Judith M.; Vanderstichele, Hugo; Reddingius, Roel E.; Pieters, Rob; van Gool, Stefdan W.

    2008-01-01

    Total Tau (t-Tau), hyperphosphorylated Tau (p-Tau((181P))) and beta-amyloid((1-42)) in cerebrospinal fluid (CSF) have shown to be markers of neuronal and axonal degeneration in various neurological and neurodegenerative diseases. The aim of this study was to evaluate the influence of the presence of

  7. CSF levels of DJ-1 and tau distinguish MSA patients from PD patients and controls.

    Science.gov (United States)

    Herbert, Megan K; Eeftens, Jorine M; Aerts, Marjolein B; Esselink, Rianne A J; Bloem, Bastiaan R; Kuiperij, H Bea; Verbeek, Marcel M

    2014-01-01

    Differential diagnosis between Parkinson's disease (PD) and multiple system atrophy (MSA) is difficult, particularly at early disease stages, but is important for therapeutic management. The protein DJ-1 is implicated in the pathology of PD but little is known about its involvement in MSA. We aimed to determine the diagnostic value of CSF DJ-1 and tau proteins for discriminating PD and MSA. DJ-1 and total tau levels were quantified in the CSF of 43 PD patients, 23 MSA patients and 30 non-neurological controls matched for age and gender. Patients were part of a study with a 3-year prospective design with extended case-review follow-up of up to 9 years, ensuring maximum accuracy of the clinical diagnosis. Our results showed that CSF DJ-1 levels could distinguish MSA from PD with a 78% sensitivity and 78% specificity (AUC = 0.84). The combination of DJ-1 and tau proteins significantly improved this discrimination to 82% sensitivity and 81% specificity to identify MSA from PD (AUC = 0.92). Our results highlight the potential benefits of a combination of DJ-1 and total tau as biomarkers for differential diagnosis of MSA and PD.

  8. CSF T-Tau/Aβ42 predicts white matter microstructure in healthy adults at risk for Alzheimer's disease.

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    Barbara B Bendlin

    Full Text Available Cerebrospinal fluid (CSF biomarkers T-Tau and Aβ(42 are linked with Alzheimer's disease (AD, yet little is known about the relationship between CSF biomarkers and structural brain alteration in healthy adults. In this study we examined the extent to which AD biomarkers measured in CSF predict brain microstructure indexed by diffusion tensor imaging (DTI and volume indexed by T1-weighted imaging. Forty-three middle-aged adults with parental family history of AD received baseline lumbar puncture and MRI approximately 3.5 years later. Voxel-wise image analysis methods were used to test whether baseline CSF Aβ(42, total tau (T-Tau, phosphorylated tau (P-Tau and neurofilament light protein predicted brain microstructure as indexed by DTI and gray matter volume indexed by T1-weighted imaging. T-Tau and T-Tau/Aβ(42 were widely correlated with indices of brain microstructure (mean, axial, and radial diffusivity, notably in white matter regions adjacent to gray matter structures affected in the earliest stages of AD. None of the CSF biomarkers were related to gray matter volume. Elevated P-Tau and P-Tau/Aβ(42 levels were associated with lower recognition performance on the Rey Auditory Verbal Learning Test. Overall, the results suggest that CSF biomarkers are related to brain microstructure in healthy adults with elevated risk of developing AD. Furthermore, the results clearly suggest that early pathological changes in AD can be detected with DTI and occur not only in cortex, but also in white matter.

  9. Characterization of novel CSF Tau and ptau biomarkers for Alzheimer's disease.

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    Jere E Meredith

    Full Text Available Cerebral spinal fluid (CSF Aβ42, tau and p181tau are widely accepted biomarkers of Alzheimer's disease (AD. Numerous studies show that CSF tau and p181tau levels are elevated in mild-to-moderate AD compared to age-matched controls. In addition, these increases might predict preclinical AD in cognitively normal elderly. Despite their importance as biomarkers, the molecular nature of CSF tau and ptau is not known. In the current study, reverse-phase high performance liquid chromatography was used to enrich and concentrate tau prior to western-blot analysis. Multiple N-terminal and mid-domain fragments of tau were detected in pooled CSF with apparent sizes ranging from <20 kDa to ~40 kDa. The pattern of tau fragments in AD and control samples were similar. In contrast, full-length tau and C-terminal-containing fragments were not detected. To quantify levels, five tau ELISAs and three ptau ELISAs were developed to detect different overlapping regions of the protein. The discriminatory potential of each assay was determined using 20 AD and 20 age-matched control CSF samples. Of the tau ELISAs, the two assays specific for tau containing N-terminal sequences, amino acids 9-198 (numbering based on tau 441 and 9-163, exhibited the most significant differences between AD and control samples. In contrast, CSF tau was not detected with an ELISA specific for a more C-terminal region (amino acids 159-335. Significant discrimination was also observed with ptau assays measuring amino acids 159-p181 and 159-p231. Interestingly, the discriminatory potential of p181 was reduced when measured in the context of tau species containing amino acids 9-p181. Taken together, these results demonstrate that tau in CSF occurs as a series of fragments and that discrimination of AD from control is dependent on the subset of tau species measured. These assays provide novel tools to investigate CSF tau and ptau as biomarkers for other neurodegenerative diseases.

  10. Total and phosphorylated tau protein as biological markers of Alzheimer's disease.

    LENUS (Irish Health Repository)

    Hampel, Harald

    2012-02-01

    Advances in our understanding of tau-mediated neurodegeneration in Alzheimer\\'s disease (AD) are moving this disease pathway to center stage for the development of biomarkers and disease modifying drug discovery efforts. Immunoassays were developed detecting total (t-tau) and tau phosphorylated at specific epitopes (p-tauX) in cerebrospinal fluid (CSF), methods to analyse tau in blood are at the experimental beginning. Clinical research consistently demonstrated CSF t- and p-tau increased in AD compared to controls. Measuring these tau species proved informative for classifying AD from relevant differential diagnoses. Tau phosphorylated at threonine 231 (p-tau231) differentiated between AD and frontotemporal dementia, tau phosphorylated at serine 181 (p-tau181) enhanced classification between AD and dementia with Lewy bodies. T- and p-tau are considered "core" AD biomarkers that have been successfully validated by controlled large-scale multi-center studies. Tau biomarkers are implemented in clinical trials to reflect biological activity, mechanisms of action of compounds, support enrichment of target populations, provide endpoints for proof-of-concept and confirmatory trials on disease modification. World-wide quality control initiatives are underway to set required methodological and protocol standards. Discussions with regulatory authorities gain momentum defining the role of tau biomarkers for trial designs and how they may be further qualified for surrogate marker status.

  11. Standardization of Assay Procedures for Analysis of the CSF Biomarkers Amyloid β(1-42, Tau, and Phosphorylated Tau in Alzheimer's Disease: Report of an International Workshop

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    Charlotte E. Teunissen

    2010-01-01

    Full Text Available Large variation in assay performance and outcomes of CSF Aβ1-42, total Tau (Tau, and phosphorylated Tau (pTau (at amino acid 181 levels is observed between laboratories. The aim of this study was to assess the differences in assay procedures between several experienced international laboratories, as potential sources of error. 14 groups performed the Aβ42, Tau, and pTau assays according to the guidelines of the manufacturer. Differences in analytical procedures between the laboratories were monitored. At least 23 items in assay procedures were identified that varied between the laboratories, including procedures for washing, pipetting, incubation, finishing, and sample handing. In general, the inter- and intra-assay variation between the groups was generally below 10% for all three assays. We concluded that 17 international centers that use the same assays for Aβ42, Tau and pTau on a regular basis do not uniformly adhere to the procedures recommended by the manufacturer. For harmonization of intercenter results of these biomarkers standardization of protocols is highly needed.

  12. Antibody-free quantification of seven tau peptides in human CSF using targeted mass spectrometry

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    Pauline eBros

    2015-09-01

    Full Text Available Tau protein concentration in cerebrospinal fluid (CSF is currently used as a sensitive and specific biomarker for Alzheimer's disease. Its detection currently relies on ELISA but the perspective of using mass spectrometry (MS to detect its different proteoforms represents an interesting alternative. This is however an analytical challenge because of its low concentration in the CSF, a biological fluid collected in small volume by lumbar puncture, and with a high structural heterogeneity. To overcome these issues, instead of using immunocapture as previously done, we rather relied on an original two steps pre-fractionation technique of CSF: perchloric acid followed by micro solid phase extraction (µSPE. We could then measure seven tau trypsic peptides by Multiple Reaction Monitoring (MRM on a triple quadrupole mass spectrometer. Quantification was performed using isotopically labelled 15N- recombinant Tau protein as internal standard and validated using CSF pools with low, medium or high tau concentrations. Repeatability, intermediate precision, linearity, limit of quantification and recovery were calculated for the different peptides. This new MRM assay, which allowed for the first time CSF tau protein quantification without immunocapture, has important potential application to follow tau metabolism in both diagnostic and therapeutic research.

  13. Antibody-free quantification of seven tau peptides in human CSF using targeted mass spectrometry.

    Science.gov (United States)

    Bros, Pauline; Vialaret, Jérôme; Barthelemy, Nicolas; Delatour, Vincent; Gabelle, Audrey; Lehmann, Sylvain; Hirtz, Christophe

    2015-01-01

    Tau protein concentration in cerebrospinal fluid (CSF) is currently used as a sensitive and specific biomarker for Alzheimer's disease. Its detection currently relies on ELISA but the perspective of using mass spectrometry (MS) to detect its different proteoforms represents an interesting alternative. This is however an analytical challenge because of its low concentration in the CSF, a biological fluid collected in small volume by lumbar puncture, and with a high structural heterogeneity. To overcome these issues, instead of using immunocapture as previously done, we rather relied on an original two steps pre-fractionation technique of CSF: perchloric acid (PCA) followed by micro solid phase extraction (μSPE). We could then measure seven tau trypsic peptides by Multiple Reaction Monitoring (MRM) on a triple quadrupole mass spectrometer. Quantification was performed using isotopically labeled (15)N- recombinant tau protein as internal standard and validated using CSF pools with low, medium, or high tau concentrations (HTCs). Repeatability, intermediate precision, linearity, limit of quantification (LOQ), and recovery were calculated for the different peptides. This new MRM assay, which allowed for the first time CSF tau protein quantification without immunocapture, has important potential application to follow tau metabolism in both diagnostic and therapeutic research.

  14. Diagnostic Utility of CSF Tau and A in Dementia: A Meta-Analysis

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    Rachna Agarwal

    2011-01-01

    Full Text Available CSF tau and Aβ42 are considered as important markers to diagnose Alzheimer’s disease in early stages. Hence, it is important to assess their status in different types of dementia. The main objective of this study was to assess whether these CSF biomarkers can be used to make the differential diagnosis of AD. In the present study, articles published from 1998 till 2009 were taken and meta-analysis was performed to clarify the consistency in trends of biomarkers- CSF tau and Aβ42 in AD and other dementias and whether the same can be used as diagnostic biomarkers for its early diagnosis. 11 out of 60 for CSF tau and 07 out of 40 for CSF Aβ42, dementia case-control studies were selected for final analysis. Descriptive statistics shows that median effect size (raw mean difference of CSF tau was 429 pg/mL (range: 32 to 910 pg/mL in AD whereas in Dementia due to other causes (DOC studies it was 69 pg/mL (range: −53 to 518 pg/mL. Similarly the median effect size of CSF Aβ42 levels was −442 pg/mL (range: −652 to −41.200 pg/mL whereas in DOC studies it was −193 pg/mL (range: −356 to −33 pg/mL.

  15. CSF neurofilament light chain and tau differentiate multiple system atrophy from Parkinson's disease.

    NARCIS (Netherlands)

    Abdo, W.; Bloem, B.R.; Geel, W.J.A. van; Esselink, R.A.J.; Verbeek, M.M.

    2007-01-01

    BACKGROUND: In early disease stages it can be clinically difficult to differentiate idiopathic Parkinson's disease (IPD) from patients with multiple system atrophy predominated by parkinsonism (MSA-P). METHODS: In CSF of 31 patients with IPD, 19 patients with MSA-P, we analyzed tau, neurofilament

  16. CSF neurofilament light chain and tau differentiate multiple system atrophy from Parkinson's disease.

    NARCIS (Netherlands)

    Abdo, W.; Bloem, B.R.; Geel, W.J.A. van; Esselink, R.A.J.; Verbeek, M.M.

    2007-01-01

    BACKGROUND: In early disease stages it can be clinically difficult to differentiate idiopathic Parkinson's disease (IPD) from patients with multiple system atrophy predominated by parkinsonism (MSA-P). METHODS: In CSF of 31 patients with IPD, 19 patients with MSA-P, we analyzed tau, neurofilament li

  17. Baseline CSF p-tau levels independently predict progression of hippocampal atrophy in Alzheimer disease

    Science.gov (United States)

    Henneman, W J.P.; Vrenken, H; Barnes, J; Sluimer, I C.; Verwey, N A.; Blankenstein, M A.; Klein, M; Fox, N C.; Scheltens, P; Barkhof, F; van der Flier, W M.

    2009-01-01

    Objective: To investigate whether baseline CSF biomarkers are associated with hippocampal atrophy rate as a measure of disease progression in patients with Alzheimer disease (AD), patients with mild cognitive impairment (MCI), and controls, controlling for baseline neuropsychological and MRI findings. Methods: We assessed data from 31 patients with AD, 25 patients with MCI, and 19 controls (mean age 68 ± 8 years; 39 [52%] female) who visited our memory clinic and had received serial MRI scanning (scan interval 1.7 ± 0.7 years). At baseline, CSF biomarkers (amyloid β 1-42, tau, and tau phosphorylated at threonine 181 [p-tau]) were obtained, as well as neuropsychological data. Baseline MRI scans were assessed using visual rating scales for medial temporal lobe atrophy (MTA), global cortical atrophy, and white matter hyperintensities. Hippocampal atrophy rates were estimated using regional nonlinear “fluid” registration of follow-up scan to baseline scan. Results: Stepwise multiple linear regression, adjusted for age and sex, showed that increased CSF p-tau levels (β [standard error]: −0.79 [0.35]) at baseline was independently associated with higher subsequent hippocampal atrophy rates (p < 0.05), together with poorer memory performance (0.09 [0.04]) and more severe MTA (−0.60 [0.21]). The association of memory function with hippocampal atrophy rate was explained by the link with diagnosis, because it disappeared from the model after we additionally corrected for diagnosis. Conclusions: Baseline CSF levels of tau phosphorylated at threonine 181 are independently associated with subsequent disease progression, as reflected by hippocampal atrophy rate. This effect is independent of baseline neuropsychological and MRI predictors. Our results imply that predicting disease progression can best be achieved by combining information from different modalities. GLOSSARY Aβ1-42 = amyloid β 1-42; AD = Alzheimer disease; FOV = field of view; GCA = global cortical

  18. Changes in PINCH and hpTau levels in the CSF of HIV patients correlate with CD4 count

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    Adiga, Radhika; Ozdemir, Ahmet Y.; Carides, Alexandra; Wasilewski, Melissa; Yen, William; Chitturi, Pallavi; Ellis, Ronald; Langford, Dianne

    2014-01-01

    Several studies report associations between the PINCH (particularly interesting new cysteine histidine-rich) protein and HIV-associated CNS disease. PINCH is detected in the CSF of HIV patients and changes in levels during disease may be indicative of changes in disease status over time. PINCH binds hyperphosphorylated Tau (hpTau) in the brain and CSF, but little is known about the relevance of these interactions to HIV CNS disease. In this study, PINCH and hpTau levels were assessed in three separate CSF samples collected longitudinally from 20 HIV+ participants before and after initiating antiretroviral therapy, or before and after a change in the current regimen. The intervals were approximately 1 (T2), and 3-7 (T3) months from the initial visit (baseline, T1). Correlational analyses were conducted for CSF levels of PINCH and hpTau and other variables including blood CD4+ T-cell count, plasma and CSF viral burden, CSF neopterin, white blood cell (WBC) count, and antiretroviral CNS penetration-effectiveness (CPE). Values for PINCH and hpTau were determined for each patient by calculating the fold changes between the second (T2) and third measurements (T3) from the baseline measurement (T1). Statistical analyses showed that the fold-change in CSF PINCH protein from T1 to T2 were significantly higher in participants with CD4 counts >200 cells/mm3 at T2 compared to those with CD4 counts <200 cells/mm3 at T2. This trend persisted irrespective of plasma or CSF viral burden or anti-retroviral therapy CPE scores. The fold-changes in PINCH levels between T1 and T2, and T1 and T3 were highly correlated to the fold changes in hpTau at T2/T1 and T3/T1 (correlation co-efficient = 0.69, p-value < 0.001, correlation co-efficient = 0.83, p-value <0.0001, respectively). In conclusion, in these HIV participants, changes in CSF levels of PINCH appear to correlate with changes in blood CD4 count and with changes in CSF hpTau levels, but not with plasma or CSF viral burden

  19. Cerebrospinal Fluid Amyloid-β 42, Total Tau and Phosphorylated Tau are Low in Patients with Normal Pressure Hydrocephalus: Analogies and Differences with Alzheimer's Disease.

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    Santangelo, Roberto; Cecchetti, Giordano; Bernasconi, Maria Paola; Cardamone, Rosalinda; Barbieri, Alessandra; Pinto, Patrizia; Passerini, Gabriella; Scomazzoni, Francesco; Comi, Giancarlo; Magnani, Giuseppe

    2017-01-01

    Co-existence of Alzheimer's disease (AD) in normal pressure hydrocephalus (NPH) is a frequent finding, thus a common pathophysiological basis between AD and NPH has been postulated. We measured CSF amyloid-β 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) concentrations in a sample of 294 patients with different types of dementia and 32 subjects without dementia. We then compared scores on neuropsychological tests of NPH patients with pathological and normal CSF Aβ42 values. Aβ42 levels were significantly lower in NPH than in control patients, with no significant differences between AD and NPH. On the contrary, t-tau and p-tau levels were significantly lower in NPH than in AD, with no differences between NPH and controls. NPH patients with pathological Aβ42 levels did not perform worse than NPH patients with normal Aβ42 levels in any cognitive domains. Our data seem to support the hypothesis of amyloid accumulation in brains of NPH patients. Nevertheless, amyloid does not seem to play a pathogenetic role in the development of cognitive deficits in NPH.

  20. Tau protein

    DEFF Research Database (Denmark)

    Frederiksen, Jette Lautrup Battistini; Kristensen, Kim; Bahl, Jmc

    2011-01-01

    Background: Tau protein has been proposed as biomarker of axonal damage leading to irreversible neurological impairment in MS. CSF concentrations may be useful when determining risk of progression from ON to MS. Objective: To investigate the association between tau protein concentration and 14......-3-3 protein in the cerebrospinal fluid (CSF) of patients with monosymptomatic optic neuritis (ON) versus patients with monosymptomatic onset who progressed to multiple sclerosis (MS). To evaluate results against data found in a complete literature review. Methods: A total of 66 patients with MS and/or ON from...... the Department of Neurology of Glostrup Hospital, University of Copenhagen, Denmark, were included. CSF samples were analysed for tau protein and 14-3-3 protein, and clinical and paraclinical information was obtained from medical records. Results: The study shows a significantly increased concentration of tau...

  1. Total-tau and phospho-tau(181Thr) in cerebrospinal fluid of neurologically intact population increase with age.

    Science.gov (United States)

    Jaworski, J; Psujek, M; Bartosik-Psujek, H

    2009-01-01

    Tau protein is a microtubule-associated molecule playing a crucial role in maintenance of neuronal integrity and in many neurodegenerative processes; its pathology has become a hallmark feature at the tissue level. The aim of the study was to estimate total tau and phospho-tau (Thr181) concentrations in cerebrospinal fluid of healthy population. Cerebrospinal fluid samples were taken from 129 subjects (age 18-77 years) without known neurologic or psychiatric condition. Both total-tau and phospho-tau levels showed significant correlation with age, which was more pronounced in older population.

  2. Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease.

    Science.gov (United States)

    Brier, Matthew R; Gordon, Brian; Friedrichsen, Karl; McCarthy, John; Stern, Ari; Christensen, Jon; Owen, Christopher; Aldea, Patricia; Su, Yi; Hassenstab, Jason; Cairns, Nigel J; Holtzman, David M; Fagan, Anne M; Morris, John C; Benzinger, Tammie L S; Ances, Beau M

    2016-05-11

    Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. Until recently, only Aβ could be studied in humans using positron emission tomography (PET) imaging owing to a lack of tau PET imaging agents. Clinical pathological studies have linked tau pathology closely to the onset and progression of cognitive symptoms in patients with AD. We report PET imaging of tau and Aβ in a cohort of cognitively normal older adults and those with mild AD. Multivariate analyses identified unique disease-related stereotypical spatial patterns (topographies) for deposition of tau and Aβ. These PET imaging tau and Aβ topographies were spatially distinct but correlated with disease progression. Cerebrospinal fluid measures of tau, often used to stage preclinical AD, correlated with tau deposition in the temporal lobe. Tau deposition in the temporal lobe more closely tracked dementia status and was a better predictor of cognitive performance than Aβ deposition in any region of the brain. These data support models of AD where tau pathology closely tracks changes in brain function that are responsible for the onset of early symptoms in AD.

  3. Increased CSF alpha-synuclein levels in Alzheimer's disease : Correlation with tau levels

    NARCIS (Netherlands)

    Slaets, Sylvie; Vanmechelen, Eugeen; Le Bastard, Nathalie; Decraemer, Hilde; Vandijck, Manu; Martin, Jean-Jacques; De Deyn, Peter Paul; Engelborghs, Sebastiaan

    2014-01-01

    Background: Given the difficult clinical differential diagnosis between Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), growing interest resulted in research on alpha-synuclein as a potential cerebrospinal fluid biomarker (CSF) for synucleinopathies. Methods: CSF alpha-synuclein-140 co

  4. Variability of CSF Alzheimer's disease biomarkers: implications for clinical practice.

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    Stephanie J B Vos

    Full Text Available BACKGROUND: Cerebrospinal fluid (CSF biomarkers are increasingly being used for diagnosis of Alzheimer's disease (AD. OBJECTIVE: We investigated the influence of CSF intralaboratory and interlaboratory variability on diagnostic CSF-based AD classification of subjects and identified causes of this variation. METHODS: We measured CSF amyloid-β (Aβ 1-42, total tau (t-tau, and phosphorylated tau (p-tau by INNOTEST enzyme-linked-immunosorbent assays (ELISA in a memory clinic population (n = 126. Samples were measured twice in a single or two laboratories that served as reference labs for CSF analyses in the Netherlands. Predefined cut-offs were used to classify CSF biomarkers as normal or abnormal/AD pattern. RESULTS: CSF intralaboratory variability was higher for Aβ1-42 than for t-tau and p-tau. Reanalysis led to a change in biomarker classification (normal vs. abnormal of 26% of the subjects based on Aβ1-42, 10% based on t-tau, and 29% based on p-tau. The changes in absolute biomarker concentrations were paralleled by a similar change in levels of internal control samples between different assay lots. CSF interlaboratory variability was higher for p-tau than for Aβ1-42 and t-tau, and reanalysis led to a change in biomarker classification of 12% of the subjects based on Aβ1-42, 1% based on t-tau, and 22% based on p-tau. CONCLUSIONS: Intralaboratory and interlaboratory CSF variability frequently led to change in diagnostic CSF-based AD classification for Aβ1-42 and p-tau. Lot-to-lot variation was a major cause of intralaboratory variability. This will have implications for the use of these biomarkers in clinical practice.

  5. Pharmacologic reductions of total tau levels; implications for the role of microtubule dynamics in regulating tau expression

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    Dickey Chad A

    2006-07-01

    Full Text Available Abstract The microtubule-associated protein tau (MAPT is a pathological component of several neurodegenerative diseases and clinical dementias. Here, we have investigated the effects of a series of commercially available FDA-approved compounds and natural products on total tau protein levels using a cell-based approach that allows for the rapid and efficient measurement of changes in protein expression. Results The compounds that reduced tau largely fell within 3 functional categories with the largest percentage being microtubule regulators. Several of these candidates were validated in both a human neuroglioma and a human neuroblastoma cell line. While these drugs lead to a rapid reduction in tau protein levels, a selective decrease in MAPT mRNA expression was also observed. Conclusion These findings suggest that the identified compounds that reduce tau levels may act either through direct effects on the MAPT promoter itself or by altering a feedback transcriptional mechanism regulating MAPT transcription. This is particularly interesting in light of recent evidence suggesting that MAPT 5' UTR mutations in late-onset PD and PSP cases alter the expression of tau mRNA. In fact, one of the compounds we identified, rotenone, has been used extensively to model PD in rodents. These observations may provide key insights into the mechanism of tau turnover within the neuron while also providing the first evidence that selectively reducing tau protein levels may be possible using compounds that are FDA-approved for other uses.

  6. Combined Analysis of CSF Tau, Aβ42, Aβ1–42% and Aβ1–40ox% in Alzheimer's Disease, Dementia with Lewy Bodies and Parkinson's Disease Dementia

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    Mirko Bibl

    2010-01-01

    Full Text Available We studied the diagnostic value of CSF Aβ42/tau versus low Aβ1–42% and high Aβ1–40ox% levels for differential diagnosis of Alzheimer's disease (AD and dementia with Lewy bodies (DLB, respectively. CSF of 45 patients with AD, 15 with DLB, 21 with Parkinson's disease dementia (PDD, and 40 nondemented disease controls (NDC was analyzed by Aβ-SDS-PAGE/immunoblot and ELISAs (Aβ42 and tau. Aβ42/tau lacked specificity in discriminating AD from DLB and PDD. Best discriminating biomarkers were Aβ1–42% and Aβ1–40ox% for AD and DLB, respectively. AD and DLB could be differentiated by both Aβ1–42% and Aβ1–40ox% with an accuracy of 80% at minimum. Thus, we consider Aβ1–42% and Aβ1–40ox% to be useful biomarkers for AD and DLB, respectively. We propose further studies on the integration of Aβ1–42% and Aβ1–40ox% into conventional assay formats. Moreover, future studies should investigate the combination of Aβ1–40ox% and CSF alpha-synuclein for the diagnosis of DLB.

  7. Amyloid and tau cerebrospinal fluid biomarkers in HIV infection

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    Rosengren Lars

    2009-12-01

    Full Text Available Abstract Background Because of the emerging intersections of HIV infection and Alzheimer's disease, we examined cerebrospinal fluid (CSF biomarkers related of amyloid and tau metabolism in HIV-infected patients. Methods In this cross-sectional study we measured soluble amyloid precursor proteins alpha and beta (sAPPα and sAPPβ, amyloid beta fragment 1-42 (Aβ1-42, and total and hyperphosphorylated tau (t-tau and p-tau in CSF of 86 HIV-infected (HIV+ subjects, including 21 with AIDS dementia complex (ADC, 25 with central nervous system (CNS opportunistic infections and 40 without neurological symptoms and signs. We also measured these CSF biomarkers in 64 uninfected (HIV- subjects, including 21 with Alzheimer's disease, and both younger and older controls without neurological disease. Results CSF sAPPα and sAPPβ concentrations were highly correlated and reduced in patients with ADC and opportunistic infections compared to the other groups. The opportunistic infection group but not the ADC patients had lower CSF Aβ1-42 in comparison to the other HIV+ subjects. CSF t-tau levels were high in some ADC patients, but did not differ significantly from the HIV+ neuroasymptomatic group, while CSF p-tau was not increased in any of the HIV+ groups. Together, CSF amyloid and tau markers segregated the ADC patients from both HIV+ and HIV- neuroasymptomatics and from Alzheimer's disease patients, but not from those with opportunistic infections. Conclusions Parallel reductions of CSF sAPPα and sAPPβ in ADC and CNS opportunistic infections suggest an effect of CNS immune activation or inflammation on neuronal amyloid synthesis or processing. Elevation of CSF t-tau in some ADC and CNS infection patients without concomitant increase in p-tau indicates neural injury without preferential accumulation of hyperphosphorylated tau as found in Alzheimer's disease. These biomarker changes define pathogenetic pathways to brain injury in ADC that differ from those

  8. Do CSF levels of t-Tau, p-Tau and β{sub 1-42} amyloid correlate with dopaminergic system impairment in patients with a clinical diagnosis of Parkinson disease? A {sup 123}I-FP-CIT study in the early stages of the disease

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    Chiaravalloti, Agostino; Fiorentini, Alessandro; Lacanfora, Annamaria [University Tor Vergata, Department of Biomedicine and Prevention, Rome (Italy); Stefani, Alessandro [University Tor Vergata, Department of Neurosciences, Rome (Italy); IRCCS Santa Lucia, Rome (Italy); Stanzione, Paolo [University Tor Vergata, Department of Neurosciences, Rome (Italy); Schillaci, Orazio [University Tor Vergata, Department of Biomedicine and Prevention, Rome (Italy); IRCCS Neuromed, Pozzilli (Italy)

    2014-11-15

    To investigate the relationships among cerebrospinal fluid (CSF) levels of t-Tau, p-Tau and Aβ{sub 1-42} amyloid peptide and {sup 123}I-FP-CIT uptake. The study included 58 subjects (31 men and 27 women, age 67 ± 9 years) with a clinical diagnosis of Parkinson disease diagnosed according to the United Kingdom Parkinson Disease Society Brain Bank criteria. All subjects underwent a CSF assay 28 ± 3 days before {sup 123}I-FP-CIT SPECT scanning. The relationships were evaluated by means of linear regression analysis and Pearson correlation. Striatal {sup 123}I-FP-CIT was positively related to both t-Tau and p-Tau CSF values with low levels of t-Tau and p-Tau being related to a low uptake of {sup 123}I-FP-CIT. In particular, differences with higher statistical significance were found for the striatum between the contralateral side and the side mainly affected on clinical examination (P < 0.001). No significant relationships were found between Aβ{sub 1-42} amyloid peptide and {sup 123}I-FP-CIT binding. The results of our study suggest that the presynaptic dopaminergic system is more involved in Parkinson disease patients with lower t-Tau and p-Tau CSF values while values of Aβ{sub 1-42} amyloid peptide seems not to be related to nigrostriatal degeneration in our series. (orig.)

  9. Cerebrospinal fluid (CSF 25-hydroxyvitamin D concentration and CSF acetylcholinesterase activity are reduced in patients with Alzheimer's disease.

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    Per Johansson

    Full Text Available BACKGROUND: Little is known of vitamin D concentration in cerebrospinal fluid (CSF in Alzheimer's disease (AD and its relation with CSF acetylcholinesterase (AChE activity, a marker of cholinergic function. METHODS: A cross-sectional study of 52 consecutive patients under primary evaluation of cognitive impairment and 17 healthy controls. The patients had AD dementia or mild cognitive impairment (MCI diagnosed with AD dementia upon follow-up (n = 28, other dementias (n = 12, and stable MCI (SMCI, n = 12. We determined serum and CSF concentrations of calcium, parathyroid hormone (PTH, 25-hydroxyvitamin D (25OHD, and CSF activities of AChE and butyrylcholinesterase (BuChE. FINDINGS: CSF 25OHD level was reduced in AD patients (P < 0.05, and CSF AChE activity was decreased both in patients with AD (P < 0.05 and other dementias (P < 0.01 compared to healthy controls. None of the measured variables differed between BuChE K-variant genotypes whereas the participants that were homozygous in terms of the apolipoprotein E (APOE ε4 allele had decreased CSF AChE activity compared to subjects lacking the APOE ε4 allele (P = 0.01. In AD patients (n=28, CSF AChE activity correlated positively with CSF levels of total tau (T-tau (r = 0.44, P < 0.05 and phosphorylated tau protein (P-tau (r = 0.50, P < 0.01, but CSF activities of AChE or BuChE did not correlate with serum or CSF levels of 25OHD. CONCLUSIONS: In this pilot study, both CSF 25OHD level and CSF AChE activity were reduced in AD patients. However, the lack of correlations between 25OHD levels and CSF activities of AChE or BuChE might suggest different mechanisms of action, which could have implications for treatment trials.

  10. Brillouin spectroscopy as a new method of screening for increased CSF total protein during bacterial meningitis.

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    Steelman, Zachary; Meng, Zhaokai; Traverso, Andrew J; Yakovlev, Vladislav V

    2015-05-01

    Bacterial meningitis is a disease of pronounced clinical significance, especially in the developing world. Immediate treatment with antibiotics is essential, and no single test can provide a conclusive diagnosis. It is well established that elevated total protein in cerebrospinal fluid (CSF) is associated with bacterial meningitis. Brillouin spectroscopy is a widely used optical technique for noninvasive determination of the elastic moduli of materials. We found that elevated protein levels in CSF alter the fluid elasticity sufficiently to be measurable by Brillouin spectroscopy, with model healthy and diseased fluids distinguishable to marked significance (P = 0.014), which increases with sample concentration by dialysis. Typical raw output of a 2-stage VIPA Brillouin spectrometer: inelastically scattered Brillouin peaks (arrows) and elastically scattered incident radiation (center cross). © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  11. Tau Rather than TDP-43 Proteins are Potential Cerebrospinal Fluid Biomarkers for Frontotemporal Lobar Degeneration Subtypes: A Pilot Study.

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    Kuiperij, H Bea; Versleijen, Alexandra A M; Beenes, Marijke; Verwey, Nicolaas A; Benussi, Luisa; Paterlini, Anna; Binetti, Giuliano; Teunissen, Charlotte E; Raaphorst, Joost; Schelhaas, Helenius J; Küsters, Benno; Pijnenburg, Yolande A L; Ghidoni, Roberta; Verbeek, Marcel M

    2017-01-01

    Frontotemporal dementia (FTD) is a heterogeneous disease both at the clinical, genetic, and pathobiological level. The underlying pathological spectrum (termed FTLD, frontotemporal lobar degeneration) is in most cases defined by accumulation of either tau (FTLD-tau) or TDP-43 proteins (FTLD-TDP). Biomarkers to differentiate these subtypes are not yet available, whereas these are essential requirements to study the natural course of disease and for homogeneous inclusion of patients in clinical studies. To study if a combination of total (t-) and phosphorylated (p-)tau, and t-TDP-43 and p-TDP-43 proteins in cerebrospinal fluid (CSF) is suitable to discriminate FTLD-tau and FTLD-TDP subtypes. We developed immunoassays for the quantification of t-TDP-43 and p-TDP-43 proteins and used commercially available assays for the quantification of t-tau and p-tau proteins. We quantified these proteins in ventricular CSF samples from neuropathologically defined FTLD-tau and FTLD-TDP cases to study the reflection of underlying brain pathology in CSF composition, and in lumbar CSF samples from FTLD-tau and FTLD-TDP patients to study the diagnostic potential of CSF biomarkers. In ventricular CSF, t-TDP-43 and t-tau levels, when combined into one model, were significantly different between neuropathologically-defined FTLD-tau and FTLD-TDP cases. In a pilot study using lumbar CSF, the p-tau/t-tau ratio, but not t-TDP-43 levels, were significantly different between FTLD-TDP and FTLD-tau patients. We conclude that with current available methods, CSF tau, rather than TDP-43 proteins, may have diagnostic value in the differentiation of FTLD patients with either tau or TDP-43 pathology.

  12. CSF Neurofilament Proteins Levels are Elevated in Sporadic Creutzfeldt-Jakob Disease

    NARCIS (Netherlands)

    van Eijk, Jeroen J. J.; van Everbroeck, Bart; Abdo, W. Farid; Kremer, Berry P. H.; Verbeek, Marcel M.

    2010-01-01

    In this study we investigated the cerebrospinal fluid (CSF) levels of neurofilament light (NFL) and heavy chain (NFHp35), total tau (t-tau), and glial fibrillary acidic protein (GFAP) to detect disease specific profiles in sporadic Creutzfeldt Jakob disease (sCJD) patients and Alzheimer's disease

  13. CSF neurofilament proteins levels are elevated in sporadic Creutzfeldt-Jakob disease.

    NARCIS (Netherlands)

    Eijk, J.J.J. van; Everbroeck, B. van; Abdo, W.; Kremer, H.P.H.; Verbeek, M.M.

    2010-01-01

    In this study we investigated the cerebrospinal fluid (CSF) levels of neurofilament light (NFL) and heavy chain (NFHp35), total tau (t-tau), and glial fibrillary acidic protein (GFAP) to detect disease specific profiles in sporadic Creutzfeldt Jakob disease (sCJD) patients and Alzheimer's disease

  14. CSF Neurofilament Proteins Levels are Elevated in Sporadic Creutzfeldt-Jakob Disease

    NARCIS (Netherlands)

    van Eijk, Jeroen J. J.; van Everbroeck, Bart; Abdo, W. Farid; Kremer, Berry P. H.; Verbeek, Marcel M.

    2010-01-01

    In this study we investigated the cerebrospinal fluid (CSF) levels of neurofilament light (NFL) and heavy chain (NFHp35), total tau (t-tau), and glial fibrillary acidic protein (GFAP) to detect disease specific profiles in sporadic Creutzfeldt Jakob disease (sCJD) patients and Alzheimer's disease (A

  15. Association of cerebrospinal fluid β-amyloid 1-42, T-tau, P-tau181, and α-synuclein levels with clinical features of drug-naive patients with early Parkinson disease.

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    Kang, Ju-Hee; Irwin, David J; Chen-Plotkin, Alice S; Siderowf, Andrew; Caspell, Chelsea; Coffey, Christopher S; Waligórska, Teresa; Taylor, Peggy; Pan, Sarah; Frasier, Mark; Marek, Kenneth; Kieburtz, Karl; Jennings, Danna; Simuni, Tanya; Tanner, Caroline M; Singleton, Andrew; Toga, Arthur W; Chowdhury, Sohini; Mollenhauer, Brit; Trojanowski, John Q; Shaw, Leslie M

    2013-10-01

    We observed a significant correlation between cerebrospinal fluid (CSF) levels of tau proteins and α-synuclein, but not β-amyloid 1-42 (Aβ1-42), and lower concentration of CSF biomarkers, as compared with healthy controls, in a cohort of entirely untreated patients with Parkinson disease (PD) at the earliest stage of the disease studied so far. To evaluate the baseline characteristics and relationship to clinical features of CSF biomarkers (Aβ1-42, total tau [T-tau], tau phosphorylated at threonine 181 [P-tau181], and α-synuclein) in drug-naive patients with early PD and demographically matched healthy controls enrolled in the Parkinson's Progression Markers Initiative (PPMI) study. Cross-sectional study of the initial 102 research volunteers (63 patients with PD and 39 healthy controls) of the PPMI cohort. The CSF biomarkers were measured by INNO-BIA AlzBio3 immunoassay (Aβ1-42, T-tau, and P-tau181; Innogenetics Inc) or by enzyme-linked immunosorbent assay (α-synuclein). Clinical features including diagnosis, demographic characteristics, motor, neuropsychiatric, and cognitive assessments, and DaTscan were systematically assessed according to the PPMI study protocol. Slightly, but significantly, lower levels of Aβ1-42, T-tau, P-tau181, α-synuclein, and T-tau/Aβ1-42 were seen in subjects with PD compared with healthy controls but with a marked overlap between groups. Using multivariate regression analysis, we found that lower Aβ1-42 and P-tau181 levels were associated with PD diagnosis and that decreased CSF T-tau and α-synuclein were associated with increased motor severity. Notably, when we classified patients with PD by their motor phenotypes, lower CSF Aβ1-42 and P-tau181 concentrations were associated with the postural instability-gait disturbance-dominant phenotype but not with the tremor-dominant or intermediate phenotype. Finally, we found a significant correlation of the levels of α-synuclein with the levels of T-tau and P-tau181. In this

  16. Cerebrospinal fluid amyloid beta42/phosphorylated tau ratio discriminates between Alzheimer's disease and vascular dementia.

    NARCIS (Netherlands)

    Jong, D. de; Jansen, R.W.M.M.; Kremer, H.P.H.; Verbeek, M.M.

    2006-01-01

    BACKGROUND: The differentiation of Alzheimer's disease (AD) from vascular dementia (VaD) is hampered by clinical diagnostic criteria with disappointing sensitivity and specificity. The objective of this study was to investigate whether cerebrospinal fluid (CSF) levels of total tau protein (t-tau),

  17. Cerebrospinal fluid amyloid beta42/phosphorylated tau ratio discriminates between Alzheimer's disease and vascular dementia

    NARCIS (Netherlands)

    de Jong, Daniëlle; Jansen, René W M M; Kremer, H P H; Verbeek, Marcel M

    BACKGROUND: The differentiation of Alzheimer's disease (AD) from vascular dementia (VaD) is hampered by clinical diagnostic criteria with disappointing sensitivity and specificity. The objective of this study was to investigate whether cerebrospinal fluid (CSF) levels of total tau protein (t-tau),

  18. Haematological effects of rhGM-CSF in dogs exposed to total-body irradiation with a dose of 2. 4 Gy

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    Nothdurft, W.; Selig, C.; Fliedner, T.M.; Kreja, L.; Weinsheimer, W. (Ulm Univ. (Germany)); Hintz-Obertreis, P.; Krumwieh, D.; Kurrle, R.; Seiler, F.R. (Ulm Univ. (Germany). Inst. of Occupational and Social Medicine)

    1992-04-01

    It was the aim of this study to test the stimulatory effects of recombinant human GM-CSF (rhGM-CSF) on haemopoietic regeneration in dogs which had received total-body irradiation (TBI) with a dose of 2.4 Gy. Results indicate that treatment with GM-CSF can be an effective biological monotherapy for radiation-induced bone marrow failure, but that for higher radiation doses the number of GM-CSF responsive target cells will become a critical determinant of therapeutic efficacy. (author).

  19. Cognitive Reserve Modifies Age-Related Alterations in CSF Biomarkers of Alzheimer's Disease

    Science.gov (United States)

    Almeida, Rodrigo P.; Schultz, Stephanie A.; Austin, Benjamin P.; Boots, Elizabeth A.; Dowling, N. Maritza; Gleason, Carey E.; Bendlin, Barbara B.; Sager, Mark; Hermann, Bruce P.; Zetterberg, Henrik; Carlsson, Cindy; Johnson, Sterling; Asthana, Sanjay; Okonkwo, Ozioma C.

    2015-01-01

    Importance Although advancing age is the strongest risk factor for the development of symptomatic Alzheimer's disease (AD), recent studies have shown that there are individual differences in susceptibility to age-related alterations in the biomarkers of AD pathophysiology. Objective In this study, we investigated whether cognitive reserve modifies the adverse influence of age on key cerebrospinal fluid (CSF) biomarkers of AD. Design, Setting, and Participants Cross-sectional cohort of 268 individuals (211 cognitively normal and 57 cognitively impaired) from the Wisconsin Registry for Alzheimer's Prevention and the Wisconsin Alzheimer's Disease Research Center participated in this study. They underwent lumbar puncture for collection of CSF samples, from which amyloid-β 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) were immunoassayed. Additionally, we computed t-tau/Aβ42 and p-tau/Aβ42 ratios. Cognitive reserve was indexed by years of education, with ≥16 years taken to confer high reserve. Covariate-adjusted regression analyses were used to test whether the effect of age on CSF biomarkers was modified by cognitive reserve. Main outcome measures CSF levels of Aβ42, t-tau, p-tau, t-tau/Aβ42, and p-tau/Aβ42. Results There were significant age*cognitive reserve interactions for CSF t-tau (p=.019), p-tau (p=.009), t-tau/Aβ42 (p=.021), and p-tau/Aβ42 (p=.004). Specifically, with advancing age, individuals with high cognitive reserve exhibited attenuated adverse alterations in these CSF biomarkers compared with individuals with low cognitive reserve. This attenuation of age effects by cognitive reserve tended to be more pronounced in the cognitively-impaired group compared with the cognitively-normal group. Lastly, there was modest evidence of a dose response relationship such that the effect of age on the biomarkers was progressively attenuated given additional years of schooling. Conclusions and Relevance In a sample comprised of both cognitively

  20. Do CSF Biomarkers Predict Progression to Cognitive Impairment in Parkinson's disease patients? A Systematic Review.

    Science.gov (United States)

    Leaver, Katherine; Poston, Kathleen L

    2015-12-01

    Many patients with Parkinson's disease (PD) will develop cognitive impairment. Cross-sectional studies have shown that certain protein levels are altered in the cerebrospinal fluid (CSF) of PD patients with dementia and are thought to represent potential biomarkers of underlying pathogenesis. Recent studies suggest that CSF biomarker levels may be predictive of future risk of cognitive decline in non-demented PD patients. However, the strength of this evidence and difference between specific CSF biomarkers is not well delineated. We therefore performed a systematic review to assess if levels of specific CSF protein biomarkers are predictive of progression to cognitive impairment. Nine articles were identified that met inclusion criteria for the review. Findings from the review suggest a convergence of evidence that a low baseline Aβ42 in the CSF of non-demented PD patients predicts development of cognitive impairment over time. Conversely, there is limited evidence that CSF levels of tau, either total tau or phosphorylated tau, is a useful predictive biomarker. There are mixed results for other CSF biomarkers such as α-synuclein, Neurofilament light chain, and Heart fatty acid-binding protein. Overall the results of this review show that certain CSF biomarkers have better predictive ability to identify PD patients who are at risk for developing cognitive impairment. Given the interest in developing disease-modifying therapies, identifying this group will be important for clinical trials as initiation of therapy prior to the onset of cognitive decline is likely to be more efficacious.

  1. Beta-amyloid and phosphorylated tau metabolism changes in narcolepsy over time.

    Science.gov (United States)

    Liguori, Claudio; Placidi, Fabio; Izzi, Francesca; Nuccetelli, Marzia; Bernardini, Sergio; Sarpa, Maria Giovanna; Cum, Fabrizio; Marciani, Maria Grazia; Mercuri, Nicola Biagio; Romigi, Andrea

    2016-03-01

    The aim od this study is to test whether metabolism of beta-amyloid and tau proteins changes in narcolepsy along with the disease course. We analyzed a population of narcoleptic drug-naïve patients compared to a sample of healthy controls. Patients and controls underwent lumbar puncture for assessment of cerebrospinal fluid (CSF) beta-amyloid1-42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) levels. Moreover, based on the median disease duration of the whole narcolepsy group, the patients were divided into two subgroups: patients with a short disease duration (SdN, 5 years). We found significantly lower CSF Aβ42 levels in the whole narcolepsy group with respect to controls. Taking into account the patient subgroups, we documented reduced CSF Aβ42 levels in SdN compared to both LdN and controls. Even LdN patients showed lower CSF Aβ42 levels with respect to controls. Moreover, we documented higher CSF p-tau levels in LdN patients compared to both SdN and controls. Finally, a significant positive correlation between CSF Aβ42 levels and disease duration was evident. We hypothesize that beta-amyloid metabolism and cascade may be impaired in narcolepsy not only at the onset but also along with the disease course, although they show a compensatory profile over time. Concurrently, also CSF biomarkers indicative of neural structure (p-tau) appear to be altered in narcolepsy patients with a long disease duration. However, the mechanism underlying beta-amyloid and tau metabolism impairment in narcolepsy remains still unclear and deserves to be better elucidated.

  2. CSF Biomarkers and Its Associations with 18F-AV133 Cerebral VMAT2 Binding in Parkinson’s Disease—A Preliminary Report

    Science.gov (United States)

    Gao, Rui; Zhang, Guangjian; Chen, Xueqi; Yang, Aimin; Smith, Gwenn; Wong, Dean F.; Zhou, Yun

    2016-01-01

    Objective Cerebrospinal fluid (CSF) biomarkers, such as α-synuclein (α-syn), amyloid beta peptide 1–42 (Aβ1–42), phosphorylated tau (181P) (p-tau), and total tau (t-tau), have long been associated with the development of Parkinson disease (PD) and other neurodegenerative diseases. In this investigation, we reported the assessment of CSF biomarkers and their correlations with vesicular monoamine transporter 2 (VMAT2) bindings measured with 18F-9-fluoropropyl-(+)-dihydrotetrabenazine (18F-AV133) that is being developed as a biomarker for PD. We test the hypothesis that monoaminergic degeneration was correlated with CSF biomarker levels in untreated PD patients. Methods The available online data from the Parkinson’s Progression Markers Initiative study (PPMI) project were collected and analyzed, which include demographic information, clinical evaluations, CSF biomarkers (α-syn, Aβ1–42, p-tau, and t-tau), 18F-AV133 brain PET, and T1 weighted MRIs. Region of interest (ROI) and voxel-wise Pearson correlation between standardized uptake value ratio (SUVR) and CSF biomarkers were calculated. Results Our major findings are: 1) Compared with controls, CSF α-syn and tau levels decreased significantly in PD; 2) α-syn was closely correlated with Aβ1–42 and tau in PD, especially in early-onset patients; and 3) hypothesis-driven ROI analysis found a significant negative correlation between CSF Aβ1–42 levels and VMAT2 densities in post cingulate, left caudate, left anterior putamen, and left ventral striatum in PDs. CSF t-tau and p-tau levels were significantly negatively related to VMAT2 SUVRs in substantia nigra and left ventral striatum, respectively. Voxel-wise analysis showed that left caudate, parahippocampal gyrus, insula and temporal lobe were negatively correlated with Aβ1–42. In addition, superior frontal gyrus and transverse temporal gyrus were negatively correlated with CSF p-tau levels. Conclusion These results suggest that monoaminergic

  3. Chemokines in CSF of Alzheimer's disease patients

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    Jôice Dias Corrêa

    2011-06-01

    Full Text Available Some studies have linked the presence of chemokines to the early stages of Alzheimer's disease (AD. Then, the identification of these mediators may contribute to diagnosis. Our objective was to evaluate the levels of beta-amyloid (BA, tau, phospho-tau (p-tau and chemokines (CCL2, CXCL8 and CXCL10 in the cerebrospinal fluid (CSF of patients with AD and healthy controls. The correlation of these markers with clinical parameters was also evaluated. The levels of p-tau were higher in AD compared to controls, while the tau/p-tau ratio was decreased. The expression of CCL2 was increased in AD. A positive correlation was observed between BA levels and all chemokines studied, and between CCL2 and p-tau levels. Our results suggest that levels of CCL2 in CSF are involved in the pathogenesis of AD and it may be an additional useful biomarker for monitoring disease progression.

  4. Cerebrospinal fluid tau, neurogranin, and neurofilament light in Alzheimer's disease.

    Science.gov (United States)

    Mattsson, Niklas; Insel, Philip S; Palmqvist, Sebastian; Portelius, Erik; Zetterberg, Henrik; Weiner, Michael; Blennow, Kaj; Hansson, Oskar

    2016-10-01

    Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). It is unknown whether these biomarkers provide similar or complementary information in AD. We examined 93 patients with AD, 187 patients with mild cognitive impairment, and 109 controls. T-tau, Ng, and NFL were all predictors of AD diagnosis. Combinations improved the diagnostic accuracy (AUC 85.5% for T-tau, Ng, and NFL) compared to individual biomarkers (T-tau 80.8%; Ng 71.4%; NFL 77.7%). T-tau and Ng were highly correlated (ρ = 0.79, P NFL on the other hand was not associated with Aβ pathology and was associated with cognitive decline and brain atrophy independent of Aβ. T-tau, Ng, and NFL provide partly independent information about neuronal injury and may be combined to improve the diagnostic accuracy for AD. T-tau and Ng reflect Aβ-dependent neurodegeneration, while NFL reflects neurodegeneration independently of Aβ pathology. © 2016 The Authors. Published under the terms of the CC BY 4.0 license.

  5. CSF markers of Alzheimer’s pathology and microglial activation are associated with altered white matter microstructure in asymptomatic adults at risk for Alzheimer’s disease

    Science.gov (United States)

    Melah, Kelsey E; Lu, Sharon Yuan-Fu; Hoscheidt, Siobhan M; Alexander, Andrew L; Adluru, Nagesh; Destiche, Daniel J; Carlsson, Cynthia M; Zetterberg, Henrik; Blennow, Kaj; Okonkwo, Ozioma C; Gleason, Carey E; Dowling, N Maritza; Bratzke, Lisa C; Rowley, Howard A; Sager, Mark A; Asthana, Sanjay; Johnson, Sterling C; Bendlin, Barbara B

    2015-01-01

    Background The immune response in Alzheimer’s disease (AD) involves activation of microglia which may remove β-amyloid. However, overproduction of inflammatory compounds may exacerbate neural damage in Alzheimer’s disease. AD pathology accumulates years before diagnosis, yet the extent to which neuroinflammation is involved in the earliest disease stages is unknown. Objective To determine whether neuroinflammation exacerbates neural damage in preclinical AD. Methods We utilized cerebrospinal fluid (CSF) and magnetic resonance imaging collected in 192 asymptomatic late-middle-aged adults (mean age=60.98 years). Neuroinflammatory markers chitinase-3-like protein 1 (YKL-40) and monocyte chemoattractant protein-1 (MCP-1) in CSF were utilized as markers of neuroinflammation. Neural cell damage was assessed using CSF neurofilament light chain protein (NFL), CSF total tau (T-Tau), and neural microstructure assessed with diffusion tensor imaging (DTI). With regard to AD pathology, CSF Aβ42 and tau phosphorylated at threonine 181 (P-Tau181) were used as markers of amyloid and tau pathology, respectively. We hypothesized that higher YKL-40 and MCP-1 in the presence of AD pathology would be associated with higher NFL, T-Tau, and altered microstructure on DTI. Results Neuroinflammation was associated with markers of neural damage. Higher CSF YKL-40 was associated with both higher CSF NFL and T-Tau. Inflammation interacted with AD pathology, such that greater MCP-1 and lower Aβ42 was associated with altered microstructure in bilateral frontal and right temporal lobe and that greater MCP-1 and greater P-Tau181 was associated with altered microstructure in precuneus. Conclusion Inflammation may play a role in neural damage in preclinical AD. PMID:26836182

  6. CSF biomarkers associated with disease heterogeneity in early Parkinson's disease: the Parkinson's Progression Markers Initiative study.

    Science.gov (United States)

    Kang, Ju-Hee; Mollenhauer, Brit; Coffey, Christopher S; Toledo, Jon B; Weintraub, Daniel; Galasko, Douglas R; Irwin, David J; Van Deerlin, Vivianna; Chen-Plotkin, Alice S; Caspell-Garcia, Chelsea; Waligórska, Teresa; Taylor, Peggy; Shah, Nirali; Pan, Sarah; Zero, Pawel; Frasier, Mark; Marek, Kenneth; Kieburtz, Karl; Jennings, Danna; Tanner, Caroline M; Simuni, Tanya; Singleton, Andrew; Toga, Arthur W; Chowdhury, Sohini; Trojanowski, John Q; Shaw, Leslie M

    2016-06-01

    The development of biomarkers to predict the progression of Parkinson's disease (PD) from its earliest stage through its heterogeneous course is critical for research and therapeutic development. The Parkinson's Progression Markers Initiative (PPMI) study is an ongoing international multicenter, prospective study to validate biomarkers in drug-naïve PD patients and matched healthy controls (HC). We quantified cerebrospinal fluid (CSF) alpha-synuclein (α-syn), amyloid-beta1-42 (Aβ1-42), total tau (t-tau), and tau phosphorylated at Thr181 (p-tau) in 660 PPMI subjects at baseline, and correlated these data with measures of the clinical features of these subjects. We found that CSF α-syn, t-tau and p-tau levels, but not Aβ1-42, were significantly lower in PD compared with HC, while the diagnostic value of the individual CSF biomarkers for PD diagnosis was limited due to large overlap. The level of α-syn, but not other biomarkers, was significantly lower in PD patients with non-tremor-dominant phenotype compared with tremor-dominant phenotype. In addition, in PD patients the lowest Aβ1-42, or highest t-tau/Aβ1-42 and t-tau/α-syn quintile in PD patients were associated with more severe non-motor dysfunction compared with the highest or lowest quintiles, respectively. In a multivariate regression model, lower α-syn was significantly associated with worse cognitive test performance. APOE ε4 genotype was associated with lower levels of Aβ1-42, but neither with PD diagnosis nor cognition. Our data suggest that the measurement of CSF biomarkers in early-stage PD patients may relate to disease heterogeneity seen in PD. Longitudinal observations in PPMI subjects are needed to define their prognostic performance.

  7. Plasmin system of Alzheimer's disease patients: CSF analysis.

    Science.gov (United States)

    Martorana, Alessandro; Sancesario, Giulia M; Esposito, Zaira; Nuccetelli, Marzia; Sorge, Roberto; Formosa, Amanda; Dinallo, Vincenzo; Bernardi, Giorgio; Bernardini, Sergio; Sancesario, Giuseppe

    2012-07-01

    Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by the extracellular deposit of Amyloid beta (Aβ), mainly of the Amyloid beta(1-42) (Aβ(1-42)) peptide in the hippocampus and neocortex leading to progressive cognitive decline and dementia. The possible imbalance between the Aβ production/degradation process was suggested to contribute to the pathogenesis of AD. Among others, the serine protease plasmin has shown to be involved in Aβ(1-42) clearance, a hypothesis strengthened by neuropathological studies on AD brains. To explore whether there is a change in plasmin system in CSF of AD patients, we analyzed CSF samples from AD and age-matched controls, looking at plasminogen, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) protein levels and t-PA and urokinase plasminogen activator (u-PA) enzymatic activities. We also measured Aβ(1-42), total-tau and phospho-tau (181) CSF levels and sought for a possible relationship between them and plasmin system values. Our findings showed that t-PA, plasminogen and PAI-1 levels, as t-PA enzymatic activity, remained unchanged in AD with respect to controls; u-PA activity was not detected. We conclude that CSF analysis of plasminogen system does not reflect changes observed post-mortem. Unfortunately, the CSF detection of plasmin system could not be a useful biomarker for either AD diagnosis or disease progression. However, these findings do not exclude the possible involvement of the plasmin system in AD.

  8. CSF biomarkers cutoffs: the importance of coincident neuropathological diseases.

    Science.gov (United States)

    Toledo, Jon B; Brettschneider, Johannes; Grossman, Murray; Arnold, Steven E; Hu, William T; Xie, Sharon X; Lee, Virginia M-Y; Shaw, Leslie M; Trojanowski, John Q

    2012-07-01

    The effects of applying clinical versus neuropathological diagnosis and the inclusion of cases with coincident neuropathological diagnoses have not been assessed specifically when studying cerebrospinal fluid (CSF) biomarker classification cutoffs for patients with neurodegenerative diseases that cause dementia. Thus, 142 neuropathologically diagnosed neurodegenerative dementia patients [71 Alzheimer's disease (AD), 29 frontotemporal lobar degeneration (FTLD), 3 amyotrophic lateral sclerosis, 7 dementia with Lewy bodies, 32 of which cases also had coincident diagnoses] were studied. 96 % had enzyme-linked immunosorbant assay (ELISA) CSF data and 77 % had Luminex CSF data, with 43 and 46 controls for comparison, respectively. Aβ(42), total, and phosphorylated tau(181) were measured. Clinical and neuropathological diagnoses showed an 81.4 % overall agreement. Both assays showed high sensitivity and specificity to classify AD subjects against FTLD subjects and controls, and moderate sensitivity and specificity for classifying FTLD subjects against controls. However, among the cases with neuropathological diagnoses of AD plus another pathology (26.8 % of the sample), 69.4 % (ELISA) and 96.4 % (Luminex) were classified as AD according to their biomarker profiles. Use of clinical diagnosis instead of neuropathological diagnosis led to a 14-17 % underestimation of the biomarker accuracy. These results show that while CSF Aβ and tau assays are useful for diagnosis of AD and neurodegenerative diseases even at MCI stages, CSF diagnostic analyte panels that establish a positive diagnosis of Lewy body disease and FTLD are also needed, and must be established based on neuropathological rather than clinical diagnoses.

  9. Chasing the effects of Pre-analytical Confounders - a Multicentre Study on CSF-AD biomarkers

    Directory of Open Access Journals (Sweden)

    Maria Joao Leitao

    2015-07-01

    Full Text Available Core cerebrospinal fluid (CSF biomarkers-Aβ42, Tau and pTau–have been recently incorporated in the revised criteria for Alzheimer’s disease (AD. However, their widespread clinical application lacks standardization. Pre-analytical sample handling and storage play an important role in the reliable measurement of these biomarkers across laboratories. In this study, we aim to surpass the efforts from previous studies, by employing a multicentre approach to assess the impact of less studied CSF pre-analytical confounders in AD-biomarkers quantification. Four different centres participated in this study and followed the same established protocol. CSF samples were analysed for three biomarkers (Aβ42, Tau and pTau and tested for different spinning conditions (temperature: Room temperature (RT vs. 4oC; speed: 500g vs. 2000g vs. 3000g, storage volume variations (25%, 50% and 75% of tube total volume as well as freezing-thaw cycles (up to 5 cyles. The influence of sample routine parameters, inter-centre variability and relative value of each biomarker (reported as normal/abnormal, was analysed. Centrifugation conditions did not influence biomarkers levels, except for samples with a high CSF total protein content, where either non centrifugation or centrifugation at RT, compared to 4ºC, led to higher Aβ42 levels. Reducing CSF storage volume from 75% to 50% of total tube capacity, decreased Aβ42 concentration (within analytical CV of the assay, whereas no change in Tau or pTau was observed. Moreover, the concentration of Tau and pTau appears to be stable up to 5 freeze-thaw cycles, whereas Aβ42 levels decrease if CSF is freeze-thawed more than 3 times. This systematic study reinforces the need for CSF centrifugation at 4ºC prior to storage and highlights the influence of storage conditions in Aβ42 levels. This study contributes to the establishment of harmonized standard operating procedures that will help reducing inter-lab variability of CSF

  10. PHOSPHORYLATED TAU: CANDIDATE BIOMARKER FOR AMYOTROPHIC LATERAL SCLEROSIS

    Science.gov (United States)

    Grossman, Murray; Elman, Lauren; McCluskey, Leo; McMillan, Corey T.; Boller, Ashley; Powers, John; Rascovsky, Katya; Hu, William; Shaw, Les; Irwin, David J.; Lee, Virginia M.-Y.; Trojanowski, John Q.

    2014-01-01

    IMPORTANCE An increasingly varied clinical spectrum of cases with amyotrophic lateral sclerosis (ALS) has been identified, and objective criteria for clinical trial eligibility is necessary. OBJECTIVE We sought to develop a cerebrospinal fluid (CSF) biomarker sensitive and specific for the diagnosis of ALS. DESIGN Case-control study. SETTING Academic medical center. PARTICIPANTS 51 individuals with ALS and 23 individuals with a disorder associated with a four-repeat tauopathy (4R-tau). MAIN OUTCOME MEASURE CSF level of tau phosophorylated at threonine 181 (ptau), and ratio of ptau to total tau (ttau). RESULTS Using a cross-validation prediction procedure, we found significantly reduced CSF levels of ptau and ptau:ttau in ALS relative to 4R-tau and to controls. In the validation cohort, the receiver operating characteristic area under the curve for the ptau:ttau ratio was 0.916, and the comparison of ALS to 4R-tau showed sensitivity=92% and specificity=91.7%. Correct classification based on low CSF ptau:ttau was confirmed in 18 (85.7%) of 21 cases with autopsy-proven or genetically-determined disease. In patients with available measures, ptau:ttau in ALS correlated with clinical measures of disease severity such as Mini Mental State Exam (n=51) and ALS Functional Rating Scale-Revised (n=42), and regression analyses related ptau:ttau to MRI (n=10) evidence of disease in the corticospinal tract and white matter projections involving prefrontal cortex. CONCLUSIONS AND RELEVANCE CSF ptau:ttau may be a candidate biomarker to provide objective support for the diagnosis of ALS. PMID:24492862

  11. The predictive value of T-tau and AB1-42 levels in idiopathic normal pressure hydrocephalus.

    Science.gov (United States)

    Craven, Claudia L; Baudracco, Irene; Zetterberg, Henrik; Lunn, Michael P T; Chapman, Miles D; Lakdawala, Neghat; Watkins, Laurence D; Toma, Ahmed K

    2017-09-09

    Idiopathic normal pressure hydrocephalus (INPH) has no reliable biomarker to assist in the selection of patients who could benefit from ventriculo-peritoneal (VP) shunt insertion. The neurodegenerative markers T-tau and Aβ1-42 have been found to successfully differentiate between Alzheimer's disease (AD) and INPH and therefore are candidate biomarkers for prognosis and shunt response in INPH. The aim of this study was to test the predictive value of cerebrospinal fluid (CSF) T-tau and Aβ1-42 for shunt responsiveness. In particular, we pay attention to the subset of INPH patients with raised T-tau, who are often expected to be poor surgical candidates. Single-centre retrospective analysis of probable INPH patients with CSF samples collected from 2006 to 2016. CSF levels of T-tau and Aβ1-42. Reference standard: postoperative outcome. ROC analysis assessed the predictive value. A total of 144 CSF samples from INPH patients were analysed. Lumbar T-tau was a good predictor of post-operative mobility (AUROC 0.80). The majority of patients with a co-existing neurodegenerative disease responded well, including those with high T-tau levels. INPH patients tended to exhibit low levels of CSF T-tau, and this can be a good predictor outcome. However levels are highly variable between individuals. Raised T-tau and being shunt-responsive are not mutually exclusive, and such patients ought not necessarily be excluded from having a VP shunt. A combined panel of markers may be a more specific method for aiding selection of patients for VP shunt insertion. This is the most comprehensive presentation of CSF samples from INPH patients to date, thus providing further reference values to the current literature.

  12. Body mass index is associated with biological CSF markers of core brain pathology of Alzheimer's disease.

    Science.gov (United States)

    Ewers, Michael; Schmitz, Susanne; Hansson, Oskar; Walsh, Cathal; Fitzpatrick, Annette; Bennett, David; Minthon, Lennart; Trojanowski, John Q; Shaw, Leslie M; Faluyi, Yetunde O; Vellas, Bruno; Dubois, Bruno; Blennow, Kaj; Buerger, Katharina; Teipel, Stefan J; Weiner, Michael; Hampel, Harald

    2012-08-01

    Weight changes are common in aging and Alzheimer's disease (AD) and postmortem findings suggest a relation between lower body mass index (BMI) and increased AD brain pathology. In the current multicenter study, we tested whether lower BMI is associated with higher core AD brain pathology as assessed by cerebrospinal fluid (CSF)-based biological markers of AD in 751 living subjects: 308 patients with AD, 296 subjects with amnestic mild cognitive impairment (MCI), and 147 elderly healthy controls (HC). Based upon a priori cutoff values on CSF concentration of total tau and beta-amyloid (Aβ(1-42)), subjects were binarized into a group with abnormal CSF biomarker signature (CSF+) and those without (CSF-). Results showed that BMI was significantly lower in the CSF+ when compared with the CSF- group (F = 27.7, df = 746, p < 0.001). There was no interaction between CSF signature and diagnosis or apolipoprotein E (ApoE) genotype. In conclusion, lower BMI is indicative of AD pathology as assessed with CSF-based biomarkers in demented and nondemented elderly subjects.

  13. Cerebrospinal Fluid (CSF) Neuronal Biomarkers across the Spectrum of HIV Infection: Hierarchy of Injury and Detection

    Science.gov (United States)

    Peterson, Julia; Gisslen, Magnus; Zetterberg, Henrik; Fuchs, Dietmar; Shacklett, Barbara L.; Hagberg, Lars; Yiannoutsos, Constantin T.; Spudich, Serena S.; Price, Richard W.

    2014-01-01

    The character of central nervous system (CNS) HIV infection and its effects on neuronal integrity vary with evolving systemic infection. Using a cross-sectional design and archived samples, we compared concentrations of cerebrospinal fluid (CSF) neuronal biomarkers in 143 samples from 8 HIV-infected subject groups representing a spectrum of untreated systemic HIV progression and viral suppression: primary infection; four groups of chronic HIV infection neuroasymptomatic (NA) subjects defined by blood CD4+ T cells of >350, 200–349, 50–199, and NFL), total and phosphorylated tau (t-tau, p-tau), soluble amyloid precursor proteins alpha and beta (sAPPα, sAPPβ) and amyloid beta (Aβ) fragments 1–42, 1–40 and 1–38. Comparison of the biomarker changes showed a hierarchy of sensitivity in detection and suggested evolving mechanisms with progressive injury. NFL was the most sensitive neuronal biomarker. Its CSF concentration exceeded age-adjusted norms in all HAD patients, 75% of NA CD4NFL with CD4 decline in the absence of HAD, and were not decreased in PHI. The CSF Aβ peptides and p-tau concentrations did not differ among the groups, distinguishing the HIV CNS injury profile from Alzheimer's disease. These CSF biomarkers can serve as useful tools in selected research and clinical settings for patient classification, pathogenetic analysis, diagnosis and management. PMID:25541953

  14. Hyperphosphorylation and cleavage at D421 enhance tau secretion.

    Directory of Open Access Journals (Sweden)

    Vanessa Plouffe

    Full Text Available It is well established that tau pathology propagates in a predictable manner in Alzheimer's disease (AD. Moreover, tau accumulates in the cerebrospinal fluid (CSF of AD's patients. The mechanisms underlying the propagation of tau pathology and its accumulation in the CSF remain to be elucidated. Recent studies have reported that human tau was secreted by neurons and non-neuronal cells when it was overexpressed indicating that tau secretion could contribute to the spreading of tau pathology in the brain and could lead to its accumulation in the CSF. In the present study, we showed that the overexpression of human tau resulted in its secretion by Hela cells. The main form of tau secreted by these cells was cleaved at the C-terminal. Surprisingly, secreted tau was dephosphorylated at several sites in comparison to intracellular tau which presented a strong immunoreactivity to all phospho-dependent antibodies tested. Our data also revealed that phosphorylation and cleavage of tau favored its secretion by Hela cells. Indeed, the mimicking of phosphorylation at 12 sites known to be phosphorylated in AD enhanced tau secretion. A mutant form of tau truncated at D421, the preferential cleavage site of caspase-3, was also significantly more secreted than wild-type tau. Taken together, our results indicate that hyperphosphorylation and cleavage of tau by favoring its secretion could contribute to the propagation of tau pathology in the brain and its accumulation in the CSF.

  15. CSF analysis

    Science.gov (United States)

    Cerebrospinal fluid analysis ... Analysis of CSF can help detect certain conditions and diseases. All of the following can be, but ... An abnormal CSF analysis result may be due to many different causes, ... Encephalitis (such as West Nile and Eastern Equine) Hepatic ...

  16. Cerebrospinal fluid tau proteins in status epilepticus.

    Science.gov (United States)

    Monti, Giulia; Tondelli, Manuela; Giovannini, Giada; Bedin, Roberta; Nichelli, Paolo F; Trenti, Tommaso; Meletti, Stefano; Chiari, Annalisa

    2015-08-01

    Tau protein is a phosphorylated microtubule-associated protein, principally localized at neuronal level in the central nervous system (CNS). Tau levels in the cerebrospinal fluid (CSF) are considered to index both axonal and neuronal damage. To date, however, no study has specifically evaluated the CSF levels of tau proteins in patients with status epilepticus (SE). We evaluated these established biomarkers of neuronal damage in patients with SE who received a lumbar puncture during SE between 2007 and 2014. Status epilepticus cases due to acute structural brain damage, including CNS infection, were excluded. Clinical, biological, therapeutic, and follow-up data were collected. Group comparison between patients stratified according to SE response to antiepileptic drugs (AEDs), disability, and epilepsy outcomes were performed. Twenty-eight patients were considered for the analyses (mean age 56 years): 14 patients had abnormally high CSF t-tau level, six patients had abnormally high CSF p-tau level, and only three patients had abnormally low Aβ1-42 level. Cerebrospinal fluid t-tau value was higher in patients who developed a refractory SE compared to patients with seizures controlled by AED. Cerebrospinal fluid t-tau values were positively correlated with SE duration and were higher in patients treated with propofol anesthesia compared to patients that had not received this treatment. Patients with higher CSF t-tau had higher risk of developing disability (OR = 32.5, p = 0.004) and chronic epilepsy (OR = 12; p = 0.016) in comparison with patients with lower CSF t-tau level. Our results suggest that CSF t-tau level might be proposed as a biomarker of SE severity and prognosis. Prospective studies are needed to evaluate the effects of propofol on tau pathology in this setting. This article is part of a Special Issue entitled "Status Epilepticus".

  17. CSF biomarkers associated with disease heterogeneity in early Parkinson’s disease: the Parkinson’s Progression Markers Initiative study

    Science.gov (United States)

    Kang, Ju-Hee; Mollenhauer, Brit; Coffey, Christopher S.; Toledo, Jon B.; Weintraub, Daniel; Galasko, Douglas R.; Irwin, David J.; Van Deerlin, Vivianna; Chen-Plotkin, Alice S.; Caspell-Garcia, Chelsea; Waligórska, Teresa; Taylor, Peggy; Shah, Nirali; Pan, Sarah; Zero, Pawel; Frasier, Mark; Marek, Kenneth; Kieburtz, Karl; Jennings, Danna; Tanner, Caroline M.; Simuni, Tanya; Singleton, Andrew; Toga, Arthur W.; Chowdhury, Sohini; Trojanowski, John Q.; Shaw, Leslie M.

    2016-01-01

    The development of biomarkers to predict the progression of Parkinson’s disease (PD) from its earliest stage through its heterogeneous course is critical for research and therapeutic development. The Parkinson’s Progression Markers Initiative (PPMI) study is an ongoing international multicenter, prospective study to validate biomarkers in drug-naïve PD patients and matched healthy controls (HC). We quantified cerebrospinal fluid (CSF) alpha-synuclein (α-syn), amyloid-beta1–42 (Aβ1–42), total tau (t-tau), and tau phosphorylated at Thr181 (p-tau) in 660 PPMI subjects at baseline, and correlated these data with measures of the clinical features of these subjects. We found that CSF α-syn, t-tau and p-tau levels, but not Aβ1–42, were significantly lower in PD compared with HC, while the diagnostic value of the individual CSF biomarkers for PD diagnosis was limited due to large overlap. The level of α-syn, but not other biomarkers, was significantly lower in PD patients with non-tremor-dominant phenotype compared with tremor-dominant phenotype. In addition, in PD patients the lowest Aβ1–42, or highest t-tau/Aβ1–42 and t-tau/α-syn quintile in PD patients were associated with more severe non-motor dysfunction compared with the highest or lowest quintiles, respectively. In a multivariate regression model, lower α-syn was significantly associated with worse cognitive test performance. APOE ε4 genotype was associated with lower levels of Aβ1–42, but neither with PD diagnosis nor cognition. Our data suggest that the measurement of CSF biomarkers in early-stage PD patients may relate to disease heterogeneity seen in PD. Longitudinal observations in PPMI subjects are needed to define their prognostic performance. PMID:27021906

  18. Association between FDG uptake, CSF biomarkers and cognitive performance in patients with probable Alzheimer's disease

    Energy Technology Data Exchange (ETDEWEB)

    Arlt, Soenke; Jahn, Holger; Eichenlaub, Martin [University Medical Center Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Hamburg (Germany); Brassen, Stefanie [University Medical Center Hamburg-Eppendorf, Institute for Systems Neuroscience, Hamburg (Germany); Wilke, Florian; Apostolova, Ivayla; Buchert, Ralph [University Medical Center Hamburg-Eppendorf, Department of Nuclear Medicine, Hamburg (Germany); Wenzel, Fabian; Young, Stewart [Philips Research, Digital Imaging Department, Hamburg (Germany); Thiele, Frank [Philips Research, Molecular Imaging Department, Aachen (Germany)

    2009-07-15

    Brain imaging of FDG uptake and cerebrospinal fluid (CSF) concentration of amyloid-beta 1-42 (A{beta}{sub 1-42}) or tau proteins are promising biomarkers in the diagnosis of Alzheimer's disease (AD). There is still uncertainty regarding any association between decreased FDG uptake and alterations in CSF markers. The relationship between FDG uptake, CSF A{beta}{sub 1-42} and total tau (T-tau), as well as the Mini-Mental State Examination (MMSE) score was investigated in 34 subjects with probable AD using step-wise linear regression. FDG uptake was scaled to the pons. Scaled FDG uptake was significantly reduced in the probable AD subjects compared to 17 controls bilaterally in the precuneus/posterior cingulate area, angular gyrus/inferior parietal cortex, inferior temporal/midtemporal cortex, midfrontal cortex, and left caudate. Voxel-based single-subject analysis of the probable AD subjects at p < 0.001 (uncorrected) revealed a total volume of significant hypometabolism ranging from 0 to 452 ml (median 70 ml). The total hypometabolic volume was negatively correlated with the MMSE score, but it was not correlated with the CSF measures. VOI-based step-wise linear regression revealed that scaled FDG uptake in the precuneus/posterior cingulate was negatively correlated with CSF A{beta}{sub 1-42}. Scaled FDG uptake in the caudate was positively correlated with CSF T-tau. The extent and local severity of the reduction in FDG uptake in probable AD subjects are associated with cognitive impairment. In addition, there appears to be a relationship between local FDG uptake and CSF biomarkers which differs between different brain regions. (orig.)

  19. CSF Neurofilament Light Chain but not FLT3 Ligand Discriminates Parkinsonian Disorders

    Science.gov (United States)

    Herbert, Megan K.; Aerts, Marjolein B.; Beenes, Marijke; Norgren, Niklas; Esselink, Rianne A. J.; Bloem, Bastiaan R.; Kuiperij, H. Bea; Verbeek, Marcel M.

    2015-01-01

    The differentiation between multiple system atrophy (MSA) and Parkinson’s disease (PD) is difficult, particularly in early disease stages. Therefore, we aimed to evaluate the diagnostic value of neurofilament light chain (NFL), fms-like tyrosine kinase ligand (FLT3L), and total tau protein (t-tau) in cerebrospinal fluid (CSF) as biomarkers to discriminate MSA from PD. Using commercially available enzyme-linked immunosorbent assays, we measured CSF levels of NFL, FLT3L, and t-tau in a discovery cohort of 36 PD patients, 27 MSA patients, and 57 non-neurological controls and in a validation cohort of 32 PD patients, 25 MSA patients, 15 PSP patients, 5 CBS patients, and 56 non-neurological controls. Cut-offs obtained from individual assays and binary logistic regression models developed from combinations of biomarkers were assessed. CSF levels of NFL were substantially increased in MSA and discriminated between MSA and PD with a sensitivity of 74% and specificity of 92% (AUC = 0.85) in the discovery cohort and with 80% sensitivity and 97% specificity (AUC = 0.94) in the validation cohort. FLT3L levels in CSF were significantly lower in both PD and MSA compared to controls in the discovery cohort, but not in the validation cohort. t-tau levels were significantly higher in MSA than PD and controls. Addition of either FLT3L or t-tau to NFL did not improve discrimination of PD from MSA above NFL alone. Our findings show that increased levels of NFL in CSF offer clinically relevant, high accuracy discrimination between PD and MSA. PMID:25999911

  20. CSF neurofilament light chain but not FLT3 ligand discriminates Parkinsonian disorders

    Directory of Open Access Journals (Sweden)

    Megan Kristy Herbert

    2015-05-01

    Full Text Available The differentiation between multiple system atrophy (MSA and Parkinson’s disease (PD is difficult, particularly in early disease stages. Therefore, we aimed to evaluate the diagnostic value of neurofilament light chain (NFL, fms-like tyrosine kinase ligand (FLT3L and total tau protein (t-tau in cerebrospinal fluid (CSF as biomarkers to discriminate MSA from PD. Using commercially available enzyme-linked immunoassays (ELISAs, we measured CSF levels of NFL, FLT3L and t-tau in a discovery cohort of 36 PD patients, 27 MSA patients and 57 non-neurological controls and in a validation cohort of 32 PD patients, 25 MSA patients, 15 PSP patients, 5 CBS patients, and 56 non-neurological controls. Cut-offs obtained from individual assays and binary logistic regression models developed from combinations of biomarkers were assessed. CSF levels of NFL were substantially increased in MSA and discriminated between MSA and PD with a sensitivity of 74% and specificity of 92% (AUC = 0.85 in the discovery cohort and with 80% sensitivity and 97% specificity (AUC = 0.94 in the validation cohort. FLT3L levels in CSF were significantly lower in both PD and MSA compared to controls in the discovery cohort, but not in the validation cohort. T-tau levels were significantly higher in MSA than PD and controls. Addition of either FLT3L or t-tau to NFL did not improve discrimination of PD from MSA above NFL alone. Our findings show that increased levels of NFL in CSF offer clinically relevant, high accuracy discrimination between PD and MSA.

  1. CSF Analysis

    Science.gov (United States)

    ... a chronic disease, such as multiple sclerosis or Alzheimer disease . Depending on a person's history, a healthcare provider may order CSF analysis when some combination of the following signs and symptoms appear, especially when accompanied by flu-like symptoms ...

  2. CSF leak

    Science.gov (United States)

    ... rarely). Drainage of CSF from the nose (rarely). Exams and Tests The health care provider will perform ... usually recommended. Drinking more fluids, especially drinks with caffeine, can help slow or stop the leak and ...

  3. CSF markers in Alzheimer disease patients are not related to the different degree of cognitive impairment.

    Science.gov (United States)

    Stefani, Alessandro; Martorana, Alessandro; Bernardini, Sergio; Panella, Marta; Mercati, Flavio; Orlacchio, Antonio; Pierantozzi, Mariangela

    2006-12-21

    Standard markers in cerebrospinal fluid (CSF), as soluble amyloid beta 1-42 (Abeta1-42) and total tau protein (t-tau), may contribute to dementia subtypes diagnostic accuracy. Yet, their sensitivity to assess the different degree of cognitive deficit is not fully clarified. Our study analyses Abeta1-42 and t-tau CSF levels in different cohorts of Alzheimer's disease (AD) patients, distinguished as early AD (mild cognitively impaired subjects recently converted to AD), mild AD (MMSE or =18), and moderately advanced AD (MMSEstage. In early AD patients, Abeta1-42 levels were already significantly low, if compared to the control group (336 vs 867 ng/L; pdiffer between AD subgroups, and in particular between mild to moderate AD. A significant progressive increase of t-tau concentration was found when comparing early AD (269 ng/L) to more advanced AD stages (468 ng/L and 495 ng/L for mild and moderate AD, respectively). Our findings confirm that the impairment of amyloidogenic cascade is an early, even pre-clinical process, but suggest that soluble Abeta1-42 concentration has a negligible correlation with the clinical progression. Conversely, t-tau concentration correlates with the transition towards marked cognitive impairment.

  4. Increased CSF-BACE1 activity associated with decreased hippocampus volume in Alzheimer's disease.

    LENUS (Irish Health Repository)

    Ewers, Michael

    2012-02-01

    The enzyme beta-secretase (BACE1) is essentially involved in the production of cerebral amyloidogenic pathology in Alzheimer\\'s disease (AD). The measurement of BACE1 activity in cerebrospinal fluid (CSF) has been reported, which may render CSF measurement of BACE1 a potential biomarker candidate of AD. In order to investigate whether BACE1 protein activity is correlated with regional brain atrophy in AD, we investigated the association between CSF levels of BACE1 and MRI-assessed hippocampus volume in patients with AD (n = 30). An increase in CSF-BACE1 activity was associated with decreased left and right hippocampus volume corrected for global head volume in the AD patients. Boot-strapped regression analysis showed that increased CSF levels of BACE1 activity were associated with increased CSF concentration of total tau but not amyloid-beta1-42 in AD. White matter hyperintensities did not influence the results. BACE1 activity and protein levels were significantly increased in AD compared to 19 elderly healthy controls. Thus, the CSF biomarker candidate of BACE1 activity was associated with hippocampus atrophy in AD in a robust manner and may reflect neurotoxic amyloid-beta-related processes.

  5. Tau structures

    Directory of Open Access Journals (Sweden)

    Jesus Avila

    2016-11-01

    Full Text Available Tau is a microtubule-associated protein that plays an important role in axonal stabilization, neuronal development, and neuronal polarity. In this review, we focus on the primary, secondary, tertiary and quaternary tau structures. We describe the structure of tau from its specific residues until its conformation in dimers, oligomers and larger polymers in physiological and pathological situations.

  6. Tau protein concentrations in cerebrospinal fluid of patients with amyotrophic lateral sclerosis.

    Science.gov (United States)

    Jiménez-Jiménez, F J; Hernánz, A; Medina-Acebrón, S; de Bustos, F; Zurdo, J M; Alonso, H; Puertas, I; Barcenilla, B; Sayed, Y; Cabrera-Valdivia, F

    2005-02-01

    To elucidate whether cerebrospinal fluid (CSF) concentrations of the microtubule-associated tau protein are related to the risk for sporadic amyotrophic lateral sclerosis (SALS). We measured tau concentrations in the CSF of 18 patients with SALS and 75 age- and sex-matched controls, using a specific ELISA method. The mean CSF concentrations of tau protein did not differ significantly between SALS patient and control groups, were not influenced by the clinical form (spinal vs bulbar) of ALS, and were not correlated with age, age at onset, and duration of the disease. CSF tau concentrations are not a biochemical marker of ALS.

  7. CSF beta-amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?

    Science.gov (United States)

    Liguori, Claudio; Placidi, Fabio; Albanese, Maria; Nuccetelli, Marzia; Izzi, Francesca; Marciani, Maria Grazia; Mercuri, Nicola Biagio; Bernardini, Sergio; Romigi, Andrea

    2014-08-01

    Narcolepsy is characterized by hypocretin deficiency due to the loss of hypothalamic orexinergic neurons, and is associated with both the human leucocyte antigen DQB1*06:02 and the T cell receptor polymorphism. The above relationship suggests autoimmune/inflammatory processes underlying the loss of orexinergic neurons in narcolepsy. To test the autoimmune/inflammatory hypothesis by means of cerebrospinal fluid (CSF) levels of beta-amyloid1-42 and/or total tau proteins in a sample of narcoleptic patients, we analysed 16 narcoleptic patients and 16 healthy controls. Beta-amyloid1-42 CSF levels were significantly lower in narcoleptic patients compared with healthy controls. We also documented pathologically low levels of CSF beta-amyloid1-42 (narcolepsy and the prevalence of an 'amyloidogenic' pathway caused by the deficiency of the alpha-secretases enzymes.

  8. Cerebrospinal fluid (CSF neuronal biomarkers across the spectrum of HIV infection: hierarchy of injury and detection.

    Directory of Open Access Journals (Sweden)

    Julia Peterson

    Full Text Available The character of central nervous system (CNS HIV infection and its effects on neuronal integrity vary with evolving systemic infection. Using a cross-sectional design and archived samples, we compared concentrations of cerebrospinal fluid (CSF neuronal biomarkers in 143 samples from 8 HIV-infected subject groups representing a spectrum of untreated systemic HIV progression and viral suppression: primary infection; four groups of chronic HIV infection neuroasymptomatic (NA subjects defined by blood CD4+ T cells of >350, 200-349, 50-199, and <50 cells/µL; HAD; treatment-induced viral suppression; and 'elite' controllers. Samples from 20 HIV-uninfected controls were also examined. The neuronal biomarkers included neurofilament light chain protein (NFL, total and phosphorylated tau (t-tau, p-tau, soluble amyloid precursor proteins alpha and beta (sAPPα, sAPPβ and amyloid beta (Aβ fragments 1-42, 1-40 and 1-38. Comparison of the biomarker changes showed a hierarchy of sensitivity in detection and suggested evolving mechanisms with progressive injury. NFL was the most sensitive neuronal biomarker. Its CSF concentration exceeded age-adjusted norms in all HAD patients, 75% of NA CD4<50, 40% of NA CD4 50-199, and 42% of primary infection, indicating common neuronal injury with untreated systemic HIV disease progression as well as transiently during early infection. By contrast, only 75% of HAD subjects had abnormal CSF t-tau levels, and there were no significant differences in t-tau levels among the remaining groups. sAPPα and β were also abnormal (decreased in HAD, showed less marked change than NFL with CD4 decline in the absence of HAD, and were not decreased in PHI. The CSF Aβ peptides and p-tau concentrations did not differ among the groups, distinguishing the HIV CNS injury profile from Alzheimer's disease. These CSF biomarkers can serve as useful tools in selected research and clinical settings for patient classification, pathogenetic

  9. Beneficial effect of bilingualism on Alzheimer's disease CSF biomarkers and cognition.

    Science.gov (United States)

    Estanga, Ainara; Ecay-Torres, Mirian; Ibañez, Almudena; Izagirre, Andrea; Villanua, Jorge; Garcia-Sebastian, Maite; Iglesias Gaspar, M Teresa; Otaegui-Arrazola, Ane; Iriondo, Ane; Clerigue, Monserrat; Martinez-Lage, Pablo

    2017-02-01

    Bilingualism as a component of cognitive reserve has been claimed to delay the onset of Alzheimer's disease (AD). However, its effect on cerebrospinal fluid (CSF) AD-biomarkers has not been investigated. We assessed cognitive performance and CSF AD-biomarkers, and potential moderation effect of bilingualism on the association between age, CSF AD-biomarkers, and cognition. Cognitively healthy middle-aged participants classified as monolinguals (n = 100, nCSF = 59), early (n = 81, nCSF = 55) and late bilinguals (n = 97, nCSF = 52) were evaluated. Models adjusted for confounders showed that bilinguals performed better than monolinguals on digits backwards (early-bilinguals p = 0.003), Judgment of Line Orientation (JLO) (early-bilinguals p = 0.018; late-bilinguals p = 0.004), and Trail Making Test-B (late-bilinguals p = 0.047). Early bilingualism was associated with lower CSF total-tau (p = 0.019) and lower prevalence of preclinical AD (NIA-AA classification) (p = 0.02). Bilingualism showed a moderation effect on the relationship between age and CSF AD-biomarkers and the relationship between age and executive function. We conclude that bilingualism contributes to cognitive reserve enhancing executive and visual-spatial functions. For the first time, this study reveals that early bilingualism is associated with more favorable CSF AD-biomarker profile.

  10. False recognition correlates with Beta-Amyloid (1-42), but not with total Tau in CSF of patients with dementia and mild cognitive impairment

    NARCIS (Netherlands)

    Hildebrandt, H.; Haldenwanger, A.; Eling, P.A.T.M.

    2009-01-01

    Severe memory impairment forms the core symptom of Alzheimer's disease (AD), which is present early in the disease course. Recent studies show that AD patients not only suffer from forgetfulness, but also differ in their response bias, when having to decide whether information has been perceived rec

  11. Phosphorylated tau as a candidate biomarker for amyotrophic lateral sclerosis.

    Science.gov (United States)

    Grossman, Murray; Elman, Lauren; McCluskey, Leo; McMillan, Corey T; Boller, Ashley; Powers, John; Rascovsky, Katya; Hu, William; Shaw, Les; Irwin, David J; Lee, Virginia M-Y; Trojanowski, John Q

    2014-04-01

    An increasingly varied clinical spectrum of cases with amyotrophic lateral sclerosis (ALS) has been identified, and objective criteria for clinical trial eligibility are necessary. To develop a cerebrospinal fluid (CSF) biomarker sensitive and specific for the diagnosis of ALS. A case-control study including 51 individuals with ALS and 23 individuals with a disorder associated with a 4-repeat tauopathy was conducted at an academic medical center. The CSF level of tau phosphorylated at threonine 181 (ptau) and ratio of ptau to total tau (ttau). Using a cross-validation prediction procedure, we found significantly reduced CSF levels of ptau and the ptau:ttau ratio in ALS relative to 4-repeat tauopathy and to controls. In the validation cohort, the receiver operating characteristic area under the curve for the ptau:ttau ratio was 0.916, and the comparison of ALS with 4-repeat tauopathy showed 92.0% sensitivity and 91.7% specificity. Correct classification based on a low CSF ptau:ttau ratio was confirmed in 18 of 21 cases (86%) with autopsy-proved or genetically determined disease. In patients with available measures, ptau:ttau in ALS correlated with clinical measures of disease severity, such as the Mini-Mental State Examination (n = 51) and ALS Functional Rating Scale-Revised (n = 42), and regression analyses related the ptau:ttau ratio to magnetic resonance imaging (n = 10) evidence of disease in the corticospinal tract and white matter projections involving the prefrontal cortex. The CSF ptau:ttau ratio may be a candidate biomarker to provide objective support for the diagnosis of ALS.

  12. Changes of cerebrospinal fluid Aβ42, t-tau, and p-tau in Parkinson's disease patients with cognitive impairment relative to those with normal cognition: a meta-analysis.

    Science.gov (United States)

    Hu, Xiaohui; Yang, Yan; Gong, Daokai

    2017-08-14

    The cerebrospinal fluid (CSF) signature of reduced amyloid beta 1-42 (Aβ42), elevated total tau (t-tau), and phosphorylated tau181 (p-tau) is important for the early diagnosis of Alzheimer's disease (AD). Aβ42, t-tau, and p-tau have been reported in numerous studies to contribute to predicting cognitive impairment in Parkinson's disease (PDCI). However, no consistent conclusion can be drawn so far. Literatures regarding Aβ42, t-tau, and p-tau in CSF were systematically reviewed, and a meta-analysis was thus performed to evaluate the changes of these biomarkers in PDCI patients, including PD with mild cognitive impairment (PDMCI) and PD dementia (PDD) patients, relative to PD with normal cognition (PDNC) patients. Databases of "PubMed," "EBSCO," and "Springer" were retrieved for articles concerning Aβ42, t-tau, and p-tau in PDCI patients relative to those in PDNC patients published from January 1, 2000 to February 1, 2017. The following keywords were set, namely, "dementia" or "cognitive impairment" or "mild cognitive impairment" and "cerebrospinal fluid" and "Parkinson*." Sixteen articles comprising 590 PDCI patients and 1182 PDNC patients were included. The results showed that CSF Aβ42 level in PDCI cohort was lower than that in PDNC cohort (pooled Std.MD = -0.44, 95% CI [-0.61, -0.26], p < 0.00001). Reduced Aβ42 (pooled Std.MD = -0.60, 95% CI [-0.75, -0.45], p < 0.00001) as well as elevated t-tau (pooled Std.MD = 0.21, 95% CI [0.06, 0.35], p = 0.006) and p-tau (pooled Std.MD = 0.36, 95% CI [0.02, 0.69], p = 0.04) could be observed in PDD cohort compared with PDNC cohort. Therefore, amyloid pathology and tauopathy may participate in the development of PDD, which is similar to AD.

  13. Mapping CSF biomarker profiles onto NIA-AA guidelines for Alzheimer's disease.

    Science.gov (United States)

    Alexopoulos, Panagiotis; Roesler, Jennifer; Thierjung, Nathalie; Werle, Lukas; Buck, Dorothea; Yakushev, Igor; Gleixner, Lena; Kagerbauer, Simone; Ortner, Marion; Grimmer, Timo; Kübler, Hubert; Martin, Jan; Laskaris, Nikolaos; Kurz, Alexander; Perneczky, Robert

    2016-10-01

    The National Institute on Aging-Alzheimer's Association (NIA-AA) guidelines for Alzheimer's disease (AD) propose the categorization of individuals according to their biomarker constellation. Though the NIA-AA criteria for preclinical AD and AD dementia have already been applied in conjunction with imaging AD biomarkers, the application of the criteria using comprehensive cerebrospinal fluid (CSF) biomarker information has not been thoroughly studied yet. The study included a monocentric cohort with healthy (N = 41) and disease (N = 22) controls and patients with AD dementia (N = 119), and a multicentric sample with healthy controls (N = 116) and patients with AD dementia (N = 102). The CSF biomarkers β-amyloid 1-42, total tau, and phosphorylated tau at threonine 181 were measured with commercially available assays. Biomarker values were trichotomized into positive for AD, negative, or borderline. In controls the presence of normal CSF profiles varied between 13.6 and 25.4 % across the studied groups, while up to 8.6 % of them had abnormal CSF biomarkers. In 40.3-52.9 % of patients with AD dementia, a typical CSF profile for AD was detected. Approximately 40 % of the potential biomarker constellations are not considered in the NIA-AA guidelines, and more than 40 % of participants could not be classified into the NIA-AA categories with distinct biomarker constellations. Here, a refined scheme covering all potential biomarker constellations is proposed. These results enrich the discussion on the NIA-AA guidelines and point to a discordance between clinical symptomatology and CSF biomarkers even in patients with full-blown AD dementia, who are supposed to have a clearly positive for AD neurochemical profile.

  14. Neuropsychological and behavioural correlates of CSF biomarkers in dementia.

    Science.gov (United States)

    Engelborghs, Sebastiaan; Maertens, Karen; Vloeberghs, Ellen; Aerts, Tony; Somers, Nore; Mariën, Peter; De Deyn, Peter P

    2006-03-01

    To improve clinical, neuropsychological and behavioural characterisation of the cerebrospinal fluid (CSF) biomarkers beta-amyloid((1-42)) protein (Abeta42), protein tau (tau) and tau phosphorylated at threonine 181 (P-tau181) across diagnostic dementia categories, a prospective study was set up. Patients with probable Alzheimer's disease (AD) (n=201), AD with cerebrovascular disease (CVD) (AD+CVD) (n=33), frontotemporal dementia (FTD) (n=27), dementia with Lewy bodies (DLB) (n=22) and healthy controls (n=148) were included. All patients underwent neuropsychological examination and behavioural assessment by means of a battery of behavioural assessment scales. CSF was obtained by lumbar puncture and levels of Abeta42, tau and P-tau181 were determined with commercially available ELISA kits. Negative correlations between CSF Abeta42 levels and aggressiveness (Spearman: r=-0.223; p=0.002) and positive correlations with age at inclusion (r=0.195; p=0.006), age at onset (r=0.205; p=0.003) and MMSE scores (r=0.198; p=0.005) were found in AD. In AD+CVD, CSF Abeta42 levels were correlated with MMSE (r=0.482; p=0.006), Hierarchic Dementia Scale (r=0.503; p=0.017) and Boston Naming Test (r=0.516; p=0.012) scores. In controls, age was positively correlated with CSF tau (r=0.465; pbiomarker levels were obtained in healthy controls compared to AD patients, indicating that AD-induced pathophysiological processes change age-dependent regulation of CSF biomarker levels.

  15. CSF clearance in Alzheimer Disease measured with dynamic PET.

    Science.gov (United States)

    de Leon, Mony J; Li, Yi; Okamura, Nobuyuki; Tsui, Wai H; Saint Louis, Les A; Glodzik, Lidia; Osorio, Ricardo S; Fortea, Juan; Butler, Tracy; Pirraglia, Elizabeth; Fossati, Silvia; Kim, Hee-Jin; Carare, Roxana O; Nedergaard, Maiken; Benveniste, Helene; Rusinek, Henry

    2017-03-16

    Evidence supporting the hypothesis that reduced cerebrospinal fluid (CSF) clearance is involved in the pathophysiology of Alzheimer's disease (AD) comes from primarily from rodent models. However, unlike rodents where predominant extra-cranial CSF egress is via olfactory nerves traversing the cribriform plate, human CSF clearance pathways are not well characterized. Using dynamic Positron Emission Tomography (PET) with (18)F-THK5117 a tracer for tau pathology, the ventricular CSF time activity was used as a biomarker for CSF clearance. We tested three hypotheses: 1. Extra-cranial CSF is detected at the superior turbinates; 2. CSF clearance is reduced in AD; and 3. CSF clearance is inversely associated with amyloid deposition. Methods: 15 subjects, 8 with AD and 7 normal control volunteers were examined with (18)F-THK5117. 10 subjects additionally received (11)C-PiB PET scans and 8 were PiB positive. Ventricular time activity curves (TAC) of (18)F-THK5117 were used to identify highly correlated TAC from extra-cranial voxels. Results: For all subjects, the greatest density of CSF positive extra-cranial voxels was in the nasal turbinates. Tracer concentration analyses validated the superior nasal turbinate CSF signal intensity. AD patients showed ventricular tracer clearance reduced by 23% and 66% fewer superior turbinate CSF egress sites. Ventricular CSF clearance was inversely associated with amyloid deposition. Conclusion: The human nasal turbinate is part of the CSF clearance system. Lateral ventricle and superior nasal turbinates CSF clearance abnormalities are found in AD. Ventricular CSF clearance reductions are associated with increased brain amyloid depositions. These data suggest that PET measured CSF clearance is a biomarker of potential interest in AD and other neurodegenerative diseases.

  16. Insulin resistance is associated with higher cerebrospinal fluid tau levels in asymptomatic APOE ε4 carriers

    Science.gov (United States)

    Starks, Erika J.; O'Grady, J. Patrick; Hoscheidt, Siobhan M.; Racine, Annie M.; Carlsson, Cindy M.; Zetterberg, Henrik; Blennow, Kaj; Okonkwo, Ozioma C.; Puglielli, Luigi; Asthana, Sanjay; Dowling, N. Maritza; Gleason, Carey E.; Anderson, Rozalyn M.; Davenport-Sis, Nancy J.; DeRungs, LeAnn M.; Sager, Mark A.; Johnson, Sterling C.; Bendlin, Barbara B.

    2015-01-01

    Background Insulin resistance (IR) is linked with the occurrence of pathological features observed in Alzheimer's disease (AD), including neurofibrillary tangles and amyloid plaques. However, the extent to which IR is associated with AD pathology in the cognitively asymptomatic stages of preclinical AD remains unclear. Objective To determine the extent to which IR is linked with amyloid and tau pathology in late-middle-age. Method Cerebrospinal fluid (CSF) samples collected from 113 participants enrolled in the Wisconsin Registry for Alzheimer's Prevention study (mean age = 60.6 years), were assayed for AD-related markers of interest: Aβ42, P-Tau181, and T-Tau. IR was determined using the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR). Linear regression was used to test the effect of IR, and APOE ε4, on tau and amyloid pathology. We hypothesized that greater IR would be associated with higher CSF P-Tau181 and T-Tau, and lower CSF Aβ42. Results No significant main effects of HOMA-IR on P-Tau181, T-Tau, or Aβ42 were observed; however, significant interactions were observed between HOMA-IR and APOE ε4 on CSF markers related to tau. Among APOE ε4 carriers, higher HOMA-IR was associated with higher P-Tau181 and T-Tau. Among APOE ε4 non-carriers, HOMA-IR was negatively associated with P-Tau181 and T-Tau. We found no effects of IR on Aβ42 levels in CSF. Conclusion IR among asymptomatic APOE ε4 carriers was associated with higher P-Tau181 and T-Tau in late-middle age. The results suggest that IR may contribute to tau-related neurodegeneration in preclinical AD. The findings may have implications for developing prevention strategies aimed at modifying IR in mid-life. PMID:25812851

  17. Passive immunization with phospho-tau antibodies reduces tau pathology and functional deficits in two distinct mouse tauopathy models.

    Science.gov (United States)

    Sankaranarayanan, Sethu; Barten, Donna M; Vana, Laurel; Devidze, Nino; Yang, Ling; Cadelina, Gregory; Hoque, Nina; DeCarr, Lynn; Keenan, Stefanie; Lin, Alan; Cao, Yang; Snyder, Bradley; Zhang, Bin; Nitla, Magdalena; Hirschfeld, Gregg; Barrezueta, Nestor; Polson, Craig; Wes, Paul; Rangan, Vangipuram S; Cacace, Angela; Albright, Charles F; Meredith, Jere; Trojanowski, John Q; Lee, Virginia M-Y; Brunden, Kurt R; Ahlijanian, Michael

    2015-01-01

    In Alzheimer's disease (AD), an extensive accumulation of extracellular amyloid plaques and intraneuronal tau tangles, along with neuronal loss, is evident in distinct brain regions. Staging of tau pathology by postmortem analysis of AD subjects suggests a sequence of initiation and subsequent spread of neurofibrillary tau tangles along defined brain anatomical pathways. Further, the severity of cognitive deficits correlates with the degree and extent of tau pathology. In this study, we demonstrate that phospho-tau (p-tau) antibodies, PHF6 and PHF13, can prevent the induction of tau pathology in primary neuron cultures. The impact of passive immunotherapy on the formation and spread of tau pathology, as well as functional deficits, was subsequently evaluated with these antibodies in two distinct transgenic mouse tauopathy models. The rTg4510 transgenic mouse is characterized by inducible over-expression of P301L mutant tau, and exhibits robust age-dependent brain tau pathology. Systemic treatment with PHF6 and PHF13 from 3 to 6 months of age led to a significant decline in brain and CSF p-tau levels. In a second model, injection of preformed tau fibrils (PFFs) comprised of recombinant tau protein encompassing the microtubule-repeat domains into the cortex and hippocampus of young P301S mutant tau over-expressing mice (PS19) led to robust tau pathology on the ipsilateral side with evidence of spread to distant sites, including the contralateral hippocampus and bilateral entorhinal cortex 4 weeks post-injection. Systemic treatment with PHF13 led to a significant decline in the spread of tau pathology in this model. The reduction in tau species after p-tau antibody treatment was associated with an improvement in novel-object recognition memory test in both models. These studies provide evidence supporting the use of tau immunotherapy as a potential treatment option for AD and other tauopathies.

  18. Passive immunization with phospho-tau antibodies reduces tau pathology and functional deficits in two distinct mouse tauopathy models.

    Directory of Open Access Journals (Sweden)

    Sethu Sankaranarayanan

    Full Text Available In Alzheimer's disease (AD, an extensive accumulation of extracellular amyloid plaques and intraneuronal tau tangles, along with neuronal loss, is evident in distinct brain regions. Staging of tau pathology by postmortem analysis of AD subjects suggests a sequence of initiation and subsequent spread of neurofibrillary tau tangles along defined brain anatomical pathways. Further, the severity of cognitive deficits correlates with the degree and extent of tau pathology. In this study, we demonstrate that phospho-tau (p-tau antibodies, PHF6 and PHF13, can prevent the induction of tau pathology in primary neuron cultures. The impact of passive immunotherapy on the formation and spread of tau pathology, as well as functional deficits, was subsequently evaluated with these antibodies in two distinct transgenic mouse tauopathy models. The rTg4510 transgenic mouse is characterized by inducible over-expression of P301L mutant tau, and exhibits robust age-dependent brain tau pathology. Systemic treatment with PHF6 and PHF13 from 3 to 6 months of age led to a significant decline in brain and CSF p-tau levels. In a second model, injection of preformed tau fibrils (PFFs comprised of recombinant tau protein encompassing the microtubule-repeat domains into the cortex and hippocampus of young P301S mutant tau over-expressing mice (PS19 led to robust tau pathology on the ipsilateral side with evidence of spread to distant sites, including the contralateral hippocampus and bilateral entorhinal cortex 4 weeks post-injection. Systemic treatment with PHF13 led to a significant decline in the spread of tau pathology in this model. The reduction in tau species after p-tau antibody treatment was associated with an improvement in novel-object recognition memory test in both models. These studies provide evidence supporting the use of tau immunotherapy as a potential treatment option for AD and other tauopathies.

  19. CSF neurofilament concentration reflects disease severity in frontotemporal degeneration

    Science.gov (United States)

    Scherling, Carole S.; Hall, Tracey; Berisha, Flora; Klepac, Kristen; Karydas, Anna; Coppola, Giovanni; Kramer, Joel H.; Rabinovici, Gil; Ahlijanian, Michael; Miller, Bruce L.; Seeley, William; Grinberg, Lea T.; Rosen, Howard; Meredith, Jere; Boxer, Adam L.

    2014-01-01

    Objective Cerebrospinal fluid (CSF) neurofilament light chain (NfL) concentration is elevated in neurological disorders including frontotemporal degeneration (FTD). We investigated the clinical correlates of elevated CSF NfL levels in FTD. Methods CSF NfL, amyloid-β42 (Aβ42), tau and phosphorylated tau (ptau) concentrations were compared in 47 normal controls (NC), 8 asymptomatic gene carriers (NC2) of FTD-causing mutations, 79 FTD (45 behavioral variant frontotemporal dementia [bvFTD], 18 progressive nonfluent aphasia [PNFA], 16 semantic dementia [SD]), 22 progressive supranuclear palsy, 50 Alzheimer’s disease, 6 Parkinson’s disease and 17 corticobasal syndrome patients. Correlations between CSF analyte levels were performed with neuropsychological measures and the Clinical Dementia Rating scale sum of boxes (CDRsb). Voxel-based morphometry of structural MR images determined the relationship between brain volume and CSF NfL. Results Mean CSF NfL concentrations were higher in bvFTD, SD and PNFA than other groups. NfL in NC2 was similar to NC. CSF NfL, but not other CSF measures, correlated with CDRsb and neuropsychological measures in FTD, and not in other diagnostic groups. Analyses in two independent FTD cohorts and a group of autopsy verified or biomarker enriched cases confirmed the larger group analysis. In FTD, gray and white matter volume negatively correlated with CSF NfL concentration, such that individuals with highest NfL levels exhibited the most atrophy. Interpretation CSF NfL is elevated in symptomatic FTD and correlates with disease severity. This measurement may be a useful surrogate endpoint of disease severity in FTD clinical trials. Longitudinal studies of CSF NfL in FTD are warranted. PMID:24242746

  20. Sensitive quantitative assays for tau and phospho-tau in transgenic mouse models

    Science.gov (United States)

    Acker, Christopher M.; Forest, Stefanie K.; Zinkowski, Ray; Davies, Peter; d’Abramo, Cristina

    2012-01-01

    Transgenic mouse models have been an invaluable resource in elucidating the complex roles of Aβ and tau in Alzheimer’s disease. While many laboratories rely on qualitative or semi-quantitative techniques when investigating tau pathology, we have developed four Low-Tau Sandwich ELISAs that quantitatively assess different epitopes of tau relevant to Alzheimer’s disease: total tau, pSer-202, pThr-231, pSer-396/404. In this study, after comparing our assays to commercially available ELISAs, we demonstrate our assays high specificity and quantitative capabilities using brain homogenates from tau transgenic mice, htau, JNPL3, tau KO mice. All four ELISAs show excellent specificity for mouse and human tau, with no reactivity to tau KO animals. An age dependent increase of serum tau in both tau transgenic models was also seen. Taken together, these assays are valuable methods to quantify tau and phospho-tau levels in transgenic animals, by examining tau levels in brain and measuring tau as a potential serum biomarker. PMID:22727277

  1. Effects of CSF proteins on brain atrophy rates in cognitively healthy older adults

    Science.gov (United States)

    Mattsson, Niklas; Insel, Philip; Nosheny, Rachel; Trojanowski, John Q.; Shaw, Leslie M.; Jack, Clifford R.; Tosun, Duygu; Weiner, Michael

    2013-01-01

    Biomarkers associated with Alzheimer’s disease (AD)-like brain atrophy in healthy people may identify mechanisms involved in early stage AD. Aside from cerebrospinal fluid (CSF) β-amyloid42 (Aβ42) and tau, no studies have tested associations between CSF proteins and AD-like brain atrophy. We studied 90 healthy elders, who underwent lumbar puncture at baseline, and serial magnetic resonance imaging scans for up to 4 years. We tested statistical effects of baseline CSF proteins (N=70 proteins related to Aβ42-metabolism, microglial activity and synaptic/neuronal function) on atrophy rates in 7 AD-related regions. Besides effects of Aβ42 and phosphorylated tau (P-tau) that were seen in several regions, novel CSF proteins were found to have effects in inferior and middle temporal cortex (including Apolipoprotein CIII, Apolipoprotein D and Apolipoprotein H). Several proteins (including S100β and Matrix Metalloproteinase-3) had effects that depended on the presence of brain Aβ pathology, as measured by CSF Aβ42. Other proteins (including P-tau and Apolipoprotein D) had effects even after adjusting for CSF Aβ42. The statistical effects in this exploratory study were mild and not significant after correction for multiple comparisons, but some of the identified proteins may be associated with brain atrophy in healthy people. Proteins interacting with CSF Aβ42 may be related to Aβ brain pathology, while proteins associated with atrophy even after adjusting for CSF Aβ42 may be related to Aβ-independent mechanisms. PMID:24094581

  2. Recommendations for CSF AD biomarkers in the diagnostic evaluation of dementia

    DEFF Research Database (Denmark)

    Simonsen, Anja Hviid; Herukka, Sanna-Kaisa; Andreasen, Niels

    2017-01-01

    This article presents recommendations, based on the Grading of Recommendations, Assessment, Development, and Evaluation method, for the clinical application of cerebrospinal fluid (CSF) amyloid-β1-42, tau, and phosphorylated tau in the diagnostic evaluation of patients with dementia. The recommen...

  3. Association between cortical thickness and CSF biomarkers in mild cognitive impairment and Alzheimer’s disease

    DEFF Research Database (Denmark)

    Mohades, Sara; Dubois, Jonathan; Parent, Maxime;

    between cortical thinning, amyloidosis or tau hyperphosphorylation depends on cortical regions and clinical stages of AD. Methods: T1-weighed MRIs and associated CSF markers from individuals with mild cognitive impairment (MCI; 16), Alzheimer Disease (AD; n¼7) and age-matched cognitively normal subjects...... regional cortical thinning (CT) measured by Magnetic Resonance Imaging (MRI) and brain amyloidosis (measured by CSF Ab 1-42 concentrations), or tau hyperphosphorylation (tau 181; p-tau) in Alzheimer’s Disease (AD) and Mild Cognitive Impairment (MCI) patients. We test the hypothesis that the association...... (CN; n¼8) were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort. Cortical surface reconstruction and group registration were generated using Freesurfer. A general linear model was used to conduct regressions between CSF markers and cortical thickness. Results: Correlation...

  4. CSF Biomarkers for Alzheimer's Disease Diagnosis

    Directory of Open Access Journals (Sweden)

    A. Anoop

    2010-01-01

    Full Text Available Alzheimer's disease (AD is the most common form of dementia that affects several million people worldwide. The major neuropathological hallmarks of AD are the presence of extracellular amyloid plaques that are composed of Aβ40 and Aβ42 and intracellular neurofibrillary tangles (NFT, which is composed of hyperphosphorylated protein Tau. While the amyloid plaques and NFT could define the disease progression involving neuronal loss and dysfunction, significant cognitive decline occurs before their appearance. Although significant advances in neuroimaging techniques provide the structure and physiology of brain of AD cases, the biomarker studies based on cerebrospinal fluid (CSF and plasma represent the most direct and convenient means to study the disease progression. Biomarkers are useful in detecting the preclinical as well as symptomatic stages of AD. In this paper, we discuss the recent advancements of various biomarkers with particular emphasis on CSF biomarkers for monitoring the early development of AD before significant cognitive dysfunction.

  5. Observation of W{yields} {tau}{nu}{sub {tau}} decays with the ATLAS experiment

    Energy Technology Data Exchange (ETDEWEB)

    Nunes Hanninger, Guilherme

    2011-04-15

    Physics studies of processes with {tau} leptons in the final state, while challenging at hadron colliders, are of great importance at the LHC. The {tau} leptons provide important signatures in searches for the Higgs boson as well as for new physics in a wide range of theoretical models. Decays of Standard Model particles to {tau} leptons, in particular Z {yields} {tau}{tau} and W {yields} {tau}{nu}{sub {tau}}, are important background processes in those searches and their cross sections need to be measured first. This thesis reports the first observation of W {yields} {tau}{nu}{sub {tau}} decays and of hadronically decaying {tau} leptons with the ATLAS experiment at the LHC. The analysis is based on a data sample corresponding to an integrated luminosity of 546 nb{sup -1}, which was recorded at a proton-proton centre-of-mass energy of 7TeV. A total of 78 data events are selected, with an estimated background of 11.1 {+-} 2.3{sub (stat.)} {+-} 3.2{sub (syst.)} events from QCD processes, and of 11.8 {+-} 0.4{sub (stat.)} {+-} 3.7{sub (syst.)} events from other W and Z decays. The observed excess of data events over the total background is compatible with the SM expectation for W {yields} {tau}{nu}{sub {tau}} decays, both in the number of events and in the shapes of distributions of characteristic variables. (orig.)

  6. No support for premature central nervous system aging in HIV-1 when measured by cerebrospinal fluid phosphorylated tau (p-tau)

    OpenAIRE

    Krut, J. J.; Price, R W; Zetterberg, H; Fuchs, D.; Hagberg, L.; YILMAZ, A.; Cinque, P.; Nilsson, S; Gisslén, M.

    2016-01-01

    BACKGROUND: The prevalence of neurocognitive deficits are reported to be high in HIV-1 positive patients, even with suppressive antiretroviral treatment, and it has been suggested that HIV can cause accelerated aging of the brain. In this study we measured phosphorylated tau (p-tau) in cerebrospinal fluid (CSF) as a potential marker for premature central nervous system (CNS) aging. P-tau increases with normal aging but is not affected by HIV-associated neurocognitive disorders. METHODS: With ...

  7. Estimation of Tau and Phosphorylated Tau181 in Serum of Alzheimer's Disease and Mild Cognitive Impairment Patients.

    Directory of Open Access Journals (Sweden)

    Shashank Shekhar

    Full Text Available The elevated level of cerebrospinal fluid (CSF Tau and phosphorylated Tau181 (p-Tau181 proteins are well established hallmarks of Alzheimer's disease (AD. Elevated level of p-Tau181 can differentiate AD from other neurodegenerative disease. However, the expression level of these proteins in serum of AD patient is not well set up. This study sought to evaluate the level of Tau and p-Tau181 in serum of AD, and mild cognitive impairment (MCI patients for an alternative approach to establish protein-based markers by convenient way. Blood samples were collected from 39 AD patients, 37 MCI patients and 37 elderly individuals as controls. The levels of Tau and p-Tau181 in the serum of the different groups were measured by label free real time Surface Plasmon Resonance technology by using specific antibodies, and were further confirmed by the conventional western blot method. An appropriate statistical analysis, including Receiver Operating Characteristic (ROC, was performed. The concentrations of serum Tau and p-Tau181 were significantly higher (p<0.00001 in AD (Tau; 47.49±9.00ng/μL, p-Tau181; 0.161±0.04 ng/μL compared to MCI (Tau; 39.26±7.78 ng/μL, p-Tau181; 0.135±0.02 ng/μL and were further higher compared to elderly controls (Tau; 34.92±6.58 ng/μL, p-Tau181; 0.122±0.01 ng/ μL. A significant (p<0.0001 downhill correlation was found between Tau as well as p-Tau181 levels with HMSE and MoCA score. This study for the first time reports the concentration of Tau and p-Tau181 in serum of AD and MCI patients. The cutoff values of Tau and p-Tau181 of AD and MCI patients with sensitivity and specificity reveal that serum level of these proteins can be used as a predictive marker for AD and MCI.

  8. Correlations between serum levels of beta amyloid, cerebrospinal levels of tau and phospho tau, and delayed response tasks in young and aged cynomolgus monkeys (Macaca fascicularis)

    DEFF Research Database (Denmark)

    Darusman, Huda Shalahudin; Sajuthi, D; Kalliokoski, O

    2013-01-01

    In an attempt to explore cynomolgus monkeys as an animal model for Alzheimer's disease, the present study focused on the Alzheimer's biomarkers beta amyloid 1-42 (Aβ42 ) in serum, and total tau (t-tau) and phosphorylated tau (p-tau) levels in cerebrospinal fluid.......In an attempt to explore cynomolgus monkeys as an animal model for Alzheimer's disease, the present study focused on the Alzheimer's biomarkers beta amyloid 1-42 (Aβ42 ) in serum, and total tau (t-tau) and phosphorylated tau (p-tau) levels in cerebrospinal fluid....

  9. Cerebrospinal fluid P-tau(181P) : biomarker for improved differential dementia diagnosis

    NARCIS (Netherlands)

    Struyfs, Hanne; Niemantsverdriet, Ellis; Goossens, Joery; Fransen, Erik; Martin, Jean-Jacques; De Deyn, Peter P.; Engelborghs, Sebastiaan

    2015-01-01

    The goal of this study is to investigate the value of tau phosphorylated at threonine 181 (P-tau(181p)) in the Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarker panel for differential dementia diagnosis in autopsy confirmed AD and non-AD patients. The study population consisted of 140 aut

  10. Comparison of Cerebrospinal Fluid Levels of Tau and Aß1-42 in Alzheimer’s disease and Frontotemporal Degeneration Using Two Analytical Platforms

    Science.gov (United States)

    Irwin, David J.; McMillan, Corey T.; Toledo, Jon B.; Arnold, Steven E.; Shaw, Leslie M.; Wang, Li-San; Lee, Virginia M.-Y.; Trojanowski, John Q.; Grossman, Murray

    2012-01-01

    Objective To utilize values of cerebrospinal fluid (CSF) tau and ß-amyloid obtained from two different analytical immunoassays to differentiate Alzheimer’s disease (AD) from frontotemporal lobar degeneration (FTLD). Design CSF values of total tau (t-tau) and ß-amyloid (Aß1-42) obtained using the INNOTEST® ELISA were transformed using a linear regression model to equivalent values obtained using the INNO-BIA AlzBio3™ (xMAP Luminex) assay. Cutoff values obtained from the xMAP assay were developed in a series of autopsy-confirmed cases and cross-validated in another series of autopsy-confirmed samples using transformed ELISA values to assess sensitivity and specificity for differentiating AD from FTLD. Setting Tertiary memory disorders clinics and neuropathological and biomarker core centers. Participants 75 samples from patients with CSF data obtained from both assays were used for transformation of ELISA values. 40 autopsy-confirmed cases (30 AD, 10 FTLD) were used to establish diagnostic cutoff values, and then cross-validated in a second sample set of 21 autopsy-confirmed cases (11 AD, 10 FTLD) with transformed ELISA values. Main outcome measure Diagnostic accuracy using transformed biomarker values. Results Data obtained from both assays were highly correlated. The t-tau:Aß1-42 ratio had the highest correlation between measures (r=0.928, p<0.001) and high reliability of transformation (ICC=0.89). A cutoff of 0.34 for the t-tau:Aß1-42 ratio had 90% and 100% sensitivity and 96.7% and 91% specificity to differentiate FTLD cases in the validation and cross-validation samples, respectively. Conclusions Values from two analytical platforms can be transformed into equivalent units, which can distinguish AD from FTLD more accurately than the clinical diagnosis. PMID:22490326

  11. Cerebrospinal Fluid Amyloid β1-42, Tau, and Alpha-Synuclein Predict the Heterogeneous Progression of Cognitive Dysfunction in Parkinson's Disease.

    Science.gov (United States)

    Kang, Ju-Hee

    2016-05-01

    Parkinson's disease (PD) is a neurodegenerative disease with heterogeneous pathological and clinical features. Cognitive dysfunction, a frequent non-motor complication, is a risk factor for poor prognosis and shows inter-individual variation in its progression. Of the clinical studies performed to identify biomarkers of PD progression, the Parkinson's Progression Markers Initiative (PPMI) study is the largest study that enrolled drug-naïve and very early stage PD patients. The baseline characteristics of the PPMI cohort were recently published. The diagnostic utility of cerebrospinal fluid (CSF) biomarkers, including alpha-synuclein (α-syn), total tau, phosphorylated tau at Thr181, and amyloid β1-42, was not satisfactory. However, the baseline data on CSF biomarkers in the PPMI study suggested that the measurement of the CSF biomarkers enables the prediction of future cognitive decline in PD patients, which was consistent with previous studies. To prove the hypothesis that the interaction between Alzheimer's pathology and α-syn pathology is important to the progression of cognitive dysfunction in PD, longitudinal observational studies must be followed. In this review, the neuropathological nature of heterogeneous cognitive decline in PD is briefly discussed, followed by a summarized interpretation of baseline CSF biomarkers derived from the data in the PPMI study. The combination of clinical, biochemical, genetic and imaging biomarkers of PD constitutes a feasible strategy to predict the heterogeneous progression of PD.

  12. Tau protein concentrations in cerebrospinal fluid of patients with multiple sclerosis.

    Science.gov (United States)

    Jiménez-Jiménez, F J; Zurdo, J M; Hernanz, A; Medina-Acebrón, S; de Bustos, F; Barcenilla, B; Sayed, Y; Ayuso-Peralta, L

    2002-12-01

    FUNDAMENTALS AND OBJECTIVE: Multiple sclerosis (MS) is the prototype of demyelinating disease, but recently, it has been shown that the existence of axonal lesions contribute to irreversible central nervous system damage in this disease. Tau proteins are considered to be important for maintaining the stability of axonal microtubules involved in the mediation of fast axonal transport of synaptic constituents. There have been reports of increased cerebrospinal fluid (CSF) tau concentrations in patients with MS, and it has been suggested that this could be a marker of axonal damage. The objective of the present study was to elucidate whether CSF tau levels could be a marker of MS activity. We measured tau concentrations in the CSF of 20 patients with MS (nine in the first, seven in the second, one in the fourth exacerbation, and three patients with chronic progressive course) and 32 age- and sex-matched controls, using a specific enzyme-linked immunosorbent assay method. The CSF tau concentrations of patients with MS did not differ from those of controls, and they were not correlated with age at onset and duration of the disease. CSF tau concentrations are not a marker of MS activity. Copyright Blackwell Munksgaard 2002

  13. Propagation of tau pathology in Alzheimer's disease: identification of novel therapeutic targets.

    Science.gov (United States)

    Pooler, Amy M; Polydoro, Manuela; Wegmann, Susanne; Nicholls, Samantha B; Spires-Jones, Tara L; Hyman, Bradley T

    2013-01-01

    Accumulation and aggregation of the microtubule-associated protein tau are a pathological hallmark of neurodegenerative disorders such as Alzheimer's disease (AD). In AD, tau becomes abnormally phosphorylated and forms inclusions throughout the brain, starting in the entorhinal cortex and progressively affecting additional brain regions as the disease progresses. Formation of these inclusions is thought to lead to synapse loss and cell death. Tau is also found in the cerebrospinal fluid (CSF), and elevated levels are a biomarker for AD. Until recently, it was thought that the presence of tau in the CSF was due to the passive release of aggregated tau from dead or dying tangle-bearing neurons. However, accumulating evidence from different AD model systems suggests that tau is actively secreted and transferred between synaptically connected neurons. Transgenic mouse lines with localized expression of aggregating human tau in the entorhinal cortex have demonstrated that, as these animals age, tau becomes mislocalized from axons to cell bodies and dendrites and that human tau-positive aggregates form first in the entorhinal cortex and later in downstream projection targets. Numerous in vitro and in vivo studies have provided insight into the mechanisms by which tau may be released and internalized by neurons and have started to provide insight into how tau pathology may spread in AD. In this review, we discuss the evidence for regulated tau release and its specific uptake by neurons. Furthermore, we identify possible therapeutic targets for preventing the propagation of tau pathology, as inhibition of tau transfer may restrict development of tau tangles in a small subset of neurons affected in early stages of AD and therefore prevent widespread neuron loss and cognitive dysfunction associated with later stages of the disease.

  14. Tau hadronic branching ratios

    CERN Document Server

    Buskulic, Damir; De Bonis, I; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Odier, P; Pietrzyk, B; Ariztizabal, F; Chmeissani, M; Crespo, J M; Efthymiopoulos, I; Fernández, E; Fernández-Bosman, M; Gaitan, V; Martínez, M; Orteu, S; Pacheco, A; Padilla, C; Palla, Fabrizio; Pascual, A; Perlas, J A; Sánchez, F; Teubert, F; Colaleo, A; Creanza, D; De Palma, M; Farilla, A; Gelao, G; Girone, M; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Natali, S; Nuzzo, S; Ranieri, A; Raso, G; Romano, F; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Bonvicini, G; Cattaneo, M; Comas, P; Coyle, P; Drevermann, H; Engelhardt, A; Forty, Roger W; Frank, M; Hagelberg, R; Harvey, J; Jacobsen, R; Janot, P; Jost, B; Kneringer, E; Knobloch, J; Lehraus, Ivan; Markou, C; Martin, E B; Mato, P; Minten, Adolf G; Miquel, R; Oest, T; Palazzi, P; Pater, J R; Pusztaszeri, J F; Ranjard, F; Rensing, P E; Rolandi, Luigi; Schlatter, W D; Schmelling, M; Schneider, O; Tejessy, W; Tomalin, I R; Venturi, A; Wachsmuth, H W; Wiedenmann, W; Wildish, T; Witzeling, W; Wotschack, J; Ajaltouni, Ziad J; Bardadin-Otwinowska, Maria; Barrès, A; Boyer, C; Falvard, A; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rossignol, J M; Saadi, F; Fearnley, Tom; Hansen, J B; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Kyriakis, A; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Zachariadou, K; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Passalacqua, L; Rougé, A; Rumpf, M; Tanaka, R; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Focardi, E; Parrini, G; Corden, M; Delfino, M C; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Pepé-Altarelli, M; Dorris, S J; Halley, A W; ten Have, I; Knowles, I G; Lynch, J G; Morton, W T; O'Shea, V; Raine, C; Reeves, P; Scarr, J M; Smith, K; Smith, M G; Thompson, A S; Thomson, F; Thorn, S; Turnbull, R M; Becker, U; Braun, O; Geweniger, C; Graefe, G; Hanke, P; Hepp, V; Kluge, E E; Putzer, A; Rensch, B; Schmidt, M; Sommer, J; Stenzel, H; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Colling, D J; Dornan, Peter J; Konstantinidis, N P; Moneta, L; Moutoussi, A; Nash, J; San Martin, G; Sedgbeer, J K; Stacey, A M; Dissertori, G; Girtler, P; Kuhn, D; Rudolph, G; Bowdery, C K; Brodbeck, T J; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Sloan, Terence; Whelan, E P; Williams, M I; Galla, A; Greene, A M; Kleinknecht, K; Quast, G; Raab, J; Renk, B; Sander, H G; Wanke, R; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Bencheikh, A M; Benchouk, C; Bonissent, A; Bujosa, G; Calvet, D; Carr, J; Diaconu, C A; Etienne, F; Thulasidas, M; Nicod, D; Payre, P; Rousseau, D; Talby, M; Abt, I; Assmann, R W; Bauer, C; Blum, Walter; Brown, D; Dietl, H; Dydak, Friedrich; Ganis, G; Gotzhein, C; Jakobs, K; Kroha, H; Lütjens, G; Lutz, Gerhard; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Saint-Denis, R; Wolf, G; Alemany, R; Boucrot, J; Callot, O; Cordier, A; Courault, F; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Jacquet, M; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Musolino, G; Nikolic, I A; Park, H J; Park, I C; Schune, M H; Simion, S; Veillet, J J; Videau, I; Abbaneo, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Rizzo, G; Sanguinetti, G; Sciabà, A; Spagnolo, P; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Triggiani, G; Vannini, C; Verdini, P G; Walsh, J; Betteridge, A P; Blair, G A; Bryant, L M; Cerutti, F; Gao, Y; Green, M G; Johnson, D L; Medcalf, T; Mir, L M; Perrodo, P; Strong, J A; Bertin, V; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Edwards, M; Maley, P; Norton, P R; Thompson, J C; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Marx, B; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Johnson, R P; Kim, H Y; Litke, A M; McNeil, M A; Taylor, G; Beddall, A; Booth, C N; Boswell, R; Cartwright, S L; Combley, F; Dawson, I; Köksal, A; Letho, M; Newton, W M; Rankin, C; Thompson, L F; Böhrer, A; Brandt, S; Cowan, G D; Feigl, E; Grupen, Claus; Lutters, G; Minguet-Rodríguez, J A; Rivera, F; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Ragusa, F; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Bellantoni, L; Elmer, P; Feng, Z; Ferguson, D P S; Gao, Y S; González, S; Grahl, J; Harton, J L; Hayes, O J; Hu, H; McNamara, P A; Nachtman, J M; Orejudos, W; Pan, Y B; Saadi, Y; Schmitt, M; Scott, I J; Sharma, V; Turk, J; Walsh, A M; Wu Sau Lan; Wu, X; Yamartino, J M; Zheng, M; Zobernig, G

    1996-01-01

    From 64492 selected \\tau-pair events, produced at the Z^0 resonance, the measurement of the tau decays into hadrons from a global analysis using 1991, 1992 and 1993 ALEPH data is presented. Special emphasis is given to the reconstruction of photons and \\pi^0's, and the removal of fake photons. A detailed study of the systematics entering the \\pi^0 reconstruction is also given. A complete and consistent set of tau hadronic branching ratios is presented for 18 exclusive modes. Most measurements are more precise than the present world average. The new level of precision reached allows a stringent test of \\tau-\\mu universality in hadronic decays, g_\\tau/g_\\mu \\ = \\ 1.0013 \\ \\pm \\ 0.0095, and the first measurement of the vector and axial-vector contributions to the non-strange hadronic \\tau decay width: R_{\\tau ,V} \\ = \\ 1.788 \\ \\pm \\ 0.025 and R_{\\tau ,A} \\ = \\ 1.694 \\ \\pm \\ 0.027. The ratio (R_{\\tau ,V} - R_{\\tau ,A}) / (R_{\\tau ,V} + R_{\\tau ,A}), equal to (2.7 \\pm 1.3) \\ \\%, is a measure of the importance of Q...

  15. $\\tau$ physics at LHCb

    CERN Document Server

    Harrison, Jonathan

    2015-01-01

    We report on the first searches for lepton flavour violating $\\tau^-$ decays at a hadron collider. These include searches for the lepton flavour violating decay $\\tau^-\\to \\mu^+\\mu^-\\mu^-$ and the lepton flavour and baryon number violating decays $\\tau^-\\to \\bar{p}\\mu^+\\mu^-$ and $\\tau^-\\to p\\mu^-\\mu^-$. Upper limits of ${\\cal B}(\\tau^-\\to \\mu^+\\mu^-\\mu^-) < 4.6 \\times 10^{-8}$, ${\\cal B}(\\tau^-\\to \\bar{p}\\mu^+\\mu^-) < 3.4 \\times 10^{-7}$ and ${\\cal B}(\\tau^-\\to p\\mu^-\\mu^-) < 4.6 \\times 10^{-7}$ are set at 90% confidence level. A measurement of the inclusive $Z\\to\\tau^+\\tau^-$ cross-section at 7 TeV is also reported and is found to be consistent with the Standard Model. The ratio of the $Z\\to\\tau^+\\tau^-$ cross-section to the $Z\\to\\mu^+\\mu^-$ cross-section is found to be consistent with lepton universality.

  16. Cerebrospinal fluid tau protein as a biomarker for severity of spinal cord injury in dogs with intervertebral disc herniation.

    Science.gov (United States)

    Roerig, A; Carlson, R; Tipold, A; Stein, V M

    2013-08-01

    Intervertebral disc herniation (IVDH) is a common cause of spinal cord injury (SCI) in dogs. Microtubule-associated protein tau derives predominantly from neurons and axons, making it a potential marker of neuronal injury. A retrospective study, including 51 dogs with thoracolumbar or cervical IVDH and 12 clinically normal dogs, was designed to describe associations between cerebrospinal fluid (CSF) tau concentration, degree of neurological signs and motor functional recovery in dogs with IVDH. Signalment, degree of neurological dysfunction and outcome were recorded. Cisternal CSF tau values were determined by ELISA. Associations between CSF tau concentration and various clinical parameters were evaluated. Receiver-operating characteristics curve (ROC) analyses were performed to assess the validity of protein tau measurements. CSF tau concentrations were significantly higher in dogs showing plegia (median, 79.9 pg/mL; range, 0-778.7 pg/mL; P=0.016) compared to healthy dogs and dogs with paresis (median, 30.1 pg/mL; range, 0-193.1 pg/mL; P=0.025). Plegic dogs that improved by one neurological grade within 1 week had significantly lower tau protein levels compared to plegic dogs that needed more time for recovery or did not show an improvement (P=0.008). A CSF tau concentration >41.3 pg/mL had a sensitivity of 86% and specificity of 83% to predict an unsuccessful outcome in plegic dogs based on ROC analysis (area under the curve, 0.887; P=0.007, 95% confidence interval [CI] 0.717-1.057). CSF protein tau levels are positively associated with the severity of spinal cord damage and may serve as a prognostic indicator in dogs with IVDH.

  17. Propagation of Tau aggregates.

    Science.gov (United States)

    Goedert, Michel; Spillantini, Maria Grazia

    2017-05-30

    Since 2009, evidence has accumulated to suggest that Tau aggregates form first in a small number of brain cells, from where they propagate to other regions, resulting in neurodegeneration and disease. Propagation of Tau aggregates is often called prion-like, which refers to the capacity of an assembled protein to induce the same abnormal conformation in a protein of the same kind, initiating a self-amplifying cascade. In addition, prion-like encompasses the release of protein aggregates from brain cells and their uptake by neighbouring cells. In mice, the intracerebral injection of Tau inclusions induced the ordered assembly of monomeric Tau, followed by its spreading to distant brain regions. Short fibrils constituted the major species of seed-competent Tau. The existence of several human Tauopathies with distinct fibril morphologies has led to the suggestion that different molecular conformers (or strains) of aggregated Tau exist.

  18. Amyloidogenesis of Tau protein.

    Science.gov (United States)

    Nizynski, Bartosz; Dzwolak, Wojciech; Nieznanski, Krzysztof

    2017-08-17

    The role of microtubule-associated protein Tau in neurodegeneration has been extensively investigated since the discovery of Tau amyloid aggregates in the brains of patients with Alzheimer's disease (AD). The process of formation of amyloid fibrils is known as amyloidogenesis and attracts much attention as a potential target in the prevention and treatment of neurodegenerative conditions linked to protein aggregation. Cerebral deposition of amyloid aggregates of Tau is observed not only in AD but also in numerous other tauopathies and prion diseases. Amyloidogenesis of intrinsically unstructured monomers of Tau can be triggered by mutations in the Tau gene, post-translational modifications, or interactions with polyanionic molecules and aggregation-prone proteins/peptides. The self-assembly of amyloid fibrils of Tau shares a number of characteristic features with amyloidogenesis of other proteins involved in neurodegenerative diseases. For example, in vitro experiments have demonstrated that the nucleation phase, which is the rate-limiting stage of Tau amyloidogenesis, is shortened in the presence of fragmented preformed Tau fibrils acting as aggregation templates ("seeds"). Accordingly, Tau aggregates released by tauopathy-affected neurons can spread the neurodegenerative process in the brain through a prion-like mechanism, originally described for the pathogenic form of prion protein. Moreover, Tau has been shown to form amyloid strains-structurally diverse self-propagating aggregates of potentially various pathological effects, resembling in this respect prion strains. Here, we review the current literature on Tau aggregation and discuss mechanisms of propagation of Tau amyloid in the light of the prion-like paradigm. © 2017 The Protein Society.

  19. Tau leptonic branching ratios

    CERN Document Server

    Buskulic, Damir; De Bonis, I; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Odier, P; Pietrzyk, B; Ariztizabal, F; Chmeissani, M; Crespo, J M; Efthymiopoulos, I; Fernández, E; Fernández-Bosman, M; Gaitan, V; Garrido, L; Martínez, M; Orteu, S; Pacheco, A; Padilla, C; Palla, Fabrizio; Pascual, A; Perlas, J A; Sánchez, F; Teubert, F; Colaleo, A; Creanza, D; De Palma, M; Farilla, A; Gelao, G; Girone, M; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Natali, S; Nuzzo, S; Ranieri, A; Raso, G; Romano, F; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Bonvicini, G; Cattaneo, M; Comas, P; Coyle, P; Drevermann, H; Engelhardt, A; Forty, Roger W; Frank, M; Hagelberg, R; Harvey, J; Jacobsen, R; Janot, P; Jost, B; Kneringer, E; Knobloch, J; Lehraus, Ivan; Markou, C; Martin, E B; Mato, P; Minten, Adolf G; Miquel, R; Oest, T; Palazzi, P; Pater, J R; Pusztaszeri, J F; Ranjard, F; Rensing, P E; Rolandi, Luigi; Schlatter, W D; Schmelling, M; Schneider, O; Tejessy, W; Tomalin, I R; Venturi, A; Wachsmuth, H W; Wiedenmann, W; Wildish, T; Witzeling, W; Wotschack, J; Ajaltouni, Ziad J; Bardadin-Otwinowska, Maria; Barrès, A; Boyer, C; Falvard, A; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rossignol, J M; Saadi, F; Fearnley, Tom; Hansen, J B; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Kyriakis, A; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Zachariadou, K; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Passalacqua, L; Rougé, A; Rumpf, M; Tanaka, R; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Focardi, E; Parrini, G; Corden, M; Delfino, M C; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Pepé-Altarelli, M; Dorris, S J; Halley, A W; ten Have, I; Knowles, I G; Lynch, J G; Morton, W T; O'Shea, V; Raine, C; Reeves, P; Scarr, J M; Smith, K; Smith, M G; Thompson, A S; Thomson, F; Thorn, S; Turnbull, R M; Becker, U; Braun, O; Geweniger, C; Graefe, G; Hanke, P; Hepp, V; Kluge, E E; Putzer, A; Rensch, B; Schmidt, M; Sommer, J; Stenzel, H; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Colling, D J; Dornan, Peter J; Konstantinidis, N P; Moneta, L; Moutoussi, A; Nash, J; San Martin, G; Sedgbeer, J K; Stacey, A M; Dissertori, G; Girtler, P; Kuhn, D; Rudolph, G; Bowdery, C K; Brodbeck, T J; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Sloan, Terence; Whelan, E P; Williams, M I; Galla, A; Greene, A M; Kleinknecht, K; Quast, G; Raab, J; Renk, B; Sander, H G; Wanke, R; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Bencheikh, A M; Benchouk, C; Bonissent, A; Bujosa, G; Calvet, D; Carr, J; Diaconu, C A; Etienne, F; Thulasidas, M; Nicod, D; Payre, P; Rousseau, D; Talby, M; Abt, I; Assmann, R W; Bauer, C; Blum, Walter; Brown, D; Dietl, H; Dydak, Friedrich; Ganis, G; Gotzhein, C; Jakobs, K; Kroha, H; Lütjens, G; Lutz, Gerhard; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Saint-Denis, R; Wolf, G; Alemany, R; Boucrot, J; Callot, O; Cordier, A; Courault, F; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Jacquet, M; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Musolino, G; Nikolic, I A; Park, H J; Park, I C; Schune, M H; Simion, S; Veillet, J J; Videau, I; Abbaneo, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Rizzo, G; Sanguinetti, G; Sciabà, A; Spagnolo, P; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Triggiani, G; Vannini, C; Verdini, P G; Walsh, J; Betteridge, A P; Blair, G A; Bryant, L M; Cerutti, F; Gao, Y; Green, M G; Johnson, D L; Medcalf, T; Mir, L M; Perrodo, P; Strong, J A; Bertin, V; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Edwards, M; Maley, P; Norton, P R; Thompson, J C; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Marx, B; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Johnson, R P; Kim, H Y; Litke, A M; McNeil, M A; Taylor, G; Beddall, A; Booth, C N; Boswell, R; Cartwright, S L; Combley, F; Dawson, I; Köksal, A; Letho, M; Newton, W M; Rankin, C; Thompson, L F; Böhrer, A; Brandt, S; Cowan, G D; Feigl, E; Grupen, Claus; Lutters, G; Minguet-Rodríguez, J A; Rivera, F; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Ragusa, F; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Bellantoni, L; Elmer, P; Feng, Z; Ferguson, D P S; Gao, Y S; González, S; Grahl, J; Harton, J L; Hayes, O J; Hu, H; McNamara, P A; Nachtman, J M; Orejudos, W; Pan, Y B; Saadi, Y; Schmitt, M; Scott, I J; Sharma, V; Turk, J; Walsh, A M; Wu Sau Lan; Wu, X; Yamartino, J M; Zheng, M; Zobernig, G

    1996-01-01

    A sample of 62249 \\tau-pair events is selected from data taken with the ALEPH detector in 1991, 1992 and 1993. The measurement of the branching fractions for \\tau decays into electrons and muons is presented with emphasis on the study of systematic effects from selection, particle identification and decay classification. Combined with the most recent ALEPH determination of the \\tau lifetime, these results provide a relative measurement of the leptonic couplings in the weak charged current for transverse W bosons.

  20. Use of amyloid-PET to determine cutpoints for CSF markers

    DEFF Research Database (Denmark)

    Zwan, Marissa D; Rinne, Juha O; Hasselbalch, Steen G;

    2016-01-01

    , 99 with mild cognitive impairment, 195 with Alzheimer disease [AD] dementia, and 82 with non-AD dementia) from 5 European centers. We calculated for each center and for the pooled cohort CSF Aβ42 and Aβ42/tau ratio cutpoints for cortical amyloid deposition based on visual interpretation of [11C...

  1. [Tau Positron Emission Tomography].

    Science.gov (United States)

    Higuchi, Makoto

    2017-07-01

    Accumulation of fibrillar tau protein aggregates is a neuropathological hallmark of Alzheimer's disease (AD) and related neurodegenerative dementias, including a subgroup of frontotemporal lobar degeneration (FTLD). Visualization of tau lesions in the brains of living subjects enables a pathology-based diagnosis of dementing illnesses in the prodromal stage, and offers objective measures of disease progression and outcomes of disease-modifying therapies. With this rationale, diverse classes of low-molecular-weight chemicals capable of binding to a β-pleated sheet structure have been developed to be used for in vivo positron emission tomography (PET) of tau pathologies. Clinical PET studies of AD patients with such tau probes have provided the following insights: (1) Tau fibrils accumulate in the hippocampal formation in an age-dependent manner that is independent of amyloid-beta peptide (Aβ) pathology; (2) The deposition of Aβ may trigger a spatial expansion of tau pathology, in transition from normal aging to advanced AD; and (3) Tau accumulation is intimately associated with local neuronal loss, leading to cortical atrophy and focal symptoms. In contrast, studies of FTLD have shown a limited performance of first-generation PET probes in capturing non-AD-type tau lesions. New compounds have accordingly been developed and clinically tested, proving to yield a high contrast for tau deposits with high specificity. These second-generation probes are being evaluated primarily by pharmaceutical companies, in line with their growing demands for neuroimaging-based biomarkers serving for clinical trials of anti-Aβ and anti-tau therapies. Meanwhile, a consortium flexibly linking academia and industry to facilitate the utilization of research tools, including tau PET probes, has been established in Japan, for the ultimate purpose of elucidating the molecular etiology of tauopathies and creating diagnostic and therapeutic agents based on such an understanding.

  2. Search for the decays $B_s^0\\to\\tau^+\\tau^-$ and $B^0\\to\\tau^+\\tau^-$

    CERN Document Server

    Aaij, Roel; Adinolfi, Marco; Ajaltouni, Ziad; Akar, Simon; Albrecht, Johannes; Alessio, Federico; Alexander, Michael; Ali, Suvayu; Alkhazov, Georgy; Alvarez Cartelle, Paula; Alves Jr, Antonio Augusto; Amato, Sandra; Amerio, Silvia; Amhis, Yasmine; An, Liupan; Anderlini, Lucio; Andreassi, Guido; Andreotti, Mirco; Andrews, Jason; Appleby, Robert; Archilli, Flavio; d'Argent, Philippe; Arnau Romeu, Joan; Artamonov, Alexander; Artuso, Marina; Aslanides, Elie; Auriemma, Giulio; Baalouch, Marouen; Babuschkin, Igor; Bachmann, Sebastian; Back, John; Badalov, Alexey; Baesso, Clarissa; Baker, Sophie; Balagura, Vladislav; Baldini, Wander; Baranov, Alexander; Barlow, Roger; Barschel, Colin; Barsuk, Sergey; Barter, William; Baryshnikov, Fedor; Baszczyk, Mateusz; Batozskaya, Varvara; Batsukh, Baasansuren; Battista, Vincenzo; Bay, Aurelio; Beaucourt, Leo; Beddow, John; Bedeschi, Franco; Bediaga, Ignacio; Beiter, Andrew; Bel, Lennaert; Bellee, Violaine; Belloli, Nicoletta; Belous, Konstantin; Belyaev, Ivan; Ben-Haim, Eli; Bencivenni, Giovanni; Benson, Sean; Beranek, Sarah; Berezhnoy, Alexander; Bernet, Roland; Bertolin, Alessandro; Betancourt, Christopher; Betti, Federico; Bettler, Marc-Olivier; van Beuzekom, Martinus; Bezshyiko, Iaroslava; Bifani, Simone; Billoir, Pierre; Birnkraut, Alex; Bitadze, Alexander; Bizzeti, Andrea; Blake, Thomas; Blanc, Frederic; Blouw, Johan; Blusk, Steven; Bocci, Valerio; Boettcher, Thomas; Bondar, Alexander; Bondar, Nikolay; Bonivento, Walter; Bordyuzhin, Igor; Borgheresi, Alessio; Borghi, Silvia; Borisyak, Maxim; Borsato, Martino; Bossu, Francesco; Boubdir, Meriem; Bowcock, Themistocles; Bowen, Espen Eie; Bozzi, Concezio; Braun, Svende; Britton, Thomas; Brodzicka, Jolanta; Buchanan, Emma; Burr, Christopher; Bursche, Albert; Buytaert, Jan; Cadeddu, Sandro; Calabrese, Roberto; Calvi, Marta; Calvo Gomez, Miriam; Camboni, Alessandro; Campana, Pierluigi; Campora Perez, Daniel Hugo; Capriotti, Lorenzo; Carbone, Angelo; Carboni, Giovanni; Cardinale, Roberta; Cardini, Alessandro; Carniti, Paolo; Carson, Laurence; Carvalho Akiba, Kazuyoshi; Casse, Gianluigi; Cassina, Lorenzo; Castillo Garcia, Lucia; Cattaneo, Marco; Cavallero, Giovanni; Cenci, Riccardo; Chamont, David; Charles, Matthew; Charpentier, Philippe; Chatzikonstantinidis, Georgios; Chefdeville, Maximilien; Chen, Shanzhen; Cheung, Shu-Faye; Chobanova, Veronika; Chrzaszcz, Marcin; Chubykin, Alexsei; Cid Vidal, Xabier; Ciezarek, Gregory; Clarke, Peter; Clemencic, Marco; Cliff, Harry; Closier, Joel; Coco, Victor; Cogan, Julien; Cogneras, Eric; Cogoni, Violetta; Cojocariu, Lucian; Collins, Paula; Comerma-Montells, Albert; Contu, Andrea; Cook, Andrew; Coombs, George; Coquereau, Samuel; Corti, Gloria; Corvo, Marco; Costa Sobral, Cayo Mar; Couturier, Benjamin; Cowan, Greig; Craik, Daniel Charles; Crocombe, Andrew; Cruz Torres, Melissa Maria; Cunliffe, Samuel; Currie, Robert; D'Ambrosio, Carmelo; Da Cunha Marinho, Franciole; Dall'Occo, Elena; Dalseno, Jeremy; David, Pieter; Davis, Adam; De Bruyn, Kristof; De Capua, Stefano; De Cian, Michel; De Miranda, Jussara; De Paula, Leandro; De Serio, Marilisa; De Simone, Patrizia; Dean, Cameron Thomas; Decamp, Daniel; Deckenhoff, Mirko; Del Buono, Luigi; Dembinski, Hans Peter; Demmer, Moritz; Dendek, Adam; Derkach, Denis; Deschamps, Olivier; Dettori, Francesco; Dey, Biplab; Di Canto, Angelo; Di Nezza, Pasquale; Dijkstra, Hans; Dordei, Francesca; Dorigo, Mirco; Dosil Suárez, Alvaro; Dovbnya, Anatoliy; Dreimanis, Karlis; Dufour, Laurent; Dujany, Giulio; Dungs, Kevin; Durante, Paolo; Dzhelyadin, Rustem; Dziewiecki, Michal; Dziurda, Agnieszka; Dzyuba, Alexey; Déléage, Nicolas; Easo, Sajan; Ebert, Marcus; Egede, Ulrik; Egorychev, Victor; Eidelman, Semen; Eisenhardt, Stephan; Eitschberger, Ulrich; Ekelhof, Robert; Eklund, Lars; Ely, Scott; Esen, Sevda; Evans, Hannah Mary; Evans, Timothy; Falabella, Antonio; Farley, Nathanael; Farry, Stephen; Fay, Robert; Fazzini, Davide; Ferguson, Dianne; Fernandez, Gerard; Fernandez Prieto, Antonio; Ferrari, Fabio; Ferreira Rodrigues, Fernando; Ferro-Luzzi, Massimiliano; Filippov, Sergey; Fini, Rosa Anna; Fiore, Marco; Fiorini, Massimiliano; Firlej, Miroslaw; Fitzpatrick, Conor; Fiutowski, Tomasz; Fleuret, Frederic; Fohl, Klaus; Fontana, Marianna; Fontanelli, Flavio; Forshaw, Dean Charles; Forty, Roger; Franco Lima, Vinicius; Frank, Markus; Frei, Christoph; Fu, Jinlin; Funk, Wolfgang; Furfaro, Emiliano; Färber, Christian; Gallas Torreira, Abraham; Galli, Domenico; Gallorini, Stefano; Gambetta, Silvia; Gandelman, Miriam; Gandini, Paolo; Gao, Yuanning; Garcia Martin, Luis Miguel

    2017-06-21

    A search for the rare decays $B_s^0\\to\\tau^+\\tau^-$ and $B^0\\to\\tau^+\\tau^-$ is performed using proton$-$proton collision data collected with the LHCb detector. The data sample corresponds to an integrated luminosity of 3fb$^{-1}$ collected in 2011 and 2012. The $\\tau$ leptons are reconstructed through the decay $\\tau^-\\to\\pi^-\\pi^+\\pi^-\

  3. 脑脊液tau蛋白预测阿尔茨海默病的Meta分析%Clinical value of tau protein in cerebrospinal fluid for prediction of Alzheimer's disease: a Meta-analysis

    Institute of Scientific and Technical Information of China (English)

    耿劲松; 董建成; 倪衡建; 施李丽; 吴辉群; 蒋葵

    2011-01-01

    Objective To evaluate the efficiency and accuracy of total tau (t-tau) and phosphorylated tau (p-tau) proteins in cerebrospinal fluid (CSF) as biomarkers for predicting Alzheimer's disease (AD). Methods The published clinical literatures which aimed to investigate the concentration of tau protein to predict the conversion of mild cognitive impairment (MCI) to AD were retrieved. The quality of all the included literatures was assessed. Meta-analysis was carried out by the software Review Manager 5. 1 and Meta Disk 1.4. Results Fifteen literatures that met the inclusion criteria were included in this study. The baseline concentrations (pg,/mL) of both t-tau and p-tau in MCI to AD patients were higher than those in control group. The weighted mean difference (WMD) of t-tau in MCI to AD patients was 320.7, 95%CI: 274.2-367.3, and WMD of p-tau was 32.8, 95%CI: 29.5-36.0). Overall diagnostic odds ratios (DOR) of t-tau and p-tau were 14.1 (95% CI: 8.2-24.4) and 22.4 (95% CI: 10.4-48.3) respectively. Conclusion Tau in CSF may be an important diagnostic marker for predicting AD.%目的 评价脑脊液(CSF)总tau蛋白(t-tau)和磷酸化tau蛋白(P-tau)浓度预测阿尔茨海默病(Alzheimer'S disease,AD)的有效性和准确性.方法 全面检索tau蛋白浓度预测轻度认知功能障碍(mild cognitive impairment,MCI)转化为AD的诊断性试验文献,评价纳入文献的质量,用Review Manager 5.1和Meta Disk 1.4软件进行Meta分析,计算合并效应量.结果 共纳入15项研究,MCI进展为AD的t-tau基线浓度(pg/mL)高于对照组[加权均数差(WMD):320.7;95%CI:274.2~367.3],p-tau基线浓度(pg/mL)亦高于时照组(WMD:32.8;95%CI:29.5~36.0).t-tau预测AD的诊断优势比(diagnostic odds ration,DOR)为14.1(95%CI:8.2~24.4);p-tau的DOR为22.4(95%CI:10.4~48.3).结果 CSF中tau蛋白可作为预测AD发生的重要指标.

  4. Measurement of the $Z \\to \\tau\\tau$ Cross Section with the ATLAS Detector

    CERN Document Server

    Aad, Georges; Abdallah, Jalal; Abdelalim, Ahmed Ali; Abdesselam, Abdelouahab; Abdinov, Ovsat; Abi, Babak; Abolins, Maris; Abramowicz, Halina; Abreu, Henso; Acerbi, Emilio; Acharya, Bobby Samir; Adams, David; Addy, Tetteh; Adelman, Jahred; Aderholz, Michael; Adomeit, Stefanie; Adragna, Paolo; Adye, Tim; Aefsky, Scott; Aguilar-Saavedra, Juan Antonio; Aharrouche, Mohamed; Ahlen, Steven; Ahles, Florian; Ahmad, Ashfaq; Ahsan, Mahsana; Aielli, Giulio; Akdogan, Taylan; Akesson, Torsten Paul; Akimoto, Ginga; Akimov, Andrei; Akiyama, Kunihiro; Alam, Mohammad; Alam, Muhammad Aftab; Albert, Justin; Albrand, Solveig; Aleksa, Martin; Aleksandrov, Igor; Alessandria, Franco; Alexa, Calin; Alexander, Gideon; Alexandre, Gauthier; Alexopoulos, Theodoros; Alhroob, Muhammad; Aliev, Malik; Alimonti, Gianluca; Alison, John; Aliyev, Magsud; Allport, Phillip; Allwood-Spiers, Sarah; Almond, John; Aloisio, Alberto; Alon, Raz; Alonso, Alejandro; Alviggi, Mariagrazia; Amako, Katsuya; Amaral, Pedro; Amelung, Christoph; Ammosov, Vladimir; Amorim, Antonio; Amoros, Gabriel; Amram, Nir; Anastopoulos, Christos; Andari, Nansi; Andeen, Timothy; Anders, Christoph Falk; Anderson, Kelby; Andreazza, Attilio; Andrei, George Victor; Andrieux, Marie-Laure; Anduaga, Xabier; Angerami, Aaron; Anghinolfi, Francis; Anjos, Nuno; Annovi, Alberto; Antonaki, Ariadni; Antonelli, Mario; Antonov, Alexey; Antos, Jaroslav; Anulli, Fabio; Aoun, Sahar; Aperio Bella, Ludovica; Apolle, Rudi; Arabidze, Giorgi; Aracena, Ignacio; Arai, Yasuo; Arce, Ayana; Archambault, John-Paul; Arfaoui, Samir; Arguin, Jean-Francois; Arik, Engin; Arik, Metin; Armbruster, Aaron James; Arnaez, Olivier; Arnault, Christian; Artamonov, Andrei; Artoni, Giacomo; Arutinov, David; Asai, Shoji; Asfandiyarov, Ruslan; Ask, Stefan; Asman, Barbro; Asquith, Lily; Assamagan, Ketevi; Astbury, Alan; Astvatsatourov, Anatoli; Atoian, Grigor; Aubert, Bernard; Auerbach, Benjamin; Auge, Etienne; Augsten, Kamil; Aurousseau, Mathieu; Austin, Nicholas; Avolio, Giuseppe; Avramidou, Rachel Maria; Axen, David; Ay, Cano; Azuelos, Georges; Azuma, Yuya; Baak, Max; Baccaglioni, Giuseppe; Bacci, Cesare; Bach, Andre; Bachacou, Henri; Bachas, Konstantinos; Bachy, Gerard; Backes, Moritz; Backhaus, Malte; Badescu, Elisabeta; Bagnaia, Paolo; Bahinipati, Seema; Bai, Yu; Bailey, David; Bain, Travis; Baines, John; Baker, Oliver Keith; Baker, Mark; Baker, Sarah; Baltasar Dos Santos Pedrosa, Fernando; Banas, Elzbieta; Banerjee, Piyali; Banerjee, Swagato; Banfi, Danilo; Bangert, Andrea Michelle; Bansal, Vikas; Bansil, Hardeep Singh; Barak, Liron; Baranov, Sergei; Barashkou, Andrei; Galtieri, Angela Barbaro; Barber, Tom; Barberio, Elisabetta Luigia; Barberis, Dario; Barbero, Marlon; Bardin, Dmitri; Barillari, Teresa; Barisonzi, Marcello; Barklow, Timothy; Barlow, Nick; Barnett, Bruce; Barnett, Michael; Baroncelli, Antonio; Barone, Gaetano; Barr, Alan; Barreiro, Fernando; Barreiro Guimaraes da Costa, Joao; Barrillon, Pierre; Bartoldus, Rainer; Barton, Adam Edward; Bartsch, Detlef; Bartsch, Valeria; Bates, Richard; Batkova, Lucia; Batley, Richard; Battaglia, Andreas; Battistin, Michele; Battistoni, Giuseppe; Bauer, Florian; Bawa, Harinder Singh; Beare, Brian; Beau, Tristan; Beauchemin, Pierre-Hugues; Beccherle, Roberto; Bechtle, Philip; Beck, Hans Peter; Beckingham, Matthew; Becks, Karl-Heinz; Beddall, Andrew; Beddall, Ayda; Bedikian, Sourpouhi; Bednyakov, Vadim; Bee, Christopher; Begel, Michael; Behar Harpaz, Silvia; Behera, Prafulla; Beimforde, Michael; Belanger-Champagne, Camille; Bell, Paul; Bell, William; Bella, Gideon; Bellagamba, Lorenzo; Bellina, Francesco; Bellomo, Massimiliano; Belloni, Alberto; Beloborodova, Olga; Belotskiy, Konstantin; Beltramello, Olga; Ben Ami, Sagi; Benary, Odette; Benchekroun, Driss; Benchouk, Chafik; Bendel, Markus; Benedict, Brian Hugues; Benekos, Nektarios; Benhammou, Yan; Benjamin, Douglas; Benoit, Mathieu; Bensinger, James; Benslama, Kamal; Bentvelsen, Stan; Berge, David; Bergeaas Kuutmann, Elin; Berger, Nicolas; Berghaus, Frank; Berglund, Elina; Beringer, Jurg; Bernardet, Karim; Bernat, Pauline; Bernhard, Ralf; Bernius, Catrin; Berry, Tracey; Bertin, Antonio; Bertinelli, Francesco; Bertolucci, Federico; Besana, Maria Ilaria; Besson, Nathalie; Bethke, Siegfried; Bhimji, Wahid; Bianchi, Riccardo-Maria; Bianco, Michele; Biebel, Otmar; Bieniek, Stephen Paul; Biesiada, Jed; Biglietti, Michela; Bilokon, Halina; Bindi, Marcello; Binet, Sebastien; Bingul, Ahmet; Bini, Cesare; Biscarat, Catherine; Bitenc, Urban; Black, Kevin; Blair, Robert; Blanchard, Jean-Baptiste; Blanchot, Georges; Blazek, Tomas; Blocker, Craig

    2011-01-01

    The Z to tau tau cross section is measured with the ATLAS experiment at the LHC in four different final states determined by the decay modes of the tau leptons: muon-hadron, electron-hadron, electron-muon, and muon-muon. The analysis is based on a data sample corresponding to an integrated luminosity of 36 pb^(-1), at a proton-proton center-of-mass energy of sqrt(s) = 7 TeV. Cross sections are measured separately for each final state in fiducial regions of high detector acceptance, as well as in the full phase space, over the mass region 66 - 116 GeV. The individual cross sections are combined and the product of the total Z production cross section and Z to tau tau branching fraction is measured to be 0.97 +/- 0.07(stat) +/- 0.06(syst) +/- 0.03(lumi), in agreement with NNLO calculations.

  5. Tau flavored dark matter and its impact on tau Yukawa coupling

    CERN Document Server

    Chao, Wei; Li, Hao-Lin

    2016-01-01

    In this paper we preform a systematic study of the tau flavored dark matter model by introducing two kinds of mediators (a scalar doublet and a charged scalar singlet). The electromagnetic properties of the dark matter, as well as their implications in dark matter direct detections, are analyzed in detail. The model turns out contributing a significant radiative correction to the tau lepton mass, in addition to loosing the tension between the measured dark matter relic density and constraints of dark matter direct detections. The loop corrections can be ${\\cal O}(10\\%)$ of the total tau mass. Signal rates of the Higgs measurements from the LHC in the $h\\to\\tau \\tau$ and $h\\to \\gamma \\gamma$ channels, relative to the Standard Model expectations, can be explained in this model.

  6. $\\tau$ appearance and CNGS

    CERN Document Server

    Komatsu, M

    2002-01-01

    In December 1999, the CERN Council approved the CNGS project to explore neutrino oscillation physics in tau neutrino appearance. Super-KAMIOKANDE result indicate that the most probable solution in atmospheric neutrino disappearance is muon neutrino oscillation into a tau neutrino. CNGS is designed to detect nu /sub mu / to nu /sub tau / oscillations by a long baseline appearance experiment. CNGS a more is unique project than the other disappearance projects like K2K and NuMI. At least two experiments are in preparation in the CNGS project at LNGS. One is OPERA which was already approved in Feb. 2001 as CNGS1 using emulsion techniques which have proven their tau detection capability in Fermilab E872 DONUT. The other is ICARUS which was approved at LNGS using a liquid argon TPC. Both experiments will detect tau neutrino signal in theCNGS beam. (5 refs).

  7. Molecular CsF 5 and CsF 2 +

    KAUST Repository

    Rogachev, Andrey Yu.

    2015-06-03

    D5h star-like CsF5, formally isoelectronic with known XeF5− ion, is computed to be a local minimum on the potential energy surface of CsF5, surrounded by reasonably large activation energies for its exothermic decomposition to CsF+2 F2, or to CsF3 (three isomeric forms)+F2, or for rearrangement to a significantly more stable isomer, a classical Cs+ complex of F5−. Similarly the CsF2+ ion is computed to be metastable in two isomeric forms. In the more symmetrical structures of these molecules there is definite involvement in bonding of the formally core 5p levels of Cs.

  8. Orbital motions and light curves of young binaries XZ Tau and VY Tau

    CERN Document Server

    Dodin, A V; Zharova, A V; Lamzin, S A; Malogolovets, E V; Roe, J M

    2015-01-01

    The results of our speckle interferometric observations of young binaries VY Tau and XZ Tau are presented. For the first time, we found a relative displacement of VY Tau components as well as a preliminary orbit for XZ Tau. It appeared that the orbit is appreciably non-circular and is inclined by $i \\lesssim 47^o$ from the plane of the sky. It means that the rotation axis of XZ Tau A and the axis of its jet are significantly non-perpendicular to the orbital plane. We found that the average brightness of XZ Tau had been increasing from the beginning of the last century up to the mid-thirties and then it decreased by $\\Delta B > 2$ mag. The maximal brightness has been reached significantly later on the time of periastron passage. The total brightness of XZ Tau's components varied in a non-regular way from 1970 to 1985 when eruptions of hot gas from XZ Tau A presumably had occurred. In the early nineties the variations became regular following which a chaotic variability had renewed. We also report that a flare ...

  9. Improved measurement of $\\psi (2S)$ decays into $\\tau ^{+}\\tau ^{-}$

    CERN Document Server

    Ablikim, M; Ban, Y; Bian, J G; Cai, X; Chen, H F; Chen, H S; Chen, H X; Chen, J C; Jin, C; Chen, Y B; Chi, S P; Chu, Y P; Cui, X Z; Dai, Y S; Diao, L Y; Deng, Z Y; Dong, Q F; Du, S X; Fang, J; Fang, S S; Fu, C D; Gao, C S; Gao, Y N; Gu, S D; Gu, Y T; Guo, Y N; Guo, Y Q; Guo, Z J; Harris, F A; He, K L; He, M; Heng, Y K; Hu, H M; Hu, T; Huang, G S; Huang, X T; Ji, X B; Jiang, X S; Jiang, X Y; Jiao, J B; Jin, D P; Jin, S; Yi, J; Lai, Y F; Li, G; Li, H B; Li, H H; Li, J; Li, R Y; Li, S M; Li, W D; Li, W G; Li, X L; Li, X N; Li, X Q; Li, Y L; Liang, Y F; Liao, H B; Liu, B J; Liu, C X; Liu, F; Fang, L; Liu, H H; Liu, H M; Liu, J; Liu, J B; Liu, J P; Liu, Q; Liu, R G; Liu, Z A; Lou, Y C; Lu, F; Lu, G R; Lu, J G; Luo, C L; Ma, F C; Ma, H L; Ma, L L; Ma, Q M; Ma, X B; Mao, Z P; Mo, X H; Nie, J; Olsen, S L; Peng, H P; Ping, R G; Qi, N D; Qin, H; Qiu, J F; Ren, Z Y; Rong, G; Shan, L Y; Shang, L; Shen, C P; Shen, D L; Shen, X Y; Sheng, H Y; Sun, H S; Sun, J F; Sun, S S; Sun, Y Z; Sun, Z J; Tan, Z Q; Tang, X; Tong, G L; Varner, G S; Wang, D Y; Wang, L; Wang, L L; Wang, L S; Wang, M; Wang, P; Wang, P L; Wang, W F; Wang, Y F; Wang, Z; Wang, Z Y; Zhe, W Z W; Wei, C L; Wei, D H; Wu, N; Xia, X M; Xie, X X; Xu, G F; Xu, X P; Xu, Y; Yan, M L; Yang, H X; Yang, Y X; Ye, M H; Ye, Y X; Yi, Z Y; Yu, G W; Yuan, C Z; Yuan, J M; Yuan, Y; Zang, S L; Zeng, Y; Zhang, B X; Zhang, B Y; Zhang, C C; Zhang, D H; Zhang, H Q; Zhang, H Y; Zhang, J W; Zhang, J Y; Zhang, S H; Zhang, X M; Zhang, X Y; Yiyun, Z; Zhang, Z P; Zhao, D X; Zhao, J W; Zhao, M G; Zhao, P P; Zhao, W R; Zhao, Z G; Zheng, H Q; Zheng, J P; Zheng, Z P; Zhou, L; Zhou, N F; Zhu, K J; Zhu, Q M; Zhu, Y C; Zhu, Y S; Yingchun, Z; Zhu, Z A; Zhuang, B A; Zhuang, X A; Zou, B S

    2006-01-01

    Using 14M $\\psi (2S)$ events collected at BESII, the branching fraction of $\\psi (2S)\\to \\tau ^{+}\\tau ^{-}$ is measured to be $Br_{\\tau \\tau}=(3.10\\pm 0.21\\pm 0.38)\\times 10^{-3}$, where the first error is statistical and the second is systematic.

  10. Humanized Chronic Graft-versus-Host Disease in NOD-SCID il2rγ-/- (NSG Mice with G-CSF-Mobilized Peripheral Blood Mononuclear Cells following Cyclophosphamide and Total Body Irradiation.

    Directory of Open Access Journals (Sweden)

    Hisaki Fujii

    Full Text Available Chronic graft-versus-host disease (cGvHD is the major source of late phase morbidity and mortality after allogeneic hematopoietic stem cell transplantation. Humanized acute GvHD (aGvHD in vivo models using NOD-SCID il2rγ-/- (NSG mice are well described and are important tools for investigating pathogenicity of human cells in vivo. However, there have been only few reported humanized cGvHD mouse models. We evaluated if prolonged inflammation driven by low dose G-CSF-mobilized human PBMCs (G-hPBMCs would lead to cGvHD following cyclophosphamide (CTX administration and total body irradiation (TBI in NSG mice. Engraftment was assessed in peripheral blood (PB and in specific target organs by either flow cytometry or immunohistochemistry (IHC. Tissue samples were harvested 56 days post transplantation and were evaluated by a pathologist. Some mice were kept for up to 84 days to evaluate the degree of fibrosis. Mice that received CTX at 20mg/kg did not show aGvHD with stable expansion of human CD45+ CD3+ T-cells in PB (mean; 5.8 to 23.2%. The pathology and fibrosis scores in the lung and the liver were significantly increased with aggregation of T-cells and hCD68+ macrophages. There was a correlation between liver pathology score and the percentage of hCD68+ cells, suggesting the role of macrophage in fibrogenesis in NSG mice. In order to study long-term survival, 6/9 mice who survived more than 56 days showed increased fibrosis in the lung and liver at the endpoint, which suggests the infiltrating hCD68+ macrophages may be pathogenic. It was shown that the combination of CTX and TBI with a low number of G-hPBMCs (1x106 leads to chronic lung and liver inflammation driven by a high infiltration of human macrophage and mature human T cells from the graft, resulting in fibrosis of lung and liver in NSG mice. In conclusion this model may serve as an important pre-clinical model to further current understanding of the roles of human macrophages in cGvHD.

  11. Humanized Chronic Graft-versus-Host Disease in NOD-SCID il2rγ-/- (NSG) Mice with G-CSF-Mobilized Peripheral Blood Mononuclear Cells following Cyclophosphamide and Total Body Irradiation.

    Science.gov (United States)

    Fujii, Hisaki; Luo, Zhi-Juan; Kim, Hye Jin; Newbigging, Susan; Gassas, Adam; Keating, Armand; Egeler, R Maarten

    2015-01-01

    Chronic graft-versus-host disease (cGvHD) is the major source of late phase morbidity and mortality after allogeneic hematopoietic stem cell transplantation. Humanized acute GvHD (aGvHD) in vivo models using NOD-SCID il2rγ-/- (NSG) mice are well described and are important tools for investigating pathogenicity of human cells in vivo. However, there have been only few reported humanized cGvHD mouse models. We evaluated if prolonged inflammation driven by low dose G-CSF-mobilized human PBMCs (G-hPBMCs) would lead to cGvHD following cyclophosphamide (CTX) administration and total body irradiation (TBI) in NSG mice. Engraftment was assessed in peripheral blood (PB) and in specific target organs by either flow cytometry or immunohistochemistry (IHC). Tissue samples were harvested 56 days post transplantation and were evaluated by a pathologist. Some mice were kept for up to 84 days to evaluate the degree of fibrosis. Mice that received CTX at 20mg/kg did not show aGvHD with stable expansion of human CD45+ CD3+ T-cells in PB (mean; 5.8 to 23.2%). The pathology and fibrosis scores in the lung and the liver were significantly increased with aggregation of T-cells and hCD68+ macrophages. There was a correlation between liver pathology score and the percentage of hCD68+ cells, suggesting the role of macrophage in fibrogenesis in NSG mice. In order to study long-term survival, 6/9 mice who survived more than 56 days showed increased fibrosis in the lung and liver at the endpoint, which suggests the infiltrating hCD68+ macrophages may be pathogenic. It was shown that the combination of CTX and TBI with a low number of G-hPBMCs (1x106) leads to chronic lung and liver inflammation driven by a high infiltration of human macrophage and mature human T cells from the graft, resulting in fibrosis of lung and liver in NSG mice. In conclusion this model may serve as an important pre-clinical model to further current understanding of the roles of human macrophages in cGvHD.

  12. BACE1 gene variants do not influence BACE1 activity, levels of APP or Aβ isoforms in CSF in Alzheimer's disease

    Directory of Open Access Journals (Sweden)

    Minthon Lennart

    2010-09-01

    Full Text Available Abstract The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD. BACE1 is the most important β-secretase responsible for the generation of Alzheimer-associated amyloid β-proteins (Aβ and may play a role in the amyloidogenic process in AD. We hypothesized that BACE1 gene variants might influence BACE1 activity or other markers for APP metabolism in the cerebrospinal fluid (CSF and thereby contribute to the development of AD. We genotyped a Swedish sample of 269 AD patients for the rs638405 single nucleotide polymorphism (SNP in the BACE1 gene and correlated genotype data to a broad range of amyloid-related biomarkers in CSF, including BACE1 activity, levels of Aβ40, Aβ42, α- and β-cleaved soluble APP (α-sAPP and β-sAPP, as well as markers for Alzheimer-type axonal degeneration, i.e., total-tau and phospho-tau181. Gene variants of BACE1 were neither associated with amyloid-related biomarkers, nor with markers for axonal degeneration in AD.

  13. The ATLAS Tau Trigger

    CERN Document Server

    Rados, PK; The ATLAS collaboration

    2014-01-01

    Physics processes involving tau leptons play a crucial role in understanding particle physics at the high energy frontier. The ability to efficiently trigger on events containing hadronic tau decays is therefore of particular importance to the ATLAS experiment. During the 2012 run, the Large Hadronic Collder (LHC) reached instantaneous luminosities of nearly $10^{34} cm^{-2}s^{-1}$ with bunch crossings occurring every $50 ns$. This resulted in a huge event rate and a high probability of overlapping interactions per bunch crossing (pile-up). With this in mind it was necessary to design an ATLAS tau trigger system that could reduce the event rate to a manageable level, while efficiently extracting the most interesting physics events in a pile-up robust manner. In this poster the ATLAS tau trigger is described, its performance during 2012 is presented, and the outlook for the LHC Run II is briefly summarized.

  14. The disk around the brown dwarf KPNO Tau 3

    CERN Document Server

    Broekhoven-Fiene, Hannah; Duchene, Gaspard; Di Francesco, James; Scholz, Aleks; Chrysostomou, Antonio; Jayawardhana, Ray

    2014-01-01

    We present submillimeter observations of the young brown dwarfs KPNO Tau 1, KPNO Tau 3, and KPNO Tau 6 at 450 micron and 850 micron taken with the Submillimeter Common-User Bolometer Array on the James Clerke Maxwell Telescope. KPNO Tau 3 and KPNO Tau 6 have been previously identified as Class II objects hosting accretion disks, whereas KPNO Tau 1 has been identified as a Class III object and shows no evidence of circumsubstellar material. Our 3 sigma detection of cold dust around KPNO Tau 3 implies a total disk mass of (4.0 +/- 1.1) x 10^{-4} Msolar (assuming a gas to dust ratio of 100:1). We place tight constraints on any disks around KPNO Tau 1 or KPNO Tau 6 of <2.1 x 10^{-4} Msolar and <2.7 x 10^{-4} Msolar, respectively. Modeling the spectral energy distribution of KPNO Tau 3 and its disk suggests the disk properties (geometry, dust mass, and grain size distribution) are consistent with observations of other brown dwarf disks and low-mass T-Tauri stars. In particular, the disk-to-host mass ratio fo...

  15. Critical role of acetylation in tau-mediated neurodegeneration and cognitive deficits.

    Science.gov (United States)

    Min, Sang-Won; Chen, Xu; Tracy, Tara E; Li, Yaqiao; Zhou, Yungui; Wang, Chao; Shirakawa, Kotaro; Minami, S Sakura; Defensor, Erwin; Mok, Sue Ann; Sohn, Peter Dongmin; Schilling, Birgit; Cong, Xin; Ellerby, Lisa; Gibson, Bradford W; Johnson, Jeffrey; Krogan, Nevan; Shamloo, Mehrdad; Gestwicki, Jason; Masliah, Eliezer; Verdin, Eric; Gan, Li

    2015-10-01

    Tauopathies, including frontotemporal dementia (FTD) and Alzheimer's disease (AD), are neurodegenerative diseases in which tau fibrils accumulate. Recent evidence supports soluble tau species as the major toxic species. How soluble tau accumulates and causes neurodegeneration remains unclear. Here we identify tau acetylation at Lys174 (K174) as an early change in AD brains and a critical determinant in tau homeostasis and toxicity in mice. The acetyl-mimicking mutant K174Q slows tau turnover and induces cognitive deficits in vivo. Acetyltransferase p300-induced tau acetylation is inhibited by salsalate and salicylate, which enhance tau turnover and reduce tau levels. In the PS19 transgenic mouse model of FTD, administration of salsalate after disease onset inhibited p300 activity, lowered levels of total tau and tau acetylated at K174, rescued tau-induced memory deficits and prevented hippocampal atrophy. The tau-lowering and protective effects of salsalate were diminished in neurons expressing K174Q tau. Targeting tau acetylation could be a new therapeutic strategy against human tauopathies.

  16. Z' to tau tau - emu final state

    CERN Document Server

    CMS Collaboration

    2015-01-01

    A search for new physics beyond the standard model in the high-mass ditau final state with one tau decaying in the electron channel and one tau decaying in the muon channel is performed using proton-proton collisions at $\\sqrt{s}$ = 8 TeV recorded by the CMS experiment at the LHC. The data correspond to an integrated luminosity of 19.7 fb$^{-1}$. The data are in good agreement with the standard model prediction. An upper limit at 95$\\%$ CL on the product of cross section times branching fraction into tau pairs is calculated as a function of the resonance mass for the Sequential Standard Model $Z'$ ($Z'_{SSM}$ masses excluded up to 1300 GeV) and for the GUT-inspired $E_6$ model ($Z'_{\\psi}$ masses excluded up to 810 GeV). The results are further interpreted in terms of the Arkani-Hamed, Dimopolous, and Dvali (ADD) model, setting an exclusion limit on the parameter $\\Lambda_T$ up to 2800 GeV.

  17. Measurements of the tau Mass and Mass Difference of the tau^+ and tau^- at BABAR

    Energy Technology Data Exchange (ETDEWEB)

    Aubert, B.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; /Annecy, LAPP; Garra Tico, J.; Grauges, E.; /Barcelona U., ECM; Martinelli, M.; Palano, A.; Pappagallo, M.; /INFN, Bari /Bari U.; Eigen, G.; Stugu, B.; Sun, L.; /Bergen U.; Battaglia, M.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /INFN, Naples /Naples U. /INFN, Naples /INFN, Naples /Naples U. /NIKHEF, Amsterdam /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /Pennsylvania U. /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2009-10-30

    The authors present the result of a precision measurement of the mass of the {tau} lepton, M{sub {tau}}, based on 423 fb{sup -1} of data recorded at the {Upsilon}(4S) resonance with the BABAR detector. Using a pseudomass endpoint method, they determine the mass to be 1776.68 {+-} 0.12(stat) {+-} 0.41(syst) MeV. They also measure the mass difference between the {tau}{sup +} and {tau}{sup -}, and obtain (M{sub {tau}{sup +}} - M{sub {tau}{sup -}})/M{sub AVG}{sup {tau}} = (-3.4 {+-} 1.3(stat) {+-} 0.3(syst)) x 10{sup -4}, where M{sub AVG}{sup {tau}} is the average value of M{sub {tau}{sup +}} and M{sub {tau}{sup -}}.

  18. Study of tau-pair production at HERA

    Energy Technology Data Exchange (ETDEWEB)

    Abramowicz, H. [Tel Aviv Univ. (Israel). School of Physics; Max Planck Institute for Physics, Munich (Germany); Adamczyk, L. [AGH-Univ. of Science and Technology, Cracow (Poland). Faculty of Physics and Applied Computer Science; Adamus, M. [Institute for Nuclear Studies, Warsaw (PL)] (and others)

    2010-12-15

    A study of events containing two tau leptons with high transverse momentum has been performed with the ZEUS detector at HERA, using a data sample corresponding to an integrated luminosity of 0.33 fb{sup -1}. The tau candidates were identified from their decays into electrons, muons or hadronic jets. The number of tau-pair candidates has been compared with the prediction from the Standard Model, where the largest contribution is expected from Bethe-Heitler processes. The total visible cross section was extracted. Standard Model expectations agree well with the measured distributions, also at high invariant mass of the tau pair. (orig.)

  19. Tau-positive nuclear indentations in P301S tauopathy mice.

    Science.gov (United States)

    Fernández-Nogales, Marta; Santos-Galindo, María; Merchán-Rubira, Jesús; Hoozemans, Jeroen J M; Rábano, Alberto; Ferrer, Isidro; Avila, Jesús; Hernández, Félix; Lucas, José J

    2016-06-24

    Increased incidence of neuronal nuclear indentations is a well-known feature of the striatum of Huntington's disease (HD) brains and, in Alzheimer's disease (AD), neuronal nuclear indentations have recently been reported to correlate with neurotoxicity caused by improper cytoskeletal/nucleoskeletal coupling. Initial detection of rod-shaped tau immunostaining in nuclei of cortical and striatal neurons of HD brains and in hippocampal neurons of early Braak stage AD led us to coin the term "tau nuclear rods (TNRs)." Although TNRs traverse nuclear space, they in fact occupy narrow cytoplasmic extensions that fill indentations of the nuclear envelope and we will here refer to this histological hallmark as Tau-immunopositive nuclear indentations (TNIs). We reasoned that TNI formation is likely secondary to tau alterations as TNI detection in HD correlates with an increase in total tau, particularly of the isoforms with four tubulin binding repeats (4R-tau). Here we analyze transgenic mice that overexpress human 4R-tau with a frontotemporal lobar degeneration-tau point mutation (P301S mice) to explore whether tau alteration is sufficient for TNI formation. Immunohistochemistry with various tau antibodies, immunoelectron microscopy and double tau-immunofluorescence/DAPI-nuclear counterstaining confirmed that excess 4R-tau in P301S mice is sufficient for the detection of abundant TNIs that fill nuclear indentations. Interestingly, this does not correlate with an increase in the number of nuclear indentations, thus suggesting that excess total tau or an isoform imbalance in favor of 4R-tau facilitates tau detection inside preexisting nuclear indentations but does not induce formation of the latter. In summary, here we demonstrate that tau alteration is sufficient for TNI detection and our results suggest that the neuropathological finding of TNIs becomes a possible indicator of increased total tau and/or increased 4R/3R-tau ratio in the affected neurons apart from being an

  20. Hyperphosphorylation-induced tau oligomers

    Directory of Open Access Journals (Sweden)

    Khalid eIqbal

    2013-08-01

    Full Text Available In normal adult brain the microtubule associated protein tau contains 2–3 phosphates per mole of the protein and at this level of phosphorylation it is a soluble cytosolic protein. The normal brain tau interacts with tubulin and promotes its assembly into microtubules and stabilizes these fibrils. In Alzheimer disease (AD brain tau is three to four fold hyperphosphorylated. The abnormally hyperphosphorylated tau binds to normal tau instead of the tubulin and this binding leads to the formation of tau oligomers. The tau oligomers can be sedimented at 200,000 x g whereas the normal tau under these conditions remains in the supernatant. The abnormally hyperphosphorylated tau is capable of sequestering not only normal tau but also microtubule associated protein (MAP MAP1 and MAP2 and causing disruption of the microtubule network promoted by these proteins. Unlike ABeta and prion protein (PrP oligomers, tau oligomerization in AD and related tauopathies is hyperphosphorylation-dependent; in vitro dephosphorylation of AD P-tau with protein phosphatase 2A (PP2A inhibits and rehyperphosphorylation of the PP2A-AD P-tau with more than one combination of tau protein kinases promotes its oligomerization. In physiological assembly conditions the AD P-tau readily self-assembles into paired helical filaments. Missense tau mutations found in frontotemporal dementia apparently lead to tau oligomerization and neurofibrillary pathology by promoting its abnormal hyperphosphorylation. Dysregulation of the alternative splicing of tau that alters the 1 : 1 ratio of the 3-repeat : 4-repeat taus such as in Down syndrome, Pick disease and progressive supranuclear palsy leads to the abnormal hyperphosphorylation of tau.

  1. Hyperphosphorylation-induced tau oligomers.

    Science.gov (United States)

    Iqbal, Khalid; Gong, Cheng-Xin; Liu, Fei

    2013-01-01

    In normal adult brain the microtubule associated protein (MAP) tau contains 2-3 phosphates per mol of the protein and at this level of phosphorylation it is a soluble cytosolic protein. The normal brain tau interacts with tubulin and promotes its assembly into microtubules and stabilizes these fibrils. In Alzheimer disease (AD) brain tau is three to fourfold hyperphosphorylated. The abnormally hyperphosphorylated tau binds to normal tau instead of the tubulin and this binding leads to the formation of tau oligomers. The tau oligomers can be sedimented at 200,000 × g whereas the normal tau under these conditions remains in the supernatant. The abnormally hyperphosphorylated tau is capable of sequestering not only normal tau but also MAP MAP1 and MAP2 and causing disruption of the microtubule network promoted by these proteins. Unlike Aβ and prion protein (PrP) oligomers, tau oligomerization in AD and related tauopathies is hyperphosphorylation-dependent; in vitro dephosphorylation of AD P-tau with protein phosphatase 2A (PP2A) inhibits and rehyperphosphorylation of the PP2A-AD P-tau with more than one combination of tau protein kinases promotes its oligomerization. In physiological assembly conditions the AD P-tau readily self-assembles into paired helical filaments. Missense tau mutations found in frontotemporal dementia apparently lead to tau oligomerization and neurofibrillary pathology by promoting its abnormal hyperphosphorylation. Dysregulation of the alternative splicing of tau that alters the 1:1 ratio of the 3-repeat: 4-repeat taus such as in Down syndrome, Pick disease, and progressive supranuclear palsy leads to the abnormal hyperphosphorylation of tau.

  2. Tau passive immunotherapy in mutant P301L mice: antibody affinity versus specificity.

    Directory of Open Access Journals (Sweden)

    Cristina d'Abramo

    Full Text Available The use of antibodies to treat neurodegenerative diseases has undergone rapid development in the past decade. To date, immunotherapeutic approaches to Alzheimer's disease have mostly targeted amyloid beta as it is a secreted protein that can be found in plasma and CSF and is consequently accessible to circulating antibodies. Few recent publications have suggested the utility of treatment of tau pathology with monoclonal antibodies to tau. Our laboratory has begun a systematic study of different classes of tau monoclonal antibodies using mutant P301L mice. Three or seven months old mutant tau mice were inoculated weekly with tau monoclonal antibodies at a dose of 10 mg/Kg, until seven or ten months of age were reached respectively. Our data strongly support the notion that in P301L animals treated with MC1, a conformational monoclonal antibody specific for PHF-tau, the rate of development of tau pathology is effectively reduced, while injecting DA31, a high affinity tau sequence antibody, does not exert such benefit. MC1 appears superior to DA31 in overall effects, suggesting that specificity is more important than affinity in therapeutic applications. Unfortunately the survival rate of the P301L treated mice was not improved when immunizing either with MC1 or PHF1, a high affinity phospho-tau antibody previously reported to be efficacious in reducing pathological tau. These data demonstrate that passive immunotherapy in mutant tau models may be efficacious in reducing the development of tau pathology, but a great deal of work remains to be done to carefully select the tau epitopes to target.

  3. NIA-AA staging of preclinical Alzheimer disease: discordance and concordance of CSF and imaging biomarkers.

    Science.gov (United States)

    Vos, Stephanie J B; Gordon, Brian A; Su, Yi; Visser, Pieter Jelle; Holtzman, David M; Morris, John C; Fagan, Anne M; Benzinger, Tammie L S

    2016-08-01

    The National Institute of Aging and Alzheimer's Association (NIA-AA) criteria for Alzheimer disease (AD) treat neuroimaging and cerebrospinal fluid (CSF) markers of AD pathology as if they would be interchangeable. We tested this assumption in 212 cognitively normal participants who have both neuroimaging and CSF measures of β-amyloid (CSF Aβ1-42 and positron emission tomography imaging with Pittsburgh Compound B) and neuronal injury (CSF t-tau and p-tau and structural magnetic resonance imaging) with longitudinal clinical follow-up. Participants were classified in preclinical AD stage 1 (β-amyloidosis) or preclinical AD stage 2+ (β-amyloidosis and neuronal injury) using the NIA-AA criteria, or in the normal or suspected non-Alzheimer disease pathophysiology group (neuronal injury without β-amyloidosis). At baseline, 21% of participants had preclinical AD based on CSF and 28% based on neuroimaging. Between modalities, staging was concordant in only 47% of participants. Disagreement resulted from low concordance between biomarkers of neuronal injury. Still, individuals in stage 2+ using either criterion had an increased risk for clinical decline. This highlights the heterogeneity of the definition of neuronal injury and has important implications for clinical trials using biomarkers for enrollment or as surrogate end point measures. Copyright © 2016 Elsevier Inc. All rights reserved.

  4. Tau Pathology and Parietal White Matter Lesions Have Independent but Synergistic Effects on Early Development of Alzheimer's Disease

    Directory of Open Access Journals (Sweden)

    Joakim Hertze

    2013-04-01

    Full Text Available Background: White matter lesions (WMLs are a common finding in patients with dementia. This study investigates the relationship between WMLs, hyperphosphorylated tau (P-tau in cerebrospinal fluid (CSF and apolipoprotein E (APOE ε4 genotype in prodromal Alzheimer's disease (AD. Methods: Baseline levels of tau, P-tau and β-amyloid 1-42 in CSF, the presence of WMLs in the brain, and the APOE genotype were ascertained in 159 patients with mild cognitive impairment (MCI and 38 cognitively healthy controls. Results: After 5.7 years, 58 patients had developed AD. In this group, patients with normal levels of CSF P-tau had higher levels of WMLs in the parietal regions than those with pathological P-tau levels (p Conclusions: We suggest that WMLs in parietal lobes and tau pathology likely have independent but synergistic effects on the reduction of the cognitive reserve capacity of the brain. In patients with a more low-grade AD pathology, WMLs in the parietal lobes might increase the risk of developing dementia.

  5. Glycemia and Levels of Cerebrospinal Fluid Amyloid and Tau in Patients Attending a Memory Clinic

    NARCIS (Netherlands)

    Exalto, Lieza G.; van der Flier, Wiesje M.; Scheltens, Phillip; Biessels, Geert Jan

    2010-01-01

    OBJECTIVES: To determine the association between markers of glycemia and cerebrospinal fluid (CSF) amyloid beta 1-42 (A beta 42) and tau levels in patients attending a memory clinic. DESIGN: Cross-sectional study. SETTING: Memory clinic. PARTICIPANTS: Two hundred forty-five consecutive patients atte

  6. A surgical method to improve the homeostasis of CSF for the treatment of Alzheimer’s disease

    Directory of Open Access Journals (Sweden)

    Yang Qin

    2016-11-01

    Full Text Available Reduced cerebrospinal fluid (CSF production and increased resistance to CSF outflow are considered to be associated with aging, and are also characteristics of Alzheimer disease (AD. These changes probably result in a decrease in the efficiency of the mechanism by which CSF removes toxic molecules such as amyloid-β (Aβ and tau from the interstitial fluid space. Soluble Aβ is potently neurotoxic and dysfunction in CSF circulation can accelerate the progression of AD. Current therapies for AD exhibit poor efficiency; therefore, a surgical method to improve the homeostasis of CSF is worthy of investigation. To achieve this, we conceived a novel device, which consists of a ventriculo-peritoneal shunt, an injection port and a portable infusion pump. Artificial CSF is pumped into the ventricles and the artificial CSF composition, infusion modes and pressure threshold of shunting can be adjusted according to the intracranial pressure and CSF contents. We hypothesize that this active treatment for CSF circulation dysfunction will significantly retard the progression of AD.

  7. Correlation between Cognitive Impairment and CSF Biomarkers in Amnesic MCI, non-Amnesic MCI, and Alzheimer's Disease

    NARCIS (Netherlands)

    Haldenwanger, A.; Eling, P.A.T.M.; Kastrup, A.; Hildebrandt, H.

    2010-01-01

    Decreased delayed recall, decreased amyloid-beta peptides (A beta(1-42)), and increased tau protein concentration in cerebrospinal fluid (CSF) are generally regarded to be valid neuropsychological and biological markers for Alzheimer's disease (AD). Previous studies failed to demonstrate clear-cut c

  8. A Search for the Decay B+ --> tau+ nu_tau

    CERN Document Server

    Aubert, B; Boutigny, D; Couderc, F; Karyotakis, Yu; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Graugès-Pous, E; Palano, A; Pappagallo, M; Pompili, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Breon, A B; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Gritsan, A V; Groysman, Y; Jacobsen, R G; Kadel, R W; Kadyk, J; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Morgan, S E; Watson, A T; Fritsch, M; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schröder, T; Steinke, M; Boyd, J T; Burke, J P; Chevalier, N; Cottingham, W N; Çuhadar-Dönszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Teodorescu, L; Blinov, A E; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Kravchenko, E A; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Yushkov, A N; Best, D; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M A; Mommsen, R K; Röthel, W; Stoker, D P; Buchanan, C; Hartfiel, B L; Weinstein, A J R; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; Del Re, D; Hadavand, H K; Hill, E J; MacFarlane, D B; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Mazur, M A; Richman, J D; Verkerke, W; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dubois-Felsmann, G P; Dvoretskii, A; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Andreassen, R; Jayatilleke, S M; Mancinelli, G; Meadows, B T; Sokoloff, M D; Blanc, F; Bloom, P; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nauenberg, U; Olivas, A; Rankin, P; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Zeng, Q; Altenburg, D; Feltresi, E; Hauke, A; Spaan, B; Brandt, T; Brose, J; Dickopp, M; Klose, V; Lacker, H M; Nogowski, R; Otto, S; Petzold, A; Schott, G; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Bernard, D; Bonneaud, G R; Grenier, P; Schrenk, S; Thiebaux, C; Vasileiadis, G; Verderi, M; Bard, D J; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Xie, Y; Andreotti, M; Azzolini, V; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Piemontese, L; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; De, R; Sangro; Finocchiaro, G; Patteri, P; Peruzzi, I M; Piccolo, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Lo Vetere, M; Macri, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Morii, M; Won, E; Wu, J; Dubitzky, R S; Langenegger, U; Marks, J; Schenk, S; Uwer, U; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Gaillard, J R; Morton, G W; Nash, J A; Nikolich, M B; Taylor, G P; Vazquez, W P; Charles, M J; Mader, W F; Mallik, U; Mohapatra, A K; Cochran, J; Crawley, H B; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Yi, J; Arnaud, N; Davier, M; Giroux, X; Grosdidier, G; Höcker, A; Le Diberder, F R; Lepeltier, V; Lutz, A M; Oyanguren, A; Petersen, T C; Pierini, M; Plaszczynski, S; Rodier, S; Roudeau, P; Schune, M H; Stocchi, A; Wormser, G; Cheng, C H; Lange, D J; Simani, M C; Wright, D M; Bevan, A J; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Parry, R J; Payne, D J; Schofield, K C; Touramanis, C; Cormack, C M; Di Lodovico, F; Menges, W; Sacco, R; Brown, C L; Cowan, G; Flächer, H U; Green, M G; Hopkins, D A; Jackson, P S; McMahon, T R; Ricciardi, S; Salvatore, F; Brown, D; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Edgar, C L; Hodgkinson, M C; Kelly, M P; Lafferty, G D; Naisbit, M T; Williams, J C; Chen, C; Hulsbergen, W D; Jawahery, A; Kovalskyi, D; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Kofler, R; Koptchev, V B; Li, X; Moore, T B; Saremi, S; Stängle, H; Willocq, S; Cowan, R; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Taras, P; Viaud, B; Nicholson, H; Cavallo, N; De Nardo, Gallieno; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M; Bulten, H; Raven, G; Snoek, H L; Wilden, L; Jessop, C P; LoSecco, J M; Allmendinger, T; Benelli, G; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Pulliam, T; Rahimi, A M; Ter-Antonian, R; Wong, Q K; Brau, J E; Frey, R; Igonkina, O; Lu, M; Potter, C T; Sinev, N B; Strom, D; Strube, J; Torrence, E; Galeazzi, F; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; Del Buono, L; La Vaissière, C de; Hamon, O; John, M J J; Leruste, P; Malcles, J; Ocariz, J; Roos, L; Therin, G; Behera, P K; Gladney, L; Guo, Q H; Panetta, J; Biasini, M; Covarelli, R; Pacetti, S; Pioppi, M; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Morganti, M; Neri, N; Paoloni, E; Rama, M; Rizzo, G; Walsh, J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y P; Lü, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Safai-Tehrani, F; Voena, C; Schröder, H; Wagner, G; Waldi, R; Adye, T; De Groot, N; Franek, B; Gopal, G P; Olaiya, E O; Wilson, F F; Aleksan, Roy; Emery, S; Gaidot, A; Ganzhur, S F; Giraud, P F; Graziani, G; Hamel de Monchenault, G; Kozanecki, Witold; Legendre, M; London, G W; Mayer, B; Vasseur, G; Yéche, C; Zito, M; Purohit, M V; Weidemann, A W; Wilson, J R; Yumiceva, F X; Abe, T; Allen, M T; Aston, D; Bakel, N; Bartoldus, R; Berger, N; Boyarski, A M; Buchmüller, O L; Claus, R; Coleman, J P; Convery, M R; Cristinziani, M; Dingfelder, J C; Dong, D; Dorfan, J; Dujmic, D; Dunwoodie, W M; Fan, S; Field, R C; Glanzman, T; Gowdy, S J; Hadig, T; Halyo, V; Hast, C; Hrynóva, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Libby, J; Luitz, S; Lüth, V; Lynch, H L; Marsiske, H; Messner, R; Müller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S; Thompson, J M; Vavra, J; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Roat, C; Ahmed, M; Ahmed, S; Alam, M S; Ernst, J A; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Bóna, M; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Vitale, L; Martínez-Vidal, F; Panvini, R S; Banerjee, S; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R V; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Eichenbaum, A M; Flood, K T; Graham, M; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Mellado, B; Mihályi, A; Pan, Y; Prepost, R; Tan, P; Von Wimmersperg-Töller, J H; Wu, S L; Yu, Z; Neal, H

    2006-01-01

    We search for the rare leptonic decay B+ --> tau+ nu_tau in a sample of 232x10^6 BBbar pairs collected with the BABAR detector at the SLAC PEP-II B-Factory. Signal events are selected by examining the properties of the B meson recoiling against the semileptonic decay B- --> D*0 l- nu_lbar. We find no evidence for a signal and set an upper limit on the branching fraction of BR(B+ --> tau+ nu_tau) tau+ nu_tau to give an upper limit of BR(B+ --> tau+ nu_tau) < 2.6x10^{-4} at the 90% confidence level.

  9. The ATLAS Tau Trigger

    CERN Document Server

    Rados, PK; The ATLAS collaboration

    2013-01-01

    The tau lepton plays a crucial role in understanding particle physics at the Tera scale. One of the most promising probes of the Higgs boson coupling to fermions is with detector signatures involving taus. In addition, many theories beyond the Standard Model, such as supersymmetry and exotic particles (Wʹ′ and Zʹ′), predict new physics with large couplings to taus. The ability to trigger on hadronic tau decays is therefore critical to achieving the physics goals of the ATLAS experiment. The higher instantaneous luminosities of proton-proton collisions achieved by the Large Hadron Collider (LHC) in 2012 resulted in a larger probability of overlap (pile-up) between bunch crossings, and so it was critical for ATLAS to have an effective tau trigger strategy. The details of this strategy are summarized in this poster, and the latest performance measurements are presented.

  10. The ATLAS Tau Trigger

    CERN Document Server

    Rados, PK; The ATLAS collaboration

    2013-01-01

    The tau lepton plays a crucial role in understanding particle physics at the Tera scale. One of the most promising probes of the Higgs boson coupling to fermions is with detector signatures involving taus. In addition, many theories beyond the Standard Model, such as supersymmetry and exotic particles (Wʹ and Zʹ), predict new physics with large couplings to taus. The ability to trigger on hadronic tau decays is therefore critical to achieving the physics goals of the ATLAS experiment. The higher instantaneous luminosities of proton-proton collisions achieved by the Large Hadron Collider (LHC) in 2012 resulted in a larger probability of overlap (pile-up) between bunch crossings, and so it was critical for ATLAS to have an effective tau trigger strategy. The details of this strategy are summarized in this paper, and the results of the latest performance measurements are presented.

  11. CSF and brain structural imaging markers of the Alzheimer's pathological cascade.

    Directory of Open Access Journals (Sweden)

    Xianfeng Yang

    Full Text Available Cerebral spinal fluid (CSF and structural imaging markers are suggested as biomarkers amended to existing diagnostic criteria of mild cognitive impairment (MCI and Alzheimer's disease (AD. But there is no clear instruction on which markers should be used at which stage of dementia. This study aimed to first investigate associations of the CSF markers as well as volumes and shapes of the hippocampus and lateral ventricles with MCI and AD at the baseline and secondly apply these baseline markers to predict MCI conversion in a two-year time using the Alzheimer's Disease Neuroimaging Initiative (ADNI cohort. Our results suggested that the CSF markers, including Aβ42, t-tau, and p-tau, distinguished MCI or AD from NC, while the Aβ42 CSF marker contributed to the differentiation between MCI and AD. The hippocampal shapes performed better than the hippocampal volumes in classifying NC and MCI, NC and AD, as well as MCI and AD. Interestingly, the ventricular volumes were better than the ventricular shapes to distinguish MCI or AD from NC, while the ventricular shapes showed better accuracy than the ventricular volumes in classifying MCI and AD. As the CSF markers and the structural markers are complementary, the combination of them showed great improvements in the classification accuracies of MCI and AD. Moreover, the combination of these markers showed high sensitivity but low specificity for predicting conversion from MCI to AD in two years. Hence, it is feasible to employ a cross-sectional sample to investigate dynamic associations of the CSF and imaging markers with MCI and AD and to predict future MCI conversion. In particular, the volumetric information may be good for the early stage of AD, while morphological shapes should be considered as markers in the prediction of MCI conversion to AD together with the CSF markers.

  12. Tau reconstruction and identification algorithm

    Indian Academy of Sciences (India)

    Raman Khurana

    2012-11-01

    CMS has developed sophisticated tau identification algorithms for tau hadronic decay modes. Production of tau lepton decaying to hadrons are studied at 7 TeV centre-of-mass energy with 2011 collision data collected by CMS detector and has been used to measure the performance of tau identification algorithms by measuring identification efficiency and misidentification rates from electrons, muons and hadronic jets. These algorithms enable extended reach for the searches for MSSM Higgs, and other exotic particles.

  13. Decays of the tau lepton

    Energy Technology Data Exchange (ETDEWEB)

    Burchat, P.R.

    1986-02-01

    Previous measurements of the branching fractions of the tau lepton result in a discrepancy between the inclusive branching fraction and the sum of the exclusive branching fractions to final states containing one charged particle. The sum of the exclusive branching fractions is significantly smaller than the inclusive branching fraction. In this analysis, the branching fractions for all the major decay modes are measured simultaneously with the sum of the branching fractions constrained to be one. The branching fractions are measured using an unbiased sample of tau decays, with little background, selected from 207 pb/sup -1/ of data accumulated with the Mark II detector at the PEP e/sup +/e/sup -/ storage ring. The sample is selected using the decay products of one member of the ..gamma../sup +/..gamma../sup -/ pair produced in e/sup +/e/sup -/ annihilation to identify the event and then including the opposite member of the pair in the sample. The sample is divided into subgroups according to charged and neutral particle multiplicity, and charged particle identification. The branching fractions are simultaneously measured using an unfold technique and a maximum likelihood fit. The results of this analysis indicate that the discrepancy found in previous experiments is possibly due to two sources. First, the leptonic branching fractions measured in this analysis are about one standard deviation higher than the world average. The measured leptonic branching fractions correspond to a tau lifetime of (3.0 +- 0.2) x 10/sup -13/ s. Secondly, the total branching fraction to one charged hadron plus at least one neutral particle is measured to be (7 +- 3)% higher than the branching fraction expected from a combination of previous measurements and theoretical predictions. It is shown that decay modes involving the eta are not expected to contribute more than 3% to this excess.

  14. ATLAS Tau Trigger

    CERN Document Server

    Belanger-Champagne, C; Bosman, M; Brenner, R; Casado, MP; Czyczula, Z; Dam, M; Demers, S; Farrington, S; Igonkina, O; Kalinowski, A; Kanaya, N; Osuna, C; Pérez, E; Ptacek, E; Reinsch, A; Saavedra, A; Sopczak, A; Strom, D; Torrence, E; Tsuno, S; Vorwerk, V; Watson, A; Xella, S

    2008-01-01

    Moving to the high energy scale of the LHC, the identification of tau leptons will become a necessary and very powerful tool, allowing a discovery of physics beyond Standard Model. Many models, among them light SM Higgs and various SUSY models, predict an abundant production of taus with respect to other leptons. The reconstruction of hadronic tau decays, although a very challenging task in hadronic enviroments, allows to increase a signal efficiency by at least of factor 2, and provides an independent control sample to disantangle lepton tau decays from prompt electrons and muons. Thanks to the advanced calorimetry and tracking, the ATLAS experiment has developed tools to efficiently identify hadronic taus at the trigger level. In this presentation we will review the characteristics of taus and the methods to suppress low-multiplicity, low-energy jets contributions as well as we will address the tau trigger chain which provide a rejection rate of 10^5. We will further present plans for commissioning the ATLA...

  15. Measurement of $\\tau$ Polarisation in $Z/\\gamma^*\\rightarrow\\tau\\tau$ Decays with the ATLAS Detector

    CERN Document Server

    Winter, Benedict Tobias; The ATLAS collaboration

    2017-01-01

    A measurement of the $\\tau$ polarisation in $Z/\\gamma^*\\rightarrow\\tau\\tau$ decays is presented. The analysis is based on the $20.2$ fb$^{-1}$ of proton$-$proton collision data collected at a centre-of-mass energy of $\\sqrt{s}=8$ TeV by the ATLAS experiment at the CERN Large Hadron Collider in 2012. Events with one leptonic $\\tau$ decay and one hadronic $\\tau$ decay with a single charged particle in the final state are selected. The $\\tau$ polarisation is measured using the kinematic configuration of the hadronic decay. A polarisation of $P_\\tau~=-0.14\\;\\pm~0.02\\;(\\textrm{stat})\\;\\pm~0.04\\;(\\textrm{syst})$ is measured in the mass range $66 < m_{Z/\\gamma^*} < 116$ GeV. It agrees with the Standard Model prediction of $P_\\tau~=-0.1517\\pm0.0014\\;(\\textrm{stat})\\pm0.0013\\;(\\textrm{syst})$.

  16. Neuronal activity enhances tau propagation and tau pathology in vivo.

    Science.gov (United States)

    Wu, Jessica W; Hussaini, S Abid; Bastille, Isle M; Rodriguez, Gustavo A; Mrejeru, Ana; Rilett, Kelly; Sanders, David W; Cook, Casey; Fu, Hongjun; Boonen, Rick A C M; Herman, Mathieu; Nahmani, Eden; Emrani, Sheina; Figueroa, Y Helen; Diamond, Marc I; Clelland, Catherine L; Wray, Selina; Duff, Karen E

    2016-08-01

    Tau protein can transfer between neurons transneuronally and trans-synaptically, which is thought to explain the progressive spread of tauopathy observed in the brain of patients with Alzheimer's disease. Here we show that physiological tau released from donor cells can transfer to recipient cells via the medium, suggesting that at least one mechanism by which tau can transfer is via the extracellular space. Neuronal activity has been shown to regulate tau secretion, but its effect on tau pathology is unknown. Using optogenetic and chemogenetic approaches, we found that increased neuronal activity stimulates the release of tau in vitro and enhances tau pathology in vivo. These data have implications for disease pathogenesis and therapeutic strategies for Alzheimer's disease and other tauopathies.

  17. Crystallization of M-CSF.alpha.

    Science.gov (United States)

    Pandit, Jayvardhan; Jancarik, Jarmila; Kim, Sung-Hou; Koths, Kirston; Halenbeck, Robert; Fear, Anna Lisa; Taylor, Eric; Yamamoto, Ralph; Bohm, Andrew

    1999-01-01

    The present invention is directed to methods for crystallizing macrophage colony stimulating factor (M-CSF) and to a crystalline M-CSF produced thereby. The present invention is also directed to methods for designing and producing M-CSF agonists and antagonists using information derived from the crystallographic structure of M-CSF. The invention is also directed to methods for screening M-CSF agonists and antagonists. In addition, the present invention is directed to an isolated, purified, soluble and functional M-CSF receptor.

  18. Influence of APOE Genotype on Alzheimer’s Disease CSF Biomarkers in a Spanish Population

    Directory of Open Access Journals (Sweden)

    J. A. Monge-Argilés

    2016-01-01

    Full Text Available Objectives. To evaluate the association between apolipoprotein E (APOE genotype and cerebrospinal fluid (CSF levels of Alzheimer’s disease (AD biomarkers and to study the influence of APOE genotype on the development of AD in a Spanish population. Material and Methods. The study comprised 29 amnestic mild cognitive impairment (MCI patients and 27 control subjects. Using ELISA methodology, CSF biomarkers and tau/Aβ ratios were obtained. ANOVA and adjusted odds ratios were calculated. Results. We observed the effect of APOE genotype and age on CSF AD variables. The progression to AD was more clearly influenced by CSF AD variables than by age or APOE status. Conclusions. APOE status influences CSF AD variables. However, the presence of APOE ε4 does not appear to be a deterministic factor for the development of AD, because CSF variables have a greater influence on progression to the disease. These results confirm previous observations and, to our knowledge, are the first published in a Spanish population.

  19. Paediatric Crohn disease patients with stricturing behaviour exhibit ileal granulocyte–macrophage colony-stimulating factor (GM-CSF) autoantibody production and reduced neutrophil bacterial killing and GM-CSF bioactivity

    Science.gov (United States)

    Jurickova, I; Collins, M H; Chalk, C; Seese, A; Bezold, R; Lake, K; Allmen, D; Frischer, J S; Falcone, R A; Trapnell, B C; Denson, L A

    2013-01-01

    Granulocyte–macrophage colony-stimulating factor (GM-CSF) autoantibodies are associated with stricturing behaviour in Crohn disease (CD). We hypothesized that CD ileal lamina propria mononuclear cells (LPMC) would produce GM-CSF autoantibodies and peripheral blood (PB) samples would contain GM-CSF neutralizing capacity (NC). Paediatric CD and control PBMC and ileal biopsies or LPMC were isolated and cultured and GM-CSF, immunoglobulin (Ig)G and GM-CSF autoantibodies production were measured by enzyme-linked immunosorbent assay (ELISA). Basal and GM-CSF-primed neutrophil bacterial killing and signal transducer and activator of transcription 5 (STAT5) tyrosine phosphorylation (pSTAT5) were measured by flow cytometry. GM-CSF autoantibodies were enriched within total IgG for LPMC isolated from CD ileal strictures and proximal margins compared to control ileum. Neutrophil bacterial killing was reduced in CD patients compared to controls. Within CD, neutrophil GM-CSF-dependent STAT5 activation and bacterial killing were reduced as GM-CSF autoantibodies increased. GM-CSF stimulation of pSTAT5 did not vary between controls and CD patients in washed PB granulocytes in which serum was removed. However, GM-CSF stimulation of pSTAT5 was reduced in whole PB samples from CD patients. These data were used to calculate the GM-CSF NC. CD patients with GM-CSF NC greater than 25% exhibited a fourfold higher rate of stricturing behaviour and surgery. The likelihood ratio (95% confidence interval) for stricturing behaviour for patients with elevation in both GM-CSF autoantibodies and GM-CSF NC was equal to 5 (2, 11). GM-CSF autoantibodies are produced by LPMC isolated from CD ileal resection specimens and are associated with reduced neutrophil bacterial killing. CD peripheral blood contains GM-CSF NC, which is associated with increased rates of stricturing behaviour. PMID:23600834

  20. Serum tau protein as a marker of disease activity in enterohemorrhagic Escherichia coli O111-induced hemolytic uremic syndrome.

    Science.gov (United States)

    Kuroda, Mondo; Shimizu, Masaki; Inoue, Natsumi; Ikeno, Iku; Nakagawa, Hiroyasu; Yokoi, Ayano; Niida, Yo; Konishi, Michio; Kaneda, Hisashi; Igarashi, Noboru; Yamahana, Junya; Taneichi, Hiromichi; Kanegane, Hirokazu; Ito, Mika; Saito, Shigeru; Furuichi, Kengo; Wada, Takashi; Nakagawa, Masaru; Yokoyama, Hitoshi; Yachie, Akihiro

    2015-01-01

    Tau protein levels in cerebrospinal fluid (CSF) and serum are elevated in patients with various central nervous system diseases. We investigated whether serum tau protein levels are useful for predicting and assessing disease activity of acute encephalopathy (AE) in enterohemorrhagic Escherichia coli (EHEC) O111-induced hemolytic uremic syndrome (HUS; EHEC encephalopathy). Serum samples were obtained from 14 patients with EHEC O111/HUS, 20 patients with non-EHEC-related AE, and 20 age- and sex-matched healthy controls. CSF samples were obtained from 2 patients with EHEC encephalopathy and 20 patients with non-EHEC-related AE. Tau protein levels and levels of several proinflammatory cytokines were quantified by enzyme-linked immunosorbent assays. Results were compared with the clinical features of EHEC encephalopathy, including magnetic resonance image (MRI) findings. Serum tau levels in patients with EHEC encephalopathy were significantly elevated compared with those in patients with EHEC O111/HUS without encephalopathy, patients with non-EHEC-related AE, and healthy controls. The ratio of CSF tau levels to serum tau levels was >1.0 in all patients with non-EHEC-related AE but encephalopathy. Serum tau protein levels increased rapidly and markedly in patients with severe EHEC 0111/HUS and encephalopathy when HUS occurred, but were not elevated in mild patients, even in the HUS phase. Furthermore, changes in serum tau protein levels in patients with EHEC encephalopathy were consistent with abnormalities on brain MRI and were positively correlated with proinflammatory cytokine levels. Our results indicate that serum tau protein might be useful to predict and assess disease activity of EHEC encephalopathy. Copyright © 2015 Elsevier Ltd. All rights reserved.

  1. Propofol directly increases tau phosphorylation.

    Directory of Open Access Journals (Sweden)

    Robert A Whittington

    Full Text Available In Alzheimer's disease (AD and other tauopathies, the microtubule-associated protein tau can undergo aberrant hyperphosphorylation potentially leading to the development of neurofibrillary pathology. Anesthetics have been previously shown to induce tau hyperphosphorylation through a mechanism involving hypothermia-induced inhibition of protein phosphatase 2A (PP2A activity. However, the effects of propofol, a common clinically used intravenous anesthetic, on tau phosphorylation under normothermic conditions are unknown. We investigated the effects of a general anesthetic dose of propofol on levels of phosphorylated tau in the mouse hippocampus and cortex under normothermic conditions. Thirty min following the administration of propofol 250 mg/kg i.p., significant increases in tau phosphorylation were observed at the AT8, CP13, and PHF-1 phosphoepitopes in the hippocampus, as well as at AT8, PHF-1, MC6, pS262, and pS422 epitopes in the cortex. However, we did not detect somatodendritic relocalization of tau. In both brain regions, tau hyperphosphorylation persisted at the AT8 epitope 2 h following propofol, although the sedative effects of the drug were no longer evident at this time point. By 6 h following propofol, levels of phosphorylated tau at AT8 returned to control levels. An initial decrease in the activity and expression of PP2A were observed, suggesting that PP2A inhibition is at least partly responsible for the hyperphosphorylation of tau at multiple sites following 30 min of propofol exposure. We also examined tau phosphorylation in SH-SY5Y cells transfected to overexpress human tau. A 1 h exposure to a clinically relevant concentration of propofol in vitro was also associated with tau hyperphosphorylation. These findings suggest that propofol increases tau phosphorylation both in vivo and in vitro under normothermic conditions, and further studies are warranted to determine the impact of this anesthetic on the acceleration of

  2. Neutral Higgs boson searches in the H{yields}{tau}{tau}{yields}{mu}{mu} decay channel

    Energy Technology Data Exchange (ETDEWEB)

    Bethani, Agni

    2013-10-15

    This dissertation describes the search for Higgs bosons decaying to a pair of {tau} leptons both decaying to muons. The analysis was performed using events recorded by the CMS detector at the LHC in 2011 and 2012, at center-of-mass energy 7 TeV and 8 TeV respectively. The dataset corresponds to total integrated luminosity of 17 fb{sup -1}, 4.9 fb{sup -1} taken at 7 TeV center-of-mass energy and 12.1 fb{sup -1} at 8 TeV. The results were interpreted in the context of both the Standard Model and the Minimal Supersymmetric Standard Model. Upper limits were set to the Higgs production cross section in the former case and on the (tan {beta}, m{sub A}) plane in the latter. The update of this analysis with more data, combined with other {tau}{tau} final states, lead to the first evidence of the Higgs coupling to {tau} leptons. Included in this document is also the study of the Z boson production followed by Z {yields} {tau}{tau} decay with two muons in the final state. This analysis was performed with 36 pb{sup -1} of data collected in 2010, at center-of-mass energy 7 TeV, by the CMS experiment. The result of this study was the measurement of the Z production cross section in proton-proton collisions. The analysis procedures developed for the Z boson decay to {tau} leptons were used to commission the Higgs boson searches in the same decay channel.

  3. IIH with normal CSF pressures?

    Directory of Open Access Journals (Sweden)

    Soh Youn Suh

    2013-01-01

    Full Text Available Idiopathic intracranial hypertension (IIH is a condition of raised intracranial pressure (ICP in the absence of space occupying lesions. ICP is usually measured by lumbar puncture and a cerebrospinal fluid (CSF pressure above 250 mm H 2 O is one of the diagnostic criteria of IIH. Recently, we have encountered two patients who complained of headaches and exhibited disc swelling without an increased ICP. We prescribed acetazolamide and followed both patients frequently; because of the definite disc swelling with IIH related symptoms. Symptoms and signs resolved in both patients after they started taking acetazolamide. It is generally known that an elevated ICP, as measured by lumbar puncture, is the most important diagnostic sign of IIH. However, these cases caution even when CSF pressure is within the normal range, that suspicion should be raised when a patient has papilledema with related symptoms, since untreated papilledema may cause progressive and irreversible visual loss.

  4. $\\tau$ decays with neutral kaons

    CERN Document Server

    Abbiendi, G.; Akesson, P.F.; Alexander, G.; Allison, John; Anderson, K.J.; Arcelli, S.; Asai, S.; Ashby, S.F.; Axen, D.; Azuelos, G.; Bailey, I.; Ball, A.H.; Barberio, E.; Barlow, Roger J.; Batley, J.R.; Baumann, S.; Behnke, T.; Bell, Kenneth Watson; Bella, G.; Bellerive, A.; Bentvelsen, S.; Bethke, S.; Betts, S.; Biebel, O.; Biguzzi, A.; Bloodworth, I.J.; Bock, P.; Bohme, J.; Boeriu, O.; Bonacorsi, D.; Boutemeur, M.; Braibant, S.; Bright-Thomas, P.; Brigliadori, L.; Brown, Robert M.; Burckhart, H.J.; Capiluppi, P.; Carnegie, R.K.; Carter, A.A.; Carter, J.R.; Chang, C.Y.; Charlton, David G.; Chrisman, D.; Ciocca, C.; Clarke, P.E.L.; Clay, E.; Cohen, I.; Conboy, J.E.; Cooke, O.C.; Couchman, J.; Couyoumtzelis, C.; Coxe, R.L.; Cuffiani, M.; Dado, S.; Dallavalle, G.Marco; Dallison, S.; Davis, R.; de Roeck, A.; Dervan, P.; Desch, K.; Dienes, B.; Dixit, M.S.; Donkers, M.; Dubbert, J.; Duchovni, E.; Duckeck, G.; Duerdoth, I.P.; Estabrooks, P.G.; Etzion, E.; Fabbri, F.; Fanfani, A.; Fanti, M.; Faust, A.A.; Feld, L.; Ferrari, P.; Fiedler, F.; Fierro, M.; Fleck, I.; Frey, A.; Furtjes, A.; Futyan, D.I.; Gagnon, P.; Gary, J.W.; Gaycken, G.; Geich-Gimbel, C.; Giacomelli, G.; Giacomelli, P.; Gingrich, D.M.; Glenzinski, D.; Goldberg, J.; Gorn, W.; Grandi, C.; Graham, K.; Gross, E.; Grunhaus, J.; Gruwe, M.; Hajdu, C.; Hanson, G.G.; Hansroul, M.; Hapke, M.; Harder, K.; Harel, A.; Hargrove, C.K.; Harin-Dirac, M.; Hauschild, M.; Hawkes, C.M.; Hawkings, R.; Hemingway, R.J.; Herten, G.; Heuer, R.D.; Hildreth, M.D.; Hill, J.C.; Hobson, P.R.; Hocker, James Andrew; Hoffman, Kara Dion; Homer, R.J.; Honma, A.K.; Horvath, D.; Hossain, K.R.; Howard, R.; Huntemeyer, P.; Igo-Kemenes, P.; Imrie, D.C.; Ishii, K.; Jacob, F.R.; Jawahery, A.; Jeremie, H.; Jimack, M.; Jones, C.R.; Jovanovic, P.; Junk, T.R.; Kanaya, N.; Kanzaki, J.; Karapetian, G.; Karlen, D.; Kartvelishvili, V.; Kawagoe, K.; Kawamoto, T.; Kayal, P.I.; Keeler, R.K.; Kellogg, R.G.; Kennedy, B.W.; Kim, D.H.; Klier, A.; Kobayashi, T.; Kobel, M.; Kokott, T.P.; Kolrep, M.; Komamiya, S.; Kowalewski, Robert V.; Kress, T.; Krieger, P.; von Krogh, J.; Kuhl, T.; Kupper, M.; Kyberd, P.; Lafferty, G.D.; Landsman, H.; Lanske, D.; Lauber, J.; Lawson, I.; Layter, J.G.; Lellouch, D.; Letts, J.; Levinson, L.; Liebisch, R.; Lillich, J.; List, B.; Littlewood, C.; Lloyd, A.W.; Lloyd, S.L.; Loebinger, F.K.; Long, G.D.; Losty, M.J.; Lu, J.; Ludwig, J.; Macchiolo, A.; Macpherson, A.; Mader, W.; Mannelli, M.; Marcellini, S.; Marchant, T.E.; Martin, A.J.; Martin, J.P.; Martinez, G.; Mashimo, T.; Mattig, Peter; McDonald, W.John; McKenna, J.; Mckigney, E.A.; McMahon, T.J.; McPherson, R.A.; Meijers, F.; Mendez-Lorenzo, P.; Merritt, F.S.; Mes, H.; Meyer, I.; Michelini, A.; Mihara, S.; Mikenberg, G.; Miller, D.J.; Mohr, W.; Montanari, A.; Mori, T.; Nagai, K.; Nakamura, I.; Neal, H.A.; Nisius, R.; O'Neale, S.W.; Oakham, F.G.; Odorici, F.; Ogren, H.O.; Okpara, A.; Oreglia, M.J.; Orito, S.; Pasztor, G.; Pater, J.R.; Patrick, G.N.; Patt, J.; Perez-Ochoa, R.; Petzold, S.; Pfeifenschneider, P.; Pilcher, J.E.; Pinfold, J.; Plane, David E.; Poli, B.; Polok, J.; Przybycien, M.; Quadt, A.; Rembser, C.; Rick, H.; Robins, S.A.; Rodning, N.; Roney, J.M.; Rosati, S.; Roscoe, K.; Rossi, A.M.; Rozen, Y.; Runge, K.; Runolfsson, O.; Rust, D.R.; Sachs, K.; Saeki, T.; Sahr, O.; Sang, W.M.; Sarkisian, E.K.G.; Sbarra, C.; Schaile, A.D.; Schaile, O.; Scharff-Hansen, P.; Schieck, J.; Schmitt, S.; Schoning, A.; Schroder, Matthias; Schumacher, M.; Schwick, C.; Scott, W.G.; Seuster, R.; Shears, T.G.; Shen, B.C.; Shepherd-Themistocleous, C.H.; Sherwood, P.; Siroli, G.P.; Skuja, A.; Smith, A.M.; Snow, G.A.; Sobie, R.; Soldner-Rembold, S.; Spagnolo, S.; Sproston, M.; Stahl, A.; Stephens, K.; Stoll, K.; Strom, David M.; Strohmer, R.; Surrow, B.; Talbot, S.D.; Taras, P.; Tarem, S.; Teuscher, R.; Thiergen, M.; Thomas, J.; Thomson, M.A.; Torrence, E.; Towers, S.; Trefzger, T.; Trigger, I.; Trocsanyi, Z.; Tsur, E.; Turner-Watson, M.F.; Ueda, I.; Van Kooten, Rick J.; Vannerem, P.; Verzocchi, M.; Voss, H.; Wackerle, F.; Waller, D.; Ward, C.P.; Ward, D.R.; Watkins, P.M.; Watson, A.T.; Watson, N.K.; Wells, P.S.; Wengler, T.; Wermes, N.; Wetterling, D.; White, J.S.; Wilson, G.W.; Wilson, J.A.; Wyatt, T.R.; Yamashita, S.; Zacek, V.; Zer-Zion, D.

    2000-01-01

    The branching ratio of the tau lepton to a neutral K meson is measured from a sample of approximately 200,000 tau decays recorded by the OPAL detector at centre-of-mass energies near the Z0 resonance. The measurement is based on two samples which identify one-prong tau decays with KL and KS mesons. The combined branching ratios are measured to be B(tau- -->pi- K0bar nutau) = (9.33+-0.68+-0.49)x10^-3 B(tau- -->pi- K0bar [>=1pi0] nutau) = (3.24+-0.74+-0.66)x10^-3 B(tau- -->K- K0bar [>=0pi0] nutau) = (3.30+-0.55+-0.39)x10^-3 where the first error is statistical and the second systematic.

  5. Ischemic cardiac complications following G-CSF.

    Science.gov (United States)

    Eckman, Peter M; Bertog, Stefan C; Wilson, Robert F; Henry, Timothy D

    2010-07-01

    Granulocyte-colony stimulating factor (G-CSF) is commonly used in bone marrow transplant donors to increase the number of circulating progenitor cells. G-CSF has also been studied following myocardial infarction, but concern has been raised about the risks of G-CSF administration in patients with coronary artery disease. We present two cases of ischemic cardiac complications that are likely to be related to administration of G-CSF and provide a contemporary overview of the literature on the cardiovascular risks of G-CSF.

  6. The cellular distribution and Ser262 phosphorylation of tau protein are regulated by BDNF in vitro.

    Directory of Open Access Journals (Sweden)

    Qian Chen

    Full Text Available The brain-enriched microtubule-associated protein tau, a critical regulator of cytoskeletal dynamics, forms insoluble aggregates in a number of neurodegenerative diseases termed tauopathies, including Alzheimer's disease (AD. Hyperphosphorylation of tau protein is an important mechanism for aggregation, so many studies on the pathogenesis of AD and other tauopathies have focused on regulation of tau phosphorylation by kinases and phosphatases. Less studied are mechanisms of tau transcriptional and post-transcriptional regulation by extracellular signals such as BDNF and how such changes alter neuronal function. Previously, we reported that tau is required for morphological plasticity induced by BDNF. Here, we further explore tau modification during BDNF-induced changes in neuronal cell morphology. In undifferentiated SH-SY5Y cells lacking neurites, tau formed a sphere within the soma as revealed by immunocytochemistry. In contrast, tau was enriched in the neurites and sparse in the soma of SH-SY5Y cells induced to differentiate by retinoic acid (RA. Treatment with RA also increased total tau protein levels but decreased expression of tau phosphorylated at Ser262 as determined by Western blot. Both effects were further enhanced by subsequent BDNF treatment. Upregulation of tau protein and downregulation of p-Ser262 tau were correlated with total neurite length (R = .94 and R = -.98, respectively. When primary E18 hippocampal neurons were treated with nocodazole, a blocker of microtubule polymerization, nascent neurites were lost and tau shifted to the soma. This process of retrograde tau movement away from neurites was reversed by BDNF. These results indicate that tau is redistributed to neurites and dephosphorylated during RA- and BDNF-mediated differentiation.

  7. Decays of the heavy lepton, tau (1785)

    Energy Technology Data Exchange (ETDEWEB)

    Blocker, C.A.

    1980-04-01

    The structure of the weak hadronic current coupled to the tau is investigated via some of the hadronic decays of the tau. The vector current coupling is determined by measuring the tau ..-->.. rho ..nu../sub tau/ branching ratio. The axial-vector coupling is determined by measuring the tau ..-->.. ..pi.. ..nu../sub tau/ branching ratio. The Cabibbo structure of the hadronic current is established by observing the decay tau ..-->.. K*(890)..nu../sub tau/ and measuring its branching ratio. The branching ratios for the decays tau ..-->.. e anti ..nu../sub e/..nu../sub tau/ and tau ..-->.. ..mu.. anti ..nu../sub ..mu../..nu../sub tau/ are measured as a normalization for the hadronic decays and as a check on the validity of the measurements. The leptonic branching ratios agree well with previous experiments. From a kinematic fit to the pion energy spectrum in the decay tau ..-->.. ..pi.. ..nu../sub tau/, an upper limit (95% confidence level) of 245 MeV is placed on the tau neutrino mass. From a simultaneous fit of the center of mass energy dependence of the tau production cross section and the pion energy spectrum in the decay tau ..-->.. ..pi.. ..nu../sub tau/, the tau mass is determined to be 1.787 +- .010 GeV/c. All properties of the tau measured here are consistent with it being a sequential lepton coupled to the ordinary weak hadronic current.

  8. Decays of the heavy lepton, tau (1785)

    Energy Technology Data Exchange (ETDEWEB)

    Blocker, C.A.

    1980-04-01

    The structure of the weak hadronic current coupled to the tau is investigated via some of the hadronic decays of the tau. The vector current coupling is determined by measuring the tau ..-->.. rho ..nu../sub tau/ branching ratio. The axial-vector coupling is determined by measuring the tau ..-->.. ..pi.. ..nu../sub tau/ branching ratio. The Cabibbo structure of the hadronic current is established by observing the decay tau ..-->.. K*(890)..nu../sub tau/ and measuring its branching ratio. The branching ratios for the decays tau ..-->.. e anti ..nu../sub e/..nu../sub tau/ and tau ..-->.. ..mu.. anti ..nu../sub ..mu../..nu../sub tau/ are measured as a normalization for the hadronic decays and as a check on the validity of the measurements. The leptonic branching ratios agree well with previous experiments. From a kinematic fit to the pion energy spectrum in the decay tau ..-->.. ..pi.. ..nu../sub tau/, an upper limit (95% confidence level) of 245 MeV is placed on the tau neutrino mass. From a simultaneous fit of the center of mass energy dependence of the tau production cross section and the pion energy spectrum in the decay tau ..-->.. ..pi.. ..nu../sub tau/, the tau mass is determined to be 1.787 +- .010 GeV/c. All properties of the tau measured here are consistent with it being a sequential lepton coupled to the ordinary weak hadronic current.

  9. Search for $B^{+}\\rightarrow K^{+} \\tau^{+}\\tau^{-}$ at the BaBar experiment

    CERN Document Server

    ,

    2016-01-01

    We search for the rare flavor-changing neutral current process $B^{+}\\rightarrow K^{+}\\tau^{+}\\tau^{-}$ using data from the BABAR experiment. The data sample, collected at the center-of-mass energy of the $\\Upsilon{(4S)}$ resonance, corresponds to a total integrated luminosity of 424 fb$^{-1}$ and to 471 million $B\\overline{B}$ pairs. We reconstruct one $B$ meson, produced in the $\\Upsilon{(4S)}\\rightarrow B^{+} B^{-}$ decay, in one of many hadronic decay modes and search for activity compatible with a $B^{+}\\rightarrow K^{+} \\tau^{+}\\tau^{-}$ decay in the rest of the event. Each $\\tau$ lepton is required to decay leptonically into an electron or muon and neutrinos. Comparing the expected number of background events with the data sample after applying the selection criteria, we do not find evidence for a signal. The measured branching fraction is ($1.31^{+0.66}_{-0.61}$( stat.)$^{+0.35}_{-0.25}$( sys.)$) \\times 10^{-3}$ with an upper limit, at the 90\\% confidence level, of $\\mathcal{B}(B^{+}\\rightarrow K^{+}\\...

  10. Tau imaging in neurodegenerative diseases

    Energy Technology Data Exchange (ETDEWEB)

    Dani, M.; Edison, P. [Imperial College London, Neurology Imaging Unit, Division of Neuroscience, London (United Kingdom); Brooks, D.J. [Imperial College London, Neurology Imaging Unit, Division of Neuroscience, London (United Kingdom); Aarhus University, Institute of Clinical Medicine, Aarhus (Denmark)

    2016-06-15

    Aggregated tau protein is a major neuropathological substrate central to the pathophysiology of neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal dementia, progressive supranuclear palsy, corticobasal degeneration and chronic traumatic encephalopathy. In AD, it has been shown that the density of hyperphosphorylated tau tangles correlates closely with neuronal dysfunction and cell death, unlike β-amyloid. Until now, diagnostic and pathologic information about tau deposition has only been available from invasive techniques such as brain biopsy or autopsy. The recent development of selective in-vivo tau PET imaging ligands including [{sup 18}F]THK523, [{sup 18}F]THK5117, [{sup 18}F]THK5105 and [{sup 18}F]THK5351, [{sup 18}F]AV1451(T807) and [{sup 11}C]PBB3 has provided information about the role of tau in the early phases of neurodegenerative diseases, and provided support for diagnosis, prognosis, and imaging biomarkers to track disease progression. Moreover, the spatial and longitudinal relationship of tau distribution compared with β - amyloid and other pathologies in these diseases can be mapped. In this review, we discuss the role of aggregated tau in tauopathies, the challenges posed in developing selective tau ligands as biomarkers, the state of development in tau tracers, and the new clinical information that has been uncovered, as well as the opportunities for improving diagnosis and designing clinical trials in the future. (orig.)

  11. First Measurement of the Branching Fraction of the Decay $\\psi(2S) \\to \\tau\\tau$

    CERN Document Server

    Bai, J Z; Bian, J G; Blum, I K; Chen, G P; Chen, H F; Chen, J; Chen Jia Chao; Chen, Y; Chen, Y B; Chen, Y Q; Cheng Bao Sen; Cui, X Z; Ding, H L; Dong, L Y; Du, Z Z; Dunwoodie, W M; Gao, C S; Gao, M L; Gao, S Q; Gratton, P; Gu, J H; Gu, S D; Gu, W X; Gu, Y F; Guo, Z J; Guo, Y N; Han, S W; Han, Y; Harris, F A; He, J; He, J T; He, K L; He, M; Heng, Y K; Hitlin, D G; Hu, G Y; Hu, H M; Hu, J L; Hu, Q H; Hu, T; Hu Xiao Qing; Huang, G S; Huang, Y Z; Izen, J M; Jiang, C H; Jin, Y; Jones, B D; Ju, X; Ke, Z J; Kelsey, M H; Kim, B K; Kong, D; Lai, Y F; Lang, P F; Lankford, A J; Li, C G; Li, D; Li, H B; Li, J; Li, J C; Li, P Q; Li, R B; Li, W; Li, W G; Li, X H; Li Xiao Nan; Liu, H M; Liu, J; Liu, R G; Liu, Y; Lou, X C; Lowery, B; Lu, F; Lu, J G; Luo, X L; Ma, E C; Ma, J M; Malchow, R; Mao, H S; Mao, Z P; Meng, X C; Nie, J; Olsen, S L; Oyang, J Y T; Paluselli, D; Pan, L J; Panetta, J; Porter, F; Qi, N D; Qi, X R; Qian, C D; Qiu, J F; Qu, Y H; Que, Y K; Rong, G; Schernau, M; Shao, Y Y; Shen, B W; Shen, D L; Shen, H; Shen, X Y; Sheng, H Y; Shi, H Z; Song, X F; Standifird, J; Sun, F; Sun, H S; Sun, Y; Sun, Y Z; Tang, S Q; Toki, W; Tong, G L; Varner, G S; Wang, F; Wang, L S; Wang, L Z; Wang, M; Wang, P; Wang, P L; Wang, S M; Wang, T J; Wang, Y Y; Weaver, M; Wei, C L; Wu, J M; Wu, N; Wu, Y G; Xi, D M; Xia, X M; Xie, P P; Xie, Y; Xie, Y H; Xu, G F; Xue, S T; Yan, J; Yan, W G; Yang, C M; Yang, C Y; Yang, H X; Yang, J; Yang, W; Yang, X F; Ye, M H; Ye Shu Wei; Ye, Y X; Yu, C S; Yu, C X; Yu, G W; Yu Yu Hei; Yu, Z Q; Yuan, C Z; Yuan, Y; Zhang Bing Yun; Zhang, C; Zhang, C C; Zhang, D H; Zhang, H L; Zhang, J; Zhang, J W; Zhang, L; Zhang, L S; Zhang, P; Zhang, Q J; Zhang, S Q; Zhang, X Y; Zhang, Y Y; Zhao, D X; Zhao, H W; Zhao Jia Wei; Zhao, M; Zhao Wei Ren; Zhao, Z G; Zheng Jian Ping; Zheng Lin Sheng; Zheng Zhi Peng; Zhou, B Q; Zhou, G P; Zhou, H S; Zhou, L; Zhu, K J; Zhu, Q M; Zhu, Y C; Zhu, Y S; Zhuang, B A

    2002-01-01

    The branching fraction of the psi(2S) decay into tau pair has been measured for the first time using the BES detector at the Beijing Electron-Positron Collider. The result is $B_{\\tau\\tau}=(2.71\\pm 0.43 \\pm 0.55) \\times 10^{-3}$, where the first error is statistical and the second is systematic. This value, along with those for the branching fractions into e+e- and mu+mu of this resonance, satisfy well the relation predicted by the sequential lepton hypothesis. Combining all these values with the leptonic width of the resonance the total width of the psi(2S) is determined to be $(252 \\pm 37)$ keV.

  12. Tau flavored dark matter and its impact on tau Yukawa coupling

    Science.gov (United States)

    Chao, Wei; Guo, Huai-Ke; Li, Hao-Lin

    2017-02-01

    In this paper we perform a systematic study of the tau flavored dark matter (DM) model by introducing two kinds of mediators (a scalar doublet and a charged scalar singlet). The electromagnetic properties of the DM, as well as their implications in DM direct detections, are analyzed in detail. The model turns out contributing a significant radiative correction to the tau lepton mass, in addition to loosing the tension between the measured DM relic density and constraints of DM direct detections. The loop corrections can be Script O(10%) of the total tau mass. Signal rates of the Higgs measurements from the LHC in the h→τ τ and h→ γ γ channels, relative to the Standard Model expectations, can be explained in this model.

  13. UX Tau A

    Science.gov (United States)

    2007-01-01

    This is an artist's rendition of the one-million-year-old star system called UX Tau A, located approximately 450 light-years away. Observations from NASA's Spitzer Space Telescope showed a gap in the dusty planet-forming disk swirling around the system's central sun-like star. Spitzer saw a gap in UX Tau A's disk that extends from 0.2 to 56 astronomical units (an astronomical unit is the distance between the sun and Earth). The gap extends from the equivalent of Mercury to Pluto in our solar system, and is sandwiched between thick inner and outer disks on either side. Astronomers suspect that the gap was carved out by one or more forming planets. Such dusty disks are where planets are thought to be born. Dust grains clump together like snowballs to form larger rocks, and then the bigger rocks collide to form the cores of planets. When rocks revolve around their central star, they act like cosmic vacuum cleaners, picking up all the gas and dust in their path and creating gaps. Although gaps have been detected in disks swirling around young stars before, UX Tau A is special because the gap is sandwiched between two thick disks of dust. An inner thick dusty disk hugs the central star, then, moving outward, there is a gap, followed by another thick doughnut-shaped disk. Other systems with gaps contain very little to no dust near the central star. In other words, those gaps are more like big holes in the centers of disks. Some scientists suspect that these holes could have been carved out by a process called photoevaporation. Photoevaporation occurs when radiation from the central star heats up the gas and dust around it to the point where it evaporates away. The fact that there is thick disk swirling extremely close to UX Tau A's central star rules out the photoevaporation scenario. If photoevaporation from the star played a role, then large amounts of dust would not be floating so close to the star.

  14. LHCb; Neutral Higgs $ \\to \\tau \\tau$ Limits at LHCb

    CERN Multimedia

    Ilten, P

    2013-01-01

    LHCb is fully instrumented in the forward region, $2 \\leq \\eta \\leq 5$, and provides compelentary results to the central measurements of ATLAS and CMS. Preliminary limits are presented on neutral Higgs production usint $\\tau \\tau$ final states in the forward region of LHCb.

  15. Measurement of the [tau]-lepton mass

    Energy Technology Data Exchange (ETDEWEB)

    Balest, R.; Daoudi, M.; Ford, W.T.; Johnson, D.R.; Lingel, K.; Lohner, M.; Rankin, P.; Smith, J.G.; Alexander, J.P.; Bebek, C.; Berkelman, K.; Besson, D.; Browder, T.E.; Cassel, D.G.; Cho, H.A.; Coffman, D.M.; Drell, P.S.; Ehrlich, R.; Galik, R.S.; Garcia-Sciveres, M.; Geiser, B.; Gittelman, B.; Gray, S.W.; Hartill, D.L.; Heltsley, B.K.; Honscheid, K.; Jones, C.D.; Kandaswamy, J.; Katayama, N.; Kim, P.C.; Kreinick, D.L.; Ludwig, G.S.; Masui, J.; Mevissen, J.; Mistry, N.B.; Ng, C.R.; Nordberg, E.; Ogg, M.; O' Grady, C.; Patterson, J.R.; Peterson, D.; Riley, D.; Sapper, M.; Selen, M.; Worden, H.; Worris, M.; Wuerthwein, F.; Avery, P.; Freyberger, A.; Rodriguez, J.; Stephens, R.; Yelton, J.; Cinabro, D.; Henderson, S.; Kinoshita, K.; Liu, T.; Saulnier, M.; Wilson, R.; Yamamoto, H.; Sadoff, A.J.; Ammar, R.; Ball, S.; Baringer, P.; Coppage, D.; Copty, N.; Davis, R.; Hancock, N.; Kelly, M.; Kwak, N.; Lam, H.; Kubota, Y.; Lattery, M.; Nelson, J.K.; Patton, S.; Perticone, D.; Poling, R.; Savino; (CLEO Collaboration)

    1993-05-01

    Using data from the CLEO II detector at CESR, we measure the [tau]-lepton mass by exploiting the unique kinematics of events in which both [tau]'s decay hadronically. The result is [ital m][sub [tau

  16. The ATLAS tau trigger

    CERN Document Server

    Tsuno, S; The ATLAS collaboration

    2009-01-01

    The ATLAS tau trigger has three levels: the first one (L1) is hardware based and uses FPGAs, while the second (L2) and third levels (EF -Event Filter-) are software based and use commodity computers (2 x Intel Harpertown quad-core 2.5 GHz), running scientific linux 4. In this contribution we discuss both the physics characteristics of tau leptons and the technical solutions to quick data access and fast algorithms. We show that L1 selects narrow jets in the calorimeter with an overall rejection against QCD jets of 300, whilst L2 and EF (referred together as High Level Trigger -HLT-) use all the detectors with full granularity and apply a typical rejection of 15 within the stringent timing requirements of the LHC. In the HLT there are two complementary approaches: specialized, fast algorithms are used at L2, while more refined and sophisticated algorithms, imported from the offline, are utilized in the EF.

  17. Tau identification at the Tevatron

    Energy Technology Data Exchange (ETDEWEB)

    Levy, Stephen; /Chicago U., EFI

    2005-07-01

    Methods for reconstructing and identifying the hadronic decays of tau leptons with the CDF and D0 detectors at the Fermilab Tevatron collider in Run II are described. Precision electroweak measurements of W and Z gauge boson cross sections are presented as well as results of searches for physics beyond the Standard Model with hadronically decaying tau leptons in the final state.

  18. A Meta-analysis of Tau Protein in Cerebrospinal Fluid in Predicting Alzheimer’s Disease%脑脊液tau蛋白预测轻度认知障碍进展为阿尔茨海默病的Meta分析

    Institute of Scientific and Technical Information of China (English)

    蔡芳芳; 温仲民

    2015-01-01

    Aim To evaluate the level of tau protein in cerebrospinal lfuid in predicting mild cognitive impairment patients progressing to Alzheimer’s disease. Methods The published literature about predicting the conversion of mild cognitive impairment to Alzheimer’s disease by cerebrospinal lfuid tau protein was retrieved comprehensively in databases such as PubMed, Cochrane Library, Web of Science. Data of tau protein were collected and analyzed by Meta-analysis by using Stata11.0. Publication bias was estimated by Egger’s regression test and sensitivity analysis was made. Results Eleven studies met inclusion criteria, 9 of them provided complete CSF total tau protein and phosphorylated tau protein concentration data. The other two studies provided the total tau protein concentration only, did not provide the phosphorylated tau protein levels. The baseline concentrations of both t-tau and p-tau in MCI to AD patients were higher than those in stable -MCI patients. (t-tau: SMD=1.063, 95%CI:0.902~1.223, Z=13.00, P<0.001; p-tau:SMD=1.335, 95%CI:0.983~1.687, Z=7.44, P<0.001). Conclusion Tau protein in cerebrospinal lfuid may be an important diagnostic biomarker for predicting the conversion from mild cognitive impairment to Alzheimer’s disease.%目的:评价脑脊液总tau(t-tau)蛋白和磷酸化tau(p-tau)蛋白预测轻度认知障碍(MCI)患者进展为阿尔茨海默病(AD)的临床价值。方法全面检索2000至2014年PubMed、Cochrane Library、Web of Science 数据库、Ovid全文电子期刊、中国知网全文数据(CNKI)和万方数据库中有关脑脊液tau蛋白预测MCI患者进展为AD的文献,收集每项研究中tau蛋白水平数据,用Stata11.0软件对数据进行Meta分析,计算合并效应量。采用Egger法对漏斗图作对称性检验评估发表偏倚、并进行敏感性分析。结果共纳入11项研究,其中9项研究完整提供了脑脊液总t-tau蛋白和p-tau蛋白浓度数据,另外2项

  19. An improved mass reconstruction technique for a heavy resonance decaying to $\\tau^+\\tau^-$

    CERN Document Server

    Xia, Li-Gang

    2016-01-01

    For a resonance decaying to $\\tau^+\\tau^-$, it is difficult to reconstruct its mass accurately because of the presence of neutrinos in the decay products of the $\\tau$ leptons. If the resonance is heavy enough, we show that its mass can be well determined by the magnitude of the momentum of the invisible decay products, $|\\vec{p}_{inv}|$, and the mass of the visible/invsible decay products, $m_{vis/inv}$, for $\\tau$ decaying to hadrons/leptons (4 unknowns in total). We do not need to know all the components of $\\vec{p}_{inv}$s and $m_{vis/inv}$s (8 unknonws in total). By sampling all kinematically allowed values of $|\\vec{p}_{inv}|$ and $m_{vis/inv}$ according to their distributions in the MC simulations, the mass of the mother resonance is assumed to lie at the postion with the maximal probability. This new mass reconstruction technique inherits the similar idea from the Missing Mass Calculator Technique (MMCT). It has a better performance, since it neither relies on the assumption that only the neutrinos fr...

  20. Measurement of the tau tag efficiency using the Z ->tau tau -> mu + hadrons +X events

    CERN Document Server

    Kalinowski, Artur

    2006-01-01

    A method for the measurement of the tau tag efficiency for the taus coming from the Z boson decay is presented. Full simulation studies show that the tau tag efficiency can be measured with the precision of 9% including the systematic uncertainties due to the calorimetry scale uncertainty.

  1. A Precise Measurement of the Tau Lifetime

    CERN Document Server

    Abdallah, J; Adam, W; Adzic, P; Albrecht, T; Alderweireld, T; Alemany-Fernandez, R; Allmendinger, T; Allport, P P; Amaldi, Ugo; Amapane, N; Amato, S; Anashkin, E; Andreazza, A; Andringa, S; Anjos, N; Antilogus, P; Apel, W D; Arnoud, Y; Ask, S; Åsman, B; Augustin, J E; Augustinus, A; Baillon, Paul; Ballestrero, A; Bambade, P; Barbier, R; Bardin, Dimitri Yuri; Barker, G J; Baroncelli, A; Battaglia, Marco; Baubillier, M; Becks, K H; Begalli, M; Behrmann, A; Ben-Haim, E; Benekos, N C; Benvenuti, Alberto C; Bérat, C; Berggren, M; Berntzon, L; Bertrand, D; Besançon, M; Besson, N; Bloch, D; Blom, M; Bluj, M; Bonesini, M; Boonekamp, M; Booth, P S L; Borisov, G; Botner, O; Bouquet, B; Bowcock, T J V; Boyko, I; Bracko, M; Brenner, R; Brodet, E; Brückman, P; Brunet, J M; Bugge, L; Buschmann, P; Calvi, M; Camporesi, T; Canale, V; Carena, F; Castro, N; Cavallo, F R; Chapkin, M M; Charpentier, P; Checchia, P; Chierici, R; Shlyapnikov, P; Chudoba, J; Chung, S U; Cieslik, K; Collins, P; Contri, R; Cosme, G; Cossutti, F; Costa, M J; Crennell, D J; Cuevas-Maestro, J; D'Hondt, J; Dalmau, J; Da Silva, T; Da Silva, W; Della Ricca, G; De Angelis, A; de Boer, Wim; De Clercq, C; De Lotto, B; De Maria, N; De Min, A; De Paula, L S; Di Ciaccio, L; Di Simone, A; Doroba, K; Drees, J; Dris, M; Eigen, G; Ekelöf, T J C; Ellert, M; Elsing, M; Espirito-Santo, M C; Fanourakis, G K; Fassouliotis, D; Feindt, M; Fernández, J; Ferrer, A; Ferro, F; Flagmeyer, U; Föth, H; Fokitis, E; Fulda-Quenzer, F; Fuster, J A; Gandelman, M; García, C; Gavillet, P; Gazis, E N; Gokieli, R; Golob, B; Gómez-Ceballos, G; Gonçalves, P; Graziani, E; Grosdidier, G; Grzelak, K; Guy, J; Haag, C; Hallgren, A; Hamacher, K; Hamilton, K; Haug, S; Hauler, F; Hedberg, V; Hennecke, M; Herr, H; Hoffman, J; Holmgren, S O; Holt, P J; Houlden, M A; Hultqvist, K; Jackson, J N; Jarlskog, G; Jarry, P; Jeans, D; Johansson, E K; Johansson, P D; Jonsson, P; Joram, C; Jungermann, L; Kapusta, F; Katsanevas, S; Katsoufis, E C; Kernel, G; Kersevan, B P; Kerzel, U; Kiiskinen, A P; King, B T; Kjaer, N J; Kluit, P; Kokkinias, P; Kourkoumelis, C; Kuznetsov, O; Krumshtein, Z; Kucharczyk, M; Lamsa, J; Leder, G; Ledroit, F; Leinonen, L; Leitner, R; Lemonne, J; Lepeltier, V; Lesiak, T; Liebig, W; Liko, D; Lipniacka, A; Lopes, J H; López, J M; Loukas, D; Lutz, P; Lyons, L; MacNaughton, J; Malek, A; Maltezos, S; Mandl, F; Marco, J; Marco, R; Maréchal, B; Margoni, M; Marin, J C; Mariotti, C; Markou, A; Martínez-Rivero, C; Masik, J; Mastroyiannopoulos, N; Matorras, F; Matteuzzi, C; Mazzucato, F; Mazzucato, M; McNulty, R; Meroni, C; Migliore, E; Mitaroff, W A; Mjörnmark, U; Moa, T; Moch, M; Mönig, K; Monge, R; Montenegro, J; Moraes, D; Moreno, S; Morettini, P; Müller, U; Münich, K; Mulders, M; Mundim, L; Murray, W; Muryn, B; Myatt, G; Myklebust, T; Nassiakou, M; Navarria, Francesco Luigi; Nawrocki, K; Nicolaidou, R; Nikolenko, M; Oblakowska-Mucha, A; Obraztsov, V F; Olshevskii, A G; Onofre, A; Orava, R; Österberg, K; Ouraou, A; Oyanguren, A; Paganoni, M; Paiano, S; Palacios, J P; Palka, H; Papadopoulou, T D; Pape, L; Parkes, C; Parodi, F; Parzefall, U; Passeri, A; Passon, O; Peralta, L; Perepelitsa, V F; Perrotta, A; Petrolini, A; Piedra, J; Pieri, L; Pierre, F; Pimenta, M; Piotto, E; Podobnik, T; Poireau, V; Pol, M E; Polok, G; Pozdnyakov, V; Pukhaeva, N; Pullia, A; Rames, J; Read, A; Rebecchi, P; Rehn, J; Reid, D; Reinhardt, R; Renton, P B; Richard, F; Rídky, J; Rivero, M; Rodríguez, D; Romero, A; Ronchese, P; Roudeau, P; Rovelli, T; Ruhlmann-Kleider, V; Ryabtchikov, D; Sadovskii, A; Salmi, L; Salt, J; Sander, C; Savoy-Navarro, A; Schwickerath, U; Segar, A; Sekulin, R L; Siebel, M; Sissakian, A N; Smadja, G; Smirnova, O G; Sokolov, A; Sopczak, A; Sosnowski, R; Spassoff, Tz; Stanitzki, M; Stocchi, A; Strauss, J; Stugu, B; Szczekowski, M; Szeptycka, M; Szumlak, T; Tabarelli de Fatis, T; Taffard, A C; Tegenfeldt, F; Timmermans, J; Tkatchev, L G; Tobin, M; Todorovova, S; Tomé, B; Tonazzo, A; Tortosa, P; Travnicek, P; Treille, D; Tristram, G; Trochimczuk, M; Troncon, C; Turluer, M L; Tyapkin, I A; Tyapkin, P; Tzamarias, S; Uvarov, V; Valenti, G; van Dam, P; Van Eldik, J; Van Lysebetten, A; Van Remortel, N; Van Vulpen, I; Vegni, G; Veloso, F; Venus, W A; Verdier, P; Verzi, V; Vilanova, D; Vitale, L; Vrba, V; Wahlen, H; Washbrook, A J; Weiser, C; Wicke, D; Wickens, J H; Wilkinson, G; Winter, M; Witek, M; Yushchenko, O P; Zalewska-Bak, A; Zalewski, P; Zavrtanik, D; Zhuravlov, V; Zimin, N I; Zintchenko, A; Zupan, M

    2004-01-01

    The tau lepton lifetime has been measured with the e+e- -> tau+tau- events collected by the DELPHI detector at LEP in the years 1991-1995. Three different methods have been exploited, using both one-prong and three-prong tau decay channels. Two measurements have been made using events in which both taus decay to a single charged particle. Combining these measurements gave tau_tau (1 prong) = 291.8 +/- 2.3 (stat) +/- 1.5 (sys) fs. A third measurement using taus which decayed to three charged particles yielded tau_tau (3 prong) = 288.6 +/- 2.4 (stat) +/- 1.3 (sys) fs. These were combined with previous DELPHI results to measure the tau lifetime, using the full LEP1 data sample, to be tau_tau = 290.9 +/- 1.4 (stat) +/- 1.0 (sys) fs.

  2. Higgs $\\to \\tau \\tau $ Analysis in the CMS Experiment

    CERN Document Server

    Olszewski, Michal

    2016-01-01

    In July 2012, the CMS and ATLAS collaborations announced the discovery of a Higgs boson with a mass of about 125 GeV and properties in agreement with expected from the Standard Model. In this note, we review the analysis performed for the H $\\to \\tau \\tau$ decay mode during the first stage of the LHC operation in the CMS. Further, we present the work done during the First Long Shutdown and the first stage of Run 2 of the LHC on the field of hadronic tau lepton offline reconstruction.

  3. Measurement of the $W \\to \\tau \

    CERN Document Server

    Aad, Georges; Abdallah, Jalal; Abdelalim, Ahmed Ali; Abdesselam, Abdelouahab; Abdinov, Ovsat; Abi, Babak; Abolins, Maris; Abramowicz, Halina; Abreu, Henso; Acerbi, Emilio; Acharya, Bobby Samir; Adams, David; Addy, Tetteh; Adelman, Jahred; Aderholz, Michael; Adomeit, Stefanie; Adragna, Paolo; Adye, Tim; Aefsky, Scott; Aguilar-Saavedra, Juan Antonio; Aharrouche, Mohamed; Ahlen, Steven; Ahles, Florian; Ahmad, Ashfaq; Ahsan, Mahsana; Aielli, Giulio; Akdogan, Taylan; Åkesson, Torsten Paul Ake; Akimoto, Ginga; Akimov, Andrei; Akiyama, Kunihiro; Alam, Mohammad; Alam, Muhammad Aftab; Albert, Justin; Albrand, Solveig; Aleksa, Martin; Aleksandrov, Igor; Alessandria, Franco; Alexa, Calin; Alexander, Gideon; Alexandre, Gauthier; Alexopoulos, Theodoros; Alhroob, Muhammad; Aliev, Malik; Alimonti, Gianluca; Alison, John; Aliyev, Magsud; Allport, Phillip; Allwood-Spiers, Sarah; Almond, John; Aloisio, Alberto; Alon, Raz; Alonso, Alejandro; Alviggi, Mariagrazia; Amako, Katsuya; Amaral, Pedro; Amelung, Christoph; Ammosov, Vladimir; Amorim, Antonio; Amorós, Gabriel; Amram, Nir; Anastopoulos, Christos; Ancu, Lucian Stefan; Andari, Nansi; Andeen, Timothy; Anders, Christoph Falk; Anders, Gabriel; Anderson, Kelby; Andreazza, Attilio; Andrei, George Victor; Andrieux, Marie-Laure; Anduaga, Xabier; Angerami, Aaron; Anghinolfi, Francis; Anjos, Nuno; Annovi, Alberto; Antonaki, Ariadni; Antonelli, Mario; Antonov, Alexey; Antos, Jaroslav; Anulli, Fabio; Aoun, Sahar; Aperio Bella, Ludovica; Apolle, Rudi; Arabidze, Giorgi; Aracena, Ignacio; Arai, Yasuo; Arce, Ayana; Archambault, John-Paul; Arfaoui, Samir; Arguin, Jean-Francois; Arik, Engin; Arik, Metin; Armbruster, Aaron James; Arnaez, Olivier; Arnault, Christian; Artamonov, Andrei; Artoni, Giacomo; Arutinov, David; Asai, Shoji; Asfandiyarov, Ruslan; Ask, Stefan; Åsman, Barbro; Asquith, Lily; Assamagan, Ketevi; Astbury, Alan; Astvatsatourov, Anatoli; Atoian, Grigor; Aubert, Bernard; Auge, Etienne; Augsten, Kamil; Aurousseau, Mathieu; Austin, Nicholas; Avolio, Giuseppe; Avramidou, Rachel Maria; Axen, David; Ay, Cano; Azuelos, Georges; Azuma, Yuya; Baak, Max; Baccaglioni, Giuseppe; Bacci, Cesare; Bach, Andre; Bachacou, Henri; Bachas, Konstantinos; Bachy, Gerard; Backes, Moritz; Backhaus, Malte; Badescu, Elisabeta; Bagnaia, Paolo; Bahinipati, Seema; Bai, Yu; Bailey, David; Bain, Travis; Baines, John; Baker, Oliver Keith; Baker, Mark; Baker, Sarah; Banas, Elzbieta; Banerjee, Piyali; Banerjee, Swagato; Banfi, Danilo; Bangert, Andrea Michelle; Bansal, Vikas; Bansil, Hardeep Singh; Barak, Liron; Baranov, Sergei; Barashkou, Andrei; Barbaro Galtieri, Angela; Barber, Tom; Barberio, Elisabetta Luigia; Barberis, Dario; Barbero, Marlon; Bardin, Dmitri; Barillari, Teresa; Barisonzi, Marcello; Barklow, Timothy; Barlow, Nick; Barnett, Bruce; Barnett, Michael; Baroncelli, Antonio; Barone, Gaetano; Barr, Alan; Barreiro, Fernando; Barreiro Guimarães da Costa, João; Barrillon, Pierre; Bartoldus, Rainer; Barton, Adam Edward; Bartsch, Detlef; Bartsch, Valeria; Bates, Richard; Batkova, Lucia; Batley, Richard; Battaglia, Andreas; Battistin, Michele; Battistoni, Giuseppe; Bauer, Florian; Bawa, Harinder Singh; Beare, Brian; Beau, Tristan; Beauchemin, Pierre-Hugues; Beccherle, Roberto; Bechtle, Philip; Beck, Hans Peter; Beckingham, Matthew; Becks, Karl-Heinz; Beddall, Andrew; Beddall, Ayda; Bedikian, Sourpouhi; Bednyakov, Vadim; Bee, Christopher; Begel, Michael; Behar Harpaz, Silvia; Behera, Prafulla; Beimforde, Michael; Belanger-Champagne, Camille; Bell, Paul; Bell, William; Bella, Gideon; Bellagamba, Lorenzo; Bellina, Francesco; Bellomo, Massimiliano; Belloni, Alberto; Beloborodova, Olga; Belotskiy, Konstantin; Beltramello, Olga; Ben Ami, Sagi; Benary, Odette; Benchekroun, Driss; Benchouk, Chafik; Bendel, Markus; Benekos, Nektarios; Benhammou, Yan; Benjamin, Douglas; Benoit, Mathieu; Bensinger, James; Benslama, Kamal; Bentvelsen, Stan; Berge, David; Bergeaas Kuutmann, Elin; Berger, Nicolas; Berghaus, Frank; Berglund, Elina; Beringer, Jürg; Bernardet, Karim; Bernat, Pauline; Bernhard, Ralf; Bernius, Catrin; Berry, Tracey; Bertin, Antonio; Bertinelli, Francesco; Bertolucci, Federico; Besana, Maria Ilaria; Besson, Nathalie; Bethke, Siegfried; Bhimji, Wahid; Bianchi, Riccardo-Maria; Bianco, Michele; Biebel, Otmar; Bieniek, Stephen Paul; Bierwagen, Katharina; Biesiada, Jed; Biglietti, Michela; Bilokon, Halina; Bindi, Marcello; Binet, Sebastien; Bingul, Ahmet; Bini, Cesare; Biscarat, Catherine; Bitenc, Urban; Black, Kevin; Blair, Robert; Blanchard, Jean-Baptiste; Blanchot, Georges; Blazek, Tomas; Blocker, Craig; Blocki, Jacek

    2011-01-01

    The cross section for the production of W bosons with subsequent decay W to tau nu is measured with the ATLAS detector at the LHC. The analysis is based on a data sample that was recorded in 2010 at a proton-proton center-of-mass energy of sqrt(s) = 7 TeV and corresponds to an integrated luminosity of 34 pb^-1. The cross section is measured in a region of high detector acceptance and then extrapolated to the full phase space. The product of the total W production cross section and the W to tau nu branching ratio is measured to be 11.1 +/- 0.3 (stat) +/- 1.7 (syst) +/- 0.4 (lumi) nb.

  4. Specialized psychosocial treatment plus treatment as usual (TAU) versus TAU for patients with cannabis use disorder and psychosis

    DEFF Research Database (Denmark)

    Hjorthøj, C R; Fohlmann, A; Larsen, Anne-Mette

    2013-01-01

    of motivational interviewing and cognitive behaviour therapy (CBT). TAU was targeted primarily at the psychotic disorder. The primary outcome was self-reported days with cannabis use in the preceding month. RESULTS: Pre-randomization cannabis use frequency was 14.9 [95% confidence interval (CI) 12.7-17.1] days......BACKGROUND: Cannabis abuse in psychotic patients is associated with rehospitalizations, reduced adherence and increased symptom severity. Previous psychosocial interventions have been ineffective in cannabis use, possibly because of low sample sizes and short interventions. We investigated whether...... adding CapOpus to treatment as usual (TAU) reduces cannabis use in patients with cannabis use disorder and psychosis. Method A total of 103 patients with psychosis and cannabis use disorder were centrally randomized to 6 months of CapOpus plus TAU (n = 52) or TAU (n = 51). CapOpus consisted mainly...

  5. Tau-er of Power

    OpenAIRE

    Kosik, Kenneth S.

    2015-01-01

    Editor’s Note: Tau protein helps nerve cells in the brain maintain their function and structure. When tau turns toxic, replicates, and spreads, neurons misfire and die. If neuroscientists can pinpoint the reasons for toxicity, identify what our author calls “a staggering number of possible modified tau states,” and find a way to block tau’s movement from cell to cell, then progress can be made in fighting any number of neurological disorders linked to this protein, including frontotemporal de...

  6. The relationship between cerebrospinal fluid markers of Alzheimer pathology and positron emission tomography tau imaging.

    Science.gov (United States)

    Gordon, Brian A; Friedrichsen, Karl; Brier, Matthew; Blazey, Tyler; Su, Yi; Christensen, Jon; Aldea, Patricia; McConathy, Jonathan; Holtzman, David M; Cairns, Nigel J; Morris, John C; Fagan, Anne M; Ances, Beau M; Benzinger, Tammie L S

    2016-08-01

    The two primary molecular pathologies in Alzheimer's disease are amyloid-β plaques and tau-immunoreactive neurofibrillary tangles. Investigations into these pathologies have been restricted to cerebrospinal fluid assays, and positron emission tomography tracers that can image amyloid-β plaques. Tau tracers have recently been introduced into the field, although the utility of the tracer and its relationship to other Alzheimer biomarkers are still unknown. Here we examined tau deposition in 41 cognitively normal and 11 cognitively impaired older adults using the radioactive tau ligand (18)F-AV-1451 (previously known as T807) who also underwent a lumbar puncture to assess cerebrospinal fluid levels of total tau (t-tau), phosphorylated tau181 (p-tau181) and amyloid-β42 Voxel-wise statistical analyses examined spatial patterns of tau deposition associated with cognitive impairment. We then related the amount of tau tracer uptake to levels of cerebrospinal fluid biomarkers. All analyses controlled for age and gender and, when appropriate, the time between imaging and lumbar puncture assessments. Symptomatic individuals (Clinical Dementia Rating > 0) demonstrated markedly increased levels of tau tracer uptake. This elevation was most prominent in the temporal lobe and temporoparietal junction, but extended more broadly into parietal and frontal cortices. In the entire cohort, there were significant relationships among all cerebrospinal fluid biomarkers and tracer uptake, notably for tau-related cerebrospinal fluid markers. After controlling for levels of amyloid-β42, the correlations with tau uptake were r = 0.490 (P < 0.001) for t-tau and r = 0.492 (P < 0.001) for p-tau181 Within the cognitively normal cohort, levels of amyloid-β42, but not t-tau or p-tau181, were associated with elevated tracer binding that was confined primarily to the medial temporal lobe and adjacent neocortical regions. AV-1451 tau binding in the medial temporal, parietal, and frontal cortices

  7. Photometric and spectroscopic monitoring of AA Tau, DN Tau, UX Tau A, T Tau, RY Tau, Lk Ca 4, and Lk Ca 7

    Science.gov (United States)

    Vrba, F. J.; Chugainov, P. F.; Weaver, W. B.; Stauffer, J. S.

    1993-01-01

    We report the results of a UBVRI photometric monitoring campaign for three classical T Tauri stars (AA Tau, DN Tau, and UX Tau A) and two weak emission line T Tauri stars (Lk Ca 4 and Lk Ca 7). Observations were obtained at three sites during a core observing period spanning UT 1985 October 14 through UT 1985 December 25, with additional observations continuing until UT 1986 April 6. Concurrent spectrophotometric observations were obtained for all main program stars except Lk Ca 7 and additionally for T Tau, RW Aur, and RY Tau. Periodic photometric variability, assumed to be the stars' rotation periods, were found for AA Tau, DN Tau, Lk Ca 4, and Lk Ca 7, respectively, as 8.2, 6.3, 3.4, and 5.7 days. Several U-filter flares were observed for Lk Ca 4 and Lk Ca 7, which are strongly concentrated toward phases of minimum light. Correlations are found between H-alpha line strengths and V magnitudes for AA Tau and RY Tau. An analysis of absolute color variations of classical T Tauri stars confirms that hot spots are the predominant cause of these stars' variability. Our overall results are consistent with earlier findings that long-lived cool spots are responsible for most of the variability found for weak-emission T Tauri stars, while temporal hot spots are primarily responsible for the observed variability found in classical T Tauri stars.

  8. Unique pathological tau conformers from Alzheimer’s brains transmit tau pathology in nontransgenic mice

    Science.gov (United States)

    Changolkar, Lakshmi; Stieber, Anna; Iba, Michiyo; McBride, Jennifer D.

    2016-01-01

    Filamentous tau aggregates are hallmark lesions in numerous neurodegenerative diseases, including Alzheimer’s disease (AD). Cell culture and animal studies showed that tau fibrils can undergo cell-to-cell transmission and seed aggregation of soluble tau, but this phenomenon was only robustly demonstrated in models overexpressing tau. In this study, we found that intracerebral inoculation of tau fibrils purified from AD brains (AD-tau), but not synthetic tau fibrils, resulted in the formation of abundant tau inclusions in anatomically connected brain regions in nontransgenic mice. Recombinant human tau seeded by AD-tau revealed unique conformational features that are distinct from synthetic tau fibrils, which could underlie the differential potency in seeding physiological levels of tau to aggregate. Therefore, our study establishes a mouse model of sporadic tauopathies and points to important differences between tau fibrils that are generated artificially and authentic ones that develop in AD brains. PMID:27810929

  9. Unique pathological tau conformers from Alzheimer's brains transmit tau pathology in nontransgenic mice.

    Science.gov (United States)

    Guo, Jing L; Narasimhan, Sneha; Changolkar, Lakshmi; He, Zhuohao; Stieber, Anna; Zhang, Bin; Gathagan, Ronald J; Iba, Michiyo; McBride, Jennifer D; Trojanowski, John Q; Lee, Virginia M Y

    2016-11-14

    Filamentous tau aggregates are hallmark lesions in numerous neurodegenerative diseases, including Alzheimer's disease (AD). Cell culture and animal studies showed that tau fibrils can undergo cell-to-cell transmission and seed aggregation of soluble tau, but this phenomenon was only robustly demonstrated in models overexpressing tau. In this study, we found that intracerebral inoculation of tau fibrils purified from AD brains (AD-tau), but not synthetic tau fibrils, resulted in the formation of abundant tau inclusions in anatomically connected brain regions in nontransgenic mice. Recombinant human tau seeded by AD-tau revealed unique conformational features that are distinct from synthetic tau fibrils, which could underlie the differential potency in seeding physiological levels of tau to aggregate. Therefore, our study establishes a mouse model of sporadic tauopathies and points to important differences between tau fibrils that are generated artificially and authentic ones that develop in AD brains. © 2016 Guo et al.

  10. The tau+ tau- production cross section near threshold revisited

    OpenAIRE

    Ruiz-Femenia, Pedro

    2002-01-01

    Next-to-next-to-leading contributions to the cross section sigma(e+e- -> tau+tau-) at energies close to threshold are analysed, taking into account the known non-relativistic effects and O(alpha^2) corrections. The numerical changes with respect to previous works are small, but the new corrections give a true estimate of the uncertainty in the theoretical calculation.

  11. Updated measurement of the $\\tau$ lepton lifetime

    CERN Document Server

    Barate, R; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Nief, J Y; Pietrzyk, B; Casado, M P; Chmeissani, M; Comas, P; Crespo, J M; Delfino, M C; Fernández, E; Fernández-Bosman, M; Garrido, L; Juste, A; Martínez, M; Merino, G; Miquel, R; Mir, L M; Padilla, C; Park, I C; Pascual, A; Perlas, J A; Riu, I; Sánchez, F; Teubert, F; Colaleo, A; Creanza, D; De Palma, M; Gelao, G; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Alemany, R; Becker, U; Bazarko, A O; Bright-Thomas, P G; Cattaneo, M; Cerutti, F; Dissertori, G; Drevermann, H; Forty, Roger W; Frank, M; Hagelberg, R; Hansen, J B; Harvey, J; Janot, P; Jost, B; Kneringer, E; Knobloch, J; Lehraus, Ivan; Mato, P; Minten, Adolf G; Moneta, L; Pacheco, A; Pusztaszeri, J F; Ranjard, F; Rizzo, G; Rolandi, Luigi; Rousseau, D; Schlatter, W D; Schmitt, M; Schneider, O; Tejessy, W; Tomalin, I R; Wachsmuth, H W; Wagner, A; Ajaltouni, Ziad J; Barrès, A; Boyer, C; Falvard, A; Ferdi, C; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rosnet, P; Rossignol, J M; Fearnley, Tom; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Rensch, B; Wäänänen, A; Daskalakis, G; Kyriakis, A; Markou, C; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Rougé, A; Rumpf, M; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Focardi, E; Parrini, G; Zachariadou, K; Corden, M; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Casper, David William; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Curtis, L; Dorris, S J; Halley, A W; Knowles, I G; Lynch, J G; O'Shea, V; Raine, C; Scarr, J M; Smith, K; Teixeira-Dias, P; Thompson, A S; Thomson, E; Thomson, F; Turnbull, R M; Buchmüller, O L; Dhamotharan, S; Geweniger, C; Graefe, G; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Girone, M; Goodsir, S M; Martin, E B; Moutoussi, A; Nash, J; Sedgbeer, J K; Spagnolo, P; Stacey, A M; Williams, M D; Ghete, V M; Girtler, P; Kuhn, D; Rudolph, G; Betteridge, A P; Bowdery, C K; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Sloan, Terence; Williams, M I; Galla, A; Giehl, I; Greene, A M; Hoffmann, C; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Sander, H G; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Benchouk, C; Bonissent, A; Bujosa, G; Carr, J; Coyle, P; Diaconu, C A; Etienne, F; Konstantinidis, N P; Leroy, O; Motsch, F; Payre, P; Talby, M; Sadouki, A; Thulasidas, M; Trabelsi, K; Aleppo, M; Antonelli, M; Ragusa, F; Berlich, R; Blum, Walter; Büscher, V; Dietl, H; Ganis, G; Gotzhein, C; Kroha, H; Lütjens, G; Lutz, Gerhard; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Saint-Denis, R; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Chen, S; Choi, Y; Cordier, A; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Höcker, A; Jacholkowska, A; Jacquet, M; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Nikolic, I A; Schune, M H; Simion, S; Tournefier, E; Veillet, J J; Videau, I; Zerwas, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Palla, Fabrizio; Sanguinetti, G; Sciabà, A; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Vannini, C; Venturi, A; Verdini, P G; Blair, G A; Bryant, L M; Chambers, J T; Gao, Y; Green, M G; Medcalf, T; Perrodo, P; Strong, J A; Von Wimmersperg-Töller, J H; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Norton, P R; Thompson, J C; Wright, A E; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Black, S N; Dann, J H; Johnson, R P; Kim, H Y; Litke, A M; McNeil, M A; Taylor, G; Booth, C N; Boswell, R; Brew, C A J; Cartwright, S L; Combley, F; Kelly, M S; Lehto, M H; Newton, W M; Reeve, J; Thompson, L F; Böhrer, A; Brandt, S; Cowan, G D; Grupen, Claus; Lutters, G; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Musolino, G; Pütz, J; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Charles, E; Elmer, P; Ferguson, D P S; González, S; Greening, T C; Hayes, O J; Hu, H; Jin, S; McNamara, P A; Nachtman, J M; Nielsen, J; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, J; Wu Sau Lan; Wu, X; Yamartino, J M; Zobernig, G

    1997-01-01

    A new measurement of the mean lifetime of the tau lepton is presented. Three different analysis methods are applied to a sample of 90000 tau pairs, collected in 1993 and 1994 with the ALEPH detector at LEP. The average of this measurement and those previously published by ALEPH is tau_tau = 290.1 +- 1.5 +- 1.1 fs.

  12. Induction of intracellular tau aggregation is promoted by α-synuclein seeds and provides novel insights into the hyperphosphorylation of tau.

    Science.gov (United States)

    Waxman, Elisa A; Giasson, Benoit I

    2011-05-25

    Intracytoplasmic proteinaceous inclusions, primarily composed of tau or α-synuclein (α-syn), are predominant pathological features of Alzheimer's disease (AD) and Parkinson's disease (PD), respectively. However, the coexistence of these pathological aggregates is identified in many neurodegenerative disorders, including spectrum disorders of AD and PD. Whereas α-syn can spontaneously polymerize into amyloidogenic fibrils, in vitro, tau polymerization requires an inducing agent. The current study presents a human-derived cellular model, in which recombinant, preformed α-syn fibrils cross-seed intracellular tau to promote the formation of neurofibrillary tangle-like aggregates. These aggregates were hyperphosphorylated, Triton insoluble, and thioflavin-S positive, either comingling with endogenously expressed α-syn aggregates or induced by only exogenously applied recombinant α-syn fibrils. Furthermore, filamentous, amyloidogenic tau took over the cellular soma, displacing the nucleus and isolating or displacing organelles, likely preventing cellular function. Although a significant proportion of wild-type tau formed these cellular inclusions, the P301L mutation in tau increased aggregation propensity resulting from α-syn seeds to over 50% of total tau protein. The role of phosphorylation on the development of these tau aggregates was investigated by coexpressing glycogen synthase kinase 3 β or microtubule-associated protein/microtubule affinity-regulating kinase 2. Expression of either kinase inhibited the formation of α-syn-induced tau aggregates. Analyses of phosphorylation sites suggest that multiple complex factors may be associated with this effect and that Triton-soluble versus Triton-insoluble tau may be independently targeted by kinases. The current work not only provides an exceptional cellular model of tau pathology, but also examines α-syn-induced tau inclusion formation and provides novel insights into hyperphosphorylation observed in disease.

  13. \\tau lepton decays and CVC

    OpenAIRE

    Cherepanov, V. A.; Eidelman, S. I.

    2009-01-01

    We use experimental data on $e^+e^- \\to \\eta (\\eta^{\\prime})\\pi^+\\pi^-$ and conservation of vector current to estimate the branching fractions of $\\tau^-$ decay to $\\eta (\\eta^{\\prime})\\pi^-\\pi^0\

  14. Tensor interactions and {tau} decays

    Energy Technology Data Exchange (ETDEWEB)

    Godina Nava, J.J.; Lopez Castro, G. [Departamento de Fisica, Cinvestav del IPN, Apartado Postal 14-740, 07000 Mexico, D.F. (Mexico)

    1995-09-01

    We study the effects of charged tensor weak currents on the strangeness-changing decays of the {tau} lepton. First, we use the available information on the {ital K}{sub {ital e}3}{sup +} form factors to obtain {ital B}({tau}{sup {minus}}{r_arrow}{ital K}{sup {minus}}{pi}{sup 0}{nu}{sub {tau}}){similar_to}10{sup {minus}4} when the {ital K}{pi} system is produced in an antisymmetric tensor configuration. Then we propose a mechanism for the direct production of the {ital K}{sub 2}{sup *}(1430) in {tau} decays. Using the current upper limit on this decay we set a bound on the symmetric tensor interactions.

  15. $\\tau^{-} \\to (\\pi \\pi \\pi )^{-} \

    CERN Document Server

    Gómez-Dumm, D; Portolés, J; 10.1016/j.nuclphysbps.2004.04.166

    2004-01-01

    We analyse tau to pi pi pi nu /sub tau / decays within the framework of the resonance effective theory of QCD. We have worked out the relevant Lagrangian that describes the axial-vector current hadronization contributing to these processes, and the new coupling constants that arise have been constrained by imposing the asymptotic behaviour of the corresponding spectral function within QCD. Hence we compare the theoretical framework with the experimental data, obtaining a good quality fit from the ALEPH spectral function and branching ratio. We also get values for the mass and on-shell width of the a/sub 1/(1260) resonance, and provide the tau to pi pi pi nu /sub tau / structure functions that have been measured by OPAL and CLEO-II finding an excellent agreement.

  16. Selected CSF biomarkers indicate no evidence of early neuroinflammation in Huntington disease

    DEFF Research Database (Denmark)

    Vinther-Jensen, Tua; Börnsen, Lars Svend; Budtz-Jorgensen, Esben

    2016-01-01

    Objective: To investigate CSF biomarkers of neuroinflammation and neurodegeneration in Huntington disease (HD) gene-expansion carriers compared to controls and to investigate these biomarkers in association with clinical HD rating scales and disease burden score. Methods: We collected CSF from 32...... premanifest and 48 manifest HD gene-expansion carriers and 24 gene-expansion negative at-risk controls. We examined biomarkers of neuroinflammation (matrix metalloproteinase 9, C-X-C motif chemokine 13, terminal complement complex, chitinase-3-like-protein 1 [CHI3L1], and osteopontin [OPN...... was the only biomarker that increased in premanifest stages and no evidence of early involvement of neuroinflammation in HD was found. However, we found that the biomarkers for neurodegeneration, MBP and tau, increased during the disease course in manifest HD gene-expansion carriers and were associated...

  17. $K^{0}_{S}$ production in $\\tau$ decays

    CERN Document Server

    Barate, R; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Nief, J Y; Pietrzyk, B; Boix, G; Casado, M P; Chmeissani, M; Crespo, J M; Delfino, M C; Fernández, E; Fernández-Bosman, M; Garrido, L; Graugès-Pous, E; Juste, A; Martínez, M; Merino, G; Miquel, R; Mir, L M; Park, I C; Pascual, A; Perlas, J A; Riu, I; Sánchez, F; Colaleo, A; Creanza, D; De Palma, M; Gelao, G; Iaselli, Giuseppe; Maggi, G; Maggi, M; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Alemany, R; Becker, U; Bright-Thomas, P G; Casper, David William; Cattaneo, M; Cerutti, F; Ciulli, V; Dissertori, G; Drevermann, H; Forty, Roger W; Frank, M; Hagelberg, R; Hansen, J B; Harvey, J; Janot, P; Jost, B; Lehraus, Ivan; Mato, P; Minten, Adolf G; Moneta, L; Pacheco, A; Pusztaszeri, J F; Ranjard, F; Rolandi, Luigi; Rousseau, D; Schlatter, W D; Schmitt, M; Schneider, O; Tejessy, W; Teubert, F; Tomalin, I R; Wachsmuth, H W; Wagner, A; Ajaltouni, Ziad J; Badaud, F; Chazelle, G; Deschamps, O; Falvard, A; Ferdi, C; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rosnet, P; Fearnley, Tom; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Rensch, B; Wäänänen, A; Daskalakis, G; Kyriakis, A; Markou, C; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Rougé, A; Rumpf, M; Valassi, Andrea; Verderi, M; Videau, H L; Boccali, T; Focardi, E; Parrini, G; Zachariadou, K; Corden, M; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Curtis, L; Dorris, S J; Halley, A W; Lynch, J G; Negus, P; O'Shea, V; Raine, C; Scarr, J M; Smith, K; Teixeira-Dias, P; Thompson, A S; Thomson, E; Thomson, F; Buchmüller, O L; Dhamotharan, S; Geweniger, C; Graefe, G; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Girone, M; Goodsir, S M; Martin, E B; Marinelli, N; Moutoussi, A; Nash, J; Sedgbeer, J K; Spagnolo, P; Williams, M D; Ghete, V M; Girtler, P; Kneringer, E; Kuhn, D; Rudolph, G; Betteridge, A P; Bowdery, C K; Buck, P G; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Williams, M I; Giehl, I; Greene, A M; Hoffmann, C; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Sander, H G; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Benchouk, C; Bonissent, A; Bujosa, G; Carr, J; Coyle, P; Etienne, F; Leroy, O; Motsch, F; Payre, P; Talby, M; Sadouki, A; Thulasidas, M; Trabelsi, K; Aleppo, M; Antonelli, M; Ragusa, F; Berlich, R; Blum, Walter; Büscher, V; Dietl, H; Ganis, G; Gotzhein, C; Kroha, H; Lütjens, G; Lutz, Gerhard; Mannert, C; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Chen, S; Choi, Y; Cordier, A; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Höcker, A; Jacholkowska, A; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Nikolic, I A; Schune, M H; Tournefier, E; Veillet, J J; Videau, I; Zerwas, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Palla, Fabrizio; Rizzo, G; Sanguinetti, G; Sciabà, A; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Vannini, C; Venturi, A; Verdini, P G; Blair, G A; Bryant, L M; Chambers, J T; Green, M G; Medcalf, T; Perrodo, P; Strong, J A; Von Wimmersperg-Töller, J H; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Norton, P R; Thompson, J C; Wright, A E; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Black, S N; Dann, J H; Johnson, R P; Kim, H Y; Konstantinidis, N P; Litke, A M; McNeil, M A; Taylor, G; Booth, C N; Brew, C A J; Cartwright, S L; Combley, F; Kelly, M S; Lehto, M H; Reeve, J; Thompson, L F; Affholderbach, K; Böhrer, A; Brandt, S; Cowan, G D; Grupen, Claus; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Musolino, G; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Charles, E; Elmer, P; Ferguson, D P S; Gao, Y; González, S; Greening, T C; Hayes, O J; Hu, H; Jin, S; McNamara, P A; Nachtman, J M; Nielsen, J; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, J; Wu Sau Lan; Wu, X; Yamartino, J M; Zobernig, G

    1998-01-01

    From a sample of about 160k $\\mbox{Z}\\!\\!\\to\\!\\!\\tau^+\\tau^-$ candidates collected with the ALEPH detector at LEP between 1991 and 1995, $\\tau$ lepton decays involving $K^0_S\\!\\to\\!\\pi^+\\pi^-$ are studied. The $K^0_SK^0_L$ associated production in $\\tau$ decays is also investigated. The branching ratios are measured for the inclusive decay $B(\\tau^-\\!\\!\\to\\!\\!K^0_SX^-\

  18. Closing the tau loop: the missing tau mutation.

    Science.gov (United States)

    McCarthy, Allan; Lonergan, Roisin; Olszewska, Diana A; O'Dowd, Sean; Cummins, Gemma; Magennis, Brian; Fallon, Emer M; Pender, Niall; Huey, Edward D; Cosentino, Stephanie; O'Rourke, Killian; Kelly, Brendan D; O'Connell, Martin; Delon, Isabelle; Farrell, Michael; Spillantini, Maria Grazia; Rowland, Lewis P; Fahn, Stanley; Craig, Peter; Hutton, Michael; Lynch, Tim

    2015-10-01

    Frontotemporal lobar degeneration comprises a group of disorders characterized by behavioural, executive, language impairment and sometimes features of parkinsonism and motor neuron disease. In 1994 we described an Irish-American family with frontotemporal dementia linked to chromosome 17 associated with extensive tau pathology. We named this disinhibition-dementia-parkinsonism-amyotrophy complex. We subsequently identified mutations in the MAPT gene. Eleven MAPT gene splice site stem loop mutations were identified over time except for 5' splice site of exon 10. We recently identified another Irish family with autosomal dominant early amnesia and behavioural change or parkinsonism associated with the 'missing' +15 mutation at the intronic boundary of exon 10. We performed a clinical, neuropsychological and neuroimaging study on the proband and four siblings, including two affected siblings. We sequenced MAPT and performed segregation analysis. We looked for a biological effect of the tau variant by performing real-time polymerase chain reaction analysis of RNA extracted from human embryonic kidney cells transfected with exon trapping constructs. We found a c.915+15A>C exon 10/intron 10 stem loop mutation in all affected subjects but not in the unaffected. The c.915+15A>C variant caused a shift in tau splicing pattern to a predominantly exon 10+ pattern presumably resulting in predominant 4 repeat tau and little 3 repeat tau. This strongly suggests that the c.915+15A>C variant is a mutation and that it causes frontotemporal dementia linked to chromosome 17 in this pedigree by shifting tau transcription and translation to +4 repeat tau. Tau (MAPT) screening should be considered in families where amnesia or atypical parkinsonism coexists with behavioural disturbance early in the disease process. We describe the final missing stem loop tau mutation predicted 15 years ago. Mutations have now been identified at all predicted sites within the 'stem' when the stem

  19. Comparing the performance characteristics of CSF-TRUST and CSF-VDRL for syphilis: a cross-sectional study

    Science.gov (United States)

    Gu, Weiming; Yang, Yang; Wu, Lei; Yang, Sheng; Ng, Lai-King

    2013-01-01

    Objective In this study, we aimed to determine the performance characteristics of toluidine red unheated serum test on cerebrospinal fluids (CSF-TRUST) as compared to venereal disease research laboratory test on cerebrospinal fluids (CSF-VDRL) for laboratory the diagnosis of neurosyphilis. Design A cross-sectional study. Setting Sexually transmitted infections (STIs) clinics. Participants and methods CSF and serum samples were collected from 824 individual STD clinic patients who have syphilis and are suspected to progress to neurosyphilis within a 9-month period. CSF-VDRL and CSF-TRUST were performed parallelly on the same day when collected. Treponema pallidum particle agglutination (TPPA) tests were also performed on the CSF and the serum samples, and biochemical analysis of the CSF samples was also performed. Results The overall agreement between CSF-TRUST and CSF-VDRL was 97.3%. The reactive ratios of the CSF samples were 22.1% by CSF-TRUST and 24.8% by CSF-VDRL, respectively. All CSF-TRUST-reactive cases were reactive in the CSF-VDRL. Twenty-two samples with CSF-TRUST-negative were tested CSF-VDRL-reactive with low titres (1 : 1 to 1 : 4). Over 97% of the double-reactive CSF samples (CSF-VDRL and CSF-TRUST) had an identical titre or a titre within a two-fold difference. The agreement of CSF-TPPA and CSF-VDRL was 71.9%. Similarly, the agreement of CSF-TPPA and CSF-TRUST was 69.2%. Conclusions Our results revealed that CSF-TRUST could be used as an option for CSF examination in settings without CSF-VDRL in place. PMID:23430600

  20. Comparing the performance characteristics of CSF-TRUST and CSF-VDRL for syphilis: a cross-sectional study.

    Science.gov (United States)

    Gu, Weiming; Yang, Yang; Wu, Lei; Yang, Sheng; Ng, Lai-King

    2013-01-01

    In this study, we aimed to determine the performance characteristics of toluidine red unheated serum test on cerebrospinal fluids (CSF-TRUST) as compared to venereal disease research laboratory test on cerebrospinal fluids (CSF-VDRL) for laboratory the diagnosis of neurosyphilis. A cross-sectional study. Sexually transmitted infections (STIs) clinics. CSF and serum samples were collected from 824 individual STD clinic patients who have syphilis and are suspected to progress to neurosyphilis within a 9-month period. CSF-VDRL and CSF-TRUST were performed parallelly on the same day when collected. Treponema pallidum particle agglutination (TPPA) tests were also performed on the CSF and the serum samples, and biochemical analysis of the CSF samples was also performed. The overall agreement between CSF-TRUST and CSF-VDRL was 97.3%. The reactive ratios of the CSF samples were 22.1% by CSF-TRUST and 24.8% by CSF-VDRL, respectively. All CSF-TRUST-reactive cases were reactive in the CSF-VDRL. Twenty-two samples with CSF-TRUST-negative were tested CSF-VDRL-reactive with low titres (1 : 1 to 1 : 4). Over 97% of the double-reactive CSF samples (CSF-VDRL and CSF-TRUST) had an identical titre or a titre within a two-fold difference. The agreement of CSF-TPPA and CSF-VDRL was 71.9%. Similarly, the agreement of CSF-TPPA and CSF-TRUST was 69.2%. Our results revealed that CSF-TRUST could be used as an option for CSF examination in settings without CSF-VDRL in place.

  1. Extracellular Tau Oligomers Induce Invasion of Endogenous Tau into the Somatodendritic Compartment and Axonal Transport Dysfunction.

    Science.gov (United States)

    Swanson, Eric; Breckenridge, Leigham; McMahon, Lloyd; Som, Sreemoyee; McConnell, Ian; Bloom, George S

    2017-01-01

    Aggregates composed of the microtubule associated protein, tau, are a hallmark of Alzheimer's disease and non-Alzheimer's tauopathies. Extracellular tau can induce the accumulation and aggregation of intracellular tau, and tau pathology can be transmitted along neural networks over time. There are six splice variants of central nervous system tau, and various oligomeric and fibrillar forms are associated with neurodegeneration in vivo. The particular extracellular forms of tau capable of transferring tau pathology from neuron to neuron remain ill defined, however, as do the consequences of intracellular tau aggregation on neuronal physiology. The present study was undertaken to compare the effects of extracellular tau monomers, oligomers, and filaments comprising various tau isoforms on the behavior of cultured neurons. We found that 2N4R or 2N3R tau oligomers provoked aggregation of endogenous intracellular tau much more effectively than monomers or fibrils, or of oligomers made from other tau isoforms, and that a mixture of all six isoforms most potently provoked intracellular tau accumulation. These effects were associated with invasion of tau into the somatodendritic compartment. Finally, we observed that 2N4R oligomers perturbed fast axonal transport of membranous organelles along microtubules. Intracellular tau accumulation was often accompanied by increases in the run length, run time and instantaneous velocity of membranous cargo. This work indicates that extracellular tau oligomers can disrupt normal neuronal homeostasis by triggering axonal tau accumulation and loss of the polarized distribution of tau, and by impairing fast axonal transport.

  2. Novel human neuronal tau model exhibiting neurofibrillary tangles and transcellular propagation.

    Science.gov (United States)

    Reilly, Patrick; Winston, Charisse N; Baron, Kelsey R; Trejo, Margarita; Rockenstein, Edward M; Akers, Johnny C; Kfoury, Najla; Diamond, Marc; Masliah, Eliezer; Rissman, Robert A; Yuan, Shauna H

    2017-10-01

    Tauopathies are a class of neurodegenerative diseases, including Alzheimer's disease, frontotemporal dementia and progressive supranuclear palsy, which are associated with the pathological aggregation of tau protein into neurofibrillary tangles (NFT). Studies have characterized tau as a "prion-like" protein given its ability to form distinct, stable amyloid conformations capable of transcellular and multigenerational propagation in clonal fashion. It has been proposed that progression of tauopathy could be due to the prion-like propagation of tau, suggesting the possibility that end-stage pathologies, like NFT formation, may require an instigating event such as tau seeding. To investigate this, we applied a novel human induced pluripotent stem cell (hiPSC) system we have developed to serve as a human neuronal model. We introduced the tau repeat domain (tau-RD) with P301L and V337M (tau-RD-LM) mutations into hiPSC-derived neurons and observed expression of tau-RD at levels similar to total tau in postmortem AD brains. Tau aggregation occurred without the addition of recombinant tau fibrils. The conditioned media from tau-RD cultures contained tau-RD seeds, which were capable of inducing aggregate formation in homotypic mode in non-transduced recipient neuronal cultures. The resultant NFTs were thioflavin-positive, silver stain-positive, and assumed fibrillary appearance on transmission electron microscopy (TEM) with immunogold, which revealed paired helical filament 1 (PHF1)-positive NFTs, representing possible recruitment of endogenous tau in the aggregates. Functionally, expression of tau-RD caused neurotoxicity that manifested as axon retraction, synaptic density reduction, and enlargement of lysosomes. The results of our hiPSC study were reinforced by the observation that Tau-RD-LM is excreted in exosomes, which mediated the transfer of human tau to wild-type mouse neurons in vivo. Our hiPSC human neuronal system provides a model for further studies of tau

  3. G-CSF plus preemptive plerixafor vs hyperfractionated CY plus G-CSF for autologous stem cell mobilization in multiple myeloma: effectiveness, safety and cost analysis.

    Science.gov (United States)

    Antar, A; Otrock, Z K; Kharfan-Dabaja, M A; Ghaddara, H A; Kreidieh, N; Mahfouz, R; Bazarbachi, A

    2015-06-01

    The optimal stem cell mobilization regimen for patients with multiple myeloma (MM) remains undefined. We retrospectively compared our experience in hematopoietic cell mobilization in 83 MM patients using fractionated high-dose CY and G-CSF with G-CSF plus preemptive plerixafor. All patients in the CY group (n=56) received fractionated high-dose CY (5 g/m(2) divided into five doses of 1 g/m(2) every 3 h) with G-CSF. All patients in the plerixafor group (n=27) received G-CSF and plerixafor preemptively based on an established algorithm. Compared with plerixafor, CY use was associated with higher total CD34+ cell yield (7.5 × 10(6) vs 15.5 × 10(6) cells/kg, P=0.005). All patients in both groups yielded ⩾4 × 10(6) CD34+ cells/kg. Conversely, CY use was associated with high frequency of febrile neutropenia, blood and platelet transfusions need and hospitalizations. The average total cost of mobilization in Lebanon was slightly higher in the plerixafor group ($7886 vs $7536; P=0.16). Our data indicate robust stem cell mobilization in MM patients with either fractionated high-dose CY and G-CSF or G-CSF alone with preemptive plerixafor. The chemo-mobilization approach was associated with twofold stem cell yield, slightly lower cost but significantly increased toxicity.

  4. Multiplexed immunoassay panel identifies novel CSF biomarkers for Alzheimer's disease diagnosis and prognosis.

    Directory of Open Access Journals (Sweden)

    Rebecca Craig-Schapiro

    Full Text Available Clinicopathological studies suggest that Alzheimer's disease (AD pathology begins ∼10-15 years before the resulting cognitive impairment draws medical attention. Biomarkers that can detect AD pathology in its early stages and predict dementia onset would, therefore, be invaluable for patient care and efficient clinical trial design. We utilized a targeted proteomics approach to discover novel cerebrospinal fluid (CSF biomarkers that can augment the diagnostic and prognostic accuracy of current leading CSF biomarkers (Aβ42, tau, p-tau181.Using a multiplexed Luminex platform, 190 analytes were measured in 333 CSF samples from cognitively normal (Clinical Dementia Rating [CDR] 0, very mildly demented (CDR 0.5, and mildly demented (CDR 1 individuals. Mean levels of 37 analytes (12 after Bonferroni correction were found to differ between CDR 0 and CDR>0 groups. Receiver-operating characteristic curve analyses revealed that small combinations of a subset of these markers (cystatin C, VEGF, TRAIL-R3, PAI-1, PP, NT-proBNP, MMP-10, MIF, GRO-α, fibrinogen, FAS, eotaxin-3 enhanced the ability of the best-performing established CSF biomarker, the tau/Aβ42 ratio, to discriminate CDR>0 from CDR 0 individuals. Multiple machine learning algorithms likewise showed that the novel biomarker panels improved the diagnostic performance of the current leading biomarkers. Importantly, most of the markers that best discriminated CDR 0 from CDR>0 individuals in the more targeted ROC analyses were also identified as top predictors in the machine learning models, reconfirming their potential as biomarkers for early-stage AD. Cox proportional hazards models demonstrated that an optimal panel of markers for predicting risk of developing cognitive impairment (CDR 0 to CDR>0 conversion consisted of calbindin, Aβ42, and age.Using a targeted proteomic screen, we identified novel candidate biomarkers that complement the best current CSF biomarkers for distinguishing very

  5. Lack of association between TDP-43 pathology and tau mis-splicing in Alzheimer's disease.

    Science.gov (United States)

    Niblock, Michael; Hortobágyi, Tibor; Troakes, Claire; Al-Sarraj, Safa; Spickett, Carl; Jones, Rebecca; Shaw, Christopher E; Gallo, Jean-Marc

    2016-01-01

    A proportion of Alzheimer's disease cases displays inclusions of the RNA-binding protein, TDP-43. Considering the pathogenic role of tau mis-splicing, we compared tau isoform expression between Alzheimer's disease cases with or without TDP-43 inclusions. The average ratio of tau isoforms containing or lacking exon 10 (4R/3R ratio) or the total level of tau mRNA was not significantly different between cases with or without TDP-43 pathology in any of the brain regions examined. Although TDP-43 functions may be affected, TDP-43 does not critically regulate expression or splicing of tau in Alzheimer's disease suggesting that TDP-43 contributes to Alzheimer's disease through mechanisms independent of tau. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

  6. CSF/serum quotient graphs for the evaluation of intrathecal C4 synthesis

    Directory of Open Access Journals (Sweden)

    Rey Alexis

    2009-07-01

    Full Text Available Abstract Background Cerebrospinal fluid (CSF/serum quotient graphs have been used previously to determine local synthesis in brain of immunoglobulins and C3 complement component. The aim of this study was to use the same technique to construct quotient graphs, or Reibergrams, for the beta globulin C4 and to evaluate the method for assessing intrathecal synthesis in neurological disease. Methods The constants in the previously-defined Reibergram for immunoglobulin IgA were used to calculate the CSF/serum quotient for C4. CSF and serum were analyzed for C4, IgA and albumin from a total of 12 patients with meningoencephalitis caused by encapsulated microorganisms and 10 subjects without infections or inflammatory neurological disease, some of which had dysfunction of the blood-CSF barrier, Results The formula and C4 Reibergram with the constants previously found for IgA, determined the intrathecal C4 synthesis in CSF. The intrathecal C4 fraction in CSF (C4 loc in mg/l was compared to the C4-Index (fraction of CSF: serum for C 4/fraction of CSF: serum for albumin. There was a significant correlation between the two formulae. The CSF/Serum quotient graph was superior for detecting intrathecal synthesis of C4 under variable conditions of blood-CSF barrier permeability. Conclusion The C4 Reibergram can be used to quantify the intrathecal synthesis of this component of the complement system in different infectious diseases of the central nervous system and is especially useful for patients with blood-brain barrier dysfunction.

  7. $H \\rightarrow \\tau^+ \\tau^- \\gamma$ as a Probe of the $\\tau$ Magnetic Dipole Moment

    CERN Document Server

    Galon, Iftah; Tait, Tim M P

    2016-01-01

    Low energy observables involving the Standard Model fermions which are chirality-violating, such as anomalous electromagnetic moments, necessarily involve an insertion of the Higgs in order to maintain $SU(2) \\times U(1)$ gauge invariance. As the result, the properties of the Higgs boson measured at the LHC impact our understanding of the associated low-energy quantities. We illustrate this feature with a discussion of the electromagnetic moments of the $\\tau$-lepton, as probed by the rare decay $H \\rightarrow \\tau^+ \\tau^- \\gamma$. We assess the feasibility of measuring this decay at the LHC, and show that the current bounds from lower energy measurements imply that $13~\\rm{TeV}$ running is very likely to improve our understanding of new physics contributing to the anomalous magnetic moment of the tau.

  8. Tau Induces Cooperative Taxol Binding to Microtubules

    Science.gov (United States)

    Ross, Jennifer; Santangelo, Christian; Victoria, Makrides; Fygenson, Deborah

    2004-03-01

    Taxol and tau are two ligands which stabilize the microtubule (MT) lattice. Taxol is an anti-mitotic drug that binds β tubulin in the MT interior. Tau is a MT-associated protein that binds both α and β tubulin on the MT exterior. Both taxol and tau reduce MT dynamics and promote tubulin polymerization. Tau alone also acts as a buttress to bundle, stiffen, and space MTs. A structural study recently suggested that taxol and tau may interact by binding to the same site. Using fluorescence recovery after photobleaching, we find that tau induces taxol to bind MTs cooperatively depending on the tau concentration. We develop a model that correctly fits the data in the absence of tau and yields a measure of taxol cooperativity when tau is present.

  9. Insulin dysfunction and Tau pathology

    Directory of Open Access Journals (Sweden)

    Noura eEl Khoury

    2014-02-01

    Full Text Available The neuropathological hallmarks of Alzheimer's disease (AD include senile plaques of β-amyloid (Aβ peptides (a cleavage product of the Amyloid Precursor Protein, or APP and neurofibrillary tangles (NFT of hyperphosphorylated Tau protein assembled in paired helical filaments (PHF. NFT pathology is important since it correlates with the degree of cognitive impairment in AD.Only a small proportion of AD is due to genetic variants, whereas the large majority of cases (~99% is late onset and sporadic in origin. The cause of sporadic AD is likely to be multifactorial, with external factors interacting with biological or genetic susceptibilities to accelerate the manifestation of the disease.Insulin dysfunction, manifested by diabetes mellitus (DM might be such factor, as there is extensive data from epidemiological studies suggesting that DM is associated with an increased relative risk for AD. Type 1 diabetes (T1DM and type 2 diabetes (T2DM are known to affect multiple cognitive functions in patients. In this context, understanding the effects of diabetes on Tau pathogenesis is important since tau pathology show a strong relationship to dementia in AD, and to memory loss in normal aging and mild cognitive impairment.Here, we reviewed preclinical studies that link insulin dysfunction to Tau protein pathogenesis, one of the major pathological hallmarks of AD. We found more than 30 studies reporting on Tau phosphorylation in a mouse or rat model of insulin dysfunction. We also payed attention to potential sources of artifacts, such as hypothermia and anesthesia, that were demonstrated to results in Tau hyperphosphorylation and could major confounding experimental factors. We found that very few studies reported the temperature of the animals, and only a handful did not use anesthesia. Overall, most published studies showed that insulin dysfunction can promote Tau hyperphosphorylation and pathology, both directly and indirectly, through hypothermia.

  10. Neoplastic Meningitis: How MRI and CSF Cytology Are Influenced by CSF Cell Count and Tumor Type

    Directory of Open Access Journals (Sweden)

    P. Prömmel

    2013-01-01

    Full Text Available Background. Although CSF cytology and MRI are standard methods to diagnose neoplastic meningitis (NM, this complication of neoplastic disease remains difficult to detect. We therefore reevaluated the sensitivity of gadolinium (GD-enhanced MRI and cerebrospinal-fluid (CSF-cytology and the relevance of tumor type and CSF cell count. Methods. We retrospectively identified 111 cases of NM diagnosed in our CSF laboratory since 1990 with complete documentation of both MRI and CSF cytology. 37 had haematological and 74 solid neoplasms. CSF cell counts were increased in 74 and normal in 37 patients. Results. In hematological neoplasms, MRI was positive in 49% and CSF cytology in 97%. In solid tumors, the sensitivity of MRI was 80% and of cytology 78%. With normal CSF cell counts, MRI was positive in 59% (50% hematological, 72% solid malignancies and CSF cytology in 76% (92% in hematological, 68% in solid neoplasms. In cases of elevated cell counts, the sensitivity of MRI was 72% (50% for hematological, 83% for solid malignancies and of CSF cytology 91% (100% for haematological and 85% for solid neoplasms. 91% of cytologically positive cases were diagnosed at first and another 7% at second lumbar puncture. Routine protein analyses had a low sensitivity in detecting NM. Conclusions. The high overall sensitivity of MRI was only confirmed for NM from solid tumors and for elevated CSF cell counts. With normal cell counts and haematological neoplasms, CSF-cytology was superior to MRI. None of the analysed routine CSF proteins had an acceptable sensitivity and specificity in detecting leptomeningeal disease.

  11. SNPs associated with cerebrospinal fluid phospho-tau levels influence rate of decline in Alzheimer's disease.

    Directory of Open Access Journals (Sweden)

    Carlos Cruchaga

    2010-09-01

    Full Text Available Alzheimer's Disease (AD is a complex and multifactorial disease. While large genome-wide association studies have had some success in identifying novel genetic risk factors for AD, case-control studies are less likely to uncover genetic factors that influence progression of disease. An alternative approach to identifying genetic risk for AD is the use of quantitative traits or endophenotypes. The use of endophenotypes has proven to be an effective strategy, implicating genetic risk factors in several diseases, including anemia, osteoporosis and heart disease. In this study we identify a genetic factor associated with the rate of decline in AD patients and present a methodology for identification of other such factors. We have used an established biomarker for AD, cerebrospinal fluid (CSF tau phosphorylated at threonine 181 (ptau(181 levels as an endophenotype for AD, identifying a SNP, rs1868402, in the gene encoding the regulatory sub-unit of protein phosphatase B, associated with CSF ptau(181 levels in two independent CSF series (P(combined = 1.17 x 10(-05. We show no association of rs1868402 with risk for AD or age at onset, but detected a very significant association with rate of progression of disease that is consistent in two independent series (P(combined = 1.17 x 10(-05. Our analyses suggest that genetic variants associated with CSF ptau(181 levels may have a greater impact on rate of progression, while genetic variants such as APOE4, that are associated with CSF Aβ(42 levels influence risk and onset but not the rate of progression. Our results also suggest that drugs that inhibit or decrease tau phosphorylation may slow cognitive decline in individuals with very mild dementia or delay the appearance of memory problems in elderly individuals with low CSF Aβ(42 levels. Finally, we believe genome-wide association studies of CSF tau/ptau(181 levels should identify novel genetic variants which will likely influence rate of progression of

  12. Modelling $Z\\to\\tau\\tau$ processes in ATLAS with $\\tau$-embedded $Z\\to\\mu\\mu$ data

    CERN Document Server

    Aad, Georges; Abdallah, Jalal; Abdinov, Ovsat; Aben, Rosemarie; Abolins, Maris; AbouZeid, Ossama; Abramowicz, Halina; Abreu, Henso; Abreu, Ricardo; Abulaiti, Yiming; Acharya, Bobby Samir; Adamczyk, Leszek; Adams, David; Adelman, Jahred; Adomeit, Stefanie; Adye, Tim; Affolder, Tony; Agatonovic-Jovin, Tatjana; Agricola, Johannes; Aguilar-Saavedra, Juan Antonio; Ahlen, Steven; Ahmadov, Faig; Aielli, Giulio; Akerstedt, Henrik; Åkesson, Torsten Paul Ake; Akimov, Andrei; Alberghi, Gian Luigi; Albert, Justin; Albrand, Solveig; Alconada Verzini, Maria Josefina; Aleksa, Martin; Aleksandrov, Igor; Alexa, Calin; Alexander, Gideon; Alexopoulos, Theodoros; Alhroob, Muhammad; Alimonti, Gianluca; Alio, Lion; Alison, John; Alkire, Steven Patrick; Allbrooke, Benedict; Allport, Phillip; Aloisio, Alberto; Alonso, Alejandro; Alonso, Francisco; Alpigiani, Cristiano; Altheimer, Andrew David; Alvarez Gonzalez, Barbara; Άlvarez Piqueras, Damián; Alviggi, Mariagrazia; Amadio, Brian Thomas; Amako, Katsuya; Amaral Coutinho, Yara; Amelung, Christoph; Amidei, Dante; Amor Dos Santos, Susana Patricia; Amorim, Antonio; Amoroso, Simone; Amram, Nir; Amundsen, Glenn; Anastopoulos, Christos; Ancu, Lucian Stefan; Andari, Nansi; Andeen, Timothy; Anders, Christoph Falk; Anders, Gabriel; Anders, John Kenneth; Anderson, Kelby; Andreazza, Attilio; Andrei, George Victor; Angelidakis, Stylianos; Angelozzi, Ivan; Anger, Philipp; Angerami, Aaron; Anghinolfi, Francis; Anisenkov, Alexey; Anjos, Nuno; Annovi, Alberto; Antonelli, Mario; Antonov, Alexey; Antos, Jaroslav; Anulli, Fabio; Aoki, Masato; Aperio Bella, Ludovica; Arabidze, Giorgi; Arai, Yasuo; Araque, Juan Pedro; Arce, Ayana; Arduh, Francisco Anuar; Arguin, Jean-Francois; Argyropoulos, Spyridon; Arik, Metin; Armbruster, Aaron James; Arnaez, Olivier; Arnal, Vanessa; Arnold, Hannah; Arratia, Miguel; Arslan, Ozan; Artamonov, Andrei; Artoni, Giacomo; Asai, Shoji; Asbah, Nedaa; Ashkenazi, Adi; Åsman, Barbro; Asquith, Lily; Assamagan, Ketevi; Astalos, Robert; Atkinson, Markus; Atlay, Naim Bora; Auerbach, Benjamin; Augsten, Kamil; Aurousseau, Mathieu; Avolio, Giuseppe; Axen, Bradley; Ayoub, Mohamad Kassem; Azuelos, Georges; Baak, Max; Baas, Alessandra; Baca, Matthew John; Bacci, Cesare; Bachacou, Henri; Bachas, Konstantinos; Backes, Moritz; Backhaus, Malte; Bagiacchi, Paolo; Bagnaia, Paolo; Bai, Yu; Bain, Travis; Baines, John; Baker, Oliver Keith; Baldin, Evgenii; Balek, Petr; Balestri, Thomas; Balli, Fabrice; Banas, Elzbieta; Banerjee, Swagato; Bannoura, Arwa A E; Bansil, Hardeep Singh; Barak, Liron; Barberio, Elisabetta Luigia; Barberis, Dario; Barbero, Marlon; Barillari, Teresa; Barisonzi, Marcello; Barklow, Timothy; Barlow, Nick; Barnes, Sarah Louise; Barnett, Bruce; Barnett, Michael; Barnovska, Zuzana; Baroncelli, Antonio; Barone, Gaetano; Barr, Alan; Barreiro, Fernando; Barreiro Guimarães da Costa, João; Bartoldus, Rainer; Barton, Adam Edward; Bartos, Pavol; Basalaev, Artem; Bassalat, Ahmed; Basye, Austin; Bates, Richard; Batista, Santiago Juan; Batley, Richard; Battaglia, Marco; Bauce, Matteo; Bauer, Florian; Bawa, Harinder Singh; Beacham, James Baker; Beattie, Michael David; Beau, Tristan; Beauchemin, Pierre-Hugues; Beccherle, Roberto; Bechtle, Philip; Beck, Hans Peter; Becker, Anne Kathrin; Becker, Maurice; Becker, Sebastian; Beckingham, Matthew; Becot, Cyril; Beddall, Andrew; Beddall, Ayda; Bednyakov, Vadim; Bee, Christopher; Beemster, Lars; Beermann, Thomas; Begel, Michael; Behr, Janna Katharina; Belanger-Champagne, Camille; Bell, William; Bella, Gideon; Bellagamba, Lorenzo; Bellerive, Alain; Bellomo, Massimiliano; Belotskiy, Konstantin; Beltramello, Olga; Benary, Odette; Benchekroun, Driss; Bender, Michael; Bendtz, Katarina; Benekos, Nektarios; Benhammou, Yan; Benhar Noccioli, Eleonora; Benitez Garcia, Jorge-Armando; Benjamin, Douglas; Bensinger, James; Bentvelsen, Stan; Beresford, Lydia; Beretta, Matteo; Berge, David; Bergeaas Kuutmann, Elin; Berger, Nicolas; Berghaus, Frank; Beringer, Jürg; Bernard, Clare; Bernard, Nathan Rogers; Bernius, Catrin; Bernlochner, Florian Urs; Berry, Tracey; Berta, Peter; Bertella, Claudia; Bertoli, Gabriele; Bertolucci, Federico; Bertsche, Carolyn; Bertsche, David; Besana, Maria Ilaria; Besjes, Geert-Jan; Bessidskaia Bylund, Olga; Bessner, Martin Florian; Besson, Nathalie; Betancourt, Christopher; Bethke, Siegfried; Bevan, Adrian John; Bhimji, Wahid; Bianchi, Riccardo-Maria; Bianchini, Louis; Bianco, Michele; Biebel, Otmar; Biedermann, Dustin; Bieniek, Stephen Paul; Biglietti, Michela; Bilbao De Mendizabal, Javier; Bilokon, Halina

    2015-01-01

    This paper describes the concept, technical realisation and validation of a largely data-driven method to model events with $Z\\to\\tau\\tau$ decays. In $Z\\to\\mu\\mu$ events selected from proton-proton collision data recorded at $\\sqrt{s}=8$ TeV with the ATLAS experiment at the LHC in 2012, the $Z$ decay muons are replaced by $\\tau$ leptons from simulated $Z\\to\\tau\\tau$ decays at the level of reconstructed tracks and calorimeter cells. The $\\tau$ lepton kinematics are derived from the kinematics of the original muons. Thus, only the well-understood decays of the $Z$ boson and $\\tau$ leptons as well as the detector response to the $\\tau$ decay products are obtained from simulation. All other aspects of the event, such as the $Z$ boson and jet kinematics as well as effects from multiple interactions, are given by the actual data. This so-called $\\tau$-embedding method is particularly relevant for Higgs boson searches and analyses in $\\tau\\tau$ final states, where $Z\\to\\tau\\tau$ decays constitute a large irreducible...

  13. Study of tau lepton decay into leptons and K{sup 0}{sub L}; Etude des desintegrations du lepton tau en leptons et en K{sup 0}{sub L}

    Energy Technology Data Exchange (ETDEWEB)

    Park, H.J.

    1995-03-21

    In this thesis the {tau} lepton is identified from its decay products and the decay rates into electrons, muons and final states containing K{sub L}{sup 0} (kaons neutral long-lived) are measured. A {tau}{tau} pair is produced in the LEP storage ring from the electron-positron annihilation to a Z{sup 0} boson, e{sup +}e{sup -} {yields} Z{sup 0} {yields} {tau}{sup +}{tau}{sup -}. Each {tau} then decays, {tau} {yields} {nu}{sub {tau}}X where in this thesis only the final states X = e anti{nu}{sub e}, {mu} anti {nu}{sub {mu}}, and {pi}/K({pi}{sup d}eg)K{sub L}{sup 0} are considered. About 62000 {tau}{tau} pairs have been detected by the ALEPH (a detector for LEP physics) period 1991-93 at a center-of-mass energy of about 91 GeV, around the Z{sup 0} boson mass. The total systematic error on the leptonic {tau} decay fractions is 2.9 per mill for B{sub e} and 2.6 per mill for B{sub {mu}}, dominated by Monte Carlo statistics (1.4 per mill), non-{tau} backgrounds (1.4 per mill) and {tau}{tau} selection uncertainty (1.2 per mill). Finally, the following branching ratios are obtained: B{sub e} = (17.79 {+-} 0.13)%, B{sub {mu}} = (17.31 {+-} 0.12)%. These measurements allow to test precisely the e-{mu}-{tau} universality in the charged weak current couplings (Wl anti{nu}{sub l}), g{mu}/g{sub e} = 1.0003 {+-} 0.0051, g{tau}/g{mu} = 0.9979 {+-} 0.0027(world av. {tau}{sub {tau}}) {+-} 0.0023(B{sub l}) {+-} 0.0004(m{tau}) where unity corresponds to perfect e-{mu} and {mu}-{tau} universalities. In addition, a hadronic {tau} final state containing a K{sub L}{sup 0} is studied, which nicely demonstrates the ALEPH capabilities of K{sub L}{sup 0} identification. (authors). 66 refs., 115 figs., 49 tabs.

  14. The ATLAS Hadronic Tau Trigger

    CERN Document Server

    Brost, E; The ATLAS collaboration

    2014-01-01

    As proton-proton collisions at the LHC reach luminosities close to 10$^{\\mathrm{34}}$ cm$^{\\mathrm{-2}}$ s $^{\\mathrm{-1}}$, the strategies for triggering have become more important than ever for physics analyses. Simplistic single tau lepton triggers suffer from severe rate limitation, despite the sophisticated algorithms used in the tau identification. The development of further fast algorithms and the design of topological selections are the main challenges to allow a large program of physics analysis. The tau triggers provide many opportunities to study new physics beyond the Standard Model, and to get precise measurements of the properties of the Higgs boson decaying to tau-leptons. We present the performance of the hadronic tau trigger taken in Run 1 data with the ATLAS detector at $\\sqrt{s}$ = 8 TeV pp collision. One of the major challenges is to sustain high efficiencies in events with multiple interactions. To do this we introduced faster tracking methods, multivariate selection techniques, and new t...

  15. The effects of G-CSF combined with SB203580 on the immune system of mice received 4 Gy total body irradiation%G-CSF联合SB203580对4Gy照射小鼠免疫系统的作用

    Institute of Scientific and Technical Information of China (English)

    李德冠; 路璐; 吴红英; 张俊伶; 孟爱民

    2014-01-01

    Objective To observe the effects of G-CSF combined with SB203580(SB) on the immune system of mice received 4 Gy total body irradiation (TBI).Methods Thirty male C57BL/6 mice were randomly divided into control group,irradiated group,combined group.The mice in irradiated and combined group received 4 Gy TBI.In combined group,G-CSF (1 μg/each) was intraperitoneally (ip) injected twice one day for 5 days,SB (15 mg/kg) was ip injected every other day after 4 Gy TBI for 5 times.After 4 Gy TBI 10 days,the peripheral bloods were counted,the CD4,CD8,B220 cells in WBC and CD4,CD8 in thymocytes were analyzed by flowcytometry.The reactive oxygen species levels (ROS) of bone marrow cells were detected by microplate reader.Results Compared to the control group,the proportion of CD8,B220 and WBC in the irradiated mice significantly decreased,CD4+CD8+ thymocytes and ROS levels of bone marrow cells increased significantly.Compared to irradiation group,red blood,platelet,CD4 and CD8 cells in peripheral blood,CD4+CD8+ thymocytes decreased in the combined group.Conclusion G-CSF combined with SB has protective effects on the radiation-induced injury in immune system.%目的 研究G-CSF联合p38抑制剂SB203580 (SB)对免疫细胞辐射损伤的作用.方法 C57BL/6雄性小鼠按体质量随机分为对照组、照射组和给药组.照射组和给药组给予4 Gy全身照射.给药组小鼠给予腹腔注射G-CSF和SB,G-CSF于4Gy照射后2h和6h给药(1μg/只),每天2次,连续给药5d,SB于照射后24h给药(15 mg/kg),隔日给药,共给药5次.照射后10d测外周血计数,进行白细胞CD4、CD8、B220检测、胸腺细胞CD4、CD8检测和骨髓细胞活性氧检测.结果 照射组外周血计数和CD8、B220比例下降,而胸腺细胞中CD4+CD8+细胞比例及骨髓细胞活性氧水平显著增加.与照射组相比,联合给药组外周血红细胞数、血小板、CD4、CD8细胞比例升高,胸腺细胞中CD4+CD8+细胞比例下降.结论 G-CSF联合SB对4 Gy照射

  16. Neurocysticercosis: relationship between Taenia antigen levels in CSF and MRI

    Energy Technology Data Exchange (ETDEWEB)

    Abraham, Ronaldo, E-mail: rnabraham@uol.com.b [University of Taubate (UNITAU), Taubate, SP (Brazil). Medicine Dept.; Livramento, Jose Antonio; Machado, Luis dos Ramos [University of Sao Paulo (USP), Sao Paulo, SP (Brazil). Medical School. Neurology Dept.; Leite, Claudia da Costa [University of Sao Paulo (USP), Sao Paulo, SP (Brazil). Medical School. Radiology Dept.; Pardini, Alessandra Xavier; Vaz, Adelaide Jose [University of Sao Paulo (USP), Sao Paulo, SP (Brazil). Biomedical Science Institute. Immunology Dept.

    2010-02-15

    Objective: to determine the relationship between Taenia antigen (TA) detection in cerebrospinal fluid (CSF) and magnetic resonance imaging (MRI) findings in patients with definite diagnosis of neurocysticercosis (NC). Method: sixty-three patients with definite diagnosis of NC were submitted to a MRI of the brain, and to a CSF examination, with a meticulous search for TA by ELISA. Results: TA detection was positive in 36 patients (57.1%). A total of 836 lesions were analyzed, greatly within the cerebral parenchyma (98.7 of the lesions). Intact or non-degenerating cysts were the most common evolutive phase observed (50.4% of all lesions), 22.1% were degenerating cysts and 19.5% calcified cysts. We observed a significant relationship between TA levels detected and the total number of lesions and the number of non-degenerating cysts, but not with calcified lesions. Conclusion: according to our results, we propose at least four important types of contribution: TA detection may allow etiologic diagnosis in transitional phases of NC, with non-characteristic images; in final stages of evolution of cysticercoids in the CNS, lesions may not appear on CT or MRI, and TA detection may contribute to a definite etiologic diagnosis; TA detection may permit diagnosis of NC in some patients with previous negative tests for antibody detection in CSF; TA detection may represent an accurate marker of disease activity in the epileptic form of NC. (author)

  17. CSF Markers in Guillain-Barre Syndrome

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2007-01-01

    Full Text Available A positive 14-3-3 protein assay of CSF was observed in 29 of 38 patients with GBS and in 4 with motor neuron disease and other neuropathies studied at Universities of Milan and Verona, Italy.

  18. CSF Obstruction and Malabsorption in Congenital Hydrocephalus

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2006-11-01

    Full Text Available The relative contribution of CSF malabsorption and obstruction in three different etiological groups of neonatal high-pressure hydrocephalus (HC was assessed in a study at University of Bonn, Germany, and University of Groningen, The Netherlands.

  19. Confirmed viral meningitis with normal CSF findings.

    Science.gov (United States)

    Dawood, Naghum; Desjobert, Edouard; Lumley, Janine; Webster, Daniel; Jacobs, Michael

    2014-07-17

    An 18-year-old woman presented with a progressively worsening headache, photophobia feverishness and vomiting. Three weeks previously she had returned to the UK from a trip to Peru. At presentation, she had clinical signs of meningism. On admission, blood tests showed a mild lymphopenia, with a normal C reactive protein and white cell count. Chest X-ray and CT of the head were normal. Cerebrospinal fluid (CSF) microscopy was normal. CSF protein and glucose were in the normal range. MRI of the head and cerebral angiography were also normal. Subsequent molecular testing of CSF detected enterovirus RNA by reverse transcriptase PCR. The patient's clinical syndrome correlated with her virological diagnosis and no other cause of her symptoms was found. Her symptoms were self-limiting and improved with supportive management. This case illustrates an important example of viral central nervous system infection presenting clinically as meningitis but with normal CSF microscopy.

  20. CSF levels of DJ-1 and tau distinguish MSA patients from PD patients and controls

    NARCIS (Netherlands)

    Herbert, M.K.; Eeftens, J.M.; Aerts, M.B.; Esselink, R.A.J.; Bloem, B.R.; Kuiperij, H.B.; Verbeek, M.M.

    2014-01-01

    Differential diagnosis between Parkinson's disease (PD) and multiple system atrophy (MSA) is difficult, particularly at early disease stages, but is important for therapeutic management. The protein DJ-1 is implicated in the pathology of PD but little is known about its involvement in MSA. We aimed

  1. Characterization of tau fibrillization in vitro.

    Science.gov (United States)

    Xu, Shaohua; Brunden, Kurt R; Trojanowski, John Q; Lee, Virginia M-Y

    2010-03-01

    The assembly of tau proteins into paired helical filaments, the building blocks of neurofibrillary tangles, is linked to neurodegeneration in Alzheimer's disease and related tauopathies. A greater understanding of this assembly process could identify targets for the discovery of drugs to treat Alzheimer's disease and related disorders. By using recombinant human tau, we have delineated events leading to the conversion of normal soluble tau into tau fibrils. Atomic force microscopy and transmission electron microscopy methodologies were used to determine the structure of tau assemblies that formed when soluble tau was incubated with heparin for increasing lengths of time. Tau initially oligomerizes into spherical nucleation units of 18- to 21-nm diameter that appear to assemble linearly into nascent fibrils. Among the earliest tau fibrils are species that resemble a string of beads formed by linearly aligned spheres that with time seem to coalesce to form straight and twisted ribbon-like filaments, as well as paired helical filaments similar to those found in human tauopathies. An analysis of fibril cross sections at later incubation times revealed three fundamental axial structural features. By monitoring tau fibrillization, we showed that different tau filament morphologies coexist. Temporal changes in the predominant tau structural species suggest that tau fibrillization involves the generation of structural intermediates, resulting in the formation of tau fibrils with verisimilitude to their authentic human counterparts. 2010 The Alzheimer's Association. All rights reserved.

  2. Tau decays into K* mesons

    Science.gov (United States)

    Albrecht, H.; Hamacher, T.; Hofmann, R. P.; Kirchhoff, T.; Mankel, R.; Nau, A.; Nowak, S.; Schröder, H.; Schulz, H. D.; Walter, M.; Wurth, R.; Hast, C.; Kapitza, H.; Kolanoski, H.; Kosche, A.; Lange, A.; Lindner, A.; Schieber, M.; Siegmund, T.; Spaan, B.; Thurn, H.; Töpfer, D.; Wegener, D.; Eckstein, P.; Schubert, K. R.; Schwierz, R.; Waldi, R.; Reim, K.; Wegener, H.; Eckmann, R.; Kuipers, H.; Mai, O.; Mundt, R.; Oest, T.; Reiner, R.; Schmidt-Parzefall, W.; Stiewe, J.; Werner, S.; Ehret, K.; Hofmann, W.; Hüpper, A.; Knöpfle, K. T.; Spengler, J.; Krieger, P.; Macfarlane, D. B.; Saull, P. R. B.; Tzamariudaki, K.; van de Water, R. G.; Yoon, T.-S.; Frankl, C.; Reßing, D.; Schmidtler, M.; Schneider, M.; Weseler, S.; Kernel, G.; Križan, P.; Križnič, E.; Podobnik, T.; Živko, T.; Balagura, V.; Belyaev, I.; Schechelnitsky, S.; Danilov, M.; Doutskoy, A.; Gershtein, Yu.; Golutvin, A.; Korolko, I.; Kostina, G.; Litvintsev, D.; Lubimov, V.; Pakhlov, P.; Semenov, S.; Snizhko, A.; Tichomirov, I.; Zaitsev, Yu.

    1995-06-01

    Using the ARGUS detector at the storage ring DORIS II we have measured τ decays into three charged mesons containing K * mesons. Exploiting the good particle identification capabilities of the detector we have determined the following branching ratios:Brleft( {tau ^ - to overline {K^{*0} } π ^ - v_tau } right) = left( {0.25 ± 0.10 ± 0.05} right)% , B r (τ-→ K *0 K - v τ)= (0.20±0.05±0.04)%, and B r (τ-→ K *- X 0 v τ) =(1.15±0.15-0.18 +0.13)%.

  3. Analisi del decadimento $W -> \\tau \

    CERN Document Server

    Coscetti, Simone

    Questo lavoro di tesi si e' svolto nell'ambito dell'esperimento CMS a LHC, ed in particolare verte sullo studio delle strategie di identificazione off-line del leptone tau, atteso tra i prodotti di decadimento del bosone di Higgs, cosi' come di altre particelle previste in altri modelli teorici. Il canale utilizzato per testare la procedura di identificazione del tau e' il decadimento semileptonico del bosone vettore W. Infine, sulla base dei risultati ottenuti viene presentata una stima quantitativa della sezione d'urto di produzione pp-> W + X

  4. Tau-Id performance with full 2016 dataset using $Z\\to\\tau_{\\mu}\\tau_{h}$ events

    CERN Document Server

    CMS Collaboration

    2017-01-01

    This note presents performance of tau reconstruction and identification algorithm using $Z\\to\\tau_{\\mu}\\tau_{h}$ events with 36.8~fb$^{-1}$ of pp data at $\\sqrt{s}$=13~TeV collected by the CMS detector in 2016.

  5. Neurofilament Light Chain in Blood and CSF as Marker of Disease Progression in Mouse Models and in Neurodegenerative Diseases.

    Science.gov (United States)

    Bacioglu, Mehtap; Maia, Luis F; Preische, Oliver; Schelle, Juliane; Apel, Anja; Kaeser, Stephan A; Schweighauser, Manuel; Eninger, Timo; Lambert, Marius; Pilotto, Andrea; Shimshek, Derya R; Neumann, Ulf; Kahle, Philipp J; Staufenbiel, Matthias; Neumann, Manuela; Maetzler, Walter; Kuhle, Jens; Jucker, Mathias

    2016-07-01

    A majority of current disease-modifying therapeutic approaches for age-related neurodegenerative diseases target their characteristic proteopathic lesions (α-synuclein, Tau, Aβ). To monitor such treatments, fluid biomarkers reflecting the underlying disease process are crucial. We found robust increases of neurofilament light chain (NfL) in CSF and blood in murine models of α-synucleinopathies, tauopathy, and β-amyloidosis. Blood and CSF NfL levels were strongly correlated, and NfL increases coincided with the onset and progression of the corresponding proteopathic lesions in brain. Experimental induction of α-synuclein lesions increased CSF and blood NfL levels, while blocking Aβ lesions attenuated the NfL increase. Consistently, we also found NfL increases in CSF and blood of human α-synucleinopathies, tauopathies, and Alzheimer's disease. Our results suggest that CSF and particularly blood NfL can serve as a reliable and easily accessible biomarker to monitor disease progression and treatment response in mouse models and potentially in human proteopathic neurodegenerative diseases.

  6. Cost and clinical analysis of autologous hematopoietic stem cell mobilization with G-CSF and plerixafor compared to G-CSF and cyclophosphamide.

    Science.gov (United States)

    Shaughnessy, Paul; Islas-Ohlmayer, Miguel; Murphy, Julie; Hougham, Maureen; MacPherson, Jill; Winkler, Kurt; Silva, Matthew; Steinberg, Michael; Matous, Jeffrey; Selvey, Sheryl; Maris, Michael; McSweeney, Peter A

    2011-05-01

    Plerixafor plus granulocyte-colony stimulating factor (G-CSF) has been shown to mobilize more CD34(+) cells than G-CSF alone for autologous hematopoietic stem cell transplantation (HSCT). However, many centers use chemotherapy followed by G-CSF to mobilize CD34(+) cells prior to HSCT. We performed a retrospective study of patients who participated in the expanded access program (EAP) of plerixafor and G-CSF for initial mobilization of CD34(+) cells, and compared outcomes to matched historic controls mobilized with cyclophosphamide 3-5 g/m(2) and G-CSF at 2 centers that participated in the EAP Control patients were matched for age, sex, disease, disease stage, and number of prior therapies. Mobilization costs were defined to be the costs of medical procedures, resource utilization, and medications. Median national CMS reimbursement rates were used to establish the costs of procedures, hospitalization, provider visits, apheresis, CD34(+) cell processing and cryopreservation. Average sale price was used for G-CSF, plerixafor, cyclophosphamide, MESNA, antiemetics, and antimicrobials. A total of 33 patients from the EAP and 33 matched controls were studied. Two patients in the control group were hospitalized for neutropenic fever during the mobilization period. Apheresis started on the scheduled day in 33 (100%) study patients and in 29 (88%) control patients (P = 0.04). Sixteen (48%) control patients required weekend apheresis. There was no difference in number of CD34(+) cells collected between the groups, and all patients proceeded to HSCT with no difference in engraftment outcomes. Median total cost of mobilization was not different between the plerixafor/G-CSF and control groups ($14,224 versus $18,824; P = .45). In conclusion, plerixafor/G-CSF and cyclophosphamide/G-CSF for upfront mobilization of CD34(-) cells resulted in similar numbers of cells collected, costs of mobilization, and clinical outcomes. Additionally, plerixafor/G-CSF mobilization resulted in more

  7. CSF concentration gradients of monoamine metabolites in patients with hydrocephalus.

    Science.gov (United States)

    Malm, J; Kristensen, B; Ekstedt, J; Wester, P

    1994-09-01

    Concentration gradients of homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG), were assessed in 762 successive CSF fractions (2 ml lumbar CSF) from 15 patients with the adult hydrocephalus syndrome (AHS) and 11 patients with hydrocephalus of other causes (mixed group). A mean volume of 49.6 (SD 11.8) ml CSF was removed in the AHS group and 56.4 (10.2) ml in the mixed group. The CSF was collected with a specially designed carousel fraction collector and the corresponding CSF dynamics were continuously registered by a constant pressure CSF infusion method. Pronounced gradients in CSF HVA and CSF 5-HIAA were seen in both patient groups in the first 25 ml of CSF removed. The concentration curves levelled off, despite the removal of larger amounts of CSF and stabilised at about twice the initial concentrations. This phenomenon has not been described before. Concentrations of HVA and 5-HIAA in the first CSF fraction correlated strongly with concentrations in fractions up to about 40 ml. A positive correlation between the first fraction of CSF HVA and CSF 5-HIAA concentrations and CSF outflow conductance was found in the AHS group. There was no gradient in MHPG. It is suggested that the rostrocaudal gradients in CSF HVA and 5-HIAA may be explained by a downward flow of CSF along the spinal cord with absorption of metabolites occurring during passage. Mixing of CSF from different CSF compartments, extraventricular production sites of CSF, clearance of metabolites to venous blood or extracellular fluid, and CSF outflow conductance are probably important determinants of the plateau phase in patients with hydrocephalus. It is concluded that lumbar CSF does not exclusively reflect the concentrations of HVA, 5-HIAA, or MHPG in the ventricles. It should be noted that these results obtained in patients with hydrocephalus may not be applicable to other groups of patients or normal subjects.

  8. Vitamin B12 Inhibits Tau Fibrillization via Binding to Cysteine Residues of Tau.

    Science.gov (United States)

    Rafiee, Saharnaz; Asadollahi, Kazem; Riazi, Gholamhossein; Ahmadian, Shahin; Saboury, Ali Akbar

    2017-09-06

    Two mechanisms underlie the inhibitory/acceleratory action of chemical compounds on tau aggregation including the regulation of cellular kinases and phosphatases activity and direct binding to tau protein. Vitamin B12 is one of the tau polymerization inhibitors, and its deficiency is linked to inactivation of protein phosphatase 2A and subsequently hyperphosphorylation and aggregation of tau protein. Regarding the structure and function of vitamin B12 and tau protein, we assumed that vitamin B12 is also able to directly bind to tau protein. Hence, we investigated the interaction of vitamin B12 with tau protein in vitro using fluorometry and circular dichrosim. Interaction studies was followed by investigation into the effect of vitamin B12 on tau aggregation using ThT fluorescence, circular dichroism, transmission electron microscopy, and SDS-PAGE. The results indicated that vitamin B12 interacts with tau protein and prevents fibrillization of tau protein. Blocking the cysteine residues of tau confirmed the cysteine-mediated binding of vitamin B12 to tau and showed that binding to cysteine is essential for inhibitory effect of vitamin B12 on tau aggregation. SDS-PAGE analysis indicated that vitamin B12 inhibits tau aggregation and that tau oligomers formed in the presence of vitamin B12 are mostly SDS-soluble. We propose that direct binding of vitamin B12 is another mechanism underlying the inhibitory role of vitamin B12 on tau aggregation and neurodegeneration.

  9. P70 S6 kinase mediates tau phosphorylation and synthesis

    DEFF Research Database (Denmark)

    Pei, Jin-Jing; An, Wen-Lin; Zhou, Xin-Wen;

    2006-01-01

    of total S6 and tau but not global proteins in SH-SY5Y cells. The requirement of p70S6K activation was confirmed in the SH-SY5Y cells that overexpress wild-type htau40. Level of p-p70S6K (T421/S424) was only significantly correlated with p-tau at S262, S214, and T212, but not T212/S214, in Alzheimer......Currently, we found that the 70-kDa p70 S6 kinase (p70S6K) directly phosphorylates tau at S262, S214, and T212 sites in vitro. By immunoprecipitation, p-p70S6K (T421/S424) showed a close association with p-tau (S262 and S396/404). Zinc-induced p70S6K activation could only upregulate translation......'s disease (AD) brains. These suggested that p70S6K might contribute to tau related pathologies in AD brains....

  10. One-prong $\\tau$ decays with kaons

    CERN Document Server

    Barate, R.; Ghez, Philippe; Goy, C.; Lees, J.P.; Merle, E.; Minard, M.N.; Pietrzyk, B.; Alemany, R.; Casado, M.P.; Chmeissani, M.; Crespo, J.M.; Fernandez, E.; Fernandez-Bosman, M.; Garrido, L.; Grauges, E.; Juste, A.; Martinez, M.; Merino, G.; Miquel, R.; Mir, L.M.; Pacheco, A.; Park, I.C.; Riu, I.; Colaleo, A.; Creanza, D.; De Palma, M.; Gelao, G.; Iaselli, G.; Maggi, G.; Maggi, M.; Nuzzo, S.; Ranieri, A.; Raso, G.; Ruggieri, F.; Selvaggi, G.; Silvestris, L.; Tempesta, P.; Tricomi, A.; Zito, G.; Huang, X.; Lin, J.; Ouyang, Q.; Wang, T.; Xie, Y.; Xu, R.; Xue, S.; Zhang, J.; Zhang, L.; Zhao, W.; Abbaneo, D.; Becker, U.; Boix, G.; Cattaneo, M.; Ciulli, V.; Dissertori, G.; Drevermann, H.; Forty, R.W.; Frank, M.; Halley, A.W.; Hansen, J.B.; Harvey, John; Janot, P.; Jost, B.; Lehraus, I.; Leroy, O.; Mato, P.; Minten, A.; Moutoussi, A.; Ranjard, F.; Rolandi, Gigi; Rousseau, D.; Schlatter, D.; Schmitt, M.; Schneider, O.; Tejessy, W.; Teubert, F.; Tomalin, I.R.; Tournefier, E.; Wright, A.E.; Ajaltouni, Z.; Badaud, F.; Chazelle, G.; Deschamps, O.; Falvard, A.; Ferdi, C.; Gay, P.; Guicheney, C.; Henrard, P.; Jousset, J.; Michel, B.; Monteil, S.; Montret, J.C.; Pallin, D.; Perret, P.; Podlyski, F.; Hansen, J.D.; Hansen, J.R.; Hansen, P.H.; Nilsson, B.S.; Rensch, B.; Waananen, A.; Daskalakis, G.; Kyriakis, A.; Markou, C.; Simopoulou, E.; Siotis, I.; Vayaki, A.; Blondel, A.; Bonneaud, G.; Brient, J.C.; Rouge, A.; Rumpf, M.; Swynghedauw, M.; Verderi, M.; Videau, H.; Focardi, E.; Parrini, G.; Zachariadou, K.; Cavanaugh, R.; Corden, M.; Georgiopoulos, C.; Antonelli, A.; Bencivenni, G.; Bologna, G.; Bossi, F.; Campana, P.; Capon, G.; Cerutti, F.; Chiarella, V.; Laurelli, P.; Mannocchi, G.; Murtas, F.; Murtas, G.P.; Passalacqua, L.; Pepe-Altarelli, M.; Curtis, L.; Lynch, J.G.; Negus, P.; O'Shea, V.; Raine, C.; Teixeira-Dias, P.; Thompson, A.S.; Buchmuller, O.; Dhamotharan, S.; Geweniger, C.; Hanke, P.; Hansper, G.; Hepp, V.; Kluge, E.E.; Putzer, A.; Sommer, J.; Tittel, K.; Werner, S.; Wunsch, M.; Beuselinck, R.; Binnie, D.M.; Cameron, W.; Dornan, P.J.; Girone, M.; Goodsir, S.; Martin, E.B.; Marinelli, N.; Sedgbeer, J.K.; Spagnolo, P.; Thomson, Evelyn J.; Williams, M.D.; Ghete, V.M.; Girtler, P.; Kneringer, E.; Kuhn, D.; Rudolph, G.; Betteridge, A.P.; Bowdery, C.K.; Buck, P.G.; Colrain, P.; Crawford, G.; Finch, A.J.; Foster, F.; Hughes, G.; Jones, R.W.L.; Robertson, N.A.; Williams, M.I.; Giehl, I.; Hoffmann, C.; Jakobs, K.; Kleinknecht, K.; Quast, G.; Renk, B.; Rohne, E.; Sander, H.G.; van Gemmeren, P.; Wachsmuth, H.; Zeitnitz, C.; Aubert, J.J.; Benchouk, C.; Bonissent, A.; Carr, J.; Coyle, P.; Etienne, F.; Motsch, F.; Payre, P.; Talby, M.; Thulasidas, M.; Aleppo, M.; Antonelli, M.; Ragusa, F.; Berlich, R.; Buescher, Volker; Dietl, H.; Ganis, G.; Huttmann, K.; Lutjens, G.; Mannert, C.; Manner, W.; Moser, H.G.; Schael, S.; Settles, R.; Seywerd, H.; Stenzel, H.; Wiedenmann, W.; Wolf, G.; Azzurri, P.; Boucrot, J.; Callot, O.; Chen, S.; Cordier, A.; Davier, M.; Duflot, L.; Grivaz, J.F.; Heusse, P.; Hocker, Andreas; Jacholkowska, A.; Kim, D.W.; Le Diberder, F.; Lefrancois, J.; Lutz, A.M.; Schune, M.H.; Veillet, J.J.; Videau, I.; Zerwas, D.; Bagliesi, Giuseppe; Bettarini, S.; Boccali, T.; Bozzi, C.; Calderini, G.; Dell'Orso, R.; Ferrante, I.; Foa, L.; Giassi, A.; Gregorio, A.; Ligabue, F.; Lusiani, A.; Marrocchesi, P.S.; Messineo, A.; Palla, F.; Rizzo, G.; Sanguinetti, G.; Sciaba, A.; Sguazzoni, G.; Tenchini, R.; Vannini, C.; Venturi, A.; Verdini, P.G.; Blair, G.A.; Cowan, G.; Green, M.G.; Medcalf, T.; Strong, J.A.; von Wimmersperg-Toeller, J.H.; Botterill, D.R.; Clifft, R.W.; Edgecock, T.R.; Norton, P.R.; Thompson, J.C.; Bloch-Devaux, Brigitte; Colas, P.; Emery, S.; Kozanecki, W.; Lancon, E.; Lemaire, M.C.; Locci, E.; Perez, P.; Rander, J.; Renardy, J.F.; Roussarie, A.; Schuller, J.P.; Schwindling, J.; Trabelsi, A.; Vallage, B.; Black, S.N.; Dann, J.H.; Johnson, R.P.; Kim, H.Y.; Konstantinidis, N.; Litke, A.M.; McNeil, M.A.; Taylor, G.; Booth, C.N.; Cartwright, S.; Combley, F.; Kelly, M.S.; Lehto, M.; Thompson, L.F.; Affholderbach, K.; Boehrer, Armin; Brandt, S.; Grupen, C.; Prange, G.; Giannini, G.; Gobbo, B.; Rothberg, J.; Wasserbaech, S.; Armstrong, S.R.; Charles, E.; Elmer, P.; Ferguson, D.P.S.; Gao, Y.; Gonzalez, S.; Greening, T.C.; Hayes, O.J.; Hu, H.; Jin, S.; McNamara, P.A., III; Nachtman, J.M.; Nielsen, J.; Orejudos, W.; Pan, Y.B.; Saadi, Y.; Scott, I.J.; Walsh, J.; Wu, Sau Lan; Wu, X.; Zobernig, G.

    1999-01-01

    One-prong $\\tau$ decays into final states involving kaons are studied with about 161k $\\tau^+\\tau^-$ events collected by the ALEPH detector from 1991 to 1995. Charged kaons are identified by dE/dx measurement, while $K^0_L$'s are detected through their interaction in calorimeters. Branching ratios are measured for the inclusive mode, $B(\\tau^-\\rightarrow K^-X\

  11. A Tau-Charm Factory at CEBAF

    Energy Technology Data Exchange (ETDEWEB)

    Seth, K.K. [Northwestern Univ., Evanston, IL (United States)

    1994-04-01

    It is proposed that a Tau Charm Factory represents a natural extension of CEBAF into higher energy domains. The exciting nature of the physics of charm quarks and tau leptons is briefly reviewed and it is suggested that the concept of a linac-ring collider as a Tau Charm Factory at CEBAF should be seriously studied.

  12. Measurement of the Absolute Branching Fraction of D_s^+ --> tau^+ nu_tau Decay

    CERN Document Server

    Ecklund, K M; Savinov, V; López, A; Méndez, H; Ramírez, J; Ge, J Y; Miller, D H; Shipsey, I P J; Xin, B; Adams, G S; Anderson, M; Cummings, J P; Danko, I; Hu, D; Moziak, B; Napolitano, J; He, Q; Insler, J; Muramatsu, H; Park, C S; Thorndike, E H; Yang, F; Artuso, M; Blusk, S; Khalil, S; Li, J; Mountain, R; Nisar, S; Randrianarivony, K; Sultana, N; Skwarnicki, T; Stone, S; Wang, J C; Zhang, L M; Bonvicini, G; Cinabro, D; Dubrovin, M; Lincoln, A; Rademacker, J; Asner, D M; Edwards, K W; Naik, P; Reed, J; Briere, R A; Ferguson, T; Tatishvili, G; Vogel, H; Watkins, M E; Rosner, J L; Alexander, J P; Cassel, D G; Duboscq, J E; Ehrlich, R; Fields, L; Gibbons, L; Gray, R; Gray, S W; Hartill, D L; Heltsley, B K; Hertz, D; Jones, C D; Kandaswamy, J; Kreinick, D L; Kuznetsov, V E; Mahlke-Krüger, H; Mohapatra, D; Onyisi, P U E; Patterson, J R; Peterson, D; Riley, D; Ryd, A; Sadoff, A J; Shi, X; Stroiney, S; Sun, W M; Wilksen, T; Athar, S B; Patel, R; Yelton, J; Rubin, P; Eisenstein, B I; Karliner, I; Mehrabyan, S; Lowrey, N; Selen, M; White, E J; Wiss, J; Mitchell, R E; Shepherd, M R; Besson, D; Pedlar, T K; Cronin-Hennessy, D; Gao, K Y; Hietala, J; Kubota, Y; Klein, T; Lang, B W; Poling, R; Scott, A W; Zweber, P; Dobbs, S; Metreveli, Z; Seth, K K; Tomaradze, A G; Libby, J; Powell, A; Wilkinson, G

    2007-01-01

    Using a sample of tagged D_s decays collected near the D^*_s D_s peak production energy with the CLEO-c detector, we study the leptonic decay D^+_s to tau^+ nu_tau via the decay channel tau^+ to e^+ nu_e bar{nu}_tau. We measure B(D^+_s to tau^+ nu_tau) = (6.17 +- 0.71 +- 0.34) %. Combining with our measurements of D^+_s to mu^+ nu_mu and D^+_s to tau^+ nu_tau (via tau^+ to pi^+ bar{nu}_tau), we determine f_{D_s} = 274 +- 10 +- 5 MeV.

  13. Mild cognitive impairment and Alzheimer patients display different levels of redox-active CSF iron.

    Science.gov (United States)

    Lavados, Manuel; Guillón, Marta; Mujica, María Cristina; Rojo, Leonel E; Fuentes, Patricio; Maccioni, Ricardo B

    2008-03-01

    Oxidative stress constitutes a hallmark of Alzheimer's disease (AD). Recent studies also point to redox active metals such as iron, copper and zinc in mediating oxidative stress in AD pathogenesis. However, the reactivity of cerebrospinal fluid (CSF) iron and its possible correlation with the severity of cognitive decline in both Alzheimer's patients and subjects with mild cognitive impairment (MCI) is still unknown. Here we show that different stages of cognitive and functional impairment are associated with changes in CSF reactive iron. In this work, we compared CSF samples from 56 elders, classified into 4 groups according to their scores on the Clinical Dementia Rating scale (CDR). Total CSF iron was analyzed by atomic absorption spectrometry. Redox-active iron was analyzed by a novel fluorimetric assay. One-way ANOVA was used to test differences in mean values, and Newman-Keuls Multiple Comparison Test was used for multi group comparisons. No difference in total CSF iron was found between different groups. Significant amounts of redox-active iron were found in CSF and their levels correlated with the extent of cognitive impairment. Redox-active CSF iron levels increased with the degree of cognitive impairment from normal to MCI subjects, while AD patients showed an abrupt decrease to levels close to zero. Given the relevance of oxidative damage in neurodegeneration, it might be possible to associate the development of cognitive and functional decline with the presence of redox-active iron in the CSF. The decrease in redox-active iron found in AD patients may represent a terminal situation, whereby the central nervous system attempts to minimize iron-associated toxicity.

  14. Neurofibrillary tangle-like tau pathology induced by synthetic tau fibrils in primary neurons over-expressing mutant tau.

    Science.gov (United States)

    Guo, Jing L; Lee, Virginia M Y

    2013-03-18

    Increasing evidence demonstrates the transmissibility of fibrillar species of tau protein, but this has never been directly tested in neurons, the cell type most affected by formation of tau inclusions in neurodegenerative tauopathies. Here we show that synthetic tau fibrils made from recombinant protein not only time-dependently recruit normal tau into neurofibrillary tangle-like insoluble aggregates in primary hippocampal neurons over-expressing human tau, but also induce neuritic tau pathology in non-transgenic neurons. This study provides highly compelling support for the protein-only hypothesis of pathological tau transmission in primary neurons and describes a useful neuronal model for studying the pathogenesis of tauopathies. Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

  15. Selected CSF biomarkers indicate no evidence of early neuroinflammation in Huntington disease

    Science.gov (United States)

    Vinther-Jensen, Tua; Börnsen, Lars; Budtz-Jørgensen, Esben; Ammitzbøll, Cecilie; Larsen, Ida U.; Hjermind, Lena E.; Sellebjerg, Finn

    2016-01-01

    Objective: To investigate CSF biomarkers of neuroinflammation and neurodegeneration in Huntington disease (HD) gene-expansion carriers compared to controls and to investigate these biomarkers in association with clinical HD rating scales and disease burden score. Methods: We collected CSF from 32 premanifest and 48 manifest HD gene-expansion carriers and 24 gene-expansion negative at-risk controls. We examined biomarkers of neuroinflammation (matrix metalloproteinase 9, C-X-C motif chemokine 13, terminal complement complex, chitinase-3-like-protein 1 [CHI3L1], and osteopontin [OPN]) and neurodegeneration (microtubule-associated protein tau, neurofilament light polypeptide [NFL], and myelin basic protein [MBP]). The study was approved by the Ethics Committee of the Capital Region of Denmark (H2-2011-085) and written informed consent was obtained from each participant before enrollment. Results: NFL was the only biomarker that increased in premanifest stages and no evidence of early involvement of neuroinflammation in HD was found. However, we found that the biomarkers for neurodegeneration, MBP and tau, increased during the disease course in manifest HD gene-expansion carriers and were associated with an increase of the neuroinflammation biomarkers CHI3L1 and OPN. Tau was also increased in all gene-expansion carriers with psychiatric symptoms compared to gene-expansion carriers without psychiatric symptoms. Conclusions: Neuroinflammation, which seems not to be an early event in our cohort, may be secondary to neurodegeneration in late HD. NFL is a possible disease burden correlate in HD, reflecting neuronal loss even before motor symptom onset, and may be useful as a dynamic biomarker in intervention studies. PMID:27734023

  16. Evidence for B+ --> tau+ nu_tau Decays using Hadronic B Tags

    Energy Technology Data Exchange (ETDEWEB)

    del Amo Sanchez, P.; Lees, J.P.; Poireau, V.; Prencipe, E.; Tisserand, V.; /Annecy, LAPP; Garra Tico, J.; Grauges, E.; /Barcelona U., ECM; Martinelli, M.; Milanes, D.A.; Palano, A.; Pappagallo, M.; /INFN, Bari /Bari U.; Eigen, G.; Stugu, B.; Sun, L.; /Bergen U.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; /UC, Berkeley; Koch, H.; Schroeder, T.; /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Indian Inst. Tech., Guwahati /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /INFN, Naples /Naples U. /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Southern Methodist U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2011-08-11

    We present a search for the decay B{sup +} --> {tau}{sup +} {nu}{sub {tau}} using 467.8 x 10{sup 6} B{anti B} pairs collected at the {Upsilon}(4S) resonance with the BABAR detector at the SLAC PEP-II B-Factory. We select a sample of events with on completely reconstructed B{sup -} in an hadronic decay mode (B{sup -} --> D{sup (*)0}X{sup -} and B{sup -} --> J/{psi} X{sup -}). We examine the rest of the event to search for a B{sup +} --> {tau}{sup +} {nu}{sub {tau}} decay. We identify the {tau}{sup +} lepton in the following modes: {tau}{sup +} --> e{sup +} {nu}{sub e}{anti {nu}}{sub {tau}}, {tau}{sup +} --> {mu}{sup +} {nu}{sub {mu}}{anti {nu}}{sub {tau}}, {tau}{sup +} --> {pi}{sup +}{anti {nu}}{sub {tau}} and {tau}{sup +} --> {rho}{anti {nu}}{sub {tau}}. We find an excess of events with respect to expected background, which excludes the null signal hypothesis at the level of 3.3 {sigma} and can be converted to a branching fraction central value of B(B{sup +} --> {tau}{sup +} {nu}{sub {tau}})= (1.80{sup + 0.57}{sub - 0.54}(stat.) {+-} 0.26 (syst.)) x 10{sup -4}.

  17. Amyloid-β peptides and tau protein as biomarkers in cerebrospinal and interstitial fluid following traumatic brain injury: A review of experimental and clinical studies

    Directory of Open Access Journals (Sweden)

    Parmenion P. Tsitsopoulos

    2013-06-01

    Full Text Available Traumatic brain injury (TBI survivors frequently suffer from life-long deficits in cognitive functions and a reduced quality of life. Axonal injury, observed in most severe TBI patients, results in accumulation of amyloid precursor protein (APP. Post-injury enzymatic cleavage of APP can generate amyloid-β (Aβ peptides, a hallmark finding in Alzheimer’s disease (AD. At autopsy, brains of AD and a subset of TBI victims display some similarities including accumulation of Aβ peptides and neurofibrillary tangles of hyperphosphorylated tau proteins. Most epidemiological evidence suggests a link between TBI and AD, implying that TBI has neurodegenerative sequelae. Aβ peptides and tau may be used as biomarkers in interstitial fluid (ISF using cerebral microdialysis and/or cerebrospinal fluid (CSF following clinical TBI. In the present review, the available clinical and experimental literature on Aβ peptides and tau as potential biomarkers following TBI is comprehensively analyzed. Elevated CSF and ISF tau protein levels have been observed following severe TBI and suggested to correlate with clinical outcome. Although Aβ peptides are produced by normal neuronal metabolism, high levels of long and/or fibrillary Aβ peptides may be neurotoxic. Increased CSF and/or ISF Aβ levels post-injury may be related to neuronal activity and/or the presence of axonal injury. The heterogeneity of animal models, clinical cohorts, analytical techniques and the complexity of TBI in available studies make the clinical value of tau and Aβ as biomarkers uncertain at present. Additionally, the link between early post-injury changes in tau and Aβ peptides and the future risk of developing AD remains unclear. Future studies using e.g. rapid biomarker sampling combined with enhanced analytical techniques and/or novel pharmacological tools could provide additional information on the importance of Aβ peptides and tau protein in both the acute pathophysiology and long

  18. Rosiglitazone ameliorates diffuse axonal injury by reducing loss of tau and up-regulating caveolin-1 expression

    Directory of Open Access Journals (Sweden)

    Yong-lin Zhao

    2016-01-01

    Full Text Available Rosiglitazone up-regulates caveolin-1 levels and has neuroprotective effects in both chronic and acute brain injury. Therefore, we postulated that rosiglitazone may ameliorate diffuse axonal injury via its ability to up-regulate caveolin-1, inhibit expression of amyloid-beta precursor protein, and reduce the loss and abnormal phosphorylation of tau. In the present study, intraperitoneal injection of rosiglitazone significantly reduced the levels of amyloid-beta precursor protein and hyperphosphorylated tau (phosphorylated at Ser 404 (p-tau (S 404 , and it increased the expression of total tau and caveolin-1 in the rat cortex. Our results show that rosiglitazone inhibits the expression of amyloid-beta precursor protein and lowers p-tau (S 404 levels, and it reduces the loss of total tau, possibly by up-regulating caveolin-1. These actions of rosiglitazone may underlie its neuroprotective effects in the treatment of diffuse axonal injury.

  19. Measurement of the {tau} lifetime at SLD

    Energy Technology Data Exchange (ETDEWEB)

    Abe, K.; Abt, I.; Ahn, C.J.; Akagi, T.; Allen, N.J.; Ash, W.W.; Aston, D.; Baird, K.G.; Baltay, C.; Band, H.R.; Barakat, M.B.; Baranko, G.; Bardon, O.; Barklow, T.; Bazarko, A.O.; Ben-David, R.; Benvenuti, A.C.; Bienz, T.; Bilei, G.M.; Bisello, D.; Blaylock, G.; Bogart, J.R.; Bolton, T.; Bower, G.R.; Brau, J.E.; Breidenbach, M.; Bugg, W.M.; Burke, D.; Burnett, T.H.; Burrows, P.N.; Busza, W.; Calcaterra, A.; Caldwell, D.O.; Calloway, D.; Camanzi, B.; Carpinelli, M.; Cassell, R.; Castaldi, R.; Castro, A.; Cavalli-Sforza, M.; Church, E.; Cohn, H.O.; Coller, J.A.; Cook, V.; Cotton, R.; Cowan, R.F.; Coyne, D.G.; D`Oliveira, A.; Damerell, C.J.S.; Daoudi, M.; De Sangro, R.; De Simone, P.; Dell`Orso, R.; Dima, M.; Du, P.Y.C.; Dubois, R.; Eisenstein, B.I.; Elia, R.; Etzion, E.; Falciai, D.; Fero, M.J.; Frey, R.; Furuno, K.; Gillman, T.; Gladding, G.; Gonzalez, S.; Hallewell, G.D.; Hart, E.L.; Hasegawa, Y.; Hedges, S.; Hertzbach, S.S.; Hildreth, M.D.; Huber, J.; Huffer, M.E.; Hughes, E.W.; Hwang, H.; Iwasaki, Y.; Jackson, D.J.; Jacques, P.; Jaros, J.; Johnson, A.S.; Johnson, J.R.; Johnson, R.A.; Junk, T.; Kajikawa, R.; Kalelkar, M.; Kang, H.J.; Karliner, I.; Kawahara, H.; Kendall, H.W.; Kim, Y.; King, M.E.; King, R.; Kofler, R.R.; Krishna, N.M.; Kroeger, R.S.; Labs, J.F.; Langston, M.; Lath, A.; Lauber, J.A.; Leith, D.W.G.; Liu, M.X.; Liu, X.; Loreti, M.; Lu, A.; Lynch, H.L.; Ma, J.; Mancinelli, G.; Manly, S.; Mantovani, G.; Markiewicz, T.W.; Maruyama, T.; Massetti, R.; Masuda, H.; Mazzucato, E.; McKemey, A.K.; Meadows, B.T.; Messner, R.; Mockett, P.M.; Moffeit, K.C.; Mours, B.; Mueller, G.; Muller, D.; Nagamine, T.; Nauenberg, U.; Neal, H.; Nussbaum, M.; Ohnishi, Y.; Osborne, L.S.; Panvini, R.S.; Park, H.; Pavel, T.J.; Peruzzi, I.; Piccolo, M.; Piemontese, L.; Pieroni, E.; Pitts, K.T.; Plano, R.J.; Prepost, R.; Prescott, C.Y.; Punkar, G.D.; Quigley, J.; Ratcliff, B.N.; Reeves, T.W.; Reidy, J.; Rensing, P.E.; Rochester, L.S.; Rothberg, J.E.; Rowson, P.C.; (The SLD Collabor...

    1995-11-01

    A measurement of the lifetime of the {tau} lepton has been made using a sample of 1671 {ital Z}{sup 0}{r_arrow}{tau}{sup +}{tau}{sup {minus}} decays collected by the SLD detector at the SLC. The measurement benefits from the small and stable collision region at the SLC and the precision pixel vertex detector of the SLD. Three analysis techniques have been used: decay length, impact parameter, and impact parameter difference methods. The combined result is {tau}{sub {tau}}=297{plus_minus}9 (stat){plus_minus}5(syst) fs.

  20. Tau physics at the LHC with ATLAS

    CERN Document Server

    Lai, Stan

    2009-01-01

    The presence of tau leptons in the final state is an important signature in searches for physics beyond the Standard Model. Hadronically decaying tau leptons can be reconstructed over a wide kinematic range at ATLAS. The reconstruction algorithm for hadronically decaying tau leptons and the performance of tau lepton identification is described. A review of physics processes with tau lepton final states is given, ranging from Standard Model processes in early data, such as W and Z boson production, to searches for new phenomena beyond the Standard Model.

  1. rhCSF3 accelerates the proliferation of human melanocytes in culture through binding CSF3R and the expression of CSF3R transcripts.

    Science.gov (United States)

    Lu, Yan; Guo, Ze; Zhou, Mei-Hua; Li, Xue; Sun, Jie; Gong, Qing-Li; Zhu, Wen-Yuan

    2015-05-01

    Melanogenic paracrine and autocrine cytokine networks have recently been discovered in vitro between melanocytes and other types of skin cells. Granulocyte colony-stimulating factor receptor (CSF3R) controls the survival, proliferation and differentiation of many kinds of cells, including neutrophils. To understand the function of CSF3R and recombinant human granulocyte colony-stimulating factor (rhCSF3) on melanocyte proliferation, this study compared the expression of CSF3R and the effects of rhCSF3 in primary human melanocytes, neutrophils and HEL 92.1.7 cells. The results show that CSF3R is localized in the cytoplasm and on cell membranes of melanocytes and neutrophils. The percentage of CSF3R(+) melanocytes was higher than CSF3R(+) HEL 92.1.7 cells, but was lower than CSF3R(+) neutrophils. Both CSF3R mRNA and CSF3R protein levels in melanocytes were higher than in HEL 92.1.7 cells, but were lower than in neutrophils. Treatment with rhCSF3 increased the proliferation of human melanocytes, but not their tyrosinase activity. Transcripts of CSF3R in human melanocytes, M14, A375 melanoma and A431 squamous cell carcinoma cells were also detected. Expression of the CSF3R V3 transcript was lower in melanocytes than in M14, A375 melanoma and A431 squamous cell carcinoma cells. In conclusion, rhCSF3 can promote melanocyte proliferation through CSF3R without affecting tyrosinase activity.

  2. Low CSF levels of both α-synuclein and the α-synuclein cleaving enzyme neurosin in patients with synucleinopathy.

    Directory of Open Access Journals (Sweden)

    Malin Wennström

    Full Text Available Neurosin is a protease that in vitro degrades α-synuclein, the main constituent of Lewy bodies found in brains of patients with synucleinopathy including Parkinson's disease (PD and dementia with Lewy bodies (DLB. Several studies have reported reduced cerebrospinal fluid (CSF levels of α-synuclein in synucleinopathy patients and recent data also proposes a significant role of α-synuclein in the pathophysiology of Alzheimer's disease (AD. To investigate potential links between neurosin and its substrate α-synuclein in vivo we used a commercially available sandwich ELISA and an in-house developed direct ELISA to quantify CSF levels of α-synuclein and neurosin in patients diagnosed with DLB, PD and PD dementia (PDD versus AD patients and non-demented controls. We found that patients with synucleinopathy displayed lower CSF levels of neurosin and α-synuclein compared to controls and AD patients. In contrast, AD patients demonstrated significantly increased CSF α-synuclein but similar neurosin levels compared to non-demented controls. Further, CSF neurosin and α-synuclein concentrations were positively associated in controls, PD and PDD patients and both proteins were highly correlated to CSF levels of phosphorylated tau in all investigated groups. We observed no effect of gender or presence of the apolipoprotein Eε4 allele on neither neurosin or α-synuclein CSF levels. In concordance with the current literature our study demonstrates decreased CSF levels of α-synuclein in synucleinopathy patients versus AD patients and controls. Importantly, decreased α-synuclein levels in patients with synucleinopathy appear linked to low levels of the α-synuclein cleaving enzyme neurosin. In contrast, elevated levels of α-synuclein in AD patients were not related to any altered CSF neurosin levels. Thus, altered CSF levels of α-synuclein and neurosin in patients with synucleinopathy versus AD may not only mirror disease-specific neuropathological

  3. Advances in tau-based drug discovery

    Science.gov (United States)

    Noble, Wendy; Pooler, Amy M.; Hanger, Diane P.

    2011-01-01

    Introduction Tauopathies, including Alzheimer’s disease (AD) and some frontotemporal dementias, are neurodegenerative diseases characterised by pathological lesions comprised of tau protein. There is currently a significant and urgent unmet need for disease-modifying therapies for these conditions and recently attention has turned to tau as a potential target for intervention. Areas covered Increasing evidence has highlighted pathways associated with tau-mediated neurodegeneration as important targets for drug development. Here, the authors review recently published papers in this area and summarise the genetic and pharmacological approaches that have shown efficacy in reducing tau-associated neurodegeneration. These include the use of agents to prevent abnormal tau processing and increase tau clearance, therapies targeting the immune system, and the manipulation of tau pre-mRNA to modify tau isoform expression. Expert opinion Several small molecule tau-based treatments are currently being assessed in clinical trials, the outcomes of which are eagerly awaited. Current evidence suggests that therapies targeting tau are likely, at least in part, to form the basis of an effective and safe treatment for Alzheimer’s disease and related neurodegenerative disorders in which tau deposition is evident. PMID:22003359

  4. CP violation in hadronic tau decays

    CERN Document Server

    Kiers, Ken

    2013-01-01

    We consider CP-violating effects in tau -> 3 pi nu_ tau and 4 pi nu_ tau (Delta S = 0), and tau -> K pi pi nu_tau (Delta S = 1), assuming that the usual Standard Model amplitudes for these processes interfere with analogous amplitudes mediated by a charged Higgs boson. In the Delta S = 0 case we focus specifically on the intermediate resonant processes tau -> V pi nu_tau (with V=omega, rho, and a_1), and consider three CP-odd observables -- the partial rate asymmetry, a polarization-dependent asymmetry and a triple-product asymmetry. In the Delta S = 1 case we examine the partial rate asymmetry, two "modified" rate asymmetries, and a triple-product asymmetry. The partial rate asymmetry is expected to be small for both the Delta S = 0 and Delta S = 1 cases. Evaluation of the other asymmetries indicates that they could potentially be measurable.

  5. Hadronization in tau -> K K pi nu_tau decays

    CERN Document Server

    Roig, Pablo

    2008-01-01

    Hadronization in tau -> K K pi nu_tau decays is driven by both vector and axial-vector currents that we study, guided by the following principles: The 1/N_C expansion -worked out at leading order, considering only the contribution of the lightest spin one resonances-, approximate chiral symmetry at low energies and the appropriate asymptotic behaviour we demand to the associated form factors. All these features are implemented in the resonance theory. Most of its couplings are determined by imposing the short-distance requirements of vector and axial-vector spectral functions within QCD. We plan to improve our prediction of the hadronic spectra using recently available experimental data.

  6. Search for tau-neutrino induced cascades in the IceCube detector

    Energy Technology Data Exchange (ETDEWEB)

    Usner, Marcel; Kowalski, Marek [DESY, Zeuthen (Germany); Collaboration: IceCube-Collaboration

    2016-07-01

    The IceCube Neutrino Observatory at the South Pole is a Cherenkov detector built to measure high-energy neutrinos from cosmic sources. A total volume of about one cubic kilometer of the Antarctic ice is instrumented with 5160 optical modules. A tau lepton is created in the charged current interaction of a tau neutrino with an ice nucleus. The Double Bang signature links two subsequent cascades from the hadronic interaction and the tau decay within the detection volume. It can only be resolved at the highest energies around 1 PeV where the decay length of the tau is about 50 m. The work is focused on optimizing reconstruction methods of Double Bang events incorporating the latest ice model. The goal is to measure a flavor ratio that, for the first time, is sensitive to tau neutrinos.

  7. TTBK2: A Tau Protein Kinase beyond Tau Phosphorylation

    Directory of Open Access Journals (Sweden)

    Jung-Chi Liao

    2015-01-01

    Full Text Available Tau tubulin kinase 2 (TTBK2 is a kinase known to phosphorylate tau and tubulin. It has recently drawn much attention due to its involvement in multiple important cellular processes. Here, we review the current understanding of TTBK2, including its sequence, structure, binding sites, phosphorylation substrates, and cellular processes involved. TTBK2 possesses a casein kinase 1 (CK1 kinase domain followed by a ~900 amino acid segment, potentially responsible for its localization and substrate recruitment. It is known to bind to CEP164, a centriolar protein, and EB1, a microtubule plus-end tracking protein. In addition to autophosphorylation, known phosphorylation substrates of TTBK2 include tau, tubulin, CEP164, CEP97, and TDP-43, a neurodegeneration-associated protein. Mutations of TTBK2 are associated with spinocerebellar ataxia type 11. In addition, TTBK2 is essential for regulating the growth of axonemal microtubules in ciliogenesis. It also plays roles in resistance of cancer target therapies and in regulating glucose and GABA transport. Reported sites of TTBK2 localization include the centriole/basal body, the midbody, and possibly the mitotic spindles. Together, TTBK2 is a multifunctional kinase involved in important cellular processes and demands augmented efforts in investigating its functions.

  8. Rescue of tau-induced synaptic transmission pathology by paclitaxel

    Directory of Open Access Journals (Sweden)

    Hdas eErez

    2014-02-01

    Full Text Available Behavioral and electrophysiological studies of Alzheimer’s disease (AD and other tauopathies have revealed that the onset of cognitive decline correlates better with synaptic dysfunctions than with hallmark pathologies such as extracellular amyloid-β plaques, intracellular hyperphosphorylated tau or neuronal loss. Recent experiments have also demonstrated that anti-cancer microtubule-stabilizing drugs can rescue tau-induced behavioral decline and hallmark neuron pathologies. Nevertheless, the mechanisms underlying tau-induced synaptic dysfunction as well as those involved in the rescue of cognitive decline by microtubules stabilizing drugs remain unclear. Here we began to study these mechanisms using the glutaminergic sensory-motoneuron synapse derived from Aplysia ganglia, electrophysiological methods, the expression of mutant-human-tau (mt-htau either pre- or post-synaptically and the antimitotic drug paclitaxel. Expression of mt-htau in the presynaptic neurons led to reduced excitatory postsynaptic potential (EPSP amplitude generated by rested synapses within 3 days of mt-htau expression, and to deeper levels of homosynaptic depression. mt-htau-induced synaptic weakening correlated with reduced releasable presynaptic vesicle pools as revealed by the induction of asynchronous neurotransmitter release by hypertonic sucrose solution. Paclitaxel totally rescued tau-induced synaptic weakening by maintaining the availability of the presynaptic vesicle stores. Postsynaptic expression of mt-htau did not impair the above described synaptic-transmission parameters for up to 5 days. Along with earlier confocal microscope observations from our laboratory, these findings suggest that tau-induced synaptic dysfunction is the outcome of impaired axoplasmic transport and the ensuing reduction in the releasable presynaptic vesicle stores rather than the direct effects of mt-htau or paclitaxel on the synaptic release mechanisms.

  9. Extracellular monomeric tau protein is sufficient to initiate the spread of tau protein pathology.

    Science.gov (United States)

    Michel, Claire H; Kumar, Satish; Pinotsi, Dorothea; Tunnacliffe, Alan; St George-Hyslop, Peter; Mandelkow, Eckhard; Mandelkow, Eva-Maria; Kaminski, Clemens F; Kaminski Schierle, Gabriele S

    2014-01-10

    Understanding the formation and propagation of aggregates of the Alzheimer disease-associated Tau protein in vivo is vital for the development of therapeutics for this devastating disorder. Using our recently developed live-cell aggregation sensor in neuron-like cells, we demonstrate that different variants of exogenous monomeric Tau, namely full-length Tau (hTau40) and the Tau-derived construct K18 comprising the repeat domain, initially accumulate in endosomal compartments, where they form fibrillar seeds that subsequently induce the aggregation of endogenous Tau. Using superresolution imaging, we confirm that fibrils consisting of endogenous and exogenous Tau are released from cells and demonstrate their potential to spread Tau pathology. Our data indicate a greater pathological risk and potential toxicity than hitherto suspected for extracellular soluble Tau.

  10. Synaptic Amyloid-β Oligomers Precede p-Tau and Differentiate High Pathology Control Cases

    Science.gov (United States)

    Bilousova, Tina; Miller, Carol A.; Poon, Wayne W.; Vinters, Harry V.; Corrada, Maria; Kawas, Claudia; Hayden, Eric Y.; Teplow, David B.; Glabe, Charles; Albay, Ricardo; Cole, Gregory M.; Teng, Edmond; Gylys, Karen H.

    2017-01-01

    Amyloid-β (Aβ) and hyperphosphorylated tau (p-tau) aggregates form the two discrete pathologies of Alzheimer disease (AD), and oligomeric assemblies of each protein are localized to synapses. To determine the sequence by which pathology appears in synapses, Aβ and p-tau were quantified across AD disease stages in parietal cortex. Nondemented cases with high levels of AD-related pathology were included to determine factors that confer protection from clinical symptoms. Flow cytometric analysis of synaptosome preparations was used to quantify Aβ and p-tau in large populations of individual synaptic terminals. Soluble Aβ oligomers were assayed by a single antibody sandwich enzyme-linked immunosorbent assay. Total in situ Aβ was elevated in patients with early- and late-stage AD dementia, but not in high pathology nondemented controls compared with age-matched normal controls. However, soluble Aβ oligomers were highest in early AD synapses, and this assay distinguished early AD cases from high pathology controls. Overall, synapse-associated p-tau did not increase until late-stage disease in human and transgenic rat cortex, and p-tau was elevated in individual Aβ-positive synaptosomes in early AD. These results suggest that soluble oligomers in surviving neocortical synaptic terminals are associated with dementia onset and suggest an amyloid cascade hypothesis in which oligomeric Aβ drives phosphorylated tau accumulation and synaptic spread. These results indicate that antiamyloid therapies will be less effective once p-tau pathology is developed. PMID:26718979

  11. Seeding of Normal Tau by Pathological Tau Conformers Drives Pathogenesis of Alzheimer-like Tangles*

    Science.gov (United States)

    Guo, Jing L.; Lee, Virginia M.-Y.

    2011-01-01

    Neurofibrillary tangles (NFTs) in Alzheimer disease and related tauopathies are composed of insoluble hyperphosphorylated Tau protein, but the mechanisms underlying the conversion of highly soluble Tau into insoluble NFTs remain elusive. Here, we demonstrate that introduction of minute quantities of misfolded preformed Tau fibrils (Tau pffs) into Tau-expressing cells rapidly recruit large amounts of soluble Tau into filamentous inclusions resembling NFTs with unprecedented efficiency, suggesting a “seeding”-recruitment process as a highly plausible mechanism underlying NFT formation in vivo. Consistent with the emerging concept of prion-like transmissibility of disease-causing amyloidogenic proteins, we found that spontaneous uptake of Tau pffs into cells is likely mediated by endocytosis, suggesting a potential mechanism for the propagation of Tau lesions in tauopathy brains. Furthermore, sequestration of soluble Tau by pff-induced Tau aggregates attenuates microtubule overstabilization in Tau-expressing cells, supporting the hypothesis of a Tau loss-of-function toxicity in cells harboring NFTs. In summary, our study establishes a cellular system that robustly develops authentic NFT-like Tau aggregates, which provides mechanistic insights into NFT pathogenesis and a potential tool for identifying Tau-based therapeutics. PMID:21372138

  12. Prefibrillar Tau oligomers alter the nucleic acid protective function of Tau in hippocampal neurons in vivo.

    Science.gov (United States)

    Violet, Marie; Chauderlier, Alban; Delattre, Lucie; Tardivel, Meryem; Chouala, Meliza Sendid; Sultan, Audrey; Marciniak, Elodie; Humez, Sandrine; Binder, Lester; Kayed, Rakez; Lefebvre, Bruno; Bonnefoy, Eliette; Buée, Luc; Galas, Marie-Christine

    2015-10-01

    The accumulation of DNA and RNA oxidative damage is observed in cortical and hippocampal neurons from Alzheimer's disease (AD) brains at early stages of pathology. We recently reported that Tau is a key nuclear player in the protection of neuronal nucleic acid integrity in vivo under physiological conditions and hyperthermia, a strong inducer of oxidative stress. In a mouse model of tauopathy (THY-Tau22), we demonstrate that hyperthermia selectively induces nucleic acid oxidative damage and nucleic acid strand breaks in the nucleus and cytoplasm of hippocampal neurons that display early Tau phosphorylation but no Tau fibrils. Nucleic acid-damaged neurons were exclusively immunoreactive for prefibrillar Tau oligomers. A similar association between prefibrillar Tau oligomers and nucleic acid oxidative damage was observed in AD brains. Pretreatment with Methylene Blue (MB), a Tau aggregation inhibitor and a redox cycler, reduced hyperthermia-induced Tau oligomerization as well as nucleic acid damage. This study clearly highlights the existence of an early and critical time frame for hyperthermia-induced Tau oligomerization, which most likely occurs through increased oxidative stress, and nucleic acid vulnerability during the progression of Tau pathology. These results suggest that at early stages of AD, Tau oligomerization triggers the loss of the nucleic acid protective function of monomeric Tau. This study highlights the existence of a short therapeutic window in which to prevent the formation of pathological forms of Tau and their harmful consequences on nucleic acid integrity during the progression of Tau pathology. Copyright © 2015 Elsevier Inc. All rights reserved.

  13. Measurement of the spectral functions of axial-vector hadronic $\\tau$ decays and determination of $\\alpha_{s}(M^2_\\tau)$

    CERN Document Server

    Barate, R; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Merle, E; Minard, M N; Nief, J Y; Pietrzyk, B; Alemany, R; Boix, G; Casado, M P; Chmeissani, M; Crespo, J M; Delfino, M C; Fernández, E; Fernández-Bosman, M; Garrido, L; Graugès-Pous, E; Juste, A; Martínez, M; Merino, G; Miquel, R; Mir, L M; Park, I C; Pascual, A; Perlas, J A; Riu, I; Sánchez, F; Colaleo, A; Creanza, D; De Palma, M; Gelao, G; Iaselli, Giuseppe; Maggi, G; Maggi, M; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Becker, U; Bright-Thomas, P G; Casper, David William; Cattaneo, M; Ciulli, V; Dissertori, G; Drevermann, H; Forty, Roger W; Frank, M; Hagelberg, R; Hansen, J B; Harvey, J; Janot, P; Jost, B; Lehraus, Ivan; Mato, P; Minten, Adolf G; Moneta, L; Pacheco, A; Pusztaszeri, J F; Ranjard, F; Rolandi, Luigi; Rousseau, D; Schlatter, W D; Schmitt, M; Schneider, O; Tejessy, W; Teubert, F; Tomalin, I R; Wachsmuth, H W; Wagner, A; Ajaltouni, Ziad J; Badaud, F; Chazelle, G; Deschamps, O; Falvard, A; Ferdi, C; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rosnet, P; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Rensch, B; Wäänänen, A; Daskalakis, G; Kyriakis, A; Markou, C; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Rougé, A; Rumpf, M; Valassi, Andrea; Verderi, M; Videau, H L; Focardi, E; Parrini, G; Zachariadou, K; Corden, M; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Cerutti, F; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Curtis, L; Halley, A W; Lynch, J G; Negus, P; O'Shea, V; Raine, C; Scarr, J M; Smith, K; Teixeira-Dias, P; Thompson, A S; Thomson, E; Buchmüller, O L; Dhamotharan, S; Geweniger, C; Graefe, G; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Girone, M; Goodsir, S M; Martin, E B; Marinelli, N; Moutoussi, A; Nash, J; Sedgbeer, J K; Spagnolo, P; Williams, M D; Ghete, V M; Girtler, P; Kneringer, E; Kuhn, D; Rudolph, G; Betteridge, A P; Bowdery, C K; Buck, P G; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Williams, M I; Giehl, I; Greene, A M; Hoffmann, C; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Sander, H G; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Benchouk, C; Bonissent, A; Bujosa, G; Carr, J; Coyle, P; Etienne, F; Leroy, O; Motsch, F; Payre, P; Talby, M; Sadouki, A; Thulasidas, M; Trabelsi, K; Aleppo, M; Antonelli, M; Ragusa, F; Berlich, R; Blum, Walter; Büscher, V; Dietl, H; Ganis, G; Kroha, H; Lütjens, G; Mannert, C; Männer, W; Moser, H G; Schael, S; Settles, Ronald; Seywerd, H C J; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Chen, S; Cordier, A; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Höcker, A; Jacholkowska, A; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Schune, M H; Tournefier, E; Veillet, J J; Videau, I; Zerwas, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Boccali, T; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Palla, Fabrizio; Rizzo, G; Sanguinetti, G; Sciabà, A; Tenchini, Roberto; Tonelli, G; Vannini, C; Venturi, A; Verdini, P G; Blair, G A; Bryant, L M; Chambers, J T; Green, M G; Medcalf, T; Perrodo, P; Strong, J A; Von Wimmersperg-Töller, J H; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Norton, P R; Thompson, J C; Wright, A E; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Black, S N; Dann, J H; Johnson, R P; Kim, H Y; Konstantinidis, N P; Litke, A M; McNeil, M A; Taylor, G; Booth, C N; Brew, C A J; Cartwright, S L; Combley, F; Kelly, M S; Lehto, M H; Reeve, J; Thompson, L F; Affholderbach, K; Böhrer, A; Brandt, S; Cowan, G D; Grupen, Claus; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Musolino, G; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Charles, E; Elmer, P; Ferguson, D P S; Gao, Y; González, S; Greening, T C; Hayes, O J; Hu, H; Jin, S; McNamara, P A; Nachtman, J M; Nielsen, J; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, J; Wu Sau Lan; Wu, X; Zobernig, G

    1998-01-01

    An analysis based on 124000 selected tau pairs recorded by the ALEPH detector at LEP provides the vector (V) and axial-vector (A) spectral functions of hadronic tau decays together with their total widths. This allows the evaluation of finite energy chiral sum rules that are weighted integrals over the (V-A) spectral functions. In addition, a precise measurement of alpha_s along with a determination of nonperturbative contributions at the tau mass scale is performed. The experimentally and theoretically most robust determination of alpha_s(M_tau^2) is obtained from the (V+A) fit that yields alpha_s(M_tau^2) = 0.334 +/- 0.022 giving alpha_s(M_Z^2) = 0.1202 +/- 0.0027 after the extrapolation to the mass of the Z boson. The approach of the Operator Product Expansion (OPE) is tested experimentally studying the evolution of the tau hadronic widths to masses smaller than the tau mass.

  14. Flow cytometry of cerebrospinal fluid (CSF) lymphocytes: alterations of blood/CSF ratios of lymphocyte subsets in inflammation disorders of human central nervous system (CNS).

    Science.gov (United States)

    Kleine, T O; Albrecht, J; Zöfel, P

    1999-03-01

    Flow cytometry was adapted to measure lymphocytes in human cerebrospinal fluid (CSF). The method was sufficiently precise, reproducible and accurate despite low cell counts. In lumbar CSF of controls with 500 to 3500 (10(3)/l) leukocytes, lymphocyte counts correlated with those in corresponding venous blood: blood/CSF ratios of approximately 2000 : 1 were found for total T cells (CD3+) and CD3+ HLA-DR-, CD3+4+, CD3+8+ subsets, ratios were increased for the lymphocyte subsets CD3+ HLA-DR+ blood-brain and blood-CSF barriers) to blood lymphocyte subsets which favor the transfer of T subsets. Correlation of the subset ratios to the CD3+ ratio indicates distinct barrier properties which changed differently with acute and subacute inflammations and neuroimmunological diseases of central nervous system (CNS) in lumbar or ventricular CSF, but not with simple protein barrier disturbance. HLA DR+ T ratios were higher than HLA DR- T ratios only with controls and some neuroimmunological diseases. Lymphocyte barrier characteristics were related to protein leakage situated at the same barriers, indicating for the lymphocyte subsets selective transfer routes in control subjects and non-selective routes in patients with CNS inflammation where altered ratios revealed a mixture of both routes.

  15. The Effect of Forskolin on tau Phosphorylation and tau Inclusion Body Formation%毛喉萜对tau蛋白磷酸化及聚集的影响

    Institute of Scientific and Technical Information of China (English)

    郭海涛; 于富敏; 李晶超; 杨柳

    2011-01-01

    目的:本实验旨在细胞水平研究毛喉萜(forskolin)对tau蛋白磷酸化、聚集体形成及tau蛋白与微管结合能力的影响.方法:利用基因转染技术建立过度表达人类最长tau(tau441)的人肾母细胞瘤细胞(HEK293),免疫印迹技术检测细胞内tau蛋白的磷酸化状况,tau与微管结合能力改变;免疫荧光技术和thioflavin染色检测细胞内tau蛋白聚集体形成情况.结果:在HEK293转tau细胞株, 总tau蛋白的表达没有明显改变,tau蛋白在Ser214、Ser262和Ser396/404位点过度磷酸化.与此同时,随着tau蛋白的过度磷酸化,tau蛋白与微管的结合能力下降,细胞内有磷酸化的tau蛋白聚集增加.结论:蛋白激酶A的激活可以引起tau蛋白的过度磷酸化,磷酸化的位点包括蛋白激酶A和非蛋白激酶A的磷酸化位点,而过度磷酸化的tau蛋白又损害了tau与微管结合,形成了大量细胞内聚集体,提示了蛋白激酶A的激活可能是超早期阿尔茨海默病病理发展过程的关键因素之一.%Aim: To investigate the effect of forskolin on tau phosphorylation, tau inclusion body formation and tau function in cultured cells. Methods : Human embryonic kidney cells (HEK293) were stably transfected with the longest human isoform of tau (tau441) (HEK293/tau441). Tau phosphorylation and microtubule binding activity of tau were detected by Western blotting. Tau aggregates formation was determined by immunofluorescence and thioflavin staining. Results : Western blotting results demonstrated that the level of total tauwas not altered significantly, but the levels of phosphorylated tau at various sites detected by a panel of site-specific tau antibodies (PS214 PS262 and PHF-1) were significantly increased after forskolin incubation The microtubule-binding activity of tau was decreased and tau accumulation was increased. Conclusion: These results indicate that in vitro activation of PKA can induce tau hyperphosphorylation not only at PKA site

  16. Therapeutic applications of macrophage colony-stimulating factor-1 (CSF-1) and antagonists of CSF-1 receptor (CSF-1R) signaling.

    Science.gov (United States)

    Hume, David A; MacDonald, Kelli P A

    2012-02-23

    Macrophage-colony stimulating factor (CSF-1) signaling through its receptor (CSF-1R) promotes the differentiation of myeloid progenitors into heterogeneous populations of monocytes, macrophages, dendritic cells, and bone-resorbing osteoclasts. In the periphery, CSF-1 regulates the migration, proliferation, function, and survival of macrophages, which function at multiple levels within the innate and adaptive immune systems. Macrophage populations elicited by CSF-1 are associated with, and exacerbate, a broad spectrum of pathologies, including cancer, inflammation, and bone disease. Conversely, macrophages can also contribute to immunosuppression, disease resolution, and tissue repair. Recombinant CSF-1, antibodies against the ligand and the receptor, and specific inhibitors of CSF-1R kinase activity have been each been tested in a range of animal models and in some cases, in patients. This review examines the potential clinical uses of modulators of the CSF-1/CSF-1R system. We conclude that CSF-1 promotes a resident-type macrophage phenotype. As a treatment, CSF-1 has therapeutic potential in tissue repair. Conversely, inhibition of CSF-1R is unlikely to be effective in inflammatory disease but may have utility in cancer.

  17. The promotion of breast cancer metastasis caused by inhibition of CSF-1R/CSF-1 signaling is blocked by targeting the G-CSF receptor.

    Science.gov (United States)

    Swierczak, Agnieszka; Cook, Andrew D; Lenzo, Jason C; Restall, Christina M; Doherty, Judy P; Anderson, Robin L; Hamilton, John A

    2014-08-01

    Treatment options are limited for patients with breast cancer presenting with metastatic disease. Targeting of tumor-associated macrophages through the inhibition of colony-stimulating factor-1 receptor (CSF-1R), a key macrophage signaling pathway, has been reported to reduce tumor growth and metastasis, and these treatments are now in clinical trials. Here, we report that, surprisingly, treatment with neutralizing anti-CSF-1R and anti-CSF-1 antibodies, or with two different small-molecule inhibitors of CSF-1R, could actually increase spontaneous metastasis without altering primary tumor growth in mice bearing two independently derived mammary tumors. The blockade of CSF-1R or CSF-1 led to increased levels of serum G-CSF, increased frequency of neutrophils in the primary tumor and in the metastasis-associated lung, as well as increased numbers of neutrophils and Ly6C(hi) monocytes in the peripheral blood. Neutralizing antibody against the G-CSF receptor, which regulates neutrophil development and function, reduced the enhanced metastasis and neutrophil numbers that resulted from CSF-1R blockade. These results indicate that the role of the CSF-1R/CSF-1 system in breast cancer is far more complex than originally proposed, and requires further investigation as a therapeutic target.

  18. CSF-biomarkers in Olympic boxing: diagnosis and effects of repetitive head trauma.

    Science.gov (United States)

    Neselius, Sanna; Brisby, Helena; Theodorsson, Annette; Blennow, Kaj; Zetterberg, Henrik; Marcusson, Jan

    2012-01-01

    Sports-related head trauma is common but still there is no established laboratory test used in the diagnostics of minimal or mild traumatic brain injuries. Further the effects of recurrent head trauma on brain injury markers are unknown. The purpose of this study was to investigate the relationship between Olympic (amateur) boxing and cerebrospinal fluid (CSF) brain injury biomarkers. The study was designed as a prospective cohort study. Thirty Olympic boxers with a minimum of 45 bouts and 25 non-boxing matched controls were included in the study. CSF samples were collected by lumbar puncture 1-6 days after a bout and after a rest period for at least 14 days. The controls were tested once. Biomarkers for acute and chronic brain injury were analysed. NFL (mean ± SD, 532±553 vs 135±51 ng/L p = 0.001), GFAP (496±238 vs 247±147 ng/L pboxing compared to controls. NFL (402±434 ng/L p = 0.004) and GFAP (369±113 ng/L p = 0.001) concentrations remained elevated after the rest period. Increased CSF levels of T-tau, NFL, GFAP, and S-100B in >80% of the boxers demonstrate that both the acute and the cumulative effect of head trauma in Olympic boxing may induce CSF biomarker changes that suggest minor central nervous injuries. The lack of normalization of NFL and GFAP after the rest period in a subgroup of boxers may indicate ongoing degeneration. The recurrent head trauma in boxing may be associated with increased risk of chronic traumatic brain injury.

  19. [MRI evaluation of cervicothoracic CSF hypotension].

    Science.gov (United States)

    Maraval, A; Brugieres, P; Combes, C; Thomas, P; Blanc, R; Gaston, A

    2006-06-01

    We propose studying signs of cervicothoracic CSF hypotension by MRI. Axial T1-weighted GRE sequence with and without saturation bands positioned above and below the selected image plane, MR venography and MR Angiography with contrast administration are helpful to confirm the venous nature of the epidural thickening and to make the differential diagnosis with infectious or neoplastic epiduritis.

  20. CP violation in $h\\to \\tau\\tau$ and LFV $h\\to \\mu\\tau$

    CERN Document Server

    Hayreter, Alper; Valencia, German

    2016-01-01

    The CMS collaboration has reported a possible lepton flavour violating (LFV) signal $h\\to\\mu\\tau$. Whereas this does not happen in the standard model (SM), we point out that new physics responsible for this type of decay would, in general, also produce charge-parity (CP) violation in $h\\to \\tau\\tau$. We estimate the size of this effect in a model independent manner and find that a large asymmetry, of order 40\\%, is allowed by current constraints.

  1. Glycation alter the process of Tau phosphorylation to change Tau isoforms aggregation property.

    Science.gov (United States)

    Liu, Kefu; Liu, Yutong; Li, Lingyun; Qin, Peibin; Iqbal, Javed; Deng, Yulin; Qing, Hong

    2016-02-01

    The risk of tauopathies depends in part on the levels and modified composition of six Tau isoforms in the human brain. Abnormal phosphorylation of the Tau protein and the shift of the ratio of 3R Tau to 4R Tau are presumed to result in neurofibrillary pathology and neurodegeneration. Glycation has recently been linked to dementia and metabolic syndrome. To determine the contribution of Tau protein glycation and phosphorylation on Tau aggregation propensity, the assembled kinetics were examined in vitro using Thioflavin T fluorescence assays. We found that glycation and phosphorylation have different effects on aggregation propensity in different Tau isoforms. Different Tau proteins play important parts in each tauopathies, but 3R0N, fetal Tau protein, has no effect on tauopathies. Conversely, 4R2N has more modified sites and a higher tendency to aggregate, playing the most important role in 4R tauopathies. Finally, Glycation, which could modulate Tau phosphorylation, may occur before any other modification. It also regulates the 3R to 4R ratio and promotes 4R2N Tau protein aggregation. Decreasing the sites of glycation, as well as shifting other Tau proteins to 3R0N Tau proteins has potential therapeutic implications for tauopathies.

  2. Extracellular association of APP and tau fibrils induces intracellular aggregate formation of tau.

    Science.gov (United States)

    Takahashi, Muneaki; Miyata, Haruka; Kametani, Fuyuki; Nonaka, Takashi; Akiyama, Haruhiko; Hisanaga, Shin-ichi; Hasegawa, Masato

    2015-06-01

    Alzheimer's disease (AD) is characterized by extracellular amyloid β (Aβ) deposition and intracellular tau aggregation. Many studies have indicated some association between these processes, but it remains unknown how the two pathologies are linked. In this study, we investigated whether expression of amyloid precursor protein (APP) influences extracellular seed-dependent intracellular tau accumulation in cultured cells. Treatment of tau-expressing SH-SY5Y cells with Aβ fibrils did not induce intracellular tau aggregation. On the other hand, in cells expressing both tau and APP, treatment with tau fibrils or Sarkosyl-insoluble tau from AD brains induced intracellular tau aggregation. The seed-dependent intracellular tau aggregation was not induced by expression of APP lacking the extracellular domain. The amount of phosphorylated tau aggregates in cultured cells was dose dependently elevated in response to increased levels of APP on the cell membrane. Our results indicate that the extracellular region of APP is involved in uptake of tau fibrils into cells, raising the possibility that APP, but not Aβ, influences cell-to-cell spreading of tau pathologies in AD by serving as a receptor of abnormal tau aggregates.

  3. Search for neutrinoless {tau} decays: {tau}{r_arrow}e{gamma} and {tau}{r_arrow}{mu}{gamma}

    Energy Technology Data Exchange (ETDEWEB)

    Edwards, K.W. [Carleton University, Ottawa, Ontario, K1S 5B6 (CANADA); Bellerive, A.; Janicek, R.; MacFarlane, D.B.; McLean, K.W.; Patel, P.M. [McGill University, Montreal, Quebec, H3A 2T8 (CANADA); Sadoff, A.J. [Ithaca College, Ithaca, New York 14850 (United States); Ammar, R.; Baringer, P.; Bean, A.; Besson, D.; Coppage, D.; Darling, C.; Davis, R.; Hancock, N.; Kotov, S.; Kravchenko, I.; Kwak, N. [University of Kansas, Lawrence, Kansas 66045 (United States); Anderson, S.; Kubota, Y.; Lattery, M.; ONeill, J.J.; Patton, S.; Poling, R.; Riehle, T.; Savinov, V.; Smith, A. [University of Minnesota, Minneapolis, Minnesota 55455 (United States); Alam, M.S.; Athar, S.B.; Ling, Z.; Mahmood, A.H.; Severini, H.; Timm, S.; Wappler, F. [State University of New York at Albany, Albany, New York 12222 (United States); Anastassov, A.; Blinov, S.; Duboscq, J.E.; Fujino, D.; Fulton, R.; Gan, K.K.; Hart, T.; Honscheid, K.; Kagan, H.; Kass, R.; Lee, J.; Spencer, M.B.; Sung, M.; Undrus, A.; Wanke, R.; Wolf, A.; Zoeller, M.M. [Ohio State University, Columbus, Ohio 43210 (United States); Nemati, B.; Richichi, S.J.; Ross, W.R.; Skubic, P.; Wood, M. [University of Oklahoma, Norman, Oklahoma 73019 (United States); Bishai, M.; Fast, J.; Gerndt, E.; Hinson, J.W.; Menon, N.; Miller, D.H.; Shibata, E.I.; Shipsey, I.P.; Yurko, M. [Purdue University, West Lafayette, Indiana 47907 (United States); Gibbons, L.; Johnson, S.D.; Kwon, Y.; Roberts, S.; Thorndike, E.H. [University of Rochester, Rochester, New York 14627 (United States); Jessop, C.P.; Lingel, K.; Marsiske, H.; Perl, M.L.; Schaffner, S.F.; Ugolini, D.; Wang, R.; Zhou, X. [Stanford Linear Accelerator Center, Stanford University, Stanford, California 94309 (United States); Coan, T.E.; Fadeyev, V.; Korolkov, I.; Maravin, Y.; Narsky, I.; Shelkov, V.; Staeck, J.; Stroynowski, R.; Volobouev, I.; Ye, J. [Southern Methodist University, Dallas, Texas 75275 (United States); Artuso, M.; Efimov, A.; Frasconi, F.; Gao, M.

    1997-04-01

    A search for the lepton-family-number-violating decays {tau}{r_arrow}e{gamma} and {tau}{r_arrow}{mu}{gamma} has been performed using CLEO II data. No evidence of a signal has been found and the corresponding upper limits are B({tau}{r_arrow}e{gamma}){lt}2.7{times}10{sup {minus}6} and B({tau}{r_arrow}{mu}{gamma}){lt}3.0{times}10{sup {minus}6} at 90{percent} C.L. {copyright} {ital 1997} {ital The American Physical Society}

  4. Hyperphosphorylation of tau protein in the ipsilateral thalamus after focal cortical infarction in rats.

    Science.gov (United States)

    Dong, Da-Wei; Zhang, Yu-Sheng; Yang, Wan-Yong; Wang-Qin, Run-Qi; Xu, An-Ding; Ruan, Yi-Wen

    2014-01-16

    Hyperphosphorylation of tau has been considered as an important risk factor for neurodegenerative diseases. It has been found also in the cortex after focal cerebral ischemia. The present study is aimed at investigating changes of tau protein expression in the ipsilateral thalamus remote from the primary ischemic lesion site after distal middle cerebral artery occlusion (MCAO). The number of neurons in the ventroposterior thalamic nucleus (VPN) was evaluated using Nissl staining and neuronal nuclei (NeuN) immunostaining. Total tau and phosphorylated tau at threonine 231 (p-T231-tau) and serine 199 (p-S199-tau) levels, respectively, in the thalamus were measured using immunostaining and immunoblotting. Moreover, apoptosis was detected with terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling (TUNEL) assay. It was found that the numbers of intact neurons and NeuN(+) cells within the ipsilateral VPN were reduced significantly compared with the sham-operated group, but the levels of p-T231-tau and p-S199-tau in the ipsilateral thalamus were increased significantly in rats subjected to ischemia for 3 days, 7 days and 28 days. Furthermore, the number of TUNEL-positive cells was increased in the ipsilateral VPN at 7 days and 28 days after MCAO. Thus, hyperphosphorylated tau protein is observed in ipsilateral thalamus after focal cerebral infarction in this study. Our findings suggest that the expression of hyperphosphorylated tau protein induced by ischemia may be associated with the secondary thalamic damage after focal cortical infarction via an apoptotic pathway.

  5. Increased CSF levels of phosphorylated neurofilament heavy protein following bout in amateur boxers.

    Directory of Open Access Journals (Sweden)

    Sanna Neselius

    Full Text Available INTRODUCTION: Diagnosis of mild TBI is hampered by the lack of imaging or biochemical measurements for identifying or quantifying mild TBI in a clinical setting. We have previously shown increased biomarker levels of protein reflecting axonal (neurofilament light protein and tau and glial (GFAP and S-100B damage in cerebrospinal fluid (CSF after a boxing bout. The aims of this study were to find other biomarkers of mild TBI, which may help clinicians diagnose and monitor mild TBI, and to calculate the role of APOE ε4 allele genotype which has been associated with poor outcome after TBI. MATERIALS AND METHODS: Thirty amateur boxers with a minimum of 45 bouts and 25 non-boxing matched controls were included in a prospective cohort study. CSF and blood were collected at one occasion between 1 and 6 days after a bout, and after a rest period for at least 14 days (follow up. The controls were tested once. CSF levels of neurofilament heavy (pNFH, amyloid precursor proteins (sAPPα and sAPPβ, ApoE and ApoA1 were analyzed. In blood, plasma levels of Aβ42 and ApoE genotype were analyzed. RESULTS: CSF levels of pNFH were significantly increased between 1 and 6 days after boxing as compared with controls (p<0.001. The concentrations decreased at follow up but were still significantly increased compared to controls (p = 0.018. CSF pNFH concentrations correlated with NFL (r =  0.57 after bout and 0.64 at follow up, p<0.001. No significant change was found in the other biomarkers, as compared to controls. Boxers carrying the APOE ε4 allele had similar biomarker concentrations as non-carriers. CONCLUSIONS: Subconcussive repetitive trauma in amateur boxing causes a mild TBI that may be diagnosed by CSF analysis of pNFH, even without unconsciousness or concussion symptoms. Possession of the APOE ε4 allele was not found to influence biomarker levels after acute TBI.

  6. Higgs Pair Production in the $H(\\rightarrow \\tau\\tau)H(\\rightarrow b\\bar{b})$ channel at the High-Luminosity LHC

    CERN Document Server

    The ATLAS collaboration

    2015-01-01

    Prospects studies are presented for the observation of double Higgs production in the channel $H(\\rightarrow b \\overline{b})H(\\rightarrow \\tau \\tau)$ for a total integrated luminosity of 3000~fb$ ^{-1}$ of $\\sqrt{s}=$14~TeV proton-proton collisions at the HL-LHC. A cut-based analysis strategy using MC data and a parametrisation of the ATLAS detector provide assessment to the measurement prospects performed under different assumptions for the trilinear Higgs couplings values. Assuming SM background and SM signal, we expect to set an upper limit of the cross section for the di-Higgs production of $4.3 \\times \\sigma(HH \\rightarrow b\\bar{b}\\tau^+\\tau^-)$ at 95\\% Confidence Level. Using an effective Lagrangian for the Higgs potential, and allowing its trilinear coupling to vary, we can project an exclusion of $\\lambda_{HHH}/\\lambda_{SM} \\leq -4$ and $\\lambda_{HHH}/\\lambda_{SM} \\geq 12$.

  7. Data-driven background estimation for the H -> tau+tau- -> lh search at 7 TeV with the ATLAS detector

    CERN Document Server

    The ATLAS collaboration

    2010-01-01

    Events characterised by the presence of an electron or muon, plus a hadronically decaying tau lepton and large missing transverse momentum are searched for in 7 TeV proton-proton collision data at the LHC. This event topology is of interest to the search for Higgs bosons with H -> tau+tau- -> lh (l=e,mu and h=hadronically decaying tau). The total integrated luminosity of the analysed data is 310 nb-1. Candidate events with missing transverse momentum above 20 GeV were found, 12 in the electron and 17 in the muon channels. The sum is consistent with 25+-9 expected from a data-driven background estimation and the observed visible mass distribution is agreed with the shape from the estimation. This note describes how this estimation is made, using information from data and Monte Carlo simulation.

  8. Cerebrospinal fluid tau and phosphorylated tau protein are elevated in corticobasal syndrome

    NARCIS (Netherlands)

    Aerts, M.B.; Esselink, R.A.J.; Bloem, B.R.; Verbeek, M.M.

    2011-01-01

    Differentiating corticobasal syndrome (CBS) from progressive supranuclear palsy (PSP) and idiopathic Parkinson's disease (PD) can be difficult. To investigate the additional value of cerebrospinal fluid (CSF) biomarkers in the diagnostic differentiation of parkinsonism, we analyzed the CSF concentra

  9. CSF neurofilament protein analysis in the differential diagnosis of ALS.

    NARCIS (Netherlands)

    Reijn, T.S.M.; Abdo, W.; Schelhaas, H.J.; Verbeek, M.M.

    2009-01-01

    BACKGROUND: Cerebrospinal fluid (CSF) biomarkers have been studied to differentiate between patients with ALS and neurological controls, but not in comparison to clinically more relevant disorders mimicking ALS. METHODS: In this retrospective study, CSF concentrations of various brain-specific

  10. CSF neurofilament proteins in the differential diagnosis of dementia

    NARCIS (Netherlands)

    de Jong, D; Jansen, R W M M; Pijnenburg, Y A L; van Geel, W J A; Borm, G F; Kremer, Berry; Verbeek, M.

    BACKGROUND: Neurofilament (NF) proteins are major cytoskeletal constituents of neurons. Increased CSF NF levels may reflect neuronal degeneration. OBJECTIVE: To investigate the diagnostic value of CSF NF analysis to discriminate in relatively young dementia patients between frontotemporal lobe

  11. CSF neurofilament proteins in the differential diagnosis of dementia.

    NARCIS (Netherlands)

    Jong, D. de; Jansen, R.W.M.M.; Pijnenburg, Y.A.; Geel, W.J.A. van; Borm, G.F.; Kremer, H.P.H.; Verbeek, M.M.

    2007-01-01

    BACKGROUND: Neurofilament (NF) proteins are major cytoskeletal constituents of neurons. Increased CSF NF levels may reflect neuronal degeneration. OBJECTIVE: To investigate the diagnostic value of CSF NF analysis to discriminate in relatively young dementia patients between frontotemporal lobe

  12. CSF-1R Inhibitor Development: Current Clinical Status.

    Science.gov (United States)

    Peyraud, Florent; Cousin, Sophie; Italiano, Antoine

    2017-09-05

    Colony-stimulating factor 1 receptor (CSF-1R) and its ligands, CSF-1 and interleukin 34 (IL-34), regulate the function and survival of tumor-associated macrophages, which are involved in tumorigenesis and in the suppression of antitumor immunity. Moreover, the CSF-1R/CSF-1 axis has been implicated in the pathogenesis of pigmented villonodular synovitis (PVNS), a benign tumor of the synovium. As advanced or metastatic malignant solid tumors and relapsed/refractory PVNS remain unresolved therapeutic problems, new approaches are needed to improve the outcome of patients with these conditions. In solid tumors, targeting CSF-1R via either small molecules or antibodies has shown interesting results in vitro but limited antitumor activity in vivo. Concerning PVNS, clinical trials assessing CSF-1R inhibitors have revealed promising initial outcomes. Blocking CSF-1/CSF-1R signaling represents a promising immunotherapy approach and several new potential combination therapies for future clinical testing.

  13. Measurement of B- -> tau- nu_tau-bar Decay With a Semileptonic Tagging Method

    CERN Document Server

    Adachi, I; Anipko, D; Arinstein, K; Aso, T; Aulchenko, V; Aushev, T; Aziz, T; Bahinipati, S; Bakich, A M; Balagura, V; Ban, Y; Barberio, E; Bay, A; Bedny, I; Belous, K S; Bhardwaj, V; Bitenc, U; Blyth, S; Bondar, A; Bozek, A; Bracko, M; Brodzicka, J; Browder, T E; Chang, M C; Chang, P; Chang, Y W; Chao, Y; Chen, A; Chen, K F; Cheon, B G; Chiang, C C; Chistov, R; Cho, I S; Choi, S K; Choi, Y; Choi, Y K; Cole, S; Dalseno, J; Danilov, M; Das, A; Dash, M; Drutskoy, A; Dungel, W; Eidelman, S; Epifanov, D; Esen, S; Fratina, S; Fujii, H; Fujikawa, M; Gabyshev, N; Garmash, A; Goldenzweig, P; Golob, B; Grosse-Perdekamp, M; Guler, H; Guo, H; Ha, H; Haba, J; Hara, K; Hara, T; Hasegawa, Y; Hastings, N C; Hayasaka, K; Hayashii, H; Hazumi, M; Heffernan, D; Higuchi, T; Hodlmoser, H; Hokuue, T; Horii, Y; Hoshi, Y; Hoshina, K; Hou, W S; Hsiung, Y B; Hyun, H J; Igarashi, Y; Iijima, T; Ikado, K; Inami, K; Ishikawa, A; Ishino, H; Itoh, R; Iwabuchi, M; Iwasaki, M; Iwasaki, Y; Jacoby, C; Joshi, N J; Kaga, M; Kah, D H; Kaji, H; Kakuno, H; Kang, J H; Kapusta, P; Kataoka, S U; Katayama, N; Kawai, H; Kawasaki, T; Kibayashi, A; Kichimi, H; Kim, H J; Kim, H O; Kim, J H; Kim, S K; Kim, Y I; Kim, Y J; Kinoshita, K; Korpar, S; Kozakai, Y; Krizan, P; Krokovny, P; Kumar, R; Kurihara, E; Kuroki, Y; Kuzmin, A; Kwon, Y J; Kyeong, S H; Lange, J S; Leder, G; Lee, J; Lee, J S; Lee, M J; Lee, S E; Lesiak, T; Li, J; Limosani, A; Lin, S W; Liu, C; Liu, Y; Liventsev, D; MacNaughton, J; Mandl, F; Marlow, D; Matsumura, T; Matyja, A; McOnie, S; Medvedeva, T; Mikami, Y; Miyabayashi, K; Miyata, H; Miyazaki, Y; Mizuk, R; Moloney, G R; Mori, T; Nagamine, T; Nagasaka, Y; Nakahama, Y; Nakamura, I; Nakano, E; Nakao, M; Nakayama, H; Nakazawa, H; Natkaniec, Z; Neichi, K; Nishida, S; Nishimura, K; Nishio, Y; Nishizawa, I; Nitoh, O; Noguchi, S; Nozaki, T; Ogawa, A; Ogawa, S; Ohshima, T; Okuno, S; Olsen, S L; Ono, S; Ostrowicz, W; Ozaki, H; Pakhlov, P; Pakhlova, G; Palka, H; Park, C W; Park, H; Park, H K; Park, K S; Parslow, N; Peak, L S; Pernicka, M; Pestotnik, R; Peters, M; Piilonen, L E; Poluektov, A; Rorie, J; Rózanska, M; Sahoo, H; Sakai, Y; Sasao, N; Sayeed, K; Schietinger, T; Schneider, O; Schonmeier, P; Schümann, J; Schwanda, C; Schwartz, A J; Seidl, R; Sekiya, A; Senyo, K; Sevior, M E; Shang, L; Shapkin, M; Shebalin, V; Shen, C P; Shibuya, H; Shinomiya, S; Shiu, J G; Shwartz, B; Sidorov, V; Singh, J B; Sokolov, A; Somov, A; Stanic, S; Staric, M; Stypula, J; Sugiyama, A; Sumisawa, K; Sumiyoshi, T; Suzuki, S; Suzuki, S Y; Tajima, O; Takasaki, F; Tamai, K; Tamura, N; Tanaka, M; Taniguchi, N; Taylor, G N; Teramoto, Y; Tikhomirov, I; Trabelsi, K; Tse, Y F; Tsuboyama, T; Uchida, Y; Uehara, S; Ueki, Y; Ueno, K; Uglov, T; Unno, Y; Uno, S; Urquijo, P; Ushiroda, Y; Usov, Yu; Varner, G; Varvell, K E; Vervink, K; Villa, S; Vinokurova, A; Wang, C C; Wang, C H; Wang, J; Wang, M Z; Wang, P; Wang, X L; Watanabe, M; Watanabe, Y; Wedd, R; Wei, J T; Wicht, J; Widhalm, L; Wiechczynski, J; Won, E; Yabsley, B D; Yamaguchi, A; Yamamoto, H; Yamaoka, M; Yamashita, Y; Yamauchi, M; Yuan, C Z; Yusa, Y; Zhang, C C; Zhang, L M; Zhang, Z P; Zhilich, V; Zhulanov, V; Zivko, T; Zupanc, A; Zwahlen, N; Zyukova, O

    2008-01-01

    We present a new measurement of the decay B- -> tau- nu_tau-bar with a semileptonic B tagging method, using a data sample containing 657*10^6 BB-bar pairs collected at the (4S) resonance with the Belle detector at the KEKB asymmetric e+e- collider. A sample of BB pairs are tagged by reconstructing one B meson decaying semileptonically. We detect the B- -> tau- nu_tau-bar candidate in the recoil. We obtain a signal with a signicance of 3.8 standard deviations including systematics, and measure the branching fraction to be B(B- -> tau- nu_tau-bar)=(1.65+0.38-0.37(stat)+0.35-0.37(syst))*10^4. This result confirms the evidence for B- -> tau- nu_tau-bartained in the previous Belle measurement with a hadronic B tagging method.

  14. CSF monoamine metabolites, cholinesterases and lactate in the adult hydrocephalus syndrome (normal pressure hydrocephalus) related to CSF hydrodynamic parameters.

    Science.gov (United States)

    Malm, J; Kristensen, B; Ekstedt, J; Adolfsson, R; Wester, P

    1991-03-01

    Monoamine metabolites, cholinesterases and lactic acid in lumbar cerebrospinal fluid (CSF) were investigated on patients with the adult hydrocephalus syndrome (idiopathic normal pressure syndrome; AHS, n = 15), Alzheimer's disease (AD, n = 14), multi-infarct dementia (MID, n = 13) and controls (n = 21). Patients had clinical and CSF hydrodynamic investigations. Monoamine concentrations were determined by reversed-phase liquid chromatography, cholinesterases and lactate were determined photometrically. In the AHS patients, CSF monoamine concentrations were not significantly different compared with controls, AD or MID patients. AHS and AD patients showed a similar reduction of CSF acetylcholinesterase activity compared with controls. Positive correlations were found in concentrations of CSF homovanillic acid, CSF 5-hydroxyindoleacetic acid and CSF lactic acid versus CSF outflow conductance (that is, resistance against CSF outflow) in the AHS patients. A similar pattern was observed in a subgroup of MID patients characterised by dilated ventricles and disturbed CSF hydrodynamics. These data suggest that a low CSF outflow conductance may facilitate the clearance of acidic substances from the arachnoid space at the probenecid sensitive active transport site. Alternative explanations would be that a pathologically low CSF outflow conductance is accompanied by an inverse caudorostral flow of CSF or a compromised trans-ependymal diffusion.

  15. Distinct Therapeutic Mechanisms of Tau Antibodies

    Science.gov (United States)

    Funk, Kristen E.; Mirbaha, Hilda; Jiang, Hong; Holtzman, David M.; Diamond, Marc I.

    2015-01-01

    Tauopathies are neurodegenerative diseases characterized by accumulation of Tau amyloids, and include Alzheimer disease and certain frontotemporal dementias. Trans-neuronal propagation of amyloid mediated by extracellular Tau may underlie disease progression. Consistent with this, active and passive vaccination studies in mouse models reduce pathology, although by unknown mechanisms. We previously reported that intracerebroventricular administration of three anti-Tau monoclonal antibodies (HJ8.5, HJ9.3, and HJ9.4) reduces pathology in a model overexpressing full-length mutant (P301S) human Tau. We now study effects of these three antibodies and a negative control antibody (HJ3.4) on Tau aggregate uptake into BV2 microglial-like cells and primary neurons. Antibody-independent Tau uptake into BV2 cells was blocked by heparin, consistent with a previously described role for heparan sulfate proteoglycans. Two therapeutic antibodies (HJ8.5 and HJ9.4) promoted uptake of full-length Tau fibrils into microglia via Fc receptors. Surprisingly, HJ9.3 promoted uptake of fibrils composed of the Tau repeat domain or Alzheimer disease-derived Tau aggregates, but failed to influence full-length recombinant Tau fibrils. Size fractionation of aggregates showed that antibodies preferentially promote uptake of larger oligomers (n ≥∼20-mer) versus smaller oligomers (n ∼10-mer) or monomer. No antibody inhibited uptake of full-length recombinant fibrils into primary neurons, but HJ9.3 blocked neuronal uptake of Tau repeat domain fibrils and Alzheimer disease-derived Tau. Antibodies thus have multiple potential mechanisms, including clearance via microglia and blockade of neuronal uptake. However these effects are epitope- and aggregate size-dependent. Establishing specific mechanisms of antibody activity in vitro may help in design and optimization of agents that are more effective in vivo. PMID:26126828

  16. Modulation of tau phosphorylation by environmental copper

    OpenAIRE

    Voss, Kellen; Harris, Christopher; Ralle, Martina; Duffy, Megan; Murchison, Charles; Joseph F. Quinn

    2014-01-01

    Background The transition metal copper enhances amyloid β aggregation and neurotoxicity, and in models of concomitant amyloid and tau pathology, copper also promotes tau aggregation. Since it is not clear if the effects of environmental copper upon tau pathology are dependent on the presence of pathological amyloid β, we tested the effects of copper overload and complexing in disease models which lack pathological amyloid β. Methods We used cell culture and transgenic murine models to test th...

  17. ANAESTHESIA MANAGEMENT OF CSF RHINORRHEA REPAIR : A CASE REPORT

    Directory of Open Access Journals (Sweden)

    Kirti Arvind

    2015-09-01

    Full Text Available Anaesthesiologist plays a major role in Cerebrospinal Fluid (CSF rhinorrhea repair surgery as the prognosis of which is dependent on provision of clear bloodless surgical field and surgeons satisfaction. Anaesthesiologist also plays vital role in the management of CSF Lumbar drain. This case highlights the importance of hypotensive anaesthesia during endoscopic repair of a case of spontaneous CSF Rhinorrhea with successful perioperative management of Lumbar drainage of CSF

  18. Neurosyphilis in AIDS patients: initial CSF VDRL may be negative.

    Science.gov (United States)

    Feraru, E R; Aronow, H A; Lipton, R B

    1990-03-01

    We report 2 HIV-seropositive patients with neurosyphilis whose initial CSF VDRL tests were negative. The CSF VDRL became positive after 12 days of IV penicillin treatment for syphilitic meningitis in the 1st patient. The 2nd patient developed syphilitic polyradiculopathy and a positive CSF VDRL 3 months after treatment with IV penicillin. Serial CSF VDRL determinations may be required in AIDS patients when a diagnosis of neurosyphilis is suspected.

  19. Correlated angular distributions in {tau}{sup +}{tau}{sup -} semileptonic decays

    Energy Technology Data Exchange (ETDEWEB)

    Dova, M.T. [La Plata Univ. Nacional (Argentina). Dept. de Fisica; Epele, L.N. [La Plata Univ. Nacional (Argentina). Dept. de Fisica; Fanchiotti, H. [La Plata Univ. Nacional (Argentina). Dept. de Fisica; Garcia Canal, C.A. [La Plata Univ. Nacional (Argentina). Dept. de Fisica; Lacentre, P.E. [La Plata Univ. Nacional (Argentina). Dept. de Fisica

    1995-06-01

    The spin correlated angular distribution for {tau}{sup -}{tau}{sup +} pairs at energies of the Z{sup 0} resonance, both decaying semi-leptonically up to 3 hadrons in each final state, was derived assuming general vector and axial vector couplings. The use of these distributions to test the V - A structure of the {tau}-W-{nu}{sub {tau}} vertex at LEP energies is analized. (orig.)

  20. Pade-Improved Extraction of $\\alpha_s(M_\\tau)$ from $R_\\tau$

    OpenAIRE

    Steele, T. G.; Elias, V.

    1999-01-01

    The perturbative series used to extract $\\alpha_s(M_\\tau)$ from the $\\tau$ hadronic width exhibits slow convergence. Asymptotic Pade-approximant and Pade summation techniques provide an estimate of these unknown higher-order effects, leading to values for $\\alpha_s(M_\\tau)$ that are about 10% smaller than current estimates. Such a reduction improves the agreement of $\\alpha_s(M_\\tau)$ with the QCD evolution of the strong coupling constant from $\\alpha_s(M_z)$.

  1. Search for the rare decays $B^0_{(s)}\\to\\tau^+\\tau^-$

    CERN Document Server

    De Bruyn, Kristof; The LHCb Collaboration

    2016-01-01

    A search for the rare decays $B^0_{(s)}\\to\\tau^+\\tau^-$ is performed using $pp$ collision data, corresponding to an integrated luminosity of 3.0 fb$^{-1}$ collected by the LHCb detector in 2011 and 2012 at centre-of-mass energies of 7 and 8 TeV, respectively. The $\\tau$ leptons are reconstructed through the hadronic decay $\\tau^+\\to\\pi^+\\pi^-\\pi^+\\overline\

  2. The Polyphenol Altenusin Inhibits in Vitro Fibrillization of Tau and Reduces Induced Tau Pathology in Primary Neurons.

    Science.gov (United States)

    Chua, Sook Wern; Cornejo, Alberto; van Eersel, Janet; Stevens, Claire H; Vaca, Inmaculada; Cueto, Mercedes; Kassiou, Michael; Gladbach, Amadeus; Macmillan, Alex; Lewis, Lev; Whan, Renee; Ittner, Lars M

    2017-04-19

    In Alzheimer's disease, the microtubule-associated protein tau forms intracellular neurofibrillary tangles (NFTs). A critical step in the formation of NFTs is the conversion of soluble tau into insoluble filaments. Accordingly, a current therapeutic strategy in clinical trials is aimed at preventing tau aggregation. Here, we assessed altenusin, a bioactive polyphenolic compound, for its potential to inhibit tau aggregation. Altenusin inhibits aggregation of tau protein into paired helical filaments in vitro. This was associated with stabilization of tau dimers and other oligomers into globular structures as revealed by atomic force microscopy. Moreover, altenusin reduced tau phosphorylation in cells expressing pathogenic tau, and prevented neuritic tau pathology induced by incubation of primary neurons with tau fibrils. However, treatment of tau transgenic mice did not improve neuropathology and functional deficits. Taken together, altenusin prevents tau fibrillization in vitro and induced tau pathology in neurons.

  3. A Search for B+ -> tau+ nu

    CERN Document Server

    Aubert, B; Boutigny, D; Karyotakis, Yu; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Garra Tico, J; Graugès-Pous, E; López, L; Palano, A; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes-Pegna, D; Lynch, G; Mir, L M; Orimoto, T J; Ronan, M T; Tackmann, K; Wenzel, W A; Del Amo-Sánchez, P; Hawkes, C M; Watson, A T; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Schröder, T; Steinke, M; Walker, D; Asgeirsson, D J; Çuhadar-Dönszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M A; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Liu, F; Long, O; Shen, B C; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Williams, D C; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Zeng, Q; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Brandt, T; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, C; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; De Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Flack, R L; Nash, J A; Nikolich, M B; Panduro-Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Meyer, N T; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bequilleux, J; Davier, M; Grosdidier, G; Höcker, A; Lepeltier, V; Le Diberder, F R; Lutz, A M; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Menges, W; Sacco, R; Cowan, G; Flächer, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; Zheng, Y; Mclachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, Gallieno; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; LoSecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Wong, Q K; Blount, N L; Brau, J E; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; La Vaissière, C de; Hamon, O; Leruste, P; Malcles, J; Ocariz, J; Pérez, A; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Haire, M; Biesiada, J; Elmer, P; Lau, Y P; Lü, C; Olsen, J; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; D'Orazio, A; Del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Ricciardi, S; Röthel, W; Wilson, F F; Aleksan, R; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yéche, C; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Hast, C; Hrynóva, T; Innes, W R; Kaminski, J; Kelsey, M H; Kim, H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Luitz, S; Lüth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Müller, D R; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Vavra, J; Van Bakel, N; Wagner, A P; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martínez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R V; Nugent, I M; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Pappagallo, M; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    2007-01-01

    We present a search for the decay B+ -> tau+ nu using 383x10^6 BBbar pairs collected at the Y(4S) resonance with the BABAR detector at the SLAC PEP-II B-Factory. A sample of events with one reconstructed semileptonic B decay (B- -> D0 l nu X)) is selected, and in the recoil a search for B+ -> tau+ nu is performed. The tau is identified in the following channels: tau+ -> e nu nubar, tau+ -> mu nu nubar, tau+ -> pi+ nu, and tau+ -> pi+ pi0 nu. We measure a branching fraction of B(B+ -> tau+ nu)=(0.9 +- 0.6(stat.) +- 0.1(syst.)) x 10^-4. In the absence of a significant signal, we calculate an upper limit at the 90% confidence level of B(B+ -> tau+ nu) < 1.7 x 10^-4. We calculate the product of the B meson decay constant f_B and |V_ub| to be f_B x |V_ub| = (7.2^{+2.0}_{-2.8}(stat.) +- 0.2 (syst.)) x 10^-4 GeV.

  4. Tau Lepton Reconstruction and Identification at ATLAS

    Directory of Open Access Journals (Sweden)

    Friedrich Felix

    2012-07-01

    Full Text Available Tau leptons play an important role in the physics program at the LHC. They are used in searches for new phenomena like the Higgs boson or Supersymmetry and in electroweak measurements. Identifying hadronically decaying tau leptons with good performance is an essential part of these analyses. We present the current status of the tau reconstruction and identification at the LHC with the ATLAS detector. The tau identification efficiencies and their systematic uncertainties are measured using W → τv and Z → ττ events, and compared with the predictions from Monte Carlo simulations.

  5. Folding of the Tau Protein on Microtubules.

    Science.gov (United States)

    Kadavath, Harindranath; Jaremko, Mariusz; Jaremko, Łukasz; Biernat, Jacek; Mandelkow, Eckhard; Zweckstetter, Markus

    2015-08-24

    Microtubules are regulated by microtubule-associated proteins. However, little is known about the structure of microtubule-associated proteins in complex with microtubules. Herein we show that the microtubule-associated protein Tau, which is intrinsically disordered in solution, locally folds into a stable structure upon binding to microtubules. While Tau is highly flexible in solution and adopts a β-sheet structure in amyloid fibrils, in complex with microtubules the conserved hexapeptides at the beginning of the Tau repeats two and three convert into a hairpin conformation. Thus, binding to microtubules stabilizes a unique conformation in Tau. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  6. Tau regulates the subcellular localization of calmodulin

    Energy Technology Data Exchange (ETDEWEB)

    Barreda, Elena Gomez de [Centro de Biologia Molecular ' Severo Ochoa' , CSIC/UAM, Universidad Autonoma de Madrid, Cantoblanco, 28049 Madrid (Spain); Avila, Jesus, E-mail: javila@cbm.uam.es [Centro de Biologia Molecular ' Severo Ochoa' , CSIC/UAM, Universidad Autonoma de Madrid, Cantoblanco, 28049 Madrid (Spain); CIBER de Enfermedades Neurodegenerativas, 28031 Madrid (Spain)

    2011-05-13

    Highlights: {yields} In this work we have tried to explain how a cytoplasmic protein could regulate a cell nuclear function. We have tested the role of a cytoplasmic protein (tau) in regulating the expression of calbindin gene. We found that calmodulin, a tau-binding protein with nuclear and cytoplasmic localization, increases its nuclear localization in the absence of tau. Since nuclear calmodulin regulates calbindin expression, a decrease in nuclear calmodulin, due to the presence of tau that retains it at the cytoplasm, results in a change in calbindin expression. -- Abstract: Lack of tau expression in neuronal cells results in a change in the expression of few genes. However, little is known about how tau regulates gene expression. Here we show that the presence of tau could alter the subcellular localization of calmodulin, a protein that could be located at the cytoplasm or in the nucleus. Nuclear calmodulin binds to co-transcription factors, regulating the expression of genes like calbindin. In this work, we have found that in neurons containing tau, a higher proportion of calmodulin is present in the cytoplasm compared with neurons lacking tau and that an increase in cytoplasmic calmodulin correlates with a higher expression of calbindin.

  7. A New Search for tau -> mu gamma and tau -> e gamma Decays at Belle

    CERN Document Server

    Abe, K; Aihara, H; Anipko, D; Aoki, K; Arakawa, T; Arinstein, K; Asano, Y; Aso, T; Aulchenko, V M; Aushev, T; Aziz, T; Bahinipati, S; Bakich, A M; Balagura, V; Ban, Y; Banerjee, S; Barberio, E; Barbero, M; Bay, A; Bedny, I; Belous, K S; Bitenc, U; Bizjak, I; Blyth, S; Bondar, A; Bozek, A; Bracko, M; Brodzicka, J; Browder, T E; Chang, M C; Chang, P; Chao, Y; Chen, A; Chen, K F; Chen, W T; Cheon, B G; Chistov, R; Choi, J H; Choi, S K; Choi, Y; Choi, Y K; Chuvikov, A; Cole, S; Dalseno, J; Danilov, M; Dash, M; Dowd, R; Dragic, J; Drutskoy, A; Eidelman, S; Enari, Y; Epifanov, D A; Fratina, S; Fujii, H; Fujikawa, M; Gabyshev, N; Garmash, A; Gershon, T; Go, A; Gokhroo, G; Goldenzweig, P; Golob, B; Gorisek, A; Grosse-Perdekamp, M; Guler, H; Ha, H; Haba, J; Hara, K; Hara, T; Hasegawa, Y; Hastings, N C; Hayasaka, K; Hayashii, H; Hazumi, M; Heffernan, D; Higuchi, T; Hinz, L; Hokuue, T; Hoshi, Y; Hoshina, K; Hou, S; Hou, W S; Hsiung, Y B; Igarashi, Y; Iijima, T; Ikado, K; Imoto, A; Inami, K; Ishikawa, A; Ishino, H; Itoh, K; Itoh, R; Iwabuchi, M; Iwasaki, M; Iwasaki, Y; Jacoby, C; Jones, M; Kakuno, H; Kang, J H; Kang, J S; Kapusta, P; Kataoka, S U; Katayama, N; Kawai, H; Kawasaki, T; Khan, H R; Kibayashi, A; Kichimi, H; Kikuchi, N; Kim, H J; Kim, H O; Kim, J H; Kim, S K; Kim, T H; Kim, Y J; Kinoshita, K; Kishimoto, N; Korpar, S; Kozakai, Y; Krizan, P; Krokovnyi, P P; Kubota, T; Kulasiri, R; Kumar, R; Kuo, C C; Kurihara, E; Kusaka, A; Kuzmin, A; Kwon, Y J; Lange, J S; Leder, G; Lee, J; Lee, S E; Lee, Y J; Lesiak, T; Li, J; Limosani, A; Lin, C Y; Lin, S W; Liu, Y; Liventsev, D; MacNaughton, J; Majumder, G; Mandl, F; Marlow, D; Matsumoto, T; Matyja, A; McOnie, S; Medvedeva, T; Mikami, Y; Mitaroff, W A; Miyabayashi, K; Miyake, H; Miyata, H; Miyazaki, Y; Mizuk, R; Mohapatra, D; Moloney, G R; Mori, T; Müller, J; Murakami, A; Nagamine, T; Nagasaka, Y; Nakagawa, T; Nakahama, Y; Nakamura, I; Nakano, E; Nakao, M; Nakazawa, H; Natkaniec, Z; Neichi, K; Nishida, S; Nishimura, K; Nitoh, O; Noguchi, S; Nozaki, T; Ogawa, A; Ogawa, S; Ohshima, T; Okabe, T; Okuno, S; Olsen, S L; Ono, S; Ostrowicz, W; Ozaki, H; Pakhlov, P; Pakhlova, G; Palka, H; Park, C W; Park, H; Park, K S; Parslow, N; Peak, L S; Pernicka, M; Pestotnik, R; Peters, M; Piilonen, L E; Poluektov, A; Ronga, F J; Root, N; Rorie, J; Rózanska, M; Sahoo, H; Saitoh, S; Sakai, Y; Sakamoto, H; Sakaue, H; Sarangi, T R; Sato, N; Satoyama, N; Sayeed, K; Schietinger, T; Schneider, O; Schonmeier, P; Schümann, J; Schwanda, C; Schwartz, A J; Seidl, R; Seki, T; Senyo, K; Sevior, M E; Shapkin, M; Shen, Y T; Shibuya, H; Shwartz, B; Sidorov, V; Singh, J B; Sokolov, A; Somov, A; Soni, N; Stamen, R; Stanic, S; Staric, M; Stöck, H; Sugiyama, A; Sumisawa, K; Sumiyoshi, T; Suzuki, S; Suzuki, S Y; Tajima, O; Takada, N; Takasaki, F; Tamai, K; Tamura, N; Tanabe, K; Tanaka, M; Taylor, G N; Teramoto, Y; Tian, X C; Tikhomirov, I; Trabelsi, K; Tsai, Y T; Tse, Y F; Tsuboyama, T; Tsukamoto, T; Uchida, K; Uchida, Y; Uehara, S; Uglov, T; Ueno, K; Unno, Y; Uno, S; Urquijo, P; Ushiroda, Y; Usov, Yu; Varner, G; Varvell, K E; Villa, S; Wang, C C; Wang, C H; Wang, M Z; Watanabe, M; Watanabe, Y; Wicht, J; Widhalm, L; Wiechczynski, J; Won, E; Wu, C H; Xie, Q L; Yabsley, B D; Yamaguchi, A; Yamamoto, H; Yamamoto, S; Yamashita, Y; Yamauchi, M; Heyoung Yang; Yoshino, S; Yuan, Y; Yusa, Y; Zang, S L; Zhang, C C; Zhang, J; Zhang, L M; Zhang, Z P; Zhilich, V; Ziegler, T; Zupanc, A; Zürcher, D

    2006-01-01

    We update our search for the lepton flavor violating tau -> mu gamma and tau -> e gamma decays based on 535/fb of data accumulated at the Belle experiment. No signal is found and we set preliminary 90% confidence level upper limits: B(tau -> mu gamma) e gamma) < 1.2x 10^-7.

  8. Hybrid chernoff tau-leap

    KAUST Repository

    Moraes, Alvaro

    2014-01-01

    Markovian pure jump processes model a wide range of phenomena, including chemical reactions at the molecular level, dynamics of wireless communication networks, and the spread of epidemic diseases in small populations. There exist algorithms such as Gillespie\\'s stochastic simulation algorithm (SSA) and Anderson\\'s modified next reaction method (MNRM) that simulate a single path with the exact distribution of the process, but this can be time consuming when many reactions take place during a short time interval. Gillespie\\'s approximated tau-leap method, on the other hand, can be used to reduce computational time, but it may lead to nonphysical values due to a positive one-step exit probability, and it also introduces a time discretization error. Here, we present a novel hybrid algorithm for simulating individual paths which adaptively switches between the SSA and the tau-leap method. The switching strategy is based on a comparison of the expected interarrival time of the SSA and an adaptive time step derived from a Chernoff-type bound for the one-step exit probability. Because this bound is nonasymptotic, we do not need to make any distributional approximation for the tau-leap increments. This hybrid method allows us (i) to control the global exit probability of any simulated path and (ii) to obtain accurate and computable estimates of the expected value of any smooth observable of the process with minimal computational work. We present numerical examples that illustrate the performance of the proposed method. © 2014 Society for Industrial and Applied Mathematics.

  9. Role of CSF-CRP as a bedside diagnostic test in children with meningitis.

    Directory of Open Access Journals (Sweden)

    Piyush Sadat

    2013-01-01

    Full Text Available Meningitis is a formidable illness with high mortality and morbidity in India. Delay in distinguishing pyogenic meningitis from tuberculous and viral meningitis and delay in starting therapy on one hand and irrational use of antibiotics on the other hand may have irrevocable consequences, so, early diagnosis and appropriate treatment of pyogenic meningitis is very vital to prevent permanent neurological deficits. Detection of C-reative protein in CSF is a bed side rapid diagnostic test to distinguish pyogenic from tuberculous and viral meningitis. So, present study was undertaken to study the usefulness of c-reactive protein in CSF as a rapid diagnostic test in differentiating pyogenic from tuberculous and viral meningitis.This study was conducted at Smt Shardaben Hospital from Sept-2008 to Nov-2010. Total 150 cases admitted in paediatric department and neonates admitted to the sick nursery suspected of having meningitis were included. Samples of CSF were taken for bed side diagnostic test of CSF-CRP. The major advantage of this method is rapid two minute reaction time. Our study revealed that out of 150 cases of suspected meningitis 64 (42.66% patient were having meningitis out of which 18 (12% patients were diagnosed as pyogenic meningitis and CSF CRP was positive in 10 (55.55 % patients out of 18 pyogenic meningitis patients and CSF-CRP was negative in all other groups Applying chisquare test, correlation between CSF-CRP positivity and pyoganic meningitis was highly significant (x2 = 31(i.e.> 3.84

  10. Aminopeptidases do not directly degrade tau protein

    Directory of Open Access Journals (Sweden)

    Hersh Louis B

    2010-11-01

    Full Text Available Abstract Background Tau hyperphosphorylation and aggregation to form intracellular neurofibrillar tangles is prevalent in a number of tauopathies. Thus there is current interest in the mechanisms involved in Tau clearance. It was recently reported that Tau can be degraded by an aminopeptidase known as the puromycin sensitive aminopeptidase (PSA. Until now PSA has been reported to only cleave peptides, with the largest reported substrates having 30-50 amino acids. We have studied this unique PSA cleavage reaction using a number of different PSA preparations. Results An N-terminally His tagged-PSA was expressed and purified from Sf9 insect cells. Although this PSA preparation cleaved Tau, product analysis with N and C terminal Tau antibodies coupled with mass spectrometry showed an endoproteolytic cleavage atypical for an aminopeptidase. Furthermore, the reaction was not blocked by the general aminopeptidase inhibitor bestatin or the specific PSA inhibitor puromycin. In order to test whether Tau hydrolysis might be caused by a protease contaminant the enzyme was expressed in E. coli as glutathione S-transferase and maltose binding protein fusion proteins or in Sf9 cells as a C-terminally His-tagged protein. After purification to near homogeneity none of these other recombinant forms of PSA cleaved Tau. Further, Tau-cleaving activity and aminopeptidase activities derived from the Sf9 cell expression system were separable by molecular sieve chromatography. When tested in a cellular context we again failed to see a PSA dependent cleavage of Tau. A commercial preparation of a related aminopeptidase, aminopeptidase N, also exhibited Tau cleaving activity, but this activity could also be separated from aminopeptidase activity. Conclusion It is concluded that PSA does not directly cleave Tau.

  11. RNA stores tau reversibly in complex coacervates.

    Science.gov (United States)

    Zhang, Xuemei; Lin, Yanxian; Eschmann, Neil A; Zhou, Hongjun; Rauch, Jennifer N; Hernandez, Israel; Guzman, Elmer; Kosik, Kenneth S; Han, Songi

    2017-07-01

    Nonmembrane-bound organelles that behave like liquid droplets are widespread among eukaryotic cells. Their dysregulation appears to be a critical step in several neurodegenerative conditions. Here, we report that tau protein, the primary constituent of Alzheimer neurofibrillary tangles, can form liquid droplets and therefore has the necessary biophysical properties to undergo liquid-liquid phase separation (LLPS) in cells. Consonant with the factors that induce LLPS, tau is an intrinsically disordered protein that complexes with RNA to form droplets. Uniquely, the pool of RNAs to which tau binds in living cells are tRNAs. This phase state of tau is held in an approximately 1:1 charge balance across the protein and the nucleic acid constituents, and can thus be maximal at different RNA:tau mass ratios, depending on the biopolymer constituents involved. This feature is characteristic of complex coacervation. We furthermore show that the LLPS process is directly and sensitively tuned by salt concentration and temperature, implying it is modulated by both electrostatic interactions between the involved protein and nucleic acid constituents, as well as net changes in entropy. Despite the high protein concentration within the complex coacervate phase, tau is locally freely tumbling and capable of diffusing through the droplet interior. In fact, tau in the condensed phase state does not reveal any immediate changes in local protein packing, local conformations and local protein dynamics from that of tau in the dilute solution state. In contrast, the population of aggregation-prone tau as induced by the complexation with heparin is accompanied by large changes in local tau conformations and irreversible aggregation. However, prolonged residency within the droplet state eventually results in the emergence of detectable β-sheet structures according to thioflavin-T assay. These findings suggest that the droplet state can incubate tau and predispose the protein toward the

  12. Cerebrospinal fluid tau and amyloid-β1-42 in patients with dementia.

    Science.gov (United States)

    Skillbäck, Tobias; Farahmand, Bahman Y; Rosén, Christoffer; Mattsson, Niklas; Nägga, Katarina; Kilander, Lena; Religa, Dorota; Wimo, Anders; Winblad, Bengt; Schott, Jonathan M; Blennow, Kaj; Eriksdotter, Maria; Zetterberg, Henrik

    2015-09-01

    Progressive cognitive decline in combination with a cerebrospinal fluid biomarker pattern of low levels of amyloid-β1-42 and high levels of total tau and phosphorylated tau is typical of Alzheimer's disease. However, several neurodegenerative disorders may overlap with Alzheimer's disease both in regards to clinical symptoms and neuropathology. In a uniquely large cohort of dementia patients, we examined the associations of cerebrospinal fluid biomarkers for Alzheimer's disease molecular pathology with clinical dementia diagnoses and disease severity. We cross-referenced the Swedish Dementia Registry with the clinical laboratory database at the Sahlgrenska University Hospital. The final data set consisted of 5676 unique subjects with a clinical dementia diagnosis and a complete set of measurements for cerebrospinal fluid amyloid-β1-42, total tau and phosphorylated tau. In cluster analysis, disregarding clinical diagnosis, the optimal natural separation of this data set was into two clusters, with the majority of patients with early onset Alzheimer's disease (75%) and late onset Alzheimer's disease (73%) assigned to one cluster and the patients with vascular dementia (91%), frontotemporal dementia (94%), Parkinson's disease dementia (94%) and dementia with Lewy bodies (87%) to the other cluster. Frontotemporal dementia had the highest cerebrospinal fluid levels of amyloid-β1-42 and the lowest levels of total tau and phosphorylated tau. The highest levels of total tau and phosphorylated tau and the lowest levels of amyloid-β1-42 and amyloid-β1-42:phosphorylated tau ratios were found in Alzheimer's disease. Low amyloid-β1-42, high total tau and high phosphorylated tau correlated with low Mini-Mental State Examination scores in Alzheimer's disease. In Parkinson's disease dementia and vascular dementia low cerebrospinal fluid amyloid-β1-42 was associated with low Mini-Mental State Examination score. In the vascular dementia, frontotemporal dementia, dementia with

  13. Selected Topics in Tau Physics from BaBar

    Energy Technology Data Exchange (ETDEWEB)

    Paramesvaran, S.; /Royal Holloway, U. of London

    2012-04-06

    Selected results from {tau} analyses performed using the BABAR detector at the SLAC National Accelerator Laboratory are presented. A precise measurement of the {tau} mass and the {tau}{sup +}{tau}{sup -} mass difference is undertaken using the hadronic decay mode {tau}{sup {+-}} {yields} {pi}{sup +}{pi}{sup -}{pi}{sup {+-}}{nu}{sub {tau}}. In addition an investigation into the strange decay modes {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{pi}{sup 0}{nu}{sub {tau}} and {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{nu}{sub {tau}} is also presented, including a fit to the {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{nu}{sub {tau}} invariant mass spectrum. Precise values for M(K*(892)) and {Lambda}(K*(892)) are obtained.

  14. Influence of Water Quality on Cholesterol-Induced Tau Pathology: Preliminary Data

    Directory of Open Access Journals (Sweden)

    D. Larry Sparks

    2011-01-01

    Full Text Available The studies employed the cholesterol-fed rabbit model of Alzheimer's disease (AD to investigate the relationship between AD-like neurofibrillary tangle (NFT neuropathology and tau protein levels as the main component of NFT. We measured brain and plasma tau levels and semiquantified NFT-like neuropathology in cholesterol-fed rabbits administered drinking water of varying quality (distilled, tap, and distilled+copper compared to animals receiving normal chow and local tap water. Total tau levels in plasma were increased in all cholesterol-fed rabbits compared to animals on normal chow, regardless of quality of water. In contrast, increased tau in brain and increased AT8 immunoreactive NFT-like lesions were greatest in cholesterol-fed rabbits administered distilled water. A substantial decrease in brain tau and incidence and density of AT8 immunoreactive NFT-like lesions occurred in cholesterol-fed rabbits administered copper water, and an even greater decrease was observed in cholesterol-fed animals on local tap water. These studies suggest the possibility that circulating tau could be the source of the tau accumulating in the brain.

  15. Exclusive branching-fraction measurements of semileptonic tau decays into three charged hadrons, into phipi(-)nu tau, and into phi K(-)nu tau.

    Science.gov (United States)

    Aubert, B; Bona, M; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Gill, M S; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Pegna, D Lopes; Lynch, G; Mir, L M; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; del Amo Sanchez, P; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Watson, A T; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Cottingham, W N; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Sherwood, D J; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Best, D S; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Roethel, W; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; Hadavand, H K; Hill, E J; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Cheng, C H; Dvoretskii, A; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Zeng, Q; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Brandt, T; Klose, V; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Lee, C L; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Nash, J A; Nikolich, M B; Vazquez, W Panduro; Behera, P K; Chai, X; Charles, M J; Mallik, U; Meyer, N T; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gritsan, A V; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Davier, M; Grosdidier, G; Höcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Oyanguren, A; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; Clarke, C K; Di Lodovico, F; Menges, W; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Jackson, P S; McMahon, T R; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; Naisbit, M T; Williams, J C; Yi, J I; Chen, C; Hulsbergen, W D; Jawahery, A; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Saremi, S; Staengle, H; Cowan, R; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; McLachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; LoSecco, J M; Benelli, G; Corwin, L A; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Rahimi, A M; Regensburger, J J; Ter-Antonyan, R; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Potter, C T; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; Del Buono, L; de la Vaissière, Ch; Hamon, O; Hartfiel, B L; Leruste, Ph; Malclès, J; Ocariz, J; Roos, L; Therin, G; Gladney, L; Biasini, M; Covarelli, R; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y P; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Gioi, L Li; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Tehrani, F Safai; Voena, C; Ebert, M; Schröder, H; Waldi, R; Adye, T; Franek, B; Olaiya, E O; Ricciardi, S; Wilson, F F; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; de Monchenault, G Hamel; Kozanecki, W; Legendre, M; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dujmic, D; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Leith, D W G S; Li, S; Luitz, S; Luth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; van Bakel, N; Wagner, A P; Weaver, M; Weinstein, A J R; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Pappagallo, M; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Flood, K T; Hollar, J J; Kutter, P E; Mellado, B; Mihalyi, A; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Yu, Z; Neal, H

    2008-01-11

    Using a data sample corresponding to an integrated luminosity of 342 fb(-1) collected with the BABAR detector at the SLAC PEP-II electron-positron storage ring operating at a center-of-mass energy near 10.58 GeV, we measure B(tau(-)--> pi(-)pi(-)pi+nu(tau)(ex.K(S0))=(8.83+/-0.01+/-0.13)%, B(tau(-) -->K(-)pi(-)pi+nu tau(ex.K(S0))=(0.273+/-0.002+/-0.009)%, B(tau(-) -->K(-)pi(-)K+nu tau)=(0.1346+/-0.0010+/-0.0036)%, and B(tau(-) -->K(-)K(-)K+nu tau)=(1.58+/-0.13+/-0.12)x10;{-5}, where the uncertainties are statistical and systematic, respectively. These include significant improvements over previous measurements and a first measurement of B(tau(-) -->K(-)K(-)K+nu tau) in which no resonance structure is assumed. We also report a first measurement of B(tau(-) -->var phi(-)nu tau)=(3.42+/-0.55+/-0.25)x10(-5), a new measurement of B(tau(-) -->var phi K(-)nu tau)=(3.39+/-0.20+/-0.28)x10(-5) and a first upper limit on B(tau(-) -->K(-)K(-)K+nu tau(ex.var phi)).

  16. A precision measurement of the Z{sup 0} lineshape parameters for the process Z{sup 0} {r_arrow} {tau}{sup +}{tau}{sup {minus}}

    Energy Technology Data Exchange (ETDEWEB)

    Lahmann, R.

    1996-12-31

    In this dissertation, a measurement of the partial decay width of the process Z{sup 0} {r_arrow} {tau}{sup +}{tau}{sup {minus}} using data collected during 1993 and 1994 at the OPAL detector at CERN is described. The cross sections of this process at three center-of-mass energies near the Z{sup 0} resonance were determined, and from a fit to those cross sections, the mass of the Z{sup 0}, its total decay width and its partial decay width into {tau}{sup +}{tau}{sup {minus}} final states were determined as M{sub Z} = 91.183 {+-} 0.020 GeV, {Lambda}{sub tot} = 2.514 {+-} 0.018 GeV and {Lambda}{sub {tau}{tau}} = 84.54 {+-} 0.59 MeV. Using published results for M{sub Z}, and {Lambda}{sub tot} with higher accuracy, a value for the partial decay width of {Lambda}{sub {tau}{tau}} = 84.02 {+-} 0.20 MeV was obtained. Further using published results for the decay width of the Z{sup 0} into quark pair final states, the invisible decay width of the Z{sup 0} was determined as {Lambda}{sub inv} = 496.9 {+-} 4.1 MeV, and the number of neutrino generations was determined as N{sub {nu}} = 2.974 {+-} 0.025(exp) {+-} 0.007 (m{sub top}, M{sub Higgs}). All results were found to be in good agreement with the Standard Model predictions and were consistent with the assumption of lepton universality within the Standard Model framework.

  17. Distributed cavity phase frequency shifts of the caesium fountain PTB-CSF2

    CERN Document Server

    Weyers, S; Nemitz, N; Li, R; Gibble, K

    2011-01-01

    We evaluate the frequency error from distributed cavity phase in the caesium fountain clock PTB-CSF2 at the Physikalisch-Technische Bundesanstalt with a combination of frequency measurements and ab initio calculations. The associated uncertainty is 1.3E-16, with a frequency bias of 0.4E-16. The agreement between the measurements and calculations explains the previously observed frequency shifts at elevated microwave amplitude. We also evaluate the frequency bias and uncertainty due to the microwave lensing of the atomic wavepackets. We report a total PTB-CSF2 systematic uncertainty of 4.1E-16.

  18. Lepton flavor violation in $\\tau$ decays

    CERN Document Server

    Chen, C H; Chen, Chuan-Hung; Geng, Chao-Qiang

    2006-01-01

    We study the lepton flavor violation (LFV) in tau decays in the framework of the supersymmetric seesaw mechanism with a large $\\tan\\beta$. By the mixture of sleptons induced at the unified scale, we examine the nonholomorphic terms from the couplings between the Higgs and leptons. We explicitly analyze two decay modes $\\tau\\to \\ell f_0(980)$ and $\\tau\\to \\ell K^{+} K^{-}$ produced by the scalar bosons, along with $\\tau\\to \\ell \\eta^{(\\prime)}$ governed by the pseudoscalar boson, to probe the lepton flavor violating effects. We find that the decay branching ratios of the two modes could be not only as large as the current upper limits $O(10^{-7})$, but also larger than those of $\\tau\\to \\ell \\eta^{(\\prime)}$. Furthermore, we discover that the decay branching ratios of $\\tau\\to \\ell \\mu^{+} \\mu^{-}$ are related to those of $\\tau\\to \\ell \\eta$ and $\\tau\\to \\ell f_0(980)$.

  19. Physics with tau leptons at CDF

    Energy Technology Data Exchange (ETDEWEB)

    Hays, C.P.; /Oxford U.

    2007-04-01

    The {radical}s = 1.96 TeV p{bar p} collisions produced by the Tevatron result in many processes with tau leptons in the final state. The CDF Collaboration has studied these final states in Z and t{bar t} production, and has used tau leptons to search for evidence of Higgs, sparticle, and Z{prime} production.

  20. Mitochondrial DNA in CSF distinguishes LRRK2 from idiopathic Parkinson's disease.

    Science.gov (United States)

    Podlesniy, Petar; Vilas, Dolores; Taylor, Peggy; Shaw, Leslie M; Tolosa, Eduard; Trullas, Ramon

    2016-10-01

    Mitochondrial DNA regulates mitochondrial function which is altered in both idiopathic and familial forms of Parkinson's disease. To investigate whether these two disease forms exhibit an altered regulation of mitochondrial DNA we measured cell free mitochondrial DNA content in cerebrospinal fluid (CSF) from idiopathic and LRRK2-related Parkinson's disease patients. The concentration of mitochondrial DNA was measured using a digital droplet polymerase chain reaction technique in a total of 98 CSF samples from a cohort of subjects including: 20 LRRK2(G2019S) mutation carriers with Parkinson's disease, 26 asymptomatic LRRK2(G2019S) mutation carriers, 31 patients with idiopathic Parkinson's disease and 21 first-degree relatives of LRRK2 Parkinson's disease patients without the mutation. Here we report that LRRK2(G2019S) mutation carriers with Parkinson's disease exhibit a high concentration of mitochondrial DNA in CSF compared with asymptomatic LRRK2(G2019S) mutation carriers and with idiopathic Parkinson's disease patients. In addition, idiopathic, but not LRRK2 Parkinson's disease is associated with low CSF concentration of α-synuclein. These results show that high mitochondrial DNA content in CSF distinguishes idiopathic from LRRK2-related Parkinson's disease suggesting that different biochemical pathways underlie neurodegeneration in these two disorders.

  1. Benign spinal meningioma without dural attachment presenting delayed CSF dissemination and malignant transformation.

    Science.gov (United States)

    Tsuda, Kyoji; Akutsu, Hiroyoshi; Yamamoto, Tetsuya; Ishikawa, Eiichi; Saito, Atsushi; Nakai, Kei; Takano, Shingo; Matsumura, Akira

    2013-07-01

    Benign spinal meningiomas have good prognoses, with low rates of recurrence and no cerebrospinal fluid (CSF) dissemination. However, we experienced an extremely rare case of initially benign non-dura-based spinal meningioma that showed multiple CSF disseminated lesions, which progressed for 14 years. A 29-year-old woman without neurofibromatosis presented with progressing dysesthesia in her lower limbs, low back pain, and intermittent claudication. Magnetic resonance imaging (MRI) showed an intradural extramedullary mass lesion at the Th10/11 level. The patient underwent a tumor resection. Intraoperative findings indicated that the tumor had no dural attachment. Histopathological diagnosis after gross total removal was microcystic meningioma (grade I, WHO 2007). Seven years after the first operation, other lesions appeared at the levels of Th11/12, L1, and L2/3 in MRI. These tumors were slow growing and became symptomatic; thus, a second surgery was performed 14 years after the first operation. The histopathological diagnosis was atypical meningioma (grade II, WHO 2007). Benign spinal meningiomas show CSF dissemination extremely rarely, although some authors have reported non-dura-based intraspinal clear-cell meningiomas showing CSF dissemination. However, even in cases of WHO grade I, neurosurgeons should pay attention to late CSF dissemination and malignant transformation after surgical removal of non-dura-based intraspinal meningiomas.

  2. Intrinsic Tau Acetylation Is Coupled to Auto-Proteolytic Tau Fragmentation.

    Directory of Open Access Journals (Sweden)

    Todd J Cohen

    Full Text Available Tau proteins are abnormally aggregated in a range of neurodegenerative tauopathies including Alzheimer's disease (AD. Recently, tau has emerged as an extensively post-translationally modified protein, among which lysine acetylation is critical for normal tau function and its pathological aggregation. Here, we demonstrate that tau isoforms have different propensities to undergo lysine acetylation, with auto-acetylation occurring more prominently within the lysine-rich microtubule-binding repeats. Unexpectedly, we identified a unique intrinsic property of tau in which auto-acetylation induces proteolytic tau cleavage, thereby generating distinct N- and C-terminal tau fragments. Supporting a catalytic reaction-based mechanism, mapping and mutagenesis studies showed that tau cysteines, which are required for acetyl group transfer, are also essential for auto-proteolytic tau processing. Further mass spectrometry analysis identified the C-terminal 2nd and 4th microtubule binding repeats as potential sites of auto-cleavage. The identification of acetylation-mediated auto-proteolysis provides a new biochemical mechanism for tau self-regulation and warrants further investigation into whether auto-catalytic functions of tau are implicated in AD and other tauopathies.

  3. TauSpinner program for studies on spin effect in tau production at the LHC

    CERN Document Server

    Czyczula, Z; Was, Z

    2012-01-01

    Final states involving tau leptons are important components of searches for new particles at the Large Hadron Collider (LHC). A proper treatment of tau spin effects in the Monte Carlo (MC) simulations is important for understanding the detector acceptance as well as for the measurements of tau polarization and tau spin correlations. In this note we present a TauSpinner package designed to simulate the spin effects. It relies on the availability of the four-momenta of the taus and their decay products in the analyzed data. The flavor and the four-momentum of the boson decaying to the tau-tau+ or tau+- nu pair need to be known. In the Z/gamma* case the initial state quark configuration is attributed from the intermediate boson kinematics, and the parton distribution functions (PDF's). TauSpinner is the first algorithm suitable for emulation of tau spin effects in tau-embedded samples. It is also the first tool that offers the user the flexibility to simulate a desired spin effect at the analysis level. An algor...

  4. Search for resonant Higgs boson pair production in the $\\mathrm{b\\overline{b}}\\tau^+\\tau^-$ final state

    CERN Document Server

    CMS Collaboration

    2016-01-01

    A search for resonant Higgs boson pair production in proton-proton collisions in the $\\mathrm{b\\overline{b}}\\tau^+\\tau^-$ final state is presented. The search assumes the existence of a new heavy scalar boson H, which decays into a pair of the known h bosons. The search for $\\mathrm{pp} \\to \\mathrm{H} \\to \\mathrm{hh} \\to \\mathrm{b\\overline{b}}\\tau^+\\tau^-$ is performed using three $\\tau\\tau$ final states, $e\\tau_{h}$, $\\mu\\tau_{h}$, and $\\tau_{h}\\tau_{h}$, where $\\tau_{h}$ indicates a $\\tau$ lepton decaying into hadrons. The analysis uses proton-proton collision data collected with the CMS detector at the LHC in 2015 at a centre-of-mass energy of $13~\\mathrm{TeV}$ and corresponding to an integrated luminosity of $2.7~\\mathrm{fb}^{-1}$.

  5. Draft genome sequence of the fish pathogen Flavobacterium columnare strain CSF-298-10

    Science.gov (United States)

    We announce the genome assembly of Flavobacterium columnare strain CSF-298-10, a strain isolated from an outbreak of Columnaris disease at a commercial trout farm in Snake River Valley Idaho, USA. The complete genome consists of 13 contigs totaling 3,284,579 bp, average G+C content of 31.5% and 2933...

  6. Measurement of the transverse spin correlations in the decay $Z \\rightarrow \\tau^+\\tau^-$

    CERN Document Server

    Barate, R; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Nief, J Y; Pietrzyk, B; Casado, M P; Chmeissani, M; Comas, P; Crespo, J M; Delfino, M C; Fernández, E; Fernández-Bosman, M; Garrido, L; Juste, A; Martínez, M; Miquel, R; Mir, L M; Orteu, S; Padilla, C; Park, I C; Pascual, A; Perlas, J A; Riu, I; Sánchez, F; Teubert, F; Colaleo, A; Creanza, D; De Palma, M; Gelao, G; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Alemany, R; Becker, U; Bazarko, A O; Bright-Thomas, P G; Cattaneo, M; Cerutti, F; Dissertori, G; Drevermann, H; Forty, Roger W; Frank, M; Hagelberg, R; Hansen, J B; Harvey, J; Janot, P; Jost, B; Kneringer, E; Knobloch, J; Lehraus, Ivan; Lutters, G; Mato, P; Minten, Adolf G; Moneta, L; Pacheco, A; Pusztaszeri, J F; Ranjard, F; Rizzo, G; Rolandi, Luigi; Rousseau, D; Schlatter, W D; Schmitt, M; Schneider, O; Tejessy, W; Tomalin, I R; Wachsmuth, H W; Wagner, A; Ajaltouni, Ziad J; Barrès, A; Boyer, C; Falvard, A; Ferdi, C; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rosnet, P; Rossignol, J M; Fearnley, Tom; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Rensch, B; Wäänänen, A; Daskalakis, G; Kyriakis, A; Markou, C; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Rougé, A; Rumpf, M; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Focardi, E; Parrini, G; Zachariadou, K; Corden, M; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Casper, David William; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Curtis, L; Dorris, S J; Halley, A W; Knowles, I G; Lynch, J G; O'Shea, V; Raine, C; Scarr, J M; Smith, K; Teixeira-Dias, P; Thompson, A S; Thomson, E; Thomson, F; Turnbull, R M; Geweniger, C; Graefe, G; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Schmidt, M; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Girone, M; Goodsir, S M; Martin, E B; Moutoussi, A; Nash, J; Sedgbeer, J K; Spagnolo, P; Stacey, A M; Williams, M D; Ghete, V M; Girtler, P; Kuhn, D; Rudolph, G; Betteridge, A P; Bowdery, C K; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Sloan, Terence; Williams, M I; Galla, A; Giehl, I; Greene, A M; Hoffmann, C; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Sander, H G; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Benchouk, C; Bonissent, A; Bujosa, G; Calvet, D; Carr, J; Coyle, P; Diaconu, C A; Etienne, F; Konstantinidis, N P; Leroy, O; Motsch, F; Payre, P; Talby, M; Sadouki, A; Thulasidas, M; Trabelsi, K; Aleppo, M; Ragusa, F; Berlich, R; Blum, Walter; Büscher, V; Dietl, H; Ganis, G; Gotzhein, C; Kroha, H; Lütjens, G; Lutz, Gerhard; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Saint-Denis, R; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Chen, S; Choi, Y; Cordier, A; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Höcker, A; Jacholkowska, A; Jacquet, M; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Nikolic, I A; Schune, M H; Simion, S; Tournefier, E; Veillet, J J; Videau, I; Zerwas, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Palla, Fabrizio; Sanguinetti, G; Sciabà, A; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Vannini, C; Venturi, A; Verdini, P G; Blair, G A; Bryant, L M; Chambers, J T; Gao, Y; Green, M G; Medcalf, T; Perrodo, P; Strong, J A; Von Wimmersperg-Töller, J H; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Maley, P; Norton, P R; Thompson, J C; Wright, A E; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Black, S N; Dann, J H; Johnson, R P; Kim, H Y; Litke, A M; McNeil, M A; Taylor, G; Booth, C N; Boswell, R; Brew, C A J; Cartwright, S L; Combley, F; Kelly, M S; Lehto, M H; Newton, W M; Reeve, J; Thompson, L F; Böhrer, A; Brandt, S; Cowan, G D; Grupen, Claus; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Musolino, G; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Charles, E; Elmer, P; Ferguson, D P S; González, S; Greening, T C; Hayes, O J; Hu, H; Jin, S; McNamara, P A; Nachtman, J M; Nielsen, J; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, J; Wu Sau Lan; Wu, X; Yamartino, J M; Zobernig, G

    1997-01-01

    For tau leptons produced in e^+e^- -> tau^+ tau^- interactions there are, in addition to the longitudinal spin correlations, two independent transverse spin correlations associated with the transverse (within the production plane) and normal (to the production plane) polarization components. A measurement of the transverse-transverse and transverse-normal tau spin correlations in the decay Z -> tau^+ tau^-, C_{TT} and C_{TN}, is presented based on the aplanarity angle of the decay products of both tau leptons. Using 80 pb^{-1} of data collected by ALEPH on the peak of the Z resonance, the results are C_{TT} = 1.06 +- 0.13 (stat) +- 0.05 (syst), and C_{TN} = 0.08 +- 0.13 (stat) +- 0.04 (syst). These values are in agreement with the Standard Model predictions, C_{TT} = 0.99 and C_{TN} = -0.01.

  7. [Present and future of the tau dementia therapy].

    Science.gov (United States)

    Takashima, Akihiko

    2013-01-01

    Neurofibrillarly tangles (NFTs) are seen most patients, who shows dementia, while β amyloid deposition observed specifically in AD patients. NFTs observe first from coeruleus and entorhinal cortex, and then spread to neocortex, which well explain clinical progression of AD, such as memory problem to dementia. Tau fibrils are the major component of NFT. Before forming tau fibrils, tau binds together, form soluble tau oligomer, and then granular tau oligomer. The soluble tau oligomer associates with synapse loss, and granular tau formation induces neuronal loss. Therefore, tau aggregation inhibitor is expected to halt the clinical progression of AD.

  8. Tau phosphorylation affects its axonal transport and degradation

    Science.gov (United States)

    Rodríguez-Martín, Teresa; Cuchillo-Ibáñez, Inmaculada; Noble, Wendy; Nyenya, Fanon; Anderton, Brian H.; Hanger, Diane P.

    2013-01-01

    Phosphorylated forms of microtubule-associated protein tau accumulate in neurofibrillary tangles in Alzheimer's disease. To investigate the effects of specific phosphorylated tau residues on its function, wild type or phosphomutant tau was expressed in cells. Elevated tau phosphorylation decreased its microtubule binding and bundling, and increased the number of motile tau particles, without affecting axonal transport kinetics. In contrast, reducing tau phosphorylation enhanced the amount of tau bound to microtubules and inhibited axonal transport of tau. To determine whether differential tau clearance is responsible for the increase in phosphomimic tau, we inhibited autophagy in neurons which resulted in a 3-fold accumulation of phosphomimic tau compared with wild type tau, and endogenous tau was unaffected. In autophagy-deficient mouse embryonic fibroblasts, but not in neurons, proteasomal degradation of phosphomutant tau was also reduced compared with wild type tau. Therefore, autophagic and proteasomal pathways are involved in tau degradation, with autophagy appearing to be the primary route for clearing phosphorylated tau in neurons. Defective autophagy might contribute to the accumulaton of tau in neurodegenerative diseases. PMID:23601672

  9. Measurement of the W{yields}{tau}{nu}{sub {tau}} cross section in proton-proton collisions at ATLAS and development of the HepMCAnalysis tool

    Energy Technology Data Exchange (ETDEWEB)

    Johnert, Sebastian

    2012-04-15

    prediction of (10.46{+-}0.52) nb. Furthermore, the W{yields}{tau}{nu}{sub {tau}} branching ratio was determined, using a total W boson production cross section of 100 nb with an uncertainty of 5%, to be (11.1{+-}0.3(stat.){+-}1.8(syst.) {+-}0.4(lumi.))%, also in agreement with the SM expectation of 10.83%.

  10. Tau Identification at CMS in Run II

    CERN Document Server

    Ojalvo, Isabel

    2016-01-01

    During LHC Long Shutdown 1 necessary upgrades to the CMS detector were made. CMS also took the opportunity to improve further particle reconstruction. A number of improvements were made to the Hadronic Tau reconstruction and Identification algorithms. In particular, electromag- netic strip reconstruction of the Hadron plus Strips (HPS) algorithm was improved to better model signal of pi0 from tau decays. This modification improves energy response and removes the tau footprint from isolation area. In addition to this, improvement to discriminators combining iso- lation and tau life time variables, and anti-electron in MultiVariate Analysis technique was also developed. The results of these improvements are presented and validation of Tau Identification using a variety of techniques is shown.

  11. Reduced number of axonal mitochondria and tau hypophosphorylation in mouse P301L tau knockin neurons.

    Science.gov (United States)

    Rodríguez-Martín, Teresa; Pooler, Amy M; Lau, Dawn H W; Mórotz, Gábor M; De Vos, Kurt J; Gilley, Jonathan; Coleman, Michael P; Hanger, Diane P

    2016-01-01

    Expression of the frontotemporal dementia-related tau mutation, P301L, at physiological levels in adult mouse brain (KI-P301L mice) results in overt hypophosphorylation of tau and age-dependent alterations in axonal mitochondrial transport in peripheral nerves. To determine the effects of P301L tau expression in the central nervous system, we examined the kinetics of mitochondrial axonal transport and tau phosphorylation in primary cortical neurons from P301L knock-in (KI-P301L) mice. We observed a significant 50% reduction in the number of mitochondria in the axons of cortical neurons cultured from KI-P301L mice compared to wild-type neurons. Expression of murine P301L tau did not change the speed, direction of travel or likelihood of movement of mitochondria. Notably, the angle that defines the orientation of the mitochondria in the axon, and the volume of individual moving mitochondria, were significantly increased in neurons expressing P301L tau. We found that murine tau phosphorylation in KI-P301L mouse neurons was diminished and the ability of P301L tau to bind to microtubules was also reduced compared to tau in wild-type neurons. The P301L mutation did not influence the ability of murine tau to associate with membranes in cortical neurons or in adult mouse brain. We conclude that P301L tau is associated with mitochondrial changes and causes an early reduction in murine tau phosphorylation in neurons coupled with impaired microtubule binding of tau. These results support the association of mutant tau with detrimental effects on mitochondria and will be of significance for the pathogenesis of tauopathies. Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.

  12. The Co-chaperone BAG2 Mediates Cold-Induced Accumulation of Phosphorylated Tau in SH-SY5Y Cells.

    Science.gov (United States)

    de Paula, Cesar Augusto Dias; Santiago, Fernando Enrique; de Oliveira, Adriele Silva Alves; Oliveira, Fernando Augusto; Almeida, Maria Camila; Carrettiero, Daniel Carneiro

    2016-05-01

    Inclusions of phosphorylated tau (p-tau) are a hallmark of many neurodegenerative disorders classified as "tauopathy," of which Alzheimer's disease is the most prevalent form. Dysregulation of tau phosphorylation disrupts neuron structure and function, and hyperphosphorylated tau aggregates to form neurotoxic inclusions. The abundance of ubiquitin in tau inclusions suggests a defect in ubiquitin-mediated tau protein degradation by the proteasome. Under the temperature of 37 °C, the co-chaperone BAG2 protein targets phosphorylated tau for degradation via by a more-efficient, ubiquitin-independent pathway. In both in vivo and in vitro studies, cold exposure induces the accumulation of phosphorylated tau protein. The SH-SY5Y cell line differentiates into neuron-like cells on treatment with retinoic acid and is an established model for research on the effects of cold on tau phosphorylation. The aim of the present study was to investigate whether BAG2 mediates the cold-induced accumulation of phosphorylated tau protein. Our findings show that cold exposure causes a decrease in BAG2 expression in undifferentiated cells. Conversely, BAG2 expression is increased in differentiated cells exposed to cold. Further, undifferentiated cells exposed to cold had an increased proportion of p-tau to total tau, suggesting an accumulation of p-tau that is consistent with decreased levels of BAG2. Overexpression of BAG2 in cold-exposed undifferentiated cells restored levels of p-tau to those of 37 °C undifferentiated control. Interestingly, although BAG2 expression increased in differentiated cells, this increase was not accompanied by a decrease in the proportion of p-tau to total tau. Further, overexpression of BAG2 in cold exposed differentiated cells showed no significant difference in p-tau levels compared to 37 °C controls. Taken together, these data show that expression of BAG2 is differently regulated in a differentiation-dependent context. Our results suggest that

  13. Characteristics of Tau and Its Ligands in PET Imaging

    Directory of Open Access Journals (Sweden)

    Ryuichi Harada

    2016-01-01

    Full Text Available Tau deposition is one of the neuropathological hallmarks in Alzheimer’s disease as well as in other neurodegenerative disorders called tauopathies. Recent efforts to develop selective tau radiopharmaceuticals have allowed the visualization of tau deposits in vivo. In vivo tau imaging allows the assessment of the regional distribution of tau deposits in a single human subject over time for determining the pathophysiology of tau accumulation in aging and neurodegenerative conditions as well as for application in drug discovery of anti-dementia drugs as surrogate markers. However, tau deposits show complicated characteristics because of different isoform composition, histopathology, and ultrastructure in various neurodegenerative conditions. In addition, since tau radiopharmaceuticals possess different chemotype classes, they may show different binding characteristics with heterogeneous tau deposits. In this review, we describe the characteristics of tau deposits and their ligands that have β-sheet binding properties, and the status of tau imaging in clinical studies.

  14. The Dynamics and Turnover of Tau Aggregates in Cultured Cells

    Science.gov (United States)

    Guo, Jing L.; Buist, Arjan; Soares, Alberto; Callaerts, Kathleen; Calafate, Sara; Stevenaert, Frederik; Daniels, Joshua P.; Zoll, Bryan E.; Crowe, Alex; Brunden, Kurt R.; Moechars, Diederik; Lee, Virginia M. Y.

    2016-01-01

    Filamentous tau aggregates, the hallmark lesions of Alzheimer disease (AD), play key roles in neurodegeneration. Activation of protein degradation systems has been proposed to be a potential strategy for removing pathological tau, but it remains unclear how effectively tau aggregates can be degraded by these systems. By applying our previously established cellular model system of AD-like tau aggregate induction using preformed tau fibrils, we demonstrate that tau aggregates induced in cells with regulated expression of full-length mutant tau can be gradually cleared when soluble tau expression is suppressed. This clearance is at least partially mediated by the autophagy-lysosome pathway, although both the ubiquitin-proteasome system and the autophagy-lysosome pathway are deficient in handling large tau aggregates. Importantly, residual tau aggregates left after the clearance phase leads to a rapid reinstatement of robust tau pathology once soluble tau expression is turned on again. Moreover, we succeeded in generating monoclonal cells persistently carrying tau aggregates without obvious cytotoxicity. Live imaging of GFP-tagged tau aggregates showed that tau inclusions are dynamic structures constantly undergoing “fission” and “fusion,” which facilitate stable propagation of tau pathology in dividing cells. These findings provide a greater understanding of cell-to-cell transmission of tau aggregates in dividing cells and possibly neurons. PMID:27129267

  15. $\\tau$ Anomalous Couplings and Radiation Zeros in the $e^+e^- \\to \\tau \\bar\\tau \\gamma$ process

    CERN Document Server

    Rodriguez, I D

    2003-01-01

    The process $e^+e^- \\to \\tau \\bar\\tau \\gamma$ contains configurations of the four-momenta for which the scattering amplitude vanishes (Radiation Zeros or Null Zone). These Radiation Zeros only occur for couplings given by a gauge theory, in particular the standard model. Therefore they are sensitive to physics beyond the standard model as the anomalous magnetic and weak moment of the $\\tau$ lepton. In this article we compute the effect of these anomalous interactions on the Radiation Zeros in the above mentioned process.

  16. A study of the weak boson fusion, with H->tau tau and tau->e(mu)

    CERN Document Server

    Klute, Markus

    2002-01-01

    The sensitivity of the ATLAS experiment for a discovery of the SM Higgs boson in the weak boson fusion qqH with H to tau tau and tau to e,mu is studied. The tagging of two high energy forward jets and a veto of soft jets in the central region of the detector provide powerful tools for background suppression. In addition the two lepton final state with missing energy allows the reconstruction of the Higgs mass with a resolution of 10 %. Signal and background rates as well as the final signal significance are evaluated for a SM Higgs boson in the mass range between 110 and 150 GeV.

  17. Tau and Charm physics highlights

    CERN Document Server

    Roudeau, Patrick

    2002-01-01

    In tau physics, we are at the frontier between the completion of the LEP program and the start of analyses from b-factories, which are expected to produce results in the coming years. Nice results from CLEO are steadily delivered in the meantime. For charm, impressive progress have been achieved by fixed target experiments in the search for CP violation and D^0 - \\bar D^0 oscillations. First results from b-factories demonstrate the power of these facilities in such areas. The novel measurement of the D* width by CLEO happens to be rather different from current expectations. The absence of a charm factory explains the lack or the very slow progress in the absolute scale determinations for charm decays.

  18. The effect of systemic administration of G-CSF on a full-thickness cartilage defect in a rabbit model MSC proliferation as presumed mechanism: G-CSF for cartilage repair.

    Science.gov (United States)

    Sasaki, T; Akagi, R; Akatsu, Y; Fukawa, T; Hoshi, H; Yamamoto, Y; Enomoto, T; Sato, Y; Nakagawa, R; Takahashi, K; Yamaguchi, S; Sasho, T

    2017-03-01

    The aim of this study was to investigate the effect of granulocyte-colony stimulating factor (G-CSF) on mesenchymal stem cell (MSC) proliferation in vitro and to determine whether pre-microfracture systemic administration of G-CSF (a bone marrow stimulant) could improve the quality of repaired tissue of a full-thickness cartilage defect in a rabbit model. MSCs from rabbits were cultured in a control medium and medium with G-CSF (low-dose: 4 μg, high-dose: 40 μg). At one, three, and five days after culturing, cells were counted. Differential potential of cultured cells were examined by stimulating them with a osteogenic, adipogenic and chondrogenic medium.A total of 30 rabbits were divided into three groups. The low-dose group (n = 10) received 10 μg/kg of G-CSF daily, the high-dose group (n = 10) received 50 μg/kg daily by subcutaneous injection for three days prior to creating cartilage defects. The control group (n = 10) was administered saline for three days. At 48 hours after the first injection, a 5.2 mm diameter cylindrical osteochondral defect was created in the femoral trochlea. At four and 12 weeks post-operatively, repaired tissue was evaluated macroscopically and microscopically. The cell count in the low-dose G-CSF medium was significantly higher than that in the control medium. The differentiation potential of MSCs was preserved after culturing them with G-CSF.Macroscopically, defects were filled and surfaces were smoother in the G-CSF groups than in the control group at four weeks. At 12 weeks, the quality of repaired cartilage improved further, and defects were almost completely filled in all groups. Microscopically, at four weeks, defects were partially filled with hyaline-like cartilage in the G-CSF groups. At 12 weeks, defects were repaired with hyaline-like cartilage in all groups. G-CSF promoted proliferation of MSCs in vitro. The systemic administration of G-CSF promoted the repair of damaged cartilage possibly through increasing the number

  19. Phosphorylated tau/amyloid beta 1-42 ratio in ventricular cerebrospinal fluid reflects outcome in idiopathic normal pressure hydrocephalus

    Directory of Open Access Journals (Sweden)

    Patel Sunil

    2012-03-01

    Full Text Available Abstract Background Idiopathic normal pressure hydrocephalus (iNPH is a potentially reversible cause of dementia and gait disturbance that is typically treated by operative placement of a ventriculoperitoneal shunt. The outcome from shunting is variable, and some evidence suggests that the presence of comorbid Alzheimer's disease (AD may impact shunt outcome. Evidence also suggests that AD biomarkers in cerebrospinal fluid (CSF may predict the presence of AD. The aim of this study was to investigate the relationship between the phosphorylated tau/amyloid beta 1-42 (ptau/Aβ1-42 ratio in ventricular CSF and shunt outcome in patients with iNPH. Methods We conducted a prospective trial with a cohort of 39 patients with suspected iNPH. Patients were clinically and psychometrically assessed prior to and approximately 4 months after ventriculoperitoneal shunting. Lumbar and ventricular CSF obtained intraoperatively, and tissue from intraoperative cortical biopsies were analyzed for AD biomarkers. Outcome measures included performance on clinical symptom scales, supplementary gait measures, and standard psychometric tests. We investigated relationships between the ptau/Aβ1-42 ratio in ventricular CSF and cortical AD pathology, initial clinical features, shunt outcome, and lumbar CSF ptau/Aβ1-42 ratios in the patients in our cohort. Results We found that high ptau/Aβ1-42 ratios in ventricular CSF correlated with the presence of cortical AD pathology. At baseline, iNPH patients with ratio values most suggestive of AD presented with better gait performance but poorer cognitive performance. Patients with high ptau/Aβ1-42 ratios also showed a less robust response to shunting on both gait and cognitive measures. Finally, in a subset of 18 patients who also underwent lumbar puncture, ventricular CSF ratios were significantly correlated with lumbar CSF ratios. Conclusions Levels of AD biomarkers in CSF correlate with the presence of cortical AD pathology

  20. A rapid latex agglutination test for the detection of anti-cysticercus antibodies in cerebrospinal fluid (CSF

    Directory of Open Access Journals (Sweden)

    ROCHA Sérgio M.

    2002-01-01

    Full Text Available Simple and rapid latex-based diagnostic tests have been used for detecting specific antigens or antibodies in several diseases. In this article, we present the preliminary results obtained with a latex agglutination test (LAT for diagnosing neurocysticercosis by detection of antibodies in CSF. A total of 43 CSF samples were assayed by the LAT: 19 CSF samples from patients with neurocysticercosis and 24 CSF samples from patients with other neurologic disorders (neurosyphilis, n = 8; neurotoxoplasmosis, n = 3; viral meningitis, n = 4, chronic headache, n = 9. The LAT exhibited 89.5% sensitivity and 75% specificity. The use of LAT seems to be an additional approach for the screening of neurocysticercosis with advantage of simplicity and rapidity. Further studies could be performed using purified antigens and serum samples.

  1. Proteopathic tau seeding predicts tauopathy in vivo.

    Science.gov (United States)

    Holmes, Brandon B; Furman, Jennifer L; Mahan, Thomas E; Yamasaki, Tritia R; Mirbaha, Hilda; Eades, William C; Belaygorod, Larisa; Cairns, Nigel J; Holtzman, David M; Diamond, Marc I

    2014-10-14

    Transcellular propagation of protein aggregates, or proteopathic seeds, may drive the progression of neurodegenerative diseases in a prion-like manner. In tauopathies such as Alzheimer's disease, this model predicts that tau seeds propagate pathology through the brain via cell-cell transfer in neural networks. The critical role of tau seeding activity is untested, however. It is unknown whether seeding anticipates and correlates with subsequent development of pathology as predicted for a causal agent. One major limitation has been the lack of a robust assay to measure proteopathic seeding activity in biological specimens. We engineered an ultrasensitive, specific, and facile FRET-based flow cytometry biosensor assay based on expression of tau or synuclein fusions to CFP and YFP, and confirmed its sensitivity and specificity to tau (∼ 300 fM) and synuclein (∼ 300 pM) fibrils. This assay readily discriminates Alzheimer's disease vs. Huntington's disease and aged control brains. We then carried out a detailed time-course study in P301S tauopathy mice, comparing seeding activity versus histological markers of tau pathology, including MC1, AT8, PG5, and Thioflavin S. We detected robust seeding activity at 1.5 mo, >1 mo before the earliest histopathological stain. Proteopathic tau seeding is thus an early and robust marker of tauopathy, suggesting a proximal role for tau seeds in neurodegeneration.

  2. Propagation of Tau Aggregates and Neurodegeneration.

    Science.gov (United States)

    Goedert, Michel; Eisenberg, David S; Crowther, R Anthony

    2017-07-25

    A pathway from the natively unfolded microtubule-associated protein Tau to a highly structured amyloid fibril underlies human Tauopathies. This ordered assembly causes disease and represents the gain of toxic function. In recent years, evidence has accumulated to suggest that Tau inclusions form first in a small number of brain cells, from where they propagate to other regions, resulting in neurodegeneration and disease. Propagation of pathology is often called prion-like, which refers to the capacity of an assembled protein to induce the same abnormal conformation in a protein of the same kind, initiating a self-amplifying cascade. In addition, prion-like encompasses the release of protein aggregates from brain cells and their uptake by neighboring cells. In mice, the intracerebral injection of Tau inclusions induces the ordered assembly of monomeric Tau, followed by its spreading to distant brain regions. Conformational differences between Tau aggregates from transgenic mouse brain and in vitro assembled recombinant protein account for the greater seeding potency of brain aggregates. Short fibrils constitute the major species of seed-competent Tau in the brains of transgenic mice. The existence of multiple human Tauopathies with distinct fibril morphologies has led to the suggestion that different molecular conformers (or strains) of aggregated Tau exist.

  3. Tau energy Calibration in the ATLAS Experiment

    CERN Document Server

    Brennan, A; The ATLAS collaboration

    2013-01-01

    Here we describe the energy scale calibration of hadronic $\\tau$ decays and the associated uncertainty in 4.5 fb$^{−1}$ of data at $\\sqrt{s}$ = 8 TeV recorded in 2012 with the ATLAS detector at the LHC. The calibration is based on simulated $\\tau$ decays, while the systematic uncertainty is estimated by propagating single particle response measurements to the individual $\\tau$ decay products, namely charged and neutral pions. The systematic uncertainty on the hadronic $\\tau$ energy scale for $p^\\tau_T$ > 20 GeV and |$\\eta^tau$ | < 2.5 is found to be ≤ 3% for the hadronic decay modes with exactly one reconstructed track, and ≤ 4% for the hadronic decay modes with at least two reconstructed tracks. The systematic uncertainty is obtained with a deconvolution method, and is checked using an in-situ analysis of the visible mass of reconstructed Z boson decays into one leptonically and one hadronically decaying $\\tau$. These two methods yield results that are compatible within the calculated uncertainties.

  4. Effect of granulocyte colony stimulating factor (G-CSF on IVF outcomes in infertile women: An RCT

    Directory of Open Access Journals (Sweden)

    Maryam Eftekhar

    2016-05-01

    Full Text Available Background: Despite major advances in assisted reproductive techniques, the implantation rates remain relatively low. Some studies have demonstrated that intrauterine infusion of granulocyte colony stimulating factor (G-CSF improves implantation in infertile women. Objective: To assess the G-CSF effects on IVF outcomes in women with normal endometrial thickness. Materials and methods: In this randomized controlled clinical trial, 100 infertile women with normal endometrial thickness who were candidate for IVF were evaluated in two groups. Exclusion criteria were positive history of repeated implantation failure (RIF, endocrine disorders, severe endometriosis, congenital or acquired uterine anomaly and contraindication for G-CSF (renal disease, sickle cell disease, or malignancy. In G-CSF group (n=50, 300 μg trans cervical intrauterine of G-CSF was administered at the oocyte retrieval day. Controls (n=50 were treated with standard protocol. Chemical, clinical and ongoing pregnancy rates, implantation rate, and miscarriage rate were compared between groups. Results: Number of total and mature oocytes (MII, two pronuclei (2PN, total embryos, transferred embryos, quality of transferred embryos, and fertilization rate did not differ significantly between two groups. So there were no significant differences between groups in chemical, clinical and ongoing pregnancy rate, implantation rate, and miscarriage rate Conclusion: our result showed in normal IVF patients with normal endometrial thickness, the intrauterine infusion of G-CSF did not improve pregnancy outcomes.

  5. Effect of granulocyte colony stimulating factor (G-CSF) on IVF outcomes in infertile women: An RCT

    Science.gov (United States)

    Eftekhar, Maryam; Hosseinisadat, Robabe; Baradaran, Ramesh; Naghshineh, Elham

    2016-01-01

    Background: Despite major advances in assisted reproductive techniques, the implantation rates remain relatively low. Some studies have demonstrated that intrauterine infusion of granulocyte colony stimulating factor (G-CSF) improves implantation in infertile women. Objective: To assess the G-CSF effects on IVF outcomes in women with normal endometrial thickness. Materials and methods: In this randomized controlled clinical trial, 100 infertile women with normal endometrial thickness who were candidate for IVF were evaluated in two groups. Exclusion criteria were positive history of repeated implantation failure (RIF), endocrine disorders, severe endometriosis, congenital or acquired uterine anomaly and contraindication for G-CSF (renal disease, sickle cell disease, or malignancy). In G-CSF group (n=50), 300 µg trans cervical intrauterine of G-CSF was administered at the oocyte retrieval day. Controls (n=50) were treated with standard protocol. Chemical, clinical and ongoing pregnancy rates, implantation rate, and miscarriage rate were compared between groups. Results: Number of total and mature oocytes (MII), two pronuclei (2PN), total embryos, transferred embryos, quality of transferred embryos, and fertilization rate did not differ significantly between two groups. So there were no significant differences between groups in chemical, clinical and ongoing pregnancy rate, implantation rate, and miscarriage rate Conclusion: our result showed in normal IVF patients with normal endometrial thickness, the intrauterine infusion of G-CSF did not improve pregnancy outcomes. PMID:27326420

  6. Intracerebral injection of preformed synthetic tau fibrils initiates widespread tauopathy and neuronal loss in the brains of tau transgenic mice.

    Science.gov (United States)

    Peeraer, Eve; Bottelbergs, Astrid; Van Kolen, Kristof; Stancu, Ilie-Cosmin; Vasconcelos, Bruno; Mahieu, Michel; Duytschaever, Hilde; Ver Donck, Luc; Torremans, An; Sluydts, Ellen; Van Acker, Nathalie; Kemp, John A; Mercken, Marc; Brunden, Kurt R; Trojanowski, John Q; Dewachter, Ilse; Lee, Virginia M Y; Moechars, Diederik

    2015-01-01

    Neurofibrillary tangles composed of hyperphosphorylated fibrillized tau are found in numerous tauopathies including Alzheimer's disease. Increasing evidence suggests that tau pathology can be transmitted from cell-to-cell; however the mechanisms involved in the initiation of tau fibrillization and spreading of disease linked to progression of tau pathology are poorly understood. We show here that intracerebral injections of preformed synthetic tau fibrils into the hippocampus or frontal cortex of young tau transgenic mice expressing mutant human P301L tau induces tau hyperphosphorylation and aggregation around the site of injection, as well as a time-dependent propagation of tau pathology to interconnected brain areas distant from the injection site. Furthermore, we show that the tau pathology as a consequence of injection of tau preformed fibrils into the hippocampus induces selective loss of CA1 neurons. Together, our data confirm previous studies on the seeded induction and the spreading of tau pathology in a different tau transgenic mouse model and reveals neuronal loss associated with seeded tau pathology in tau transgenic mouse brain. These results further validate the utility of the tau seeding model in studying disease transmission, and provide a more complete in vivo tauopathy model with associated neurodegeneration which can be used to investigate the mechanisms involved in tau aggregation and spreading, as well as aid in the search for disease modifying treatments for Alzheimer's disease and related tauopathies. Copyright © 2014 Elsevier Inc. All rights reserved.

  7. Cine-MR imaging aqueductal CSF flow in normal pressure hydrocephalus syndrome before and after CSF shunt

    Energy Technology Data Exchange (ETDEWEB)

    Mascalchi, M. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy)); Arnetoli, G. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy)); Inzitari, D. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy)); Dal Pozzo, G. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy)); Lolli, F. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy)); Caramella, D. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy)); Bartolozzi, C. (Sezione di Radiodiagnostica, Dipt. di Fisiopatologia Clinica, and Dipt. di Scienze Neurologiche, Florence Univ. (Italy))

    1993-11-01

    Reproducibility of the aqueductal CSF signal intensity on a gradient echo cine-MR sequence exploiting through plane inflow enhancement was tested in 11 patients with normal or dilated ventricles. Seven patients with normal pressure hydrocephalus (NPH) syndrome were investigated with the sequence before and after CSF shunting. Two patients exhibiting central flow void within a hyperintense aqueductal CSF improved after surgery and the flow void disappeared after shunting. One patient with increased maximum and minimum aqueductal CSF signal as compared to 18 healthy controls also improved and the aqueductal CSF signal was considerably decreased after shunting. Three patients with aqueductal CSF values similar to those in the controls did not improve, notwithstanding their maximum aqueductal CSF signals decreasing slightly after shunting. No appreciable aqueductal CSF flow related enhancement consistent with non-communicating hydrocephalus was found in the last NPH patient who improved after surgery. Cine-MR with inflow technique yields a reproducible evaluation of flow-related aqueductal CSF signal changes which might help in identifying shunt responsive NPH patients. These are likely to be those with hyperdynamic aqueductal CSF or aqueductal obstruction. (orig.).

  8. Observation of the Semileptonic Decays B --> D* tau nubar and Evidence for B --> D tau nubar

    CERN Document Server

    Aubert, B; Boutigny, D; Karyotakis, Yu; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Garra Tico, J; Graugès-Pous, E; López, L; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes-Pegna, D; Lynch, G; Mir, L M; Orimoto, T J; Osipenkov, I L; Ronan, M T; Tackmann, K; Tanabé, T; Wenzel, W A; Del Amo-Sánchez, P; Hawkes, C M; Watson, A T; Koch, H; Schröder, T; Walker, D; Asgeirsson, D J; Çuhadar-Dönszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Barrett, M; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Gary, J W; Liu, F; Long, O; Shen, B C; Vitug, G M; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, C; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Watson, J E; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; De Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Flack, R L; Nash, J A; Panduro-Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bequilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Höcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, L; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Sacco, R; Cowan, G; Flächer, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; Zheng, Y; Mclachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, Gallieno; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; LoSecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Sekula, S J; Wong, Q K; Blount, N L; Brau, J E; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; De La Vaissière, C; Hamon, O; Leruste, P; Malcles, J; Ocariz, J; Pérez, A; Prendki, J; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Biesiada, J; Elmer, P; Lau, Y P; Lü, C; Olsen, J; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; Del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Röthel, W; Wilson, F F; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yéche, C; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Hast, C; Innes, W R; Kaminski, J; Kelsey, M H; Kim, H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Luitz, S; Lüth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Müller, D R; Nelson, S; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Vavra, J; Wagner, A P; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Ziegler, V; Burchat, P R; Edwards, A J; Majewski, S A; Miyashita, T S; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martínez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    2007-01-01

    We present measurements of the semileptonic decays B- --> D0 tau- nubar, B- --> D*0 tau- nubar, B0bar --> D+ tau- nubar, and B0bar --> D*+ tau- nubar, which are potentially sensitive to non--Standard Model amplitudes. The data sample comprises 232x10^6 Upsilon(4S) --> BBbar decays collected with the BaBar detector. From a combined fit to B- and B0bar channels, we obtain the branching fractions B(B --> D tau- nubar) = (0.86 +/- 0.24 +/- 0.11 +/- 0.06)% and B(B --> D* tau- nubar) = (1.62 +/- 0.31 +/- 0.10 +/- 0.05)% (normalized for the B0bar), where the uncertainties are statistical, systematic, and normalization-mode-related.

  9. Search for the Decay tau- --> 3pi- 2pi+ 2pi0 nu_tau

    CERN Document Server

    Aubert, B; Bóna, M; Boutigny, D; Couderc, F; Karyotakis, Yu; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Graugès-Pous, E; Palano, A; Pappagallo, M; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Morgan, S E; Watson, A T; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schröder, T; Steinke, M; Boyd, J T; Burke, J P; Cottingham, W N; Walker, D; Çuhadar-Dönszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Best, D S; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M A; Mommsen, R K; Röthel, W; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; Hadavand, H K; Hill, E J; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dvoretskii, A; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Andreassen, R; Mancinelli, G; Meadows, B T; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nauenberg, U; Olivas, A; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Zeng, Q; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Spaan, B; Brandt, T; Klose, V; Lacker, H M; Mader, W F; Nogowski, R; Petzold, A; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Grenier, P; Latour, E; Thiebaux, C; Verderi, M; Bard, D J; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; De Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Gaillard, J R; Nash, J A; Nikolich, M B; Panduro-Vazquez, W; Chai, X; Charles, M J; Mallik, U; Meyer, N T; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gritsan, A V; Fritsch, M; Schott, G; Arnaud, N; Davier, M; Grosdidier, G; Höcker, A; Le Diberder, F R; Lepeltier, V; Lutz, A M; Oyanguren, A; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Stocchi, A; Wang, W F; Wormser, G; Cheng, C H; Lange, D J; Wright, D M; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; Di Lodovico, F; Menges, W; Sacco, R; Brown, C L; Cowan, G; Flächer, H U; Hopkins, D A; Jackson, P S; McMahon, T R; Ricciardi, S; Salvatore, F; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Kelly, M P; Lafferty, G D; Naisbit, M T; Williams, J C; Yi, J I; Chen, C; Hulsbergen, W D; Jawahery, A; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Saremi, S; Stängle, H; Willocq, S Y; Cowan, R; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; Patel, P M; Potter, C T; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; Cavallo, N; De Nardo, Gallieno; Del Re, D; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M; Bulten, H; Raven, G; Snoek, H L; Jessop, C P; LoSecco, J M; Allmendinger, T; Benelli, G; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Pulliam, T; Rahimi, A M; Ter-Antonian, R; Wong, Q K; Blount, N L; Brau, J E; Frey, R; Igonkina, O; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Galeazzi, F; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Chauveau, J; David, P; Del Buono, L; La Vaissière, C de; Hamon, O; Hartfiel, B L; John, M J J; Leruste, P; Malcles, J; Ocariz, J; Roos, L; Therin, G; Behera, P K; Gladney, L; Panetta, J; Biasini, M; Covarelli, R; Pioppi, M; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y P; Lü, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Safai-Tehrani, F; Voena, C; Ebert, M; Schröder, H; Waldi, R; Adye, T; De Groot, N; Franek, B; Olaiya, E O; Wilson, F F; Emery, S; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, Witold; Legendre, M; Mayer, B; Vasseur, G; Yéche, C; Zito, M; Park, W; Purohit, M V; Weidemann, A W; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Boyarski, A M; Claus, R; Coleman, J P; Convery, M R; Cristinziani, M; Dingfelder, J C; Dong, D; Dorfan, J; Dubois-Felsmann, G P; Dujmic, D; Dunwoodie, W M; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Halyo, V; Hast, C; Hrynóva, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Libby, J; Luitz, S; Lüth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Müller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Vavra, J; Van Bakel, N; Weaver, M; Weinstein, A J R; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Roat, C; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schilling, C J; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Vitale, L; Azzolini, V; Martínez-Vidal, F; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R V; Nugent, I M; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Eichenbaum, A M; Flood, K T; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Mellado, B; Mihályi, A; Mohapatra, A K; Pan, Y; Pierini, M; Prepost, R; Tan, P; Wu, S L; Yu, Z; Neal, H

    2006-01-01

    A search for the decay of the tau lepton to five charged and two neutral pions is performed using data collected by the BABAR detector at the PEP-II asymmetric-energy e+e- collider. The analysis uses 232 fb-1 of data at center-of-mass energies on or near the Y(4S) resonance. We observe 10 events with an expected background of 6.5^{+2.0}_{-1.4} events. In the absence of a signal, we set the limit on the branching ratio B(tau- --> 3pi- 2pi+ 2pi0 nu_tau) 2omega pi- nu_tau. We observe 1 event with an expected background of 0.4^{+1.0}_{-0.4} events and calculate the upper limit B(tau- --> 2omega pi- nu_tau) < 5.4x10^{-7} at the 90% confidence level. This is the first upper limit for this mode.

  10. Reconstruction and Identification of Tau Leptons in ATLAS

    CERN Document Server

    Limbach, C; The ATLAS collaboration

    2014-01-01

    These slides give a brief overview over the tau trigger, reconstruction and identification in the ATLAS experiment at the LHC. First the tau lepton, its importance in high energy physics and QCD jets as main source of background are introduced. The basic concepts of the tau trigger are explained together with a trigger efficiency measurement. A visual explanation of the tau reconstruction procedure is followed by an explanation of the tau identification method and the corresponding performance. Before concluding with an outlook on the new tau reconstruction for 2015 and later, a measurement of the tau energy scale is presented.

  11. Measurement of the tau lifetime with the DELPHI detector

    CERN Document Server

    Andreazza, Attilio

    2005-01-01

    The tau lepton lifetime has been measured with the $e^{+}e^{-}$ to tau /sup +/ tau /sup -/ events collected by the DELPHI detector at LEP in the years 1991-1995. Three different methods have been exploited, using both one-prong and three-prong tau decay channels. These are combined with previously published DELPHI results to provide a tau lifetime measurement of tau /sub tau /=290.9+or-1.4/sub stat/+or-1.0/sub sys/ fs, using the full LEP1 data sample.

  12. Comparison of the cerebrospinal fluid (CSF) toluidine red unheated serum test and the CSF rapid plasma reagin test with the CSF venereal disease research laboratory test for diagnosis of neurosyphilis among HIV-negative syphilis patients in China.

    Science.gov (United States)

    Zhu, Lin; Gu, Xin; Peng, Rui-Rui; Wang, Cuini; Gao, Zixiao; Zhou, Pingyu; Gao, Ying; Shi, Mei; Guan, Zhifang; Seña, Arlene C

    2014-03-01

    In this study, we aimed to investigate the performance of nontreponemal antibody tests in cerebrospinal fluid (CSF) specimens from syphilis patients. From September 2009 to September 2012, CSF specimens were collected at the Shanghai Skin Disease Hospital in Shanghai, China, from 1,132 syphilis patients without HIV infection, including 154 with symptomatic and 56 with asymptomatic neurosyphilis. All of the CSF specimens underwent testing with a rapid plasma reagin (RPR) test, an RPR-V (commercial RPR antigen diluted 1:2 in 10% saline) test, the toluidine red unheated serum test (TRUST), and the Venereal Disease Research Laboratory (VDRL) test. Specificities, sensitivities, positive predictive values (PPVs), negative predictive values (NPVs), and kappa values were calculated to determine the performances of the tests. We compared results of the CSF-VDRL, CSF-RPR, CSF-RPR-V, and CSF-TRUST among patients with symptomatic and asymptomatic neurosyphilis who had reactive CSF-Treponema pallidum particle agglutination (TPPA) test results. Overall, the CSF-VDRL test was reactive in 261 patients (23.1%). There were no cases in which the CSF-VDRL was nonreactive and CSF-RPR, CSF-RPR-V, or CSF-TRUST was reactive. Agreement between the results of CSF-TRUST and CSF-RPR was almost perfect (κ=0.861), with substantial agreement between the results of CSF-RPR and CSF-RPR-V (κ=0.740). The sensitivities of CSF-VDRL, CSF-RPR, CSF-RPR-V, and CSF-TRUST were 81.4%, 76.2%, 79.5%, and 76.2%, respectively. Compared to CSF-VDRL, CSF-RPR, CSF-RPR-V, and CSF-TRUST had comparable PPVs and NPVs. However, the specificity of CSF-VDRL (90.3%) was significantly lower than those of the other tests (92.7 to 93.4%). Therefore, CSF-RPR, CSF-RPR-V, and CSF-TRUST can be considered alternative tests for neurosyphilis diagnosis in HIV-negative populations, particularly when the CSF-VDRL is not available.

  13. Upward and Horizontal Tau Airshowers by UHE Neutrinos

    CERN Document Server

    Fargion, D

    2001-01-01

    Upward and Horizontal Tau Air-showers (UPTAUS and HORTAUS) emerging from the Earth crust, mountain chains or deep plate boundaries are the most powerful signals of Ultra High Energy UHE anti neutrinos electron at PeV and neutrino and anti-neutrino tau at energies near and above 10^{15}-10^{19}eV. The large tau Air-showers multiplicity N in secondaries N_opt =10^{12} E_{tau}/ PeV, N_{gamma}= 10^8 E_{tau}/PeV, N_{e^- e^+}= 2 10^7 E_{tau}/PeV, N_{mu} = 3 \\cdot 10^5 E_{tau}/PeV^{0.85}, make easy their discover. UHE nu_{tau}, nu_{tau} because neutrino flavor mixing, (nu_{mu} nu_{tau}), should be as abundant as nu_{mu}, bar\

  14. Search for the rare decay B0-->tau+tau- at BABAR.

    Science.gov (United States)

    Aubert, B; Barate, R; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Pappagallo, M; Pompili, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Breon, A B; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Gritsan, A V; Groysman, Y; Jacobsen, R G; Kadel, R W; Kadyk, J; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Morgan, S E; Watson, A T; Fritsch, M; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Chevalier, N; Cottingham, W N; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Teodorescu, L; Blinov, A E; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Kravchenko, E A; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Yushkov, A N; Best, D; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Mommsen, R K; Roethel, W; Stoker, D P; Buchanan, C; Hartfiel, B L; Weinstein, A J R; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; del Re, D; Hadavand, H K; Hill, E J; MacFarlane, D B; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Mazur, M A; Richman, J D; Verkerke, W; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dubois-Felsmann, G P; Dvoretskii, A; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Andreassen, R; Mancinelli, G; Meadows, B T; Sokoloff, M D; Blanc, F; Bloom, P; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nauenberg, U; Olivas, A; Rankin, P; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Harton, J L; Soffer, A; Toki, W H; Wilson, R J; Zeng, Q; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; Giraud, P-F; Graziani, G; Hamel de Monchenault, G; Kozanecki, W; Legendre, M; London, G W; Mayer, B; Vasseur, G; Yeche, Ch; Zito, M; Altenburg, D; Feltresi, E; Hauke, A; Spaan, B; Brandt, T; Brose, J; Dickopp, M; Klose, V; Lacker, H M; Nogowski, R; Otto, S; Petzold, A; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Bernard, D; Bonneaud, G R; Grenier, P; Schrenk, S; Thiebaux, Ch; Vasileiadis, G; Verderi, M; Bard, D J; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Xie, Y; Andreotti, M; Azzolini, V; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Piemontese, L; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Patteri, P; Peruzzi, I M; Piccolo, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Lo Vetere, M; Macri, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Morii, M; Won, E; Wu, J; Dubitzky, R S; Langenegger, U; Marks, J; Schenk, S; Uwer, U; Martinez-Vidal, F; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Gaillard, J R; Morton, G W; Nash, J A; Nikolich, M B; Taylor, G P; Vazquez, W P; Charles, M J; Mader, W F; Mallik, U; Mohapatra, A K; Cochran, J; Crawley, H B; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Yi, J; Biasini, M; Covarelli, R; Pacetti, S; Pioppi, M; Arnaud, N; Davier, M; Giroux, X; Grosdidier, G; Höcker, A; Le Diberder, F; Lepeltier, V; Lutz, A M; Oyanguren, A; Petersen, T C; Pierini, M; Plaszczynski, S; Rodier, S; Roudeau, P; Schune, M H; Stocchi, A; Wormser, G; Cheng, C H; Lange, D J; Simani, M C; Wright, D M; Bevan, A J; Chavez, C A; Forster, Ian J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Parry, R J; Payne, D J; Schofield, K C; Touramanis, C; Cormack, C M; Di Lodovico, F; Menges, W; Sacco, R; Brown, C L; Cowan, G; Flaecher, H U; Green, M G; Hopkins, D A; Jackson, P S; McMahon, T R; Ricciardi, S; Salvatore, F; Brown, D; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Edgar, C L; Hodgkinson, M C; Kelly, M P; Lafferty, G D; Naisbit, M T; Williams, J C; Chen, C; Hulsbergen, W D; Jawahery, A; Kovalskyi, D; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Kofler, R; Koptchev, V B; Li, X; Moore, T B; Saremi, S; Staengle, H; Willocq, S; Cowan, R; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Cote, D; Taras, P; Viaud, B; Nicholson, H; Baak, M; Bulten, H; Raven, G; Snoek, H L; Wilden, L; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Jessop, C P; LoSecco, J M; Allmendinger, T; Benelli, G; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Pulliam, T; Rahimi, A M; Ter-Antonyan, R; Wong, Q K; Brau, J; Frey, R; Igonkina, O; Lu, M; Potter, C T; Sinev, N B; Strom, D; Strube, J; Torrence, E; Galeazzi, F; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; de la Vaissiere, C; Del Buono, L; Hamon, O; John, M J J; Leruste, Ph; Malcles, J; Ocariz, J; Roos, L; Therin, G; Behera, P K; Gladney, L; Guo, Q H; Panetta, J; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Morganit, M; Neri, N; Paoloni, E; Rama, M; Rizzo, G; Walsh, J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Safai Tehrani, F; Voena, C; Schröder, H; Wagner, G; Waldi, R; Adye, T; De Groot, N; Franek, B; Gopal, G P; Olaiya, E O; Wilson, F F; Purohit, M V; Weidemann, A W; Wilson, J R; Yumiceva, F X; Abe, T; Allen, M T; Aston, D; Bartoldus, R; Berger, N; Boyarski, A M; Buchmueller, O L; Claus, R; Coleman, J P; Convery, M R; Cristinziani, M; Dingfelder, J C; Dong, D; Dorfan, J; Dujmic, D; Dunwoodie, W; Fan, S; Field, R C; Glanzman, T; Gowdy, S J; Hadig, T; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Libby, J; Luitz, S; Luth, V; Lynch, H L; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; van Bakel, N; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Roat, C; Ahmed, M; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Bona, M; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Vitale, L; Panvini, R S; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Eichenbaum, A M; Flood, K T; Graham, M; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Mellado, B; Mihalyi, A; Pan, Y; Prepost, R; Tan, P; von Wimmersperg-Toeller, J H; Wu, S L; Yu, Z; Neal, H; Schott, G

    2006-06-23

    We present the results of a search for the decay B0-->tau+tau- in a data sample of (232+/-3)x10(6) Upsilon(4S)-->BB decays using the BABAR detector. Certain extensions of the standard model predict measurable levels of this otherwise rare decay. We reconstruct fully one neutral B meson and seek evidence for the signal decay in the rest of the event. We find no evidence for signal events and obtain Beta(B0->tau+tau-)<4.1x10(-3) at the 90% confidence level.

  15. Measurement of the tau- --> K- pi0 nu_tau Branching Fraction

    CERN Document Server

    Aubert, B; Boutigny, D; Karyotakis, Yu; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Garra Tico, J; Graugès-Pous, E; López, L; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes-Pegna, D; Lynch, G; Mir, L M; Orimoto, T J; Osipenkov, I L; Ronan, M T; Tackmann, K; Tanabé, T; Wenzel, W A; Del Amo-Sánchez, P; Hawkes, C M; Watson, A T; Held, T; Koch, H; Pelizaeus, M; Schröder, T; Steinke, M; Walker, D; Asgeirsson, D J; Çuhadar-Dönszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Liu, F; Long, O; Shen, B C; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, C; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Watson, J E; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; De Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Flack, R L; Nash, J A; Panduro-Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bequilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Höcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Menges, W; Sacco, R; Cowan, G; Flächer, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; Zheng, Y; Mclachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, Gallieno; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; LoSecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Wong, Q K; Blount, N L; Brau, J E; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; De La Vaissière, C; Hamon, O; Leruste, P; Malcles, J; Ocariz, J; Pérez, A; Prendki, J; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Haire, M; Biesiada, J; Elmer, P; Lau, Y P; Lü, C; Olsen, J; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; Del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Ricciardi, S; Röthel, W; Wilson, F F; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hame lde Monchenault, G; Kozanecki, W; Vasseur, G; Yéche, C; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Hast, C; Hrynóva, T; Innes, W R; Kaminski, J; Kelsey, M H; Kim, H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Luitz, S; Lüth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Müller, D R; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Vavra, J; Van Bakel, N; Wagner, A P; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martínez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    2007-01-01

    A measurement of the tau- --> K- pi0 nu_tau branching fraction has been made using 230.2 fb-1 of data recorded by the BABAR detector at the PEP-II e+ e- collider, located at the Stanford Linear Accelerator Center (SLAC), at a center of mass energy sqrt{s} close to 10.58 GeV. We measure BF(tau- --> K- pi0 nu_tau) = (0.416 +/- 0.003 (stat) +/- 0.018 (syst)) %.

  16. A Search for the rare decay B0 --> tau+tau- at BABAR

    CERN Document Server

    Aubert, B; Abrams, G S; Adye, T; Ahmed, M; Ahmed, S; Alam, M S; Albert, J; Aleksan, Roy; Allen, M T; Allison, J; Allmendinger, T; Altenburg, D; Andreassen, R; Andreotti, M; Angelini, C; Anulli, F; Arnaud, N; Aston, D; Azzolini, V; BULA, R; Baak, M; Back, J J; Baldini-Ferroli, R; Band, H R; Banerjee, Sw; Barate, R; Bard, D J; Barlow, N R; Barlow, R J; Barrett, M; Bartoldus, R; Batignani, G; Battaglia, M; Bauer, J M; Beck, T W; Behera, P K; Bellini, F; Benayoun, M; Benelli, G; Berger, N; Bernard, D; Berryhill, J W; Best, D; Bettarini, S; Bettoni, D; Bevan, A J; Bhimji, W; Bhuyan, B; Bianchi, F; Biasini, M; Biesiada, J; Blanc, F; Blaylock, G; Blinov, A E; Blinov, V E; Bloom, P; Bomben, M; Bondioli, M; Bonneaud, G R; Bosisio, L; Boutigny, D; Bowerman, D A; Boyarski, A M; Boyd, J T; Bozzi, C; Brandenburg, G; Brandt, T; Brau, J E; Breon, A B; Briand, H; Brose, J; Brown, C L; Brown, C M; Brown, D; Brown, D N; Bruinsma, M; Brunet, S; Bucci, F; Buchanan, C; Buchmüller, O L; Bugg, W; Bukin, A D; Bulten, H; Burchat, P R; Burke, J P; Button-Shafer, J; Buzzo, A; Bóna, M; Cahn, R N; Calabrese, R; Calcaterra, A; Calderini, G; Campagnari, C; Capra, R; Carpinelli, M; Cartaro, C; Cavallo, N; Cavoto, G; Cenci, R; Chaisanguanthum, K S; Chao, M; Charles, E; Charles, M J; Chauveau, J; Chavez, C A; Chen, A; Chen, C; Chen, E; Chen, J C; Chen, S; Chen, X; Cheng, B; Cheng, C H; Chevalier, N; Cibinetto, G; Clark, P J; Claus, R; Cochran, J; Coleman, J P; Contri, R; Convery, M R; Cormack, C M; Cossutti, F; Cottingham, W N; Couderc, F; Covarelli, R; Cowan, G; Cowan, R; Crawley, H B; Cremaldi, L; Cristinziani, M; Cunha, A; Curry, S; Côté, D; D'Orazio, A; Dahmes, B; Dallapiccola, C; Danielson, N; Dasu, S; Datta, M; Dauncey, P D; David, P; Davier, M; Davis, C L; Day, C T; De Groot, N; De Nardo, Gallieno; De Sangro, R; Del Buono, L; Del Re, D; Della Ricca, G; Di Lodovico, F; Di Marco, E; Dickopp, M; Dingfelder, J C; Dittongo, S; Dong, D; Dorfan, J; Druzhinin, V P; Dubitzky, R S; Dubois-Felsmann, G P; Dujmic, D; Dunwoodie, W M; Dvoretskii, A; Eckhart, E A; Eckmann, R; Edgar, C L; Edwards, A J; Egede, U; Eichenbaum, A M; Eigen, G; Eisner, A M; Elmer, P; Emery, S; Ernst, J A; Eschenburg, V; Eschrich, I; Eyges, V; Fabozzi, F; Faccini, R; Fan, S; Feltresi, E; Ferrarotto, F; Ferroni, F; Field, R C; Finocchiaro, G; Flacco, C J; Flack, R L; Flächer, H U; Flood, K T; Ford, K E; Ford, W T; Forster, Ian J; Forti, F; Fortin, D; Foulkes, S D; Franek, B; Frey, R; Fritsch, M; Fry, J R; Fulsom, B G; Gabathuler, E; Gaidot, A; Gaillard, J R; Galeazzi, F; Gallo, F; Gamba, D; Gamet, R; Gan, K K; Ganzhur, S F; Gary, J W; Gaspero, M; Gatto, C; George, K A; Gill, M S; Giorgi, M A; Giraud, P F; Giroux, X; Gladney, L; Glanzman, T; Godang, R; Goetzen, K; Golubev, V B; Gopal, G P; Gowdy, S J; Gradl, W; Graham, M; Grancagnolo, S; Graugès-Pous, E; Graziani, G; Green, M G; Grenier, P; Gritsan, A V; Grosdidier, G; Groysman, Y; Guo, Q H; Hadavand, H K; Hadig, T; Haire, M; Halyo, V; Hamano, K; Hamel de Monchenault, G; Hamon, O; Harrison, P F; Harrison, T J; Hart, A J; Hartfiel, B L; Harton, J L; Hast, C; Hauke, A; Hawkes, C M; Hearty, C; Held, T; Hertzbach, S S; Heusch, C A; Hill, E J; Hirschauer, J F; Hitlin, D G; Hodgkinson, M C; Hollar, J J; Hong, T M; Honscheid, K; Hopkins, D A; Hrynóva, T; Hufnagel, D; Hulsbergen, W D; Hutchcroft, D E; Höcker, A; Igonkina, O; Innes, W R; Izen, J M; Jackson, P D; Jackson, P S; Jacobsen, R G; Jawahery, A; Jessop, C P; John, M J J; Johnson, J R; Judd, D; Kadel, R W; Kadyk, J; Kagan, H; Karyotakis, Yu; Kass, R; Kelly, M P; Kelsey, M H; Kerth, L T; Khan, A; Kim, H; Kim, P; Kirkby, D; Kitayama, I; Klose, V; Knecht, N S; Koch, H; Kocian, M L; Koeneke, K; Kofler, R; Kolomensky, Yu G; Koptchev, V B; Kovalskyi, D; Kowalewski, R V; Kozanecki, Witold; Kravchenko, E A; Kreisel, A; Krishnamurthy, M; Kroeger, R; Kroseberg, J; Kukartsev, G; Kutter, P E; Kyberd, P; LI, X; LU, M; La Vaissière, C de; Lacker, H M; Lae, C K; Lafferty, G D; Lanceri, L; Lange, D J; Langenegger, U; Lankford, A J; Latham, T E; Lau, Y; Lazzaro, A; Le Diberder, F R; Lees, J P; Legendre, M; Leith, D W G S; Lepeltier, V; Leruste, P; Lewandowski, B; Li Gioi, L; Li, H; Libby, J; Lista, L; Liu, R; Lo Vetere, M; LoSecco, J M; Lockman, W S; Lombardo, V; London, G W; Long, O; Lou, X C; Luitz, S; Lund, P; Luppi, E; Lusiani, A; Lutz, A M; Lynch, G; Lynch, H L; Lü, C; Lüth, V; MacFarlane, D B; Macri, M; Mader, W F; Majewski, S A; Malcles, J; Mallik, U; Mancinelli, G; Mandelkern, M A; Marchiori, G; Margoni, M; Marks, J; Marsiske, H; Martínez-Vidal, F; Mattison, T S; Mayer, B; Mazur, M A; Mazzoni, M A; McKenna, J A; McMahon, T R; Meadows, B T; Mellado, B; Menges, W; Messner, R; Meyer, W T; Mihályi, A; Mir, L M; Mohanty, G B; Mohapatra, A K; Mommsen, R K; Monge, M R; Monorchio, D; Moore, T B; Morandin, M; Morgan, S E; Morganit, M; Morganti, S; Morii, M; Morton, G W; Muheim, F; Müller, D R; Naisbit, M T; Narsky, I; Nash, J A; Nauenberg, U; Neal, H; Negrini, M; Neri, N; Nesom, G; Nicholson, H; Nikolich, M B; Nogowski, R; O'Grady, C P; Ocariz, J; Oddone, P J; Ofte, I; Olaiya, E O; Olivas, A; Olsen, J; Onuchin, A P; Orimoto, T J; Otto, S; Oyanguren, A; Ozcan, V E; Paar, H P; Pacetti, S; Palano, A; Palombo, F; Pan, Y; Panetta, J; Panvini, R S; Paoloni, E; Paolucci, P; Pappagallo, M; Parry, R J; Passaggio, S; Patel, P M; Patrignani, C; Patteri, P; Payne, D J; Pelizaeus, M; Perazzo, A; Perl, M; Peruzzi, I M; Peters, K; Petersen, B A; Petersen, T C; Petzold, A; Piatenko, T; Piccolo, D; Piccolo, M; Piemontese, L; Pierini, M; Pioppi, M; Piredda, G; Plaszczynski, S; Playfer, S; Poireau, V; Polci, F; Pompili, A; Porter, F C; Posocco, M; Potter, C T; Prell, S; Prepost, R; Pripstein, M; Pulliam, T; Purohit, M V; Qi, N D; Rahatlou, S; Rahimi, A M; Rama, M; Rankin, P; Ratcliff, B N; Raven, G; Reidy, J; Ricciardi, S; Richman, J D; Ritchie, J L; Rizzo, G; Roat, C; Roberts, D A; Robertson, S H; Robutti, E; Rodier, S; Roe, N A; Ronan, M T; Roney, J M; Rong, G; Roodman, A; Roos, L; Rosenberg, E I; Rotondo, M; Roudeau, P; Rubin, A E; Ruddick, W O; Ryd, A; Röthel, W; Sacco, R; Saeed, M A; Safai-Tehrani, F; Saleem, M; Salnikov, A A; Salvatore, F; Samuel, A; Sanders, D A; Santroni, A; Saremi, S; Satpathy, A; Schalk, T; Schenk, S; Schindler, R H; Schofield, K C; Schott, G; Schrenk, S; Schröder, T; Schröder, H; Schubert, J; Schubert, K R; Schumm, B A; Schune, M H; Schwiening, J; Schwierz, R; Schwitters, R F; Sciacca, C; Sciolla, G; Seiden, A; Sekula, S J; Serednyakov, S I; Sharma, V; Shen, B C; Simani, M C; Simi, G; Simonetto, F; Sinev, N B; Skovpen, Yu I; Smith, A J S; Smith, J G; Snoek, H L; Snyder, A; Sobie, R J; Soffer, A; Sokoloff, M D; Solodov, E P; Spaan, B; Spanier, S M; Spitznagel, M; Spradlin, P; Steinke, M; Stelzer, J; Stocchi, A; Stoker, D P; Stroili, R; Strom, D; Strube, J; Stugu, B; Stängle, H; Su, D; Sullivan, M K; Summers, D J; Sundermann, J E; Suzuki, K; Swain, S K; Tan, P; Taras, P; Taylor, F; Taylor, G P; Telnov, A V; Teodorescu, L; Ter-Antonian, R; Therin, G; Thiebaux, C; Thompson, J M; Tisserand, V; Toki, W H; Torrence, E; Tosi, S; Touramanis, C; Ulmer, K A; Uwer, U; Van Bakel, N; Vasileiadis, G; Vasseur, G; Vavra, J; Vazquez, W P; Verderi, M; Verkerke, W; Viaud, B; Vitale, L; Voci, C; Voena, C; Von Wimmersperg-Töller, J H; Wagner, G; Wagner, S R; Wagoner, D E; Waldi, R; Walsh, J; Wang, K; Wang, P; Wappler, F R; Watson, A T; Weaver, M; Weidemann, A W; Weinstein, A J R; Wenzel, W A; Wilden, L; Williams, D C; Williams, J C; Willocq, S; Wilson, F F; Wilson, J R; Wilson, M G; Wilson, R J; Wisniewski, W J; Wittgen, M; Won, E; Wong, Q K; Wormser, G; Wright, D H; Wright, D M; Wu, J; Wu, S L; Xie, Y; Yamamoto, R K; Yarritu, A K; Ye, S; Yi, J; Yi, K; Young, C C; Yu, Z; Yumiceva, F X; Yushkov, A N; Yéche, C; Zain, S B; Zallo, A; Zeng, Q; Zghiche, A; Zhang, J; Zhang, L; Zhao, H W; Zhu, Y S; Zito, M; Çuhadar-Dönszelmann, T

    2006-01-01

    We present the results of a search for the decay B0 --> tau+tau- in a data sample of (232 +- 3) x 10^6 Upsilon(4S) --> BBbar decays using the BABAR detector. Certain extensions of the Standard Model predict measurable levels of this otherwise rare decay. We reconstruct fully one neutral B meson and seek evidence for the signal decay in the rest of the event. We find no evidence for signal events and obtain B(B0 --> tau+tau-) < 3.2 x 10^-3 at the 90% confidence level.

  17. An upper limit on the $\\tau$ neutrino mass from three- and five-prong tau decays

    CERN Document Server

    Barate, R; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Nief, J Y; Pietrzyk, B; Casado, M P; Chmeissani, M; Comas, P; Crespo, J M; Delfino, M C; Fernández, E; Fernández-Bosman, M; Garrido, L; Juste, A; Martínez, M; Merino, G; Miquel, R; Mir, L M; Padilla, C; Park, I C; Pascual, A; Perlas, J A; Riu, I; Sánchez, F; Colaleo, A; Creanza, D; De Palma, M; Gelao, G; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Alemany, R; Becker, U; Bright-Thomas, P G; Casper, David William; Cattaneo, M; Cerutti, F; Dissertori, G; Drevermann, H; Forty, Roger W; Frank, M; Hagelberg, R; Hansen, J B; Harvey, J; Janot, P; Jost, B; Lehraus, Ivan; Mato, P; Minten, Adolf G; Moneta, L; Pacheco, A; Pusztaszeri, J F; Ranjard, F; Rolandi, Luigi; Rousseau, D; Schlatter, W D; Schmitt, M; Schneider, O; Tejessy, W; Teubert, F; Tomalin, I R; Wachsmuth, H W; Wagner, A; Ajaltouni, Ziad J; Barrès, A; Boyer, C; Falvard, A; Ferdi, C; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rosnet, P; Rossignol, J M; Fearnley, Tom; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Rensch, B; Wäänänen, A; Daskalakis, G; Kyriakis, A; Markou, C; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Rougé, A; Rumpf, M; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Boccali, T; Focardi, E; Parrini, G; Zachariadou, K; Corden, M; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Curtis, L; Dorris, S J; Halley, A W; Lynch, J G; O'Shea, V; Raine, C; Scarr, J M; Smith, K; Teixeira-Dias, P; Thompson, A S; Thomson, E; Thomson, F; Buchmüller, O L; Dhamotharan, S; Geweniger, C; Graefe, G; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Girone, M; Goodsir, S M; Martin, E B; Moutoussi, A; Nash, J; Sedgbeer, J K; Spagnolo, P; Stacey, A M; Williams, M D; Ghete, V M; Girtler, P; Kneringer, E; Kuhn, D; Rudolph, G; Betteridge, A P; Bowdery, C K; Buck, P G; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Sloan, Terence; Williams, M I; Giehl, I; Greene, A M; Hoffmann, C; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Sander, H G; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Benchouk, C; Bonissent, A; Bujosa, G; Carr, J; Coyle, P; Diaconu, C A; Etienne, F; Leroy, O; Motsch, F; Payre, P; Talby, M; Sadouki, A; Thulasidas, M; Trabelsi, K; Aleppo, M; Antonelli, M; Ragusa, F; Berlich, R; Blum, Walter; Büscher, V; Dietl, H; Ganis, G; Gotzhein, C; Kroha, H; Lütjens, G; Lutz, Gerhard; Mannert, C; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Chen, S; Choi, Y; Cordier, A; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Höcker, A; Jacholkowska, A; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Nikolic, I A; Schune, M H; Tournefier, E; Veillet, J J; Videau, I; Zerwas, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Palla, Fabrizio; Rizzo, G; Sanguinetti, G; Sciabà, A; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Vannini, C; Venturi, A; Verdini, P G; Blair, G A; Bryant, L M; Chambers, J T; Green, M G; Medcalf, T; Perrodo, P; Strong, J A; Von Wimmersperg-Töller, J H; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Norton, P R; Thompson, J C; Wright, A E; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Black, S N; Dann, J H; Johnson, R P; Kim, H Y; Konstantinidis, N P; Litke, A M; McNeil, M A; Taylor, G; Booth, C N; Brew, C A J; Cartwright, S L; Combley, F; Kelly, M S; Lehto, M H; Reeve, J; Thompson, L F; Affholderbach, K; Böhrer, A; Brandt, S; Cowan, G D; Grupen, Claus; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Musolino, G; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Charles, E; Elmer, P; Ferguson, D P S; Gao, Y; González, S; Greening, T C; Hayes, O J; Hu, H; Jin, S; McNamara, P A; Nachtman, J M; Nielsen, J; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, J; Wu Sau Lan; Wu, X; Yamartino, J M; Zobernig, G

    1998-01-01

    A bound on the tau neutrino mass is established using the data collected from 1991 to 1995 at Ecm = M(Z) with the ALEPH detector. Two separate limits are derived by fitting the distribution of visible energy vs invariant mass in tau+ -> pi+ pi+ pi- nu and tau+ -> pi+ pi+ pi- pi- pi+ (pi0) nu decays. The two results are combined to obtain a 95 % confidence level upper limit of 18.2 MeV/c^2 on the mass of the tau neutrino.

  18. First Observation of Upsilon(3S) --> tau tau and Tests of Lepton Universality in Upsilon Decays

    CERN Document Server

    Besson, D; Cronin-Hennessy, D; Gao, K Y; Gong, D T; Hietala, J; Kubota, Y; Klein, T; Lang, B W; Poling, R; Scott, A W; Smith, A; Zweber, P; Dobbs, S; Metreveli, Z V; Seth, K K; Tomaradze, A G; Ernst, J; Severini, H; Dytman, S A; Love, W; Savinov, V; Aquines, O; Li, Z; López, A; Mehrabyan, S S; Méndez, H; Ramírez, J; Huang, G S; Miller, D H; Pavlunin, V; Sanghi, B; Shipsey, I P J; Xin, B; Adams, G S; Anderson, M; Cummings, J P; Danko, I; Napolitano, J; He, Q; Insler, J; Muramatsu, H; Park, C S; Thorndike, E H; Yang, F; Coan, T E; Gao, Y S; Liu, F; Artuso, M; Blusk, S; Butt, J; Horwitz, N; Li, J; Menaa, N; Mountain, R; Nisar, S; Randrianarivony, K; Redjimi, R; Sia, R; Skwarnicki, T; Stone, S; Wang, J C; Zhang, K; Csorna, S E; Bonvicini, G; Cinabro, D; Dubrovin, M; Lincoln, A; Asner, D M; Edwards, K W; Briere, R A; Brock, I; Chen, J; Ferguson, T; Tatishvili, G T; Vogel, H; Watkins, M E; Rosner, J L; Adam, N E; Alexander, J P; Berkelman, K; Cassel, D G; Duboscq, J E; Ecklund, K M; Ehrlich, R; Fields, L; Galik, R S; Gibbons, L; Gray, R; Gray, S W; Hartill, D L; Heltsley, B K; Hertz, D; Jones, C D; Kandaswamy, J; Kreinick, D L; Kuznetsov, V E; Mahlke-Krüger, H; Meyer, T O; Onyisi, P U E; Patterson, J R; Peterson, D; Pivarski, J; Riley, D; Ryd, A; Sadoff, A J; Schwarthoff, H; Shi, X; Stroiney, S; Sun, W M; Wilksen, T; Weinberger, M; Athar, S B; Patel, R; Potlia, V; Yelton, J; Rubin, P; Cawlfield, C; Eisenstein, B I; Karliner, I; Kim, D; Lowrey, N; Naik, P; Sedlack, C; Selen, M; White, E J; Wiss, J; Shepherd, M R

    2007-01-01

    Using data collected with the CLEO-III detector at the CESR e+e- collider, we report on a first observation of the decay of the Upsilon(3S) to tau tau, and precisely measure the ratio of branching fractions of Upsilon(nS),n=1,2,3 to tau tau and mu mu final states, finding agreement with expectations from lepton universality. We derive absolute branching fractions for these decays, and also set a limit on the influence of a low mass CP-odd Higgs boson in the decay of the Upsilon(1S).

  19. GM-CSF in sickle cell anemia patients with elevated Hb F.

    Science.gov (United States)

    Haider, M Z; Raghupathy, R; Azizieh, F; Abdelsalam, R; D'Souza, T M; Adekile, A D

    2000-01-01

    We estimated plasma GM-CSF levels in a group of 28 steady-state sickle cell anemia (SS) patients in Kuwait, using an ELISA technique. There were 24 age-matched Hb AA controls, 14 of whom were healthy while 10 were acutely ill at the time of the study. Five SS patients were also studied during 6 episodes of painful crisis. Among the SS patients, 82.1% were homozygous for the Saudi Arabia/India (SAI) haplotype with Hb F ranging from 15 to 35% and total Hb from 8.5 to 11 g/dl. Three patients (siblings) were SAI/Benin compound heterozygotes with Hb F of 9-23% and total Hb >10 g/dl. One patient each was homozygous for the Benin or the Bantu haplotype; they had Hb F <2% and total Hb of 6.6 and 7.2 g/dl, respectively. Four (14. 3%) steady-state SS patients had detectable plasma GM-CSF ranging from 75 to 1,817.6 pg/ml. These included the 2 patients with Hb F <2. 0% and 2 with the SAI/Benin compound heterozygotes with Hb F of 11 and 9%, respectively. Four (66.7%) SS patients in crisis, 6 (42.9%) healthy controls and 6 (60%) acutely ill controls had detectable plasma GM-CSF. A clearcut association of GM-CSF with Hb F level or degree of anemia in steady-state SS patients could not be established. The appearance of GM-CSF in the plasma of patients in crisis and also among control subjects raises the possibility that other factors are involved in the production of this cytokine in the subjects studied.

  20. Measurement of the Tau Polarisation at LEP

    CERN Document Server

    Heister, A; Barate, R; De Bonis, I; Décamp, D; Ghez, P; Goy, C; Merle, E; Pietrzyk, B; Alemany, R; Bravo, S; Casado, M P; Chmeissani, M; Crespo, J M; Fernández, E; Graugès-Pous, E; Martínez, M; Merino, G; Miquel, R; Pacheco, A; Ruiz, H; Colaleo, A; Creanza, D; De Palma, M; Iaselli, Giuseppe; Maggi, G; Maggi, M; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Azzurri, P; Boix, G; Buchmüller, O L; Cattaneo, M; Cerutti, F; Clerbaux, B; Dissertori, G; Drevermann, H; Forty, Roger W; Frank, M; Greening, T C; Hansen, J B; Harvey, J; Janot, P; Jost, B; Kado, M; Mato, P; Moutoussi, A; Ranjard, F; Rolandi, Luigi; Schlatter, W D; Schmitt, M; Schneider, O; Spagnolo, P; Tejessy, W; Teubert, F; Tournefier, E; Ward, J; Wright, A E; Ajaltouni, Ziad J; Badaud, F; Falvard, A; Gay, P; Henrard, P; Jousset, J; Michel, B; Monteil, S; Pallin, D; Perret, P; Podlyski, F; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Wäänänen, A; Daskalakis, G; Kyriakis, A; Markou, C; Simopoulou, Errietta; Vayaki, Anna; Blondel, A; Bonneaud, G R; Rougé, A; Rumpf, M; Swynghedauw, M; Verderi, M; Videau, H L; Focardi, E; Parrini, G; Zachariadou, K; Antonelli, A; Antonelli, M; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Chiarella, V; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Halley, A W; Lynch, J G; Negus, P; O'Shea, V; Raine, C; Thompson, A S; Wasserbaech, S R; Cavanaugh, R J; Dhamotharan, S; Geweniger, C; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Girone, M; Marinelli, N; Sedgbeer, J K; Thompson, J C; Ghete, V M; Girtler, P; Kneringer, E; Kuhn, D; Rudolph, G; Bouhova-Thacker, E; Bowdery, C K; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Pearson, M R; Robertson, N A; Giehl, I; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Wachsmuth, H W; Zeitnitz, C; Bonissent, A; Carr, J; Coyle, P; Leroy, O; Payre, P; Rousseau, D; Talby, M; Aleppo, M; Ragusa, F; David, A; Dietl, H; Ganis, G; Hüttmann, K; Lütjens, G; Mannert, C; Männer, W; Settles, Ronald; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Chen, S; Davier, M; Duflot, L; Jacholkowska, A; Lefrançois, J; Nikolic, I A; Videau, I; Yuan, C; Bagliesi, G; Boccali, T; Calderini, G; Ciulli, V; Foà, L; Giassi, A; Ligabue, F; Messineo, A; Palla, Fabrizio; Sanguinetti, G; Sciabà, A; Sguazzoni, G; Tenchini, Roberto; Venturi, A; Verdini, P G; Blair, G A; Cowan, G D; Green, M G; Medcalf, T; Strong, J A; Clifft, R W; Edgecock, T R; Norton, P R; Tomalin, I R; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Locci, E; Pérez, P; Rander, J; Roussarie, A; Schwindling, J; Trabelsi, A; Vallage, B; Konstantinidis, N P; Litke, A M; Taylor, G; Booth, C N; Cartwright, S L; Combley, F; Lehto, M H; Thompson, L F; Affholderbach, K; Böhrer, A; Brandt, S; Grupen, Claus; Misiejuk, A; Ngac, A; Prange, G; Sieler, U; Giannini, G; Rothberg, J E; Armstrong, S R; Cranmer, K; Elmer, P; Ferguson, D P S; Gao, Y; González, S; Hayes, O J; Hu, H; Jin, S; Kile, J; McNamara, P A; Nielsen, J; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, J; Wu, X; Zobernig, G

    2001-01-01

    The polarisation of $\\tau$'s produced in Z decay is measured using 160 pb$^{-1}$ of data accumulated at LEP by the ALEPH detector between 1990 and 1995. The variation of the polarisation with polar angle yields the two parameters ${\\cal A}_e = 0.1504 \\pm 0.0068 $ and ${\\cal A}_{\\tau} = 0.1451 \\pm 0.0059$ which are consistent with the hypothesis of $e$-$\\tau$ universality. Assuming universality, the value ${\\cal A}_{e\\mbox{-}\\tau} = 0.1474 \\pm 0.0045$ is obtained from which the effective weak mixing angle $\\sin^2 {\\theta_{\\mathrm{W}}^{\\mathrm{eff}}} =0.23147 \\pm 0.00057 $ is derived.

  1. Measurement of the $\\tau$ lepton lifetime

    CERN Document Server

    Buskulic, Damir; De Bonis, I; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Odier, P; Pietrzyk, B; Ariztizabal, F; Chmeissani, M; Crespo, J M; Efthymiopoulos, I; Fernández, E; Fernández-Bosman, M; Gaitan, V; Garrido, L; Martínez, M; Orteu, S; Pacheco, A; Padilla, C; Palla, Fabrizio; Pascual, A; Perlas, J A; Sánchez, F; Teubert, F; Colaleo, A; Creanza, D; De Palma, M; Farilla, A; Gelao, G; Girone, M; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Natali, S; Nuzzo, S; Ranieri, A; Raso, G; Romano, F; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Bonvicini, G; Cattaneo, M; Comas, P; Coyle, P; Drevermann, H; Engelhardt, A; Forty, Roger W; Frank, M; Hagelberg, R; Harvey, J; Jacobsen, R; Janot, P; Jost, B; Kneringer, E; Knobloch, J; Lehraus, Ivan; Markou, C; Martin, E B; Mato, P; Minten, Adolf G; Miquel, R; Oest, T; Palazzi, P; Pater, J R; Pusztaszeri, J F; Ranjard, F; Rensing, P E; Rolandi, Luigi; Schlatter, W D; Schmelling, M; Schneider, O; Tejessy, W; Tomalin, I R; Venturi, A; Wachsmuth, H W; Wiedenmann, W; Wildish, T; Witzeling, W; Wotschack, J; Ajaltouni, Ziad J; Bardadin-Otwinowska, Maria; Barrès, A; Boyer, C; Falvard, A; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rossignol, J M; Saadi, F; Fearnley, Tom; Hansen, J B; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Kyriakis, A; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Zachariadou, K; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Passalacqua, L; Rougé, A; Rumpf, M; Tanaka, R; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Focardi, E; Parrini, G; Corden, M; Delfino, M C; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Pepé-Altarelli, M; Dorris, S J; Halley, A W; ten Have, I; Knowles, I G; Lynch, J G; Morton, W T; O'Shea, V; Raine, C; Reeves, P; Scarr, J M; Smith, K; Smith, M G; Thompson, A S; Thomson, F; Thorn, S; Turnbull, R M; Becker, U; Braun, O; Geweniger, C; Graefe, G; Hanke, P; Hepp, V; Kluge, E E; Putzer, A; Rensch, B; Schmidt, M; Sommer, J; Stenzel, H; Tittel, K; Werner, S; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Colling, D J; Dornan, Peter J; Konstantinidis, N P; Moneta, L; Moutoussi, A; Nash, J; San Martin, G; Sedgbeer, J K; Stacey, A M; Dissertori, G; Girtler, P; Kuhn, D; Rudolph, G; Bowdery, C K; Brodbeck, T J; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Sloan, Terence; Whelan, E P; Williams, M I; Galla, A; Greene, A M; Kleinknecht, K; Quast, G; Raab, J; Renk, B; Sander, H G; Wanke, R; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Bencheikh, A M; Benchouk, C; Bonissent, A; Bujosa, G; Calvet, D; Carr, J; Diaconu, C A; Etienne, F; Thulasidas, M; Nicod, D; Payre, P; Rousseau, D; Talby, M; Abt, I; Assmann, R W; Bauer, C; Blum, Walter; Brown, D; Dietl, H; Dydak, Friedrich; Ganis, G; Gotzhein, C; Jakobs, K; Kroha, H; Lütjens, G; Lutz, Gerhard; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Saint-Denis, R; Wolf, G; Alemany, R; Boucrot, J; Callot, O; Cordier, A; Courault, F; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Jacquet, M; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Musolino, G; Nikolic, I A; Park, H J; Park, I C; Schune, M H; Simion, S; Veillet, J J; Videau, I; Abbaneo, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Fidecaro, F; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Rizzo, G; Sanguinetti, G; Sciabà, A; Spagnolo, P; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Triggiani, G; Vannini, C; Verdini, P G; Walsh, J; Betteridge, A P; Blair, G A; Bryant, L M; Cerutti, F; Gao, Y; Green, M G; Johnson, D L; Medcalf, T; Mir, L M; Perrodo, P; Strong, J A; Bertin, V; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Edwards, M; Maley, P; Norton, P R; Thompson, J C; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Marx, B; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Johnson, R P; Kim, H Y; Litke, A M; McNeil, M A; Taylor, G; Beddall, A; Booth, C N; Boswell, R; Cartwright, S L; Combley, F; Dawson, I; Köksal, A; Letho, M; Newton, W M; Rankin, C; Thompson, L F; Böhrer, A; Brandt, S; Cowan, G D; Feigl, E; Grupen, Claus; Lutters, G; Minguet-Rodríguez, J A; Rivera, F; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Ragusa, F; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Bellantoni, L; Elmer, P; Feng, Z; Ferguson, D P S; Gao, Y S; González, S; Grahl, J; Harton, J L; Hayes, O J; Hu, H; McNamara, P A; Nachtman, J M; Orejudos, W; Pan, Y B; Saadi, Y; Schmitt, M; Scott, I J; Sharma, V; Turk, J; Walsh, A M; Wu Sau Lan; Wu, X; Yamartino, J M; Zheng, M; Zobernig, G

    1996-01-01

    The mean lifetime of the \\tau lepton is measured in a sample of 25700 \\tau pairs collected in 1992 with the ALEPH detector at LEP. A new analysis of the 1-1 topology events is introduced. In this analysis, the dependence of the impact parameter sum distribution on the daughter track momenta is taken into account, yielding improved precision compared to other impact parameter sum methods. Three other analyses of the one- and three-prong \\tau decays are updated with increased statistics. The measured lifetime is 293.5 \\pm 3.1 \\pm 1.7 \\fs. Including previous (1989--1991) ALEPH measurements, the combined \\tau lifetime is 293.7 \\pm 2.7 \\pm 1.6 \\fs.

  2. Measurement of $\\tau$ polarisation at LEP

    CERN Document Server

    Acciarri, M; Aguilar-Benítez, M; Ahlen, S P; Alcaraz, J; Alemanni, G; Allaby, James V; Aloisio, A; Alviggi, M G; Ambrosi, G; Anderhub, H; Andreev, V P; Angelescu, T; Anselmo, F; Arefev, A; Azemoon, T; Aziz, T; Bagnaia, P; Baksay, L; Ball, R C; Banerjee, S; Banerjee, Sw; Banicz, K; Barczyk, A; Barillère, R; Barone, L; Bartalini, P; Baschirotto, A; Basile, M; Battiston, R; Bay, A; Becattini, F; Becker, U; Behner, F; Berdugo, J; Berges, P; Bertucci, B; Betev, B L; Bhattacharya, S; Biasini, M; Biland, A; Bilei, G M; Blaising, J J; Blyth, S C; Bobbink, Gerjan J; Böck, R K; Böhm, A; Boldizsar, L; Borgia, B; Bourilkov, D; Bourquin, Maurice; Boutigny, D; Braccini, S; Branson, J G; Brigljevic, V; Brock, I C; Buffini, A; Buijs, A; Burger, J D; Burger, W J; Busenitz, J K; Cai, X D; Campanelli, M; Capell, M; Cara Romeo, G; Carlino, G; Cartacci, A M; Casaus, J; Castellini, G; Cavallari, F; Cavallo, N; Cecchi, C; Cerrada-Canales, M; Cesaroni, F; Chamizo-Llatas, M; Chang, Y H; Chaturvedi, U K; Chekanov, S V; Chemarin, M; Chen, A; Chen, G; Chen, G M; Chen, H F; Chen, H S; Chen, M; Chiefari, G; Chien, C Y; Cifarelli, Luisa; Cindolo, F; Civinini, C; Clare, I; Clare, R; Cohn, H O; Coignet, G; Colijn, A P; Colino, N; Costantini, S; Cotorobai, F; de la Cruz, B; Csilling, Akos; Dai, T S; D'Alessandro, R; De Asmundis, R; Degré, A; Deiters, K; Denes, P; De Notaristefani, F; DiBitonto, Daryl; Diemoz, M; Van Dierendonck, D N; Di Lodovico, F; Dionisi, C; Dittmar, Michael; Dominguez, A; Doria, A; Dova, M T; Drago, E; Duchesneau, D; Duinker, P; Durán, I; Dutta, S; Easo, S; Efremenko, Yu V; El-Mamouni, H; Engler, A; Eppling, F J; Erné, F C; Ernenwein, J P; Extermann, Pierre; Fabre, M; Faccini, R; Falciano, S; Favara, A; Fay, J; Fedin, O; Felcini, Marta; Fenyi, B; Ferguson, T; Ferroni, F; Fesefeldt, H S; Fiandrini, E; Field, J H; Filthaut, Frank; Fisher, P H; Fisk, I; Forconi, G; Fredj, L; Freudenreich, Klaus; Furetta, C; Galaktionov, Yu; Ganguli, S N; García-Abia, P; Gau, S S; Gentile, S; Gerald, J; Gheordanescu, N; Giagu, S; Goldfarb, S; Goldstein, J; Gong, Z F; Gougas, Andreas; Gratta, Giorgio; Grünewald, M W; Gupta, V K; Gurtu, A; Gutay, L J; Haas, D; Hartmann, B; Hasan, A; Hatzifotiadou, D; Hebbeker, T; Hervé, A; Hirschfelder, J; Van Hoek, W C; Hofer, H; Hoorani, H; Hou, S R; Hu, G; Innocente, Vincenzo; Jenkes, K; Jin, B N; Jones, L W; de Jong, P; Josa-Mutuberria, I; Kasser, A; Khan, R A; Kamrad, D; Kamyshkov, Yu A; Kapustinsky, J S; Karyotakis, Yu; Kaur, M; Kienzle-Focacci, M N; Kim, D; Kim, D H; Kim, J K; Kim, S C; Kinnison, W W; Kirkby, A; Kirkby, D; Kirkby, Jasper; Kiss, D; Kittel, E W; Klimentov, A; König, A C; Kopp, A; Korolko, I; Koutsenko, V F; Krämer, R W; Krenz, W; Kunin, A; Lacentre, P E; Ladrón de Guevara, P; Landi, G; Lapoint, C; Lassila-Perini, K M; Laurikainen, P; Lavorato, A; Lebeau, M; Lebedev, A; Lebrun, P; Lecomte, P; Lecoq, P; Le Coultre, P; Lee, H J; Leggett, C; Le Goff, J M; Leiste, R; Leonardi, E; Levchenko, P M; Li Chuan; Lin, C H; Lin, W T; Linde, Frank L; Lista, L; Liu, Z A; Lohmann, W; Longo, E; Lu, W; Lü, Y S; Lübelsmeyer, K; Luci, C; Luckey, D; Luminari, L; Lustermann, W; Ma Wen Gan; Maity, M; Majumder, G; Malgeri, L; Malinin, A; Maña, C; Mangeol, D J J; Mangla, S; Marchesini, P A; Marin, A; Martin, J P; Marzano, F; Massaro, G G G; McNally, D; Mele, S; Merola, L; Meschini, M; Metzger, W J; Von der Mey, M; Mi, Y; Migani, D; Mihul, A; Van Mil, A J W; Milcent, H; Mirabelli, G; Mnich, J; Molnár, P; Monteleoni, B; Moore, R; Moulik, T; Mount, R; Muheim, F; Muijs, A J M; Nahn, S; Napolitano, M; Nessi-Tedaldi, F; Newman, H; Niessen, T; Nippe, A; Nisati, A; Nowak, H; Oh, Yu D; Opitz, H; Organtini, G; Ostonen, R; Palit, S; Palomares, C; Pandoulas, D; Paoletti, S; Paolucci, P; Park, H K; Park, I H; Pascale, G; Passaleva, G; Patricelli, S; Paul, T; Pauluzzi, M; Paus, C; Pauss, Felicitas; Peach, D; Pei, Y J; Pensotti, S; Perret-Gallix, D; Petersen, B; Petrak, S; Pevsner, A; Piccolo, D; Pieri, M; Piroué, P A; Pistolesi, E; Plyaskin, V; Pohl, M; Pozhidaev, V; Postema, H; Produit, N; Prokofev, D; Prokofiev, D O; Quartieri, J; Rahal-Callot, G; Raja, N; Rancoita, P G; Rattaggi, M; Raven, G; Razis, P A; Read, K; Ren, D; Rescigno, M; Reucroft, S; Van Rhee, T; Riemann, S; Riles, K; Rind, O; Robohm, A; Rodin, J; Roe, B P; Romero, L; Rosier-Lees, S; Rosselet, P; Van Rossum, W; Roth, S; Rubio, Juan Antonio; Ruschmeier, D; Rykaczewski, H; Salicio, J; Sánchez, E; Sanders, M P; Sarakinos, M E; Sarkar, S; Sauvage, G; Schäfer, C; Shchegelskii, V; Schmidt-Kärst, S; Schmitz, D; Schneegans, M; Scholz, N; Schopper, Herwig Franz; Schotanus, D J; Schwenke, J; Schwering, G; Sciacca, C; Sciarrino, D; Servoli, L; Shevchenko, S; Shivarov, N; Shoutko, V; Shukla, J; Shumilov, E; Shvorob, A V; Siedenburg, T; Son, D; Soulimov, V; Smith, B; Spillantini, P; Steuer, M; Stickland, D P; Stone, H; Stoyanov, B; Strässner, A; Sudhakar, K; Sultanov, G G; Sun, L Z; Susinno, G F; Suter, H; Swain, J D; Tang, X W; Tauscher, Ludwig; Taylor, L; Ting, Samuel C C; Ting, S M; Tonwar, S C; Tóth, J; Tully, C; Tuchscherer, H; Tung, K L; Uchida, Y; Ulbricht, J; Uwer, U; Valente, E; Vesztergombi, G; Vetlitskii, I; Viertel, Gert M; Vivargent, M; Vlachos, S; Völkert, R; Vogel, H; Vogt, H; Vorobev, I; Vorobyov, A A; Vorvolakos, A; Wadhwa, M; Wallraff, W; Wang, J C; Wang, X L; Wang, Z M; Weber, A; Wu, S X; Wynhoff, S; Xu, J; Xu, Z Z; Yang, B Z; Yang, C G; Yao, X Y; Ye, J B; Yeh, S C; You, J M; Zalite, A; Zalite, Yu; Zemp, P; Zeng, Y; Zhang, Z; Zhang, Z P; Zhou, B; Zhou, Y; Zhu, G Y; Zhu, R Y; Zichichi, Antonino; Ziegler, F

    1998-01-01

    Using the data collected with the L3 detector at LEP between 1990 and 1995, corresponding to an integrated luminosity of 149 pb$^{-1}$, the $\\tau$ longitudinal polarisation has been measured as a function of the production polar angle using the $\\tau$ decays \\thad\\ ($\\rm h = \\pi, \\rho, \\aone$) and \\tlep\\ ($\\rm \\ell = e, \\mu$). From this measurement the quantities æl~and \\at, which depend on the couplings of the electron and the $\\tau$ to the Z, are determined to be $\\ael = 0.1678 \\pm 0.0127 \\pm 0.0030 $ and $\\at = 0.1476 \\pm 0.0088 \\pm 0.0062$, consistent with the hypothesis of e--$\\tau$ universality. Under this assumption a value of $\\al = 0.1540 \\pm 0.0074 \\pm 0.0044 $ is obtained, yielding the value of the effective weak mixing angle $\\swsqb = 0.2306 \\pm 0.0011$.

  3. Inhibition of tau hyperphosphorylation and beta amyloid production in rat brain by oral administration of atorvastatin

    Institute of Scientific and Technical Information of China (English)

    LU Fen; LI Xu; SUO Ai-qin; ZHANG Jie-wen

    2010-01-01

    Background Alzheimer's disease (AD) is a neurodegenerative disorder and the leading cause of dementia in the elderly. The two hallmark lesions in AD brain are deposition of amyloid plaques and neurofibrillary tangles (NFTs).Hypercholesteremia is one of the risk factors of AD. But its role in the pathogenesis of AD is largely unknown. The aim of this study was to investigate the relationship between hypercholesteremia and tau phosphorylation or β-amyloid (Aβ),and evaluate the effect of atorvastatin on the level of tau phosphorylation and Aβ in the brains of rats fed with high cholesterol diet.Methods Sprague-Dawley (SD) rats were randomly divided into normal diet control group, high cholesterol diet group,and high cholesterol diet plus atorvastatin (Lipitor, 15 mg·kg-1·d-1) treated group. Blood from caudal vein was collected to measure total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL) and high-density lipoprotein (HDL) at the end of the 3th and the 6th months by an enzymatic method. The animals were sacrificed 6 months later and brains were removed. All left brain hemispheres were fixed for immunohistochemistry. Hippocampus and cerebral cortex were separated from right hemispheres and homogenized separately. Tau phosphorylation and Aβ in the brain tissue were determined by Western blotting (using antibodies PHF-1 and Tau-1) and anti-Aβ40/anti-Aβ42, respectively.Results We found that high cholesterol diet led to hypercholesteremia of rats as well as hyperphosphorylation of tau and increased Aβ level in the brains. Treatment of the high cholesterol diet fed rats with atorvastatin prevented the changes of both tau phosphorylation and Aβ level induced by high cholesterol diet.Conclusions Hypercholesteremia could induce tau hyperphosphorylation and Aβ production in rat brain. Atorvastatin could inhibit tau hyperphosphorylation and decrease Aβ generation. It may play a protective role in the patho-process of hypercholesteremia

  4. Longitudinal assessment of tau and amyloid beta in cerebrospinal fluid of Parkinson disease.

    Science.gov (United States)

    Zhang, Jing; Mattison, Hayley A; Liu, Changqin; Ginghina, Carmen; Auinger, Peggy; McDermott, Michael P; Stewart, Tessandra; Kang, Un Jung; Cain, Kevin C; Shi, Min

    2013-11-01

    Tau gene has been consistently associated with the risk of Parkinson disease in recent genome wide association studies. In addition, alterations of the levels of total tau, phosphorylated tau [181P], and amyloid beta 1-42 in cerebrospinal fluid have been reported in patients with sporadic Parkinson disease and asymptomatic carriers of leucine-rich repeat kinase 2 mutations, in patterns that clearly differ from those typically described for patients with Alzheimer disease. To further determine the potential roles of these molecules in Parkinson disease pathogenesis and/or in tracking the disease progression, especially at early stages, the current study assessed all three proteins in 403 Parkinson disease patients enrolled in the DATATOP (Deprenyl and tocopherol antioxidative therapy of parkinsonism) placebo-controlled clinical trial, the largest cohort to date with cerebrospinal fluid samples collected longitudinally. These initially drug-naive patients at early disease stages were clinically evaluated, and cerebrospinal fluid was collected at baseline and then at endpoint, defined as the time at which symptomatic anti-Parkinson disease medications were determined to be required. General linear models were used to test for associations between baseline cerebrospinal fluid biomarker levels or their rates of change and changes in the Unified Parkinson Disease Rating Scale (total or part III motor score) over time. Robust associations among candidate markers are readily noted. Baseline levels of amyloid beta were weakly but negatively correlated with baseline Unified Parkinson Disease Rating Scale total scores. Baseline phosphorylated tau/total tau and phosphorylated tau/amyloid beta were significantly and negatively correlated with the rates of the Unified Parkinson Disease Rating Scale change. While medications (deprenyl and/or tocopherol) did not appear to alter biomarkers appreciably, a weak but significant positive correlation between the rate of change in total

  5. Search for a low-mass higgs boson in Upsilon(3S)-->gammaA(0), A(0)-->tau(+)tau(-) at BABAR.

    Science.gov (United States)

    Aubert, B; Karyotakis, Y; Lees, J P; Poireau, V; Prencipe, E; Prudent, X; Tisserand, V; Tico, J Garra; Grauges, E; Martinelli, M; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Battaglia, M; Brown, D N; Kerth, L T; Kolomensky, Yu G; Lynch, G; Osipenkov, I L; Tackmann, K; Tanabe, T; Hawkes, C M; Soni, N; Watson, A T; Koch, H; Schroeder, T; Asgeirsson, D J; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Barrett, M; Khan, A; Randle-Conde, A; Blinov, V E; Bukin, A D; Buzykaev, A R; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Atmacan, H; Gary, J W; Liu, F; Long, O; Vitug, G M; Yasin, Z; Sharma, V; Campagnari, C; Hong, T M; Kovalskyi, D; Mazur, M A; Richman, J D; Beck, T W; Eisner, A M; Heusch, C A; Kroseberg, J; Lockman, W S; Martinez, A J; Schalk, T; Schumm, B A; Seiden, A; Wang, L; Winstrom, L O; Cheng, C H; Doll, D A; Echenard, B; Fang, F; Hitlin, D G; Narsky, I; Ongmongkolkul, P; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Bloom, P C; Ford, W T; Gaz, A; Hirschauer, J F; Nagel, M; Nauenberg, U; Smith, J G; Wagner, S R; Ayad, R; Toki, W H; Wilson, R J; Feltresi, E; Hauke, A; Jasper, H; Karbach, T M; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Kobel, M J; Nogowski, R; Schubert, K R; Schwierz, R; Bernard, D; Latour, E; Verderi, M; Clark, P J; Playfer, S; Watson, J E; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Fioravanti, E; Franchini, P; Luppi, E; Munerato, M; Negrini, M; Petrella, A; Piemontese, L; Santoro, V; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Contri, R; Guido, E; Lo Vetere, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Tosi, S; Chaisanguanthum, K S; Morii, M; Adametz, A; Marks, J; Schenk, S; Uwer, U; Bernlochner, F U; Klose, V; Lacker, H M; Lueck, T; Volk, A; Bard, D J; Dauncey, P D; Tibbetts, M; Behera, P K; Charles, M J; Mallik, U; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Arnaud, N; Béquilleux, J; D'Orazio, A; Davier, M; Derkach, D; da Costa, J Firmino; Grosdidier, G; Le Diberder, F; Lepeltier, V; Lutz, A M; Malaescu, B; Pruvot, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Touramanis, C; Bevan, A J; Clarke, C K; Di Lodovico, F; Sacco, R; Sigamani, M; Cowan, G; Paramesvaran, S; Wren, A C; Brown, D N; Davis, C L; Denig, A G; Fritsch, M; Gradl, W; Hafner, A; Alwyn, K E; Bailey, D; Barlow, R J; Jackson, G; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Dallapiccola, C; Salvati, E; Cowan, R; Dujmic, D; Fisher, P H; Henderson, S W; Sciolla, G; Spitznagel, M; Yamamoto, R K; Zhao, M; Patel, P M; Robertson, S H; Schram, M; Biassoni, P; Lazzaro, A; Lombardo, V; Palombo, F; Stracka, S; Cremaldi, L; Godang, R; Kroeger, R; Sonnek, P; Summers, D J; Zhao, H W; Simard, M; Taras, P; Nicholson, H; De Nardo, G; Lista, L; Monorchio, D; Onorato, G; Sciacca, C; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; Losecco, J M; Wang, W F; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Sekula, S J; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Castelli, G; Gagliardi, N; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Del Amo Sanchez, P; Ben-Haim, E; Bonneaud, G R; Briand, H; Chauveau, J; Hamon, O; Leruste, Ph; Marchiori, G; Ocariz, J; Perez, A; Prendki, J; Sitt, S; Gladney, L; Biasini, M; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Calderini, G; Carpinelli, M; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Lopes Pegna, D; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Anulli, F; Baracchini, E; Cavoto, G; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Gioi, L Li; Mazzoni, M A; Morganti, S; Piredda, G; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Franek, B; Olaiya, E O; Wilson, F F; Emery, S; Esteve, L; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yèche, Ch; Zito, M; Allen, M T; Aston, D; Bartoldus, R; Benitez, J F; Cenci, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Sevilla, M Franco; Gabareen, A M; Graham, M T; Grenier, P; Hast, C; Innes, W R; Kaminski, J; Kelsey, M H; Kim, H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Lindquist, B; Luitz, S; Luth, V; Lynch, H L; Macfarlane, D B; Marsiske, H; Messner, R; Muller, D R; Neal, H; Nelson, S; O'Grady, C P; Ofte, I; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; West, C A; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Young, C C; Ziegler, V; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Bellis, M; Burchat, P R; Edwards, A J; Miyashita, T S; Ahmed, S; Alam, M S; Ernst, J A; Pan, B; Saeed, M A; Zain, S B; Soffer, A; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Wray, B C; Drummond, B W; Izen, J M; Lou, X C; Bianchi, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Choi, H H F; Hamano, K; King, G J; Kowalewski, R; Lewczuk, M J; Nugent, I M; Roney, J M; Sobie, R J; Gershon, T J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Puccio, E M T; Band, H R; Chen, X; Dasu, S; Flood, K T; Pan, Y; Prepost, R; Vuosalo, C O; Wu, S L

    2009-10-30

    We search for a light Higgs boson A0 in the radiative decay Upsilon(3S)-->gammaA(0), A(0)-->tau+tau-, tau+-->e+nu(e)nu(tau), or tau+-->mu+nu(mu)nu(tau). The data sample contains 122x10(6) Upsilon(3S) events recorded with the BABAR detector. We find no evidence for a narrow structure in the studied tau+tau- invariant mass region of 4.03gammaA(0))xB(A(0)-->tau+tau-)>(1.5-16)x10(-5) across the m(tau+tau-) range. We also set a 90% C.L. upper limit on the tau+tau- decay of the eta(b) at B(eta(b)-->tau+tau-)<8%.

  6. Measurement of the Weak Dipole Moments of the $\\tau$ Lepton

    CERN Document Server

    Acciarri, M; Aguilar-Benítez, M; Ahlen, S P; Alcaraz, J; Alemanni, G; Allaby, James V; Aloisio, A; Alviggi, M G; Ambrosi, G; Anderhub, H; Andreev, V P; Angelescu, T; Anselmo, F; Arefev, A; Azemoon, T; Aziz, T; Bagnaia, P; Baksay, L; Ball, R C; Banerjee, S; Banerjee, Sw; Banicz, K; Barczyk, A; Barillère, R; Barone, L; Bartalini, P; Baschirotto, A; Basile, M; Battiston, R; Bay, A; Becattini, F; Becker, U; Behner, F; Berdugo, J; Berges, P; Bertucci, B; Betev, B L; Bhattacharya, S; Biasini, M; Biland, A; Bilei, G M; Blaising, J J; Blyth, S C; Bobbink, Gerjan J; Böck, R K; Böhm, A; Boldizsar, L; Borgia, B; Bourilkov, D; Bourquin, Maurice; Boutigny, D; Braccini, S; Branson, J G; Brigljevic, V; Brock, I C; Buffini, A; Buijs, A; Burger, J D; Burger, W J; Busenitz, J K; Cai, X D; Campanelli, M; Capell, M; Cara Romeo, G; Carlino, G; Cartacci, A M; Casaus, J; Castellini, G; Cavallari, F; Cavallo, N; Cecchi, C; Cerrada-Canales, M; Cesaroni, F; Chamizo-Llatas, M; Chang, Y H; Chaturvedi, U K; Chekanov, S V; Chemarin, M; Chen, A; Chen, G; Chen, G M; Chen, H F; Chen, H S; Chen, M; Chiefari, G; Chien, C Y; Cifarelli, Luisa; Cindolo, F; Civinini, C; Clare, I; Clare, R; Cohn, H O; Coignet, G; Colijn, A P; Colino, N; Costantini, S; Cotorobai, F; de la Cruz, B; Csilling, Akos; Dai, T S; D'Alessandro, R; De Asmundis, R; Degré, A; Deiters, K; Denes, P; De Notaristefani, F; DiBitonto, Daryl; Diemoz, M; Van Dierendonck, D N; Di Lodovico, F; Dionisi, C; Dittmar, Michael; Dominguez, A; Doria, A; Dova, M T; Drago, E; Duchesneau, D; Duinker, P; Durán, I; Dutta, S; Easo, S; Efremenko, Yu V; El-Mamouni, H; Engler, A; Eppling, F J; Erné, F C; Ernenwein, J P; Extermann, Pierre; Fabre, M; Faccini, R; Falciano, S; Favara, A; Fay, J; Fedin, O; Felcini, Marta; Fenyi, B; Ferguson, T; Ferroni, F; Fesefeldt, H S; Fiandrini, E; Field, J H; Filthaut, Frank; Fisher, P H; Fisk, I; Forconi, G; Fredj, L; Freudenreich, Klaus; Furetta, C; Galaktionov, Yu; Ganguli, S N; García-Abia, P; Gau, S S; Gentile, S; Gerald, J; Gheordanescu, N; Giagu, S; Goldfarb, S; Goldstein, J; Gong, Z F; Gougas, Andreas; Gratta, Giorgio; Grünewald, M W; Gupta, V K; Gurtu, A; Gutay, L J; Haas, D; Hartmann, B; Hasan, A; Hatzifotiadou, D; Hebbeker, T; Hervé, A; Hirschfelder, J; Van Hoek, W C; Hofer, H; Hoorani, H; Hou, S R; Hu, G; Innocente, Vincenzo; Jenkes, K; Jin, B N; Jones, L W; de Jong, P; Josa-Mutuberria, I; Kasser, A; Khan, R A; Kamrad, D; Kamyshkov, Yu A; Kapustinsky, J S; Karyotakis, Yu; Kaur, M; Kienzle-Focacci, M N; Kim, D; Kim, D H; Kim, J K; Kim, S C; Kinnison, W W; Kirkby, A; Kirkby, D; Kirkby, Jasper; Kiss, D; Kittel, E W; Klimentov, A; König, A C; Kopp, A; Korolko, I; Koutsenko, V F; Krämer, R W; Krenz, W; Kunin, A; Lacentre, P E; Ladrón de Guevara, P; Landi, G; Lapoint, C; Lassila-Perini, K M; Laurikainen, P; Lavorato, A; Lebeau, M; Lebedev, A; Lebrun, P; Lecomte, P; Lecoq, P; Le Coultre, P; Lee, H J; Leggett, C; Le Goff, J M; Leiste, R; Leonardi, E; Levchenko, P M; Li Chuan; Lin, C H; Lin, W T; Linde, Frank L; Lista, L; Liu, Z A; Lohmann, W; Longo, E; Lu, W; Lü, Y S; Lübelsmeyer, K; Luci, C; Luckey, D; Luminari, L; Lustermann, W; Ma Wen Gan; Maity, M; Majumder, G; Malgeri, L; Malinin, A; Maña, C; Mangeol, D J J; Mangla, S; Marchesini, P A; Marin, A; Martin, J P; Marzano, F; Massaro, G G G; McNally, D; Mele, S; Merola, L; Meschini, M; Metzger, W J; Von der Mey, M; Mi, Y; Migani, D; Mihul, A; Van Mil, A J W; Milcent, H; Mirabelli, G; Mnich, J; Molnár, P; Monteleoni, B; Moore, R; Moulik, T; Mount, R; Muheim, F; Muijs, A J M; Nahn, S; Napolitano, M; Nessi-Tedaldi, F; Newman, H; Niessen, T; Nippe, A; Nisati, A; Oh, Yu D; Opitz, H; Organtini, G; Ostonen, R; Palit, S; Palomares, C; Pandoulas, D; Paoletti, S; Paolucci, P; Park, H K; Park, I H; Pascale, G; Passaleva, G; Patricelli, S; Paul, T; Pauluzzi, M; Paus, C; Pauss, Felicitas; Peach, D; Pei, Y J; Pensotti, S; Perret-Gallix, D; Petersen, B; Petrak, S; Pevsner, A; Piccolo, D; Pieri, M; Piroué, P A; Pistolesi, E; Plyaskin, V; Pohl, M; Pozhidaev, V; Postema, H; Produit, N; Prokofev, D; Prokofiev, D O; Quartieri, J; Rahal-Callot, G; Raja, N; Rancoita, P G; Rattaggi, M; Raven, G; Razis, P A; Read, K; Ren, D; Rescigno, M; Reucroft, S; Van Rhee, T; Riemann, S; Riles, K; Rind, O; Robohm, A; Rodin, J; Roe, B P; Romero, L; Rosier-Lees, S; Rosselet, P; Van Rossum, W; Roth, S; Rubio, Juan Antonio; Ruschmeier, D; Rykaczewski, H; Salicio, J; Sánchez, E; Sanders, M P; Sarakinos, M E; Sarkar, S; Sauvage, G; Schäfer, C; Shchegelskii, V; Schmidt-Kärst, S; Schmitz, D; Schneegans, M; Scholz, N; Schopper, Herwig Franz; Schotanus, D J; Schwenke, J; Schwering, G; Sciacca, C; Sciarrino, D; Servoli, L; Shevchenko, S; Shivarov, N; Shoutko, V; Shukla, J; Shumilov, E; Shvorob, A V; Siedenburg, T; Son, D; Soulimov, V; Smith, B; Spillantini, P; Steuer, M; Stickland, D P; Stone, H; Stoyanov, B; Strässner, A; Sudhakar, K; Sultanov, G G; Sun, L Z; Susinno, G F; Suter, H; Swain, J D; Tang, X W; Tauscher, Ludwig; Taylor, L; Ting, Samuel C C; Ting, S M; Tonwar, S C; Tóth, J; Tully, C; Tuchscherer, H; Tung, K L; Uchida, Y; Ulbricht, J; Uwer, U; Valente, E; Vesztergombi, G; Vetlitskii, I; Viertel, Gert M; Vivargent, M; Vlachos, S; Völkert, R; Vogel, H; Vogt, H; Vorobev, I; Vorobyov, A A; Vorvolakos, A; Wadhwa, M; Wallraff, W; Wang, J C; Wang, X L; Wang, Z M; Weber, A; Wu, S X; Wynhoff, S; Xu, J; Xu, Z Z; Yang, B Z; Yang, C G; Yao, X Y; Ye, J B; Yeh, S C; You, J M; Zalite, A; Zalite, Yu; Zemp, P; Zeng, Y; Zhang, Z; Zhang, Z P; Zhou, B; Zhou, Y; Zhu, G Y; Zhu, R Y; Zichichi, Antonino; Ziegler, F

    1998-01-01

    Using the data collected by the L3 experiment at LEP from 1991 to 1995 at energies around the $\\Zo$ mass, a measurement of the weak anomalous magnetic dipole moment, $a^w_{\\tau}$,~ and of the weak electric dipole moment, $d^w_{\\tau}$, of the $\\tau$ lepton is performed. These quantities are obtained from angular distributions in $e^{+}e^{-}\\rightarrow\\tau^{+}\\tau^{-} \\rightarrow h^{+} \\bar{\

  7. Ironing out Tau's Role in Parkinsonism

    Science.gov (United States)

    Stankowski, Jeannette N.; Dawson, Valina L.; Dawson, Ted M.

    2015-01-01

    Parkinson's disease affects more than five million people worldwide, yet no therapeutic has been identified that can slow or halt the progression of this debilitating disease. A new study in tau knockout mice suggests that tau deficiency causes impaired ferroportin-coupled iron export, by retention of the amyloid precursor protein, a neuronal ferroxidase partner, in the endoplasmic reticulum. This leads to parkinsonism through intracellular iron accumulation and degeneration of dopamine neurons (pages X-Y). PMID:22310680

  8. Effects of tensor interactions in {tau} decays

    Energy Technology Data Exchange (ETDEWEB)

    Lopez Castro, G.; Godina Nava, J.J. [Departamento de Fisica, Cinvestav del IPN, Mexico DF. (MEXICO)

    1996-02-01

    Recent claims for the observation of antisymmetric weak tensor currents in {pi} and {ital K} decays are considered for the case of {tau}{r_arrow}{ital K}{pi}{nu} transitions. Assuming the existence of symmetric tensor currents, a mechanism for the direct production of the {ital K}{sub 2}{sup {asterisk}}(1430) spin-2 meson in {tau} decays is proposed. {copyright} {ital 1996 American Institute of Physics.}

  9. The winds from HL Tau

    Science.gov (United States)

    Klaassen, P. D.; Mottram, J. C.; Maud, L. T.; Juhasz, A.

    2016-01-01

    Outflowing motions, whether a wind launched from the disc, a jet launched from the protostar, or the entrained molecular outflow, appear to be a ubiquitous feature of star formation. These outwards motions have a number of root causes, and how they manifest is intricately linked to their environment as well as the process of star formation itself. Using the Atacama Large Millimeter/submillimeter Array (ALMA) Science Verification data of HL Tau, we investigate the high-velocity molecular gas being removed from the system as a result of the star formation process. We aim to place these motions in context with the optically detected jet, and the disc. With these high-resolution (∼1 arcsec) ALMA observations of CO (J=1−0), we quantify the outwards motions of the molecular gas. We find evidence for a bipolar outwards flow, with an opening angle, as measured in the redshifted lobe, starting off at 90°, and narrowing to 60° further from the disc, likely because of magnetic collimation. Its outwards velocity, corrected for inclination angle is of the order of 2.4 km s−1. PMID:27559304

  10. The Winds from HL Tau

    CERN Document Server

    Klaassen, Pamela D; Maud, Luke T; Juhasz, Attila

    2016-01-01

    Outflowing motions, whether a wind launched from the disk, a jet launched from the protostar, or the entrained molecular outflow, appear to be an ubiquitous feature of star formation. These outwards motions have a number of root causes, and how they manifest is intricately linked to their environment as well as the process of star formation itself. Using the ALMA Science Verification data of HL Tau, we investigate the high velocity molecular gas being removed from the system as a result of the star formation process. We aim to place these motions in context with the optically detected jet, and the disk. With these high resolution ($\\sim 1"$) ALMA observations of CO (J=1-0), we quantify the outwards motions of the molecular gas. We find evidence for a bipolar outwards flow, with an opening angle, as measured in the red-shifted lobe, starting off at 90$^\\circ$, and narrowing to 60$^\\circ$ further from the disk, likely because of magnetic collimation. Its outwards velocity, corrected for inclination angle is of ...

  11. Tau energy scale and $\\mu \\rightarrow \\tau$ misidentification rate estimated with early 2016 data using Z events.

    CERN Document Server

    CMS Collaboration

    2016-01-01

    This note presents results of the tau energy scale ($\\tau$~ES) measured using $\\mathrm{Z\\rightarrow \\tau_{\\mu} \\tau_{h}}$, and $\\mu \\rightarrow \\tau$ misidentification rate measured using $\\mathrm{Z\\rightarrow \\mu \\mu}$. Both measurements were made with 6.3 fb$^{-1}$ of pp data at $\\mathrm{\\sqrt{s}} = 13$~TeV collected by the CMS detector in first half of 2016.

  12. Cerebrospinal Fluid Amyloid Beta and Tau Concentrations Are Not Modulated by 16 Weeks of Moderate- to High-Intensity Physical Exercise in Patients with Alzheimer Disease

    DEFF Research Database (Denmark)

    Jensen, Camilla Steen; Portelius, Erik; Siersma, Volkert

    2016-01-01

    Background: Physical exercise may have some effect on cognition in patients with Alzheimer disease (AD). However, the underlying biochemical effects are unclear. Animal studies have shown that amyloid beta (Aβ), one of the pathological hallmarks of AD, can be altered with high levels of physical...... of Life, Physical Health and Functional Ability in Alzheimer's Disease: The Effect of Physical Exercise (ADEX) study we analyzed cerebrospinal fluid samples for Aβ species, total tau (t-tau), phosphorylated tau (p-tau) and soluble amyloid precursor protein (sAPP) species. We also assessed the patients...

  13. Management and cost analysis of cancer patients treated with G-CSF: a cohort study based on the French national healthcare insurance database.

    Science.gov (United States)

    Tilleul, Patrick; Jacot, William; Emery, Corinne; Lafuma, Antoine; Gourmelen, Julie

    2017-09-04

    To describe the management and costs associated with G-CSF therapy in cancer patients in France. This study analyzed a representative random population sample from the French national healthcare insurance database, focusing on 1,612 patients with hematological or solid malignancies who were reimbursed in 2013 or 2014 for at least one G-CSF treatment dispensed in a retail pharmacy. Patient characteristics and treatment costs were analyzed according to the type of cancer. Then the costs and characteristics of patients associated with the use of different G-CSF products were analyzed in the sub-set of breast cancer patients. The most frequent malignancies in the database population were breast cancer (23.3%), hematological malignancies (22.2%), and lung cancer (12.4%). The reimbursed G-CSF was pegfilgrastim in 34.1% of cases, lenograstim in 26.7%, and filgrastim in 17.9%. More than one G-CSF product was reimbursed to 21.3% of patients. The total annual reimbursed health expenses per patient, according to the type of G-CSF, were €27,001, €24,511, and €20,802 for patients treated with filgrastim, lenograstim, and pegfilgrastim, respectively. Ambulatory care accounted for, respectively, 35%, 38%, and 41% of those costs. In patients with breast cancer, ambulatory care cost was €7,915 with filgrastim, €7,750 with lenograstim, and €6,989 with pegfilgrastim, and the respective cost of G-CSF was €1,733, €1,559, and €3,668. All available G-CSF products have been shown to be effective in cancer patients, and both daily G-CSFs and pegylated G-CSF are recommended in international guidelines. Nevertheless, this analysis of G-CSF reimbursement indicates that the choice of product can markedly affect the total cost of ambulatory care.

  14. Measurement of sigma(p(p)over-bar -> Z) center dot B(Z -> tau tau) in p(p)over-bar collisions at root s=1.96 TeV

    OpenAIRE

    Abulencia, A.; Adelman, J.; Affolder, T.; Akimoto, T.; Albrow, M. G.; Ambrose, D.; Amerio, S.; Amidei, D.; A. Anastassov; Anikeev, K.; Annovi, A.; Antos, J.; M. Aoki; Apollinari, G.; Arguin, J. F.

    2007-01-01

    We present a measurement of the inclusive production cross section for Z bosons decaying to tau leptons in p (p) over bar collisions at root s=1.96 TeV. We use a channel with one hadronically-decaying and one electronically-decaying tau. This measurement is based on 350 pb(-1) of CDF Run II data. Using a sample of 504 opposite sign e tau events with a total expected background of 190 events, we obtain sigma(p (p) ...

  15. The current G-CSF use in cancer patients with chemotherapy

    Institute of Scientific and Technical Information of China (English)

    Jing Zhang; Shiying Yu

    2014-01-01

    Objective:The purpose of the study was to survey current G-CSF use in cancer patients, investigate whether the use of granulocyte colony-stimulating factor (G-CSF) is standardized. Methods:From July 2012 to October 2012, patients in a third-grade class-A hospital were investigated by self-designed questionnaires, according to ASCO’s recommendations for white blood cellgrowth factors in 2006 and NCCN myeloid growth factors guideline in 2012. Results:Two hundred and twenty-two patients treated with 724 courses of chemotherapy were included. In prophylactic use, 259 (35.8%) cases used G-CSF that the guideline doesn’t recommend, which belonged to excessive use, the dose were 274 700 µg, accounting for 59.7%of the totle prophylactic use;105 (14.5%) didn’t use while the guideline recommend, belonging to lack of use. 89.0%of the prophylactic use were 24-72 h after chemotherapy, only a few (5.4%) on the day of chemotherapy. In therapeutic use, only 3.1%were standardized, with the dose of 23 000 µg, accounting for 7.4%of the total. So 92.6%were excessive. 14.2%of the therapeutic use were 24-72 h after chemotherapy, 21.2%on the day of chemotherapy. Conclusion:More than 50%use of G-CSF weren’t standardized, especial y the excessive use.

  16. CSF-endorphines in acute and chronic brain lesions.

    Science.gov (United States)

    Hamel, E

    1988-01-01

    In order to answer the question of an opioid influence on consciousness, a radio-immuno-assay (n = 852) of beta-endorphin and beta-LPH (beta-lipotropic hormone) in both ventricular CSF and blood plasma was carried out in 101 neurosurgical patients. The following results were obtained: I) beta-END and beta-LPH levels were found to be lower in the CSF than in blood plasma. II) beta-END and beta-LPH in the CSF was the same in both sexes. III) beta-END levels in the CSF decreased with age. IV) beta-END and beta-LPH levels showed a diurnal rhythm with a maximum in the late a. m. hours. V) beta-END levels in the ventricular CSF tend to decrease parallel to a drop in conciousness as well as with longlasting comatous states. VI) beta-END in ventricular CSF becomes higher with increasing systolic arterial blood pressure. VII) beta-END and beta-LPH levels in ventricular CSF are not correlated with the type of the disease, CSF pressure, body temperature or respiratory changes.

  17. The future of tau physics and tau-charm detector and factory design

    Energy Technology Data Exchange (ETDEWEB)

    Perl, M.L.

    1991-02-01

    Future research on the tau lepton requires large statistics, thorough investigation of systematic errors, and direct experimental knowledge of backgrounds. Only a tau-charm factory with a specially designed detector can provide all the experimental conditions to meet these requirements. This paper is a summary of three lectures delivered at the 1991 Lake Louise Winter Institute.

  18. First Observation of the Decay tau^- -> phi K^- nu_tau

    CERN Document Server

    colaboration, B

    2006-01-01

    We present the first observation of tau lepton decays to hadronic final states with a phi-meson. This analysis is based on 401 fb^-1 of data accumulated at the Belle experiment. The branching fraction obtained is B(tau- -> phi K- nu) = (4.05 +- 0.25 +- 0.26) x 10^-5.

  19. Horizontal $\\tau$ air showers from mountains in deep valley Traces of UHECR neutrino $\\tau$

    CERN Document Server

    Fargion, D; Conversano, R; Fargion, Daniele; Aiello, Andrea; Conversano, Roberto

    1999-01-01

    Ultra High Energy (UHE) Tau neutrino may lead to a very peculiar imprint in future underground $Km^3$ detectors in water and ice as well as in air: rarest secondary tau tracks and decay which may exceed the muon ones. Indeed Bremsstrahlung at high energy lead to longer tracks for heavier leptons. Radiation lenght grows nearly with the square of the lepton mass. Indeed electrons are too light and their trace in matter (liquid or rock) is negligible (tens of centimeters); muons are much better observed, while tau are too short life time and too short range to be found. However, because relativistic time expansion, UHE tau traces in matter, above $10^{17} eV$, are relativistically boosted overcoming the corresponding muon tracks, already bounded by bremsstrahlung logarithmic regime. The tau crossing for Kms in water or ice may be confused with common muon tracks; their tau decay may be misunderstood as muonic catastrophic bremsstrahlung interactions. To economize UHE tau discovery, we suggest to look the tau dec...

  20. Higgs boson measurements in $WW$, $\\tau\\tau$ and $\\mu\\mu$ channels with CMS

    CERN Document Server

    Kumar, Arun

    2017-01-01

    This note presents a search for the Standard Model (SM) Higgs boson in $WW$, $\\tau\\tau$ and $\\mu\\mu$ decay channels with proton-proton collision data collected by the CMS experiment at the LHC. The results have been derived using different amounts of luminosities for different channels.

  1. Comprehensive Soldier Fitness (CSF) Experiment: Research Biases in the Development of the CSF

    Science.gov (United States)

    2013-06-13

    and teens can compare, and ultimately be transposed through the CSF, to developing resiliency of deployed Soldiers in combat zones. These studies...added pressure of a shortened development time may contribute to unintended biases or unmitigated biases. This study will look at all of their...units. They recommended that the units designate proponents to manage the suicide prevention program, maintain vigilance by leaders and Soldier peers

  2. Stem Cell Mobilization with G-CSF versus Cyclophosphamide plus G-CSF in Mexican Children

    Directory of Open Access Journals (Sweden)

    José Eugenio Vázquez Meraz

    2016-01-01

    Full Text Available Fifty-six aphaereses were performed in 23 pediatric patients with malignant hematological and solid tumors, following three different protocols for PBPC mobilization and distributed as follows: A: seventeen mobilized with 4 g/m2 of cyclophosphamide (CFA and 10 μg/kg/day of granulocyte colony stimulating factor (G-CSF, B: nineteen with CFA + G-CSF, and C: twenty only with G-CSF when the WBC count exceeded 10 × 109/L. The average number of MNC/kg body weight (BW/aphaeresis was 0.4 × 108 (0.1–1.4, 2.25 × 108 (0.56–6.28, and 1.02 × 108 (0.34–2.5 whereas the average number of CD34+ cells/kg BW/aphaeresis was 0.18 × 106/kg (0.09–0.34, 1.04 × 106 (0.19–9.3, and 0.59 × 106 (0.17–0.87 and the count of CFU/kg BW/aphaeresis was 1.11 × 105 (0.31–2.12, 1.16 × 105 (0.64–2.97, and 1.12 × 105 (0.3–6.63 in groups A, B, and C, respectively. The collection was better in group B versus group A (p=0.007 and p=0.05, resp. and in group C versus group A (p=0.08 and p=0.05, resp.. The collection of PBPCs was more effective in the group mobilized with CFM + G-CSF when the WBC exceeded 10 × 103/μL in terms of MNC and CD34+ cells and there was no toxicity of the chemotherapy.

  3. Branching fractions of tau leptons to three charged hadrons.

    Science.gov (United States)

    Briere, R A; Chen, G P; Ferguson, T; Tatishvili, G; Vogel, H; Adam, N E; Alexander, J P; Berkelman, K; Boisvert, V; Cassel, D G; Drell, P S; Duboscq, J E; Ecklund, K M; Ehrlich, R; Galik, R S; Gibbons, L; Gittelman, B; Gray, S W; Hartill, D L; Heltsley, B K; Hsu, L; Jones, C D; Kandaswamy, J; Kreinick, D L; Magerkurth, A; Mahlke-Krüger, H; Meyer, T O; Mistry, N B; Patterson, J R; Peterson, D; Pivarski, J; Richichi, S J; Riley, D; Sadoff, A J; Schwarthoff, H; Shepherd, M R; Thayer, J G; Urner, D; Wilksen, T; Warburton, A; Weinberger, M; Athar, S B; Avery, P; Breva-Newell, L; Potlia, V; Stoeck, H; Yelton, J; Benslama, K; Eisenstein, B I; Gollin, G D; Karliner, I; Lowrey, N; Plager, C; Sedlack, C; Selen, M; Thaler, J J; Williams, J; Edwards, K W; Besson, D; Zhao, X; Anderson, S; Frolov, V V; Gong, D T; Kubota, Y; Li, S Z; Poling, R; Smith, A; Stepaniak, C J; Urheim, J; Metreveli, Z; Seth, K K; Tomaradze, A; Zweber, P; Ahmed, S; Alam, M S; Ernst, J; Jian, L; Saleem, M; Wappler, F; Arms, K; Eckhart, E; Gan, K K; Gwon, C; Honscheid, K; Hufnagel, D; Kagan, H; Kass, R; Pedlar, T K; von Toerne, E; Zoeller, M M; Severini, H; Skubic, P; Dytman, S A; Mueller, J A; Nam, S; Savinov, V; Hinson, J W; Lee, J; Miller, D H; Pavlunin, V; Sanghi, B; Shibata, E I; Shipsey, I P J; Cronin-Hennessy, D; Lyon, A L; Park, C S; Park, W; Thayer, J B; Thorndike, E H; Coan, T E; Gao, Y S; Liu, F; Maravin, Y; Stroynowski, R; Artuso, M; Boulahouache, C; Blusk, S; Bukin, K; Dambasuren, E; Mountain, R; Muramatsu, H; Nandakumar, R; Skwarnicki, T; Stone, S; Wang, J C; Mahmood, A H; Csorna, S E; Danko, I; Bonvicini, G; Cinabro, D; Dubrovin, M; McGee, S; Bornheim, A; Lipeles, E; Pappas, S P; Shapiro, A; Sun, W M; Weinstein, A J

    2003-05-09

    From electron-positron collision data collected with the CLEO detector operating at Cornell Electron Storage Ring near sqrt[s]=10.6 GeV, improved measurements of the branching fractions for tau decays into three explicitly identified hadrons and a neutrino are presented as B(tau(-)-->pi(-)pi(+)pi(-)nu(tau))=(9.13+/-0.05+/-0.46)%, B(tau(-)-->K-pi(+)pi(-)nu(tau))=(3.84+/-0.14+/-0.38) x 10(-3), B(tau(-)-->K-K+pi(-)nu(tau))=(1.55+/-0.06+/-0.09) x 10(-3), and B(tau(-)-->K-K+K-nu(tau))<3.7 x 10(-5) at 90% C.L., where the uncertainties are statistical and systematic, respectively.

  4. Simulated cytoskeletal collapse via tau degradation.

    Directory of Open Access Journals (Sweden)

    Austin Sendek

    Full Text Available We present a coarse-grained two dimensional mechanical model for the microtubule-tau bundles in neuronal axons in which we remove taus, as can happen in various neurodegenerative conditions such as Alzheimers disease, tauopathies, and chronic traumatic encephalopathy. Our simplified model includes (i taus modeled as entropic springs between microtubules, (ii removal of taus from the bundles due to phosphorylation, and (iii a possible depletion force between microtubules due to these dissociated phosphorylated taus. We equilibrate upon tau removal using steepest descent relaxation. In the absence of the depletion force, the transverse rigidity to radial compression of the bundles falls to zero at about 60% tau occupancy, in agreement with standard percolation theory results. However, with the attractive depletion force, spring removal leads to a first order collapse of the bundles over a wide range of tau occupancies for physiologically realizable conditions. While our simplest calculations assume a constant concentration of microtubule intercalants to mediate the depletion force, including a dependence that is linear in the detached taus yields the same collapse. Applying percolation theory to removal of taus at microtubule tips, which are likely to be the protective sites against dynamic instability, we argue that the microtubule instability can only obtain at low tau occupancy, from 0.06-0.30 depending upon the tau coordination at the microtubule tips. Hence, the collapse we discover is likely to be more robust over a wide range of tau occupancies than the dynamic instability. We suggest in vitro tests of our predicted collapse.

  5. EXPRESSION OF RHGM-CSF GENE IN EUKARYOCYTE BY LIPOFECTION

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    objective: To recombinant the nearly natural humangranulocyte-macrophage-colony stimulating factor (GM-CSF) for supplying more safe and steady expressed cytokine in clinic. Method: The eukaryotic recombinant pcDNA3.1-GM-CSF plasmid which was controlled by the CMV promoter was transferred into CHO cell by lipofectamine, selected by G418 and the positive clones was got. The recombinant vector which was rejoined into the groups of DNA of CHO was identified by PCR. Results: The results showed that the protein of rhGM-CSF was about 28 KD by using ELISA, SDS-PAGE and Western blot. Conclusion: rhGM-CSF was expressed steadily and highly. The rhGM-CSF will be of more use value.

  6. Selective tau tyrosine nitration in non-AD tauopathies

    Science.gov (United States)

    Geula, Changiz; Vana, Laurel; Binder, Lester I.

    2012-01-01

    Previously, we reported the characterization of two novel antibodies that react with tau nitrated at tyrosine 197 (Tau-nY197) and tyrosine 394 (Tau-nY394) in Alzheimer’s disease (AD). In this report, we examined whether tau nitration at these sites also occurs in corticobasal degeneration (CBD), progressive supranuclear palsy (PSP) and Pick’s disease (PiD), three neurodegenerative tauopathies that contain abundant tau deposits within glial and neuronal cell types but lack amyloid deposition. The reactivity of these antibodies was also compared to two previously characterized antibodies Tau-nY18 and Tau-nY29, specific for tau nitrated at tyrosine 18 and tyrosine 29, respectively. In the present experiments, Tau-nY18 did not label the classical pathological lesions of CBD or PSP but did label the neuronal lesions associated with PiD to a limited extent. In contrast, Tau-nY29 revealed some, but not all classes of tau inclusions associated with both CBD and PSP but did label numerous Pick body inclusions in PiD. Tau-nY197 was restricted to the neuropil threads in both CBD and PSP; however, similar to Tau-nY29, extensive Pick body pathology was clearly labeled. Tau-nY394 did not detect any of the lesions associated with these disorders. In contrast, extensive neuronal and glial tau pathology within these diseases was labeled by Tau-Y197, a monoclonal antibody that reacts within the Y-197-containing proline-rich region of the molecule. Based on our Western and IHC experiments, it appears that nitration of tau at tyrosine 29 is a pathological modification that might be associated with neurodegeneration. Collectively, our data suggest that site-specific tau tyrosine nitration events occur in a disease and lesion-specific manner, indicating that nitration appears to be a highly controlled modification in AD and non-AD tauopathies. PMID:22057784

  7. Low CSF oxytocin reflects high intent in suicide attempters.

    Science.gov (United States)

    Jokinen, Jussi; Chatzittofis, Andreas; Hellström, Christer; Nordström, Peter; Uvnäs-Moberg, Kerstin; Asberg, Marie

    2012-04-01

    Data from animal studies suggest that oxytocin is an important modulating neuropeptide in regulation of social interaction. One human study has reported a negative correlation between CSF oxytocin levels, life history of aggression and suicidal behaviour. We hypothesized that CSF oxytocin levels would be related to suicidal behaviour, suicide intent, lifetime interpersonal violence and suicide risk. 28 medication free suicide attempters and 19 healthy volunteers participated in this cross sectional and longitudinal study. CSF and plasma morning basal levels of oxytocin were assessed with specific radio-immunoassays. The Beck Suicide Intent Scale (SIS), the Freeman scale and the Karolinska Interpersonal Violence Scale (KIVS) were used to assess suicide intent and lifetime violent behaviour. All patients were followed up for cause of death. The mean follow-up was 21 years. Suicide attempters had lower CSF oxytocin levels compared to healthy volunteers p=0.077. In suicide attempters CSF oxytocin showed a significant negative correlation with the planning subscale of SIS. CSF oxytocin showed a significant negative correlation with suicide intent, the planning subscale of SIS and Freeman interruption probability in male suicide attempters. Correlations between plasma oxytocin levels and the planning subscale of SIS and Freeman interruption probability were significant in male suicide attempters. Lifetime violent behaviour showed a trend to negative correlation with CSF oxytocin. In the regression analysis suicide intent remained a significant predictor of CSF oxytocin corrected for age and gender whereas lifetime violent behaviour showed a trend to be a predictor of CSF oxytocin. Oxytocin levels did not differ significantly in suicide victims compared to survivors. CSF oxytocin may be an important modulator of suicide intent and interpersonal violence in suicide attempters.

  8. Parallel variation of ventricular CSF tryptophan and free serum tryptophan in man.

    Science.gov (United States)

    Young, S N; Lal, S; Feldmuller, F; Sourkes, T L; Ford, R M; Kiely, M; Martin, J B

    1976-01-01

    Tryptophan was measured in the ventricular CSE and serum and the neutral amino acids leucine, isoleucine, valine, phenylalanine, and tyrosine were measured in the serum of two cases with ventricular drains. Samples were taken every two hours for 24 hours in one case and for 16 hours in the other. The CSF tryptophan was correlated significantly with the free--that is, non-albumin-bound--serum tryptophan but not with the total serum tryptophan. CSF tryptophan was not correlated significantly with the ratio of free serum tryptophan to the sum of the neutral amino acids. These data suggest that, in man, brain tryptophan concentrations are influenced by the free and not the total serum tryptophan and that physiological variations of the neutral amino acids do not appreciably influence the concentration of brain trytophan.

  9. CSF concentrations of cAMP and cGMP are lower in patients with Creutzfeldt-Jakob disease but not Parkinson's disease and amyotrophic lateral sclerosis.

    Directory of Open Access Journals (Sweden)

    Patrick Oeckl

    Full Text Available BACKGROUND: The cyclic nucleotides cyclic adenosine-3',5'-monophosphate (cAMP and cyclic guanosine-3',5'-monophosphate (cGMP are important second messengers and are potential biomarkers for Parkinson's disease (PD, amyotrophic lateral sclerosis (ALS and Creutzfeldt-Jakob disease (CJD. METHODOLOGY/PRINCIPAL FINDINGS: Here, we investigated by liquid chromatography/tandem mass spectrometry (LC-MS/MS the cerebrospinal fluid (CSF concentrations of cAMP and cGMP of 82 patients and evaluated their diagnostic potency as biomarkers. For comparison with a well-accepted biomarker, we measured tau concentrations in CSF of CJD and control patients. CJD patients (n = 15 had lower cAMP (-70% and cGMP (-55% concentrations in CSF compared with controls (n = 11. There was no difference in PD, PD dementia (PDD and ALS cases. Receiver operating characteristic (ROC curve analyses confirmed cAMP and cGMP as valuable diagnostic markers for CJD indicated by the area under the curve (AUC of 0.86 (cAMP and 0.85 (cGMP. We calculated a sensitivity of 100% and specificity of 64% for cAMP and a sensitivity of 67% and specificity of 100% for cGMP. The combination of both nucleotides increased the sensitivity to 80% and specificity to 91% for the term cAMPxcGMP (AUC 0.92 and to 93% and 100% for the ratio tau/cAMP (AUC 0.99. CONCLUSIONS/SIGNIFICANCE: We conclude that the CSF determination of cAMP and cGMP may easily be included in the diagnosis of CJD and could be helpful in monitoring disease progression as well as in therapy control.

  10. Fat Hoffman graphs with smallest eigenvalue at least $-1-\\tau$

    CERN Document Server

    Munemasa, Akihiro; Taniguchi, Tetsuji

    2011-01-01

    In this paper, we show that all fat Hoffman graphs with smallest eigenvalue at least -1-\\tau, where \\tau is the golden ratio, can be described by a finite set of fat (-1-\\tau)-irreducible Hoffman graphs. In the terminology of Woo and Neumaier, we mean that every fat Hoffman graph with smallest eigenvalue at least -1-\\tau is an H-line graph, where H is the set of isomorphism classes of maximal fat (-1-\\tau)-irreducible Hoffman graphs. It turns out that there are 37 fat (-1-\\tau)-irreducible Hoffman graphs, up to isomorphism.

  11. Amplification of Tau fibrils from minute quantities of seeds.

    Science.gov (United States)

    Meyer, Virginia; Dinkel, Paul D; Rickman Hager, Emily; Margittai, Martin

    2014-09-16

    The propagation of Tau pathology in Alzheimer's disease (AD) is thought to proceed through templated conversion of Tau protein into fibrils and cell-to-cell transfer of elongation-competent seeds. To investigate the efficiency of Tau conversion, we adapted the protein misfolding cyclic amplification assay used for the conversion of prions. Utilizing heparin as a cofactor and employing repetitive cycles of shearing and growth, synthetic Tau fibrils and Tau fibrils in AD brain extract are progressively amplified. Concurrently, self-nucleation is suppressed. The results highlight breakage-induced replication of Tau fibrils as a potential facilitator of disease spread.

  12. Measurement of the Lifetime of the $\\tau$ Lepton

    CERN Document Server

    Acciarri, M; Aguilar-Benítez, M; Ahlen, S P; Alpat, B; Alcaraz, J; Alemanni, G; Allaby, James V; Aloisio, A; Alverson, G; Alviggi, M G; Ambrosi, G; Anderhub, H; Andreev, V P; Angelescu, T; Anselmo, F; Antreasyan, D; Arefev, A; Azemoon, T; Aziz, T; Bagnaia, P; Baksay, L; Ball, R C; Banerjee, S; Banicz, K; Barillère, R; Barone, L; Bartalini, P; Baschirotto, A; Basile, M; Battiston, R; Bay, A; Becattini, F; Becker, U; Behner, F; Berdugo, J; Berges, P; Bertucci, B; Betev, B L; Bhattacharya, S; Biasini, M; Biland, A; Bilei, G M; Blaising, J J; Blyth, S C; Bobbink, Gerjan J; Böck, R K; Böhm, A; Borgia, B; Boucham, A; Bourilkov, D; Bourquin, Maurice; Boutigny, D; Branson, J G; Brigljevic, V; Brock, I C; Buffini, A; Buijs, A; Burger, J D; Burger, W J; Busenitz, J K; Buytenhuijs, A O; Cai, X D; Campanelli, M; Capell, M; Cara Romeo, G; Caria, M; Carlino, G; Cartacci, A M; Casaus, J; Castellini, G; Cavallari, F; Cavallo, N; Cecchi, C; Cerrada-Canales, M; Cesaroni, F; Chamizo-Llatas, M; Chan, A; Chang, Y H; Chaturvedi, U K; Chemarin, M; Chen, A; Chen, G; Chen, G M; Chen, H F; Chen, H S; Chen, M; Chiefari, G; Chien, C Y; Choi, M T; Cifarelli, Luisa; Cindolo, F; Civinini, C; Clare, I; Clare, R; Cohn, H O; Coignet, G; Colijn, A P; Colino, N; Costantini, S; Cotorobai, F; de la Cruz, B; Csilling, Akos; Dai, T S; D'Alessandro, R; De Asmundis, R; De Boeck, H; Degré, A; Deiters, K; Denes, P; De Notaristefani, F; DiBitonto, Daryl; Diemoz, M; Van Dierendonck, D N; Di Lodovico, F; Dionisi, C; Dittmar, Michael; Dominguez, A; Doria, A; Dorne, I; Dova, M T; Drago, E; Duchesneau, D; Duinker, P; Durán, I; Dutta, S; Easo, S; Efremenko, Yu V; El-Mamouni, H; Engler, A; Eppling, F J; Erné, F C; Ernenwein, J P; Extermann, Pierre; Fabre, M; Faccini, R; Falciano, S; Favara, A; Fay, J; Fedin, O; Felcini, Marta; Fenyi, B; Ferguson, T; Fernández, D; Ferroni, F; Fesefeldt, H S; Fiandrini, E; Field, J H; Filthaut, Frank; Fisher, P H; Forconi, G; Fredj, L; Freudenreich, Klaus; Furetta, C; Galaktionov, Yu; Ganguli, S N; García-Abia, P; Gau, S S; Gentile, S; Gerald, J; Gheordanescu, N; Giagu, S; Goldfarb, S; Goldstein, J; Gong, Z F; Gougas, Andreas; Gratta, Giorgio; Grünewald, M W; Gupta, V K; Gurtu, A; Gutay, L J; Hangarter, K; Hartmann, B; Hasan, A; Hatzifotiadou, D; Hebbeker, T; Hervé, A; Van Hoek, W C; Hofer, H; Hoorani, H; Hou, S R; Hu, G; Innocente, Vincenzo; Janssen, H; Jin, B N; Jones, L W; de Jong, P; Josa-Mutuberria, I; Kasser, A; Khan, R A; Kamyshkov, Yu A; Kapinos, P; Kapustinsky, J S; Karyotakis, Yu; Kaur, M; Kienzle-Focacci, M N; Kim, D; Kim, J K; Kim, S C; Kim, Y G; Kinnison, W W; Kirkby, A; Kirkby, D; Kirkby, Jasper; Kiss, D; Kittel, E W; Klimentov, A; König, A C; Korolko, I; Koutsenko, V F; Krämer, R W; Krenz, W; Kuijten, H; Kunin, A; Ladrón de Guevara, P; Landi, G; Lapoint, C; Lassila-Perini, K M; Laurikainen, P; Lebeau, M; Lebedev, A; Lebrun, P; Lecomte, P; Lecoq, P; Le Coultre, P; Lee Jae Sik; Lee, K Y; Leggett, C; Le Goff, J M; Leiste, R; Leonardi, E; Levchenko, P M; Li Chuan; Lieb, E H; Lin, W T; Linde, Frank L; Lista, L; Liu, Z A; Lohmann, W; Longo, E; Lu, W; Lü, Y S; Lübelsmeyer, K; Luci, C; Luckey, D; Luminari, L; Lustermann, W; Ma Wen Gan; Maity, M; Majumder, G; Malgeri, L; Malinin, A; Maña, C; Mangla, S; Marchesini, P A; Marin, A; Martin, J P; Marzano, F; Massaro, G G G; McNally, D; Mele, S; Merola, L; Meschini, M; Metzger, W J; Von der Mey, M; Mi, Y; Mihul, A; Van Mil, A J W; Mirabelli, G; Mnich, J; Molnár, P; Monteleoni, B; Moore, R; Morganti, S; Moulik, T; Mount, R; Müller, S; Muheim, F; Nagy, E; Nahn, S; Napolitano, M; Nessi-Tedaldi, F; Newman, H; Nippe, A; Nowak, H; Organtini, G; Ostonen, R; Pandoulas, D; Paoletti, S; Paolucci, P; Park, H K; Pascale, G; Passaleva, G; Patricelli, S; Paul, T; Pauluzzi, M; Paus, C; Pauss, Felicitas; Peach, D; Pei, Y J; Pensotti, S; Perret-Gallix, D; Petrak, S; Pevsner, A; Piccolo, D; Pieri, M; Pinto, J C; Piroué, P A; Pistolesi, E; Plyaskin, V; Pohl, M; Pozhidaev, V; Postema, H; Produit, N; Prokofev, D; Prokofiev, D O; Rahal-Callot, G; Rancoita, P G; Rattaggi, M; Raven, G; Razis, P A; Read, K; Ren, D; Rescigno, M; Reucroft, S; Van Rhee, T; Riemann, S; Riemers, B C; Riles, K; Rind, O; Ro, S; Robohm, A; Rodin, J; Rodríguez-Calonge, F J; Roe, B P; Röhner, S; Romero, L; Rosier-Lees, S; Rosselet, P; Van Rossum, W; Roth, S; Rubio, Juan Antonio; Rykaczewski, H; Salicio, J; Sánchez, E; Santocchia, A; Sarakinos, M E; Sarkar, S; Sassowsky, M; Sauvage, G; Schäfer, C; Shchegelskii, V; Schmidt-Kärst, S; Schmitz, D; Schmitz, P; Schneegans, M; Schöneich, B; Scholz, N; Schopper, Herwig Franz; Schotanus, D J; Schwenke, J; Schwering, G; Sciacca, C; Sciarrino, D; Sens, Johannes C; Servoli, L; Shevchenko, S; Shivarov, N; Shoutko, V; Shukla, J; Shumilov, E; Shvorob, A V; Siedenburg, T; Son, D; Sopczak, André; Soulimov, V; Smith, B; Spillantini, P; Steuer, M; Stickland, D P; Stone, H; Stoyanov, B; Strässner, A; Strauch, K; Sudhakar, K; Sultanov, G G; Sun, L Z; Susinno, G F; Suter, H; Swain, J D; Tang, X W; Tauscher, Ludwig; Taylor, L; Ting, Samuel C C; Ting, S M; Tonisch, F; Tonutti, M; Tonwar, S C; Tóth, J; Tully, C; Tuchscherer, H; Tung, K L; Ulbricht, J; Uwer, U; Valente, E; Van de Walle, R T; Vesztergombi, G; Vetlitskii, I; Viertel, Gert M; Vivargent, M; Völkert, R; Vogel, H; Vogt, H; Vorobev, I; Vorobyov, A A; Vorvolakos, A; Wadhwa, M; Wallraff, W; Wang, J C; Wang, X L; Wang, Z M; Weber, A; Wittgenstein, F; Wu, S X; Wynhoff, S; Xu, J; Xu, Z Z; Yang, B Z; Yang, C G; Yao, X Y; Ye, J B; Yeh, S C; You, J M; Zalite, A; Zalite, Yu; Zemp, P; Zeng, Y; Zhang, Z; Zhang, Z P; Zhou, B; Zhou, Y; Zhu, G Y; Zhu, R Y; Zichichi, Antonino

    1996-01-01

    The lifetime of the tau lepton is measured using data collected in 1994 by the L3 detector at LEP. The precise track position information of the Silicon Microvertex Detector is exploited. The tau lepton lifetime is determined from the signed impact parameter distribution for 30 322 tau decays into one charged particle and from the decay length distribution for 3891 tau decays into three charged particles. Combining the two methods we obtain $\\tau_{\\tau}$ = 290.1 $\\pm$ 4.0 fs.

  13. Mitochondrial oxidative stress causes hyperphosphorylation of tau.

    Science.gov (United States)

    Melov, Simon; Adlard, Paul A; Morten, Karl; Johnson, Felicity; Golden, Tamara R; Hinerfeld, Doug; Schilling, Birgit; Mavros, Christine; Masters, Colin L; Volitakis, Irene; Li, Qiao-Xin; Laughton, Katrina; Hubbard, Alan; Cherny, Robert A; Gibson, Brad; Bush, Ashley I

    2007-06-20

    Age-related neurodegenerative disease has been mechanistically linked with mitochondrial dysfunction via damage from reactive oxygen species produced within the cell. We determined whether increased mitochondrial oxidative stress could modulate or regulate two of the key neurochemical hallmarks of Alzheimer's disease (AD): tau phosphorylation, and beta-amyloid deposition. Mice lacking superoxide dismutase 2 (SOD2) die within the first week of life, and develop a complex heterogeneous phenotype arising from mitochondrial dysfunction and oxidative stress. Treatment of these mice with catalytic antioxidants increases their lifespan and rescues the peripheral phenotypes, while uncovering central nervous system pathology. We examined sod2 null mice differentially treated with high and low doses of a catalytic antioxidant and observed striking elevations in the levels of tau phosphorylation (at Ser-396 and other phospho-epitopes of tau) in the low-dose antioxidant treated mice at AD-associated residues. This hyperphosphorylation of tau was prevented with an increased dose of the antioxidant, previously reported to be sufficient to prevent neuropathology. We then genetically combined a well-characterized mouse model of AD (Tg2576) with heterozygous sod2 knockout mice to study the interactions between mitochondrial oxidative stress and cerebral Ass load. We found that mitochondrial SOD2 deficiency exacerbates amyloid burden and significantly reduces metal levels in the brain, while increasing levels of Ser-396 phosphorylated tau. These findings mechanistically link mitochondrial oxidative stress with the pathological features of AD.

  14. Mitochondrial oxidative stress causes hyperphosphorylation of tau.

    Directory of Open Access Journals (Sweden)

    Simon Melov

    Full Text Available Age-related neurodegenerative disease has been mechanistically linked with mitochondrial dysfunction via damage from reactive oxygen species produced within the cell. We determined whether increased mitochondrial oxidative stress could modulate or regulate two of the key neurochemical hallmarks of Alzheimer's disease (AD: tau phosphorylation, and beta-amyloid deposition. Mice lacking superoxide dismutase 2 (SOD2 die within the first week of life, and develop a complex heterogeneous phenotype arising from mitochondrial dysfunction and oxidative stress. Treatment of these mice with catalytic antioxidants increases their lifespan and rescues the peripheral phenotypes, while uncovering central nervous system pathology. We examined sod2 null mice differentially treated with high and low doses of a catalytic antioxidant and observed striking elevations in the levels of tau phosphorylation (at Ser-396 and other phospho-epitopes of tau in the low-dose antioxidant treated mice at AD-associated residues. This hyperphosphorylation of tau was prevented with an increased dose of the antioxidant, previously reported to be sufficient to prevent neuropathology. We then genetically combined a well-characterized mouse model of AD (Tg2576 with heterozygous sod2 knockout mice to study the interactions between mitochondrial oxidative stress and cerebral Ass load. We found that mitochondrial SOD2 deficiency exacerbates amyloid burden and significantly reduces metal levels in the brain, while increasing levels of Ser-396 phosphorylated tau. These findings mechanistically link mitochondrial oxidative stress with the pathological features of AD.

  15. Study of $\\tau \\to KS \\pi - \

    CERN Document Server

    Epifanov, D A; Aihara, H; Arinstein, K; Aulchenko, V; Aushev, T; Bakich, A M; Balagura, V; Barberio, E; Bedny, I; Belous, K S; Bitenc, U; Bizjak, I; Bondar, A; Bozek, A; Bracko, M; Browder, T E; Chao, Y; Chen, A; Chen, K F; Chen, W T; Cheon, B G; Chiang, C C; Chistov, R; Cho, I S; Choi, Y; Choi, Y K; Dalseno, J; Dash, M; Drutskoy, A; Eidelman, S; Gokhroo, G; Golob, B; Ha, H; Haba, J; Hayasaka, K; Hayashii, H; Hazumi, M; Heffernan, D; Hokuue, T; Hoshi, Y; Hou, W S; Hsiung, Y B; Hyun, H J; Iijima, T; Ikado, K; Inami, K; Ishikawa, A; Itoh, R; Iwasaki, M; Iwasaki, Y; Kah, D H; Kaji, H; Kang, J H; Kawai, H; Kawasaki, T; Kichimi, H; Kim, H O; Kim, S K; Kim, Y J; Krizan, P; Krokovnyi, P P; Kumar, R; Kuo, C C; Kuzmin, A; Kwon, Y J; Lee, J S; Lee, M J; Lee, S E; Lesiak, T; Li, J; Limosani, A; Lin, S W; Liu, Y; Liventsev, D; Mandl, F; Marlow, D; Matsumoto, T; Matyja, A; McOnie, S; Medvedeva, T; Miyata, H; Miyazaki, Y; Mizuk, R; Moloney, G R; Mori, T; Nakano, E; Nakao, M; Nakazawa, H; Natkaniec, Z; Nishida, S; Nitoh, O; Ogawa, S; Ohshima, T; Onuki, Y; Ostrowicz, W; Ozaki, H; Pakhlov, P; Pakhlova, G; Palka, H; Park, C W; Park, H; Park, K S; Peak, L S; Pestotnik, R; Piilonen, L E; Poluektov, A; Sahoo, H; Sakai, Y; Schneider, O; Seidl, R; Senyo, K; Sevior, M E; Shapkin, M; Shibuya, H; Shwartz, B; Sokolov, A; Somov, A; Soni, N; Stanic, S; Staric, M; Stöck, H; Sumiyoshi, T; Takasaki, F; Tamai, K; Tanaka, M; Taylor, G N; Teramoto, Y; Tian, X C; Tikhomirov, I; Tsuboyama, T; Uehara, S; Ueno, K; Uglov, T; Unno, Y; Uno, S; Urquijo, P; Usov, Yu; Varner, G; Vervink, K; Villa, S; Vinokurova, A; Wang, C H; Wang, P; Watanabe, Y; Wedd, R; Won, E; Yabsley, B D; Yamaguchi, A; Yamashita, Y; Yamauchi, M; Yuan, C Z; Zhang, Z P; Zhilich, V; Zupanc, A

    2007-01-01

    We present a study of the decay tau- -> K_S pi- nu_tau using a 351 fb^-1 data sample collected with the Belle detector. The analysis is based on 53110 lepton-tagged signal events. The measured branching fraction B(tau- -> K_S pi- nu_tau)=(0.404 +- 0.002(stat.) +- 0.013(syst.))% is consistent with the world average value and has better accuracy. An analysis of the K_S pi- invariant mass spectrum reveals contributions from the K*(892)- as well as other states. For the first time the K*(892)- mass and width have been measured in tau decay: M(K*(892)-)=(895.47 +- 0.20(stat.) +- 0.44(syst.) +- 0.59(mod.)) MeV/c2, Gamma(K*(892)-)=(46.2 +- 0.6(stat.) +- 1.0(syst.) +- 0.7(mod.)) MeV. The K*(892)- mass is significantly different from the current world average value.

  16. Resolved Multifrequency Radio Observations of GG Tau

    CERN Document Server

    Andrews, Sean M; Isella, Andrea; Birnstiel, Tilman; Rosenfeld, Katherine A; Wilner, David J; Perez, Laura M; Ricci, Luca; Carpenter, John M; Calvet, Nuria; Corder, Stuartt A; Deller, Adam T; Dullemond, Cornelis P; Greaves, Jane S; Harris, Robert J; Henning, Thomas; Kwon, Woojin; Lazio, Joseph; Linz, Hendrik; Mundy, Lee G; Sargent, Anneila I; Storm, Shaye; Testi, Leonardo

    2014-01-01

    We present sub-arcsecond resolution observations of continuum emission associated with the GG Tau quadruple star system at wavelengths of 1.3, 2.8, 7.3, and 50 mm. These data confirm that the GG Tau A binary is encircled by a circumbinary ring at a radius of 235 AU with a FWHM width of ~60 AU. We find no clear evidence for a radial gradient in the spectral shape of the ring, suggesting that the particle size distribution is spatially homogeneous on angular scales of ~0.1". A central point source, likely associated with the primary component (GG Tau Aa), exhibits a composite spectrum from dust and free-free emission. Faint emission at 7.3 mm is observed toward the low-mass star GG Tau Ba, although its origin remains uncertain. Using these measurements of the resolved, multifrequency emission structure of the GG Tau A system, models of the far-infrared to radio spectrum are developed to place constraints on the grain size distribution and dust mass in the circumbinary ring. The non-negligible curvature present ...

  17. A measurement of the $\\tau^{-} \\to \\mu^{-} \

    CERN Document Server

    Abbiendi, G; Åkesson, P F; Alexander, G; Allison, J; Amaral, P; Anagnostou, G; Anderson, K J; Arcelli, S; Asai, S; Axen, D A; Azuelos, Georges; Bailey, I; Barberio, E; Barlow, R J; Batley, J Richard; Bechtle, P; Behnke, T; Bell, K W; Bell, P J; Bella, G; Bellerive, A; Benelli, G; Bethke, Siegfried; Biebel, O; Bloodworth, Ian J; Boeriu, O; Bock, P; Bonacorsi, D; Boutemeur, M; Braibant, S; Brigliadori, L; Brown, R M; Büsser, K; Burckhart, H J; Campana, S; Carnegie, R K; Caron, B; Carter, A A; Carter, J R; Chang, C Y; Charlton, D G; Csilling, Akos; Cuffiani, M; Dado, S; Dallison, S; de Roeck, A; De Wolf, E A; Desch, Klaus; Dienes, B; Donkers, M; Dubbert, J; Duchovni, E; Duckeck, G; Duerdoth, I P; Elfgren, E; Etzion, E; Fabbri, Franco Luigi; Feld, L; Ferrari, P; Fiedler, F; Fleck, I; Ford, M; Frey, A; Fürtjes, A; Gagnon, P; Gary, J W; Gaycken, G; Geich-Gimbel, C; Giacomelli, G; Giacomelli, P; Giunta, M; Goldberg, J; Gross, E; Grunhaus, Jacob; Gruwé, M; Günther, P O; Sen-Gupta, A; Hajdu, C; Hamann, M; Hanson, G G; Harder, K; Harel, A; Harin-Dirac, M; Hauschild, M; Hauschildt, J; Hawkes, C M; Hawkings, R; Hemingway, Richard J; Hensel, C; Herten, G; Heuer, R D; Hill, J C; Hoffman, K; Homer, R J; Horváth, D; Howard, R; Igo-Kemenes, P; Ishii, K; Jeremie, H; Jovanovic, P; Junk, T R; Kanaya, N; Kanzaki, J; Karapetian, G V; Karlen, Dean A; Kartvelishvili, V G; Kawagoe, K; Kawamoto, T; Keeler, Richard K; Kellogg, R G; Kennedy, B W; Kim, D H; Klein, K; Klier, A; Kluth, S; Kobayashi, T; Kobel, M; Komamiya, S; Kormos, L L; Krämer, T; Kress, T; Krieger, P; Von Krogh, J; Krop, D; Krüger, K; Kühl, T; Kupper, M; Lafferty, G D; Landsman, Hagar Yaël; Lanske, D; Layter, J G; Leins, A; Lellouch, D; Letts, J; Levinson, L; Lillich, J; Lloyd, S L; Loebinger, F K; Lü, J; Ludwig, J; MacPherson, A; Mader, W; Marcellini, S; Marchant, T E; Martin, A J; Martin, J P; Masetti, G; Mashimo, T; Mättig, P; McDonald, W J; McKenna, J A; McMahon, T J; McPherson, R A; Meijers, F; Méndez-Lorenzo, P; Menges, W; Merritt, F S; Mes, H; Michelini, Aldo; Mihara, S; Mikenberg, G; Miller, D J; Moed, S; Mohr, W; Mori, T; Mutter, A; Nagai, K; Nakamura, I; Neal, H A; Nisius, R; O'Neale, S W; Oh, A; Okpara, A N; Oreglia, M J; Orito, S; Pahl, C; Pásztor, G; Pater, J R; Patrick, G N; Pilcher, J E; Pinfold, J L; Plane, D E; Poli, B; Polok, J; Pooth, O; Przybycien, M B; Quadt, A; Rabbertz, K; Rembser, C; Renkel, P; Rick, Hartmut; Roney, J M; Rosati, S; Rozen, Y; Runge, K; Sachs, K; Saeki, T; Sahr, O; Sarkisyan-Grinbaum, E; Schaile, A D; Schaile, O; Scharff-Hansen, P; Schieck, J; Schörner-Sadenius, T; Schröder, M; Schumacher, M; Schwick, C; Scott, W G; Seuster, R; Shears, T G; Shen, B C; Sherwood, P; Siroli, G P; Skuja, A; Smith, A M; Sobie, R J; Söldner-Rembold, S; Spanó, F; Stahl, A; Stephens, K; Strom, D; Ströhmer, R; Tarem, S; Tasevsky, M; Taylor, R J; Teuscher, R; Thomson, M A; Torrence, E; Toya, D; Tran, P; Trefzger, T M; Tricoli, A; Trigger, I; Trócsányi, Z L; Tsur, E; Turner-Watson, M F; Ueda, I; Ujvári, B; Vachon, B; Vollmer, C F; Vannerem, P; Verzocchi, M; Voss, H; Vossebeld, Joost Herman; Waller, D; Ward, C P; Ward, D R; Watkins, P M; Watson, A T; Watson, N K; Wells, P S; Wengler, T; Wermes, N; Wetterling, D; Wilson, G W; Wilson, J A; Wolf, G; Wyatt, T R; Yamashita, S; Zer-Zion, D; Zivkovic, L

    2003-01-01

    The tau /sup -/ to mu /sup -/ nu /sub mu / nu /sub tau / branching ratio has been measured using data collected from 1990 to 1995 by the OPAL detector at the LEP collider. The resulting value of B( tau /sup -/ to mu /sup -/ nu /sub mu / nu /sub tau /) = 0.1734 +or- 0.0009 (stat) +or- 0.0006(syst) has been used in conjunction with other OPAL measurements to test lepton universality, yielding the coupling constant ratios g/sub mu //g/sub e/ = 1.0005 +or- 0.0044 and g/sub tau //g/sub e/ = 1.0031 +or- 0.0048, in good agreement with the Standard Model prediction of unity. A value for the Michel parameter eta = 0.004 +or- 0.037 has also been determined and used to find a limit for the mass of the charged Higgs boson, m/sub H/+or- > 1.28 tan beta , in the minimal supersymmetric standard model. (23 refs).CER 4095216 BASE L 13

  18. Measurement of Tau Polarisation in $Z/\\gamma^{*}\\rightarrow\\tau\\tau$ Decays in Proton-Proton Collisions at $\\sqrt{s}=8$ TeV with the ATLAS Detector

    CERN Document Server

    The ATLAS collaboration

    2017-01-01

    This note presents a measurement of the polarisation of $\\tau$ leptons produced in $Z/\\gamma^{*}\\rightarrow\\tau\\tau$ decays which is performed with a dataset of proton-proton collisions at $\\sqrt{s}=8$ TeV corresponding to an integrated luminosity of 20.2 fb$^{-1}$ recorded with the ATLAS detector at the LHC in 2012. The $Z/\\gamma^{*}\\rightarrow\\tau\\tau$ decays are reconstructed from a hadronically decaying $\\tau$ lepton ($\\tau \\rightarrow \\text{hadrons + } \

  19. Adenosine deaminase in CSF and pleural fluid for diagnosis of tubercular meningitis and pulmonary tuberculosis.

    Science.gov (United States)

    Nepal, A K; Gyawali, N; Poudel, B; Mahato, R V; Lamsal, M; Gurung, R; Baral, N; Majhi, S

    2012-12-01

    Tuberculosis (TB) is one of the most common infectious diseases in developing countries including Nepal. Delay in diagnosis and treatment of tuberculosis results in poor prognosis of the disease. This study was conducted to estimate diagnostic cut off values of Adenosine Deaminase (ADA) in cerebrospinal fluid (CSF) and pleural fluid and to evaluate the sensitivity, specificity, positive and negative predictive values ofADA in pleural fluid and CSF from patients with tuberculous and non-tuberculous disease. A total of 98 body fluid (CSF: 24, Pleural fluid: 74) specimens were received for the estimation of ADA. ADA activity was measured at 37 degrees C by spectrophotometric method of Guisti and Galanti, 1984 at 625nm wavelength. Among the patients enrolled for the study subjects for which CSF were received (n = 24) included 8 tuberculous meningitis (TBM), and 16 non-tubercular meningitis (NTM). Pleural fluid samples (n = 74) were received from 19 pulmonary TB with pleural effusion, 17 PTB without pleural effusion and 37 of non-tuberculous disease patients. CSF ADA activity were (11. 1 +/- 2.03 IU/L) and (5.3 +/- +1.89 IU/L) (p <00001) in TM and non-NTM groups and Pleural fluid ADA activity were (10 +/- 22.18 IU/L) and (23.79 +/- 11.62 IU/L) (p < 0.001) in PTB and non-TB groups respectively. ADA test in body fluids, which is simple, cost-effective and sensitive, specific for the tubercular disease is recommended to perform before forwarding the cumbersome and expensive procedures like culture and PCR for TB diagnosis.

  20. Untargeted 1H-NMR metabolomics in CSF: toward a diagnostic biomarker for motor neuron disease.

    Science.gov (United States)

    Blasco, Hélène; Nadal-Desbarats, Lydie; Pradat, Pierre-François; Gordon, Paul H; Antar, Catherine; Veyrat-Durebex, Charlotte; Moreau, Caroline; Devos, David; Mavel, Sylvie; Emond, Patrick; Andres, Christian R; Corcia, Philippe

    2014-04-01

    To develop a CSF metabolomics signature for motor neuron disease (MND) using (1)H-NMR spectroscopy and to evaluate the predictive value of the profile in a separate cohort. We collected CSF from patients with MND and controls and analyzed the samples using (1)H-NMR spectroscopy. We divided the total patient sample in a 4:1 ratio into a training cohort and a test cohort. First, a metabolomics signature was created by statistical modeling in the training cohort, and then the analyses tested the predictive value of the signature in the test cohort. We conducted 10 independent trials for each step. Finally, we identified the compounds that contributed most consistently to the metabolome profile. Analysis of CSF from 95 patients and 86 controls identified a diagnostic profile for MND (R(2)X > 22%, R(2)Y > 93%, Q(2) > 66%). The best model selected the correct diagnosis with mean probability of 99.31% in the training cohort. The profile discriminated between diagnostic groups with 78.9% sensitivity and 76.5% specificity in the test cohort. Metabolites linked to pathophysiologic pathways in MND (i.e., threonine, histidine, and molecules related to the metabolism of branched amino acids) were among the discriminant compounds. CSF metabolomics using (1)H-NMR spectroscopy can detect a reproducible metabolic signature for MND with reasonable performance. To our knowledge, this is the first metabolomics study that shows that a validation in separate cohorts is feasible. These data should be considered in future biomarker studies. This study provides Class III evidence that CSF metabolomics accurately distinguishes MNDs from other neurologic diseases.

  1. Tau pathology spread in PS19 tau transgenic mice following locus coeruleus (LC) injections of synthetic tau fibrils is determined by the LC's afferent and efferent connections.

    Science.gov (United States)

    Iba, Michiyo; McBride, Jennifer D; Guo, Jing L; Zhang, Bin; Trojanowski, John Q; Lee, Virginia M-Y

    2015-09-01

    Filamentous tau inclusions are hallmarks of Alzheimer's disease (AD) and other neurodegenerative tauopathies. An increasing number of studies implicate the cell-to-cell propagation of tau pathology in the progression of tauopathies. We recently showed (Iba et al., J Neurosci 33:1024-1037, 2013) that inoculation of preformed synthetic tau fibrils (tau PFFs) into the hippocampus of young transgenic (Tg) mice (PS19) overexpressing human P301S mutant tau induced robust tau pathology in anatomically connected brain regions including the locus coeruleus (LC). Since Braak and colleagues hypothesized that the LC is the first brain structure to develop tau lesions and since LC has widespread connections throughout the CNS, LC neurons could be the critical initiators of the stereotypical spreading of tau pathology through connectome-dependent transmission of pathological tau in AD. Here, we report that injections of tau PFFs into the LC of PS19 mice induced propagation of tau pathology to major afferents and efferents of the LC. Notably, tau pathology propagated along LC efferent projections was localized not only to axon terminals but also to neuronal perikarya, suggesting transneuronal transfer of templated tau pathology to neurons receiving LC projections. Further, brainstem neurons giving rise to major LC afferents also developed perikaryal tau pathology. Surprisingly, while tangle-bearing neurons degenerated in the LC ipsilateral to the injection site starting 6 months post-injection, no neuron loss was seen in the contralateral LC wherein tangle-bearing neurons gradually cleared tau pathology by 6-12 months post-injection. However, the spreading pattern of tau pathology observed in our LC-injected mice is different from that in AD brains since hippocampus and entorhinal cortex, which are affected in early stages of AD, were largely spared of tau inclusions in our model. Thus, while our study tested critical aspects of the Braak hypothesis of tau pathology spread

  2. Nerve protective effect of rhTPO and G-CSF on hypoxic ischemic brain damage in rats

    Institute of Scientific and Technical Information of China (English)

    Hong-Xia Zhou; Chun-Lai Zhang; Yue-Hong Li; Yu-Xin Zhang; Zi-Feng Wei; Xi Wang Meng Ling-Li

    2014-01-01

    Objective:To observe the protection effect of rhTPO and granulocyte colony stimulating factor (G-CSF) on brain nerve after hypoxic ischemic brain damage(HIBD) in neonatal rats, exploring new ways for the laboratory basis of treatment for hypoxic ischemic encephalopathy, and provide for possible.Methods:A total of120 newbornSD rats aging7 d were randomly divided into control group, model group,TPO group andG-CSF group, using the method of blockingleft carotid artery to establishHIBD model.The left carotid artery was only seperated rather than blocked in the control group; after modeling, saline injection, rhTPO treatment andG-CSF treatment were adopted in the model group,TPO group andG-CSF group respectively.Then10 rats of4 groups were executed atDay3,7,14 after modeling, brain tissue was extracted to observe the brain damage;Immunohistochemical method was used to observe the histopathological changes of brain tissue and changes of nest protein(nestin) expression.Results:Injured brain mass of model group,TPO group andG-CSF group were significantly higher than that of control group at corresponding time point(P<0.05).Injured brain mass ofTPO group andG-CSF group were significantly lower than that of model group(P<0.05), and with the increase of age, more significant increasing trend.AtDay3 after modeling, the expression of nestin positive cells in cerebral cortex of model group,TPO group andG-CSF group increased significantly than that of control group(P<0.05); nestin positive cells ofG-CSF group outnumberedTPO group significantly (P<0.05).Conclusions:The earlyTPO,G-CSF treatment ofHIBD rats can improve brain function after hypoxia ischemia by neural protection.G-CSF can promote the differentiation of neural cells proliferation, and reduce degeneration and necrosis of nerve cells.

  3. Aminothienopyridazines and methylene blue affect Tau fibrillization via cysteine oxidation.

    Science.gov (United States)

    Crowe, Alex; James, Michael J; Lee, Virginia M-Y; Smith, Amos B; Trojanowski, John Q; Ballatore, Carlo; Brunden, Kurt R

    2013-04-19

    Alzheimer disease and several other neurodegenerative disorders are characterized by the accumulation of intraneuronal fibrils comprised of the protein Tau. Tau is normally a soluble protein that stabilizes microtubules, with splice isoforms that contain either three (3-R) or four (4-R) microtubule binding repeats. The formation of Tau fibrils is thought to result in neuronal damage, and inhibitors of Tau fibrillization may hold promise as therapeutic agents. The process of Tau fibrillization can be replicated in vitro, and a number of small molecules have been identified that inhibit Tau fibril formation. However, little is known about how these molecules affect Tau fibrillization. Here, we examined the mechanism by which the previously described aminothieno pyridazine (ATPZ) series of compounds inhibit Tau fibrillization. Active ATPZs were found to promote the oxidation of the two cysteine residues within 4-R Tau by a redox cycling mechanism, resulting in the formation of a disulfide-containing compact monomer that was refractory to fibrillization. Moreover, the ATPZs facilitated intermolecular disulfide formation between 3-R Tau monomers, leading to dimers that were capable of fibrillization. The ATPZs also caused cysteine oxidation in molecules unrelated to Tau. Interestingly, methylene blue, an inhibitor of Tau fibrillization under evaluation in Alzheimer disease clinical trials, caused a similar oxidation of cysteines in Tau and other molecules. These findings reveal that the ATPZs and methylene blue act by a mechanism that may affect their viability as potential therapeutic agents.

  4. Distinct temporal and anatomical distributions of amyloid-β and tau abnormalities following controlled cortical impact in transgenic mice.

    Directory of Open Access Journals (Sweden)

    Hien T Tran

    Full Text Available Traumatic brain injury (TBI is a major environmental risk factor for Alzheimer's disease. Intracellular accumulations of amyloid-β and tau proteins have been observed within hours following severe TBI in humans. Similar abnormalities have been recapitulated in young 3xTg-AD mice subjected to the controlled cortical impact model (CCI of TBI and sacrificed at 24 h and 7 days post injury. This study investigated the temporal and anatomical distributions of amyloid-β and tau abnormalities from 1 h to 24 h post injury in the same model. Intra-axonal amyloid-β accumulation in the fimbria was detected as early as 1 hour and increased monotonically over 24 hours following injury. Tau immunoreactivity in the fimbria and amygdala had a biphasic time course with peaks at 1 hour and 24 hours, while tau immunoreactivity in the contralateral CA1 rose in a delayed fashion starting at 12 hours after injury. Furthermore, rapid intra-axonal amyloid-β accumulation was similarly observed post controlled cortical injury in APP/PS1 mice, another transgenic Alzheimer's disease mouse model. Acute increases in total and phospho-tau immunoreactivity were also evident in single transgenic Tau(P301L mice subjected to controlled cortical injury. These data provide further evidence for the causal effects of moderately severe contusional TBI on acceleration of acute Alzheimer-related abnormalities and the independent relationship between amyloid-β and tau in this setting.

  5. INVENTORY OF KENYAH LEPO TAU SEGMENTAL SOUNDS

    Directory of Open Access Journals (Sweden)

    Yuni Utami Asih

    2017-05-01

    Full Text Available Studies on the phonological description of Kenyah language are very limited. Initiated by Lees, she found 24 phonemes of Lepo Tau, one of Kenyah language branches are briefly explained on her article. Listing 18 consonants and 6 vowels, this article provides a preliminary analysis of the sound system of Lepo Tau. To a certain extent, Rufinus similarly states the same number of phonemes of the language. A study by Soriente in 2003 provides some more descriptions of the phonology of Kenyah language. It states that Lepo Tau language has 23 phonemes, 17 consonants and 6 vowels. Some of the result register 18 underlying forms of consonants in KLT which are phonetically realized into 23 representations of consonant. List of vowel shows 8 representations generated from 5 underlying forms of vowel. The descriptions of their representation include the nature of their 13 distinctive features.

  6. Tau identification using multivariate techniques in ATLAS

    CERN Document Server

    O'Neil, D; The ATLAS collaboration

    2011-01-01

    Tau leptons will play an important role in the physics program at the LHC. They will be used in electroweak measurements and in detector related studies like the determination of the missing transverse energy scale, but also in searches for new phenomena like the Higgs boson or Supersymmetry. Due to the huge background from QCD processes, efficient tau identification techniques with large fake rejection are essential. Tau object appear as collimated jets with low track multiplicity and single variable criteria are not enough to efficiently separate them from jets and electrons. This can be achieved using modern multivariate techniques which make optimal use of all the information available. They are particularly useful when the discriminating variables are not independent and no single variable provides good signal and background separation. In ATLAS several advanced algorithms are applied to identify taus, in particular a projective likelihood estimator and boosted decision trees. All multivariate methods ap...

  7. Tau identification using multivariate techniques in ATLAS

    CERN Document Server

    "O'Neil, D C; The ATLAS collaboration

    2011-01-01

    Tau leptons play an important role in the physics program of the LHC. They are being used in electroweak measurements, in detector related studies and in searches for new phenomena like the Higgs boson or Supersymmetry. Tau objects appear as collimated jets with low track multiplicity. Due to the background from QCD multijet processes, efficient tau identification techniques with large fake rejection are essential. Since single variable criteria are not enough to efficiently separate them from jets and electrons, modern multivariate techniques are used. In ATLAS, several advanced algorithms are applied to identify taus, including a projective likelihood estimator and boosted decision trees. All multivariate methods applied to the ATLAS simulated data perform better than the baseline cut analysis. Their performance is shown using high energy data collected at the ATLAS experiment. The strengths and weaknesses of each technique are also discussed.

  8. Reconstructing the Hsp90/Tau Machine.

    Science.gov (United States)

    Jinwal, Umesh K; Koren, John; Dickey, Chad A

    2013-01-01

    Imbalanced protein load within cells is a critical aspect for most diseases of aging. In particular, the accumulation of proteins into neurotoxic aggregates is a common thread for a host of neurodegenerative diseases. Recent work demonstrates that age-related changes to the cellular chaperone repertoire contributes to abnormal buildup of the microtubule-associated protein tau that accumulates in a group of diseases termed tauopathies, the most common being Alzheimer's disease (AD). The Hsp90 co-chaperone repertoire has diverse effects on tau stability; some co-chaperones stabilize tau while others facilitate its clearance. We propose that each of these proteins may be novel therapeutic targets. While targeting Hsp90 directly may be deleterious at the organismal level, perhaps targeting individual co-chaperone activities will be more tolerable.

  9. Tau kinase inhibitors protect hippocampal synapses despite of insoluble tau accumulation.

    Science.gov (United States)

    Hinners, Ina; Hill, Anika; Otto, Ulrike; Michalsky, Anke; Mack, Till G A; Striggow, Frank

    2008-03-01

    A better understanding of the cellular and molecular pathomechanisms of Alzheimer's disease (AD) is a prerequisite for the development of efficient treatments. We have used a novel assay system based on virus-transduced organotypic hippocampal slice cultures that mimics important aspects of tau-driven AD pathology in a short time frame. Human tau P301L, when expressed in pyramidal neurons of hippocampal slice cultures, was increasingly phosphorylated at several disease-relevant epitopes, leading to progressive neuronal dystrophy and formation of RIPA-insoluble tau. AD-like tau hyperphosphorylation was reduced by the tau kinase inhibitors lithium and SRN-003-556, but RIPA-insoluble tau remained unaffected after treatment with any of these substances. Only SRN-003-556 was able to protect hippocampal neurons from synaptic damage that was presumably caused by a toxic soluble tau fraction. These data provide first mechanistic insights towards the functional benefits of SRN-003-556 that have been observed in vivo.

  10. The Ward ansaetze and Painleve tau function

    Energy Technology Data Exchange (ETDEWEB)

    Mo, M Y [Department of Mathematics, University of Bristol, University Walk, Bristol, BS8 ITW (United Kingdom)

    2008-10-03

    We have classified a tau function for the hypergeometric solutions of the Painleve VI equation constructed by Shah and Woodhouse (2006 J. Phys. A: Math. Gen. 39, 12265-9) through twistor methods. We have shown that the tau function is the product of a Toeplitz determinant and a power of the time variable t. In a suitable trivialization of the twistor bundle, the symbol of this Toeplitz determinant is the minus of the off-diagonal entry in the patching matrix. The method can also be applied to other solutions obtained from the Ward ansaetze.

  11. Determination of the {tau}-lepton reconstruction and identification efficiency using Z {yields} {tau}{tau} events in first data at ATLAS

    Energy Technology Data Exchange (ETDEWEB)

    Fischer, Gordon

    2011-10-15

    The Large Hadron Collider (LHC) at CERN started operation in November 2009. At the same time the ATLAS experiment started data taking. Since this time a large number of Z-bosons is produced. An important decay channel of the Z-boson is the decay into two {tau} -leptons. The large mass of the {tau}-lepton allows the decay into pions or kaons. In many models considering new physics the {tau}-lepton is an important final state. The LHC is a proton-proton collider and for that reason, the hadronic {tau}-lepton decay is difficult to distinguish from QCD multi-jet background. For the selection of hadronically decaying {tau}-leptons, reconstruction and identification algorithms were developed in order to suppress this background. In order to measure the Z-boson production cross section or possible new particles decaying into {tau}-leptons, the estimation of the {tau}-lepton reconstruction and identification efficiency is required. Furthermore, for detector calibration the Z-boson as well as the {tau}-lepton are helpful probes. In this thesis two methods are discussed which provide an estimation of {tau}-lepton reconstruction and identification efficiencies from data. The full selection of Z {yields} {tau}{tau} events including data-driven techniques for background extraction is discussed. The semi-leptonic Z {yields} {tau}{tau} channel promises a good QCD multi-jet suppression because of the selected additional lepton. For that reason also the leptonically decaying {tau}-lepton is discussed. The Z-boson production cross section can be calculated with the estimated efficiencies. (orig.)

  12. CSF cortisol in Alzheimer's disease and mild cognitive impairment.

    Science.gov (United States)

    Popp, Julius; Schaper, Karsten; Kölsch, Heike; Cvetanovska, Gabriela; Rommel, Fatima; Klingmüller, Dietrich; Dodel, Richard; Wüllner, Ullrich; Jessen, Frank

    2009-03-01

    Hypercortisolaemia occurs in Alzheimer's disease (AD) and may be involved in the AD related neurodegenerative process. In order to determine whether brain structures are exposed to high cortisol concentrations early in AD, we measured cerebrospinal fluid (CSF) cortisol in 66 subjects with AD, 33 subjects with mild cognitive impairment (MCI) and 34 control subjects. CSF cortisol concentrations were higher in AD subjects compared to controls (pcortisol in MCI subjects compared with controls suggesting that the increase of CSF cortisol is not an early event in the course of AD.

  13. CSF Ascites: Review of articles and a case presentation

    Directory of Open Access Journals (Sweden)

    R Pourkhalili

    2005-09-01

    Full Text Available Cerebrospinal fluid (CSF ascites is a rare complication after ventriculopritoneal (VP shunts. Most patients have gradual abdominal protrusion without any neurological sign or symptom of shunt malfunction. We presented a girl with posterior third ventricle glioblastoma and acute hydrocephalus who developed increasingly abdominal protrusion one month after VP shunt operation. Ascites fluid examination showed characteristic findings similar to CSF with no evidence of infection or malignant cells. Ventriculo-atrial shunt revision cured patient's ascites. Review articles of patients with CSF ascites after VP shunt were presented in details. Key words: Cerebrospinal fluid, Ascites, Ventriculopritoneal Shunt

  14. Synaptic Contacts Enhance Cell-to-Cell Tau Pathology Propagation

    Directory of Open Access Journals (Sweden)

    Sara Calafate

    2015-05-01

    Full Text Available Accumulation of insoluble Tau protein aggregates and stereotypical propagation of Tau pathology through the brain are common hallmarks of tauopathies, including Alzheimer’s disease (AD. Propagation of Tau pathology appears to occur along connected neurons, but whether synaptic contacts between neurons are facilitating propagation has not been demonstrated. Using quantitative in vitro models, we demonstrate that, in parallel to non-synaptic mechanisms, synapses, but not merely the close distance between the cells, enhance the propagation of Tau pathology between acceptor hippocampal neurons and Tau donor cells. Similarly, in an artificial neuronal network using microfluidic devices, synapses and synaptic activity are promoting neuronal Tau pathology propagation in parallel to the non-synaptic mechanisms. Our work indicates that the physical presence of synaptic contacts between neurons facilitate Tau pathology propagation. These findings can have implications for synaptic repair therapies, which may turn out to have adverse effects by promoting propagation of Tau pathology.

  15. Reconstruction and Identification of Tau Leptons in ATLAS

    CERN Document Server

    Limbach, Christian; The ATLAS collaboration

    2015-01-01

    These proceedings describe the reconstruction and identification of tau leptons in the ATLAS experiment at the LHC. Tau leptons play an important role in the measurement of Standard Model processes, in the search for new physics (Supersymmetry, heavy resonances) and in the measurement of Higgs boson properties. Hadronic tau lepton decays are reconstructed calorimeter based and separation against QCD-induced jets is done relying on shapes of energy depositions in the calorimeter as well as tracking based variables. The energy scale of tau leptons is obtained by scaling the measured momentum to the simulated one and is cross-checked in data. The tau trigger makes use of the collimated nature of tau decays and relies on a combination of objects (e.g. tau + muon) to reduce the rates and thresholds. An outlook to the improved tau reconstruction to be used in the next data-taking period of ATLAS concludes the proceedings.

  16. Study of $\\tau$ Decays to Six Pions and Neutrino

    CERN Document Server

    Anastassov, A; Eckhart, E; Gan, K K; Gwon, C; Hart, T; Honscheid, K; Hufnagel, D; Kagan, H; Kass, R; Pedlar, T K; Schwarthoff, H; Thayer, J B; Von Törne, E; Zoeller, M M; Richichi, S J; Severini, H; Skubic, P L; Undrus, A; Chen, S; Fast, J; Hinson, J W; Lee, J; Miller, D H; Shibata, E I; Shipsey, I P J; Pavlunin, V; Cronin-Hennessy, D; Lyon, A L; Thorndike, E H; Jessop, C P; Savinov, V; Coan, T E; Fadeev, V; Maravin, Y; Narsky, I; Stroynowski, R; Ye, J; Wlodek, T; Artuso, M; Ayad, R; Boulahouache, C; Bukin, K; Dambasuren, E; Karamov, S; Majumder, G; Moneti, G C; Mountain, R; Schuh, S; Skwarnicki, T; Stone, S; Viehhauser, G; Wang, J C; Wolf, A; Wu, J; Kopp, S E; Mahmood, A H; Csorna, S E; Danko, I; McLean, K W; Xu, Z; Godang, R; Bonvicini, G; Cinabro, D; Dubrovin, M; McGee, S; Zhou, G J; Lipeles, E; Pappas, S P; Schmidtler, M; Shapiro, A; Sun, W M; Weinstein, A J; Würthwein, F; Jaffe, D E; Masek, G E; Paar, H P; Potter, E M; Prell, S; Asner, D M; Eppich, A; Hill, T S; Morrison, R J; Briere, R A; Chen, G P; Ford, W T; Gritsan, A; Roy, J D; Smith, J G; Alexander, J P; Baker, R; Bebek, C; Berger, B E; Berkelman, K; Blanc, F; Boisvert, V; Cassel, David G; Drell, P S; Ecklund, K M; Ehrlich, R; Foland, A D; Gaidarev, P B; Galik, R S; Gibbons, L K; Gittelman, B; Gray, S W; Hartill, D L; Heltsley, B K; Hopman, P I; Hsu, L; Jones, C D; Kreinick, D L; Lohner, M; Magerkurth, A; Meyer, T O; Mistry, N B; Nordberg, E; Patterson, J R; Peterson, D; Riley, D; Romano, A; Thayer, J G; Urner, D; Valant-Spaight, B L; Warburton, A; Avery, P; Prescott, C; Rubiera, A I; Stöck, H; Yelton, J; Brandenburg, G; Ershov, A; Gao, Y S; Kim, D Y J; Wilson, R; Bergfeld, T; Eisenstein, B I; Ernst, J; Gladding, G E; Gollin, G D; Hans, R M; Johnson, E; Karliner, I; Marsh, M A; Palmer, M; Plager, C; Sedlack, C; Selen, M; Thaler, J J; Williams, J; Edwards, K W; Janicek, R; Patel, P M; Sadoff, A J; Ammar, R; Bean, A; Besson, D; Zhao, X; Anderson, S; Frolov, V V; Kubota, Y; Lee, S J; Mahapatra, R; O'Neill, J J; Poling, R A; Riehle, T; Smith, A; Stepaniak, C J; Urheim, J; Ahmed, S; Alam, M S; Athar, S B; Jian, L; Ling, L; Saleem, M; Timm, S; Wappler, F

    2001-01-01

    The $\\tau$ decays to six-pion final states have been studied with the CLEO detector at the Cornell Electron Storage Ring. The measured branching fractions are ${\\cal B}(\\tau^-\\to 2\\pi^-\\pi^+3\\pi^0\

  17. Synaptic Contacts Enhance Cell-to-Cell Tau Pathology Propagation.

    Science.gov (United States)

    Calafate, Sara; Buist, Arjan; Miskiewicz, Katarzyna; Vijayan, Vinoy; Daneels, Guy; de Strooper, Bart; de Wit, Joris; Verstreken, Patrik; Moechars, Diederik

    2015-05-26

    Accumulation of insoluble Tau protein aggregates and stereotypical propagation of Tau pathology through the brain are common hallmarks of tauopathies, including Alzheimer's disease (AD). Propagation of Tau pathology appears to occur along connected neurons, but whether synaptic contacts between neurons are facilitating propagation has not been demonstrated. Using quantitative in vitro models, we demonstrate that, in parallel to non-synaptic mechanisms, synapses, but not merely the close distance between the cells, enhance the propagation of Tau pathology between acceptor hippocampal neurons and Tau donor cells. Similarly, in an artificial neuronal network using microfluidic devices, synapses and synaptic activity are promoting neuronal Tau pathology propagation in parallel to the non-synaptic mechanisms. Our work indicates that the physical presence of synaptic contacts between neurons facilitate Tau pathology propagation. These findings can have implications for synaptic repair therapies, which may turn out to have adverse effects by promoting propagation of Tau pathology.

  18. A study of tau decays involving eta and omega mesons

    CERN Document Server

    Buskulic, Damir; Décamp, D; Ghez, P; Goy, C; Lees, J P; Lucotte, A; Minard, M N; Nief, J Y; Odier, P; Pietrzyk, B; Casado, M P; Chmeissani, M; Crespo, J M; Delfino, M C; Efthymiopoulos, I; Fernández, E; Fernández-Bosman, M; Carrido, L; Juste, A; Martínez, M; Orteu, S; Padilla, C; Park, I C; Pascual, A; Perlas, J A; Riu, I; Sánchez, F; Teubert, F; Colaleo, A; Creanza, D; De Palma, M; Gelao, G; Girone, M; Iaselli, Giuseppe; Maggi, G; Maggi, M; Marinelli, N; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Alemany, R; Bazarko, A O; Bonvicini, G; Bright-Thomas, P G; Cattaneo, M; Comas, P; Coyle, P; Drevermann, H; Forty, Roger W; Frank, M; Hagelberg, R; Harvey, J; Janot, P; Jost, B; Kneringer, E; Knobloch, J; Lehraus, Ivan; Lutters, G; Martin, E B; Mato, P; Minten, Adolf G; Miquel, R; Mir, L M; Moneta, L; Oest, T; Pacheco, A; Pusztaszeri, J F; Ranjard, F; Rensing, P E; Rizzo, G; Rolandi, Luigi; Schlatter, W D; Schmelling, M; Schmitt, M; Schneider, O; Tejessy, W; Tomalin, I R; Venturi, A; Wachsmuth, H W; Wagner, A; Ajaltouni, Ziad J; Barrès, A; Boyer, C; Falvard, A; Gay, P; Guicheney, C; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Podlyski, F; Proriol, J; Rosnet, P; Rossignol, J M; Fearnley, Tom; Hansen, J B; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Rensch, B; Wäänänen, A; Kyriakis, A; Markou, C; Simopoulou, Errietta; Siotis, I; Vayaki, Anna; Zachariadou, K; Blondel, A; Bonneaud, G R; Brient, J C; Bourdon, P; Rougé, A; Rumpf, M; Valassi, Andrea; Verderi, M; Videau, H L; Candlin, D J; Parsons, M I; Focardi, E; Parrini, G; Corden, M; Georgiopoulos, C H; Jaffe, D E; Antonelli, A; Bencivenni, G; Bologna, G; Bossi, F; Campana, P; Capon, G; Casper, David William; Chiarella, V; Felici, G; Laurelli, P; Mannocchi, G; Murtas, F; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Curtis, L; Dorris, S J; Halley, A W; Knowles, I G; Lynch, J G; O'Shea, V; Raine, C; Reeves, P; Scarr, J M; Smith, K; Teixeira-Dias, P; Thompson, A S; Thomson, F; Thorn, S; Turnbull, R M; Becker, U; Geweniger, C; Graefe, G; Hanke, P; Hansper, G; Hepp, V; Kluge, E E; Putzer, A; Schmidt, M; Sommer, J; Tittel, K; Werner, S; Wunsch, M; Abbaneo, D; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, Peter J; Moutoussi, A; Nash, J; Sedgbeer, J K; Stacey, A M; Williams, M D; Dissertori, G; Girtler, P; Kuhn, D; Rudolph, G; Betteridge, A P; Bowdery, C K; Colrain, P; Crawford, G; Finch, A J; Foster, F; Hughes, G; Sloan, Terence; Williams, M I; Galla, A; Giehl, I; Greene, A M; Hoffmann, C; Jakobs, K; Kleinknecht, K; Quast, G; Renk, B; Rohne, E; Sander, H G; Van Gemmeren, P; Zeitnitz, C; Aubert, Jean-Jacques; Bencheikh, A M; Benchouk, C; Bonissent, A; Bujosa, G; Calvet, D; Carr, J; Diaconu, C A; Etienne, F; Konstantinidis, N P; Payre, P; Rousseau, D; Talby, M; Sadouki, A; Thulasidas, M; Trabelsi, K; Aleppo, M; Ragusa, F; Bauer, C; Berlich, R; Blum, Walter; Büscher, V; Dietl, H; Dydak, Friedrich; Ganis, G; Gotzhein, C; Kroha, H; Lütjens, G; Lutz, Gerhard; Männer, W; Moser, H G; Richter, R H; Rosado-Schlosser, A; Schael, S; Settles, Ronald; Seywerd, H C J; Saint-Denis, R; Stenzel, H; Wiedenmann, W; Wolf, G; Boucrot, J; Callot, O; Choi, Y; Cordier, A; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Höcker, A; Jacholkowska, A; Jacquet, M; Kim, D W; Le Diberder, F R; Lefrançois, J; Lutz, A M; Nikolic, I A; Park, H J; Schune, M H; Simion, S; Veillet, J J; Videau, I; Zerwas, D; Azzurri, P; Bagliesi, G; Batignani, G; Bettarini, S; Bozzi, C; Calderini, G; Carpinelli, M; Ciocci, M A; Ciulli, V; Dell'Orso, R; Fantechi, R; Ferrante, I; Foà, L; Forti, F; Giassi, A; Giorgi, M A; Gregorio, A; Ligabue, F; Lusiani, A; Marrocchesi, P S; Messineo, A; Palla, Fabrizio; Sanguinetti, G; Sciabà, A; Spagnolo, P; Steinberger, Jack; Tenchini, Roberto; Tonelli, G; Vannini, C; Verdini, P G; Walsh, J; Blair, G A; Bryant, L M; Cerutti, F; Chambers, J T; Gao, Y; Green, M G; Medcalf, T; Perrodo, P; Strong, J A; Von Wimmersperg-Töller, J H; Botterill, David R; Clifft, R W; Edgecock, T R; Haywood, S; Maley, P; Norton, P R; Thompson, J C; Wright, A E; Bloch-Devaux, B; Colas, P; Emery, S; Kozanecki, Witold; Lançon, E; Lemaire, M C; Locci, E; Marx, B; Pérez, P; Rander, J; Renardy, J F; Roussarie, A; Schuller, J P; Schwindling, J; Trabelsi, A; Vallage, B; Black, S N; Dann, J H; Johnson, R P; Kim, H Y; Litke, A M; McNeil, M A; Taylor, G; Booth, C N; Boswell, R; Brew, C A J; Cartwright, S L; Combley, F; Köksal, A; Lehto, M H; Newton, W M; Reeve, J; Thompson, L F; Böhrer, A; Brandt, S; Cowan, G D; Grupen, Claus; Minguet-Rodríguez, J A; Rivera, F; Saraiva, P; Smolik, L; Stephan, F; Apollonio, M; Bosisio, L; Della Marina, R; Giannini, G; Gobbo, B; Musolino, G; Rothberg, J E; Wasserbaech, S R; Armstrong, S R; Elmer, P; Feng, Z; Ferguson, D P S; Gao, Y S; González, S; Grahl, J; Greening, T C; Hayes, O J; Hu, H; McNamara, P A; Nachtman, J M; Orejudos, W; Pan, Y B; Saadi, Y; Scott, I J; Walsh, A M; Wu, X; Yamartino, J M; Zheng, M; Zobernig, G

    1997-01-01

    The 132 pb$^{-1}$ of data collected by ALEPH from 1991 to 1994 have been used to analyze $\\eta$ and $\\omega$ production in $\\tau$ decays. The following branching fractions have been measured: \\begin{eqnarray*} B(\\tau^-\\to\

  19. Scalar doublet models confront $\\tau$ and $b$ anomalies

    CERN Document Server

    Cline, James M

    2015-01-01

    There are indications of a possible breakdown of the standard model, suggesting that $\\tau$ lepton interactions violate flavor universality. BABAR, Belle and LHCb report high ratios of $B\\to D^{(*)}\\tau\

  20. Multiple-neutral-meson decays of the /tau/ lepton and electromagnetic calorimeter requirements at Tau-Charm Factory

    Energy Technology Data Exchange (ETDEWEB)

    Gan, K.K.

    1989-08-01

    This is a study of the physics sensitivity to the multiple-neutral-meson decays of the /tau/ lepton at the Tau-Charm Factory. The sensitivity is compared for a moderate and an ultimate electromagnetic calorimeter. With the high luminosity of the Tau- Charm Factory, a very large sample of the decays /tau//sup /minus// /yields/ /pi//sup /minus//2/pi//sup 0//nu//sub /tau// and /tau//sup /minus// /yields/ /pi//sup /minus//3/pi//sup 0//nu//sub /tau// can be collected with both detectors. However, with the ultimate detector, 2/pi//sup 0/ and 3/pi//sup 0/ can be unambiguously reconstructed with very little background. For the suppressed decay /tau//sup /minus// /yields/ /pi//sup /minus///eta//pi//sup 0//nu//sub /tau//, only the ultimate detector has the sensitivity. The ultimate detector is also sensitive to the more suppressed decay /tau//sup /minus// /yields/ K/sup /minus///eta//nu//sub /tau// and the moderate detector may have the sensitivity if the hadronic background is not significantly larger than that predicted by Lund. In the case of the highly suppressed second-class-current decay /tau//sup /minus// /yields/ /pi//sup /minus///eta//nu//sub /tau//, only the ultimate detector has sensitivity. The sensitivity can be greatly enhanced with a small-angle photon veto. 16 refs., 9 figs., 2 tabs.

  1. Spatially resolved H2 emission from the disk around T Tau N

    CERN Document Server

    Gustafsson, M; Herbst, T M; Kasper, M

    2008-01-01

    We report the detection of quiescent H2 emission in a spatially resolved ring-like structure within 100 AU of T Tau N. We present evidence to show that the emission most likely arises from shocks in the atmosphere of a nearly face-on disk around T Tau N. Using high spatial resolution 3D spectroscopic K-band data, we trace the spatial distribution of several H2 NIR rovibrational lines in the vicinity of T Tau N. We detect weak H2 emission from the v=1-0 S(0), S(1), Q(1) lines and the v=2-1 S(1) line in a ring-like structure around T Tau N between 0.1'' (~15 AU) and 0.7'' (~100AU) from the star. The v=1-0 S(0) and v=2-1 S(1) lines are detected only in the outer parts of the ring structure. Closer to the star, the strong continuum limits our sensitivity to these lines. The total flux of the v=1-0 S(1) line is 1.8 *10^{-14} ergs s^{-1}cm^{-2}, similar to previous measurements of H2 in circumstellar disks. The velocity of the H2 emitting gas around T Tau N is consistent with the rest velocity of the star, and the ...

  2. Measurement of the lifetime of the tau lepton

    Science.gov (United States)

    Acciarri, M.; Adriani, O.; Aguilar-Benitez, M.; Ahlen, S.; Alpat, B.; Alcaraz, J.; Alemanni, G.; Allaby, J.; Aloisio, A.; Alverson, G.; Alviggi, M. G.; Ambrosi, G.; Anderhub, H.; Andreev, V. P.; Angelescu, T.; Anselmo, F.; Antreasyan, D.; Arefiev, A.; Azemoon, T.; Aziz, T.; Bagnaia, P.; Baksay, L.; Ball, R. C.; Banerjee, S.; Banicz, K.; Barillère, R.; Barone, L.; Bartalini, P.; Baschirotto, A.; Basile, M.; Battiston, R.; Bay, A.; Becattini, F.; Becker, U.; Behner, F.; Berdugo, J.; Berges, P.; Bertucci, B.; Betev, B. L.; Bhattacharya, S.; Biasini, M.; Biland, A.; Bilei, G. M.; Blaising, J. J.; Blyth, S. C.; Bobbink, G. J.; Bock, R.; Böhm, A.; Borgia, B.; Boucham, A.; Bourilkov, D.; Bourquin, M.; Boutigny, D.; Branson, J. G.; Brigljevic, V.; Brock, I. C.; Buffini, A.; Buijs, A.; Burger, J. D.; Burger, W. J.; Busenitz, J.; Buytenhuijs, A.; Cai, X. D.; Campanelli, M.; Capell, M.; Cara Romeo, G.; Caria, M.; Carlino, G.; Cartacci, A. M.; Casaus, J.; Castellini, G.; Cavallari, F.; Cavallo, N.; Cecchi, C.; Cerrada, M.; Cesaroni, F.; Chamizo, M.; Chan, A.; Chang, Y. H.; Chaturvedi, U. K.; Chemarin, M.; Chen, A.; Chen, G.; Chen, G. M.; Chen, H. F.; Chen, H. S.; Chen, M.; Chiefari, G.; Chien, C. Y.; Choi, M. T.; Cifarelli, L.; Cindolo, F.; Civinini, C.; Clare, I.; Clare, R.; Cohn, H. O.; Coignet, G.; Colijn, A. P.; Colino, N.; Costantini, S.; Cotorobai, F.; de La Cruz, B.; Csilling, A.; Dai, T. S.; D'Alessandro, R.; de Asmundis, R.; de Boeck, H.; Degré, A.; Deiters, K.; Denes, P.; Denotaristefani, F.; Dibitonto, D.; Diemoz, M.; van Dierendonck, D.; di Lodovico, F.; Dionisi, C.; Dittmar, M.; Dominguez, A.; Doria, A.; Dorne, I.; Dova, M. T.; Drago, E.; Duchesneau, D.; Duinker, P.; Duran, I.; Dutta, S.; Easo, S.; Efremenko, Yu.; El Mamouni, H.; Engler, A.; Eppling, F. J.; Erné, F. C.; Ernenwein, J. P.; Extermann, P.; Fabre, M.; Faccini, R.; Falciano, S.; Favara, A.; Fay, J.; Fedin, O.; Felcini, M.; Fenyi, B.; Ferguson, T.; Fernandez, D.; Ferroni, F.; Fesefeldt, H.; Fiandrini, E.; Field, J. H.; Filthaut, F.; Fisher, P. H.; Forconi, G.; Fredj, L.; Freudenreich, K.; Furetta, C.; Galaktionov, Yu.; Ganguli, S. N.; Garcia-Abia, P.; Gau, S. S.; Gentile, S.; Gerald, J.; Gheordanescu, N.; Giagu, S.; Goldfarb, S.; Goldstein, J.; Gong, Z. F.; Gougas, A.; Gratta, G.; Gruenewald, M. W.; Gupta, V. K.; Gurtu, A.; Gutay, L. J.; Hangarter, K.; Hartmann, B.; Hasan, A.; Hatzifotiadou, D.; Hebbeker, T.; Hervé, A.; van Hoek, W. C.; Hofer, H.; Hoorani, H.; Hou, S. R.; Hu, G.; Innocente, V.; Janssen, H.; Jin, B. N.; Jones, L. W.; de Jong, P.; Josa-Mutuberria, I.; Kasser, A.; Khan, R. A.; Kamyshkov, Yu.; Kapinos, P.; Kapustinsky, J. S.; Karyotakis, Y.; Kaur, M.; Kienzle-Focacci, M. N.; Kim, D.; Kim, J. K.; Kim, S. C.; Kim, Y. G.; Kinnison, W. W.; Kirkby, A.; Kirkby, D.; Kirkby, J.; Kiss, D.; Kittel, W.; Klimentov, A.; König, A. C.; Korolko, I.; Koutsenko, V.; Kraemer, R. W.; Krenz, W.; Kuijten, H.; Kunin, A.; de Guevara, P. Ladron; Landi, G.; Lapoint, C.; Lassila-Perini, K.; Laurikainen, P.; Lebeau, M.; Lebedev, A.; Lebrun, P.; Lecomte, P.; Lecoq, P.; Le Coultre, P.; Lee, J. S.; Lee, K. Y.; Leggett, C.; Le Goff, J. M.; Leiste, R.; Leonardi, E.; Levtchenko, P.; Li, C.; Lieb, E.; Lin, W. T.; Linde, F. L.; Lista, L.; Liu, Z. A.; Lohmann, W.; Longo, E.; Lu, W.; Lu, Y. S.; Lübelsmeyer, K.; Luci, C.; Luckey, D.; Luminari, L.; Lustermann, W.; Ma, W. G.; Maity, M.; Majumder, G.; Malgeri, L.; Malinin, A.; Maña, C.; Mangla, S.; Marchesini, P.; Marin, A.; Martin, J. P.; Marzano, F.; Massaro, G. G. G.; McNally, D.; Mele, S.; Merola, L.; Meschini, M.; Metzger, W. J.; von der Mey, M.; Mi, Y.; Mihul, A.; van Mil, A. J. W.; Mirabelli, G.; Mnich, J.; Molnar, P.; Monteleoni, B.; Moore, R.; Morganti, S.; Moulik, T.; Mount, R.; Müller, S.; Muheim, F.; Nagy, E.; Nahn, S.; Napolitano, M.; Nessi-Tedaldi, F.; Newman, H.; Nippe, A.; Nowak, H.; Organtini, G.; Ostonen, R.; Pandoulas, D.; Paoletti, S.; Paolucci, P.; Park, H. K.; Pascale, G.; Passaleva, G.; Patricelli, S.; Paul, T.; Pauluzzi, M.; Paus, C.; Pauss, F.; Peach, D.; Pei, Y. J.; Pensotti, S.; Perret-Gallix, D.; Petrak, S.; Pevsner, A.; Piccolo, D.; Pieri, M.; Pinto, J. C.; Piroué, P. A.; Pistolesi, E.; Plyaskin, V.; Pohl, M.; Pojidaev, V.; Postema, H.; Produit, N.; Prokofiev, D.; Rahal-Callot, G.; Rancoita, P. G.; Rattaggi, M.; Raven, G.; Razis, P.; Read, K.; Ren, D.; Rescigno, M.; Reucroft, S.; van Rhee, T.; Riemann, S.; Riemers, B. C.; Riles, K.; Rind, O.; Ro, S.; Robohm, A.; Rodin, J.; Rodriguez, F. J.; Roe, B. P.; Röhner, S.; Romero, L.; Rosier-Lees, S.; Rosselet, Ph.; van Rossum, W.; Roth, S.; Rubio, J. A.; Rykaczewski, H.; Salicio, J.; Sanchez, E.; Santocchia, A.; Sarakinos, M. E.; Sarkar, S.; Sassowsky, M.; Sauvage, G.; Schäfer, C.; Schegelsky, V.; Schmidt-Kaerst, S.; Schmitz, D.; Schmitz, P.; Schneegans, M.; Schoeneich, B.; Scholz, N.; Schopper, H.; Schotanus, D. J.; Schwenke, J.; Schwering, G.; Sciacca, C.; Sciarrino, D.; Sens, J. C.; Servoli, L.; Shevchenko, S.; Shivarov, N.; Shoutko, V.; Shukla, J.; Shumilov, E.; Shvorob, A.; Siedenburg, T.; Son, D.; Sopczak, A.; Soulimov, V.; Smith, B.; Spillantini, P.; Steuer, M.; Stickland, D. P.; Stone, H.; Stoyanov, B.; Straessner, A.; Strauch, K.; Sudhakar, K.; Sultanov, G.; Sun, L. Z.; Susinno, G. F.; Suter, H.; Swain, J. D.; Tang, X. W.; Tauscher, L.; Taylor, L.; Ting, Samuel C. C.; Ting, S. M.; Tonisch, F.; Tonutti, M.; Tonwar, S. C.; Tóth, J.; Tully, C.; Tuchscherer, H.; Tung, K. L.; Uchida, Y.; Ulbricht, J.; Uwer, U.; Valente, E.; van de Walle, R. T.; Vesztergombi, G.; Vetlitsky, I.; Viertel, G.; Vivargent, M.; Völkert, R.; Vogel, H.; Vogt, H.; Vorobiev, I.; Vorobyov, A. A.; Vorvolakos, A.; Wadhwa, M.; Wallraff, W.; Wang, J. C.; Wang, X. L.; Wang, Z. M.; Weber, A.; Wittgenstein, F.; Wu, S. X.; Wynhoff, S.; Xu, J.; Xu, Z. Z.; Yang, B. Z.; Yang, C. G.; Yao, X. Y.; Ye, J. B.; Yeh, S. C.; You, J. M.; Zalite, An.; Zalite, Yu.; Zemp, P.; Zeng, Y.; Zhang, Z.; Zhang, Z. P.; Zhou, B.; Zhou, Y.; Zhu, G. Y.; Zhu, R. Y.; Zichichi, A.

    1996-02-01

    The lifetime of the tau lepton is measured using data collected in 1994 by the L3 detector at LEP. The precise track position information of the Silicon Microvertex Detector is exploited. The tau lepton lifetime is determined from the signed impact parameter distribution for 30 322 tau decays into one charged particle and from the decay length distribution for 3891 tau decays into three charged particles. Combining the two methods we obtain ττ = 290.1 +/- 4.0 fs.

  3. Tau Phosphorylation by GSK3 in Different Conditions

    Science.gov (United States)

    Avila, Jesús; León-Espinosa, Gonzalo; García, Esther; García-Escudero, Vega; Hernández, Félix; DeFelipe, Javier

    2012-01-01

    Almost a 20% of the residues of tau protein are phosphorylatable amino acids: serine, threonine, and tyrosine. In this paper we comment on the consequences for tau of being a phosphoprotein. We will focus on serine/threonine phosphorylation. It will be discussed that, depending on the modified residue in tau molecule, phosphorylation could be protective, in processes like hibernation, or toxic like in development of those diseases known as tauopathies, which are characterized by an hyperphosphorylation and aggregation of tau. PMID:22675648

  4. The strong coupling from tau decays without prejudice

    CERN Document Server

    Boito, Diogo; Jamin, Matthias; Mahdavi, Andisheh; Maltman, Kim; Osborne, James; Peris, Santiago

    2012-01-01

    We review our recent determination of the strong coupling \\alpha_s from the OPAL data for non-strange hadronic tau decays. We find that \\alpha_s(m^2_\\tau) =0.325+-0.018 using fixed-order perturbation theory, and \\alpha_s(m^2_\\tau)=0.347+-0.025 using contour-improved perturbation theory. At present, these values supersede any earlier determinations of the strong coupling from hadronic tau decays, including those from ALEPH data.

  5. Measurement of the Tau Lepton Polarisation at LEP2

    CERN Document Server

    Abdallah, J; Adam, W; Adzic, P; Albrecht, T; Alemany-Fernandez, R; Allmendinger, T; Allport, P P; Amaldi, Ugo; Amapane, N; Amato, S; Anashkin, E; Andreazza, A; Andringa, S; Anjos, N; Antilogus, P; Apel, W D; Arnoud, Y; Ask, S; Åsman, B; Augustin, J E; Augustinus, A; Baillon, P; Ballestrero, A; Bambade, P; Barbier, R; Bardin, D; Barker, G J; Baroncelli, A; Battaglia, M; Baubillier, M; Becks, K H; Begalli, M; Behrmann, A; Ben-Haim, E; Benekos, N; Benvenuti, A; Bérat, C; Berggren, M; Bertrand, D; Besançon, M; Besson, N; Bloch, D; Blom, M; Bluj, M; Bonesini, M; Boonekamp, M; Booth, P S L; Borisov, G; Botner, O; Bouquet, B; Bowcock, T J V; Boyko, I; Bracko, M; Brenner, R; Brodet, E; Brückman, P; Brunet, J M; Buschbeck, B; Buschmann, P; Calvi, M; Camporesi, T; Canale, V; Carena, F; Castro, N; Cavallo, F; Chapkin, M; Charpentier, P; Checchia, P; Chierici, R; Shlyapnikov, P; Chudoba, J; Chung, S U; Cieslik, K; Collins, P; Contri, R; Cosme, G; Cossutti, F; Costa, M J; Crennell, D J; Cuevas-Maestro, J; D'Hondt, J; Da Silva, T; Da Silva, W; Dedovich, D; Della Ricca, G; De Angelis, A; de Boer, Wim; De Clercq, C; De Lotto, B; De Maria, N; De Min, A; De Paula, L; Di Ciaccio, L; Di Simone, A; Doroba, K; Drees, J; Eigen, G; Ekelöf, T J C; Ellert, M; Elsing, M; Espirito-Santo, M C; Fanourakis, G K; Fassouliotis, D; Feindt, M; Fernández, J; Ferrer, A; Ferro, F; Flagmeyer, U; Föth, H; Fokitis, E; Fulda-Quenzer, F; Fuster, J; Gandelman, M; García, C; Gavillet, P; Gazis, E; Gokieli, R; Golob, B; Gómez-Ceballos, G; Gonçalves, P; Graziani, E; Grosdidier, G; Grzelak, K; Guy, J; Haag, C; Hallgren, A; Hamacher, K; Hamilton, K; Haug, S; Hauler, F; Hedberg, V; Hennecke, M; Herr, H; Hoffman, J; Holmgren, S O; Holt, P J; Houlden, M A; Jackson, J N; Jarlskog, G; Jarry, P; Jeans, D; Johansson, E K; Jonsson, P; Joram, C; Jungermann, L; Kapusta, F; Katsanevas, S; Katsoufis, E; Kernel, G; Kersevan, B P; Kerzel, U; King, B T; Kjaer, N J; Kluit, P; Kokkinias, P; Kourkoumelis, C; Kuznetsov, O; Krumshtein, Z; Kucharczyk, M; Lamsa, J; Leder, G; Ledroit, F; Leinonen, L; Leitner, R; Lemonne, J; Lepeltier, V; Lesiak, T; Liebig, W; Liko, D; Lipniacka, A; Lopes, J H; López, J M; Loukas, D; Lutz, P; Lyons, L; MacNaughton, J; Malek, A; Maltezos, S; Mandl, F; Marco, J; Marco, R; Maréchal, B; Margoni, M; Marin, J C; Mariotti, C; Markou, A; Martínez-Rivero, C; Masik, J; Mastroyiannopoulos, N; Matorras, F; Matteuzzi, C; Mazzucato, F; Mazzucato, M; McNulty, R; Meroni, C; Migliore, E; Mitaroff, W A; Mjörnmark, U; Moa, T; Moch, M; Mönig, K; Monge, R; Montenegro, J; Moraes, D; Moreno, S; Morettini, P; Müller, U; Münich, K; Mulders, M; Mundim, L; Murray, W; Muryn, B; Myatt, G; Myklebust, T; Nassiakou, M; Navarria, F; Nawrocki, K; Nicolaidou, R; Nikolenko, M; Oblakowska-Mucha, A; Obraztsov, V F; Olshevski, A; Onofre, A; Orava, R; Österberg, K; Ouraou, A; Oyanguren, A; Paganoni, M; Paiano, S; Palacios, J P; Palka, H; Papadopoulou, T D; Pape, L; Parkes, C; Parodi, F; Parzefall, U; Passeri, A; Passon, O; Peralta, L; Perepelitsa, V; Perrotta, A; Petrolini, A; Piedra, J; Pieri, L; Pierre, F; Pimenta, M; Piotto, E; Podobnik, T; Poireau, V; Pol, M E; Polok, G; Pozdnyakov, V; Pukhaeva, N; Pullia, A; Rames, J; Read, A; Rebecchi, P; Rehn, J; Reid, D; Reinhardt, R; Renton, P B; Richard, F; Rídky, J; Rivero, M; Rodríguez, D; Romero, A; Ronchese, P; Roudeau, P; Rovelli, T; Ruhlmann-Kleider, V; Ryabtchikov, D; Sadovskii, A; Salmi, L; Salt, J; Sander, C; Savoy-Navarro, A; Schwickerath, U; Sekulin, R; Siebel, M; Sisakian, A; Smadja, G; Smirnova, O; Sokolov, A; Sopczak, A; Sosnowski, R; Spassoff, Tz; Stanitzki, M; Stocchi, A; Strauss, J; Stugu, B; Szczekowski, M; Szeptycka, M; Szumlak, T; Tabarelli de Fatis, T; Tegenfeldt, F; Timmermans, J; Tkatchev, L; Tobin, M; Todorovova, S; Tomé, B; Tonazzo, A; Tortosa, P; Travnicek, P; Treille, D; Tristram, G; Trochimczuk, M; Troncon, C; Turluer, M L; Tyapkin, I A; Tyapkin, P; Tzamarias, S; Uvarov, V; Valenti, G; van Dam, P; Van Eldik, J; Van Remortel, N; Van Vulpen, I; Vegni, G; Veloso, F; Venus, W; Verdier, P; Verzi, V; Vilanova, D; Vitale, L; Vrba, V; Wahlen, H; Washbrook, A J; Weiser, C; Wicke, D; Wickens, J; Wilkinson, G; Winter, M; Witek, M; Yushchenko, O; Zalewska-Bak, A; Zalewski, P; Zavrtanik, D; Zhuravlov, V; Zimin, N I; Zintchenko, A; Zupan, M

    2008-01-01

    A first measurement of the average polarisation P_tau of tau leptons produced in e+e- annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value P_tau = -0.164 +/- 0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV.

  6. Measurement of the Tau Lepton Polarisation at LEP2

    CERN Document Server

    Abdallah, J.; Adam, W.; Adzic, P.; Albrecht, T.; Alemany-Fernandez, R.; Allmendinger, T.; Allport, P.P.; Amaldi, U.; Amapane, N.; Amato, Sandra F.; Anashkin, E.; Andreazza, A.; Andringa, S.; Anjos, N.; Antilogus, Pierre; Apel, W-D.; Arnoud, Y.; Ask, S.; Asman, B.; Augustin, Jean-Eudes; Augustinus, A.; Baillon, P.; Ballestrero, A.; Bambade, P.; Barbier, R.; Bardin, D.; Barker, G.J.; Baroncelli, Antonio; Battaglia, M.; Baubillier, M.; Becks, K-H.; Begalli, M.; Behrmann, A.; Ben-Haim, Eli; Benekos, N.; Benvenuti, A.; Berat, C.; Berggren, Mikael; Bertrand, D.; Besancon, M.; Besson, N.; Bloch, D.; Blom, M.; Bluj, Michal; Bonesini, Maurizio; Boonekamp, M.; Booth, P.S.L.; Borisov, G.; Botner, Olga; Bouquet, B.; Bowcock, T.J.V.; Boyko, I.; Bracko, Marko; Brenner, R.; Brodet, E.; Bruckman, P.; Brunet, J.M.; Buschbeck, B.; Buschmann, P.; Calvi, M.; Camporesi, Tiziano; Canale, V.; Carena, F.; Castro, Nuno Filipe; Cavallo, F.; Chapkin, M.; Charpentier, Ph.; Checchia, Paolo; Chierici, R.; Chliapnikov, P.; Chudoba, J.; Chung, Suh-Urk; Cieslik, K.; Collins, P.; Contri, Roberto; Cosme, G.; Cossutti, Fabio; Costa, M.J.; Crennell, D.; Cuevas, J.; D'Hondt, J.; da Silva, T.; Da Silva, W.; Dedovich, D.; Della Ricca, Giuseppe; De Angelis, Alessandro; De Boer, W.; De Clercq, C.; De Lotto, Barbara; De Maria, N.; De Min, A.; de Paula, L.; Di Ciaccio, L.; Di Simone, A.; Doroba, K.; Eigen, G.; Ekelof, Tord; Ellert, Mattias; Elsing, M.; Espirito Santo, Maria Catarina; Fanourakis, George K.; Feindt, Michael; Fernandez, J.; Ferrer, A.; Ferro, F.; Flagmeyer, U.; Foeth, H.; Fokitis, E.; Fulda-Quenzer, F.; Fuster, J.; Gandelman, Miriam; Garcia, C.; Gavillet, Philippe; Gazis, Evangelos; Gomez-Ceballos, G.; Goncalves, P.; Graziani, E.; Grosdidier, G.; Grzelak, K.; Guy, J.; Haag, C.; Hallgren, A.; Hamacher, Klaus; Hamilton, K.; Haug, S.; Hauler, F.; Hedberg, Vincent; Hennecke, M.; Herr, H.; Hoffman, J.; Holmgren, S-O.; Holt, P.J.; Houlden, M.A.; Jackson, John Neil; Jarlskog, Goran; Jarry, P.; Jeans, D.; Johansson, E.K.; Jonsson, P.; Joram, C.; Jungermann, L.; Kapusta, Frederic; Katsanevas, S.; Katsoufis, E.; Kernel, Gabrijel; Kerzel, U.; King, B.T.; Kjaer, N.J.; Kluit, Peter; Kokkinias, P.; Kourkoumelis, C.; Kouznetsov, O.; Krumstein, Z.; Kucharczyk, M.; Lamsa, J.; Leder, G.; Ledroit, F.; Leinonen, L.; Leitner, R.; Lemonne, Jacques; Lepeltier, V.; Lesiak, T.; Liebig, W.; Liko, D.; Lipniacka, A.; Lopes, J.H.; Lopez, J.M.; Loukas, D.; Lutz, Pierre; Lyons, Louis; MacNaughton, J.; Malek, A.; Maltezos, S.; Mandl, F.; Marco, J.; Marco, R.; Marechal, B.; Margoni, M.; Marin, J-C.; Mariotti, C.; Markou, Athanasios; Martinez-Rivero, C.; Masik, J.; Mastroyiannopoulos, N.; Matorras, Francisco; Matteuzzi, C.; Mazzucato, F.; Mazzucato, M.; Nulty, R.Mc; Meroni, C.; Migliore, E.; Mitaroff, Winfried A.; Mjoernmark, U.; Moa, T.; Moch, M.; Monge, R.; Montenegro, J.; Moraes, D.; Moreno, S.; Morettini, P.; Mueller, U.; Muenich, K.; Mulders, M.; Mundim Filho, Luiz Martins; Murray, W.; Muryn, B.; Myatt, G.; Myklebust, T.; Nassiakou, M.; Navarria, F.; Nawrocki, K.; Nicolaidou, R.; Oblakowska-Mucha, A.; Obraztsov, V.; Olshevski, A.; Onofre, A.; Orava, R.; Osterberg, K.; Ouraou, A.; Oyanguren, A.; Paganoni, M.; Paiano, S.; Palacios, J.P.; Palka, Henryk; Papadopoulou, Th.D.; Pape, L.; Parkes, C.; Parodi, F.; Parzefall, U.; Passeri, A.; Passon, O.; Peralta, L.; Perepelitsa, V.; Perrotta, Andrea; Petrolini, Alessandro; Piedra, Jonatan; Pieri, L.; Pierre, Francois; Pimenta, M.; Piotto, E.; Poireau, V.; Pol, M.E.; Polok, G.; Pozdniakov, V.; Pukhaeva, N.; Pullia, A.; Rames, J.; Read, A.; Rebecchi, P.; Rehn, J.; Reid, D.; Reinhardt, R.; Renton, Peter; Richard, F.; Ridky, Jan; Rivero, M.; Rodriguez, D.; Romero, A.; Ronchese, P.; Roudeau, P.; Rovelli, T.; Ruhlmann, Vanina; Ryabtchikov, D.; Sadovsky, A.; Salmi, L.; Salt, J.; Sander, C.; Savoy-Navarro, A.; Schwickerath, U.; Segar, A.; Sekulin, R.; Siebel, Martin; Sisakian, A.; Smadja, G.; Smirnova, O.; Sokolov, A.; Sopczak, A.; Sosnowski, R.; Spassov, T.; Stanitzki, M.; Stocchi, A.; Strauss, J.; Stugu, B.; Szczekowski, M.; Szeptycka, M.; Szumlak, T.; Tabarelli de Fatis, T.; Taffard, A.C.; Tegenfeldt, F.; Timmermans, Jan; Tkatchev, L.; Tobin, M.; Todorovova, S.; Tome, B.; Tonazzo, A.; Tortosa, P.; Travnicek, Petr; Treille, D.; Tristram, G.; Trochimczuk, M.; Troncon, Clara; Turluer, M-L.; Tyapkin, I.A.; Tyapkin, P.; Tzamarias, S.; Uvarov, V.; Valenti, Giovanni; Van Dam, P.; Van Eldik, J.; van Remortel, N.; Van Vulpen, I.; Vegni, G.; Veloso, F.; Venus, W.; Verdier, Patrice; Verzi, V.; Vilanova, D.; Vitale, Lorenzo; Vrba, V.; Wahlen, H.; Washbrook, A.J.; Weiser, C.; Wicke, D.; Wickens, J.; Wilkinson, G.; Winter, M.; Witek, M.; Yushchenko, O.; Zalewska, A.; Zalewski, P.; Zavrtanik, Danilo; Zhuravlov, V.; Zimine, N.I.; Zintchenko, Alexandre

    2008-01-01

    A first measurement of the average polarisation P_tau of tau leptons produced in e+e- annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value P_tau = -0.164 +/- 0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV.

  7. Precise predictions for B -> Xc tau nu decay distributions

    CERN Document Server

    Ligeti, Zoltan

    2014-01-01

    We derive precise standard model predictions for the dilepton invariant mass and the tau energy distributions in inclusive B -> Xc tau nu decay. We include Lambda_QCD^2/m_b^2 and alpha_s corrections using the 1S short-distance mass scheme, and estimate shape function effects near maximal tau energy. These results can improve the sensitivity of b -> c tau nu related observables to beyond standard model physics.

  8. Intracellular clusterin interacts with brain isoforms of the bridging integrator 1 and with the microtubule-associated protein Tau in Alzheimer's disease.

    Directory of Open Access Journals (Sweden)

    Yuan Zhou

    Full Text Available Sporadic or late-onset Alzheimer's disease (AD is expected to affect 50% of individuals reaching 85 years of age. The most significant genetic risk factor for late-onset AD is the e4 allele of APOE gene encoding apolipoprotein E, a lipid carrier shown to modulate brain amyloid burden. Recent genome-wide association studies have uncovered additional single nucleotide polymorphisms (SNPs linked to AD susceptibility, including those in the CLU and BIN1 genes encoding for clusterin (CLU and the bridging integrator 1 (BIN1 proteins, respectively. Because CLU has been implicated in brain amyloid-β (Aβ clearance in mouse models of amyloid deposition, we sought to investigate whether an AD-linked SNP in the CLU gene altered Aβ42 biomarker levels in the cerebrospinal fluid (CSF. Instead, we found that the CLU rs11136000 SNP modified CSF levels of the microtubule-associated protein Tau in AD patients. We also found that an intracellular form of CLU (iCLU was upregulated in the brain of Tau overexpressing Tg4510 mice, but not in Tg2576 amyloid mouse model. By overexpressing iCLU and Tau in cell culture systems we discovered that iCLU was a Tau-interacting protein and that iCLU associated with brain-specific isoforms of BIN1, also recently identified as a Tau-binding protein. Through expression analysis of CLU and BIN1 variants, we found that CLU and BIN1 interacted via their coiled-coil motifs. In co-immunoprecipitation studies using human brain tissue, we showed that iCLU and the major BIN1 isoform expressed in neurons were associated with modified Tau species found in AD. Finally, we showed that expression of certain coding CLU variants linked to AD risk led to increased levels of iCLU. Together, our findings suggest that iCLU and BIN1 interaction might impact Tau function in neurons and uncover potential new mechanisms underlying the etiology of Tau pathology in AD.

  9. Search for anomalous weak dipole moments of the $\\tau$ lepton

    CERN Document Server

    Heister, A; Barate, R; De Bonis, I; Décamp, D; Goy, C; Lees, J P; Merle, E; Minard, M N; Pietrzyk, B; Bravo, S; Casado, M P; Chmeissani, M; Crespo, J M; Fernández, E; Fernández-Bosman, M; Garrido, L; Martínez, M; Pacheco, A; Ruiz, H; Colaleo, A; Creanza, D; De Palma, M; Iaselli, Giuseppe; Maggi, G; Maggi, M; Nuzzo, S; Ranieri, A; Raso, G; Ruggieri, F; Selvaggi, G; Silvestris, L; Tempesta, P; Tricomi, A; Zito, G; Huang, X; Lin, J; Ouyang, Q; Wang, T; Xie, Y; Xu, R; Xue, S; Zhang, J; Zhang, L; Zhao, W; Abbaneo, D; Azzurri, P; Buchmüller, O L; Cattaneo, M; Cerutti, F; Clerbaux, B; Drevermann, H; Forty, R W; Frank, M; Gianotti, F; Hansen, J B; Harvey, J; Hutchcroft, D E; Janot, P; Jost, B; Kado, M; Mato, P; Moutoussi, A; Ranjard, F; Rolandi, Luigi; Schlatter, W D; Schneider, O; Sguazzoni, G; Tejessy, W; Teubert, F; Valassi, Andrea; Videau, I; Ward, J; Badaud, F; Falvard, A; Gay, P; Henrard, P; Jousset, J; Michel, B; Monteil, S; Montret, J C; Pallin, D; Perret, P; Hansen, J D; Hansen, J R; Hansen, P H; Nilsson, B S; Kyriakis, A; Markou, C; Simopoulou, Errietta; Vayaki, Anna; Zachariadou, K; Blondel, A; Bonneaud, G R; Brient, J C; Rougé, A; Rumpf, M; Swynghedauw, M; Verderi, M; Videau, H L; Ciulli, V; Focardi, E; Parrini, G; Antonelli, A; Antonelli, M; Bencivenni, G; Bossi, F; Capon, G; Chiarella, V; Laurelli, P; Mannocchi, G; Murtas, G P; Passalacqua, L; Pepé-Altarelli, M; Lynch, J G; Negus, P; O'Shea, V; Raine, C; Thompson, A S; Wasserbaech, S R; Cavanaugh, R J; Geweniger, C; Hanke, P; Hepp, V; Kluge, E E; Putzer, A; Stenzel, H; Tittel, K; Wunsch, M; Beuselinck, R; Binnie, David M; Cameron, W; Dornan, P J; Girone, M; Marinelli, N; Sedgbeer, J K; Thompson, J C; Ghete, V M; Girtler, P; Kneringer, E; Kuhn, D; Rudolph, G; Bouhova-Thacker, E; Bowdery, C K; Finch, A J; Foster, F; Hughes, G; Jones, R W L; Pearson, M R; Robertson, N A; Jakobs, K; Kleinknecht, K; Renk, B; Sander, H G; Wachsmuth, H W; Zeitnitz, C; Bonissent, A; Coyle, P; Leroy, O; Payre, P; Rousseau, D; Talby, M; Ragusa, F; David, A; Dietl, H; Ganis, G; Hüttmann, K; Lütjens, G; Männer, W; Moser, H G; Settles, Ronald; Wolf, G; Boucrot, J; Callot, O; Davier, M; Duflot, L; Grivaz, J F; Heusse, P; Jacholkowska, A; Lefrançois, J; Veillet, J J; Yuan, C; Bagliesi, G; Boccali, T; Foà, L; Giammanco, A; Giassi, A; Ligabue, F; Messineo, A; Palla, Fabrizio; Sanguinetti, G; Sciabà, A; Tenchini, Roberto; Venturi, A; Verdini, P G; Blair, G A; Cowan, G; Green, M G; Medcalf, T; Misiejuk, A; Strong, J A; Teixeira-Dias, P; Clifft, R W; Edgecock, T R; Norton, P R; Tomalin, I R; Bloch-Devaux, B; Colas, P; Lançon, E; Lemaire, M C; Locci, E; Pérez, P; Rander, J; Schuller, J P; Vallage, B; Konstantinidis, N P; Litke, A M; Taylor, G; Booth, C N; Cartwright, S L; Combley, F; Lehto, M H; Thompson, L F; Böhrer, A; Brandt, S; Grupen, Claus; Ngac, A; Prange, G; Giannini, G; Rothberg, J E; Armstrong, S R; Berkelman, K; Cranmer, K; Ferguson, D P S; Gao, Y; Gonzáles, S; Hayes, O J; Hu, H; Jin, S; Kile, J; McNamara, P A; Nielsen, J; Pan, Y B; Von Wimmersperg-Töller, J H; Wiedenmann, W; Wu, J; Wu Sau Lan; Wu, X; Zobernig, G; Dissertori, G

    2003-01-01

    The anomalous weak dipole moments of the $\\tau$ lepton are measured in a data sample collected by ALEPH from 1990 to 1995 corresponding to an integrated luminosity of 155~pb$^{-1}$. Tau leptons produced in the reaction $e^+ e^- \\rightarrow \\tau^+ \\tau^-$ at energies close to the ${\\rm Z}$ mass are studied using their semileptonic decays to $\\pi$, $\\rho$, $a_1 \\rightarrow \\pi 2\\pi^0$ or $a_1 \\rightarrow 3 \\pi$. The real and imaginary components of both the anomalous weak magnetic dipole moment and the CP-violating anomalous weak electric dipole moment, $ {\\rm Re}\\,\\mu_{\\tau}$, ${\\rm Im}\\,\\mu_{\\tau}$, ${\\rm Re}\\,d_{\\tau}$ and ${\\rm Im}\\,d_{\\tau}$, are measured simultaneously by means of a likelihood fit built from the full differential cross section. No evidence of new physics is found. The following bounds are obtained (95\\% CL): $|{\\rm Re}\\, \\mu_{\\tau} | < 1.14 \\times 10^{-3}$, $|{\\rm Im}\\, \\mu_{\\tau} | < 2.65 \\times 10^{-3}$, $|{\\rm Re}\\, d_{\\tau} | < 0.91 \\times 10^{-3}$, and $|{\\rm Im}\\, d_{\\tau} ...

  10. Enumerative geometry, tau-functions and Heisenberg-Virasoro algebra

    CERN Document Server

    Alexandrov, A

    2014-01-01

    In this paper we establish relations between three enumerative geometry tau-functions, namely the Kontsevich-Witten, Hurwitz and Hodge tau-functions. The relations allow us to describe the tau-functions in terms of matrix integrals, Virasoro constraints and Kac-Schwarz operators. All constructed operators belong to the algebra (or group) of symmetries of the KP hierarchy.

  11. Molecular insights into the reversible formation of tau protein fibrils.

    Science.gov (United States)

    Luo, Yin; Dinkel, Paul; Yu, Xiang; Margittai, Martin; Zheng, Jie; Nussinov, Ruth; Wei, Guanghong; Ma, Buyong

    2013-05-04

    We computationally and experimentally showed that tau protein fibrils can be formed at high temperature. When cooled, the fibrils dissociate back to monomers. Heparin promotes tau fibril formation and prevents its reversion. Our results revealed the physicochemical mechanism of reversible formation of tau fibrils.

  12. Comparative peptidome analyses of the profiles of the peptides ranging from 1-10 KD in CSF samples pooled from probable sporadic CJD and non-CJD patients.

    Science.gov (United States)

    Chen, Cao; Xiao, Di; Zhou, Wei; Zhang, Yong-Chan; Shi, Qi; Tian, Chan; Zhang, Jin; Zhou, Chun-Xi; Zhang, Jian-Zhong; Dong, Xiao-Ping

    2012-01-01

    The shotgun strategy applying tandem mass spectrometry has been widely used to identify the proteins that are differentially distributed among diseases for its high reliability and efficiency. To find out the potential difference of protein profiles in cerebrospinal fluids (CSF) between Creutzfeldt-Jakob disease (CJD) and non-CJD patients, especially in the fraction ranging from 1-10 KD, the CSF samples of 40 probable sporadic CJD (sCJD) patients, 32 non-CJD cases with dementia and 17 non-CJD cases without dementia were separately pooled and enriched by the magnetic beads based weak cation exchange chromatography (MB-WCX). After trypsin digestion, each enriched CSF was separated and identified by RP-HPLC-ESI-QTOF MS/MS. In total, 42, 53 and 47 signals of proteins were identified in the pooled CSF fraction less than 10 KD of probable sCJD, non-CJD with dementia and non-CJD without dementia, respectively. Compared with that of probable sCJD, the similarity of CSF protein profiles of non-CJD with dementia (76.2%) were higher than that of non-CJD without dementia (57.1%). Nine CSF proteins were found to be specially observed in probable sCJD group. Those data may help to select the potential biomarkers for diagnosis of CJD. Additionally, further studies of the small segments of cellular proteins in CSF of CJD patients may also provide scientific clues for understanding the neuropathogenesis of TSEs.

  13. Epidural blood patch for refractory low CSF pressure headache

    DEFF Research Database (Denmark)

    Madsen, Søren Aalbæk; Fomsgaard, Jonna Storm; Jensen, Rigmor

    2011-01-01

    of non-invasive/conservative measures and invasive measures with epidural blood patch providing the cornerstone of the invasive measures. In the present pilot study we therefore aimed to evaluate the treatment efficacy of epidural blood patch (EBP) in treatment-refractory low-pressure headache. Our...... reduction in frequency. An increase in days with use of medication was found. Increased awareness of low CSF pressure headache is emphasized and a controlled larger randomized study is needed to confirm the results. However the present results, allows us to conclude that EBP in treatment-refractory low CSF......Once believed an exceedingly rare disorder, recent evidence suggests that low cerebrospinal fluid (CSF) pressure headache has to be considered an important cause of new daily persistent headaches, particularly among young and middle-aged individuals. Treatment of low CSF pressure headache consists...

  14. REVIEW Interpretation and value of MR CSF flow studies for ...

    African Journals Online (AJOL)

    more specific uses of CSF flow studies is to gain information relating ... phase contrast magnetic resonance (PCMR) capabilities and analysis packages.[6] Imaging .... Note that the black or white signal for systole and diastole or representation.

  15. Epidural blood patch for refractory low CSF pressure headache

    DEFF Research Database (Denmark)

    Madsen, Søren Aalbæk; Fomsgaard, Jonna Storm; Jensen, Rigmor

    2011-01-01

    of non-invasive/conservative measures and invasive measures with epidural blood patch providing the cornerstone of the invasive measures. In the present pilot study we therefore aimed to evaluate the treatment efficacy of epidural blood patch (EBP) in treatment-refractory low-pressure headache. Our......Once believed an exceedingly rare disorder, recent evidence suggests that low cerebrospinal fluid (CSF) pressure headache has to be considered an important cause of new daily persistent headaches, particularly among young and middle-aged individuals. Treatment of low CSF pressure headache consists...... reduction in frequency. An increase in days with use of medication was found. Increased awareness of low CSF pressure headache is emphasized and a controlled larger randomized study is needed to confirm the results. However the present results, allows us to conclude that EBP in treatment-refractory low CSF...

  16. Enhanced tau neutrino appearance through invisible decay

    CERN Document Server

    Pagliaroli, Giulia; Mannarelli, Massimo

    2016-01-01

    The decay of neutrino mass eigenstates leads to a change of the conversion and survival probability of neutrino flavor eigenstates. Remarkably, we find that the neutrino decay provides an enhancement of the expected tau appearance signal with respect to the standard oscillation scenario for the long-baseline OPERA experiment. The increase of the $\

  17. Tau neurofibrillary pathology and microtubule stability.

    Science.gov (United States)

    Michaelis, Mary L; Dobrowsky, Rick T; Li, Guibin

    2002-12-01

    We previously reported that nonomolar concentrations of Taxol and several structurally diverse microtubule (MT)-stabilizing agents significantly enhanced the survival of neurons in the presence of fibrils of amyloid beta peptide (Abeta). Pretreatment of neurons with MT-stabilizing drugs also blocked Abeta-induced activation of tau hyperphosphorylation. Although tau is a substrate for several kinases, we initially focused on cdk5, as this tau kinase has been shown to be activated in Abeta-treated neurons and Alzheimer's disease (AD) brain. In an in vitro kinase assay, Taxol inhibited activation of cdk5 by Abeta. In addition, the proposed cellular cascade in which calpain activation leads to cleavage of the cdk5 regulator, p35, to the strong kinase activator p25 was also prevented. Taxol did not directly inhibit the activity of either cdk5 or calpain, indicating that other cellular components are required for the effect of the drug on Abeta activation of tau phosphorylation. Our results suggest that drugs that interact with MTs can alter signaling events in neurons, possibly because some MTs play a role in organizing protein complexes involved in responses to Abeta. Thus the cytoskeletal network may serve as a biosensor of cellular well-being.

  18. Tau identification using multivariate techniques in ATLAS

    Science.gov (United States)

    O'Neil, D. C.; ATLAS Collaboration

    2012-06-01

    Tau leptons play an important role in the physics program of the LHC. They are being used in electroweak measurements, in detector related studies and in searches for new phenomena like the Higgs boson or Supersymmetry. In th