Neurochemical alterations associated with borderline personality disorder.

Science.gov (United States)

Atmaca, Murad; Karakoc, Tevfik; Mermi, Osman; Gurkan Gurok, M; Yildirim, Hanefi

2015-01-01

In neuroimaging on borderline personality disorder, prior studies focused on the hippocampus and amygdala, as mentioned above. However, no study investigated whether there were neurochemical changes in the patients with borderline personality disorder. Therefore, in the present study, we aimed to investigate neurochemical change of patients diagnosed with borderline disorder and hypothesized that neurochemicals would change in the hippocampus region of these patients. Seventeen patients and the same number of healthy control subjects were analyzed by using a 1.5 Tesla GE Signa Imaging System. N-acetylaspartate (NAA), choline compounds (CHO), and creatine (CRE) values of hippocampal region were measured. The mean NAA/CRE ratio in the hippocampus region was significantly reduced in the patients with borderline personality disorder compared to that of healthy control subjects, In addition, NAA/CHO ratio of the patients with borderline personality disorder was also significantly reduced when compared to that of healthy subjects. There was no difference in the ratio of CHO/CRE. In summary, we present evidence for reduced NAA in the patients with borderline personality disorder. © 2015, The Author(s).

Neurochemical and Neuroanatomical Plasticity Following Memory Training and Yoga Interventions in Older Adults with Mild Cognitive Impairment.

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Yang, Hongyu; Leaver, Amber M; Siddarth, Prabha; Paholpak, Pattharee; Ercoli, Linda; St Cyr, Natalie M; Eyre, Harris A; Narr, Katherine L; Khalsa, Dharma S; Lavretsky, Helen

2016-01-01

Behavioral interventions are becoming increasingly popular approaches to ameliorate age-related cognitive decline, but their underlying neurobiological mechanisms and clinical efficiency have not been fully elucidated. The present study explored brain plasticity associated with two behavioral interventions, memory enhancement training (MET) and a mind-body practice (yogic meditation), in healthy seniors with mild cognitive impairment (MCI) using structural magnetic resonance imaging (s-MRI) and proton magnetic resonance spectroscopy ( 1 H-MRS). Senior participants (age ≥55 years) with MCI were randomized to the MET or yogic meditation interventions. For both interventions, participants completed either MET training or Kundalini Yoga (KY) for 60-min sessions over 12 weeks, with 12-min daily homework assignments. Gray matter volume and metabolite concentrations in the dorsal anterior cingulate cortex (dACC) and bilateral hippocampus were measured by structural MRI and 1 H-MRS at baseline and after 12 weeks of training. Metabolites measured included glutamate-glutamine (Glx), choline-containing compounds (Cho, including glycerophosphocholine and phosphocholine), gamma-aminobutyric acid (GABA), and N-acetyl aspartate and N-acetylaspartyl-glutamate (NAA-NAAG). In total, 11 participants completed MET and 14 completed yogic meditation for this study. Structural MRI analysis showed an interaction between time and group in dACC, indicating a trend towards increased gray matter volume after the MET intervention. 1 H-MRS analysis showed an interaction between time and group in choline-containing compounds in bilateral hippocampus, induced by significant decreases after the MET intervention. Though preliminary, our results suggest that memory training induces structural and neurochemical plasticity in seniors with MCI. Further research is needed to determine whether mind-body interventions like yoga yield similar neuroplastic changes.

[Comparison of visual impairment caused by trachoma in China between 1978 and 2006].

Science.gov (United States)

Hu, Ailian; Cai, Xiaogu; Qiao, Liya; Zhang, Ye; Zhang, Xu; Sun, Baochen; Wang, Ningli

2015-10-01

To understand the distribution of visual impairment caused by trachoma in China and provide evidences for evaluation of eliminating blinding trachoma in China in the mission of Vision 2020. Sampling study. The results from the first year 1987 and second (year 2006) national sampling surveys of disabled persons were analyzed. Chi-square test was performed using SAS 9.30 to analyze the rates of visual impairment caused by trachoma in different groups. Unifactor and multifactor analyses were applied to analyze the relevance between visual impairment caused by trachoma and risk factors, including gender and age. The rate of visual impairment caused by trachoma was 102.01 persons/100 000 in 1987 and 17.62 persons/100 000 in 2006. The percentage of trachoma in all kinds of visual impairment was 14.25% in 1987 and 1.87% in 2006, and the difference was significant (F = 1 382.6, P visual impairment caused by trachoma. H-aggregation areas included Hubei, Sichuan, Anhui, Shannxi, Guizhou, Hunan provinces and Chongqing Municipality. Survival time without trachoma between 1987 and 2006 was significantly different (F = 2 745.9, P visual impairment caused by trachoma increased with age. Except the group of > 85 years, the rate of visual impairment caused by trachoma in all age groups in 1987 was significantly higher than that in 2006. The risk of visual impairment caused by trachoma in 1987 was 5.8 times that in 2006. If the other risk factors were not involved, the risk in 1987 was 8.75 times that in 2006. The risk in females was twice that in males. Both, the rate and risk of visual impairment caused by trachoma were significantly reduced in China. Impressive progresses were achieved in trachoma prevention and control.

Clean Water Act 303(d) Listed Impaired Waters and their Causes of Impairment from All Years

Data.gov (United States)

U.S. Environmental Protection Agency — Waters identified as impaired as well as their associated causes of impairment from all approved Clean Water Act 303(d) lists submitted by the states. Includes all...

Causes of visual impairment in children: a study of 3,210 cases.

Science.gov (United States)

Haddad, Maria Aparecida Onuki; Sei, Mayumi; Sampaio, Marcos Wilson; Kara-José, Newton

2007-01-01

To determine causes of visual impairment in children at the Low Vision Service of the Ophthalmic Clinic at the University of São Paulo and at the Brazilian Association for the Visually Impaired People (Laramara), located in São Paulo, Brazil. This study evaluated 3,210 visually impaired children (49% female, 51% male; average age, 5.9 years). Visual impairment was present in 57% (visually impaired group) and 43% presented another associated disability (multiple disability group). The main causes of visual impairment in the visually impaired group were toxoplasmic macular retinochoroiditis (20.7%), retinal dystrophies (12.2%), retinopathy of prematurity (11.8%), ocular malformation (11.6%), congenital glaucoma (10.8%), optic atrophy (9.7%), and congenital cataracts (7.1%). The main causes of visual impairment in the multiple disability group were optic atrophy (37.7%), cortical visual impairment (19.7%), toxoplasmic macular retinochoroiditis (8.6%), retinopathy of prematurity (7.6%), ocular malformation (6.8%), congenital cataracts (6.1%), and degenerative disorders of the retina and macula (4.8%). The retina was the most frequently affected anatomic site in the visually impaired group (49.2%) and the optic nerve in the multiple disability group (39%). Primary, secondary, and tertiary prevention efforts for childhood blindness and visual rehabilitation must be considered in Latin America.

Neurochemical changes underpinning the development of adjunct therapies in recovery after stroke: A role for GABA?

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Johnstone, Ainslie; Levenstein, Jacob M; Hinson, Emily L; Stagg, Charlotte J

2017-01-01

Stroke is a leading cause of long-term disability, with around three-quarters of stroke survivors experiencing motor problems. Intensive physiotherapy is currently the most effective treatment for post-stroke motor deficits, but much recent research has been targeted at increasing the effects of the intervention by pairing it with a wide variety of adjunct therapies, all of which aim to increase cortical plasticity, and thereby hope to maximize functional outcome. Here, we review the literature describing neurochemical changes underlying plasticity induction following stroke. We discuss methods of assessing neurochemicals in humans, and how these measurements change post-stroke. Motor learning in healthy individuals has been suggested as a model for stroke plasticity, and we discuss the support for this model, and what evidence it provides for neurochemical changes. One converging hypothesis from animal, healthy and stroke studies is the importance of the regulation of the inhibitory neurotransmitter GABA for the induction of cortical plasticity. We discuss the evidence supporting this hypothesis, before finally summarizing the literature surrounding the use of adjunct therapies such as non-invasive brain stimulation and SSRIs in post-stroke motor recovery, both of which have been show to influence the GABAergic system.

Causes of visual impairment in children with low vision.

Science.gov (United States)

Shah, Mufarriq; Khan, Mirzaman; Khan, Muhammad Tariq; Khan, Mohammad Younas; Saeed, Nasir

2011-02-01

To determine the main causes of visual impairment in children with low vision. To assess the need of spectacles and low vision devices (LVDs) in children and to evaluate visual outcome after using their LVDs for far and near distance. Observational study. Khyber Institute of Ophthalmic Medical Sciences, Peshawar, Pakistan, from June 2006 to December 2007. The clinical record of 270 children with low vision age 4-16 years attending the Low Vision Clinic were included. All those children, aged 4-16 years, who had corrected visual acuity (VA) less than 6/18 in the better eye after medical or surgical treatment, were included in the study. WHO low vision criteria were used to classify into visually impaired, severe visually impaired and blind. Results were described as percentage frequencies. One hundred and eighty nine (70%) were males and 81 (30%) were females. The male to female ratio was 2.3:1. The main causes of visual impairment included nystagmus (15%), Stargardt's disease (14%), maculopathies (13%), myopic macular degeneration (11%) and oculocutaneous albinism (7%). The percentages of visually impaired, severe visually impaired and blind were 33.8%, 27.2% and 39.0% respectively. Spectacles were prescribed to 146 patients and telescopes were prescribed to 75 patients. Spectacles and telescope both were prescribed to 179 patients while Ocutech telescope was prescribed to 4 patients. Retinal diseases nystagmus and macular conditions were mainly responsible for low vision in children. Visually impaired children especially with hereditary/congenital ocular anomalies benefit from refraction and low vision services which facilitate vision enhancement and inclusive education.

Prevalence and causes of visual impairment and blindness among 9980 Scandinavian adults

DEFF Research Database (Denmark)

Buch, Helena; Vinding, Troels; La Cour, Morten

2004-01-01

To investigate the age-specific prevalence and causes of visual impairment and blindness in an epidemiologic study of an adult Scandinavian population.......To investigate the age-specific prevalence and causes of visual impairment and blindness in an epidemiologic study of an adult Scandinavian population....

The prevalence and causes of visual impairment in seven-year-old children.

Science.gov (United States)

Ghaderi, Soraya; Hashemi, Hassan; Jafarzadehpur, Ebrahim; Yekta, Abbasali; Ostadimoghaddam, Hadi; Mirzajani, Ali; Khabazkhoob, Mehdi

2018-05-01

To report the prevalence and causes of visual impairment in seven-year-old children in Iran and its relationship with socio-economic conditions. In a cross-sectional population-based study, first-grade students in the primary schools of eight cities in the country were randomly selected from different geographic locations using multistage cluster sampling. The examinations included visual acuity measurement, ocular motility evaluation, and cycloplegic and non-cycloplegic refraction. Using the definitions of the World Health Organization (presenting visual acuity less than or equal to 6/18 in the better eye) to estimate the prevalence of vision impairment, the present study reported presenting visual impairment in seven-year-old children. Of 4,614 selected students, 4,106 students participated in the study (response rate 89 per cent), of whom 2,127 (51.8 per cent) were male. The prevalence of visual impairment according to a visual acuity of 6/18 was 0.341 per cent (95 per cent confidence interval 0.187-0.571); 1.34 per cent (95 per cent confidence interval 1.011-1.74) of children had visual impairment according to a visual acuity of 6/18 in at least one eye. Sixty-six (1.6 per cent) and 23 (0.24 per cent) children had visual impairment according to a visual acuity of 6/12 in the worse and better eye, respectively. The most common causes of visual impairment were refractive errors (81.8 per cent) and amblyopia (14.5 per cent). Among different types of refractive errors, astigmatism was the main refractive error leading to visual impairment. According to the concentration index, the distribution of visual impairment in children from low-income families was higher. This study revealed a high prevalence of visual impairment in a representative sample of seven-year-old Iranian children. Astigmatism and amblyopia were the most common causes of visual impairment. The distribution of visual impairment was higher in children from low-income families. Cost

Behavioral metabolomics analysis identifies novel neurochemical signatures in methamphetamine sensitization

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Adkins, Daniel E.; McClay, Joseph L.; Vunck, Sarah A.; Batman, Angela M.; Vann, Robert E.; Clark, Shaunna L.; Souza, Renan P.; Crowley, James J.; Sullivan, Patrick F.; van den Oord, Edwin J.C.G.; Beardsley, Patrick M.

2014-01-01

Behavioral sensitization has been widely studied in animal models and is theorized to reflect neural modifications associated with human psychostimulant addiction. While the mesolimbic dopaminergic pathway is known to play a role, the neurochemical mechanisms underlying behavioral sensitization remain incompletely understood. In the present study, we conducted the first metabolomics analysis to globally characterize neurochemical differences associated with behavioral sensitization. Methamphetamine-induced sensitization measures were generated by statistically modeling longitudinal activity data for eight inbred strains of mice. Subsequent to behavioral testing, nontargeted liquid and gas chromatography-mass spectrometry profiling was performed on 48 brain samples, yielding 301 metabolite levels per sample after quality control. Association testing between metabolite levels and three primary dimensions of behavioral sensitization (total distance, stereotypy and margin time) showed four robust, significant associations at a stringent metabolome-wide significance threshold (false discovery rate < 0.05). Results implicated homocarnosine, a dipeptide of GABA and histidine, in total distance sensitization, GABA metabolite 4-guanidinobutanoate and pantothenate in stereotypy sensitization, and myo-inositol in margin time sensitization. Secondary analyses indicated that these associations were independent of concurrent methamphetamine levels and, with the exception of the myo-inositol association, suggest a mechanism whereby strain-based genetic variation produces specific baseline neurochemical differences that substantially influence the magnitude of MA-induced sensitization. These findings demonstrate the utility of mouse metabolomics for identifying novel biomarkers, and developing more comprehensive neurochemical models, of psychostimulant sensitization. PMID:24034544

Causes of Childhood Vision Impairment in the School for the Blind in Eritrea.

Science.gov (United States)

Gyawali, Rajendra; Moodley, Vanessa R

2017-12-01

Our study provides the much-needed evidence on causes of childhood blindness in Eritrea. This will assist authorities to plan appropriate strategies and implement preventive, curative, and rehabilitative services to address these causes of vision loss in children in this resource-limited country. This study aims to identify the causes of severe vision impairment and blindness in children attending the only school for the blind in Eritrea. All children enrolled in the school were examined, and the World Health Organization form for the examination of visually impaired children was used to record the data. Examination included visual acuity, refraction, anterior segment, and fundus assessment. Causes of vision loss for children with severe vision impairment (visual acuity blindness (visual acuity blindness. The major causes of vision loss were corneal scars (16.9%), cataract (12.7%), phthisis bulbi (11.3%), congenital eye deformities (11.3%), optic atrophy (9.3%), and presumed chorioretinal Toxoplasma scars (7.0%). Hereditary factors were the major known etiological category (15.5%) followed by the sequel of eye injuries (12.7%). Blindness due to vitamin A deficiency was not found, whereas infectious causes such as measles and ophthalmia neonatorum were relatively absent (one case each). Potentially avoidable causes of vision impairment were accounted for in 47.9% of children. This study provides the first direct evidence on childhood vision impairment in Eritrea. Despite the limitations, it is clearly shown that nearly half of the vision loss is due to avoidable causes. Thus, preventive public health strategies, specialist pediatric eye care, and rehabilitative services are recommended to address childhood vision impairment in Eritrea.

Causes of permanent childhood hearing impairment.

Science.gov (United States)

Korver, Anna M H; Admiraal, Ronald J C; Kant, Sarina G; Dekker, Friedo W; Wever, Capi C; Kunst, Henricus P M; Frijns, Johan H M; Oudesluys-Murphy, Anne Marie

2011-02-01

The causes of Permanent Childhood Hearing Impairment (PCHI) are often quoted as being hereditary in 50%, acquired in 25%, and unknown in 25% of cases. Interest in the causes of PCHI has grown recently due to increasing diagnostic possibilities. We investigated the evidence for the reported distribution of these causes. Population-based study and a systematic review. Inclusion criteria for population-based study: children born between 2003 and 2005, resident in The Netherlands at birth, known at an Audiology Center with PCHI at the age of 3-5 years. The causes of PCHI were determined prospectively by detection of congenital cytomegalovirus on dried blood spots and/or genetic diagnostic investigations in addition to reviewing data from medical records. A systematic review was carried out using three terms (hearing loss, infant, and etiology) and limited to articles published between January 1997 and July 2009. Main outcome measures were: the (weighted) proportions of the various causes of PCHI following diagnostic investigations. In the study-population (n = 185) a hereditary cause was found in 38.9%, acquired cause in 29.7%, miscellaneous cause in 7.1%, and the cause remained unknown in 24.3%. The systematic review of the literature (n = 9 articles) resulted in a weighted mean of 30.4% hereditary, 19.2% acquired, and 48.3% unknown causes of PCHI. The systematic review and the results of the population-based study provided little support for the generally accepted distribution of causes of PCHI. Copyright © 2010 The American Laryngological, Rhinological, and Otological Society, Inc.

Cerebral visual impairment in children: Causes and associated ophthalmological problems.

Science.gov (United States)

Pehere, Niranjan; Chougule, Pratik; Dutton, Gordon N

2018-06-01

The aim of this study is to identify common causes, associated ophthalmological abnormalities, and systemic comorbidities in children in Andhra Pradesh, India, with cerebral visual impairment (CVI). A retrospective review of case records of all children aged visual impairment was seen in 88.8%, and 11.2% had high functioning CVI. Fifty-eight (46.4%) patients had significant refractive errors, 40 (32.25%) had strabismus, 4 (3.2%) had visually significant cataract, and 40 (32%) had optic atrophy. Motor delay was observed in 39.5%, speech delay was evident in 22.4%, and cognitive delay in 16%. HIE is the most common cause (one-third) of CVI in our population, and the majority of them presented at age visual impairment (88.8%). A significant number of them have treatable ophthalmic conditions such as refractive errors (46.4%), accommodative insufficiency (12.1%), and cataract (3.2%), and more than one-third of them also have delay in other areas of development.

Prevalence and causes of blindness and visual impairment among school children in south-western Nigeria.

Science.gov (United States)

Ajaiyeoba, A I; Isawumi, M A; Adeoye, A O; Oluleye, T S

2005-01-01

The aim of the study was to assess the prevalence and identify the causes of blindness and visual impairment in school children of Ilesa-East Local Government Area of Osun State, Nigeria. A total of 1144 school children in primary and secondary schools were selected using a 2-stage random sampling method and examined to determine the prevalence and causes of blindness and visual impairment. A total of 17 (1.48%) children were blind or visually impaired. These comprised of 11 (0.96%) children who were visually impaired and 4 (0.3%) who were severely visually impaired. Only 2 (0.15%) school children were blind. The causes of visual impairment were refractive error 10 (0.87%) and immature cataract 1 (0.08%), causes of severe visual impairment included corneal opacities 2 (0.2%), amblyopia leading to squint 1 (0.08%) and 1 cataract 1 (0.08%). The causes of blindness in school children were corneal scars presumed to be due to vitamin A deficiency 1 (0.08%) and keratoconus 1 (0.08%). Causes of blindness and visual impairment in children attending regular schools in Nigeria were treatable. Prevention, early recognition and prompt treatment of these diseases by regular screening of school children would definitely reduce unnecessary visual handicap in Nigerian school children so that they can attain their full potential in the course of their education. Also, information from this study is relevant for the purpose of planning eye care programmes for the prevention of blindness in Nigerian school children. This will go a long way in the prevention of unnecessary blindness and visual impairment in school children.

Prevalence and Causes of Visual Impairment and Blindness in Shanxi Province, China.

Science.gov (United States)

Li, Tong; Du, Liping; Du, Lingzhen

2015-01-01

To estimate the prevalence and causes of visual impairment and blindness in Shanxi Province, China. Data were obtained from the Second National Sampling Survey of Disability conducted in 2006. Blindness and visual impairment were defined as best corrected visual acuity Visual acuity (VA) was measured using a Standard Logarithmic Visual Acuity E chart (Snellen) for subjects aged 7 years and older. Participants younger than 7 years were examined using special experiments or the Childhood Graphical Visual Chart. The prevalence of visual impairment and blindness in Shanxi was estimated to be 0.6% (466/75,016) among persons up to 80 years old. The prevalence in rural areas (0.7%; 351/48,137) was significantly higher than that in urban areas (0.4%; 115/26,879) and was higher in females (0.8%; 298/36,933) than in males (0.4%; 168/38,083). The most common cause of visual impairment and blindness was cataract (44.9%), followed by retinopathy and choroidopathy (12.5%), hereditary and developmental disorders (10.3%), corneal disease (5.2%), and refractive error (4.9%). Prevalences of visual impairment and blindness in women and in rural areas were higher than in men and urban areas, and increased with age. Cataract was the most prevalent cause of visual impairment and blindness. Based on the findings from this study, we suggest that provision of support and welfare services should be organized.

Multivoxel proton magnetic resonance spectroscopy detects thalamic neurochemical metabolic changes in patients with major depressive disorder

Directory of Open Access Journals (Sweden)

Rania E. Mohamed

2017-06-01

Conclusion: The multi-voxel 1H-MRS can provide an insight to the neurochemical metabolic changes occurring in both thalami in patients with MDD. Increased severity of depression is significantly related to these thalamic neurochemical changes.

Linking Essential Tremor to the Cerebellum: Neurochemical Evidence.

Science.gov (United States)

Marin-Lahoz, Juan; Gironell, Alexandre

2016-06-01

The pathophysiology and the exact anatomy of essential tremor (ET) is not well known. One of the pillars that support the cerebellum as the main anatomical locus in ET is neurochemistry. This review examines the link between neurochemical abnormalities found in ET and cerebellum. The review is based on published data about neurochemical abnormalities described in ET both in human and in animal studies. We try to link those findings with cerebellum. γ-aminobutyric acid (GABA) is the main neurotransmitter involved in the pathophysiology of ET. There are several studies about GABA that clearly points to a main role of the cerebellum. There are few data about other neurochemical abnormalities in ET. These include studies with noradrenaline, glutamate, adenosine, proteins, and T-type calcium channels. One single study reveals high levels of noradrenaline in the cerebellar cortex. Another study about serotonin neurotransmitter results negative for cerebellum involvement. Finally, studies on T-type calcium channels yield positive results linking the rhythmicity of ET and cerebellum. Neurochemistry supports the cerebellum as the main anatomical locus in ET. The main neurotransmitter involved is GABA, and the GABA hypothesis remains the most robust pathophysiological theory of ET to date. However, this hypothesis does not rule out other mechanisms and may be seen as the main scaffold to support findings in other systems. We clearly need to perform more studies about neurochemistry in ET to better understand the relations among the diverse systems implied in ET. This is mandatory to develop more effective pharmacological therapies.

Metabolomics reveals distinct neurochemical profiles associated with stress resilience

Directory of Open Access Journals (Sweden)

Brooke N. Dulka

2017-12-01

Full Text Available Acute social defeat represents a naturalistic form of conditioned fear and is an excellent model in which to investigate the biological basis of stress resilience. While there is growing interest in identifying biomarkers of stress resilience, until recently, it has not been feasible to associate levels of large numbers of neurochemicals and metabolites to stress-related phenotypes. The objective of the present study was to use an untargeted metabolomics approach to identify known and unknown neurochemicals in select brain regions that distinguish susceptible and resistant individuals in two rodent models of acute social defeat. In the first experiment, male mice were first phenotyped as resistant or susceptible. Then, mice were subjected to acute social defeat, and tissues were immediately collected from the ventromedial prefrontal cortex (vmPFC, basolateral/central amygdala (BLA/CeA, nucleus accumbens (NAc, and dorsal hippocampus (dHPC. Ultra-high performance liquid chromatography coupled with high resolution mass spectrometry (UPLC-HRMS was used for the detection of water-soluble neurochemicals. In the second experiment, male Syrian hamsters were paired in daily agonistic encounters for 2 weeks, during which they formed stable dominant-subordinate relationships. Then, 24 h after the last dominance encounter, animals were exposed to acute social defeat stress. Immediately after social defeat, tissue was collected from the vmPFC, BLA/CeA, NAc, and dHPC for analysis using UPLC-HRMS. Although no single biomarker characterized stress-related phenotypes in both species, commonalities were found. For instance, in both model systems, animals resistant to social defeat stress also show increased concentration of molecules to protect against oxidative stress in the NAc and vmPFC. Additionally, in both mice and hamsters, unidentified spectral features were preliminarily annotated as potential targets for future experiments. Overall, these findings

Quantitative autoradiography of neurochemicals

International Nuclear Information System (INIS)

Rainbow, T.C.; Biegon, A.; Bleisch, W.V.

1982-01-01

Several new methods have been developed that apply quantitative autoradiography to neurochemistry. These methods are derived from the 2-deoxyglucose (2DG) technique of Sokoloff (1), which uses quantitative autoradiography to measure the rate of glucose utilization in brain structures. The new methods allow the measurement of the rate of cerbral protein synthesis and the levels of particular neurotransmitter receptors by quantitative autoradiography. As with the 2DG method, the new techniques can measure molecular levels in micron-sized brain structures; and can be used in conjunction with computerized systems of image processing. It is possible that many neurochemical measurements could be made by computerized analysis of quantitative autoradiograms

Neurochemical imaging of Alzheimer's disease and other degenerative dementias

International Nuclear Information System (INIS)

Frey, K.A.; Minoshima, S.; Kuhl, D.E.

1998-01-01

A wide variety of neurochemical and functional imaging approaches have been applied to the study of progressive dementias, particularly Alzheimer's disease (Ad) and related disorders. Despite considerable progress in the past decade, the cause((s) of most cases of Ad remain undetermined and preventive or protective therapies are lacking. Specifically-designed imaging procedures have permitted the testing of pathophysiological hypotheses of the etiology and progression of Ad, and have yielded important insights in several areas including the potential roles of cerebral cortical cholinergic lesions, cellular inflammation, and losses of cortical synapses. From the perspective of clinical diagnosis, PET glucose metabolism imaging with use of ( 18 F)2-fluorodeoxyglucose (FDG) is the most sensitive and specific imaging modality yet identified. The overall performance of PET FDG is favorable for routine clinical evaluation of suspected Ad, and will likely gain increasing utilization in the near future. Assessments of glucose metabolism and other, specific aspects of neurochemistry in Ad will provide direct measures of therapeutic drug actions and may permit distinction of symptomatic versus disease-modifying therapies as they are developed and introduced in clinical trials

A diamond-based electrode for detection of neurochemicals in the human brain

Directory of Open Access Journals (Sweden)

Kevin E. Bennet

2016-03-01

Full Text Available Deep brain stimulation (DBS, a surgical technique to treat certain neurologic and psychiatric conditions, relies on pre-determined stimulation parameters in an open-loop configuration. The major advancement in DBS devices is a closed-loop system that uses neurophysiologic feedback to dynamically adjust stimulation frequency and amplitude. Stimulation-driven neurochemical release can be measured by fast-scan cyclic voltammetry (FSCV, but existing FSCV electrodes rely on carbon fiber, which degrades quickly during use and is therefore unsuitable for chronic neurochemical recording. To address this issue, we developed durable, synthetic boron-doped diamond-based electrodes capable of measuring neurochemical release in humans. Compared to carbon fiber electrodes, they were more than two orders-of-magnitude more physically-robust and demonstrated longevity in vitro without deterioration. Applied for the first time in humans, diamond electrode recordings from thalamic targets in patients (n=4 undergoing DBS for tremor produced signals consistent with adenosine release at a sensitivity comparable to carbon fiber electrodes.

Neurochemical metabolites in prefrontal cortex in patients with mild/moderate levels in first-episode depression

Directory of Open Access Journals (Sweden)

Sozeri-Varma G

2013-08-01

Full Text Available Gülfizar Sözeri-Varma,1 Nalan Kalkan-Oğuzhanoglu,1 Muharrem Efe,1 Yilmaz Kiroglu,2 Taçlan Duman11Department of Psychiatry, 2Department of Radiology, Faculty of Medicine, Pamukkale University, Denizli, TurkeyBackground: Previous studies have determined the neurochemical metabolite abnormalities in major depressive disorder (MDD. The results of studies are inconsistent. Severity of depression may relate to neurochemical metabolic changes. The aim of this study is to investigate neurochemical metabolite levels in the prefrontal cortex (PFC of patients with mild/moderate MDD.Methods: Twenty-one patients with mild MDD, 18 patients with moderate MDD, and 16 matched control subjects participated in the study. Patients had had their first episode. They had not taken treatment. The severity of depression was assessed by the Hamilton Rating Scale for Depression (HAM-D. Levels of N-acetyl aspartate (NAA, choline-containing compounds (Cho, and creatine-containing compounds (Cr were measured using proton magnetic resonance spectroscopy (1H-MRS at 1.5 T, with an 8-cm3 single voxel placed in the right PFC.Results: The moderate MDD patients had lower NAA/Cr levels than the control group. No differences were found in neurochemical metabolite levels between the mild MDD and control groups. No correlation was found between the patients’ neurochemical metabolite levels and HAM-D scores.Conclusion: Our findings suggest that NAA/Cr levels are low in moderate-level MDD in the PFC. Neurochemical metabolite levels did not change in mild depressive disorder. Our results suggest that the severity of depression may affect neuronal function and viability. Studies are needed to confirm this finding, including studies on severely depressive patients.Keywords: major depressive disorder, magnetic resonance spectroscopy, N-acetyl aspartate, creatine, choline

Effects of electroconvulsive seizures on depression-related behavior, memory and neurochemical changes in Wistar and Wistar-Kyoto rats.

Science.gov (United States)

Kyeremanteng, C; MacKay, J C; James, J S; Kent, P; Cayer, C; Anisman, H; Merali, Z

2014-10-03

Investigations in healthy outbred rat strains have shown a potential role for brain-derived neurotrophic factor (BDNF) and the hypothalamic-pituitary-adrenal (HPA) axis in the antidepressant and memory side effects of electroconvulsive therapy (ECT, or ECS in animals). The Wistar-Kyoto (WKY) rat strain is used as a genetic model of depression yet no studies to date have directly compared the impact of ECS on the WKY strain to its healthy outbred control (Wistar). The objective of this study is to examine behavioral (antidepressant and retrograde memory) and neurochemical (BDNF and HPA axis) changes immediately (1day) and at a longer delay (7days) after repeated ECS (5 daily administrations) in WKY and Wistar rats. Male Wistar and WKY rats received 5days of repeated ECS or sham treatment and were assessed 1 and 7days later for 1) depression-like behavior and mobility; 2) retrograde memory; and 3) brain BDNF protein, brain corticotropin-releasing factor (CRF) and plasma corticosterone levels. Both strains showed the expected antidepressant response and retrograde memory impairments at 1day following ECS, which were sustained at 7days. In addition, at 1day after ECS, Wistar and WKY rats showed similar elevations in brain BDNF and extra-hypothalamic CRF and no change in plasma corticosterone. At 7days after ECS, Wistar rats showed sustained elevations of brain BDNF and CRF, whereas WKY rats showed a normalization of brain BDNF, despite sustained elevations of brain CRF. The model of 5 daily ECS was effective at eliciting behavioral and neurochemical changes in both strains. A temporal association was observed between brain CRF levels, but not BDNF, and measures of antidepressant effectiveness of ECS and retrograde memory impairments suggesting that extra-hypothalamic CRF may be a potential important contributor to these behavioral effects after repeated ECS/ECT. Copyright © 2014 Elsevier Inc. All rights reserved.

Prevalence and causes of hearing impairment in Fundong Health District, North-West Cameroon.

Science.gov (United States)

Ferrite, Silvia; Mactaggart, Islay; Kuper, Hannah; Oye, Joseph; Polack, Sarah

2017-04-01

To estimate the prevalence and causes of hearing impairment in Fundong Health District, North-West Cameroon. We selected 51 clusters of 80 people (all ages) through probability proportionate to size sampling. Initial hearing screening was undertaken through an otoacoustic emission (OAE) test. Participants aged 4+ years who failed this test in both ears or for whom an OAE reading could not be taken underwent a manual pure-tone audiometry (PTA) screening. Cases of hearing impairment were defined as those with pure-tone average ≥41 dBHL in adults and ≥35 dBHL in children in the better ear, or children under age 4 who failed the OAE test in both ears. Each case with hearing loss was examined by an ear, nose and throat nurse who indicated the main likely cause. We examined 3567 (86.9%) of 4104 eligible people. The overall prevalence of hearing impairment was 3.6% (95% confidence interval [CI]: 2.8-4.6). The prevalence was low in people aged 0-17 (1.1%, 0.7-1.8%) and 18-49 (1.1%, 0.5-2.6%) and then rose sharply in people aged 50+ (14.8%, 11.7-19.1%). Among cases, the majority were classified as moderate (76%), followed by severe (15%) and profound (9%). More than one-third of cases of hearing impairment were classified as unknown (37%) or conductive (37%) causes, while sensorineural causes were less common (26%). Prevalence of hearing impairment in North-West Cameroon is in line with the WHO estimate for sub-Saharan Africa. The majority of cases with known causes are treatable, with impacted wax playing a major role. © 2017 John Wiley & Sons Ltd.

Neurochemical enhancement of conscious error awareness.

Science.gov (United States)

Hester, Robert; Nandam, L Sanjay; O'Connell, Redmond G; Wagner, Joe; Strudwick, Mark; Nathan, Pradeep J; Mattingley, Jason B; Bellgrove, Mark A

2012-02-22

How the brain monitors ongoing behavior for performance errors is a central question of cognitive neuroscience. Diminished awareness of performance errors limits the extent to which humans engage in corrective behavior and has been linked to loss of insight in a number of psychiatric syndromes (e.g., attention deficit hyperactivity disorder, drug addiction). These conditions share alterations in monoamine signaling that may influence the neural mechanisms underlying error processing, but our understanding of the neurochemical drivers of these processes is limited. We conducted a randomized, double-blind, placebo-controlled, cross-over design of the influence of methylphenidate, atomoxetine, and citalopram on error awareness in 27 healthy participants. The error awareness task, a go/no-go response inhibition paradigm, was administered to assess the influence of monoaminergic agents on performance errors during fMRI data acquisition. A single dose of methylphenidate, but not atomoxetine or citalopram, significantly improved the ability of healthy volunteers to consciously detect performance errors. Furthermore, this behavioral effect was associated with a strengthening of activation differences in the dorsal anterior cingulate cortex and inferior parietal lobe during the methylphenidate condition for errors made with versus without awareness. Our results have implications for the understanding of the neurochemical underpinnings of performance monitoring and for the pharmacological treatment of a range of disparate clinical conditions that are marked by poor awareness of errors.

Clinical characteristics and causes of visual impairment in a low vision clinic in northern Jordan.

Science.gov (United States)

Bakkar, May M; Alzghoul, Eman A; Haddad, Mera F

2018-01-01

The aim of the study was to identify causes of visual impairment among patients attending a low vision clinic in the north of Jordan and to study the relevant demographic characteristics of these patients. The retrospective study was conducted through a review of clinical records of 135 patients who attended a low vision clinic in Irbid. Clinical characteristics of the patients were collected, including age, gender, primary cause of low vision, best corrected visual acuity, and current prescribed low vision aids. Descriptive statistics analysis using numbers and percentages were calculated to summarize categorical and nominal data. A total of 135 patients (61 [45.2%] females and 74 [54.8%] males) were recruited in the study. Mean age ± standard deviation for the study population was 24.53 ± 16.245 years; age range was 5-90 years. Of the study population, 26 patients (19.3%) had mild visual impairment, 61 patients (45.2%) had moderate visual impairment, 27 patients (20.0%) had severe visual impairment, and 21 patients (15.6%) were blind. The leading causes of visual impairment across all age groups were albinism (31.9%) and retinitis pigmentosa (RP) (18.5%). Albinism also accounted for the leading cause of visual impairment among the pediatric age group (0-15 years) while albinism, RP, and keratoconus were the primary causes of visual impairment for older patients. A total of 59 patients (43.7%) were given low vision aids either for near or distance. The only prescribed low vision aids for distances were telescopes. For near, spectacle-type low vision aid was the most commonly prescribed low vision aids. Low vision services in Jordan are still very limited. A national strategy programme to increase awareness of low vision services should be implemented, and health care policies should be enforced to cover low vision aids through the national medical insurance.

Pupillometry as a glimpse into the neurochemical basis of human memory encoding.

Science.gov (United States)

Hoffing, Russell Cohen; Seitz, Aaron R

2015-04-01

Neurochemical systems are well studied in animal learning; however, ethical issues limit methodologies to explore these systems in humans. Pupillometry provides a glimpse into the brain's neurochemical systems, where pupil dynamics in monkeys have been linked with locus coeruleus (LC) activity, which releases norepinephrine (NE) throughout the brain. Here, we use pupil dynamics as a surrogate measure of neurochemical activity to explore the hypothesis that NE is involved in modulating memory encoding. We examine this using a task-irrelevant learning paradigm in which learning is boosted for stimuli temporally paired with task targets. We show that participants better recognize images that are paired with task targets than distractors and, in correspondence, that pupil size changes more for target-paired than distractor-paired images. To further investigate the hypothesis that NE nonspecifically guides learning for stimuli that are present with its release, a second procedure was used that employed an unexpected sound to activate the LC-NE system and induce pupil-size changes; results indicated a corresponding increase in memorization of images paired with the unexpected sounds. Together, these results suggest a relationship between the LC-NE system, pupil-size changes, and human memory encoding.

Prevalence and causes of blindness and visual impairment in the ...

African Journals Online (AJOL)

Public information systems, epidemiological data and funding for blindness programmes are often lacking and have hampered comprehensive blindness control programmes in the rural communities, a fact that underscores the importance of this study. Aim: To estimate the prevalence and causes of visual impairment and ...

Impaired fatty acid oxidation as a cause for lipotoxicity in cardiomyocytes

Energy Technology Data Exchange (ETDEWEB)

Haffar, T. [Université de Montreal (Canada); Montreal Heart Institute (Canada); Bérubé-Simard, F. [Montreal Heart Institute (Canada); Bousette, N., E-mail: nicolas.bousette@umontreal.ca [Université de Montreal (Canada); Montreal Heart Institute (Canada)

2015-12-04

A major cause for diabetic cardiomyopathy is excess lipid accumulation. To elucidate mechanisms of lipotoxicity mediated diabetic heart disease we need to further our understanding of how lipid metabolism is altered in the diabetic heart. Here we investigated the role of lipid clearance by oxidation as a regulator of lipid-mediated toxicity (lipotoxicity). We evaluated the effect of pre-treating rat neonatal cardiomyocytes (NCMs) with either oleate (mono-unsaturated fatty acid) or palmitate (saturated fatty acid) on fatty acid oxidation (FAO) by measuring {sup 14}C–CO{sub 2} production. We evaluated carnitine palmitoyltransferase (Cpt1b) expression by western blotting and mitochondrial membrane potential by quantitative and qualitative fluorescence analyses using the JC-1 dye. We inhibited the Cpt1b pharmacologically using etomoxir and genetically by knocking down its expression using LentiVector mediated transduction of siRNAs targeting the Cpt1b gene. We found that palmitate had a slower clearance rate from NCMs than oleate, and this was associated with a significant decrease in FAO. This impairment in FAO was not the result of either loss of Cpt1b protein or mitochondrial integrity. Enhancing FAO with either oleate or carnitine was associated with a significant attenuation of palmitate mediated lipotoxicity. In contrast impairing FAO in oleate treated NCMs caused lipotoxicity. Here we demonstrate that a major difference between non-toxic unsaturated fatty acids and toxic saturated fatty acids is there ability to stimulate or inhibit fatty acid oxidation, respectively. This has important implications for diabetic cardiomyopathy since diabetic hearts consistently exhibit elevated lipid accumulation. - Highlights: • Palmitate had a slower clearance rate from NCMs than oleate. • Palmitate caused a significant decrease in fatty acid oxidation in cardiomyocytes. • Impaired FAO was not due to loss of Cpt1b protein or mitochondrial integrity. • Enhancing FAO

Impaired fatty acid oxidation as a cause for lipotoxicity in cardiomyocytes

International Nuclear Information System (INIS)

Haffar, T.; Bérubé-Simard, F.; Bousette, N.

2015-01-01

A major cause for diabetic cardiomyopathy is excess lipid accumulation. To elucidate mechanisms of lipotoxicity mediated diabetic heart disease we need to further our understanding of how lipid metabolism is altered in the diabetic heart. Here we investigated the role of lipid clearance by oxidation as a regulator of lipid-mediated toxicity (lipotoxicity). We evaluated the effect of pre-treating rat neonatal cardiomyocytes (NCMs) with either oleate (mono-unsaturated fatty acid) or palmitate (saturated fatty acid) on fatty acid oxidation (FAO) by measuring "1"4C–CO_2 production. We evaluated carnitine palmitoyltransferase (Cpt1b) expression by western blotting and mitochondrial membrane potential by quantitative and qualitative fluorescence analyses using the JC-1 dye. We inhibited the Cpt1b pharmacologically using etomoxir and genetically by knocking down its expression using LentiVector mediated transduction of siRNAs targeting the Cpt1b gene. We found that palmitate had a slower clearance rate from NCMs than oleate, and this was associated with a significant decrease in FAO. This impairment in FAO was not the result of either loss of Cpt1b protein or mitochondrial integrity. Enhancing FAO with either oleate or carnitine was associated with a significant attenuation of palmitate mediated lipotoxicity. In contrast impairing FAO in oleate treated NCMs caused lipotoxicity. Here we demonstrate that a major difference between non-toxic unsaturated fatty acids and toxic saturated fatty acids is there ability to stimulate or inhibit fatty acid oxidation, respectively. This has important implications for diabetic cardiomyopathy since diabetic hearts consistently exhibit elevated lipid accumulation. - Highlights: • Palmitate had a slower clearance rate from NCMs than oleate. • Palmitate caused a significant decrease in fatty acid oxidation in cardiomyocytes. • Impaired FAO was not due to loss of Cpt1b protein or mitochondrial integrity. • Enhancing FAO attenuated

Neurochemical phenotype of cytoglobin‑expressing neurons in the rat hippocampus

DEFF Research Database (Denmark)

Hundahl, Christian Ansgar; Fahrenkrug, Jan; Hannibal, Jens

2014-01-01

in a subpopulation of brain neurons. Recently, it has been shown that stress upregulates Cygb expression in the brain and the majority of neuronal nitric oxide synthase (nNOS)-positive neurons, an enzyme that produces NO, co-express Cygb. However, there are more neurons expressing Cygb than nNOS, thus a large number...... of Cygb neurons remain uncharacterized by the neurochemical content. The aim of the present study was to provide an additional and more detailed neurochemical phenotype of Cygb-expressing neurons in the rat hippocampus. The rat hippocampus was chosen due to the abundance of Cygb, as well as this limbic...... structure being an important target in a number of neurodegenerative diseases. Using triple immunohistochemistry, it was demonstrated that nearly all the parvalbumin- and heme oxygenase 1-positive neurons co-express Cygb and to a large extent, these neuron populations are distinct from the population...

Clinical characteristics and causes of visual impairment in a low vision clinic in northern Jordan

Directory of Open Access Journals (Sweden)

Bakkar MM

2018-04-01

Full Text Available May M Bakkar, Eman A Alzghoul, Mera F Haddad Faculty of Applied Medical Sciences, Department of Allied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan Aim: The aim of the study was to identify causes of visual impairment among patients attending a low vision clinic in the north of Jordan and to study the relevant demographic characteristics of these patients.Subjects and methods: The retrospective study was conducted through a review of clinical records of 135 patients who attended a low vision clinic in Irbid. Clinical characteristics of the patients were collected, including age, gender, primary cause of low vision, best corrected visual acuity, and current prescribed low vision aids. Descriptive statistics analysis using numbers and percentages were calculated to summarize categorical and nominal data.Results: A total of 135 patients (61 [45.2%] females and 74 [54.8%] males were recruited in the study. Mean age ± standard deviation for the study population was 24.53 ± 16.245 years; age range was 5–90 years. Of the study population, 26 patients (19.3% had mild visual impairment, 61 patients (45.2% had moderate visual impairment, 27 patients (20.0% had severe visual impairment, and 21 patients (15.6% were blind. The leading causes of visual impairment across all age groups were albinism (31.9% and retinitis pigmentosa (RP (18.5%. Albinism also accounted for the leading cause of visual impairment among the pediatric age group (0–15 years while albinism, RP, and keratoconus were the primary causes of visual impairment for older patients. A total of 59 patients (43.7% were given low vision aids either for near or distance. The only prescribed low vision aids for distances were telescopes. For near, spectacle-type low vision aid was the most commonly prescribed low vision aids.Conclusion: Low vision services in Jordan are still very limited. A national strategy programme to increase awareness of low vision

Neurochemical dynamics of acute orofacial pain in the human trigeminal brainstem nuclear complex.

Science.gov (United States)

de Matos, Nuno M P; Hock, Andreas; Wyss, Michael; Ettlin, Dominik A; Brügger, Mike

2017-11-15

The trigeminal brainstem sensory nuclear complex is the first central relay structure mediating orofacial somatosensory and nociceptive perception. Animal studies suggest a substantial involvement of neurochemical alterations at such basal CNS levels in acute and chronic pain processing. Translating this animal based knowledge to humans is challenging. Human related examining of brainstem functions are challenged by MR related peculiarities as well as applicability aspects of experimentally standardized paradigms. Based on our experience with an MR compatible human orofacial pain model, the aims of the present study were twofold: 1) from a technical perspective, the evaluation of proton magnetic resonance spectroscopy at 3 T regarding measurement accuracy of neurochemical profiles in this small brainstem nuclear complex and 2) the examination of possible neurochemical alterations induced by an experimental orofacial pain model. Data from 13 healthy volunteers aged 19-46 years were analyzed and revealed high quality spectra with significant reductions in total N-acetylaspartate (N-acetylaspartate + N-acetylaspartylglutamate) (-3.7%, p = 0.009) and GABA (-10.88%, p = 0.041) during the pain condition. These results might reflect contributions of N-acetylaspartate and N-acetylaspartylglutamate in neuronal activity-dependent physiologic processes and/or excitatory neurotransmission, whereas changes in GABA might indicate towards a reduction in tonic GABAergic functioning during nociceptive signaling. Summarized, the present study indicates the applicability of 1 H-MRS to obtain neurochemical dynamics within the human trigeminal brainstem sensory nuclear complex. Further developments are needed to pave the way towards bridging important animal based knowledge with human research to understand the neurochemistry of orofacial nociception and pain. Copyright © 2017 Elsevier Inc. All rights reserved.

Recent Advances in Mass Spectrometry for the Identification of Neuro-chemicals and their Metabolites in Biofluids.

Science.gov (United States)

Kailasa, Suresh Kumar; Wu, Hui-Fen

2013-07-01

Recently, mass spectrometric related techniques have been widely applied for the identification and quantification of neurochemicals and their metabolites in biofluids. This article presents an overview of mass spectrometric techniques applied in the detection of neurological substances and their metabolites from biological samples. In addition, the advances of chromatographic methods (LC, GC and CE) coupled with mass spectrometric techniques for analysis of neurochemicals in pharmaceutical and biological samples are also discussed.

Neurochemical Correlates of Autistic Disorder: A Review of the Literature

Science.gov (United States)

Lam, Kristen S. L.; Aman, Michael G.; Arnold, L. Eugene

2006-01-01

Review of neurochemical investigations in autistic disorder revealed that a wide array of transmitter systems have been studied, including serotonin, dopamine, norepinephrine, acetylcholine, oxytocin, endogenous opioids, cortisol, glutamate, and gamma-aminobutyric acid (GABA). These studies have been complicated by the fact that autism is a very…

Effects of Gladiolus dalenii on the Stress-Induced Behavioral, Neurochemical, and Reproductive Changes in Rats

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David Fotsing

2017-09-01

Full Text Available Gladiolus dalenii is a plant commonly used in many regions of Cameroon as a cure for various diseases like headaches, epilepsy, schizophrenia, and mood disorders. Recent studies have revealed that the aqueous extract of G. dalenii (AEGD exhibited antidepressant-like properties in rats. Therefore, we hypothesized that the AEGD could protect from the stress-induced behavioral, neurochemical, and reproductive changes in rats. The objective of the present study was to elucidate the effect of the AEGD on behavioral, neurochemical, and reproductive characteristics, using female rats subjected to chronic immobilization stress. The chronic immobilization stress (3 h per day for 28 days was applied to induce female reproductive and behavioral impairments in rats. The immobilization stress was provoked in rats by putting them separately inside cylindrical restrainers with ventilated doors at ambient temperature. The plant extract was given to rats orally everyday during 28 days, 5 min before induction of stress. On a daily basis, a vaginal smear was made to assess the duration of the different phases of the estrous cycle and at the end of the 28 days of chronic immobilization stress, the rat’s behavior was assessed in the elevated plus maze. They were sacrificed by cervical disruption. The organs were weighed, the ovary histology done, and the biochemical parameters assessed. The findings of this research revealed that G. dalenii increased the entries and the time of open arm exploration in the elevated plus maze. Evaluation of the biochemical parameters levels indicated that there was a significant reduction in the corticosterone, progesterone, and prolactin levels in the G. dalenii aqueous extract treated rats compared to stressed rats whereas the levels of serotonin, triglycerides, adrenaline, cholesterol, glucose estradiol, follicle stimulating hormone and luteinizing hormone were significantly increased in the stressed rats treated with, G. dalenii

Induction of gram-negative bacterial growth by neurochemical containing banana (Musa x paradisiaca) extracts.

Science.gov (United States)

Lyte, M

1997-09-15

Bananas contain large quantities of neurochemicals. Extracts from the peel and pulp of bananas in increasing stages of ripening were prepared and evaluated for their ability to modulate the growth of non-pathogenic and pathogenic bacteria. Extracts from the peel, and to a much lesser degree the pulp, increased the growth of Gram-negative bacterial strains Escherichia coli O157:H7, Shigella flexneri, Enterobacter cloacae and Salmonella typhimurium, as well as two non-pathogenic E. coli strains, in direct relation to the content of norepinephrine and dopamine, but not serotonin. The growth of Gram-positive bacteria was not altered by any of the extracts. Supplementation of vehicle and pulp cultures with norepinephrine or dopamine yielded growth equivalent to peel cultures. Total organic analysis of extracts further demonstrated that the differential effects of peel and pulp on bacterial growth was not nutritionally based, but due to norepinephrine and dopamine. These results suggest that neurochemicals contained within foodstuffs may influence the growth of pathogenic and indigenous bacteria through direct neurochemical-bacterial interactions.

[Frequency and causes of blindness and visual impairment in schools for the blind in Yaoundé (Cameroon)].

Science.gov (United States)

Noche, Christelle Domngang; Bella, Assumpta Lucienne

2010-01-01

To determine the causes of blindness and visual impairment in students attending schools for the blind in Yaounde (Cameroon) and to estimate their frequencies. This study examined all 56 students at three schools for the blind in Yaoundé from September 15 through October 15, 2006. We collected data about their age, sex, medical and surgical history. Visual acuity was measured to determine their vision status according to the World Health Organization categories for blindness and visual impairment. All subjects underwent an ocular examination. Epi Info 3.5.1. was used for the statistical analysis of age, sex, visual acuity, causes of blindness and visual impairment, and etiologies. Fifty six people were examined: 37 men (66.1%) and 19 women (33.9%). Their mean age was 21.57 ± 10.53 years (min-max: 5-49), and 48.2% were in the 10-19 years age group (n = 27). In all, 87.5% were blind, 7.14% severely visually impaired, and 1.78% moderately visually impaired. The main causes of blindness and visual impairment in our sample were corneal disease (32.14%), optic nerve lesions (26.78%), cataract and its surgical complications (19.64%), retinal disorders (10.71%), glaucoma (8.92%, and malformations of the eyeball (1.78%). Their etiologies included congenital cataracts (19.64%), meningitis/fever (8.92%), glaucoma (7.14%), measles (5.35%), ocular trauma (5.35%), albinism (3.57%), Lyell syndrome (1.8%), and alcohol ingestion (1.8%). Etiology was unknown in 46.42%. Fifty per cent of these causes of blindness and visual impairment were treatable and/or preventable. Corneal lesions were the main cause of blindness and visual impairment in our sample. Fifty per cent of the causes found were treatable and/or preventable. Thus, substantial efforts are required to ensure access to better quality specialist ocular care. Furthermore, local authorities should create more centers specialised in the rehabilitation of the visual handicapped.

Thiamine Deficiency Induced Neurochemical, Neuroanatomical, and Neuropsychological Alterations: A Reappraisal

Directory of Open Access Journals (Sweden)

Raffaele Nardone

2013-01-01

Full Text Available Nutritional deficiency can cause, mainly in chronic alcoholic subjects, the Wernicke encephalopathy and its chronic neurological sequela, the Wernicke-Korsakoff syndrome (WKS. Long-term chronic ethanol abuse results in hippocampal and cortical cell loss. Thiamine deficiency also alters principally hippocampal- and frontal cortical-dependent neurochemistry; moreover in WKS patients, important pathological damage to the diencephalon can occur. In fact, the amnesic syndrome typical for WKS is mainly due to the damage in the diencephalic-hippocampal circuitry, including thalamic nuclei and mammillary bodies. The loss of cholinergic cells in the basal forebrain region results in decreased cholinergic input to the hippocampus and the cortex and reduced choline acetyltransferase and acetylcholinesterase activities and function, as well as in acetylcholine receptor downregulation within these brain regions. In this narrative review, we will focus on the neurochemical, neuroanatomical, and neuropsychological studies shedding light on the effects of thiamine deficiency in experimental models and in humans.

Causes of blindness and visual impairment among students in integrated schools for the blind in Nepal.

Science.gov (United States)

Shrestha, Jyoti Baba; Gnyawali, Subodh; Upadhyay, Madan Prasad

2012-12-01

To identify the causes of blindness and visual impairment among students in integrated schools for the blind in Nepal. A total of 778 students from all 67 integrated schools for the blind in Nepal were examined using the World Health Organization/Prevention of Blindness Eye Examination Record for Children with Blindness and Low Vision during the study period of 3 years. Among 831 students enrolled in the schools, 778 (93.6%) participated in the study. Mean age of students examined was 13.7 years, and the male to female ratio was 1.4:1. Among the students examined, 85.9% were blind, 10% had severe visual impairment and 4.1% were visually impaired. The cornea (22.8%) was the most common anatomical site of visual impairment, its most frequent cause being vitamin A deficiency, followed by the retina (18.4%) and lens (17.6%). Hereditary and childhood factors were responsible for visual loss in 27.9% and 22.0% of students, respectively. Etiology could not be determined in 46% of cases. Overall, 40.9% of students had avoidable causes of visual loss. Vision could be improved to a level better than 6/60 in 3.6% of students refracted. More than one third of students were visually impaired for potentially avoidable reasons, indicating lack of eye health awareness and eye care services in the community. The cause of visual impairment remained unknown in a large number of students, which indicates the need for introduction of modern diagnostic tools.

The prevalence and causes of visual impairment and blindness among older adults in the city of Lodz, Poland.

Science.gov (United States)

Nowak, Michal S; Smigielski, Janusz

2015-02-01

To investigate the prevalence and causes of visual impairment and blindness in a sample of Polish older adults. The study was designed in a cross-sectional and observational manner. Data concerning the vision status were assessed in 2214 eyes from 1107 subjects of European Caucasian origin; most of whom live in the city of Lodz, in central Poland. Visual impairment was defined as distance visual acuity visual acuity (BCVA) 20/200 in better-seeing eye, and blindness was defined as BCVA ≤20/200 in both eyes (United States criteria). Visual impairment was found in 27.5% subjects in the worse-seeing eye. Multiple regression analysis showed that increasing age (OR 0.98, 95% CI 0.97-0.99) and female gender (OR 1.47, 95% CI 1.11-1.93) were independent risk factors. No association was found between visual impairment and socioeconomic status of subjects. Noncorrectable visual impairment was found in 7.0% of subjects, including 5.2% of subjects with unilateral and 1.8% of subjects with bilateral visual impairment. Low vision and blindness accounted for 1.3% and 0.5%, respectively, and were only associated with older age (OR 1.05, 95% CI 1.02-1.10). Retinal diseases represented the major cause of noncorrectable visual impairment and accounted for more than half of causes of blindness. Provision of appropriate refractive correction improves visual acuity in 75% subjects presenting with visual impairment. Retinal diseases are a major cause of noncorrectable visual impairment and blindness in this older population.

Association of disease-specific causes of visual impairment and 10-year mortality amongst Indigenous Australians: the Central Australian Ocular Health Study.

Science.gov (United States)

Estevez, José; Kaidonis, Georgia; Henderson, Tim; Craig, Jamie E; Landers, John

2018-01-01

Visual impairment significantly impairs the length and quality of life, but little is known of its impact in Indigenous Australians. To investigate the association of disease-specific causes of visual impairment with all-cause mortality. A retrospective cohort analysis. A total of 1347 Indigenous Australians aged over 40 years. Participants visiting remote medical clinics underwent clinical examinations including visual acuity, subjective refraction and slit-lamp examination of the anterior and posterior segments. The major ocular cause of visual impairment was determined. Patients were assessed periodically in these remote clinics for the succeeding 10 years after recruitment. Mortality rates were obtained from relevant departments. All-cause 10-year mortality and its association with disease-specific causes of visual impairment. The all-cause mortality rate for the entire cohort was 29.3% at the 10-year completion of follow-up. Of those with visual impairment, the overall mortality rate was 44.9%. The mortality rates differed for those with visual impairment due to cataract (59.8%), diabetic retinopathy (48.4%), trachoma (46.6%), 'other' (36.2%) and refractive error (33.4%) (P visual impairment from diabetic retinopathy were any more likely to die during the 10 years of follow-up when compared with those without visual impairment (HR 1.70; 95% CI, 1.00-2.87; P = 0.049). Visual impairment was associated with all-cause mortality in a cohort of Indigenous Australians. However, diabetic retinopathy was the only ocular disease that significantly increased the risk of mortality. Visual impairment secondary to diabetic retinopathy may be an important predictor of mortality. © 2017 Royal Australian and New Zealand College of Ophthalmologists.

Kcne2 deletion impairs insulin secretion and causes type 2 diabetes mellitus.

Science.gov (United States)

Lee, Soo Min; Baik, Jasmine; Nguyen, Dara; Nguyen, Victoria; Liu, Shiwei; Hu, Zhaoyang; Abbott, Geoffrey W

2017-06-01

Type 2 diabetes mellitus (T2DM) represents a rapidly increasing threat to global public health. T2DM arises largely from obesity, poor diet, and lack of exercise, but it also involves genetic predisposition. Here we report that the KCNE2 potassium channel transmembrane regulatory subunit is expressed in human and mouse pancreatic β cells. Kcne2 deletion in mice impaired glucose tolerance as early as 5 wk of age in pups fed a Western diet, ultimately causing diabetes. In adult mice fed normal chow, skeletal muscle expression of insulin receptor β and insulin receptor substrate 1 were down-regulated 2-fold by Kcne2 deletion, characteristic of T2DM. Kcne2 deletion also caused extensive pancreatic transcriptome changes consistent with facets of T2DM, including endoplasmic reticulum stress, inflammation, and hyperproliferation. Kcne2 deletion impaired β-cell insulin secretion in vitro up to 8-fold and diminished β-cell peak outward K + current at positive membrane potentials, but also left-shifted its voltage dependence and slowed inactivation. Interestingly, we also observed an aging-dependent reduction in β-cell outward currents in both Kcne2 +/+ and Kcne2 - / - mice. Our results demonstrate that KCNE2 is required for normal β-cell electrical activity and insulin secretion, and that Kcne2 deletion causes T2DM. KCNE2 may regulate multiple K + channels in β cells, including the T2DM-linked KCNQ1 potassium channel α subunit.-Lee, S. M., Baik, J., Nguyen, D., Nguyen, V., Liu, S., Hu, Z., Abbott, G. W. Kcne2 deletion impairs insulin secretion and causes type 2 diabetes mellitus. © FASEB.

Age-related changes of neurochemically different subpopulations of cardiac spinal afferent neurons in rats.

Science.gov (United States)

Guić, Maja Marinović; Runtić, Branka; Košta, Vana; Aljinović, Jure; Grković, Ivica

2013-08-01

This study investigated the effect of aging on cardiac spinal afferent neurons in the rat. A patch loaded with retrograde tracer Fast Blue (FB) was applied to all chambers of the rat heart. Morphological and neurochemical characteristics of labeled cardiac spinal afferent neurons were assessed in young (2 months) and old (2 years) rats using markers for likely unmyelinated (isolectin B4; IB4) and myelinated (neurofilament 200; N52) neurons. The number of cardiac spinal afferent neurons decreased in senescence to 15% of that found in young rats (1604 vs. 248). The size of neuronal soma as well as proportion of IB4+ neurons increased significantly, whereas the proportion of N52+ neurons decreased significantly in senescence. Unlike somatic spinal afferents, neurochemically different populations of cardiac spinal afferent neurons experience morphological and neurochemical changes related to aging. A major decrease in total number of cardiac spinal afferent neurons occurs in senescence. The proportion of N52+ neurons decreased in senescence, but it seems that nociceptive innervation is preserved due to increased proportion and size of IB4+ unmyelinated neurons. Copyright © 2013 Elsevier Inc. All rights reserved.

Personality and neurochemicals in the human brain: A preliminary study using 1H MRS

Institute of Scientific and Technical Information of China (English)

XU Shiyong; PENG Danling; JIN Zhen; LIU Hongyan; YANG Jie

2005-01-01

To investigate the neuro-biological bases of introversion-extraversion personality traits, the concentra- tion of four neurochemicals (Cho, mI, α-Glx and NAA) in anterior cigulate gyrus between normal extroverts and introverts were examined using non-invasive 1H MRS technique. Our study revealed that introverts have significantly higher level of α-Glx, Cho and mI in the anterior cingulate gyrus than extroverts. This result provides new evidence that the anterior cingulate gyrus is related to personality traits partly in support of Eysenck's supposition that introverts have higher arousal level than extroverts. Moreover, this result offers neurochemical data for psychobiological theories of personality.

Prevalence and Causes of Visual Impairment in Fundong District, North West Cameroon: Results of a Population-Based Survey.

Science.gov (United States)

Oye, Joseph; Mactaggart, Islay; Polack, Sarah; Schmidt, Elena; Tamo, Violet; Okwen, Marvice; Kuper, Hannah

2017-12-01

To estimate the prevalence and causes of visual impairment in Fundong Health District, North West Cameroon. A total of 51 clusters of 80 people (all ages) were sampled with probability proportionate to size and compact segment sampling. Visual acuity (VA) was measured with a tumbling "E" chart. An ophthalmic nurse examined people with VAimpairments were assessed using clinical examination, and self-reported visual problems using the Washington Group Short Set. In total, 4080 people were enumerated of whom 3567 were screened (response rate 87%). The overall prevalence of visual impairment was 2.3% (95% CI 1.8-3.0%) and blindness was 0.6% (0.3-1.0%). The prevalence of both blindness and visual impairment increased rapidly with age, so that the vast majority of cases of visual impairment (84%) and blindness (82%) were in people aged 50+. Posterior segment disease and cataract were the main causes of blindness and visual impairment, with refractive error also an important cause of visual impairment. Cataract surgical coverage (proportion of all cataracts that had received surgery) was relatively high (87% of people at VAvisual impairment, 22% had a physical impairment or epilepsy and 30% had a hearing impairment. Self-reported difficulties in vision were relatively closely related to clinical measures of visual impairment. Ophthalmic programmes in Cameroon need to incorporate control of posterior segment diseases while also working to improve outcomes after cataract surgery.

Rapid recovery and altered neurochemical dependence of locomotor central pattern generation following lumbar neonatal spinal cord injury.

Science.gov (United States)

Züchner, Mark; Kondratskaya, Elena; Sylte, Camilla B; Glover, Joel C; Boulland, Jean-Luc

2018-01-15

Spinal compression injury targeted to the neonatal upper lumbar spinal cord, the region of highest hindlimb locomotor rhythmogenicity, leads to an initial paralysis of the hindlimbs. Behavioural recovery is evident within a few days and approaches normal function within about 3 weeks. Fictive locomotion in the isolated injured spinal cord cannot be elicited by a neurochemical cocktail containing NMDA, dopamine and serotonin 1 day post-injury, but can 3 days post-injury as readily as in the uninjured spinal cord. Low frequency coordinated rhythmic activity can be elicited in the isolated uninjured spinal cord by NMDA + dopamine (without serotonin), but not in the isolated injured spinal cord. In both the injured and uninjured spinal cord, eliciting bona fide fictive locomotion requires the additional presence of serotonin. Following incomplete compression injury in the thoracic spinal cord of neonatal mice 1 day after birth (P1), we previously reported that virtually normal hindlimb locomotor function is recovered within about 3 weeks despite substantial permanent thoracic tissue loss. Here, we asked whether similar recovery occurs following lumbar injury that impacts more directly on the locomotor central pattern generator (CPG). As in thoracic injuries, lumbar injuries caused about 90% neuronal loss at the injury site and increased serotonergic innervation below the injury. Motor recovery was slower after lumbar than thoracic injury, but virtually normal function was attained by P25 in both cases. Locomotor CPG status was tested by eliciting fictive locomotion in isolated spinal cords using a widely used neurochemical cocktail (NMDA, dopamine, serotonin). No fictive locomotion could be elicited 1 day post-injury, but could within 3 days post-injury as readily as in age-matched uninjured control spinal cords. Burst patterning and coordination were largely similar in injured and control spinal cords but there were differences. Notably, in both groups there

Brain Metabolism Alterations Induced by Pregnancy Swimming Decreases Neurological Impairments Following Neonatal Hypoxia-Ischemia in Very Immature Rats

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Eduardo F. Sanches

2018-06-01

Full Text Available Introduction: Prematurity, through brain injury and altered development is a major cause of neurological impairments and can result in motor, cognitive and behavioral deficits later in life. Presently, there are no well-established effective therapies for preterm brain injury and the search for new strategies is needed. Intra-uterine environment plays a decisive role in brain maturation and interventions using the gestational window have been shown to influence long-term health in the offspring. In this study, we investigated whether pregnancy swimming can prevent the neurochemical metabolic alterations and damage that result from postnatal hypoxic-ischemic brain injury (HI in very immature rats.Methods: Female pregnant Wistar rats were divided into swimming (SW or sedentary (SE groups. Following a period of adaptation before mating, swimming was performed during the entire gestation. At postnatal day (PND3, rat pups from SW and SE dams had right common carotid artery occluded, followed by systemic hypoxia. At PND4 (24 h after HI, the early neurochemical profile was measured by 1H-magnetic resonance spectroscopy. Astrogliosis, apoptosis and neurotrophins protein expression were assessed in the cortex and hippocampus. From PND45, behavioral testing was performed. Diffusion tensor imaging and neurite orientation dispersion and density imaging were used to evaluate brain microstructure and the levels of proteins were quantified.Results: Pregnancy swimming was able to prevent early metabolic changes induced by HI preserving the energetic balance, decreasing apoptotic cell death and astrogliosis as well as maintaining the levels of neurotrophins. At adult age, swimming preserved brain microstructure and improved the performance in the behavioral tests.Conclusion: Our study points out that swimming during gestation in rats could prevent prematurity related brain damage in progeny with high translational potential and possibly interesting cost

Piperine Augments the Protective Effect of Curcumin Against Lipopolysaccharide-Induced Neurobehavioral and Neurochemical Deficits in Mice.

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Jangra, Ashok; Kwatra, Mohit; Singh, Tavleen; Pant, Rajat; Kushwah, Pawan; Sharma, Yogita; Saroha, Babita; Datusalia, Ashok Kumar; Bezbaruah, Babul Kumar

2016-06-01

The aim of the present study was to investigate the protective effects of curcumin alone and in combination with piperine against lipopolysaccharide (LPS)-induced neurobehavioral and neurochemical deficits in the mice hippocampus. Mice were treated with curcumin (100, 200, and 400 mg/kg, p.o.) and piperine (20 mg/kg, p.o.) for 7 days followed by LPS (0.83 mg/kg, i.p.) administration. Animals exhibited anxiety and depressive-like phenotype after 3 and 24 h of LPS exposure, respectively. LPS administration increased the oxido-nitrosative stress as evident by elevated levels of malondialdehyde, nitrite, and depletion of glutathione level in the hippocampus. Furthermore, we found raised level of pro-inflammatory cytokines (IL-1β and TNF-α) in the hippocampus of LPS-treated mice. Pretreatment with curcumin alleviated LPS-induced neurobehavioral and neurochemical deficits. Furthermore, co-administration of curcumin with piperine significantly potentiated the neuroprotective effect of curcumin. These results demonstrate that piperine enhanced the neuroprotective effect of curcumin against LPS-induced neurobehavioral and neurochemical deficits.

Suicide: Neurochemical Approaches

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Ritabrata Banerjee

2013-10-01

Full Text Available Despite the devastating effect of suicide on numerous lives, there is still a dearthof knowledge concerning its neurochemical aspects. There is increasing evidence that brain-derived neurotrophic factor (BDNF and Nerve growth factor (NGF are involved in the pathophysiology and treatment of depression through binding and activating their cognate receptors trk B and trk A respectively. The present study was performed to examine whether the expression profiles of BDNF and/or trk B as well as NGF and/or trk A were altered in postmortem brain in subjects who commitsuicide and whether these alterations were associated with specific psychopathologic conditions. These studies were performed in hippocampus obtained 21 suicide subjects and 19 non-psychiatric control subjects. The protein and mRNA levels of BDNF, trk B and NGF, trk A were determined with Sandwich ELISA, Western Blot and RT PCR respectively. Given the importance of BDNFand NGF along with their cognate receptors in mediating physiological functions, including cell survival and synaptic plasticity, our findings of reduced expression of BDNF, Trk B and NGF, Trk A in both protein and mRNA levels of postmortem brain in suicide subjects suggest that these molecules may play an important role in the pathophysiological aspects of suicidal behavior.

Impairments of learning and memory in the rats after brain irradiation

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Takai, Nobuhiko [National Inst. of Radiological Sciences, Chiba (Japan)

2002-06-01

Clinical trials of hadrontherapy have been carried out world wide at several facilities including National Institute of Radiological Sciences (NIRS). Cerebral dysfunction is one of the major concerns associated with radiotherapy of brain tumors. However, little is known about the neurochemical basis of brain dysfunction induced by proton irradiation. We investigated and reported here the early consequences of brain damages caused by proton beam. The animals that had memorized the location of the standard position were locally irradiated to brain with either 70 MeV protons or 290 MeV carbon ions. At 24 hr after irradiation, impairment of the long-term memory was not observed in the irradiated rats compared to control. Irradiated animals, however, required substantially longer time finding out the standard position than control rats when the standard platform displaced to a position different from memorized position. This follows that a single doses of 30 Gy, either protons or carbon ions, impairs the working memory of animals. Function of muscarinic acetylcholine receptors was analyzed by an in vivo binding assay using radioligand quinuclidinyl benzilate (QNB). Irradiated rats were intravenously injected with 5.5 MBq of {sup 3}H-QNB 24 hr after the irradiation, and decapitated 60 min after tracer injection. The autoradiographic studies showed an transitional increase of {sup 3}H-QNB in vivo binding in the early phase after proton irradiation, even though no change in in-vitro {sup 3}H-QNB binding was see in brain autoradiograms of irradiated rats. The cerebral blood flow and the histrogical features of brain were also changed at 3 months post-irradiation. These results indicate that the memory impairment caused by radiation is closely related to the early change of acetylcholine receptor in vivo. (author)

Impairments of learning and memory in the rats after brain irradiation

International Nuclear Information System (INIS)

Takai, Nobuhiko

2002-01-01

Clinical trials of hadrontherapy have been carried out world wide at several facilities including National Institute of Radiological Sciences (NIRS). Cerebral dysfunction is one of the major concerns associated with radiotherapy of brain tumors. However, little is known about the neurochemical basis of brain dysfunction induced by proton irradiation. We investigated and reported here the early consequences of brain damages caused by proton beam. The animals that had memorized the location of the standard position were locally irradiated to brain with either 70 MeV protons or 290 MeV carbon ions. At 24 hr after irradiation, impairment of the long-term memory was not observed in the irradiated rats compared to control. Irradiated animals, however, required substantially longer time finding out the standard position than control rats when the standard platform displaced to a position different from memorized position. This follows that a single doses of 30 Gy, either protons or carbon ions, impairs the working memory of animals. Function of muscarinic acetylcholine receptors was analyzed by an in vivo binding assay using radioligand quinuclidinyl benzilate (QNB). Irradiated rats were intravenously injected with 5.5 MBq of 3 H-QNB 24 hr after the irradiation, and decapitated 60 min after tracer injection. The autoradiographic studies showed an transitional increase of 3 H-QNB in vivo binding in the early phase after proton irradiation, even though no change in in-vitro 3 H-QNB binding was see in brain autoradiograms of irradiated rats. The cerebral blood flow and the histrogical features of brain were also changed at 3 months post-irradiation. These results indicate that the memory impairment caused by radiation is closely related to the early change of acetylcholine receptor in vivo. (author)

Causes of vision impairment and assessment of need for low vision services for students of blind schools in Nepal.

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Kansakar, I; Thapa, H B; Salma, K C; Ganguly, S; Kandel, R P; Rajasekaran, S

The present study is first of its kind to evaluate causes of visual impairment of blind students in Nepal and assess their need for low vision rehabilitation services. To evaluate causes of vision impairment of students enrolled in blind schools in Nepal and assess the need for low vision rehabilitation services in these students. A survey was conducted in 12 blind schools in Nepal, which were registered with Nepal Association for Welfare of Blindness (NAWB).It was conducted by a team of an ophthalmologist and an optometrist, by using standard eye examination protocols of the World Health Organization Prevention of Blindness Program (WHO/PBL). Of the 345 students enrolled in 12 schools, 285 students were examined (response rate of 82.61%). The students were in the 5 - 29 years age group. Nearly three-fourth of the children had become blind within one year of age and 52.3% visually impaired at birth and 20.7% developed vision impairment within one year of age. After refraction, 26 students (9.12%) had mild visual impairment, 21 students (7.37%) had severe visual impairment and 238 students (83.51%) were blind. The main cause of vision impairment was found to be corneal 35.79% and retina diseases, mainly dystrophy, 20.35% followed by problems with the whole globe, lens and optic nerve, accounting for 13.33%, 12.63% and 12.98% respectively. The major etiological factors were those of childhood such as Vitamin A deficiency, measles and similar causes (42.11%) followed by hereditary causes (25.26%). Of the total students examined, 48.07% were visually impaired due to preventable causes and 16.14% treatable aggregating to 64.21% of avoidable blindness. Fifty seven (28.22%) students could read smaller than 2 M print size after low vision assessment for near and 33(15.78%) students benefited with telescopic trial for distance low vision. In Nepal, renewed focus on providing best possible quality of life for visually impaired children by proper low vision assessment and eye

Covertly active and progressing neurochemical abnormalities in suppressed HIV infection.

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Cysique, Lucette A; Jugé, Lauriane; Gates, Thomas; Tobia, Michael; Moffat, Kirsten; Brew, Bruce J; Rae, Caroline

2018-01-01

To assess whether HIV-related brain injury is progressive in persons with suppressed HIV infection. Seventy-three HIV+ virally suppressed men and 35 HIV- men, screened for psychiatric and alcohol/drug use disorders, underwent neuropsychological evaluation and proton magnetic resonance spectroscopy ( 1 H-MRS) at baseline and after and 23 ± 5 months. 1 H-MRS included brain regions known to be vulnerable to HIV and aging: frontal white matter (FWM), posterior cingulate cortex (PCC), and caudate area (CA). Major brain metabolites such as creatine (Cr: marker of cellular energy), N -acetyl aspartate (NAA: marker of neuronal integrity), choline (marker of cellular membrane turnover), glutamate/glutamine (excitatory/inhibitory neurotransmitter), and myo -Inositol (mI: marker of neuroinflammation) were calculated with reference to water signal. Neurocognitive decline was corrected for practice effect and baseline HIV-associated neurocognitive disorder (HAND) status. Across the study period, 44% had intact cognition, 42% stable HAND (including the single case that improved), 10% progressing HAND, and 4% incident HAND. When analyzing the neurochemical data per neurocognitive trajectories, we found decreasing PCC Cr in all subgroups compared with controls ( p < 0.002). In addition, relative to the HIV- group, stable HAND showed decreasing FWM Cr, incident HAND showed steep FWM Cr reduction, whereas progressing HAND had a sharply decreasing PCC NAA and reduced but stable CA NAA. When analyzing the neurochemical data at the group level (HIV+ vs HIV- groups), we found stable abnormal metabolite concentrations over the study period: decreased FWM and PCC Cr (both p < 0.001), decreased PCC NAA and CA NAA (both p < 0.05) and PCC mI increase ( p < 0.05). HIV duration and historical HAND had modest effects on metabolite changes. Our study reveals covertly active or progressing HIV-related brain injury in the majority of this virally suppressed cohort, reflecting ongoing

Comparison of Different Matrices as Potential Quality Control Samples for Neurochemical Dementia Diagnostics

NARCIS (Netherlands)

Lelental, Natalia; Brandner, Sebastian; Kofanova, Olga; Blennow, Kaj; Zetterberg, Henrik; Andreasson, Ulf; Engelborghs, Sebastiaan; Mroczko, Barbara; Gabryelewicz, Tomasz; Teunissen, Charlotte; Mollenhauer, Brit; Parnetti, Lucilla; Chiasserini, Davide; Molinuevo, Jose Luis; Perret-Liaudet, Armand; Verbeek, Marcel M.; Andreasen, Niels; Brosseron, Frederic; Bahl, Justyna M. C.; Herukka, Sanna-Kaisa; Hausner, Lucrezia; Froelich, Lutz; Labonte, Anne; Poirier, Judes; Miller, Anne-Marie; Zilka, Norbert; Kovacech, Branislav; Urbani, Andrea; Suardi, Silvia; Oliveira, Catarina; Baldeiras, Ines; Dubois, Bruno; Rot, Uros; Lehmann, Sylvain; Skinningsrud, Anders; Betsou, Fay; Wiltfang, Jens; Gkatzima, Olymbia; Winblad, Bengt; Buchfelder, Michael; Kornhuber, Johannes; Lewczuk, Piotr

2016-01-01

Background: Assay-vendor independent quality control (QC) samples for neurochemical dementia diagnostics (NDD) biomarkers are so far commercially unavailable. This requires that NDD laboratories prepare their own QC samples, for example by pooling leftover cerebrospinal fluid (CSF) samples.

Neurochemical Changes after Acute Binge Toluene Inhalation in Adolescent and Adult Rats: A High-Resolution Magnetic Resonance Spectroscopy Study

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O'Leary-Moore, Shonagh K.; Galloway, Matthew P.; McMechan, Andrew P.; Irtenkauf, Susan; Hannigan, John H.; Bowen, Scott E.

2009-01-01

Inhalant abuse in young people is a growing public health concern. We reported previously that acute toluene intoxication in young rats, using a pattern of exposures that approximate abuse patterns of inhalant use in humans, significantly altered neurochemical measures in select brain regions. In this study, adolescent and young adult rats were exposed similarly to an acute (2 × 15 min), high dose (8000 − 12000 ppm) of toluene and high-resolution magic angle spinning proton magnetic resonance spectroscopy (HR-MAS 1H-MRS) was used to assess neurochemical profiles of tissue samples from a number of brain regions collected immediately following solvent exposure. The current investigation focused on N-acetyl-aspartate (NAA), choline-containing compounds, creatine, glutamate, GABA, and glutamine. Contrary to our predictions, no significant alterations were found in levels of NAA, choline, creatine, glutamate, or glutamine in adolescent animals. In contrast to these minimal effects in adolescents, binge toluene exposure altered several neurochemical parameters in young adult rats, including decreased levels of choline and GABA in the frontal cortex and striatum and lowered glutamine and NAA levels in the frontal cortex. One of the more robust findings was a wide-ranging increase in lactate after toluene exposure in adult animals, an effect not observed in adolescents. These age-dependent effects of toluene are distinct from those reported previously in juvenile rats and suggest a developmental difference in vulnerability to the effects of inhalants. Specifically, the results suggest that the neurochemical response to toluene in adolescents is attenuated compared to adults, and imply an association between these neurochemical differences and age-influenced differences in solvent abuse in humans. PMID:19628036

Global causes of blindness and distance vision impairment 1990-2020: a systematic review and meta-analysis.

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Flaxman, Seth R; Bourne, Rupert R A; Resnikoff, Serge; Ackland, Peter; Braithwaite, Tasanee; Cicinelli, Maria V; Das, Aditi; Jonas, Jost B; Keeffe, Jill; Kempen, John H; Leasher, Janet; Limburg, Hans; Naidoo, Kovin; Pesudovs, Konrad; Silvester, Alex; Stevens, Gretchen A; Tahhan, Nina; Wong, Tien Y; Taylor, Hugh R

2017-12-01

Contemporary data for causes of vision impairment and blindness form an important basis of recommendations in public health policies. Refreshment of the Global Vision Database with recently published data sources permitted modelling of cause of vision loss data from 1990 to 2015, further disaggregation by cause, and forecasts to 2020. In this systematic review and meta-analysis, we analysed published and unpublished population-based data for the causes of vision impairment and blindness from 1980 to 2014. We identified population-based studies published before July 8, 2014, by searching online databases with no language restrictions (MEDLINE from Jan 1, 1946, and Embase from Jan 1, 1974, and the WHO Library Database). We fitted a series of regression models to estimate the proportion of moderate or severe vision impairment (defined as presenting visual acuity of blindness (presenting visual acuity of blind in 2015 (36·0 million [12·9 million to 65·4 million]), the leading causes were cataract (12·6 million [3·4 million to 28·7 million]), uncorrected refractive error (7·4 million [2·4 million to 14·8 million]), and glaucoma (2·9 million [0·4 million to 9·9 million]). By 2020, among the global population with moderate or severe vision impairment (237·1 million [101·5 million to 399·0 million]), the number of people affected by uncorrected refractive error is anticipated to rise to 127·7 million (51·0 million to 225·3 million), by cataract to 57·1 million (17·9 million to 124·1 million), by age-related macular degeneration to 8·8 million (0·8 million to 32·1 million), by glaucoma to 4·5 million (0·5 million to 15·4 million), and by diabetic retinopathy to 3·2 million (0·2 million to 12·9 million). By 2020, among the global population who are blind (38·5 million [13·2 million to 70·9 million]), the number of patients blind because of cataract is anticipated to rise to 13·4 million (3·3 million to 31·6 million), because of uncorrected

Investigation of spatial trends and neurochemical impacts of mercury in herring gulls across the Laurentian Great Lakes

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Rutkiewicz, Jennifer [Department of Environmental Health Sciences, University of Michigan School of Public Health, 109 S. Observatory St, Ann Arbor, MI 48109 (United States); Scheuhammer, Anton; Crump, Doug; Jagla, Magdalena [Environment Canada, National Wildlife Research Centre, Carleton University, Ottawa, ON K1A 0H3 (Canada); Basu, Niladri, E-mail: niladri@umich.ed [Department of Environmental Health Sciences, University of Michigan School of Public Health, 109 S. Observatory St, Ann Arbor, MI 48109 (United States)

2010-08-15

Herring gulls (Larus argentatus) bioaccumulate mercury (Hg) but it is unknown whether they are exposed at levels of neurological concern. Here we studied brain tissues from gulls at five Great Lakes colonies and one non-Great Lakes colony during spring of 2001 and 2003. Total brain Hg concentrations ranged from 0.14 to 2.0 {mu}g/g (dry weight) with a mean of 0.54 {mu}g/g. Gulls from Scotch Bonnet Island, on the easternmost edge of the Great Lakes, had significantly higher brain Hg than other colonies. No association was found between brain Hg concentration and [3H]-ligand binding to neurochemical receptors (N-methyl-D-aspartate, muscarinic cholinergic, nicotinic cholinergic) or nicotinic receptor {alpha}-7 relative mRNA expression as previously documented in other wildlife. In conclusion, spatial trends in Hg contamination exist in herring gulls across the Great Lakes basin, and herring gulls accumulate brain Hg but not at levels associated with sub-clinical neurochemical alterations. - Spatial trends in brain mercury exist in herring gulls across the Laurentian Great Lakes though levels are not associated with neurochemical biomarkers.

Investigation of spatial trends and neurochemical impacts of mercury in herring gulls across the Laurentian Great Lakes

International Nuclear Information System (INIS)

Rutkiewicz, Jennifer; Scheuhammer, Anton; Crump, Doug; Jagla, Magdalena; Basu, Niladri

2010-01-01

Herring gulls (Larus argentatus) bioaccumulate mercury (Hg) but it is unknown whether they are exposed at levels of neurological concern. Here we studied brain tissues from gulls at five Great Lakes colonies and one non-Great Lakes colony during spring of 2001 and 2003. Total brain Hg concentrations ranged from 0.14 to 2.0 μg/g (dry weight) with a mean of 0.54 μg/g. Gulls from Scotch Bonnet Island, on the easternmost edge of the Great Lakes, had significantly higher brain Hg than other colonies. No association was found between brain Hg concentration and [3H]-ligand binding to neurochemical receptors (N-methyl-D-aspartate, muscarinic cholinergic, nicotinic cholinergic) or nicotinic receptor α-7 relative mRNA expression as previously documented in other wildlife. In conclusion, spatial trends in Hg contamination exist in herring gulls across the Great Lakes basin, and herring gulls accumulate brain Hg but not at levels associated with sub-clinical neurochemical alterations. - Spatial trends in brain mercury exist in herring gulls across the Laurentian Great Lakes though levels are not associated with neurochemical biomarkers.

Prevalence and causes of visual impairment in a Brazilian population: The Botucatu Eye Study

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Cordeiro Ricardo

2009-08-01

Full Text Available Abstract Background This paper reports population-based data on the prevalence and causes of visual impairment among children and adults in Botucatu, Brazil. Methods A population-based cross-sectional study was conducted involving a random start point and then systematic sampling of an urban Brazilian population in the city of Botucatu. There were approximately 3 300 individuals aged 1 to 91 years who were eligible to participate in the study. Of this sample, 2485 (75.3% underwent ophthalmic examination. The ophthalmic examination included uncorrected (presenting and best corrected distance visual acuity using standardized protocols. The primary cause of decreased visual acuity was identified for all patients with visual impairment. Results Presenting low vision and presenting blindness were found in 5.2% (95% CI: 4.3–6.1 and 2.2% (95% CI: 1.6–2.8 of the population, respectively. Unilateral presenting low vision and unilateral presenting blindness were found in 8.3% (95% CI: 7.2–9.5 and 3.7% (95% CI: 2.9–4.4 of the population respectively. Best corrected low vision was found in 1.3% of the population (95% CI: 0.9–1.7 and best corrected blindness was discovered in 0.4% of people (95% CI: 0.2–0.7. The main cause of presenting low vision was refractive error (72.3% and cataract was the most prevalent cause of blindness (50%. Conclusion The main causes of low vision and blindness in this Brazilian city were uncorrected refractive errors, cataract, and retinal diseases. Programs to further reduce the burden of visual impairment need to be targeted toward the correction of refractive error and surgery for cataracts.

Causes of blindness and visual impairment in Latin America.

Science.gov (United States)

Furtado, João M; Lansingh, Van C; Carter, Marissa J; Milanese, María F; Peña, Brenda N; Ghersi, Hernán A; Bote, Paula L; Nano, María E; Silva, Juan C

2012-01-01

We review what is known in each country of the Latin American region with regards to blindness and visual impairment and make some comparisons to Hispanic populations in the United States. Prevalence of blindness varied from 1.1% in Argentina to 4.1% in Guatemala in people 50 years of age and older, with the major cause being cataract. Diabetic retinopathy and glaucoma are starting to make serious inroads, although epidemiological data are limited, and age-related macular degeneration is now a concern in some populations. Infectious diseases such as trachoma and onchocerciasis are quickly diminishing. Although progress has been made, retinopathy of prematurity remains the major cause of childhood blindness. If VISION 2020 is to succeed, many more epidemiological studies will be needed to set priorities, although some can be of the Rapid Assessment of Avoidable Blindness design. Developing the infrastructure for screening and treatment of ophthalmic disease in Latin America continues to be a challenge. Copyright © 2012 Elsevier Inc. All rights reserved.

Prevalence and causes of visual impairment and rate of wearing spectacles in schools for children of migrant workers in Shanghai, China.

Science.gov (United States)

He, Jiangnan; Lu, Lina; Zou, Haidong; He, Xiangui; Li, Qiangqiang; Wang, Weijie; Zhu, Jianfeng

2014-12-22

To assess the prevalence of visual impairment and rate of wearing spectacles in schools for children of migrant workers in Shanghai, China. Children from grade 1 to 5 in schools for children of migrant workers were randomly chosen for ocular examinations. All children were screened for uncorrected visual acuity and presenting visual acuity. After screening, the children whose uncorrected visual acuity was 20/40 or less received ocular motility evaluation, cycloplegic refraction/non-cycloplegic refraction, and external eye, anterior segment, media, and fundus examinations. A total of 9673 children were enumerated and 9512 (98.34%) participated in this study. The prevalence of uncorrected, presenting, and best-corrected visual acuity of 20/40 or worse in the better eye were 13.33%, 11.26%, and 0.63%, respectively. The rate of wearing spectacles of the children with visual impairment in one or both eyes was 15.50%. Of these, 26.05% were wearing spectacles with inaccurate prescriptions. Refractive error was a major cause of visual impairment, accounting for 89.48% of all the visual impairment causes. Other causes of visual impairment included amblyopia accounting for 10.12%; congenital cataract, 0.1%; congenital nystagmus, 0.1%; ocular prosthesis, 0.1%; macular degeneration, 0.05%; and opaque cornea, 0.05%. This is the first study of the prevalence and causes of visual impairment in schools for children of migrant workers in Shanghai, China. The visual impairment rate in schools for children of migrant workers in suburbs of Shanghai in the best eye before vision correction was lower than those of urban children in mainstream schools in Guangzhou in 2012, and higher than students in rural of Beijing in 1998 and in suburb of Chongqing in 2007. The refractive error was the principal cause of the visual impairment of the children of migrant workers. The rate of wearing spectacles was low and the percentage of inaccurate prescriptions, among those who wore spectacles, was

Mercury Vapour Long-Lasting Exposure: Lymphocyte Muscarinic Receptors as Neurochemical Markers of Accidental Intoxication

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E. Roda

2016-01-01

Full Text Available Introduction. Chronic poisoning may result in home setting after mercury (Hg vapours inhalation from damaged devices. We report a chronic, nonoccupational Hg poisoning due to 10-year indoor exposure to mercury spillage. Case Report. A 72-year-old man with polyneuropathy of suspected toxic origin. At hospitalization, toxicological clinical evaluations confirmed the altered neurological picture documented across the last decade. Periodic blood and urine Hg levels (BHg, UHg monitoring were performed from admission (t0, until 1 year later (t2, paralleled by blood neurochemical markers assessment, that is, lymphocytes muscarinic receptors (l-MRs. At t0: BHg and UHg were 27 and 1.4 microg/L, respectively (normal values: BHg 1–4.5; UHg 0.1–4.5, associated with l-MRs increase, 185.82 femtomoL/million lymphocytes (normal range: 8.0–16.0. At t1 (two days after DMSA-mobilization test, BHg weak reduction, paralleled by UHg 3.7-fold increase, was measured together with further l-MRs enhancement (205.43 femtomoL/million lymphocytes. At t2 (eight months after two cycles of DMSA chelating therapy ending, gradual improving of clinical manifestations was accompanied by progressive decrease of BHg and UHg (4.0 and 2.8 microg/L, resp. and peripheral l-MRs neurochemical marker (24.89 femtomoL/million lymphocytes. Conclusion. l-MRs modulatory effect supports their use as peripheral neurochemical marker in Hg poisoning diagnosis and chelation therapy monitoring.

SOME NEUROCHEMICAL DISTURBANCES IN MULTIPLE SCLEROSIS

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Vladimir V. Markelov

2006-04-01

Full Text Available ABSTRACTThe data presented in this manuscript suggest a pivotal role of the central nervous system (CNS in the regulation of immune status. We describe here that some neurochemical disturbances may provoke development of various diseases including multiple sclerosis. Some theoretic and practical backgrounds, how to improve the multiple sclerosis sufferers and patients with other autoimmune disorders, are also given.RESUMENLos datos que presentamos en este manuscrito, sugieren un papel guia del sistema nervioso central (SNC en la regulación del estado inmune. Describimos aquí que varias alteraciones neuroquímicas pueden provocar el desarrollo de varias enfermedades, incluyendo esclerosis múltiple. También se comenta acerca del trasfondo teórico y práctico, y cómo mejorar a víctimas y pacientes con esclerosis múltiple y otras alteraciones autoinmunes.

Large-scale neurochemical metabolomics analysis identifies multiple compounds associated with methamphetamine exposure.

Science.gov (United States)

McClay, Joseph L; Adkins, Daniel E; Vunck, Sarah A; Batman, Angela M; Vann, Robert E; Clark, Shaunna L; Beardsley, Patrick M; van den Oord, Edwin J C G

2013-04-01

Methamphetamine (MA) is an illegal stimulant drug of abuse with serious negative health consequences. The neurochemical effects of MA have been partially characterized, with a traditional focus on classical neurotransmitter systems. However, these directions have not yet led to novel drug treatments for MA abuse or toxicity. As an alternative approach, we describe here the first application of metabolomics to investigate the neurochemical consequences of MA exposure in the rodent brain. We examined single exposures at 3 mg/kg and repeated exposures at 3 mg/kg over 5 days in eight common inbred mouse strains. Brain tissue samples were assayed using high-throughput gas and liquid chromatography mass spectrometry, yielding quantitative data on >300 unique metabolites. Association testing and false discovery rate control yielded several metabolome-wide significant associations with acute MA exposure, including compounds such as lactate ( p = 4.4 × 10 -5 , q = 0.013), tryptophan ( p = 7.0 × 10 -4 , q = 0.035) and 2-hydroxyglutarate ( p = 1.1 × 10 -4 , q = 0.022). Secondary analyses of MA-induced increase in locomotor activity showed associations with energy metabolites such as succinate ( p = 3.8 × 10 -7 ). Associations specific to repeated (5 day) MA exposure included phosphocholine ( p = 4.0 × 10 -4 , q = 0.087) and ergothioneine ( p = 3.0 × 10 -4 , q = 0.087). Our data appear to confirm and extend existing models of MA action in the brain, whereby an initial increase in energy metabolism, coupled with an increase in behavioral locomotion, gives way to disruption of mitochondria and phospholipid pathways and increased endogenous antioxidant response. Our study demonstrates the power of comprehensive MS-based metabolomics to identify drug-induced changes to brain metabolism and to develop neurochemical models of drug effects.

Prenatal NMDA Receptor Antagonism Impaired Proliferation of Neuronal Progenitor, Leading to Fewer Glutamatergic Neurons in the Prefrontal Cortex

Science.gov (United States)

Toriumi, Kazuya; Mouri, Akihiro; Narusawa, Shiho; Aoyama, Yuki; Ikawa, Natsumi; Lu, Lingling; Nagai, Taku; Mamiya, Takayoshi; Kim, Hyoung-Chun; Nabeshima, Toshitaka

2012-01-01

N-methyl--aspartate (NMDA) receptor is a glutamate receptor which has an important role on mammalian brain development. We have reported that prenatal treatment with phencyclidine (PCP), a NMDA receptor antagonist, induces long-lasting behavioral deficits and neurochemical changes. However, the mechanism by which the prenatal antagonism of NMDA receptor affects neurodevelopment, resulting in behavioral deficits, has remained unclear. Here, we report that prenatal NMDA receptor antagonism impaired the proliferation of neuronal progenitors, leading to a decrease in the progenitor pool in the ventricular and the subventricular zone. Furthermore, using a PCR array focused on neurogenesis and neuronal stem cells, we evaluated changes in gene expression causing the impairment of neuronal progenitor proliferation and found aberrant gene expression, such as Notch2 and Ntn1, in prenatal PCP-treated mice. Consequently, the density of glutamatergic neurons in the prefrontal cortex was decreased, probably resulting in glutamatergic hypofunction. Prenatal PCP-treated mice displayed behavioral deficits in cognitive memory and sensorimotor gating until adulthood. These findings suggest that NMDA receptors regulate the proliferation and maturation of progenitor cells for glutamatergic neuron during neurodevelopment, probably via the regulation of gene expression. PMID:22257896

Visual impairment and blindness: an overview of prevalence and causes in Brazil

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Solange R. Salomão

2009-09-01

Full Text Available Our purpose is to provide a summary overview of blindness and visual impairment on the context of recent Brazilian ocular epidemiologic studies. Synthesis of data from two cross-sectional population-based studies - the São Paulo Eye Study and the Refractive Error in School Children Study is presented. 3678 older adults and 2441 school children were examined between July 2004 and December 2005. Prevalence of blindness in older adults using presenting visual acuity was 1.51% decreasing to 1. 07% with refractive correction. The most common causes of blindness in older adults were retinal disorders, followed by cataract and glaucoma. In school children, the prevalence of uncorrected visual impairment was 4.82% decreasing to 0.41% with refractive correction. The most common cause of visual impairment in school children was uncorrected refractive error. Visual impairment and blindness in Brazil is an important public health problem. It is a significant problem in older Brazilians, reinforcing the need to implement prevention of blindness programs for elderly people with emphasis on those without schooling. In school-children cost-effective strategies are needed to address a readily treatable cause of vision impairment - prescription and provision of glasses.Nosso objetivo é fazer uma revisão de cegueira e deficiência visual no contexto de recentes estudos epidemiológicos oculares brasileiros. É apresentada a síntese dos dados de dois estudos populacionais transversais - o Estudo Ocular de São Paulo e o Estudo de Erros Refrativos em Escolares. Entre julho de 2004 e dezembro de 2005 foram examinados 3678 adultos e 2441 escolares. A prevalência de cegueira em adultos mais velhos considerando a acuidade visual apresentada foi de 1, 51% diminuindo para 1, 07% com a correção refrativa. As causas mais comuns de cegueira em adultos mais velhos foram os distúrbios de retina, seguidos de catarata e glaucoma. Em escolares a prevalência de defici

A neurochemical map of the developing amphioxus nervous system

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Candiani Simona

2012-06-01

Full Text Available Abstract Background Amphioxus, representing the most basal group of living chordates, is the best available proxy for the last invertebrate ancestor of the chordates. Although the central nervous system (CNS of amphioxus comprises only about 20,000 neurons (as compared to billions in vertebrates, the developmental genetics and neuroanatomy of amphioxus are strikingly vertebrate-like. In the present study, we mapped the distribution of amphioxus CNS cells producing distinctive neurochemicals. To this end, we cloned genes encoding biosynthetic enzymes and/or transporters of the most common neurotransmitters and assayed their developmental expression in the embryo and early larva. Results By single and double in situ hybridization experiments, we identified glutamatergic, GABAergic/glycinergic, serotonergic and cholinergic neurons in developing amphioxus. In addition to characterizing the distribution of excitatory and inhibitory neurons in the developing amphioxus CNS, we observed that cholinergic and GABAergic/glycinergic neurons are segmentally arranged in the hindbrain, whereas serotonergic, glutamatergic and dopaminergic neurons are restricted to specific regions of the cerebral vesicle and the hindbrain. We were further able to identify discrete groups of GABAergic and glutamatergic interneurons and cholinergic motoneurons at the level of the primary motor center (PMC, the major integrative center of sensory and motor stimuli of the amphioxus nerve cord. Conclusions In this study, we assessed neuronal differentiation in the developing amphioxus nervous system and compiled the first neurochemical map of the amphioxus CNS. This map is a first step towards a full characterization of the neurotransmitter signature of previously described nerve cell types in the amphioxus CNS, such as motoneurons and interneurons.

Neuroprotective and neurochemical properties of mint extracts

DEFF Research Database (Denmark)

López, Víctor; Martín, Sara; Gómez-Serranillos, Maria Pilar

2010-01-01

(A) receptor). Mentha x piperita and Mentha aquatica produced significant (p oxidative stress. All the plants exhibited antioxidant and MAO-A inhibitory activities, M. x piperita being the most active. M. aquatica showed the highest affinity to the GABA......Mints are aromatic plants with a tradition as medicinal remedies and culinary herbs. With the aim of investigating potential central nervous system (CNS) activities of traditional medicinal plants, four species and one hybrid of the genus Mentha (M. aquatica, M. longifolia, M. pulegium, M....... suaveolens and M. x piperita) were selected. Methanolic extracts of the plants were tested for protective effects against hydrogen-peroxide-induced toxicity in PC12 cells, antioxidant activity (by ABTS and X/XO methods) and neurochemical properties (MAO-A inhibition, AChE inhibition and affinity to the GABA...

Neuropsychological Testing and Machine Learning Distinguish Alzheimer’s Disease from Other Causes for Cognitive Impairment

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Helmut Hildebrandt

2017-04-01

Full Text Available With promising results in recent treatment trials for Alzheimer’s disease (AD, it becomes increasingly important to distinguish AD at early stages from other causes for cognitive impairment. However, existing diagnostic methods are either invasive (lumbar punctures, PET or inaccurate Magnetic Resonance Imaging (MRI. This study investigates the potential of neuropsychological testing (NPT to specifically identify those patients with possible AD among a sample of 158 patients with Mild Cognitive Impairment (MCI or dementia for various causes. Patients were divided into an early stage and a late stage group according to their Mini Mental State Examination (MMSE score and labeled as AD or non-AD patients based on a post-mortem validated threshold of the ratio between total tau and beta amyloid in the cerebrospinal fluid (CSF; Total tau/Aβ(1–42 ratio, TB ratio. All patients completed the established Consortium to Establish a Registry for Alzheimer’s Disease—Neuropsychological Assessment Battery (CERAD-NAB test battery and two additional newly-developed neuropsychological tests (recollection and verbal comprehension that aimed at carving out specific Alzheimer-typical deficits. Based on these test results, an underlying AD (pathologically increased TB ratio was predicted with a machine learning algorithm. To this end, the algorithm was trained in each case on all patients except the one to predict (leave-one-out validation. In the total group, 82% of the patients could be correctly identified as AD or non-AD. In the early group with small general cognitive impairment, classification accuracy was increased to 89%. NPT thus seems to be capable of discriminating between AD patients and patients with cognitive impairment due to other neurodegenerative or vascular causes with a high accuracy, and may be used for screening in clinical routine and drug studies, especially in the early course of this disease.

Caffeine triggers behavioral and neurochemical alterations in adolescent rats.

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Ardais, A P; Borges, M F; Rocha, A S; Sallaberry, C; Cunha, R A; Porciúncula, L O

2014-06-13

Caffeine is the psychostimulant most consumed worldwide but concerns arise about the growing intake of caffeine-containing drinks by adolescents since the effects of caffeine on cognitive functions and neurochemical aspects of late brain maturation during adolescence are poorly known. We now studied the behavioral impact in adolescent male rats of regular caffeine intake at low (0.1mg/mL), moderate (0.3mg/mL) and moderate/high (1.0mg/mL) doses only during their active period (from 7:00 P.M. to 7:00 A.M.). All tested doses of caffeine were devoid of effects on locomotor activity, but triggered anxiogenic effects. Caffeine (0.3 and 1mg/mL) improved the performance in the object recognition task, but the higher dose of caffeine (1.0mg/mL) decreased the habituation to an open-field arena, suggesting impaired non-associative memory. All tested doses of caffeine decreased the density of glial fibrillary acidic protein and synaptosomal-associated protein-25, but failed to modify neuron-specific nuclear protein immunoreactivity in the hippocampus and cerebral cortex. Caffeine (0.3-1mg/mL) increased the density of brain-derived neurotrophic factor (BDNF) and proBDNF density as well as adenosine A1 receptor density in the hippocampus, whereas the higher dose of caffeine (1mg/mL) increased the density of proBDNF and BDNF and decreased A1 receptor density in the cerebral cortex. These findings document an impact of caffeine consumption in adolescent rats with a dual impact on anxiety and recognition memory, associated with changes in BDNF levels and decreases of astrocytic and nerve terminal markers without overt neuronal damage in hippocampal and cortical regions. Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

The Prevalence and Causes of Visaual Impairment and Blindness in a Rural Population in the North of Iran

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HASHEMI, Hassan; REZVAN, Farhad; YEKTA, AbbasAli; OSTADIMOGHADDAM, Hadi; SOROUSH, Sara; DADBIN, Nooshin; KHABAZKHOOB, Mehdi

2015-01-01

Background: Visual impairment is a very important public health problem. In Iran, reports of visual impairment and blindness have been published from the urban population while the prevalence of visual impairment in the rural population has not been reported. The purpose of this study to determine the prevalence and causes of visual impairment, in a rural population in district of based on age and sex Methods: In a cross-sectional population-based study, using random cluster sampling, 13 of the 83 villages of Khaf County in the north east of Iran were selected. Eye examinations were performed in a Mobile Eye Clinic (Nooravaran Salamat, 2011) and included optometric examinations such as measuring uncorrected and corrected visual acuity along with non-cycloplegic refraction. Results: The prevalence of visual impairment, low vision, and blindness was 6.3% (95% CI 5.3–7.3), 3.4% (95% CI 2.6–4.1), and 3.0% (95% CI 2.3–3.6), respectively. The prevalence of visual impairment ranged from 1.8% in the participant younger than 20 years of age to 28% in the subjects aged 60 and over (Pimpairment and low vision was significantly higher in women. The most prevalent causes of visual impairment were uncorrected refractory error (54.5%) and cataract (17.6%). Conclusion: The prevalence of visual impairment was significantly higher in the rural population of this study when compared to previous reports from Iran. It seems that provision of therapeutic facilities like cataract surgery and availability of eyeglasses in villages can considerably reduce the prevalence of visual impairment. PMID:26258099

A study on image diagnosis of lung impairment caused by aspiration

International Nuclear Information System (INIS)

Takata, Hidenao

2000-01-01

remarkably in severe patients, however, the amplitude of attenuation showed no significant change. The results reflect change in compliance of the severely impaired lung. The ventilation imbalance caused by aspiration was visualized by SGCT. Analysis of Dynamic CT images make possible evaluation of the lung function and it may contribute diagnosis of the lung impairment caused by aspiration. (author)

Neurochemical binding profiles of novel indole and benzofuran MDMA analogues.

OpenAIRE

Shimshoni, JA; Winkler, I; Golan, E; Nutt, D

2016-01-01

3,4-Methylenedioxy-N-methylamphetamine (MDMA) has been shown to be effective in the treatment of post-traumatic stress disorder (PTSD) in numerous clinical trials. In the present study, we have characterized the neurochemical binding profiles of three MDMA-benzofuran analogues (1-(benzofuran-5-yl)-propan-2-amine, 5-APB; 1-(benzofuran-6-yl)-N-methylpropan-2-amine, 6-MAPB; 1-(benzofuran-5-yl)-N-methylpropan-2-amine, 5-MAPB) and one MDMA-indole analogue (1-(1H-indol-5-yl)-2-methylamino-propan-1-...

Differential Effects of Intrauterine Growth Restriction on the Regional Neurochemical Profile of the Developing Rat Brain.

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Maliszewski-Hall, Anne M; Alexander, Michelle; Tkáč, Ivan; Öz, Gülin; Rao, Raghavendra

2017-01-01

Intrauterine growth restricted (IUGR) infants are at increased risk for neurodevelopmental deficits that suggest the hippocampus and cerebral cortex may be particularly vulnerable. Evaluate regional neurochemical profiles in IUGR and normally grown (NG) 7-day old rat pups using in vivo 1 H magnetic resonance (MR) spectroscopy at 9.4 T. IUGR was induced via bilateral uterine artery ligation at gestational day 19 in pregnant Sprague-Dawley dams. MR spectra were obtained from the cerebral cortex, hippocampus and striatum at P7 in IUGR (N = 12) and NG (N = 13) rats. In the cortex, IUGR resulted in lower concentrations of phosphocreatine, glutathione, taurine, total choline, total creatine (P regions. Persistent neurochemical changes may lead to cortex-based long-term neurodevelopmental deficits in human IUGR infants.

Causes of visual impairment and blindness in children at Instituto Benjamin Constant Blind School, Rio de Janeiro

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Daniela da Silva Verzoni

Full Text Available Abstract Objective: To determine the main causes of visual impairment and blindness in children enrolled at Instituto Benjamin Constant blind school (IBC in 2013, to aid in planning for the prevention and management of avoidable causes of blindness. Methods: Study design: cross-sectional observational study. Data was collected from medical records of students attending IBC in 2013. Causes of blindness were classified according to WHO/PBL examination record. Data were analyzed for those children aged less than 16 years using Stata 9 program. Results: Among 355 students attending IBC in 2013, 253 (73% were included in this study. Of these children, 190 (75% were blind and 63 (25% visually impaired. The major anatomical site of visual loss was retina (42%, followed by lesions of the globe (22%, optic nerve lesions (13.8%, central nervous system (8.8% and cataract/pseudophakia/aphakia (8.8%. The etiology was unknown in 41.9% and neonatal factors accounted for 30,9% of cases. Forty-eight percent of cases were potentially avoidable. Retinopathy of prematurity (ROP was the main cause of blindness and with microphthalmia, optic nerve atrophy, cataract and glaucoma accounted for more than 50% of cases. Conclusion: Provision and improvement of ROP, cataract and glaucoma screening and treatment and programs could prevent avoidable visual impairment and blindness.

Effect of the novel synthetic cannabinoids AKB48 and 5F-AKB48 on "tetrad", sensorimotor, neurological and neurochemical responses in mice. In vitro and in vivo pharmacological studies.

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Canazza, Isabella; Ossato, Andrea; Trapella, Claudio; Fantinati, Anna; De Luca, Maria Antonietta; Margiani, Giulia; Vincenzi, Fabrizio; Rimondo, Claudia; Di Rosa, Fabiana; Gregori, Adolfo; Varani, Katia; Borea, Pier Andrea; Serpelloni, Giovanni; Marti, Matteo

2016-10-01

AKB48 and its fluorinate derivate 5F-AKB48 are two novel synthetic cannabinoids belonging to a structural class with an indazole core structure. They are marketed as incense, herbal preparations or chemical supply for their psychoactive Cannabis-like effects. The present study was aimed at investigating the in vitro and in vivo pharmacological activity of AKB48 and 5F-AKB48 in male CD-1 mice and comparing their in vivo effects with those caused by the administration of Δ 9 -THC and JWH-018. In vitro competition binding experiments performed on mouse and human CB 1 and CB 2 receptors revealed a nanomolar affinity and potency of the AKB48 and 5F-AKB48. In vivo studies showed that AKB48 and 5F-AKB48, induced hypothermia, increased pain threshold to both noxious mechanical and thermal stimuli, caused catalepsy, reduced motor activity, impaired sensorimotor responses (visual, acoustic and tactile), caused seizures, myoclonia, hyperreflexia and promoted aggressiveness in mice. Moreover, microdialysis study in freely moving mice showed that systemic administration of AKB48 and 5F-AKB48 stimulated dopamine release in the nucleus accumbens. Behavioural, neurological and neurochemical effects were fully prevented by the selective CB 1 receptor antagonist/inverse agonist AM 251. For the first time, the present study demonstrates the overall pharmacological effects induced by the administration of AKB48 and 5F-AKB48 in mice and suggests that the fluorination can increase the power and/or effectiveness of SCBs. Furthermore, this study outlines the potential detrimental effects of SCBs on human health.

A neurochemical closed-loop controller for deep brain stimulation: toward individualized smart neuromodulation therapies.

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Peter Jonas Grahn

2014-06-01

Full Text Available Current strategies for optimizing deep brain stimulation (DBS therapy involve multiple postoperative visits. During each visit, stimulation parameters are adjusted until desired therapeutic effects are achieved and adverse effects are minimized. However, the efficacy of these therapeutic parameters may decline with time due at least in part to disease progression, interactions between the host environment and the electrode, and lead migration. As such, development of closed-loop control systems that can respond to changing neurochemical environments, tailoring DBS therapy to individual patients, is paramount for improving the therapeutic efficacy of DBS.Evidence obtained using electrophysiology and imaging techniques in both animals and humans suggests that DBS works by modulating neural network activity. Recently, animal studies have shown that stimulation-evoked changes in neurotransmitter release that mirror normal physiology are associated with the therapeutic benefits of DBS. Therefore, to fully understand the neurophysiology of DBS and optimize its efficacy, it may be necessary to look beyond conventional electrophysiological analyses and characterize the neurochemical effects of therapeutic and non-therapeutic stimulation. By combining electrochemical monitoring and mathematical modeling techniques, we can potentially replace the trial-and-error process used in clinical programming with deterministic approaches that help attain optimal and stable neurochemical profiles. In this manuscript, we summarize the current understanding of electrophysiological and electrochemical processing for control of neuromodulation therapies. Additionally, we describe a proof-of-principle closed-loop controller that characterizes DBS-evoked dopamine changes to adjust stimulation parameters in a rodent model of DBS. The work described herein represents the initial steps toward achieving a smart neuroprosthetic system for treatment of neurologic and

Causes of hearing impairment in the Norwegian paediatric cochlear implant program.

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Siem, Geir; Fagerheim, Toril; Jonsrud, Christoffer; Laurent, Claude; Teig, Erik; Harris, Sten; Leren, Trond P; Früh, Andreas; Heimdal, Ketil

2010-08-01

Severe to profound hearing impairment (HI) is estimated to affect around 1/2000 young children. Advances in genetics have made it possible to identify several genes related to HI. This information can cast light upon prognostic factors regarding the outcome in cochlear implantation, and provide information both for scientific and genetic counselling purposes. From 1992 to 2005, 273 children from 254 families (probands) were offered cochlear implants in Norway. An evaluation of the causes of HI, especially regarding the genes GJB2, GJB6, SLC26A4, KCNQ1, KCNE1, and the mutation A1555G in mitochondrial DNA was performed in 85% of the families. The number of probands with unknown cause of HI was thus reduced from 120 to 68 (43% reduction). Ninety-eight (46%) of the probands had an identified genetic etiology of their HI. A relatively high prevalence of Jervell and Lange-Nielsen syndrome was found. The main causes of severe and profound HI were similar to those found in other European countries. GJB2 mutations are a common cause of prelingual HI in Norwegian cochlear implanted children.

Lawn mower injuries as a cause of serious visual acuity impairment - Case reports.

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Jasielska, Monika; Winiarczyk, Mateusz; Bieliński, Paweł; Mackiewicz, Jerzy

2017-05-11

[b]Abstract Objective.[/b] The aim of the study is to present four cases of lawn mowers injuries as a cause of serious visual acuity impairment. [b]Materials and Method[/b]. A retrospective study of four patients admitted in 2013-2015 to the Department of Vitreoretinal Surgery in Lublin with severe open or closed globe injury, one with an intraocular foreign body (IOFB). The presence of eye protective equipment was assessed, as well as visual acuity, eye tissue condition before and after treatment, and applied therapy. In all cases an improvement was achieved in local conditions. The intraocular foreign body was removed, wounds sutured and damaged tissues placed in position. All eyeballs were saved. In three cases, visual acuity was improved to a usable level. Three patients underwent pars plana vitrectomy, one with IOFB removal from the vitreous cavity. [b]Conclusions[/b]. Lawn mower induced eye injuries are a significant cause of serious visual acuity impairment or blindness. The presented study shows that lawn mower eye injuries are still a therapeutic, social and economic problem, yet are very preventable with proper eye protection and patients' education. Current prevention strategies are inadequate, and therefore should be updated.

Prevalence, Causes and Social Factors of Visual Impairment among Chinese Adults: Based on a National Survey.

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Guo, Chao; Wang, Zhenjie; He, Ping; Chen, Gong; Zheng, Xiaoying

2017-09-08

Visual impairment has become a global challenge, especially for developing countries. This study aims to estimate the prevalence, causes and social factors of visual impairment among Chinese adults. Data were from a nationally representative population-based cross-sectional study. The study population were 1,909,199 non-institutionalized adults aged 18 years and older in mainland China. In the survey, low vision and blindness were checked by ophthalmologists according to the WHO best-corrected visual acuity (BCVA) criteria. Population weighted numbers and prevalence of low vision and blindness with 95% confidence intervals (CIs) were estimated where appropriate. Multivariable logistic regression analysis was used to identify the social factors of visual impairment. The weighted prevalence of visual impairment was 17.17 (95% CI, 16.84-17.50) per 1000 Chinese adults aged 18 years and older. Cataract (57.35%), disorders of choroid and retina (9.80%), and disorders of cornea (6.49%) contributed more than 70 percent to the visual impairment in Chinese adults. Older age groups, young or middle-aged male adults, female elders, illiterate, rural dwellers, non-eastern residents, singles, unemployment, and from family with lower income were associated with visual impairment. More efforts are warranted to enhance treatment and rehabilitation among people with eye disorders to prevent visual impairment.

Noonan Syndrome: An Underestimated Cause of Severe to Profound Sensorineural Hearing Impairment. Which Clues to Suspect the Diagnosis?

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Ziegler, Alban; Loundon, Natalie; Jonard, Laurence; Cavé, Hélène; Baujat, Geneviève; Gherbi, Souad; Couloigner, Vincent; Marlin, Sandrine

2017-09-01

To highlight Noonan syndrome as a clinically recognizable cause of severe to profound sensorineural hearing impairment. New clinical cases and review. Patients evaluated for etiological diagnosis by a medical geneticist in a reference center for hearing impairment. Five patients presenting with confirmed Noonan syndrome and profound sensorineural hearing impairment. Diagnostic and review of the literature. Five patients presented with profound sensorineural hearing impairment and molecularly confirmed Noonan syndrome. Sensorineural hearing impairment has been progressive for three patients. Cardiac echography identified pulmonary stenosis in two patients and was normal for the three other patients. Short stature was found in two patients. Mild intellectual disability was found in one patient. Inconspicuous clinical features as facial dysmorphism, cryptorchidism, or easy bruising were of peculiar interest to reach the diagnosis of Noonan syndrome. Profound sensorineural hearing impairment can be the main feature of Noonan syndrome. Associated features are highly variable; thus, detailed medical history and careful physical examination are mandatory to consider the diagnosis in case of a sensorineural hearing impairment.

Lawn mower injuries as a cause of serious visual acuity impairment – Case reports

Directory of Open Access Journals (Sweden)

Monika Jasielska

2017-05-01

Lawn mower induced eye injuries are a significant cause of serious visual acuity impairment or blindness. The presented study shows that lawn mower eye injuries are still a therapeutic, social and economic problem, yet are very preventable with proper eye protection and patients’ education. Current prevention strategies are inadequate, and therefore should be updated.

Transplacental exposure to AZT induces adverse neurochemical and behavioral effects in a mouse model: protection by L-acetylcarnitine.

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Anna Rita Zuena

Full Text Available Maternal-fetal HIV-1 transmission can be prevented by administration of AZT, alone or in combination with other antiretroviral drugs to pregnant HIV-1-infected women and their newborns. In spite of the benefits deriving from this life-saving prophylactic therapy, there is still considerable uncertainty on the potential long-term adverse effects of antiretroviral drugs on exposed children. Clinical and experimental studies have consistently shown the occurrence of mitochondrial dysfunction and increased oxidative stress following prenatal treatment with antiretroviral drugs, and clinical evidence suggests that the developing brain is one of the targets of the toxic action of these compounds possibly resulting in behavioral problems. We intended to verify the effects on brain and behavior of mice exposed during gestation to AZT, the backbone of antiretroviral therapy during human pregnancy. We hypothesized that glutamate, a neurotransmitter involved in excitotoxicity and behavioral plasticity, could be one of the major actors in AZT-induced neurochemical and behavioral alterations. We also assessed the antioxidant and neuroprotective effect of L-acetylcarnitine, a compound that improves mitochondrial function and is successfully used to treat antiretroviral-induced polyneuropathy in HIV-1 patients. We found that transplacental exposure to AZT given per os to pregnant mice from day 10 of pregnancy to delivery impaired in the adult offspring spatial learning and memory, enhanced corticosterone release in response to acute stress, increased brain oxidative stress also at birth and markedly reduced expression of mGluR1 and mGluR5 subtypes and GluR1 subunit of AMPA receptors in the hippocampus. Notably, administration during the entire pregnancy of L-acetylcarnitine was effective in preventing/ameliorating the neurochemical, neuroendocrine and behavioral adverse effects induced by AZT in the offspring. The present preclinical findings provide a

Causes of childhood blindness in a school for the visually impaired in Hong Kong.

Science.gov (United States)

Fan, D S P; Lai, T Y Y; Cheung, E Y Y; Lam, D S C

2005-04-01

To identify the causes of blindness in children attending a school for the blind in Hong Kong. Cross-sectional observational study. School for blind children in Hong Kong. Eighty-two blind students at the Ebenezer School and Home for the Visually Impaired were examined between December 1998 and August 1999. Demographic data were obtained from students and a questionnaire assessment made of their medical and ocular history. Visual acuity was assessed and visual loss classified according to the World Health Organization classification of visual impairment. Complete ophthalmic assessments were performed in all students including slit-lamp examination and dilated binocular indirect ophthalmoscopy. The mean age of the students was 12.2 years. Ten (12.2%) had a family history of eye disease. Major past medical illnesses were reported in 50% with prematurity and diseases of the central nervous system found in 26.8% and 11.0% of students, respectively. The most common anatomical site for visual impairment was the retina (47.6%), followed by diseases of the optic nerve (14.6%), and diseases of the anterior segment and the lens (14.6%). The pattern of childhood blindness in Hong Kong is similar to that seen in other developed countries. Preventable causes of childhood blindness, such as prematurity and birth asphyxia, were responsible for a large proportion of cases. Early diagnosis and treatment of such conditions may reduce the incidence of childhood blindness in Hong Kong.

Prevalence and causes of severe visual impairment and blindness among children in the lorestan province of iran, using the key informant method.

Science.gov (United States)

Razavi, Hessom; Kuper, Hannah; Rezvan, Farhad; Amelie, Khatere; Mahboobi-Pur, Hassan; Oladi, Mohammad Reza; Muhit, Mohammad; Hashemi, Hassan

2010-03-01

To estimate the prevalence and causes of severe visual impairment and blindness among children in Lorestan province of Iran, and to assess the feasibility of the Key Informant Method in this setting. Potential cases were identified using the Key Informant Method, in 3 counties of Lorestan province during June through August 2008, and referred for examination. Causes of severe visual impairment/blindness were determined and categorized using standard World Health Organization methods. Of 123 children referred for examination, 27 children were confirmed to have severe visual impairment/blindness or blindness. The median age was11 years (interquartile range 6-13), and 59% were girls. After adjusting for non-attenders, the estimated prevalence of severe visual impairment/blindness was 0.04% (0.03-0.05). The main site of abnormality was retina (44%), followed by disorders of the whole eye (33%). The majority of causes had a hereditary etiology (70%), which was associated with a family history of blindness (P = 0.002). Potentially avoidable causes of severe visual impairment/blindness were found in 14 children (52%). Almost all children with severe visual impairment/blindness had a history of parental consanguinity (93%). Our findings suggest a moderate prevalence of childhood blindness in the Lorestan province of Iran, a high proportion of which may be avoidable, given improved access to ophthalmic and genetic counselling services in rural areas. The Key Informant Method is feasible in Iran; future research is discussed.

Dysregulation of Brain Reward Systems in Eating Disorders: Neurochemical Information from Animal Models of Binge Eating, Bulimia Nervosa, and Anorexia Nervosa

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Avena, Nicole M.; Bocarsly, Miriam E.

2012-01-01

Food intake is mediated, in part, through brain pathways for motivation and reinforcement. Dysregulation of these pathways may underlay some of the behaviors exhibited by patients with eating disorders. Research using animal models of eating disorders has greatly contributed to the detailed study of potential brain mechanisms that many underlie the causes or consequences of aberrant eating behaviors. This review focuses on neurochemical evidence of reward-related brain dysfunctions obtained through animal models of binge eating, bulimia nervosa, or anorexia nervosa. The findings suggest that alterations in dopamine (DA), acetylcholine (ACh) and opioid systems in reward-related brain areas occur in response to binge eating of palatable foods. Moreover, animal models of bulimia nervosa suggest that while bingeing on palatable food releases DA, purging attenuates the release of ACh that might otherwise signal satiety. Animal models of anorexia nervosa suggest that restricted access to food enhances the reinforcing effects of DA when the animal does eat. The activity-based anorexia model suggests alterations in mesolimbic DA and serotonin occur as a result of starvation coupled with excessive wheel running. These findings with animal models complement data obtained through neuroimaging and pharmacotherapy studies of clinical populations. Finally, information on the neurochemical consequences of the behaviors associated with these eating disorders will be useful in understanding these complex disorders and may inform future therapeutic approaches, as discussed here. PMID:22138162

Early Postnatal Manganese Exposure Causes Lasting Impairment of Selective and Focused Attention and Arousal Regulation in Adult Rats

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Beaudin, Stephane A.; Strupp, Barbara J.; Strawderman, Myla; Smith, Donald R.

2016-01-01

Background: Studies in children and adolescents have associated early developmental manganese (Mn) exposure with inattention, impulsivity, hyperactivity, and oppositional behaviors, but causal inferences are precluded by the correlational nature of the data and generally limited control for potential confounders. Objectives: To determine whether early postnatal oral Mn exposure causes lasting attentional and impulse control deficits in adulthood, and whether continued lifelong Mn exposure exacerbates these effects, using a rat model of environmental Mn exposure. Methods: Neonates were exposed orally to 0, 25 or 50 mg Mn/kg/day during early postnatal life (PND 1–21) or throughout life from PND 1 until the end of the study. In adulthood, the animals were tested on a series of learning and attention tasks using the five-choice serial reaction time task. Results: Early postnatal Mn exposure caused lasting attentional dysfunction due to impairments in attentional preparedness, selective attention, and arousal regulation, whereas associative ability (learning) and impulse control were spared. The presence and severity of these deficits varied with the dose and duration of Mn exposure. Conclusions: This study is the first to show that developmental Mn exposure can cause lasting impairments in focused and selective attention and arousal regulation, and to identify the specific nature of the impairments. Given the importance of attention and arousal regulation in cognitive functioning, these findings substantiate concerns about the adverse effects of developmental Mn exposure in humans. Citation: Beaudin SA, Strupp BJ, Strawderman M, Smith DR. 2017. Early postnatal manganese exposure causes lasting impairment of selective and focused attention and arousal regulation in adult rats. Environ Health Perspect 125:230–237; http://dx.doi.org/10.1289/EHP258 PMID:27384154

Early Postnatal Manganese Exposure Causes Lasting Impairment of Selective and Focused Attention and Arousal Regulation in Adult Rats.

Science.gov (United States)

Beaudin, Stephane A; Strupp, Barbara J; Strawderman, Myla; Smith, Donald R

2017-02-01

Studies in children and adolescents have associated early developmental manganese (Mn) exposure with inattention, impulsivity, hyperactivity, and oppositional behaviors, but causal inferences are precluded by the correlational nature of the data and generally limited control for potential confounders. To determine whether early postnatal oral Mn exposure causes lasting attentional and impulse control deficits in adulthood, and whether continued lifelong Mn exposure exacerbates these effects, using a rat model of environmental Mn exposure. Neonates were exposed orally to 0, 25 or 50 mg Mn/kg/day during early postnatal life (PND 1-21) or throughout life from PND 1 until the end of the study. In adulthood, the animals were tested on a series of learning and attention tasks using the five-choice serial reaction time task. Early postnatal Mn exposure caused lasting attentional dysfunction due to impairments in attentional preparedness, selective attention, and arousal regulation, whereas associative ability (learning) and impulse control were spared. The presence and severity of these deficits varied with the dose and duration of Mn exposure. This study is the first to show that developmental Mn exposure can cause lasting impairments in focused and selective attention and arousal regulation, and to identify the specific nature of the impairments. Given the importance of attention and arousal regulation in cognitive functioning, these findings substantiate concerns about the adverse effects of developmental Mn exposure in humans. Citation: Beaudin SA, Strupp BJ, Strawderman M, Smith DR. 2017. Early postnatal manganese exposure causes lasting impairment of selective and focused attention and arousal regulation in adult rats. Environ Health Perspect 125:230-237; http://dx.doi.org/10.1289/EHP258.

Learning impairment in honey bees caused by agricultural spray adjuvants.

Directory of Open Access Journals (Sweden)

Timothy J Ciarlo

Full Text Available BACKGROUND: Spray adjuvants are often applied to crops in conjunction with agricultural pesticides in order to boost the efficacy of the active ingredient(s. The adjuvants themselves are largely assumed to be biologically inert and are therefore subject to minimal scrutiny and toxicological testing by regulatory agencies. Honey bees are exposed to a wide array of pesticides as they conduct normal foraging operations, meaning that they are likely exposed to spray adjuvants as well. It was previously unknown whether these agrochemicals have any deleterious effects on honey bee behavior. METHODOLOGY/PRINCIPAL FINDINGS: An improved, automated version of the proboscis extension reflex (PER assay with a high degree of trial-to-trial reproducibility was used to measure the olfactory learning ability of honey bees treated orally with sublethal doses of the most widely used spray adjuvants on almonds in the Central Valley of California. Three different adjuvant classes (nonionic surfactants, crop oil concentrates, and organosilicone surfactants were investigated in this study. Learning was impaired after ingestion of 20 µg organosilicone surfactant, indicating harmful effects on honey bees caused by agrochemicals previously believed to be innocuous. Organosilicones were more active than the nonionic adjuvants, while the crop oil concentrates were inactive. Ingestion was required for the tested adjuvant to have an effect on learning, as exposure via antennal contact only induced no level of impairment. CONCLUSIONS/SIGNIFICANCE: A decrease in percent conditioned response after ingestion of organosilicone surfactants has been demonstrated here for the first time. Olfactory learning is important for foraging honey bees because it allows them to exploit the most productive floral resources in an area at any given time. Impairment of this learning ability may have serious implications for foraging efficiency at the colony level, as well as potentially many

Exogenous hydrogen sulfide eliminates spatial memory retrieval impairment and hippocampal CA1 LTD enhancement caused by acute stress via promoting glutamate uptake.

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He, Jin; Guo, Ruixian; Qiu, Pengxin; Su, Xingwen; Yan, Guangmei; Feng, Jianqiang

2017-05-14

Acute stress impairs the hippocampus-dependent spatial memory retrieval, and its synaptic mechanisms are associated with hippocampal CA1 long-term depression (LTD) enhancement in the adult rats. Endogenous hydrogen sulfide (H 2 S) is recognized as a novel gasotransmitter and has the neural protective roles. However, very little attention has been paid to understanding the effects of H 2 S on spatial memory retrieval impairment. We observed the protective effects of NaHS (a donor of H 2 S) against spatial memory retrieval impairment caused by acute stress and its synaptic mechanisms. Our results showed that NaHS abolished spatial memory retrieval impairment and hippocampal CA1 LTD enhancement caused by acute stress, but not by glutamate transporter inhibitor l-trans-pyrrolidine-2,4-dicarboxylic (tPDC), indicating that the activation of glutamate transporters is necessary for exogenous H 2 S to exert its roles. Moreover, NaHS restored the decreased glutamate uptake in the hippocampal CA1 synaptosomal fraction caused by acute stress. Dithiothreitol (DTT, a disulfide reducing agent) abolished a decrease in the glutamate uptake caused by acute stress, and NaHS eradicated the decreased glutamate uptake caused by 5,5'-dithio-bis(2-nitrobenzoic)acid (DTNB, a thiol oxidizing agent), collectively, revealing that exogenous H 2 S increases glutamate uptake by reducing disulfide bonds of the glutamate transporters. Additionally, NaHS inhibited the increased expression level of phosphorylated c-Jun-N-terminal kinase (JNK) in the hippocampal CA1 region caused by acute stress. The JNK inhibitor SP600125 eliminated spatial memory retrieval impairment, hippocampal CA1 LTD enhancement and the decreased glutamate uptake caused by acute stress, indicating that exogenous H 2 S exerts these roles by inhibiting the activation of JNK signaling pathway. Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

Molecular and neurochemical substrates of the audiogenic seizure strains: The GASH:Sal model.

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Prieto-Martín, Ana I; Aroca-Aguilar, J Daniel; Sánchez-Sánchez, Francisco; Muñoz, Luis J; López, Dolores E; Escribano, Julio; de Cabo, Carlos

2017-06-01

Animal models of audiogenic epilepsy are useful tools to understand the mechanisms underlying human reflex epilepsies. There is accumulating evidence regarding behavioral, anatomical, electrophysiological, and genetic substrates of audiogenic seizure strains, but there are still aspects concerning their neurochemical basis that remain to be elucidated. Previous studies have shown the involved of γ-amino butyric acid (GABA) in audiogenic seizures. The aim of our research was to clarify the role of the GABAergic system in the generation of epileptic seizures in the genetic audiogenic seizure-prone hamster (GASH:Sal) strain. We studied the K + /Cl - cotransporter KCC2 and β2-GABAA-type receptor (GABAAR) and β3-GABAAR subunit expressions in the GASH:Sal both at rest and after repeated sound-induced seizures in different brain regions using the Western blot technique. We also sequenced the coding region for the KCC2 gene both in wild- type and GASH:Sal hamsters. Lower expression of KCC2 protein was found in GASH:Sal when compared with controls at rest in several brain areas: hippocampus, cortex, cerebellum, hypothalamus, pons-medulla, and mesencephalon. Repeated induction of seizures caused a decrease in KCC2 protein content in the inferior colliculus and hippocampus and an increase in the pons-medulla. When compared to controls, the basal β 2 -GABA A R subunit in the GASH:Sal was overexpressed in the inferior colliculus, rest of the mesencephalon, and cerebellum, whereas basal β 3 subunit levels were lower in the inferior colliculus and rest of the mesencephalon. Repeated seizures increased β2 both in the inferior colliculus and in the hypothalamus and β 3 in the hypothalamus. No differences in the KCC2 gene-coding region were found between GASH:Sal and wild-type hamsters. These data indicate that GABAergic system functioning is impaired in the GASH:Sal strain, and repeated seizures seem to aggravate this dysfunction. These results have potential clinical

Impaired skin capillary recruitment in essential hypertension is caused by both functional and structural capillary rarefaction

NARCIS (Netherlands)

Serne, EH; Gans, ROB; ter Maaten, JC; Tangelder, GJ; Donker, AJM; Stehouwer, CDA

Capillary rarefaction occurs in many tissues in patients with essential hypertension and may contribute to an increased vascular resistance and impaired muscle metabolism. Rarefaction may be caused by a structural (anatomic) absence of capillaries, functional nonperfusion, or both. The aim of this

Neurochemical, morphologic, and laminar characterization of cortical projection neurons in the cingulate motor areas of the macaque monkey

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Nimchinsky, E. A.; Hof, P. R.; Young, W. G.; Morrison, J. H.; Bloom, F. E. (Principal Investigator)

1996-01-01

The primate cingulate gyrus contains multiple cortical areas that can be distinguished by several neurochemical features, including the distribution of neurofilament protein-enriched pyramidal neurons. In addition, connectivity and functional properties indicate that there are multiple motor areas in the cortex lining the cingulate sulcus. These motor areas were targeted for analysis of potential interactions among regional specialization, connectivity, and cellular characteristics such as neurochemical profile and morphology. Specifically, intracortical injections of retrogradely transported dyes and intracellular injection were combined with immunocytochemistry to investigate neurons projecting from the cingulate motor areas to the putative forelimb region of the primary motor cortex, area M1. Two separate groups of neurons projecting to area M1 emanated from the cingulate sulcus, one anterior and one posterior, both of which furnished commissural and ipsilateral connections with area M1. The primary difference between the two populations was laminar origin, with the anterior projection originating largely in deep layers, and the posterior projection taking origin equally in superficial and deep layers. With regard to cellular morphology, the anterior projection exhibited more morphologic diversity than the posterior projection. Commissural projections from both anterior and posterior fields originated largely in layer VI. Neurofilament protein distribution was a reliable tool for localizing the two projections and for discriminating between them. Comparable proportions of the two sets of projection neurons contained neurofilament protein, although the density and distribution of the total population of neurofilament protein-enriched neurons was very different in the two subareas of origin. Within a projection, the participating neurons exhibited a high degree of morphologic heterogeneity, and no correlation was observed between somatodendritic morphology and

Causes of severe visual impairment and blindness in students in schools for the blind in Northwest Ethiopia.

Science.gov (United States)

Asferaw, Mulusew; Woodruff, Geoffrey; Gilbert, Clare

2017-01-01

To determine the causes of severe visual impairment and blindness (SVI/BL) among students in schools for the blind in Northwest Ethiopia and to identify preventable and treatable causes. Students attending nine schools for the blind in Northwest Ethiopia were examined and causes assigned using the standard WHO record form for children with blindness and low vision in May and June 2015. 383 students were examined, 357 (93%) of whom were severely visually impaired or blind (blind and four were SVI, total 104. The major anatomical site of visual loss among those 0-15 years was cornea/phthisis (47.1%), usually due to measles and vitamin A deficiency, followed by whole globe (22.1%), lens (9.6%) and uvea (8.7%). Among students aged 16 years and above, corneal/phthisis (76.3%) was the major anatomical cause, followed by lens (6.3%), whole globe (4.7%), uvea (3.6%) and optic nerve (3.2%). The leading underlying aetiology among students aged blindness, mainly as the result of measles and vitamin A deficiency, is still a public health problem in Northwest Ethiopia, and this has not changed as observed in other low-income countries. More than three-fourth of causes of SVI/BL in students in schools for the blind are potentially avoidable, with measles/vitamin A deficiency and cataract being the leading causes.

Causes of childhood visual impairment and unmet low-vision care in blind school students in Ghana.

Science.gov (United States)

Ntim-Amponsah, C T; Amoaku, W M K

2008-10-01

The purpose of this study was to determine the causes of childhood visual impairment and blindness in students of a school for blind children, to determine how many students had some residual vision, and to evaluate any unmet low-vision care. A survey of students in the blind school was conducted in two parts in May-June and then October 2003. The sample consisted of 201 students who became blind before the age of 16. Information was obtained from student interviews, doctors' referral notes and ophthalmic examination of all students who consented. Students with residual vision had low-vision assessments. These investigations were supplemented with active participation of the investigators in Parent-Teacher Association meetings and focus group discussions with parents. One hundred and ninety-nine students consented and were recruited, whereas two declined. Ninety-six became visually impaired within their first year of life and 33 by the age of 5 years. Pathology of the cornea and then the lens were the commonest causes of blindness. One hundred and eight students were totally blind, whereas 87 (43.7%) had some residual vision and formed the target for the second part of the study. Fifty-one out of 77 of this target group who turned up for low-vision examination had useful residual vision by the World Health Organisation (WHO) low-vision examination chart. Spectacle magnifiers aided two students to read normal print at N5 and N8, respectively. Different visual aids would help enhance the residual vision in some of the others. Emotional trauma was apparent in parents and teachers. Children who became blind later in life remained in shock for a longer time and adapted less well to their visual impairment. Visual impairment in the population is not uncommon. Some causes are preventable. There is a significant unmet need for low-vision care, particularly amongst children in Ghana, and perhaps many countries in the West Africa subregion. It is hoped that the findings from

Behavioral, neurochemical, and electrophysiological changes in an early spontaneous mouse model of nigrostriatal degeneration.

Science.gov (United States)

Sgadò, Paola; Viaggi, Cristina; Pinna, Annalisa; Marrone, Cristina; Vaglini, Francesca; Pontis, Silvia; Mercuri, Nicola Biagio; Morelli, Micaela; Corsini, Giovanni Umberto

2011-08-01

In idiopathic Parkinson's disease, clinical symptoms do not emerge until consistent neurodegeneration has occurred. The late appearance of symptoms implies the existence of a relatively long preclinical period during which several disease-induced neurochemical changes take place to mask the existence of the disease and delay its clinical manifestations. The aim of this study was to examine the neurochemical, neurophysiological, and behavioral changes induced by the loss of nigrostriatal innervation in the En1+/-;En2-/- mouse, in the 10 months following degeneration, compared to En2 null mutant mice. Behavioral analysis (Pole-test, Beam-walking test, and Inverted grid test) and field potential recordings in the striatum indicated that loss of ~70% of nigrostriatal neurons produced no significant functional effects until 8 months of age, when En1+/-;En2-/- animals started to show frank motor deficits and electrophysiological alterations in corticostriatal plasticity. Similarly, alterations in dopamine homeostasis, dopamine turnover, and dopamine innervation were observed in aged animals compared to young En1+/-;En2-/- mice. These data suggests that in En1+/-;En2-/- mice nigrostriatal degeneration in the substantia nigra is functionally compensated.

Neurochemical mechanisms underlying responses to psychostimulants

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Volkow, N.D.; Fowler, J.S.; Hitzemann, R.; Wang, G.J. [Brookhaven National Lab., Upton, NY (United States)]|[State Univ. of New York, Stony Brook, NY (United States)

1994-11-01

This study employed positron emission tomography (PET) to investigate biochemical and metabolic characteristics of the brain of individuals which could put them at risk for drug addiction. It takes advantage of the normal variability between individuals in response to psychoactive drugs to investigate relation between mental state, brain neurochemistry and metabolism and the behavioral response to drugs. We discuss its use to assess if there is an association between mental state and dompaminergic reactivity in response to the psychostimulant drug methylphenidate (MP). Changes in synaptic dopamine induced by MP were evaluated with PET and [11C]raclopride, a D{sub 2} receptor radioligand that is sensitive to endogenous dopamine. Methylpphenidate significantly decreased striatal [11C]raclopride binding. The study showed a correlation between the magnitude of the dopamine-induced changes by methylphenidate, and the mental state of the subjects. Subjects reporting high levels of anxiety and restlessness at baseline had larger changes in MP-induced dopamine changes than those that did not. Further investigations on the relation between an individual`s response to a drug and his/her mental state and personality as well as his neurochemical brain composition may enable to understand better differences in drug addiction vulnerability.

The gyri of the octopus vertical lobe have distinct neurochemical identities.

Science.gov (United States)

Shigeno, Shuichi; Ragsdale, Clifton W

2015-06-15

The cephalopod vertical lobe is the largest learning and memory structure known in invertebrate nervous systems. It is part of the visual learning circuit of the central brain, which also includes the superior frontal and subvertical lobes. Despite the well-established functional importance of this system, little is known about neuropil organization of these structures and there is to date no evidence that the five longitudinal gyri of the vertical lobe, perhaps the most distinctive morphological feature of the octopus brain, differ in their connections or molecular identities. We studied the histochemical organization of these structures in hatchling and adult Octopus bimaculoides brains with immunostaining for serotonin, octopus gonadotropin-releasing hormone (oGNRH), and octopressin-neurophysin (OP-NP). Our major finding is that the five lobules forming the vertical lobe gyri have distinct neurochemical signatures. This is most prominent in the hatchling brain, where the median and mediolateral lobules are enriched in OP-NP fibers, the lateral lobule is marked by oGNRH innervation, and serotonin immunostaining heavily labels the median and lateral lobules. A major source of input to the vertical lobe is the superior frontal lobe, which is dominated by a neuropil of interweaving fiber bundles. We have found that this neuropil also has an intrinsic neurochemical organization: it is partitioned into territories alternately enriched or impoverished in oGNRH-containing fascicles. Our findings establish that the constituent lobes of the octopus superior frontal-vertical system have an intricate internal anatomy, one likely to reflect the presence of functional subsystems within cephalopod learning circuitry. © 2015 Wiley Periodicals, Inc.

What are the causes and consequences of impaired sleep quality during and following extended hospitalisation amongst older adults?

OpenAIRE

AISLINN FELICITY LALOR

2017-01-01

Sleep is essential to everyone's health and wellbeing. Between 30-40% of people experience impaired sleep and is most common in older adults. Older adults also experience a higher number of hospitalisations in comparison to any other age group. This thesis aimed to investigate the causes and consequences of impaired sleep quality for older adults during and following hospital admission. Over 80% of older adults with self-reported poor sleep do not discuss it with any health professionals. Thi...

When psychopathy impairs moral judgments: neural responses during judgments about causing fear.

Science.gov (United States)

Marsh, Abigail A; Cardinale, Elise M

2014-01-01

Psychopathy is a disorder characterized by reduced empathy, shallow affect and behaviors that cause victims distress, like threats, bullying and violence. Neuroimaging research in both institutionalized and community samples implicates amygdala dysfunction in the etiology of psychopathic traits. Reduced amygdala responsiveness may disrupt processing of fear-relevant stimuli like fearful facial expressions. The present study links amygdala dysfunction in response to fear-relevant stimuli to the willingness of individuals with psychopathic traits to cause fear in other people. Thirty-three healthy adult participants varying in psychopathic traits underwent whole-brain fMRI scanning while they viewed statements that selectively evoke anger, disgust, fear, happiness or sadness. During scanning, participants judged whether it is morally acceptable to make each statement to another person. Psychopathy was associated with reduced activity in right amygdala during judgments of fear-evoking statements and with more lenient moral judgments about causing fear. No group differences in amygdala function or moral judgments emerged for other emotion categories. Psychopathy was also associated with increased activity in middle frontal gyrus (BA 10) during the task. These results implicate amygdala dysfunction in impaired judgments about causing distress in psychopathy and suggest that atypical amygdala responses to fear in psychopathy extend across multiple classes of stimuli.

Selective activation of M4 muscarinic acetylcholine receptors reverses MK-801-induced behavioral impairments and enhances associative learning in rodents

DEFF Research Database (Denmark)

Bubser, Michael; Bridges, Thomas M; Dencker, Ditte

2014-01-01

PAMs, enabling a more extensive characterization of M4 actions in rodent models. We used VU0467154 to test the hypothesis that selective potentiation of M4 receptor signaling could ameliorate the behavioral, cognitive, and neurochemical impairments induced by the noncompetitive NMDAR antagonist MK-801....... VU0467154 produced a robust dose-dependent reversal of MK-801-induced hyperlocomotion and deficits in preclinical models of associative learning and memory functions, including the touchscreen pairwise visual discrimination task in wild-type mice, but failed to reverse these stimulant...

Prevalence and causes of visual impairment according to World Health Organization and United States criteria in an aged, urban Scandinavian population

DEFF Research Database (Denmark)

Buch, Helena; Vinding, T; Nielsen, N V

2001-01-01

PURPOSE: To evaluate the prevalence and causes of visual impairment in an epidemiologic study of aged, urban individuals in Denmark. DESIGN: Cross-sectional study. PARTICIPANTS: The study population consisted of 1000 randomly selected residents aged 60 to 80 years in Copenhagen, Denmark. Of 976...... eligible persons, 946 (96.9%) could be examined. Information about best-corrected visual acuity (VA) was obtained from 944 cooperative persons (96.7%). METHODS: Data from the Copenhagen City Eye Study were used to assess the cause-specific prevalence of visual impairment as defined by the World Health...

Causes of Severe Visual Impairment and Blindness: Comparative Data From Bhutanese and Laotian Schools for the Blind.

Science.gov (United States)

Farmer, Lachlan David Mailey; Ng, Soo Khai; Rudkin, Adam; Craig, Jamie; Wangmo, Dechen; Tsang, Hughie; Southisombath, Khamphoua; Griffiths, Andrew; Muecke, James

2015-01-01

To determine and compare the major causes of childhood blindness and severe visual impairment in Bhutan and Laos. Independent cross-sectional surveys. This survey consists of 2 cross-sectional observational studies. The Bhutanese component was undertaken at the National Institute for Vision Impairment, the only dedicated school for the blind in Bhutan. The Laotian study was conducted at the National Ophthalmology Centre and Vientiane School for the Blind. Children younger than age 16 were invited to participate. A detailed history and examination were performed consistent with the World Health Organization Prevention of Blindness Eye Examination Record. Of the 53 children examined in both studies, 30 were from Bhutan and 23 were from Laos. Forty percent of Bhutanese and 87.1% of Laotian children assessed were blind, with 26.7% and 4.3%, respectively, being severely visually impaired. Congenital causes of blindness were the most common, representing 45% and 43.5% of the Bhutanese and Laotian children, respectively. Anatomically, the primary site of blinding pathology differed between the cohorts. In Bhutan, the lens comprised 25%, with whole globe at 20% and retina at 15%, but in Laos, whole globe and cornea equally contributed at 30.4%, followed by retina at 17.4%. There was an observable difference in the rates of blindness/severe visual impairment due to measles, with no cases observed in the Bhutanese children but 20.7% of the total pathologies in the Laotian children attributable to congenital measles infection. Consistent with other studies, there is a high rate of blinding disease, which may be prevented, treated, or ameliorated.

Visual impairment attributable to uncorrected refractive error and other causes in the Ghanaian youth: The University of Cape Coast Survey.

Science.gov (United States)

Abokyi, Samuel; Ilechie, Alex; Nsiah, Peter; Darko-Takyi, Charles; Abu, Emmanuel Kwasi; Osei-Akoto, Yaw Jnr; Youfegan-Baanam, Mathurin

2016-01-01

To determine the prevalence of visual impairment attributable to refractive error and other causes in a youthful Ghanaian population. A prospective survey of all consecutive visits by first-year tertiary students to the Optometry clinic between August, 2013 and April, 2014. Of the 4378 first-year students aged 16-39 years enumerated, 3437 (78.5%) underwent the eye examination. The examination protocol included presenting visual acuity (PVA), ocular motility, and slit-lamp examination of the external eye, anterior segment and media, and non-dilated fundus examination. Pinhole acuity and fundus examination were performed when the PVA≤6/12 in one or both eyes to determine the principal cause of the vision loss. The mean age of participants was 21.86 years (95% CI: 21.72-21.99). The prevalence of bilateral visual impairment (BVI; PVA in the better eye ≤6/12) and unilateral visual impairment UVI; PVA in the worse eye ≤6/12) were 3.08% (95% CI: 2.56-3.72) and 0.79% (95% CI: 0.54-1.14), respectively. Among 106 participants with BVI, refractive error (96.2%) and corneal opacity (3.8%) were the causes. Of the 27 participants with UVI, refractive error (44.4%), maculopathy (18.5%) and retinal disease (14.8%) were the major causes. There was unequal distribution of BVI in the different age groups, with those above 20 years having a lesser burden. Eye screening and provision of affordable spectacle correction to the youth could be timely to eliminate visual impairment. Copyright © 2014 Spanish General Council of Optometry. Published by Elsevier Espana. All rights reserved.

Carbon Nanofiber Electrode Array for Neurochemical Monitoring

Science.gov (United States)

Koehne, Jessica E.

2017-01-01

A sensor platform based on vertically aligned carbon nanofibers (CNFs) has been developed. Their inherent nanometer scale, high conductivity, wide potential window, good biocompatibility and well-defined surface chemistry make them ideal candidates as biosensor electrodes. Here, we report using vertically aligned CNF as neurotransmitter recording electrodes for application in a smart deep brain stimulation (DBS) device. Our approach combines a multiplexed CNF electrode chip, developed at NASA Ames Research Center, with the Wireless Instantaneous Neurotransmitter Concentration Sensor (WINCS) system, developed at the Mayo Clinic. Preliminary results indicate that the CNF nanoelectrode arrays are easily integrated with WINCS for neurotransmitter detection in a multiplexed array format. In the future, combining CNF based stimulating and recording electrodes with WINCS may lay the foundation for an implantable smart therapeutic system that utilizes neurochemical feedback control while likely resulting in increased DBS application in various neuropsychiatric disorders. In total, our goal is to take advantage of the nanostructure of CNF arrays for biosensing studies requiring ultrahigh sensitivity, high-degree of miniaturization, and selective biofunctionalization.

Separate neurochemical classes of sympathetic postganglionic neurons project to the left ventricle of the rat heart.

Science.gov (United States)

Richardson, R J; Grkovic, I; Allen, A M; Anderson, C R

2006-04-01

The sympathetic innervation of the rat heart was investigated by retrograde neuronal tracing and multiple label immunohistochemistry. Injections of Fast Blue made into the left ventricular wall labelled sympathetic neurons that were located along the medial border of both the left and right stellate ganglia. Cardiac projecting sympathetic postganglionic neurons could be grouped into one of four neurochemical populations, characterised by their content of calbindin and/or neuropeptide Y (NPY). The subpopulations of neurons contained immunoreactivity to both calbindin and NPY, immunoreactivity to calbindin only, immunoreactivity to NPY only and no immunoreactivity to calbindin or NPY. Sympathetic postganglionic neurons were also labelled in vitro with rhodamine dextran applied to the cut end of a cardiac nerve. The same neurochemical subpopulations of sympathetic neurons were identified by using this technique but in different proportions to those labelled from the left ventricle. Preganglionic terminals that were immunoreactive for another calcium-binding protein, calretinin, preferentially surrounded retrogradely labelled neurons that were immunoreactive for both calbindin and NPY. The separate sympathetic pathways projecting to the rat heart may control different cardiac functions.

Signal pathway of hippocampal apoptosis and cognitive impairment of mice caused by cerium chloride.

Science.gov (United States)

Cheng, Zhe; Li, Na; Cheng, Jie; Hu, Renping; Gao, Guodong; Cui, Yaling; Gong, Xiaolan; Wang, Ling; Hong, Fashui

2012-12-01

Experimental studies have demonstrated that lanthanides could impair cognitive functions of children and animals, but very little is known about the hippocampal apoptosis and its molecular mechanism. The study investigated the signal pathway of hippocampal apoptosis induced by intragastric administration of CeCl(3) for 60 consecutive days. It showed that cerium had been significantly accumulated in the mouse hippocampus, and CeCl(3) caused hippocampal apoptosis and impairment of spatial recognition memory of mice. CeCl(3) effectively activated caspase-3 and -9, inhibited Bcl-2, and increased the levels of Bax and cytochrome c, promoted accumulation of reactive oxygen species in the mouse hippocampus. It implied that CeCl(3)-induced apoptosis in the mouse hippocampus could be triggered via mitochondrion-mediated pathway. Our findings suggest the need for great caution to handle the lanthanides for workers and consumers. 2011 Wiley Periodicals, Inc

Effect of chronic psychogenic stress on some behavioral and neurochemical characteristics of rats

International Nuclear Information System (INIS)

Danchev, N.D.; Rozhanets, V.V.; Val'dman, A.V.

1986-01-01

This paper studies the behavioral, somatic, and certain neurochemical parameters in rats under conditions of unavoidable chronic stress, according to Hecht et al. in a situation of possible avoidance, with the same total number of aversive stimuli. Specific binding of tritium-flunitrazepam and tritium-dihydroalprenolol was studied. The dissociatin constant and the maximal concentration of ligand-receptor complexes were determined in Scatchard plots by means of an HP-33E computer. The protein concentration in the samples was determined by Peterson's method

Impaired working memory capacity is not caused by failures of selective attention in schizophrenia.

Science.gov (United States)

Erickson, Molly A; Hahn, Britta; Leonard, Carly J; Robinson, Benjamin; Gray, Brad; Luck, Steven J; Gold, James

2015-03-01

The cognitive impairments associated with schizophrenia have long been known to involve deficits in working memory (WM) capacity. To date, however, the causes of WM capacity deficits remain unknown. The present study examined selective attention impairments as a putative contributor to observed capacity deficits in this population. To test this hypothesis, we used an experimental paradigm that assesses the role of selective attention in WM encoding and has been shown to involve the prefrontal cortex and the basal ganglia. In experiment 1, participants were required to remember the locations of 3 or 5 target items (red circles). In another condition, 3-target items were accompanied by 2 distractor items (yellow circles), which participants were instructed to ignore. People with schizophrenia (PSZ) exhibited significant impairment in memory for the locations of target items, consistent with reduced WM capacity, but PSZ and healthy control subjects did not differ in their ability to filter the distractors. This pattern was replicated in experiment 2 for distractors that were more salient. Taken together, these results demonstrate that reduced WM capacity in PSZ is not attributable to a failure of filtering irrelevant distractors. © The Author 2014. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Neuroprotective potential of curcumin in combination with piperine against 6-hydroxy dopamine induced motor deficit and neurochemical alterations in rats.

Science.gov (United States)

Singh, Shamsher; Kumar, Puneet

2017-02-01

6-hydroxy dopamine (6-OHDA) is a neurotoxin which on intranigral administration produces severe nigrostriatal damage with motor and cognitive deficit in animals. Curcumin (CMN) in combination with bioenhancer piperine (PP) in 6-hydroxydopamine-induced Parkinsonian rats was used to investigate the antioxidant, neuromodulatory and neuroprotective mechanisms. Hemi-Parkinson's rat model was developed with intranigral infusion of 6-OHDA (8 μg/2 μl, once, unilaterally), treatment with CMN (25 and 50 mg/kg) and combination of PP (2.5 mg/kg) with CMN (25 mg/kg) was given daily for 21 days starting from the 7th day after 6-OHDA infusion. The behavioral (locomotor, grip strength, and narrow beam walk) parameters were studied on weekly basis. On 22nd day, isolated brain preparations were subjected to biochemical (lipid peroxidation, glutathione, and nitrite), neuroinflammatory (IL-1β, IL-6, and TNF- α), and neurochemical (DA, NE, 5- HT, GABA, Glutamate, DOPAC, HVA, and 5-HIAA) analysis. Oral administration of CMN had significantly prevented behavioral, neuroinflammatory, and neurochemical changes and preserved the antioxidant potential of the nigrostriatum in rats treated with 6-OHDA. In the present study, PP and CMN had afforded a better neuroprotective effect compared to alone treatment on behavior, biochemical, neuroinflammatory, and neurochemical parameters in rats.

Dysregulation of brain reward systems in eating disorders: neurochemical information from animal models of binge eating, bulimia nervosa, and anorexia nervosa.

Science.gov (United States)

Avena, Nicole M; Bocarsly, Miriam E

2012-07-01

Food intake is mediated, in part, through brain pathways for motivation and reinforcement. Dysregulation of these pathways may underlay some of the behaviors exhibited by patients with eating disorders. Research using animal models of eating disorders has greatly contributed to the detailed study of potential brain mechanisms that many underlie the causes or consequences of aberrant eating behaviors. This review focuses on neurochemical evidence of reward-related brain dysfunctions obtained through animal models of binge eating, bulimia nervosa, or anorexia nervosa. The findings suggest that alterations in dopamine (DA), acetylcholine (ACh) and opioid systems in reward-related brain areas occur in response to binge eating of palatable foods. Moreover, animal models of bulimia nervosa suggest that while bingeing on palatable food releases DA, purging attenuates the release of ACh that might otherwise signal satiety. Animal models of anorexia nervosa suggest that restricted access to food enhances the reinforcing effects of DA when the animal does eat. The activity-based anorexia model suggests alterations in mesolimbic DA and serotonin occur as a result of restricted eating coupled with excessive wheel running. These findings with animal models complement data obtained through neuroimaging and pharmacotherapy studies of clinical populations. Information on the neurochemical consequences of the behaviors associated with these eating disorders will be useful in understanding these complex disorders and may inform future therapeutic approaches, as discussed here. This article is part of a Special Issue entitled 'Central Control of Food Intake'. Copyright © 2011 Elsevier Ltd. All rights reserved.

Social isolation stress and chronic glutathione deficiency have a common effect on the glutamine-to-glutamate ratio and myo-inositol concentration in the mouse frontal cortex.

Science.gov (United States)

Corcoba, Alberto; Gruetter, Rolf; Do, Kim Q; Duarte, João M N

2017-09-01

Environmental stress can interact with genetic predisposition to increase the risk of developing psychopathology. In this work, we tested the hypothesis that social isolation stress interacts with impaired glutathione synthesis and have cumulative effects on the neurochemical profile of the frontal cortex. A mouse model with chronic glutathione deficit induced by knockout (-/-) of the glutamate-cysteine ligase modulatory subunit (Gclm) was exposed to social isolation stress from weaning to post-natal day 65. Using magnetic resonance methods at high-field (14.1 T), we analysed the neurochemical profile in the frontal cortex, brain size and ventricular volume of adult animals. Glutathione deficit was accompanied by elevated concentrations of N-acetylaspartate, alanine, and glutamine, as well as the ratio of glutamine-to-glutamate (Gln/Glu), and by a reduction in levels of myo-inositol and choline-containing compounds in the frontal cortex of -/- animals with respect to wild-type littermates. Although there was no significant interaction between social isolation stress and glutathione deficiency, mice reared in isolation displayed lower myo-inositol concentration (-8.4%, p social isolation had no effect on these parameters. We conclude that social isolation caused neurochemical alterations that may add to those associated to impaired glutathione synthesis. © 2017 International Society for Neurochemistry.

Causes of severe visual impairment and blindness in children in schools for the blind in eastern Africa: changes in the last 14 years.

Science.gov (United States)

Njuguna, Margaret; Msukwa, Gerald; Shilio, Bernadeth; Tumwesigye, Cillasy; Courtright, Paul; Lewallen, Susan

2009-01-01

To determine the causes of severe visual impairment and blindness in children attending schools for the blind in Kenya, Malawi, Uganda, and Tanzania and to compare the findings with those of a 1994 study. Children attending schools for the blind or annexes in 4 eastern African countries were examined. The major anatomical site of and underlying etiology of severe visual impairment and blindness was recorded using the standardized World Health Organization (WHO) reporting form. A total of 1062 children aged below 16 years were examined of whom 701 (65.2%) had severe visual impairment or blindness. The major anatomical sites of visual loss overall (% and 95% CI) were cornea scar/phthisis bulbi (19%,16.1-21.9), whole globe lesions (15.7%,13.0-18.4), retina (15.4 %, 12.7-18.1), lens related disorders (13.1%, 10.7-15.5), and optic nerve disorders (12.3%, 9.9-14.7). Corneal scar/phthisis was not distributed equally among the countries and was highest in Malawi, similar to findings in 1995. The major etiology of visual loss was childhood factors (29.9%) and an estimated 40% of severe visual impairment and blindness was due to potentially avoidable causes. The major causes of severe visual impairment and blindness overall have not changed appreciably since 1995. There are important differences among countries, however, and using overall estimates for planning may be misleading.

Infection related renal impairment: a major cause of acute allograft dysfunction.

Science.gov (United States)

Nampoory, Mangalathillam R N; Johny, Kaivilayil V; Costandy, Jamal N; Nair, Madhavan P; Said, Tarek; Homoud, Hani; Al-Muzairai, Ibrahim; Samhan, Mohmoud; Al-Moussawi, Mustafa

2003-06-01

We prospectively analyzed the impact of post-transplant infections on the renal function in 532 stable renal transplant recipients (M=340; F=192) over a period of 5 years. Their age ranged from 3-75 years (40+14 years). During the follow-up period, 52 patients expired and 64 lost on followup. We defined renal impairment (RI) as a persistent rise in serum creatinine above 20% from baseline value. 495 episodes of RI occurred in 269 recipients. This included 180-36% episodes of acute rejection, 53-10.7% Cyclosporine toxicity, 236-47.7% infection related renal impairment [IRRI] and 26-5.3% others. The severity of renal failure is less in IRRI (100+90.2) than that of acute rejection (166+127.1), but was more than that in cyclosporine toxicity (50+42.2). Sites of infection in IRRI were urinary (33%), respiratory (26.3%), septicemia (15.7%) and others (25.4%). Episode of IRRI occurred more frequently in LURD (159-67.4%) compared to LRD-RTR (50-21.2%). Occurrence of IRRI is more significantly higher in patients on triple drug immunosuppression (IS) (34.3%) than those on two drug IS (13.2%) (P=orEcoli (23.1%), Pseudomonas (11.1%), Salmonella (8.8%), Klebsiella (8.8%) and Staphylococai (8.3%) were the major organisms producing IRRI. IRRI is frequent (27.8%) during the first six months. Present study denotes that IRRI is a major cause of acute failure in RTR.

Cortical visual impairment

OpenAIRE

Koželj, Urša

2013-01-01

In this thesis we discuss cortical visual impairment, diagnosis that is in the developed world in first place, since 20 percent of children with blindness or low vision are diagnosed with it. The objectives of the thesis are to define cortical visual impairment and the definition of characters suggestive of the cortical visual impairment as well as to search for causes that affect the growing diagnosis of cortical visual impairment. There are a lot of signs of cortical visual impairment. ...

Autism: cause factors, early diagnosis and therapies.

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Bhat, Shreya; Acharya, U Rajendra; Adeli, Hojjat; Bairy, G Muralidhar; Adeli, Amir

2014-01-01

Autism spectrum disorder (ASD) is a complex neurobiological disorder characterized by neuropsychological and behavioral deficits. Cognitive impairment, lack of social skills, and stereotyped behavior are the major autistic symptoms, visible after a certain age. It is one of the fastest growing disabilities. Its current prevalence rate in the U.S. estimated by the Centers for Disease Control and Prevention is 1 in 68 births. The genetic and physiological structure of the brain is studied to determine the pathology of autism, but diagnosis of autism at an early age is challenging due to the existing phenotypic and etiological heterogeneity among ASD individuals. Volumetric and neuroimaging techniques are explored to elucidate the neuroanatomy of the ASD brain. Nuroanatomical, neurochemical, and neuroimaging biomarkers can help in the early diagnosis and treatment of ASD. This paper presents a review of the types of autism, etiologies, early detection, and treatment of ASD.

Behavioral and neurochemical responses to 8-OH-DPAT in restrained and unrestrained animals treated with lithium carbonate in drinking water

International Nuclear Information System (INIS)

Naz, H.; Haleem, D.J.

2012-01-01

Lithium has been suggested for mood disorders and neurodegenerative diseases. Its ability to increase the gray matter and provision of protection against neuronal death makes it tempting to be marketed as brain food. Moreover it also ameliorates the effects of stress on brain dendrites; however lithium has a narrow therapeutic range. Brain serotonin (5-HT) neurotransmission may mediate the actions of lithium. Preclinical studies have shown that single restraint stress produces behavioral and neurochemical deficits. The present study was designed to investigate a potential role of Lithium in attenuation of stress induced behavioral and neurochemical deficits in rats. Moreover the study also monitored the esponsiveness of pre and post synaptic serotonin 1 A receptor following restraint and administration of lithium carbonate. Pre stress behavioral activities were monitored after 15 and 30 days of consumption of 0.1% lithium carbonate in drinking water while post stress were monitored on day 31. Pre and post synaptic 5-HT -1 A responsiveness was monitored by injecting 0.25mg/ml/kg of 8-OH-DPAT. Although lithium produced hypo activity but attenuated stress induced behavioral deficits. Whole brain neurochemical analysis revealed that its administration increased tryptophan, 5-HT and 5-Hydroindoleacetic acid (5-HIAA). 8-OH-DPAT elicited hyperactivity and fore paw treading were enhanced in lithium treated rats. Lithium induced pre synaptic changes together with the super sensitivity of post synaptic receptors may be able to produce antidepressant effect. (author)

A High-Performance Application Specific Integrated Circuit for Electrical and Neurochemical Traumatic Brain Injury Monitoring.

Science.gov (United States)

Pagkalos, Ilias; Rogers, Michelle L; Boutelle, Martyn G; Drakakis, Emmanuel M

2018-05-22

This paper presents the first application specific integrated chip (ASIC) for the monitoring of patients who have suffered a Traumatic Brain Injury (TBI). By monitoring the neurophysiological (ECoG) and neurochemical (glucose, lactate and potassium) signals of the injured human brain tissue, it is possible to detect spreading depolarisations, which have been shown to be associated with poor TBI patient outcome. This paper describes the testing of a new 7.5 mm 2 ASIC fabricated in the commercially available AMS 0.35 μm CMOS technology. The ASIC has been designed to meet the demands of processing the injured brain tissue's ECoG signals, recorded by means of depth or brain surface electrodes, and neurochemical signals, recorded using microdialysis coupled to microfluidics-based electrochemical biosensors. The potentiostats use switchedcapacitor charge integration to record currents with 100 fA resolution, and allow automatic gain changing to track the falling sensitivity of a biosensor. This work supports the idea of a "behind the ear" wireless microplatform modality, which could enable the monitoring of currently non-monitored mobile TBI patients for the onset of secondary brain injury. ©2018 The Authors. Published by Wiley-VCH Verlag GmbH & Co. KGaA.

Trends in the incidence and causes of severe visual impairment and blindness in children from Israel.

Science.gov (United States)

Mezer, Eedy; Chetrit, Angela; Kalter-Leibovici, Ofra; Kinori, Michael; Ben-Zion, Itay; Wygnanski-Jaffe, Tamara

2015-06-01

To describe trends in the incidence and causes of legal childhood blindness in Israel, one of the few countries worldwide that maintain a national registry of the blind. We performed a historical cohort study of annual reports of the National Registry of the Blind (NRB) between 1999 and 2013. All data regarding demographic information, year of registration and cause of blindness of children 0-18 years of age registered for blind certification were obtained from the annual reports of the NRB. Causes of legal blindness analyzed were optic atrophy, retinitis pigmentosa, retinopathy of prematurity (ROP), albinism, other retinal disorders, cataract, and glaucoma. The main outcome measure was the incidence of new cases of certified legal blindness. The incidence of newly registered legally blind children in Israel almost halved from 7.7 per 100,000 in 1999 to 3.1 per 100,000 in 2013. The decline was mainly attributable to a decreased incidence of blindness resulting from retinitis pigmentosa and ROP. The incidence of registered cases due to cerebral visual impairment increased. During the past decade the incidence of severe childhood visual impairment and blindness declined in Israel. A continuous decline in consanguineous marriages among the Jewish and Arab populations in Israel may have contributed to the decrease in the rate of vision loss due to retinitis pigmentosa in children. Copyright © 2015 American Association for Pediatric Ophthalmology and Strabismus. Published by Elsevier Inc. All rights reserved.

How (and why) the immune system makes us sleep.

Science.gov (United States)

Imeri, Luca; Opp, Mark R

2009-03-01

Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value.

Noonan syndrome-causing SHP2 mutants impair ERK-dependent chondrocyte differentiation during endochondral bone growth.

Science.gov (United States)

Tajan, Mylène; Pernin-Grandjean, Julie; Beton, Nicolas; Gennero, Isabelle; Capilla, Florence; Neel, Benjamin G; Araki, Toshiyuki; Valet, Philippe; Tauber, Maithé; Salles, Jean-Pierre; Yart, Armelle; Edouard, Thomas

2018-04-12

Growth retardation is a constant feature of Noonan syndrome (NS) but its physiopathology remains poorly understood. We previously reported that hyperactive NS-causing SHP2 mutants impair the systemic production of insulin-like growth factor 1 (IGF1) through hyperactivation of the RAS/extracellular signal-regulated kinases (ERK) signalling pathway. Besides endocrine defects, a direct effect of these mutants on growth plate has not been explored, although recent studies have revealed an important physiological role for SHP2 in endochondral bone growth. We demonstrated that growth plate length was reduced in NS mice, mostly due to a shortening of the hypertrophic zone and to a lesser extent of the proliferating zone. These histological features were correlated with decreased expression of early chondrocyte differentiation markers, and with reduced alkaline phosphatase staining and activity, in NS murine primary chondrocytes. Although IGF1 treatment improved growth of NS mice, it did not fully reverse growth plate abnormalities, notably the decreased hypertrophic zone. In contrast, we documented a role of RAS/ERK hyperactivation at the growth plate level since 1) NS-causing SHP2 mutants enhance RAS/ERK activation in chondrocytes in vivo (NS mice) and in vitro (ATDC5 cells) and 2) inhibition of RAS/ERK hyperactivation by U0126 treatment alleviated growth plate abnormalities and enhanced chondrocyte differentiation. Similar effects were obtained by chronic treatment of NS mice with statins.In conclusion, we demonstrated that hyperactive NS-causing SHP2 mutants impair chondrocyte differentiation during endochondral bone growth through a local hyperactivation of the RAS/ERK signalling pathway, and that statin treatment may be a possible therapeutic approach in NS.

Chronic exposure to low frequency noise at moderate levels causes impaired balance in mice.

Directory of Open Access Journals (Sweden)

Haruka Tamura

Full Text Available We are routinely exposed to low frequency noise (LFN; below 0.5 kHz at moderate levels of 60-70 dB sound pressure level (SPL generated from various sources in occupational and daily environments. LFN has been reported to affect balance in humans. However, there is limited information about the influence of chronic exposure to LFN at moderate levels for balance. In this study, we investigated whether chronic exposure to LFN at a moderate level of 70 dB SPL affects the vestibule, which is one of the organs responsible for balance in mice. Wild-type ICR mice were exposed for 1 month to LFN (0.1 kHz and high frequency noise (HFN; 16 kHz at 70 dB SPL at a distance of approximately 10-20 cm. Behavior analyses including rotarod, beam-crossing and footprint analyses showed impairments of balance in LFN-exposed mice but not in non-exposed mice or HFN-exposed mice. Immunohistochemical analysis showed a decreased number of vestibular hair cells and increased levels of oxidative stress in LFN-exposed mice compared to those in non-exposed mice. Our results suggest that chronic exposure to LFN at moderate levels causes impaired balance involving morphological impairments of the vestibule with enhanced levels of oxidative stress. Thus, the results of this study indicate the importance of considering the risk of chronic exposure to LFN at a moderate level for imbalance.

Unique Behavioral and Neurochemical Effects Induced by Repeated Adolescent Consumption of Caffeine-Mixed Alcohol in C57BL/6 Mice.

Directory of Open Access Journals (Sweden)

Meridith T Robins

Full Text Available The number of highly caffeinated products has increased dramatically in the past few years. Among these products, highly caffeinated energy drinks are the most heavily advertised and purchased, which has resulted in increased incidences of co-consumption of energy drinks with alcohol. Despite the growing number of adolescents and young adults reporting caffeine-mixed alcohol use, knowledge of the potential consequences associated with co-consumption has been limited to survey-based results and in-laboratory human behavioral testing. Here, we investigate the effect of repeated adolescent (post-natal days P35-61 exposure to caffeine-mixed alcohol in C57BL/6 mice on common drug-related behaviors such as locomotor sensitivity, drug reward and cross-sensitivity, and natural reward. To determine changes in neurological activity resulting from adolescent exposure, we monitored changes in expression of the transcription factor ΔFosB in the dopaminergic reward pathway as a sign of long-term increases in neuronal activity. Repeated adolescent exposure to caffeine-mixed alcohol exposure induced significant locomotor sensitization, desensitized cocaine conditioned place preference, decreased cocaine locomotor cross-sensitivity, and increased natural reward consumption. We also observed increased accumulation of ΔFosB in the nucleus accumbens following repeated adolescent caffeine-mixed alcohol exposure compared to alcohol or caffeine alone. Using our exposure model, we found that repeated exposure to caffeine-mixed alcohol during adolescence causes unique behavioral and neurochemical effects not observed in mice exposed to caffeine or alcohol alone. Based on similar findings for different substances of abuse, it is possible that repeated exposure to caffeine-mixed alcohol during adolescence could potentially alter or escalate future substance abuse as means to compensate for these behavioral and neurochemical alterations.

Everyday memory impairment in patients with temporal lobe epilepsy caused by hippocampal sclerosis.

Science.gov (United States)

Rzezak, Patrícia; Lima, Ellen Marise; Gargaro, Ana Carolina; Coimbra, Erica; de Vincentiis, Silvia; Velasco, Tonicarlo Rodrigues; Leite, João Pereira; Busatto, Geraldo F; Valente, Kette D

2017-04-01

Patients with temporal lobe epilepsy caused by hippocampal sclerosis (TLE-HS) have episodic memory impairment. Memory has rarely been evaluated using an ecologic measure, even though performance on these tests is more related to patients' memory complaints. We aimed to measure everyday memory of patients with TLE-HS to age- and gender-matched controls. We evaluated 31 patients with TLE-HS and 34 healthy controls, without epilepsy and psychiatric disorders, using the Rivermead Behavioral Memory Test (RBMT), Visual Reproduction (WMS-III) and Logical Memory (WMS-III). We evaluated the impact of clinical variables such as the age of onset, epilepsy duration, AED use, history of status epilepticus, and seizure frequency on everyday memory. Statistical analyses were performed using MANCOVA with years of education as a confounding factor. Patients showed worse performance than controls on traditional memory tests and in the overall score of RBMT. Patients had more difficulties to recall names, a hidden belonging, to deliver a message, object recognition, to remember a story full of details, a previously presented short route, and in time and space orientation. Clinical epilepsy variables were not associated with RBMT performance. Memory span and working memory were correlated with worse performance on RBMT. Patients with TLE-HS demonstrated deficits in everyday memory functions. A standard neuropsychological battery, designed to assess episodic memory, would not evaluate these impairments. Impairment in recalling names, routes, stories, messages, and space/time disorientation can adversely impact social adaptation, and we must consider these ecologic measures with greater attention in the neuropsychological evaluation of patients with memory complaints. Copyright © 2017 Elsevier Inc. All rights reserved.

Association of Visual Impairment and All-Cause 10-Year Mortality Among Indigenous Australian Individuals Within Central Australia: The Central Australian Ocular Health Study.

Science.gov (United States)

Ng, Soo Khai; Kahawita, Shyalle; Andrew, Nicholas Howard; Henderson, Tim; Craig, Jamie Evan; Landers, John

2018-05-01

It is well established from different population-based studies that visual impairment is associated with increased mortality rate. However, to our knowledge, the association of visual impairment with increased mortality rate has not been reported among indigenous Australian individuals. To assess the association between visual impairment and 10-year mortality risk among the remote indigenous Australian population. Prospective cohort study recruiting indigenous Australian individuals from 30 remote communities located within the central Australian statistical local area over a 36-month period between July 2005 and June 2008. The data were analyzed in January 2017. Visual acuity, slitlamp biomicroscopy, and fundus examination were performed on all patients at recruitment. Visual impairment was defined as a visual acuity of less than 6/12 in the better eye. Mortality rate and mortality cause were obtained at 10 years, and statistical analyses were performed. Hazard ratios for 10-year mortality with 95% confidence intervals are presented. One thousand three hundred forty-seven patients were recruited from a total target population number of 2014. The mean (SD) age was 56 (11) years, and 62% were women. The total all-cause mortality was found to be 29.3% at 10 years. This varied from 21.1% among those without visual impairment to 48.5% among those with visual impairment. After adjustment for age, sex, and the presence of diabetes and hypertension, those with visual impairment were 40% more likely to die (hazard ratio, 1.40; 95% CI, 1.16-1.70; P = .001) during the 10-year follow-up period compared with those with normal vision. Bilateral visual impairment among remote indigenous Australian individuals was associated with 40% higher 10-year mortality risk compared with those who were not visually impaired. Resource allocation toward improving visual acuity may therefore aid in closing the gap in mortality outcomes between indigenous and nonindigenous Australian

In vivo and In vitro neurochemical-based assessments of wastewater effluents from the Maumee River area of concern

International Nuclear Information System (INIS)

Arini, Adeline; Cavallin, Jenna E.; Berninger, Jason P.; Marfil-Vega, Ruth; Mills, Marc; Villeneuve, Daniel L.; Basu, Niladri

2016-01-01

Wastewater treatment plant (WWTP) effluents contain potentially neuroactive chemicals though few methods are available to screen for the presence of such agents. Here, two parallel approaches (in vivo and in vitro) were used to assess WWTP exposure-related changes to neurochemistry. First, fathead minnows (FHM, Pimephales promelas) were caged for four days along a WWTP discharge zone into the Maumee River (Ohio, USA). Grab water samples were collected and extracts obtained for the detection of alkylphenols, bisphenol A (BPA) and steroid hormones. Second, the extracts were then used as a source of in vitro exposure to brain tissues from FHM and four additional species relevant to the Great Lakes ecosystem (rainbow trout (RT), river otter (RO), bald eagle (BE) and human (HU)). The ability of the wastewater (in vivo) or extracts (in vitro) to interact with enzymes (monoamine oxidase (MAO) and glutamine synthetase (GS)) and receptors (dopamine (D2) and N-methyl-D-aspartate receptor (NMDA)) involved in dopamine and glutamate-dependent neurotransmission were examined on brain homogenates. In vivo exposure of FHM led to significant decreases of NMDA receptor binding in females (24–42%), and increases of MAO activity in males (2.8- to 3.2-fold). In vitro, alkylphenol-targeted extracts significantly inhibited D2 (66% in FHM) and NMDA (24–54% in HU and RT) receptor binding, and induced MAO activity in RT, RO, and BE brains. Steroid hormone-targeted extracts inhibited GS activity in all species except FHM. BPA-targeted extracts caused a MAO inhibition in FHM, RT and BE brains. Using both in vivo and in vitro approaches, this study shows that WWTP effluents contain agents that can interact with neurochemicals important in reproduction and other neurological functions. Additional work is needed to better resolve in vitro to in vivo extrapolations (IVIVE) as well as cross-species differences. - Highlights: • We conducted in vivo and in vitro neurochemical

Brain region-specific perfluoroalkylated sulfonate (PFSA) and carboxylic acid (PFCA) accumulation and neurochemical biomarker responses in east Greenland polar bears (Ursus maritimus)

DEFF Research Database (Denmark)

Pedersen, Kathrine Eggers; Basu, Niladri; Letcher, Robert J.

2015-01-01

to bioaccumulate in lipid rich tissues of the brain among other tissues such as liver, and can reach high concentrations in top predators including the polar bear. PFCA and PFSA bioaccummulation in the brain has the potential to pose neurotoxic effects and therefore we conducted a study to investigate...... if variations in neurochemical transmitter systems i.e. the cholinergic, glutaminergic, dopaminergic and GABAergic, could be related to brain-specific bioaccumulation of PFASs in East Greenland polar bears. Nine brain regions from nine polar bears were analyzed for enzyme activity (monoamine oxidase (MAO...... regions, whereas GS activity was positively correlated with PFASs primarily in occipital lobe. Results from the present study support the hypothesis that PFAS concentrations in polar bears from East Greenland have exceeded the threshold limits for neurochemical alterations. It is not known whether...

Caffeine tolerance: behavioral, electrophysiological and neurochemical evidence

International Nuclear Information System (INIS)

Chou, D.T.; Khan, S.; Forde, J.; Hirsh, K.R.

1985-01-01

The development of tolerance to the stimulatory action of caffeine upon mesencephalic reticular neurons and upon spontaneous locomotor activity was evaluated in rats after two weeks of chronic exposure to low doses of caffeine (5-10 mg/kg/day via their drinking water). These doses are achievable through dietary intake of caffeine-containing beverages in man. Concomitant measurement of [ 3 H]-CHA binding in the mesencephalic reticular formation was also carried out in order to explore the neurochemical basis of the development of tolerance. Caffeine, 2.5 mg/kg i.v., markedly increased the firing rate of reticular neurons in caffeine naive rats but failed to modify the neuronal activity in a group exposed chronically to low doses of caffeine. In addition, in spontaneous locomotor activity studies, the data show a distinct shift to the right of the caffeine dose-response curve in caffeine pretreated rats. These results clearly indicate that tolerance develops to the stimulatory action of caffeine upon the reticular formation at the single neuronal activity level as well as upon spontaneous locomotor activity. Furthermore, in chronically caffeine exposed rats, an increase in the number of binding sites for [ 3 H]-CHA was observed in reticular formation membranes without any change in receptor affinity. 28 references, 4 figures

Development of the Wireless Instantaneous Neurotransmitter Concentration System for intraoperative neurochemical monitoring using fast-scan cyclic voltammetry.

Science.gov (United States)

Bledsoe, Jonathan M; Kimble, Christopher J; Covey, Daniel P; Blaha, Charles D; Agnesi, Filippo; Mohseni, Pedram; Whitlock, Sidney; Johnson, David M; Horne, April; Bennet, Kevin E; Lee, Kendall H; Garris, Paul A

2009-10-01

Emerging evidence supports the hypothesis that modulation of specific central neuronal systems contributes to the clinical efficacy of deep brain stimulation (DBS) and motor cortex stimulation (MCS). Real-time monitoring of the neurochemical output of targeted regions may therefore advance functional neurosurgery by, among other goals, providing a strategy for investigation of mechanisms, identification of new candidate neurotransmitters, and chemically guided placement of the stimulating electrode. The authors report the development of a device called the Wireless Instantaneous Neurotransmitter Concentration System (WINCS) for intraoperative neurochemical monitoring during functional neurosurgery. This device supports fast-scan cyclic voltammetry (FSCV) at a carbon-fiber microelectrode (CFM) for real-time, spatially and chemically resolved neurotransmitter measurements in the brain. The FSCV study consisted of a triangle wave scanned between -0.4 and 1 V at a rate of 300 V/second and applied at 10 Hz. All voltages were compared with an Ag/AgCl reference electrode. The CFM was constructed by aspirating a single carbon fiber (r = 2.5 mum) into a glass capillary and pulling the capillary to a microscopic tip by using a pipette puller. The exposed carbon fiber (that is, the sensing region) extended beyond the glass insulation by approximately 100 microm. The neurotransmitter dopamine was selected as the analyte for most trials. Proof-of-principle tests included in vitro flow injection and noise analysis, and in vivo measurements in urethane-anesthetized rats by monitoring dopamine release in the striatum following high-frequency electrical stimulation of the medial forebrain bundle. Direct comparisons were made to a conventional hardwired system. The WINCS, designed in compliance with FDA-recognized consensus standards for medical electrical device safety, consisted of 4 modules: 1) front-end analog circuit for FSCV (that is, current-to-voltage transducer); 2

Impairment of different protein domains causes variable clinical presentation within Pitt-Hopkins syndrome and suggests intragenic molecular syndromology of TCF4.

Science.gov (United States)

Bedeschi, Maria Francesca; Marangi, Giuseppe; Calvello, Maria Rosaria; Ricciardi, Stefania; Leone, Francesca Pia Chiara; Baccarin, Marco; Guerneri, Silvana; Orteschi, Daniela; Murdolo, Marina; Lattante, Serena; Frangella, Silvia; Keena, Beth; Harr, Margaret H; Zackai, Elaine; Zollino, Marcella

2017-11-01

Pitt-Hopkins syndrome is a neurodevelopmental disorder characterized by severe intellectual disability and a distinctive facial gestalt. It is caused by haploinsufficiency of the TCF4 gene. The TCF4 protein has different functional domains, with the NLS (nuclear localization signal) domain coded by exons 7-8 and the bHLH (basic Helix-Loop-Helix) domain coded by exon 18. Several alternatively spliced TCF4 variants have been described, allowing for translation of variable protein isoforms. Typical PTHS patients have impairment of at least the bHLH domain. To which extent impairment of the remaining domains contributes to the final phenotype is not clear. There is recent evidence that certain loss-of-function variants disrupting TCF4 are associated with mild ID, but not with typical PTHS. We describe a frameshift-causing partial gene deletion encompassing exons 4-6 of TCF4 in an adult patient with mild ID and nonspecific facial dysmorphisms but without the typical features of PTHS, and a c.520C > T nonsense variant within exon 8 in a child presenting with a severe phenotype largely mimicking PTHS, but lacking the typical facial dysmorphism. Investigation on mRNA, along with literature review, led us to suggest a preliminary phenotypic map of loss-of-function variants affecting TCF4. An intragenic phenotypic map of loss-of-function variants in TCF4 is suggested here for the first time: variants within exons 1-4 and exons 4-6 give rise to a recurrent phenotype with mild ID not in the spectrum of Pitt-Hopkins syndrome (biallelic preservation of both the NLS and bHLH domains); variants within exons 7-8 cause a severe phenotype resembling PTHS but in absence of the typical facial dysmorphism (impairment limited to the NLS domain); variants within exons 9-19 cause typical Pitt-Hopkins syndrome (impairment of at least the bHLH domain). Understanding the TCF4 molecular syndromology can allow for proper nosology in the current era of whole genomic investigations. Copyright �

Arid1b haploinsufficient mice reveal neuropsychiatric phenotypes and reversible causes of growth impairment.

Science.gov (United States)

Celen, Cemre; Chuang, Jen-Chieh; Luo, Xin; Nijem, Nadine; Walker, Angela K; Chen, Fei; Zhang, Shuyuan; Chung, Andrew S; Nguyen, Liem H; Nassour, Ibrahim; Budhipramono, Albert; Sun, Xuxu; Bok, Levinus A; McEntagart, Meriel; Gevers, Evelien F; Birnbaum, Shari G; Eisch, Amelia J; Powell, Craig M; Ge, Woo-Ping; Santen, Gijs We; Chahrour, Maria; Zhu, Hao

2017-07-11

Sequencing studies have implicated haploinsufficiency of ARID1B , a SWI/SNF chromatin-remodeling subunit, in short stature (Yu et al., 2015), autism spectrum disorder (O'Roak et al., 2012), intellectual disability (Deciphering Developmental Disorders Study, 2015), and corpus callosum agenesis (Halgren et al., 2012). In addition, ARID1B is the most common cause of Coffin-Siris syndrome, a developmental delay syndrome characterized by some of the above abnormalities (Santen et al., 2012; Tsurusaki et al., 2012; Wieczorek et al., 2013). We generated Arid1b heterozygous mice, which showed social behavior impairment, altered vocalization, anxiety-like behavior, neuroanatomical abnormalities, and growth impairment. In the brain, Arid1b haploinsufficiency resulted in changes in the expression of SWI/SNF-regulated genes implicated in neuropsychiatric disorders. A focus on reversible mechanisms identified Insulin-like growth factor (IGF1) deficiency with inadequate compensation by Growth hormone-releasing hormone (GHRH) and Growth hormone (GH), underappreciated findings in ARID1B patients. Therapeutically, GH supplementation was able to correct growth retardation and muscle weakness. This model functionally validates the involvement of ARID1B in human disorders, and allows mechanistic dissection of neurodevelopmental diseases linked to chromatin-remodeling.

Hearing Impairment Caused by Occupational Noise | Mets | South ...

African Journals Online (AJOL)

Occupational noise-induced hearing impairment is an insidiously developing injury which only becomes apparent when it affects the hearing of conversational speech. As no remedy is possible, prevention is the only answer. In view of the impending legislation in South Africa a review of the literature is presented. This is ...

Does extracorporeal shock wave lithotripsy cause hearing impairment?

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Tuncer, Murat; Erdogan, Banu A; Yazici, Ozgur; Sahin, Cahit; Altin, Gokhan; Faydaci, Gokhan; Eryildirim, Bilal; Sarica, Kemal

2014-07-01

To evaluate the possible effects of extracorporeal shock wave lithotripsy (ESWL) on the hearing status of the patients in this prospective controlled study. A total of 40 patients with normal hearing function were included to the study. We had 20 patients each in the study group and control group. The treatment parameters were standardized in all 3 sessions in which a total of 3000 shock waves with a rate of 90/min along with a total energy value of 126 J at the fourth energy level have been applied (Dornier Compact Sigma, Medtech, Germany). In addition to the testing of hearing functions and possible cochlear impairment by Transient Evoked Otoacoustic Emissions test at 1.0, 1.4, 2.0, 2.8, and 4.0 kHz frequencies, complications such as ear pain, tinnitus, and hearing loss have been well evaluated in each patient before the procedure and 2 hours and 1 month after the completion of the third session of ESWL in the study group. The same evaluation procedures were performed before the study and after 7-weeks in the control group. Regarding Transient Evoked Otoacoustic Emissions data obtained in study group and control group patients, there was no significant alteration in values obtained after ESWL when compared with the values before the procedure. A well-planned ESWL procedure is a safe and effective treatment in urinary stones and causes no detectable harmful effect on the hearing function of treated patients. Copyright © 2014 Elsevier Inc. All rights reserved.

Specific genetic deficiencies of the A and B isoenzymes of monoamine oxidase are characterized by distinct neurochemical and clinical phenotypes

NARCIS (Netherlands)

Lenders, J. W.; Eisenhofer, G.; Abeling, N. G.; Berger, W.; Murphy, D. L.; Konings, C. H.; Wagemakers, L. M.; Kopin, I. J.; Karoum, F.; van Gennip, A. H.; Brunner, H. G.

1996-01-01

Monoamine oxidase (MAO) exists as two isoenzymes and plays a central role in the metabolism of monoamine neurotransmitters. In this study we compared the neurochemical phenotypes of previously described subjects with genetically determined selective lack of MAO-A or a lack of both MAO-A and MAO-B

Absence of Carbohydrate Response Element Binding Protein in Adipocytes Causes Systemic Insulin Resistance and Impairs Glucose Transport

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Archana Vijayakumar

2017-10-01

Full Text Available Lower adipose-ChREBP and de novo lipogenesis (DNL are associated with insulin resistance in humans. Here, we generated adipose-specific ChREBP knockout (AdChREBP KO mice with negligible sucrose-induced DNL in adipose tissue (AT. Chow-fed AdChREBP KO mice are insulin resistant with impaired insulin action in the liver, muscle, and AT and increased AT inflammation. HFD-fed AdChREBP KO mice are also more insulin resistant than controls. Surprisingly, adipocytes lacking ChREBP display a cell-autonomous reduction in insulin-stimulated glucose transport that is mediated by impaired Glut4 translocation and exocytosis, not lower Glut4 levels. AdChREBP KO mice have lower levels of palmitic acid esters of hydroxy stearic acids (PAHSAs in serum, and AT. 9-PAHSA supplementation completely rescues their insulin resistance and AT inflammation. 9-PAHSA also normalizes impaired glucose transport and Glut4 exocytosis in ChREBP KO adipocytes. Thus, loss of adipose-ChREBP is sufficient to cause insulin resistance, potentially by regulating AT glucose transport and flux through specific lipogenic pathways.

Previous Ketamine Produces an Enduring Blockade of Neurochemical and Behavioral Effects of Uncontrollable Stress

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Dolzani, Samuel D.; Tilden, Scott; Christianson, John P.; Kubala, Kenneth H.; Bartholomay, Kristi; Sperr, Katherine; Ciancio, Nicholas; Watkins, Linda R.; Maier, Steven F.

2016-01-01

Recent interest in the antidepressant and anti-stress effects of subanesthetic doses of ketamine, an NMDA receptor antagonist, has identified mechanisms whereby ketamine reverses the effect of stress, but little is known regarding the prophylactic effect ketamine might have on future stressors. Here we investigate the prophylactic effect of ketamine against neurochemical and behavioral changes that follow inescapable, uncontrollable tail shocks (ISs) in Sprague Dawley rats. IS induces increased anxiety, which is dependent on activation of serotonergic (5-HT) dorsal raphe nucleus (DRN) neurons that project to the basolateral amygdala (BLA). Ketamine (10 mg/kg, i.p.) administered 2 h, 1 week, or 2 weeks before IS prevented the increased extracellular levels of 5-HT in the BLA typically produced by IS. In addition, ketamine administered at these time points blocked the decreased juvenile social investigation produced by IS. Microinjection of ketamine into the prelimbic (PL) region of the medial prefrontal cortex duplicated the effects of systemic ketamine, and, conversely, systemic ketamine effects were prevented by pharmacological inhibition of the PL. Although IS does not activate DRN-projecting neurons from the PL, IS did so after ketamine, suggesting that the prophylactic effect of ketamine is a result of altered functioning of this projection. SIGNIFICANCE STATEMENT The reported data show that systemic ketamine, given up to 2 weeks before a stressor, blunts behavioral and neurochemical effects of the stressor. The study also advances understanding of the mechanisms involved and suggests that ketamine acts at the prelimbic cortex to sensitize neurons that project to and inhibit the DRN. PMID:26740657

Prevalence and causes of musculoskeletal impairment in Mahabubnagar District, Telangana State, India: results of a population-based survey.

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Smythe, Tracey; Mactaggart, Islay; Kuper, Hannah; Murthy, G V S; Lavy, Christopher; Polack, Sarah

2017-11-01

Musculoskeletal impairments (MSI) are the leading contributor to global years lived with disability. Comparable epidemiological data on MSI is lacking, and are needed to inform health and rehabilitative services. This study aimed to estimate the prevalence and causes of MSI in Telangana State, India. A population-based survey used probability proportionate to size and compact-segment sampling to select 51 clusters of 80 individuals (all ages). Participants were screened using seven questions and any participant who screened positive underwent standardized examination by a physiotherapist for MSI presence, severity and diagnosis. Data were also collected on vision and hearing impairment, depression and self-reported difficulties with physical functioning. The prevalence of MSI was 19.6% (95% CI: 16.7-22.8%) and this increased with age. The majority (82%; 574/699) of MSI was classified as mild, 11% as moderate and 7% as severe. Over half (57%) of MSI diagnoses were acquired non-traumatic causes, with degenerative joint disease being the most common. There was a high unmet need for physiotherapy services (3% attended vs. 40% recommended). One-fifth (21%) of MSI cases also had at least one of vision (10%) or hearing (11%) impairment or depression (3%). MSI is common among persons living in Mahabubnagar District, particularly older adults. These estimates can inform public health initiatives for the planning of health and rehabilitation services. © The Author(s) 2018. Published by Oxford University Press on behalf of Royal Society of Tropical Medicine and Hygiene. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Wireless Amperometric Neurochemical Monitoring Using an Integrated Telemetry Circuit

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Roham, Masoud; Halpern, Jeffrey M.; Martin, Heidi B.; Chiel, Hillel J.

2015-01-01

An integrated circuit for wireless real-time monitoring of neurochemical activity in the nervous system is described. The chip is capable of conducting high-resolution amperometric measurements in four settings of the input current. The chip architecture includes a first-order ΔΣ modulator (ΔΣM) and a frequency-shift-keyed (FSK) voltage-controlled oscillator (VCO) operating near 433 MHz. It is fabricated using the AMI 0.5 μm double-poly triple-metal n-well CMOS process, and requires only one off-chip component for operation. Measured dc current resolutions of ~250 fA, ~1.5 pA, ~4.5 pA, and ~17 pA were achieved for input currents in the range of ±5, ±37, ±150, and ±600 nA, respectively. The chip has been interfaced with a diamond-coated, quartz-insulated, microneedle, tungsten electrode, and successfully recorded dopamine concentration levels as low as 0.5 μM wirelessly over a transmission distance of ~0.5 m in flow injection analysis experiments. PMID:18990633

Wireless amperometric neurochemical monitoring using an integrated telemetry circuit.

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Roham, Masoud; Halpern, Jeffrey M; Martin, Heidi B; Chiel, Hillel J; Mohseni, Pedram

2008-11-01

An integrated circuit for wireless real-time monitoring of neurochemical activity in the nervous system is described. The chip is capable of conducting high-resolution amperometric measurements in four settings of the input current. The chip architecture includes a first-order Delta Sigma modulator (Delta Sigma M) and a frequency-shift-keyed (FSK) voltage-controlled oscillator (VCO) operating near 433 MHz. It is fabricated using the AMI 0.5 microm double-poly triple-metal n-well CMOS process, and requires only one off-chip component for operation. Measured dc current resolutions of approximately 250 fA, approximately 1.5 pA, approximately 4.5 pA, and approximately 17 pA were achieved for input currents in the range of +/-5, +/-37, +/-150, and +/-600 nA, respectively. The chip has been interfaced with a diamond-coated, quartz-insulated, microneedle, tungsten electrode, and successfully recorded dopamine concentration levels as low as 0.5 microM wirelessly over a transmission distance of approximately 0.5 m in flow injection analysis experiments.

Axonal transport of TDP-43 mRNA granules in neurons is impaired by ALS-causing mutations

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Carrasco, Monica A.; Williams, Luis A.; Winborn, Christina S.; Han, Steve S. W.; Kiskinis, Evangelos; Winborn, Brett; Freibaum, Brian D.; Kanagaraj, Anderson; Clare, Alison J.; Badders, Nisha M.; Bilican, Bilada; Chaum, Edward; Chandran, Siddharthan; Shaw, Christopher E.; Eggan, Kevin C.; Maniatis, Tom; Taylor, J. Paul

2014-01-01

Summary The RNA binding protein TDP-43 regulates RNA metabolism at multiple levels, including transcription, RNA splicing, and mRNA stability. TDP-43 is a major component of the cytoplasmic inclusions characteristic of amyotrophic lateral sclerosis and some types of frontotemporal lobar degeneration. The importance of TDP-43 in disease is underscored by the fact that dominant missense mutations are sufficient to cause disease, although the role of TDP-43 in pathogenesis is unknown. Here we show that TDP-43 forms cytoplasmic mRNP granules that undergo bidirectional, microtubule-dependent transport in neurons in vitro and in vivo and facilitate delivery of target mRNA to distal neuronal compartments. TDP-43 mutations impair this mRNA transport function in vivo and in vitro, including in stem cell-derived motor neurons from ALS patients bearing any one of three different TDP-43 ALS-causing mutations. Thus, TDP43 mutations that cause ALS lead to partial loss of a novel cytoplasmic function of TDP-43. PMID:24507191

Combined exposure to endocrine disrupting pesticides impairs parturition, causes pup mortality and affects sexual differentiation in rats

DEFF Research Database (Denmark)

Jacobsen, Pernille Rosenskjold; Christiansen, Sofie; Boberg, Julie

2010-01-01

Risk assessment is currently based on the no observed adverse effect levels (NOAELs) for single compounds. Humans are exposed to a mixture of chemicals and recent studies in our laboratory have shown that combined exposure to endocrine disrupters can cause adverse effects on male sexual development...... were gavaged during gestation and lactation with five doses of a mixture of the fungicides procymidone, mancozeb, epoxyconazole, tebuconazole and prochloraz. The mixture ratio was chosen according to the doses of each individual pesticide that produced no observable effects on pregnancy length and pup...... survival in our laboratory and the dose levels used ranged from 25 to 100% of this mixture. All dose levels caused increased gestation length and dose levels above 25% caused impaired parturition leading to markedly decreased number of live born offspring and high pup perinatal mortality. The sexual...

Impaired endocannabinoid signalling in the rostral ventromedial medulla underpins genotype-dependent hyper-responsivity to noxious stimuli.

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Rea, Kieran; Olango, Weredeselam M; Okine, Bright N; Madasu, Manish K; McGuire, Iseult C; Coyle, Kathleen; Harhen, Brendan; Roche, Michelle; Finn, David P

2014-01-01

Pain is both a sensory and an emotional experience, and is subject to modulation by a number of factors including genetic background modulating stress/affect. The Wistar-Kyoto (WKY) rat exhibits a stress-hyper-responsive and depressive-like phenotype and increased sensitivity to noxious stimuli, compared with other rat strains. Here, we show that this genotype-dependent hyperalgesia is associated with impaired pain-related mobilisation of endocannabinoids and transcription of their synthesising enzymes in the rostral ventromedial medulla (RVM). Pharmacological blockade of the Cannabinoid1 (CB1) receptor potentiates the hyperalgesia in WKY rats, whereas inhibition of the endocannabinoid catabolising enzyme, fatty acid amide hydrolase, attenuates the hyperalgesia. The latter effect is mediated by CB1 receptors in the RVM. Together, these behavioural, neurochemical, and molecular data indicate that impaired endocannabinoid signalling in the RVM underpins hyper-responsivity to noxious stimuli in a genetic background prone to heightened stress/affect. Copyright © 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

[Prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Longyao County of Hebei Province:the China Nine-Province survey].

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Lü, Jian-hua; Zhao, Jia-liang; Ellwein, Leon B; Li, Shan-yu; Han, Dong; Yan, Zhong-yang; Zhang, Hong-bin; Yang, Mei; Wang, Yu; Gao, Xue-cheng

2013-09-01

To investigate the prevalence and causes of blindness and moderate and severe visual impairment among adults aged ≥ 50 years in Longyao County, Hebei Province, China. It was a population-based cross-section study.Geographically defined cluster sampling was used in randomly selecting 5527 individuals aged ≥ 50 years in Longyao County. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. All participants were enumerated through village registers followed door-to-door visits.Eligible individuals were invited to receive visual acuity measurement and eye examination. Prevalence of blindness and moderate and severe visual impairment was calculated according to different age, gender or education. And the reasons of blindness were analyzed.Statistical analyses were performed using Stata/SE Statistical Software, release 9.0. Chi-square test was used to investigate the association of age, gender and education with presenting and best corrected visual acuity. Five thousands five hundreds and twenty-seven individuals were enumerated and 5051 persons were examined, the response rate was 91.39%. Based on the criteria of World Health Organization visual impairment classification in 1973, the prevalence of blindness and moderate and severe visual impairment defined as best corrected visual acuity was 1.05% (53/5051) and 3.46% (175/5051) respectively. The prevalence of blindness and moderate and severe visual impairment defined as presenting visual acuity was 1.48% (75/5051) and 7.94% (401/5051) respectively. The prevalence of blindness and moderate and severe visual impairment was higher in aged (trend χ(2) = 897.27, P = 0.000) , female (χ(2) = 30.32, P = 0.000), illiterate (trend χ(2) = 83.20, P = 0.000) persons. Cataract was still the first leading cause of blindness. Un-corrected refractive error also was the main cause of visual impairment. The prevalence of blindness and moderate and severe

Cognitive Impairment in Chronic Alcoholics: Some Cause for Optimism.

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Goldman, Mark S.

1983-01-01

It appears that, although the cognitive functioning of many alcoholics remains impaired even after drinking has stopped, considerable recovery can occur. New findings now suggest the possibility of reducing cognitive dysfunction and enhancing alcoholism treatment outcomes. (CMG)

Neurodegeneration caused by expression of human truncated tau leads to progressive neurobehavioural impairment in transgenic rats.

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Hrnkova, Miroslava; Zilka, Norbert; Minichova, Zuzana; Koson, Peter; Novak, Michal

2007-01-26

Human truncated tau protein is an active constituent of the neurofibrillary degeneration in sporadic Alzheimer's disease. We have shown that modified tau protein, when expressed as a transgene in rats, induced AD characteristic tau cascade consisting of tau hyperphosphorylation, formation of argyrophilic tangles and sarcosyl-insoluble tau complexes. These pathological changes led to the functional impairment characterized by a variety of neurobehavioural symptoms. In the present study we have focused on the behavioural alterations induced by transgenic expression of human truncated tau. Transgenic rats underwent a battery of behavioural tests involving cognitive- and sensorimotor-dependent tasks accompanied with neurological assessment at the age of 4.5, 6 and 9 months. Behavioural examination of these rats showed altered spatial navigation in Morris water maze resulting in less time spent in target quadrant (popen field was not influenced by transgene expression. However beam walking test revealed that transgenic rats developed progressive sensorimotor disturbances related to the age of tested animals. The disturbances were most pronounced at the age of 9 months (p<0.01). Neurological alterations indicating impaired reflex responses were other added features of behavioural phenotype of this novel transgenic rat. These results allow us to suggest that neurodegeneration, caused by the non-mutated human truncated tau derived from sporadic human AD, result in the neuronal dysfunction consequently leading to the progressive neurobehavioural impairment.

Impairment of Serotonergic Transmission by the Antiparkinsonian Drug L-DOPA: Mechanisms and Clinical Implications

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Cristina Miguelez

2017-09-01

Full Text Available The link between the anti-Parkinsonian drug L-3,4-dihydroxyphenylalanine (L-DOPA and the serotonergic (5-HT system has been long established and has received increased attention during the last decade. Most studies have focused on the fact that L-DOPA can be transformed into dopamine (DA and released from 5-HT terminals, which is especially important for the management of L-DOPA-induced dyskinesia. In patients, treatment using L-DOPA also impacts 5-HT neurotransmission; however, few studies have investigated the mechanisms of this effect. The purpose of this review is to summarize the electrophysiological and neurochemical data concerning the effects of L-DOPA on 5-HT cell function. This review will argue that L-DOPA disrupts the link between the electrical activity of 5-HT neurons and 5-HT release as well as that between 5-HT release and extracellular 5-HT levels. These effects are caused by the actions of L-DOPA and DA in 5-HT neurons, which affect 5-HT neurotransmission from the biosynthesis of 5-HT to the impairment of the 5-HT transporter. The interaction between L-DOPA and 5-HT transmission is especially relevant in those Parkinson’s disease (PD patients that suffer dyskinesia, comorbid anxiety or depression, since the efficacy of antidepressants or 5-HT compounds may be affected.

Congenital hearing impairment

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Robson, Caroline D. [Children' s Hospital and Harvard Medical School, Division of Neuroradiology, Department of Radiology, Boston, MA (United States)

2006-04-15

Establishing the etiology of congenital hearing impairment can significantly improve treatment for certain causes of hearing loss and facilitates genetic counseling. High-resolution CT and MRI have contributed to the evaluation and management of hearing impairment. In addition, with the identification of innumerable genetic loci and genetic defects involved in hearing loss, genetic testing has emerged as an invaluable tool in the assessment of hearing impairment. Some of the common forms of congenital hearing loss are reviewed and their imaging features illustrated. (orig.)

Congenital hearing impairment

International Nuclear Information System (INIS)

Robson, Caroline D.

2006-01-01

Establishing the etiology of congenital hearing impairment can significantly improve treatment for certain causes of hearing loss and facilitates genetic counseling. High-resolution CT and MRI have contributed to the evaluation and management of hearing impairment. In addition, with the identification of innumerable genetic loci and genetic defects involved in hearing loss, genetic testing has emerged as an invaluable tool in the assessment of hearing impairment. Some of the common forms of congenital hearing loss are reviewed and their imaging features illustrated. (orig.)

[Prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Yongchuan District of Chongqing City: the China Nine-Province survey].

Science.gov (United States)

Yin, Zheng-qin; Zhao, Jia-liang; Li, Ping-hua; Ellwein, Leon b; Song, Sheng-fang; Li, Fu-liang; Wang, Ting-gang; Ren, Yi-ming; Yang, Mei; Wang, Yu; Gao, Xue-cheng

2013-09-01

To investigate the prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Yongchuan of Chongqing City, China. It was a population-based cross-section study.Geographically defined cluster sampling was used in randomly selecting 5663 individuals aged ≥ 50 years in Yongchuan District. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. All participants were enumerated through village registers followed door-to-door visits.Eligible individuals were invited to receive visual acuity measurement and eye examination. Prevalence of blindness and moderate and severe visual impairment was calculated according to different age, gender or education. And the reasons of blindness were analyzed.Statistical analyses were performed using Stata/SE Statistical Software, release 9.0. Chi-square test was used to investigate the association of age, gender and education with presenting and best corrected visual acuity. Five thousands six hundreds and sixty-three individuals were enumerated and 5390 persons were examined, the response rate was 95.18%. Based on the criteria of World Health Organization visual impairment classification in 1973, the prevalence of blindness and moderate and severe visual impairment defined as best corrected visual acuity was 2.12% (114/5390) and 5.40% (291/5390) respectively. The prevalence of blindness and moderate and severe visual impairment defined as presenting visual acuity was 2.49% (134/5390) and 10.71% (577/5390) respectively. The prevalence of blindness and moderate and severe visual impairment was higher in aged (trend χ(2) = 951.32, P = 0.000) , female (χ(2) = 33.35, P = 0.000) and illiterate (trend χ(2) equals; 141.32, P = 0.000) persons. Cataract was still the first leading cause of blindness and visual impairment.Un-corrected refractive error also was the main cause of visual impairment. The prevalence

[Prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Changji City of Xinjiang Uygur Autonomous Region: the China Nine-Province survey].

Science.gov (United States)

Ma, Xian-zhi; Zhao, Jia-liang; Ellwein, Leon B; Wei, Bin; Chen, Jing; Ye, Ying; Tang, Xiao-dong; Yang, Mei; Wang, Yu; Gao, Xue-cheng

2013-09-01

To investigate the prevalence and causes of blindness and moderate and severe visual impairment among adults aged ≥ 50 years in Changji City of Xinjiang Uygur Autonomous Region, China. It was a population-based cross-section study.Geographically defined cluster sampling was used in randomly selecting 5714 individuals aged ≥ 50 years in Changji City. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. All participants were enumerated through village registers followed door-to-door visits.Eligible individuals were invited to received visual acuity measurement and eye examination. Prevalence of blindness and moderate and severe visual impairment was calculated according to different age, gender or education. And the reasons of blindness were analyzed.Statistical analyses were performed using Stata/SE Statistical Software, release 9.0. Chi-square test was used to investigate the association of age, gender and education with presenting and best corrected visual acuity. Five thousands seven hundreds and fourteen individuals were enumerated and 5250 persons were examined, the response rate was 91.88%. Based on the criteria of World Health Organization visual impairment classification in 1973, the prevalence of blindness and moderate and severe visual impairment defined as best corrected visual acuity was 0.74% (39/5250) and 3.83% (201/5250) respectively. The prevalence of blindness and moderate and severe visual impairment defined as presenting visual acuity was 1.33% (70/5250) and 8.02% (421/5250) respectively. The prevalence of blindness and moderate and severe visual impairment was higher in aged (trend χ(2) = 617.06, P = 0.000) , illiterate (trend χ(2) = 222.35, P = 0.000) persons. Cataract and was the first leading cause of blindness and visual impairment, the retinal diseases, including age-related macular degeneration, high myopic retinopathy, and diabetic retinopathy, were the

Individual differences in the forced swimming test and neurochemical kinetics in the rat brain.

Science.gov (United States)

Sequeira-Cordero, Andrey; Mora-Gallegos, Andrea; Cuenca-Berger, Patricia; Fornaguera-Trías, Jaime

2014-04-10

Individual differences in the forced swimming test (FST) could be associated with differential temporal dynamics of gene expression and neurotransmitter activity. We tested juvenile male rats in the FST and classified the animals into those with low and high immobility according to the amount of immobility time recorded in FST. These groups and a control group which did not undergo the FST were sacrificed either 1, 6 or 24 h after the test. We analyzed the expression of the CRF, CRFR1, BDNF and TrkB in the prefrontal cortex, hippocampus and nucleus accumbens as well as norepinephrine, dopamine, serotonin, glutamate, GABA and glutamine in the hippocampus and nucleus accumbens. Animals with low immobility showed significant reductions of BDNF expression across time points in both the prefrontal cortex and the nucleus accumbens when compared with non-swim control. Moreover, rats with high immobility only showed a significant decrease of BDNF expression in the prefrontal cortex 6h after the FST. Regarding neurotransmitters, only accumbal dopamine turnover and hippocampal glutamate content showed an effect of individual differences (i.e. animals with low and high immobility), whereas nearly all parameters showed significant differences across time points. Correlational analyses suggest that immobility in the FST, probably reflecting despair, is related to prefrontal cortical BDNF and to the kinetics observed in several other neurochemical parameters. Taken together, our results suggest that individual differences observed in depression-like behavior can be associated not only with changes in the concentrations of key neurochemical factors but also with differential time courses of such factors. Copyright © 2014 Elsevier Inc. All rights reserved.

Mutations in OTOF, CLDN14 & SLC26A4 genes as major causes of hearing impairment in Dhadkai village, Jammu & Kashmir, India

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Nishtha Pandey

2017-01-01

Interpretation & conclusions: This study suggested considerable genetic heterogeneity in the causation of hearing loss in Dhadkai. Recessive mutations were observed in at least three genes causing hearing loss: OTOF (p.R708X, SLC26A4 (p.Y556X and CLDN14 (p.V85D. Mutation p.R708X appeared to be the major cause of hearing impairment in Dhadkai.

Hypomorphic mutation in mouse Nppc gene causes retarded bone growth due to impaired endochondral ossification

International Nuclear Information System (INIS)

Tsuji, Takehito; Kondo, Eri; Yasoda, Akihiro; Inamoto, Masataka; Kiyosu, Chiyo; Nakao, Kazuwa; Kunieda, Tetsuo

2008-01-01

Long bone abnormality (lbab/lbab) is a spontaneous mutant mouse characterized by dwarfism with shorter long bones. A missense mutation was reported in the Nppc gene, which encodes C-type natriuretic peptide (CNP), but it has not been confirmed whether this mutation is responsible for the dwarf phenotype. To verify that the mutation causes the dwarfism of lbab/lbab mice, we first investigated the effect of CNP in lbab/lbab mice. By transgenic rescue with chondrocyte-specific expression of CNP, the dwarf phenotype in lbab/lbab mice was completely compensated. Next, we revealed that CNP derived from the lbab allele retained only slight activity to induce cGMP production through its receptor. Histological analysis showed that both proliferative and hypertrophic zones of chondrocytes in the growth plate of lbab/lbab mice were markedly reduced. Our results demonstrate that lbab/lbab mice have a hypomorphic mutation in the Nppc gene that is responsible for dwarfism caused by impaired endochondral ossification

Impaired emotional empathy and related social network deficits in cocaine users.

Science.gov (United States)

Preller, Katrin H; Hulka, Lea M; Vonmoos, Matthias; Jenni, Daniela; Baumgartner, Markus R; Seifritz, Erich; Dziobek, Isabel; Quednow, Boris B

2014-05-01

Chronic cocaine users consistently display neurochemical and functional alterations in brain areas involved in social cognition (e.g. medial and orbitofrontal cortex). Although social functioning plays a crucial role in the development and treatment of drug dependence, studies investigating social cognition in cocaine users are lacking. Therefore, we investigated mental perspective taking ('theory of mind') and emotional and cognitive empathy in recreational (RCU) and dependent (DCU) cocaine users. Furthermore, we related these measures to real-life indicators of social functioning. One-hundred cocaine users (69 RCU, 31 DCU) and 68 stimulant-naïve healthy controls were tested with the Multifaceted Empathy Test (MET), Movie for the Assessment of Social Cognition (MASC) and Reading the Mind in the Eyes Test (RMET). The Social Network Questionnaire was conducted to assess social network size. Furthermore, participants provided information on committed criminal offenses. RCU and DCU showed less emotional empathy compared to controls (MET), whereas cognitive empathy was not impaired (MET, RMET). Additionally, DCU made more errors in mental perspective taking (MASC). Notably, cocaine users committed more criminal offenses and displayed a smaller social network and higher cocaine use was correlated with less social contacts. Diminished mental perspective taking was tentatively correlated with more intense cocaine use as well. Finally, younger age of onset of cocaine use was associated with more pronounced empathy impairment. In conclusion, social cognition impairments in cocaine users were related to real-life social functioning and should therefore be considered in therapy and prevention strategies. © 2013 Society for the Study of Addiction.

Brain visual impairment in childhood: mini review

OpenAIRE

Kozeis, N

2010-01-01

Cerebral visual impairment (CVI) is one of the leading causes of severe visual impairment in childhood. This article was written to highlight any new knowledge related to cerebral visual impairment in childhood.

Neurochemical properties of BDNF-containing neurons projecting to rostral ventromedial medulla in the ventrolateral periaqueductal gray

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Jun-Bin eYin

2014-11-01

Full Text Available The periaqueductal gray (PAG modulates nociception via a descending pathway that relays in the rostral ventromedial medulla (RVM and terminates in the spinal cord. Previous behavioral pharmacology and electrophysiological evidence suggests that brain-derived neurotrophic factor (BDNF plays an important role in descending pain modulation, likely through the PAG-RVM pathway. However, there still lacks detailed information on the distribution of BDNF, activation of BDNF-containing neurons projecting to RVM in the condition of pain, and neurochemical properties of these neurons within the PAG. Through fluorescent in situ hybridization (FISH and immunofluorescent staining, the homogenous distributions of BDNF mRNA and protein were observed in the four subregions of PAG. Both neurons and astrocytes expressed BDNF, but not microglias. By combining retrograde tracing methods and formalin pain model, there were more BDNF-containing neurons projecting to RVM being activated in the ventrolateral PAG (vlPAG than other subregions of PAG. The neurochemical properties of BDNF-containing projection neurons in the vlPAG were investigated. BDNF-containing projection neurons expressed auto receptor Tropomyosin-related kinase B (TrkB in addition to serotonin (5-HT, neurotensin (NT, substance P (SP, calcitonin gene related peptide (CGRP, nitric oxide synthase (NOS, and parvalbumin (PV but not tyrosine decarboxylase (TH. It is speculated that BDNF released from projection neurons in the vlPAG might participate in the descending pain modulation through enhancing the presynaptic release of other neuroactive substances (NSs in the RVM.

Phytoceramide Shows Neuroprotection and Ameliorates Scopolamine-Induced Memory Impairment

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Seikwan Oh

2011-10-01

Full Text Available The function and the role phytoceramide (PCER and phytosphingosine (PSO in the central nervous system has not been well studied. This study was aimed at investigating the possible roles of PCER and PSO in glutamate-induced neurotoxicity in cultured neuronal cells and memory function in mice. Phytoceramide showed neuro-protective activity in the glutamate-induced toxicity in cultured cortical neuronal cells. Neither phytosphingosine nor tetraacetylphytosphingosine (TAPS showed neuroproective effects in neuronal cells. PCER (50 mg/kg, p.o. recovered the scopolamine-induced reduction in step-through latency in the passive avoidance test; however, PSO did not modulate memory function on this task. The ameliorating effects of PCER on spatial memory were confirmed by the Morris water maze test. In conclusion, through behavioral and neurochemical experimental results, it was demonstrated that central administration of PCER produces amelioration of memory impairment. These results suggest that PCER plays an important role in neuroprotection and memory enhancement and PCER could be a potential new therapeutic agent for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

Prevalence, causes of blindness, visual impairment and cataract surgical services in Sindhudurg district on the western coastal strip of India

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Shailbala Patil

2014-01-01

Full Text Available Background : Konkan coast of India is geographically distinct and its pattern of blindness has never been mapped. Aim : To study the prevalence and causes of blindness and cataract surgical services in Sindhudurg district of West Coast. Subjects : Individual aged > 50 years. Materials and Methods: Rapid assessment of avoidable blindness used to map blindness pattern in the district. Statistical analysis: SPSS version 19. Results: Amongst those examined 1415 (51.7% had visual acuity (VA >20/60, 924 (33.8%, confidence interval (C.I 30.5%-36.8% had VA 20/200-<20/60(visual impairment, 266 (9.7%, C.I. 6.1%-13.3% had VA < 20/200-20/400 (severe visual impairment and 132 (4.8%, C. I. 1.1%-8.5% had VA < 20/400 (blindness by WHO standards. There was no significant gender difference in prevalence of blindness, but blindness and visual impairment was more in older and rural residing individuals. Amongst those with presenting vision < 20/200 in better eye, 309 (82.4% had cataract, 36 (9.7% had corneal scars, 13 (3.5% had diabetic retinopathyand 3 (0.8% had glaucoma. Cataract surgical coverage for the district was only 30.5%; 32% for males and 28.4% for females. Unable to afford, lack of knowledge and lack of access to services were the commonest barriers responsible for cataract patients not seeking care. Amongst those who had undergone cataract surgery, only 50% had visual acuity ≥ 20/60.46.9% of the population had spectacles for near, but only 53.3% of the population had presenting near vision < N10. Conclusion : Cataract, refractive errors and diabetes were significant causes of visual impairment and blindness.

Neuroanatomical and Neurochemical Basis of Impulsivity

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Kemal Yazici

2010-08-01

tis paradigm, the tendency to prefer small immediate rewards over larger, more delayed reinforcers is measured. İmpulsive choice is defined by a greater tendency to value or choose smaller, more immediate reinforcers. Impulsivity is a multi-faceted behaviour. This behaviour may be studied by subdividing it into different processes neuroanatomically and neurochemically. Neuroanatomical data support the suggestion that behavioral disinhibition (impulsive action / motoric impulsivity and delay-discounting (impulsive choice / decision making differ in the degree to which various components of frontostriatal loops are implicated in their regulation. The dorsal prefrontal cortex does not appear to be involved in mediating impulsive choice, yet does have some role in regulating inhibitory processes. In contrast, there appears to be a pronounced role for the orbitofrontal cortex and basolateral amygdala in controlling impulsive choice. Other structures, however, such as the nucleus accumbens and subthalamic nucleus may be common to both circuits. From the neurochemical perspective, dopamine system and dopamine- 2 (D2 receptors in particular, seems to be closely involved in making impulsive choice. When the noradrenaline system does not function optimally, it might contribute to increased impulsivity. Serotonin might act upon prefrontal cortex to decrease impulsive choices. Interactions between the serotonin and the dopamine systems are important in the regulation of impulsive behaviour. It is possible that various receptor subtypes of the serotonin system may exert differing and even contrasting effects on impulsive behaviour. Although it is very informative to study neurotransmitter systems separately, it should be kept in mind that there are very intimate interactions between the neurotransmitter systems mentioned above. Based on the fact that impulsivity is regulated through multiple neurotransmitters and even more receptors, one may suggest that pharmacotherapy of

Renal Impairment in Cirrhosis Unrelated to Hepatorenal Syndrome

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Gavin Low

2015-01-01

Full Text Available Renal impairment is common in liver disease and may occur as a consequence of the pathophysiological changes that underpin cirrhosis or secondary to a pre-existing unrelated insult. Nevertheless, the onset of renal impairment often portends a worsening prognosis. Hepatorenal syndrome remains one of the most recognized and reported causes of renal impairment in cirrhosis. However, other causes of renal impairment occur and can be classified into prerenal, intrinsic or postrenal, which are the subjects of the present review.

Caffeine consumption prevents diabetes-induced memory impairment and synaptotoxicity in the hippocampus of NONcZNO10/LTJ mice.

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João M N Duarte

Full Text Available Diabetic conditions are associated with modified brain function, namely with cognitive deficits, through largely undetermined processes. More than understanding the underlying mechanism, it is important to devise novel strategies to alleviate diabetes-induced cognitive deficits. Caffeine (a mixed antagonist of adenosine A(1 and A(2A receptors emerges as a promising candidate since caffeine consumption reduces the risk of diabetes and effectively prevents memory deficits caused by different noxious stimuli. Thus, we took advantage of a novel animal model of type 2 diabetes to investigate the behavioural, neurochemical and morphological modifications present in the hippocampus and tested if caffeine consumption might prevent these changes. We used a model closely mimicking the human type 2 diabetes condition, NONcNZO10/LtJ mice, which become diabetic at 7-11 months when kept under an 11% fat diet. Caffeine (1 g/l was applied in the drinking water from 7 months onwards. Diabetic mice displayed a decreased spontaneous alternation in the Y-maze accompanied by a decreased density of nerve terminal markers (synaptophysin, SNAP25, mainly glutamatergic (vesicular glutamate transporters, and increased astrogliosis (GFAP immunoreactivity compared to their wild type littermates kept under the same diet. Furthermore, diabetic mice displayed up-regulated A(2A receptors and down-regulated A(1 receptors in the hippocampus. Caffeine consumption restored memory performance and abrogated the diabetes-induced loss of nerve terminals and astrogliosis. These results provide the first evidence that type 2 diabetic mice display a loss of nerve terminal markers and astrogliosis, which is associated with memory impairment; furthermore, caffeine consumption prevents synaptic dysfunction and astrogliosis as well as memory impairment in type 2 diabetes.

Caffeine consumption prevents diabetes-induced memory impairment and synaptotoxicity in the hippocampus of NONcZNO10/LTJ mice.

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Duarte, João M N; Agostinho, Paula M; Carvalho, Rui A; Cunha, Rodrigo A

2012-01-01

Diabetic conditions are associated with modified brain function, namely with cognitive deficits, through largely undetermined processes. More than understanding the underlying mechanism, it is important to devise novel strategies to alleviate diabetes-induced cognitive deficits. Caffeine (a mixed antagonist of adenosine A(1) and A(2A) receptors) emerges as a promising candidate since caffeine consumption reduces the risk of diabetes and effectively prevents memory deficits caused by different noxious stimuli. Thus, we took advantage of a novel animal model of type 2 diabetes to investigate the behavioural, neurochemical and morphological modifications present in the hippocampus and tested if caffeine consumption might prevent these changes. We used a model closely mimicking the human type 2 diabetes condition, NONcNZO10/LtJ mice, which become diabetic at 7-11 months when kept under an 11% fat diet. Caffeine (1 g/l) was applied in the drinking water from 7 months onwards. Diabetic mice displayed a decreased spontaneous alternation in the Y-maze accompanied by a decreased density of nerve terminal markers (synaptophysin, SNAP25), mainly glutamatergic (vesicular glutamate transporters), and increased astrogliosis (GFAP immunoreactivity) compared to their wild type littermates kept under the same diet. Furthermore, diabetic mice displayed up-regulated A(2A) receptors and down-regulated A(1) receptors in the hippocampus. Caffeine consumption restored memory performance and abrogated the diabetes-induced loss of nerve terminals and astrogliosis. These results provide the first evidence that type 2 diabetic mice display a loss of nerve terminal markers and astrogliosis, which is associated with memory impairment; furthermore, caffeine consumption prevents synaptic dysfunction and astrogliosis as well as memory impairment in type 2 diabetes.

In vivo neurochemical characterization of clothianidin induced striatal dopamine release.

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Faro, L R F; Oliveira, I M; Durán, R; Alfonso, M

2012-12-16

Clothianidin (CLO) is a neonicotinoid insecticide with selective action on nicotinic acetylcholine receptors. The aim of this study was to determine the neurochemical basis for CLO-induced striatal dopamine release using the microdialysis technique in freely moving and conscious rats. Intrastriatal administration of CLO (3.5mM), produced an increase in both spontaneous (2462 ± 627% with respect to basal values) and KCl-evoked (4672 ± 706% with respect to basal values) dopamine release. This effect was attenuated in Ca(2+)-free medium, and was prevented in reserpine pre-treated animals or in presence of tetrodotoxin (TTX). To investigate the involvement of dopamine transporter (DAT), the effect of CLO was observed in presence of nomifensine. The coadministration of CLO and nomifensine produced an additive effect on striatal dopamine release. The results suggest that the effect of CLO on striatal dopamine release is predominantly mediated by an exocytotic mechanism, Ca(2+), vesicular and TTX-dependent and not by a mechanism mediated by dopamine transporter. Published by Elsevier Ireland Ltd.

Loss of hfe function reverses impaired recognition memory caused by olfactory manganese exposure in mice.

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Ye, Qi; Kim, Jonghan

2015-03-01

Excessive manganese (Mn) in the brain promotes a variety of abnormal behaviors, including memory deficits, decreased motor skills and psychotic behavior resembling Parkinson's disease. Hereditary hemochromatosis (HH) is a prevalent genetic iron overload disorder worldwide. Dysfunction in HFE gene is the major cause of HH. Our previous study has demonstrated that olfactory Mn uptake is altered by HFE deficiency, suggesting that loss of HFE function could alter manganese-associated neurotoxicity. To test this hypothesis, Hfe-knockout (Hfe (-/-)) and wild-type (Hfe (+/+)) mice mice were intranasally-instilled with manganese chloride (MnCl2 5 mg/kg) or water daily for 3 weeks and examined for memory function. Olfactory Mn diminished both short-term recognition and spatial memory in Hfe (+/+) mice, as examined by novel object recognition task and Barnes maze test, respectively. Interestingly, Hfe (-/-) mice did not show impaired recognition memory caused by Mn exposure, suggesting a potential protective effect of Hfe deficiency against Mn-induced memory deficits. Since many of the neurotoxic effects of manganese are thought to result from increased oxidative stress, we quantified activities of anti-oxidant enzymes in the prefrontal cortex (PFC). Mn instillation decreased superoxide dismutase 1 (SOD1) activity in Hfe (+/+) mice, but not in Hfe (-/-) mice. In addition, Hfe deficiency up-regulated SOD1 and glutathione peroxidase activities. These results suggest a beneficial role of Hfe deficiency in attenuating Mn-induced oxidative stress in the PFC. Furthermore, Mn exposure reduced nicotinic acetylcholine receptor levels in the PFC, indicating that blunted acetylcholine signaling could contribute to impaired memory associated with intranasal manganese. Together, our model suggests that disrupted cholinergic system in the brain is involved in airborne Mn-induced memory deficits and loss of HFE function could in part prevent memory loss via a potential up-regulation of

Rapid and reversible impairments of short- and long-term social recognition memory are caused by acute isolation of adult rats via distinct mechanisms.

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Shahar-Gold, Hadar; Gur, Rotem; Wagner, Shlomo

2013-01-01

Mammalian social organizations require the ability to recognize and remember individual conspecifics. This social recognition memory (SRM) can be examined in rodents using their innate tendency to investigate novel conspecifics more persistently than familiar ones. Here we used the SRM paradigm to examine the influence of housing conditions on the social memory of adult rats. We found that acute social isolation caused within few days a significant impairment in acquisition of short-term SRM of male and female rats. Moreover, SRM consolidation into long-term memory was blocked following only one day of social isolation. Both impairments were reversible, but with different time courses. Furthermore, only the impairment in SRM consolidation was reversed by systemic administration of arginine-vasopressin (AVP). In contrast to SRM, object recognition memory was not affected by social isolation. We conclude that acute social isolation rapidly induces reversible changes in the brain neuronal and molecular mechanisms underlying SRM, which hamper its acquisition and completely block its consolidation. These changes occur via distinct, AVP sensitive and insensitive mechanisms. Thus, acute social isolation of rats swiftly causes changes in their brain and interferes with their normal social behavior.

Rapid and reversible impairments of short- and long-term social recognition memory are caused by acute isolation of adult rats via distinct mechanisms.

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Hadar Shahar-Gold

Full Text Available Mammalian social organizations require the ability to recognize and remember individual conspecifics. This social recognition memory (SRM can be examined in rodents using their innate tendency to investigate novel conspecifics more persistently than familiar ones. Here we used the SRM paradigm to examine the influence of housing conditions on the social memory of adult rats. We found that acute social isolation caused within few days a significant impairment in acquisition of short-term SRM of male and female rats. Moreover, SRM consolidation into long-term memory was blocked following only one day of social isolation. Both impairments were reversible, but with different time courses. Furthermore, only the impairment in SRM consolidation was reversed by systemic administration of arginine-vasopressin (AVP. In contrast to SRM, object recognition memory was not affected by social isolation. We conclude that acute social isolation rapidly induces reversible changes in the brain neuronal and molecular mechanisms underlying SRM, which hamper its acquisition and completely block its consolidation. These changes occur via distinct, AVP sensitive and insensitive mechanisms. Thus, acute social isolation of rats swiftly causes changes in their brain and interferes with their normal social behavior.

Neurochemical metabolomics reveals disruption to sphingolipid metabolism following chronic haloperidol administration

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McClay, Joseph L.; Vunck, Sarah A.; Batman, Angela M.; Crowley, James J.; Vann, Robert E.; Beardsley, Patrick M.; van den Oord, Edwin J.

2015-01-01

Haloperidol is an effective antipsychotic drug for treatment of schizophrenia, but prolonged use can lead to debilitating side effects. To better understand the effects of long-term administration, we measured global metabolic changes in mouse brain following 3 mg/kg/day haloperidol for 28 days. These conditions lead to movement-related side effects in mice akin to those observed in patients after prolonged use. Brain tissue was collected following microwave tissue fixation to arrest metabolism and extracted metabolites were assessed using both liquid and gas chromatography mass spectrometry (MS). Over 300 unique compounds were identified across MS platforms. Haloperidol was found to be present in all test samples and not in controls, indicating experimental validity. Twenty-one compounds differed significantly between test and control groups at the p haloperidol-treated mice (p = 0.004), a marker previously associated with demyelination. This study further demonstrates the utility of murine neurochemical metabolomics as a method to advance understanding of CNS drug effects. PMID:25850894

[Prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Luxi County of Yunnan Province: the China Nine-Province survey].

Science.gov (United States)

Cai, Ning; Yuan, Yuan-sheng; Zhao, Jia-liang; Zhong, Hua; Ellwein, Leon B; Chen, Miao-miao; Dan, Ai-hua; Sun, Peng; Luo, Ting-hao; Wang, Yu; Gao, Xue-cheng

2013-09-01

To investigate the prevalence and causes of blindness and moderate and severe visual impairment among adults aged ≥ 50 years in Luxi County of Yunnan Province, China. It was a population-based cross-section study. Geographically defined cluster sampling was used in randomly selecting 5575 individuals aged ≥ 50 years in Luxi County. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. All participants were enumerated through village registers followed door-to-door visits.Eligible individuals were invited to receive visual acuity measurement and eye examination. Prevalence of blindness and moderate and severe visual impairment was calculated according to different age, gender or education. And the reasons of blindness were analyzed.Statistical analyses were performed using Stata/SE Statistical Software, release 9.0. Chi-square test was used to investigate the association of age, gender and education with presenting and best corrected visual acuity. Five thousands five hundreds and seventy-five individuals were enumerated and 5151 persons were examined, the response rate was 92.39%. Based on the criteria of World Health Organization visual impairment classification in 1973, the prevalence of blindness and moderate and severe visual impairment defined as best corrected visual acuity was 4.95% (255/5151) and 9.51% (490/5151) , respectively. The prevalence of blindness and moderate and severe visual impairment defined as presenting visual acuity was 5.40% (278/5151) and 15.84% (816/5151) , respectively. The prevalence of blindness and moderate and severe visual impairment was higher in aged (χ(2) = 1349.21, P = 0.000) , illiterate (χ(2) = 203.55, P = 0.000) persons. Cataract was still the first leading cause of blindness and visual impairment. The prevalence of blindness and moderate and severe visual impairment is highest in China Nine-Province Survey among older adults aged ≥ 50 years

Antioxidant-Rich Fraction of Urtica dioica Mediated Rescue of Striatal Mito-Oxidative Damage in MPTP-Induced Behavioral, Cellular, and Neurochemical Alterations in Rats.

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Bisht, Rohit; Joshi, Bhuwan Chandra; Kalia, Ajudhiya Nath; Prakash, Atish

2017-09-01

Parkinson's disease (PD) having a complex and multi-factorial neuropathology includes mainly the degeneration of the dopaminergic nigrostriatal pathway, which is a cumulative effect of depleted endogenous antioxidant enzymes, increased oxidative DNA damage, mitochondrial dysfunction, excitotoxicity, and neuroinflammation. The present study was designed to investigate the neuroprotective effect of a potent antioxidant from Urtica dioica in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of parkinsonism. MPTP was administered intranigrally for the induction of PD in male Wistar rats. Behavioral alterations were assessed in between the study period. Animals were sacrificed immediately after behavioral session, and different biochemical, cellular, and neurochemical parameters were measured. Intranigrally repeated administration of MPTP showed significant impairment of motor co-ordination and marked increase of mito-oxidative damage and neuroinflammation in rats. Intranigral MPTP significantly decreases the dopamine and its metabolites with impairment of dopaminergic cell density in rat brain. However, post-treatment with the potent antioxidant fraction of Urtica dioica Linn. (UD) (20, 40, 80 mg/kg) improved the motor function, mito-oxidative defense alteration significantly and dose dependently in MPTP-treated rats. In addition, the potent antioxidant fraction of UD attenuated the pro-inflammatory cytokines (TNF-α and IL-β) and restored the level of dopamine and its metabolites in MPTP-induced PD in rats. Moreover, minocycline (30 mg/kg) with lower dose of UD (20 mg/kg) had significantly potentiated the protective effect of minocycline as compared to its effect with other individual drug-treated groups. In conclusion, Urtica dioica protected the dopaminergic neurons probably by reducing mito-oxidative damage, neuroinflammation, and cellular alteration along with enhanced neurotrophic potential. The above results revealed that the antioxidant rich

Chronic choline supplementation improves cognitive and motor performance via modulating oxidative and neurochemical status in rats.

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Tabassum, Saiqa; Haider, Saida; Ahmad, Saara; Madiha, Syeda; Parveen, Tahira

2017-08-01

Choline, an essential nutrient, accounts for multiple functions in the body and brain. While its beneficial effects on healthy adults are not clear, choline supplementation is important during pregnancy for brain development, in elderly patients for support of cognitive performance and in patients with neurological disorders to reduce memory deficits. Thus, the aim of this study is to investigate whether choline administration in healthy adult rats beneficially impacts cognitive and locomotor performance, and associated oxidative and neurochemical outcomes. Two groups, control and choline, received tap water and choline bitartrate, respectively at the dose equivalent to adequate intake for five weeks. Food intake and body weight were monitored daily. Behavioral analysis comprising assessment of cognitive performance (by novel object recognition, passive avoidance and Morris Water Maze test) and locomotor performance (by Open field, Kondziela's inverted screen and beam walking test) were performed. Following testing, rats were decapitated and brain samples were collected for estimation of acetylcholine, redox profile and monoamine measurements. The results showed that chronic choline administration significantly improves cognitive and locomotor performance accompanied by a reduction in oxidative stress, enhanced cholinergic neurotransmission and monoamine levels in the brain of healthy adult rats. Hence, chronic choline intake was found to improve behavioral, oxidative and neurochemical outcomes in the normal population, so it can be suggested that choline tablets can be used as a safe and effective supplement for improving the neurological health of normal individuals and that they might also be beneficial in preventing cognitive and motor disorders later in life. Copyright © 2017 Elsevier Inc. All rights reserved.

A combination of two truncating mutations in USH2A causes more severe and progressive hearing impairment in Usher syndrome type IIa

NARCIS (Netherlands)

Hartel, B.P.; Lofgren, M.; Huygen, P.L.; Guchelaar, I.; Lo, A.N.K.N.; Sadeghi, A.M.; van Wijk, E.; Tranebjaerg, L.; Kremer, H.; Kimberling, W.J.; Cremers, C.W.R.J.; Moller, C.; Pennings, R.J.

2016-01-01

OBJECTIVES: Usher syndrome is an inherited disorder that is characterized by hearing impairment (HI), retinitis pigmentosa, and in some cases vestibular dysfunction. Usher syndrome type IIa is caused by mutations in USH2A. HI in these patients is highly heterogeneous and the present study evaluates

Biochanin-A ameliorates behavioural and neurochemical derangements in cognitive-deficit mice for the betterment of Alzheimer's disease.

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Biradar, S M; Joshi, H; Chheda, T K

2014-04-01

Biochanin-A (BCA), a potent phytoconstituent, has been previously used as an antitumour, a dopaminergic neuron protective agent, an antioxidant, an anticholinergic and on other pharmacological activities including neuroprotection. The present study was aimed to evaluate the behavioural and neurochemical evidence of BCA in cognitive-deficit mice in scopolamine challenged and natural aged-induced amnesia models in young and aged mice, respectively. BCA has exhibited decrease in the transfer latency and increase in step through latency significantly (p 0.05), BCA 10 mg kg(-1) (p betterment of Alzheimer's disease.

Harm to patients and others caused by impaired junior doctors ...

African Journals Online (AJOL)

Creative Commons licence CC-BY-NC 4.0. Harm to patients and ... enjoining doctors to 'self-report' impairment, the HPCSA Handbook on Internship .... e.g. where doctors have car accidents while driving home because they are not provided ...

Blindness and visual impairment in opera.

Science.gov (United States)

Aydin, Pinar; Ritch, Robert; O'Dwyer, John

2018-01-01

The performing arts mirror the human condition. This study sought to analyze the reasons for inclusion of visually impaired characters in opera, the cause of the blindness or near blindness, and the dramatic purpose of the blindness in the storyline. We reviewed operas from the 18 th century to 2010 and included all characters with ocular problems. We classified the cause of each character's ocular problem (organic, nonorganic, and other) in relation to the thematic setting of the opera: biblical and mythical, blind beggars or blind musicians, historical (real or fictional characters), and contemporary or futuristic. Cases of blindness in 55 characters (2 as a choir) from 38 operas were detected over 3 centuries of repertoire: 11 had trauma-related visual impairment, 5 had congenital blindness, 18 had visual impairment of unknown cause, 9 had psychogenic or malingering blindness, and 12 were symbolic or miracle-related. One opera featured an ophthalmologist curing a patient. The research illustrates that visual impairment was frequently used as an artistic device to enhance the intent and situate an opera in its time.

Jumping the gun: Smoking constituent BaP causes premature primordial follicle activation and impairs oocyte fusibility through oxidative stress

International Nuclear Information System (INIS)

Sobinoff, A.P.; Pye, V.; Nixon, B.; Roman, S.D.; McLaughlin, E.A.

2012-01-01

Benzo(a)pyrene (BaP) is an ovotoxic constituent of cigarette smoke associated with pre-mature ovarian failure and decreased rates of conception in IVF patients. Although the overall effect of BaP on female fertility has been documented, the exact molecular mechanisms behind its ovotoxicity remain elusive. In this study we examined the effects of BaP exposure on the ovarian transcriptome, and observed the effects of in vivo exposure on oocyte dysfunction. Microarray analysis of BaP cultured neonatal ovaries revealed a complex mechanism of ovotoxicity involving a small cohort of genes associated with follicular growth, cell cycle progression, and cell death. Histomorphological and immunohistochemical analysis supported these results, with BaP exposure causing increased primordial follicle activation and developing follicle atresia in vitro and in vivo. Functional analysis of oocytes obtained from adult Swiss mice treated neonatally revealed significantly increased levels of mitochondrial ROS/lipid peroxidation, and severely reduced sperm-egg binding and fusion in both low (1.5 mg/kg/daily) and high (3 mg/kg/daily) dose treatments. Our results reveal a complex mechanism of BaP induced ovotoxicity involving developing follicle atresia and accelerated primordial follicle activation, and suggest short term neonatal BaP exposure causes mitochondrial leakage resulting in reduced oolemma fluidity and impaired fertilisation in adulthood. This study highlights BaP as a key compound which may be partially responsible for the documented effects of cigarette smoke on follicular development and sub-fertility. -- Highlights: ► BaP exposure up-regulates canonical pathways linked with follicular growth/atresia. ► BaP causes primordial follicle activation and developing follicle atresia. ► BaP causes oocyte mitochondrial ROS and lipid peroxidation, impairing fertilisation. ► Short term neonatal BaP exposure compromises adult oocyte quality.

Jumping the gun: Smoking constituent BaP causes premature primordial follicle activation and impairs oocyte fusibility through oxidative stress

Energy Technology Data Exchange (ETDEWEB)

Sobinoff, A.P.; Pye, V. [Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW2308 (Australia); Nixon, B.; Roman, S.D. [Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW2308 (Australia); ARC Centre of Excellence in Biotechnology and Development, University of Newcastle, Callaghan, NSW2308 (Australia); McLaughlin, E.A., E-mail: eileen.mclaughlin@newcastle.edu.au [Reproductive Science Group, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW2308 (Australia); ARC Centre of Excellence in Biotechnology and Development, University of Newcastle, Callaghan, NSW2308 (Australia)

2012-04-01

Benzo(a)pyrene (BaP) is an ovotoxic constituent of cigarette smoke associated with pre-mature ovarian failure and decreased rates of conception in IVF patients. Although the overall effect of BaP on female fertility has been documented, the exact molecular mechanisms behind its ovotoxicity remain elusive. In this study we examined the effects of BaP exposure on the ovarian transcriptome, and observed the effects of in vivo exposure on oocyte dysfunction. Microarray analysis of BaP cultured neonatal ovaries revealed a complex mechanism of ovotoxicity involving a small cohort of genes associated with follicular growth, cell cycle progression, and cell death. Histomorphological and immunohistochemical analysis supported these results, with BaP exposure causing increased primordial follicle activation and developing follicle atresia in vitro and in vivo. Functional analysis of oocytes obtained from adult Swiss mice treated neonatally revealed significantly increased levels of mitochondrial ROS/lipid peroxidation, and severely reduced sperm-egg binding and fusion in both low (1.5 mg/kg/daily) and high (3 mg/kg/daily) dose treatments. Our results reveal a complex mechanism of BaP induced ovotoxicity involving developing follicle atresia and accelerated primordial follicle activation, and suggest short term neonatal BaP exposure causes mitochondrial leakage resulting in reduced oolemma fluidity and impaired fertilisation in adulthood. This study highlights BaP as a key compound which may be partially responsible for the documented effects of cigarette smoke on follicular development and sub-fertility. -- Highlights: ► BaP exposure up-regulates canonical pathways linked with follicular growth/atresia. ► BaP causes primordial follicle activation and developing follicle atresia. ► BaP causes oocyte mitochondrial ROS and lipid peroxidation, impairing fertilisation. ► Short term neonatal BaP exposure compromises adult oocyte quality.

Opinions of hearing parents about the causes of hearing impairment of their children with biallelic GJB2 mutations.

Science.gov (United States)

Solovyev, Aisen V; Dzhemileva, Lilya U; Posukh, Olga L; Barashkov, Nikolay A; Bady-Khoo, Marita S; Lobov, Semen L; Popova, Natalya Yu; Romanov, Georgii P; Sazonov, Nikolay N; Bondar, Alexander A; Morozov, Igor V; Tomsky, Mikhail I; Fedorova, Sardana A; Khusnutdinova, Elza K

2017-07-01

Hereditary hearing impairment (HI) caused by recessive GJB2 mutations is a frequent sensory disorder. The results of the molecular-based studies of HI are widely used in various genetic test systems. However, the ethical aspects are less described than the genetic aspects. The concerns expressed by individuals from groups with genetic risks must be included in the counseling of patients and their families. For evaluation of subjective opinions of hearing parents about the presumed causes of HI of their children, we analyze the cohort of parents having children with confirmed hereditary HI caused by biallelic recessive GJB2 mutations (in a homozygous or a compound heterozygous state). This study included 70 deaf children with HI due to mutations in the GJB2 gene and 91 questionnaires about the presumed causes of their deafness filled by their parents. Most of the parents at 78% (CI 68.4-85.4%) attributed their children's HI to "non-hereditary" causes and 22% (CI 14.7-31.6%) to "hereditary" causes (p < 0.05). Therefore, the prior opinions of the parents did not correspond to positive GJB2 genetic testing results. The subjective opinions of parents are probably partly based on family history, since respondents with deaf relatives in their pedigree more likely supposed hereditary causes for HI in their children than the respondents without deaf relatives (p < 0.001).

Selective dentate gyrus disruption causes memory impairment at the early stage of experimental multiple sclerosis.

Science.gov (United States)

Planche, Vincent; Panatier, Aude; Hiba, Bassem; Ducourneau, Eva-Gunnel; Raffard, Gerard; Dubourdieu, Nadège; Maitre, Marlène; Lesté-Lasserre, Thierry; Brochet, Bruno; Dousset, Vincent; Desmedt, Aline; Oliet, Stéphane H; Tourdias, Thomas

2017-02-01

Memory impairment is an early and disabling manifestation of multiple sclerosis whose anatomical and biological substrates are still poorly understood. We thus investigated whether memory impairment encountered at the early stage of the disease could be explained by a differential vulnerability of particular hippocampal subfields. By using experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, we identified that early memory impairment was associated with selective alteration of the dentate gyrus as pinpointed in vivo with diffusion-tensor-imaging (DTI). Neuromorphometric analyses and electrophysiological recordings confirmed dendritic degeneration, alteration in glutamatergic synaptic transmission and impaired long-term synaptic potentiation selectively in the dentate gyrus, but not in CA1, together with a more severe pattern of microglial activation in this subfield. Systemic injections of the microglial inhibitor minocycline prevented DTI, morphological, electrophysiological and behavioral impairments in EAE-mice. Furthermore, daily infusions of minocycline specifically within the dentate gyrus were sufficient to prevent memory impairment in EAE-mice while infusions of minocycline within CA1 were inefficient. We conclude that early memory impairment in EAE is due to a selective disruption of the dentate gyrus associated with microglia activation. These results open new pathophysiological, imaging, and therapeutic perspectives for memory impairment in multiple sclerosis. Copyright © 2016 Elsevier Inc. All rights reserved.

EPA Office of Water (OW): 303(d) Listed Impaired Waters by Causes of Impairment and Probable Sources

Data.gov (United States)

U.S. Environmental Protection Agency — Under Section 303(d) of the CWA, states, territories, and authorized tribes (referred to here as states) are required to develop lists of impaired waters. These are...

Dystypia: isolated typing impairment without aphasia, apraxia or visuospatial impairment.

Science.gov (United States)

Otsuki, Mika; Soma, Yoshiaki; Arihiro, Shoji; Watanabe, Yoshimasa; Moriwaki, Hiroshi; Naritomi, Hiroaki

2002-01-01

We report a 60-year-old right-handed Japanese man who showed an isolated persistent typing impairment without aphasia, agraphia, apraxia or any other neuropsychological deficit. We coined the term 'dystypia' for this peculiar neuropsychological manifestation. The symptom was caused by an infarction in the left frontal lobe involving the foot of the second frontal convolution and the frontal operculum. The patient's typing impairment was not attributable to a disturbance of the linguistic process, since he had no aphasia or agraphia. The impairment was not attributable to the impairment of the motor execution process either, since he had no apraxia. Thus, his typing impairment was deduced to be based on a disturbance of the intermediate process where the linguistic phonological information is converted into the corresponding performance. We hypothesized that there is a specific process for typing which branches from the motor programming process presented in neurolinguistic models. The foot of the left second frontal convolution and the operculum may play an important role in the manifestation of 'dystypia'. Copyright 2002 S. Karger AG, Basel

Rapid sensing of l-leucine by human and murine hypothalamic neurons: Neurochemical and mechanistic insights.

Science.gov (United States)

Heeley, Nicholas; Kirwan, Peter; Darwish, Tamana; Arnaud, Marion; Evans, Mark L; Merkle, Florian T; Reimann, Frank; Gribble, Fiona M; Blouet, Clemence

2018-04-01

Dietary proteins are sensed by hypothalamic neurons and strongly influence multiple aspects of metabolic health, including appetite, weight gain, and adiposity. However, little is known about the mechanisms by which hypothalamic neural circuits controlling behavior and metabolism sense protein availability. The aim of this study is to characterize how neurons from the mediobasal hypothalamus respond to a signal of protein availability: the amino acid l-leucine. We used primary cultures of post-weaning murine mediobasal hypothalamic neurons, hypothalamic neurons derived from human induced pluripotent stem cells, and calcium imaging to characterize rapid neuronal responses to physiological changes in extracellular l-Leucine concentration. A neurochemically diverse subset of both mouse and human hypothalamic neurons responded rapidly to l-leucine. Consistent with l-leucine's anorexigenic role, we found that 25% of mouse MBH POMC neurons were activated by l-leucine. 10% of MBH NPY neurons were inhibited by l-leucine, and leucine rapidly reduced AGRP secretion, providing a mechanism for the rapid leucine-induced inhibition of foraging behavior in rodents. Surprisingly, none of the candidate mechanisms previously implicated in hypothalamic leucine sensing (K ATP channels, mTORC1 signaling, amino-acid decarboxylation) were involved in the acute activity changes produced by l-leucine. Instead, our data indicate that leucine-induced neuronal activation involves a plasma membrane Ca 2+ channel, whereas leucine-induced neuronal inhibition is mediated by inhibition of a store-operated Ca 2+ current. A subset of neurons in the mediobasal hypothalamus rapidly respond to physiological changes in extracellular leucine concentration. Leucine can produce both increases and decreases in neuronal Ca 2+ concentrations in a neurochemically-diverse group of neurons, including some POMC and NPY/AGRP neurons. Our data reveal that leucine can signal through novel mechanisms to rapidly

Voxel Scale Complex Networks of Functional Connectivity in the Rat Brain: Neurochemical State Dependence of Global and Local Topological Properties

Directory of Open Access Journals (Sweden)

Adam J. Schwarz

2012-01-01

Full Text Available Network analysis of functional imaging data reveals emergent features of the brain as a function of its topological properties. However, the brain is not a homogeneous network, and the dependence of functional connectivity parameters on neuroanatomical substrate and parcellation scale is a key issue. Moreover, the extent to which these topological properties depend on underlying neurochemical changes remains unclear. In the present study, we investigated both global statistical properties and the local, voxel-scale distribution of connectivity parameters of the rat brain. Different neurotransmitter systems were stimulated by pharmacological challenge (d-amphetamine, fluoxetine, and nicotine to discriminate between stimulus-specific functional connectivity and more general features of the rat brain architecture. Although global connectivity parameters were similar, mapping of local connectivity parameters at high spatial resolution revealed strong neuroanatomical dependence of functional connectivity in the rat brain, with clear differentiation between the neocortex and older brain regions. Localized foci of high functional connectivity independent of drug challenge were found in the sensorimotor cortices, consistent with the high neuronal connectivity in these regions. Conversely, the topological properties and node roles in subcortical regions varied with neurochemical state and were dependent on the specific dynamics of the different functional processes elicited.

20 CFR 416.911 - Definition of disabling impairment.

Science.gov (United States)

2010-04-01

... with your age, education and work experience, would result in a finding that you are disabled under... combination of impairments that meets the requirements in §§ 416.920 (c) through (f). (b) If you are a child, a disabling impairment is an impairment (or combination of impairments) that causes marked and...

Magnitude and Causes of Low Vision Disability (Moderate and Severe Visual Impairment) among Students of Al-Noor Institute for the Blind in Al-Hassa, Saudi Arabia: A case series.

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Al-Wadani, Fahad; Khandekar, Rajiv; Al-Hussain, Muneera A; Alkhawaja, Ahmed A; Khan, Mohammed Sarfaraz; Alsulaiman, Ramzy A

2012-02-01

This study aimed to estimate the magnitude and causes of low vision disability (severe visual impairment [SVI] and moderate visual impairment [MVI]) among students at Al-Noor Institute for the Blind (NIB) in Al-Hassa, Saudi Arabia in 2006. An optometrist conducted refraction of 122 eyes of the 61 students (27 boys and 34 girls) with MVI (vision visual acuity was ≥6/18 and in 28 (23%) eyes, it was visual impairment in 16 (13.1%) and 9 (7.4%) eyes. These students were prescribed optical and non-optical low vision aids. Retinal disease was the main cause of SVI and MVI in our series. Some students at Al-Noor Institute for the Blind have curable low vision conditions. Rehabilitation of low vision disability should be different from that offered to the absolutely blind.

[Multilingualism and specific language impairment].

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Arkkila, Eva; Smolander, Sini; Laasonen, Marja

2013-01-01

Specific language impairment is one of the most common developmental disturbances in childhood. With the increase of the foreign language population group an increasing number of children assimilating several languages and causing concern in language development attend clinical examinations. Knowledge of factors underlying the specific language impairment and the specific impairment in general, special features of language development of those learning several languages, as well as the assessment and support of the linguistic skills of a multilingual child is essential. The risk of long-term problems and marginalization is high for children having specific language impairment.

Changes in neurochemicals within the ventrolateral medullary respiratory column in awake goats after carotid body denervation

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Miller, Justin Robert; Neumueller, Suzanne; Muere, Clarissa; Olesiak, Samantha; Pan, Lawrence; Hodges, Matthew R.

2013-01-01

A current and major unanswered question is why the highly sensitive central CO2/H+ chemoreceptors do not prevent hypoventilation-induced hypercapnia following carotid body denervation (CBD). Because perturbations involving the carotid bodies affect central neuromodulator and/or neurotransmitter levels within the respiratory network, we tested the hypothesis that after CBD there is an increase in inhibitory and/or a decrease in excitatory neurochemicals within the ventrolateral medullary column (VMC) in awake goats. Microtubules for chronic use were implanted bilaterally in the VMC within or near the pre-Bötzinger Complex (preBötC) through which mock cerebrospinal fluid (mCSF) was dialyzed. Effluent mCSF was collected and analyzed for neurochemical content. The goats hypoventilated (peak +22.3 ± 3.4 mmHg PaCO2) and exhibited a reduced CO2 chemoreflex (nadir, 34.8 ± 7.4% of control ΔV̇E/ΔPaCO2) after CBD with significant but limited recovery over 30 days post-CBD. After CBD, GABA and glycine were above pre-CBD levels (266 ± 29% and 189 ± 25% of pre-CBD; P 0.05) different from control after CBD. Analyses of brainstem tissues collected 30 days after CBD exhibited 1) a midline raphe-specific reduction (P < 0.05) in the percentage of tryptophan hydroxylase–expressing neurons, and 2) a reduction (P < 0.05) in serotonin transporter density in five medullary respiratory nuclei. We conclude that after CBD, an increase in inhibitory neurotransmitters and a decrease in excitatory neuromodulation within the VMC/preBötC likely contribute to the hypoventilation and attenuated ventilatory CO2 chemoreflex. PMID:23869058

Anthocyanin-rich extract from Hibiscus sabdariffa calyx counteracts UVC-caused impairments in rats.

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Ozkol, Hatice Uce; Koyuncu, Ismail; Tuluce, Yasin; Dilsiz, Nihat; Soral, Sinan; Ozkol, Halil

2015-01-01

Ultraviolet radiation (UV) was reported to cause oxidative stress. Hibiscus sabdariffa L. (Malvaceae) calyx is commonly used in traditional Asian and African medicines and possesses strong antioxidant capacity due to its anthocyanin (ANTH) content. This study researched the possible protective role of Hibiscus sabdariffa calyx extract (HSCE) in UVC exposure of rats. Levels of serum enzymes, renal function tests, and some oxidant/antioxidant biomarkers of skin, lens, and retina tissues were monitored. Rats were exposed to UVC 4 h daily for 40 d and simultaneously received HSCE containing 2.5, 5, and 10 mg doses of ANTH in drinking water. Significant (p < 0.05) increases in the levels of serum aminotransferases, lactate dehydrogenase, urea, creatinine, and uric acid were noted after UVC exposure. In skin, lens, and retina tissues, total oxidant status, oxidative stress index, lipid peroxidation, and protein oxidation escalated markedly (p < 0.05) whereas total antioxidant status, reduced glutathione, and superoxide dismutase decreased dramatically (p < 0.05) related to UVC. Co-administration of HSCE with each ANTH dose significantly (p < 0.05) reversed aforementioned parameters (except total oxidant status) almost in all tissues. The LD50 of HSCE in rats was determined to be above 5000 mg/kg. Our data revealed that HSCE has a remarkable potential to counteract UVC-caused impairments, probably through its antioxidant and free radical-defusing effects. Therefore, HSCE could be useful against some cutaneous and ocular diseases in which UV and oxidative stress have a role in the etiopathogenesis.

The mental health of UK ex-servicemen with a combat-related or a non-combat-related visual impairment: does the cause of visual impairment matter?

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Stevelink, Sharon A M; Malcolm, Estelle M; Gill, Pashyca C; Fear, Nicola T

2015-08-01

Since the start of the conflicts in Iraq and Afghanistan, the numbers of young service personnel who have sustained a combat-related visual impairment have increased. This cross-sectional study examined the mental well-being of ex-servicemen (aged 22-55 years) with a visual impairment and determined if the mental health of those with a combat-related visual impairment differed from those whose visual impairment is not combat-related. Male ex-service personnel with a visual impairment completed a telephone interview assessing the presence of depressive symptomatology, probable anxiety disorder, post-traumatic stress disorder (PTSD) symptomatology and alcohol misuse. Data were analysed using descriptive statistics. 77 participants were included in the study, reflecting a response rate of 76.2%. Of those with complete data (n=74), 20 ex-servicemen had a combat-related visual impairment. Among ex-service personnel with a combat-related visual impairment, 10.0% (95% CI 0 to 23.2) screened positive for a probable depression, 25.0% (95% CI 6.0 to 44.0) for probable anxiety and 10.0% (95% CI 0 to 23.2) for probable PTSD. The prevalence of probable depression and probable PTSD differed among those with a non-combat-related visual impairment, namely 18.5% (95% CI 8.1 to 28.9) and 16.7% (95% CI 6.8 to 26.7), respectively. Probable anxiety was 18.5% (95% CI 8.1 to 28.9) among non-combat-related visually impaired ex-service personnel. 45.0% (95% CI 23.2 to 66.8) of combat-related visually impaired personnel reported hazardous drinking, compared with 20.4% (95% CI 9.7 to 31.2) of those with a non-combat-related visual impairment. Mental health problems were prevalent among visually impaired younger ex-servicemen. No statistically significant differences were found in the prevalence of mental health problems among ex-servicemen with a combat-related visual impairment compared with those with a non-combat-related visual impairment. Published by the BMJ Publishing Group Limited

Impaired reproduction after exposure to ADHD drugs

DEFF Research Database (Denmark)

Danborg, Pia Brandt; Simonsen, Anders Lykkemark; Gøtzsche, Peter C

2017-01-01

BACKGROUND: Few studies have reported on long-term harms caused by ADHD drugs but they are known to impair growth. OBJECTIVE: To assess whether ADHD drugs impair reproduction in mammals. METHODS: Systematic review of reproduction in studies of animals treated with ADHD drugs. DATA SOURCES: Pub....... CONCLUSION: ADHD drugs impair the reproduction in animals....

[Behavioral impairments in Parkinson's disease].

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Kashihara, Kenichi

2004-09-01

Behavioral impairments in parkinsonian patients include agitation, hypersexuality, stereotypic movement, pathological gambling, abuse of antiparkinsonian drugs, REM sleep behavioral disorder, and restless legs syndrome. Dementia, psychoses, and emotional disorders, such as depression and anxiety/panic disorder, also impair behavior. Symptoms may be produced by dysfunction of the central nervous system, medication, and/or the psychosocial problems associated with Parkinson's disease. Treatment therefore should be based on the cause of the symptoms seen. In some cases, the reduction or change of antiparkinsonian drugs, or both, may be effective. Treatment of the motor symptoms of Parkinson's disease, including motor fluctuations, may reduce the risk of panic attacks being evoked in the 'off' period. Use of antidepressants, sedatives, and neuroleptics may often be effective. Physicians should identify the causes of the symptoms of behavioral impairment and select appropriate treatments.

Neurochemical Effects of Chronic Administration of Calcitriol in Rats

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Pei Jiang

2014-12-01

Full Text Available Despite accumulating data showing the various neurological actions of vitamin D (VD, its effects on brain neurochemistry are still far from fully understood. To further investigate the neurochemical influence of VD, we assessed neurotransmitter systems in the brain of rats following 6-week calcitriol (1,25-dihydroxyvitamin D administration (50 ng/kg/day or 100 ng/kg/day. Both the two doses of calcitriol enhanced VDR protein level without affecting serum calcium and phosphate status. Rats treated with calcitriol, especially with the higher dose, exhibited elevated γ-aminobutyric acid (GABA status. Correspondingly, the mRNA expression of glutamate decarboxylase (GAD 67 was increased. 100 ng/kg of calcitriol administration also increased glutamate and glutamine levels in the prefrontal cortex, but did not alter glutamine synthetase (GS expression. Additionally, calcitriol treatment promoted tyrosine hydroxylase (TH and tryptophan hydroxylase 2 (TPH2 expression without changing dopamine and serotonin status. However, the concentrations of the metabolites of dopamine and serotonin were increased and the drug use also resulted in a significant rise of monoamine oxidase A (MAOA expression, which might be responsible to maintain the homeostasis of dopaminergic and serotonergic neurotransmission. Collectively, the present study firstly showed the effects of calcitriol in the major neurotransmitter systems, providing new evidence for the role of VD in brain function.

Effect of Artificial Gravity: Central Nervous System Neurochemical Studies

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Fox, Robert A.; D'Amelio, Fernando; Eng, Lawrence F.

1997-01-01

The major objective of this project was to assess chemical and morphological modifications occurring in muscle receptors and the central nervous system of animals subjected to altered gravity (2 x Earth gravity produced by centrifugation and simulated micro gravity produced by hindlimb suspension). The underlying hypothesis for the studies was that afferent (sensory) information sent to the central nervous system by muscle receptors would be changed in conditions of altered gravity and that these changes, in turn, would instigate a process of adaptation involving altered chemical activity of neurons and glial cells of the projection areas of the cerebral cortex that are related to inputs from those muscle receptors (e.g., cells in the limb projection areas). The central objective of this research was to expand understanding of how chronic exposure to altered gravity, through effects on the vestibular system, influences neuromuscular systems that control posture and gait. The project used an approach in which molecular changes in the neuromuscular system were related to the development of effective motor control by characterizing neurochemical changes in sensory and motor systems and relating those changes to motor behavior as animals adapted to altered gravity. Thus, the objective was to identify changes in central and peripheral neuromuscular mechanisms that are associated with the re-establishment of motor control which is disrupted by chronic exposure to altered gravity.

Brain region-specific perfluoroalkylated sulfonate (PFSA) and carboxylic acid (PFCA) accumulation and neurochemical biomarker responses in east Greenland polar bears (Ursus maritimus).

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Eggers Pedersen, Kathrine; Basu, Niladri; Letcher, Robert; Greaves, Alana K; Sonne, Christian; Dietz, Rune; Styrishave, Bjarne

2015-04-01

Perfluoroalkyl substances (PFASs) is a growing class of contaminants in the Arctic environment, and include the established perfluorinated sulfonates (PFSAs; especially perfluorooctane sulfonate (PFOS)) and carboxylic acids (PFCAs). PFSAs and PFCAs of varying chain length have been reported to bioaccumulate in lipid rich tissues of the brain among other tissues such as liver, and can reach high concentrations in top predators including the polar bear. PFCA and PFSA bioaccummulation in the brain has the potential to pose neurotoxic effects and therefore we conducted a study to investigate if variations in neurochemical transmitter systems i.e. the cholinergic, glutaminergic, dopaminergic and GABAergic, could be related to brain-specific bioaccumulation of PFASs in East Greenland polar bears. Nine brain regions from nine polar bears were analyzed for enzyme activity (monoamine oxidase (MAO), acetylcholinesterase (AChE) and glutamine synthetase (GS)) and receptor density (dopamine-2 (D2), muscarinic cholinergic (mAChR) and gamma-butyric acid type A (GABA-A)) along with PFSA and PFCA concentrations. Average brain ∑PFSA concentration was 25ng/g ww where PFOS accounted for 91%. Average ∑PFCA concentration was 88ng/g ww where PFUnDA, PFDoDA and PFTrDA combined accounted for 79%. The highest concentrations of PFASs were measured in brain stem, cerebellum and hippocampus. Correlative analyses were performed both across and within brain regions. Significant positive correlations were found between PFASs and MAO activity in occipital lobe (e.g. ∑PFCA; rp=0.83, p=0.041, n=6) and across brain regions (e.g. ∑PFCA; rp=0.47, p=0.001, ∑PFSA; rp=0.44, p>0.001; n=50). GABA-A receptor density was positively correlated with two PFASs across brain regions (PFOS; rp=0.33, p=0.02 and PFDoDA; rp=0.34, p=0.014; n=52). Significant negative correlations were found between mAChR density and PFASs in cerebellum (e.g. ∑PFCA; rp=-0.95, p=0.013, n=5) and across brain regions (e.g. �

Visual impairment and blindness in Hungary.

Science.gov (United States)

Szabó, Dorottya; Sándor, Gábor László; Tóth, Gábor; Pék, Anita; Lukács, Regina; Szalai, Irén; Tóth, Georgina Zsófia; Papp, András; Nagy, Zoltán Zsolt; Limburg, Hans; Németh, János

2018-03-01

The aim of this study was to estimate the prevalence and causes of blindness, severe visual impairment (SVI), moderate visual impairment (MVI), and early visual impairment (EVI) and its causes in an established market economy of Europe. A cross-sectional population-based survey. A sample size of 3675 was calculated using the standard Rapid Assessment of Avoidable Blindness (RAAB) software in Hungary. A total of 105 clusters of 35 people aged 50 years or older were randomly selected with probability proportionate to size by the Hungarian Central Statistical Office. Households within the clusters were selected using compact segment sampling. Visual acuity (VA) was assessed with a Snellen tumbling E-chart with or without a pinhole in the households. The adjusted prevalences of bilateral blindness, SVI, MVI and EVI were 0.9% (95% CI: 0.6-1.2), 0.5% (95% CI: 0.2-0.7), 5.1% (95% CI: 4.3-5.9) and 6.9% (95% CI: 5.9-7.9), respectively. The major causes of blindness in Hungary were age-related macular degeneration (AMD; 27.3%) and other posterior segment diseases (27.3%), cataract (21.2%) and glaucoma (12.1%). Cataract was the main cause of SVI, MVI and EVI. Cataract surgical coverage (CSC) was 90.7%. Of all bilateral blindness in Hungary, 45.5% was considered avoidable. This study proved that RAAB methodology can be successfully conducted in industrialized countries, which often lack reliable epidemiologic data. The prevalence of blindness was relatively low, with AMD and other posterior segment diseases being the leading causes, and cataract is still a significant cause of visual impairment. © 2017 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

Behavioral and Neurochemical Studies in Stressed and Unstressed Rats Fed on Protein, Carbohydrate and Fat Rich Diet

Directory of Open Access Journals (Sweden)

Samia Moin§, Saida Haider*, Saima Khaliq1, Saiqa Tabassum and Darakhshan J. Haleem

2012-05-01

Full Text Available Stress produces behavioral and neurochemical deficits. To study the relationship between adaptation to stress and macronutrient intake, the present study was designed to monitor the effects of different diets on feed intake, growth rate and serotonin (5-Hydroxytryptamine, 5-HT metabolism following exposure to restraint stress in rats. Rats were divided into four groups (n=12 as control, sugar, protein and fat rich diet fed rats. After 5 weeks of treatment animals of each group were divided into unrestrained and restrained animals (n=6. Rats of restrained group were given immobilization stress for 2 hours/day for 5 days. Food intake and growth rates of unrestrained and restrained rats were monitored daily. Rats were decapitated on 6th day to collect brain samples for neurochemical estimation. Results show that sugar diet fed rats produced adaptation to stress early as compared to normal diet fed rats. Food intake and growth rates of unrestrained and restrained rats were comparable on 3rd day in sugar diet fed rats and on 4th day in normal diet fed rats. Stress decreased food intake and growth rates of protein and fat treated rats. Repeated stress did not alter brain 5-HT and 5-HIAA levels of normal diet fed rats and sugar diet fed rats. Protein diet fed restrained rats showed elevated brain 5-HT levels. Fat diet fed restrained rats significantly decreased brain TRP and 5-HIAA levels. Finding suggested that carbohydrate diet might protect against stressful conditions. Study also showed that nutritional status could alter different behaviors in response to a stressful environment.

Vascular cognitive impairment

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N.V. Vakhnina

2014-01-01

Full Text Available Vascular pathology of the brain is the second most common cause of cognitive impairment after Alzheimer's disease. The article describes the modern concepts of etiology, pathogenetic mechanisms, clinical features and approaches to diagnosis and therapy of vascular cognitive impairment (VCI. Cerebrovascular accident, chronic cerebral circulatory insufficiency and their combination, sometimes in combination with a concomitant neurodegenerative process, are shown to be the major types of brain lesions leading to VCI. The clinical presentation of VCI is characterized by the neuropsychological status dominated by impairment of the executive frontal functions (planning, control, attention in combination with focal neurological symptoms. The diagnosis is based on comparing of the revealed neuropsychological and neurological features with neuroimaging data. Neurometabolic, acetylcholinergic, glutamatergic, and other vasoactive drugs and non-pharmacological methods are widely used to treat VCI. 

[Survey on avoidable blindness and visual impairment in Panama].

Science.gov (United States)

López, Maritza; Brea, Ileana; Yee, Rita; Yi, Rodolfo; Carles, Víctor; Broce, Alberto; Limburg, Hans; Silva, Juan Carlos

2014-12-01

Determine prevalence of blindness and visual impairment in adults aged ≥ 50 years in Panama, identify their main causes, and characterize eye health services. Cross-sectional population study using standard Rapid Assessment of Avoidable Blindness methodology. Fifty people aged ≥ 50 years were selected from each of 84 clusters chosen through representative random sampling of the entire country. Visual acuity was assessed using a Snellen chart; lens and posterior pole status were assessed by direct ophthalmoscopy. Cataract surgery coverage was calculated and its quality assessed, along with causes of visual acuity blindness was 3.0% (95% CI: 2.3-3.6). The main cause of blindness was cataract (66.4%), followed by glaucoma (10.2%). Cataract (69.2%) was the main cause of severe visual impairment and uncorrected refractive errors were the main cause of moderate visual impairment (60.7%). Surgical cataract coverage in individuals was 76.3%. Of all eyes operated for cataract, 58.0% achieved visual acuity ≤ 20/60 with available correction. Prevalence of blindness in Panama is in line with average prevalence found in other countries of the Region. This problem can be reduced, since 76.2% of cases of blindness and 85.0% of cases of severe visual impairment result from avoidable causes.

The Tribal Odisha Eye Disease Study (TOES) 1: prevalence and causes of visual impairment among tribal children in an urban school in Eastern India.

Science.gov (United States)

Warkad, Vivekanand U; Panda, Lapam; Behera, Pradeep; Das, Taraprasad; Mohanta, Bikash C; Khanna, Rohit

2018-04-01

To estimate the prevalence and causes of visual impairment and other ocular comorbidities among tribal children in an urban school population in eastern India. In this cross-sectional study, vision screening tests were administered to tribal school children. Demographic data, including name, age, sex, home district, height, and weight of each child, and examination data, including unaided and pinhole visual acuity, external eye examination with a flashlight, slit-lamp examination, intraocular pressure (IOP) measurement, and undilated fundus photography, were collected. Children with visual acuity of less than 20/20, abnormal anterior or posterior segment findings, and IOP of >21 mm Hg were referred for further evaluation. Of 10,038 children (5,840 males [58.2%]) screened, 335 (median age, 9 years; range, 6-17 years) were referred. Refractive error was the most common cause of visual impairment (59.52%; 95% CI, 51.97-66.65) followed by amblyopia (17.2%; 95% CI, 12.3-23.6) and posterior segment anomaly (14.88%; 95% CI, 10.2-21.0). The prevalence of best-corrected visual acuity of 20/40 was 0.13%. The prevalence of blindness was 0.03%. Visual impairment among tribal children in this residential school is an uncommon but important disability. Copyright © 2018 American Association for Pediatric Ophthalmology and Strabismus. Published by Elsevier Inc. All rights reserved.

GABAA receptor positive allosteric modulators modify the abuse-related behavioral and neurochemical effects of methamphetamine in rhesus monkeys.

Science.gov (United States)

Berro, Laís F; Andersen, Monica L; Tufik, Sergio; Howell, Leonard L

2017-09-01

GABA A receptor positive allosteric modulators (GABA A receptor modulators) are commonly used for the treatment of insomnia. Nevertheless, the effects of these compounds on psychostimulant-induced sleep impairment are poorly understood. Because GABA A receptor modulators have been shown to decrease the abuse-related effects of psychostimulants, the aim of the present study was to evaluate the effects of temazepam (0.3, 1.0 or 3.0 mg/kg) and eszopiclone (0.3, 1.0 or 3.0 mg/kg), two GABA A receptor modulators, on the behavioral neuropharmacology of methamphetamine in adult rhesus macaques (n = 5). Sleep-like measures and general daytime activity were evaluated with Actiwatch monitors. Methamphetamine self-administration (0.03 mg/kg/inf) was evaluated during morning sessions. Methamphetamine-induced dopamine overflow was assessed through in vivo microdialysis targeting the nucleus accumbens. Nighttime treatment with either temazepam or eszopiclone was ineffective in improving sleep-like measures disrupted by methamphetamine self-administration. Acute pretreatment with a low dose of temazepam before self-administration sessions increased methamphetamine self-administration without affecting normal daytime home-cage activity. At a high dose, acute temazepam pretreatment decreased methamphetamine self-administration and attenuated methamphetamine-induced increases in dopamine in the nucleus accumbens, without decreasing general daytime activity. Acute eszopiclone treatment exerted no effects on methamphetamine intake or drug-induced increases in dopamine. Our study suggests that treatments based on GABA A receptor modulators are not effective for the treatment of sleep disruption in the context of psychostimulant use. In addition, distinct GABA A receptor modulators differentially modulated the abuse-related effects of methamphetamine, with acute treatment with the high efficacy GABA A receptor modulator temazepam decreasing the behavioral and neurochemical effects

A detailed analysis of open-field habituation and behavioral and neurochemical antidepressant-like effects in postweaning enriched rats.

Science.gov (United States)

Brenes, Juan C; Padilla, Michael; Fornaguera, Jaime

2009-01-30

Our previous work has shown that male Sprague-Dawley rats reared in social isolation, standard housing and environmental enrichment differ in their spontaneous open-field activity and in some neurobehavioral depressive-like parameters. Here, we extended this evidence by using a shorter postweaning rearing period (1 month) and including additional evaluations. First, in order to obtain a better characterization of the exploratory strategies among rearing conditions we analyzed in detail the spontaneous activity at the first minute and during the 10-min session. Second, we asked whether the changes in open-field activity were related with basal anxiety levels in the elevated plus-maze. Third, behavior in the forced-swimming test was analyzed and afterward, the tissue levels of hippocampal norepinephrine and serotonin were assessed. The possible relationship between neurotransmitters and forced-swimming behavior were explored through correlation analyses. We found that rearing conditions (i) differed on locomotor habituation and on sensory-motor exploration at the first minute and during the 10-min session without modifying the plus-maze behavior; (ii) affected differentially the grooming time, its sequential components, and the relationship between grooming and locomotor parameters; (iii) modified forced-swimming behavior and the hippocampal concentration of norepinephrine, serotonin, and its turnover; and (iv) produced different correlation patterns between both neurotransmitters and forced-swimming behaviors. Overall, environmental enrichment accelerated open-field habituation and led to behavioral and neurochemical antidepressant-like effects. In contract, isolation rearing strongly impaired habituation and simple information processing, but showed marginal effects on depressive-like behavior and on hippocampal neurochemistry. The current results suggest that differential rearing is not only a useful procedure to study behavioral plasticity or rigidity in response

[Epidemiological survey of visual impairment in Funing County, Jiangsu].

Science.gov (United States)

Yang, M; Zhang, J F; Zhu, R R; Kang, L H; Qin, B; Guan, H J

2017-07-11

Objective: To investigate the prevalence of visual impairment and factors associated with visual impairment among people aged 50 years and above in Funing County, Jiangsu Province. Methods: Cross-sectional study. Random cluster sampling was used in selecting individuals aged ≥50 years in 30 clusters, and 5 947 individuals received visual acuity testing and eye examination. Stata 13.0 software was used to analyze the data. Multivariate logistic regression was used to detect possible factors of visual impairment such as age, gender and education. Statistical significance was defined as Pvisual impairment classification and presenting visual acuity, 138 persons were diagnosed as blindness, and 1 405 persons were diagnosed as low vision. The prevalence of blindness and low vision was 2.32% and 23.63%, respectively. And the prevalence of visual impairment was 25.95%. Based on the criteria of WHO visual impairment classification and best-corrected visual acuity, 92 persons were diagnosed as blindness, and 383 persons were diagnosed as low vision. The prevalence of blindness and low vision was 1.55% and 6.44%, respectively. And the prevalence of visual impairment was 7.99%. Concerning presenting visual acuity and best-corrected visual acuity, the prevalence of blindness and low vision was higher in old people, females and less educated persons. Cataract (46.63%) was the leading cause of blindness. Uncorrected refractive error (36.51%) was also a main cause of visual impairment. Conclusion: The prevalence of visual impairment is higher in old people, females and less educated persons in Funing County, Jiangsu Province. Cataract is still the leading cause of visual impairment. (Chin J Ophthalmol, 2017, 53: 502-508) .

[Motivation and Emotional States: Structural Systemic, Neurochemical, Molecular and Cellular Mechanisms].

Science.gov (United States)

Bazyan, A S

2016-01-01

The structural, systemic, neurochemical, molecular and cellular mechanisms of organization and coding motivation and emotional states are describe. The GABA and glutamatergic synaptic systems of basal ganglia form a neural network and participate in the implementation of voluntary behavior. Neuropeptides, neurohormones and paracrine neuromodulators involved in the organization of motivation and emotional states, integrated with synaptic systems, controlled by neural networks and organizing goal-directed behavior. Structural centers for united and integrated of information in voluntary and goal-directed behavior are globus pallidus. Substantia nigra pars reticulata switches the information from corticobasal networks to thalamocortical networks, induces global dopaminergic (DA) signal and organize interaction of mesolimbic and nigostriatnoy DA systems controlled by prefrontal and motor cortex. Together with the motor cortex, substantia nigra displays information in the brainstem and spinal cord to implementation of behavior. Motivation states are formed in the interaction of neurohormonal and neuropeptide systems by monoaminergic systems of brain. Emotional states are formed by monoaminergic systems of the mid-brain, where the leading role belongs to the mesolimbic DA system. The emotional and motivation state of the encoded specific epigenetic molecular and chemical pattern of neuron.

Cigarette smoking causes hearing impairment among Bangladeshi population.

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Ahmed Faisal Sumit

Full Text Available Lifestyle including smoking, noise exposure with MP3 player and drinking alcohol are considered as risk factors for affecting hearing synergistically. However, little is known about the association of cigarette smoking with hearing impairment among subjects who carry a lifestyle without using MP3 player and drinking alcohol. We showed here the influence of smoking on hearing among Bangladeshi subjects who maintain a lifestyle devoid of using MP3 player and drinking alcohol. A total of 184 subjects (smokers: 90; non-smokers: 94 were included considering their duration and frequency of smoking for conducting this study. The mean hearing thresholds of non-smoker subjects at 1, 4, 8 and 12 kHz frequencies were 5.63 ± 2.10, 8.56±5.75, 21.06 ± 11.06, 40.79 ± 20.36 decibel (dB, respectively and that of the smokers were 7 ± 3.8, 13.27 ± 8.4, 30.66 ± 12.50 and 56.88 ± 21.58 dB, respectively. The hearing thresholds of the smokers at 4, 8 and 12 kHz frequencies were significantly (p5 years showed higher level of auditory threshold (62.16 ± 19.87 dB at 12 kHz frequency compared with that (41.52 ± 19.21 dB of the subjects smoked for 1-5 years and the difference in auditory thresholds was statistically significant (p<0.0002. In this study, the Brinkman Index (BI of smokers was from 6 to 440 and the adjusted odds ratio showed a positive correlation between hearing loss and smoking when adjusted for age and body mass index (BMI. In addition, age, but not BMI, also played positive role on hearing impairment at all frequencies. Thus, these findings suggested that cigarette smoking affects hearing level at all the frequencies tested but most significantly at extra higher frequencies.

Loss of EphA4 impairs short-term spatial recognition memory performance and locomotor habituation.

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Willi, R; Winter, C; Wieske, F; Kempf, A; Yee, B K; Schwab, M E; Singer, P

2012-11-01

EphA4 receptor (EphA4) tyrosine kinase is an important regulator of central nervous system development and synaptic plasticity in the mature brain, but its relevance to the control of normal behavior remains largely unexplored. This study is the first attempt to obtain a behavioral profile of constitutive homozygous and heterozygous EphA4 knockout mice. A deficit in locomotor habituation in the open field, impairment in spatial recognition in the Y-maze and reduced probability of spatial spontaneous alternation in the T-maze were identified in homozygous EphA4(-/-) mice, while heterozygo us EphA4(+/-) mice appeared normal on these tests in comparison with wild-type (WT) controls. The multiple phenotypes observed in EphA4(-/-) mice might stem from an underlying deficit in habituation learning, reflecting an elementary form of nonassociative learning that is in contrast to Pavlovian associative learning, which appeared unaffected by EphA4 disruption. A deficit in motor coordination on the accelerating rotarod was also demonstrated only in EphA4(-/-) mice--a finding in keeping with the presence of abnormal gait in EphA4(-/-) mice--although they were able to improve performance over training. There was no evidence for substantial changes in major neurochemical markers in various brain regions rich in EphA4 as shown by post-mortem analysis. This excludes the possibility of major neurochemical compensation in the brain of EphA4(-/-) mice. In summary, we have demonstrated for the first time the behavioral significance of EphA4 disruption, supporting further investigation of EphA4 as a possible target for behavioral interventions where habituation deficits are prominent. © 2012 The Authors. Genes, Brain and Behavior © 2012 Blackwell Publishing Ltd and International Behavioural and Neural Genetics Society.

Difficulty understanding speech in noise by the hearing impaired: underlying causes and technological solutions.

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Healy, Eric W; Yoho, Sarah E

2016-08-01

A primary complaint of hearing-impaired individuals involves poor speech understanding when background noise is present. Hearing aids and cochlear implants often allow good speech understanding in quiet backgrounds. But hearing-impaired individuals are highly noise intolerant, and existing devices are not very effective at combating background noise. As a result, speech understanding in noise is often quite poor. In accord with the significance of the problem, considerable effort has been expended toward understanding and remedying this issue. Fortunately, our understanding of the underlying issues is reasonably good. In sharp contrast, effective solutions have remained elusive. One solution that seems promising involves a single-microphone machine-learning algorithm to extract speech from background noise. Data from our group indicate that the algorithm is capable of producing vast increases in speech understanding by hearing-impaired individuals. This paper will first provide an overview of the speech-in-noise problem and outline why hearing-impaired individuals are so noise intolerant. An overview of our approach to solving this problem will follow.

Prevalence and causes of blindness, visual impairment among different ethnical minority groups in Xinjiang Uygur autonomous region, China.

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Li, Yanping; Huang, Wenyong; Qiqige, Aoyun; Zhang, Hongwei; Jin, Ling; Ti, Pula; Yip, Jennifer; Xiao, Baixiang

2018-02-13

The aim of this cross-sectional study is to ascertain the prevalence and causes of blindness, visual impairment, uptake of cataract surgery among different ethnic groups in Xinjiang Uygur Autonomous Region, China. Four thousand one hundred fifty people at 50 years and above from different minority ethnic groups were randomly selected for an eye examination. The four trained eye teams collected data using tumbling E visual chart, torch, portable slit lamp and direct ophthalmoscope in 2015. The World Health Organization's definition of blindness and visual impairment (VI) was used to classify patients in each ethnic group. Data were analyzed by different minority groups and were compared with Han Chinese. 3977 (95.8%) out of 4150 people were examined. The prevalence of blindness from the study population was 1.7% (95% confidence interval: 1.3-2.2%).There was no significant difference in prevalence of blindness between Han Chinese and people of Khazak and other minority ethnic groups, nor, between male and female. Cataract was the leading course (65.5%) of blindness and uncorrected refractive error was the most common cause of VI (36.3%) followed by myopic retinopathy. The most common barrier to cataract surgery was lack of awareness of service availability. This study documented a low blindness prevalence among people aged 50 years and over comparing to prevalence identified through studies of other regions in China. It still indicates blindness and un-operated cataract as the significant public health issue, with no evidence of eye health inequalities, but some inequities in accessing to cataract surgery amongst ethnic minority groups in Xinjiang.

The Association of Visual Impairment With Clinical Outcomes in Hemodialysis Patients.

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Hong, Yu Ah; Kim, Suk Young; Kim, Su-Hyun; Kim, Young Ok; Jin, Dong Chan; Song, Ho Chul; Choi, Euy Jin; Kim, Yong-Lim; Kim, Yon-Su; Kang, Shin-Wook; Kim, Nam-Ho; Yang, Chul Woo; Kim, Yong Kyun

2016-05-01

Visual impairment limits people's ability to perform daily tasks and affects their quality of life. We evaluated the impact of visual impairment on clinical outcomes in hemodialysis (HD) patients.HD patients were selected from the Clinical Research Center registry a prospective cohort study on dialysis patients in Korea. Visual impairment was defined as difficulty in daily life due to decreased visual acuity or blindness. The primary outcome was all-cause mortality and the secondary outcomes were cardiovascular and infection-related hospitalization.A total of 3250 patients were included. Seven hundred thirty (22.5%) of the enrolled patients had visual impairment. The median follow-up period was 30 months. The Kaplan-Meier curve and log-rank test showed that all-cause mortality rates (P visual impairment than in patients without visual impairment. In the multivariable analysis, visual impairment had significant predictive power for all-cause mortality (Hazard ratio [HR], 1.77, 95% confidence interval [CI], 1.21-2.61, P = 0.004) and cardiovascular hospitalization (HR 1.45 [1.00-1.90], P = 0.008) after adjusting for confounding variables. Of these 3250 patients, 634 patients from each group were matched by propensity scores. In the propensity score matched analysis, patients with visual impairment had independently significant associations with increased all-cause mortality (HR 1.69 [1.12-2.54], P = 0.01) and cardiovascular hospitalization (HR 1.48 [1.08-2.02], P = 0.01) compared with patients without visual impairment after adjustment for confounding variables.Our data demonstrated that visual impairment was an independent risk factor for clinical adverse outcomes in HD patients.

Convulsant activity and neurochemical alterations induced by a fraction obtained from fruit Averrhoa carambola (Oxalidaceae: Geraniales).

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Carolino, Ruither O G; Beleboni, Renê O; Pizzo, Andrea B; Vecchio, Flavio Del; Garcia-Cairasco, Norberto; Moyses-Neto, Miguel; Santos, Wagner F Dos; Coutinho-Netto, Joaquim

2005-06-01

We obtained a neurotoxic fraction (AcTx) from star fruit (Averrhoa carambola) and studied its effects on GABAergic and glutamatergic transmission systems. AcTx had no effect on GABA/glutamate uptake or release, or on glutamate binding. However, it specifically inhibited GABA binding in a concentration-dependent manner (IC(50)=0.89muM). Video-electroencephalogram recordings demonstrated that following cortical administration of AcTx, animals showed behavioral changes, including tonic-clonic seizures, evolving into status epilepticus, accompanied by cortical epileptiform activity. Chemical characterization of AcTx showed that this compound is a nonproteic molecule with a molecular weight less than 500, differing from oxalic acid. This neurotoxic fraction of star fruit may be considered a new tool for neurochemical and neuroethological research.

Bombesin administration impairs memory and does not reverse memory deficit caused by sleep deprivation.

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Ferreira, L B T; Oliveira, S L B; Raya, J; Esumi, L A; Hipolide, D C

2017-07-28

Sleep deprivation impairs performance in emotional memory tasks, however this effect on memory is not completely understood. Possible mechanisms may involve an alteration in neurotransmission systems, as shown by the fact that many drugs that modulate neural pathways can prevent memory impairment by sleep loss. Gastrin releasing peptide (GRP) is a neuropeptide that emerged as a regulatory molecule of emotional memory through the modulation of other neurotransmission systems. Thus, the present study addressed the effect of intraperitoneal (IP) administration of bombesin (BB) (2.5, 5.0 and 10.0μg/kg), a GRP agonist, on the performance of Wistar rats in a multiple trail inhibitory avoidance (MTIA) task, after sleep deprivation, using the modified multiple platforms method (MMPM). Sleep deprived animals exhibited acquisition and retention impairment that was not prevented by BB injection. In addition, non-sleep deprived animals treated with BB before and after the training session, but not before the test, have shown a retention deficit. In summary, BB did not improve the memory impairment by sleep loss and, under normal conditions, produced a memory consolidation deficit. Copyright © 2017 Elsevier B.V. All rights reserved.

Region-specific aging of the human brain as evidenced by neurochemical profiles measured noninvasively in the posterior cingulate cortex and the occipital lobe using 1H magnetic resonance spectroscopy at 7 T.

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Marjańska, Małgorzata; McCarten, J Riley; Hodges, James; Hemmy, Laura S; Grant, Andrea; Deelchand, Dinesh K; Terpstra, Melissa

2017-06-23

The concentrations of fourteen neurochemicals associated with metabolism, neurotransmission, antioxidant capacity, and cellular structure were measured noninvasively from two distinct brain regions using 1 H magnetic resonance spectroscopy. Seventeen young adults (age 19-22years) and sixteen cognitively normal older adults (age 70-88years) were scanned. To increase sensitivity and specificity, 1 H magnetic resonance spectra were obtained at the ultra-high field of 7T and at ultra-short echo time. The concentrations of neurochemicals were determined using water as an internal reference and accounting for gray matter, white matter, and cerebrospinal fluid content of the volume of interest. In the posterior cingulate cortex (PCC), the concentrations of neurochemicals associated with energy (i.e., creatine plus phosphocreatine), membrane turnover (i.e., choline containing compounds), and gliosis (i.e., myo-inositol) were higher in the older adults while the concentrations of N-acetylaspartylglutamate (NAAG) and phosphorylethanolamine (PE) were lower. In the occipital cortex (OCC), the concentration of N-acetylaspartate (NAA), a marker of neuronal viability, concentrations of the neurotransmitters Glu and NAAG, antioxidant ascorbate (Asc), and PE were lower in the older adults while the concentration of choline containing compounds was higher. Altogether, these findings shed light on how the human brain ages differently depending on region. Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

Persistent non-verbal memory impairment in remitted major depression - caused by encoding deficits?

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Behnken, Andreas; Schöning, Sonja; Gerss, Joachim; Konrad, Carsten; de Jong-Meyer, Renate; Zwanzger, Peter; Arolt, Volker

2010-04-01

While neuropsychological impairments are well described in acute phases of major depressive disorders (MDD), little is known about the neuropsychological profile in remission. There is evidence for episodic memory impairments in both acute depressed and remitted patients with MDD. Learning and memory depend on individuals' ability to organize information during learning. This study investigates non-verbal memory functions in remitted MDD and whether nonverbal memory performance is mediated by organizational strategies whilst learning. 30 well-characterized fully remitted individuals with unipolar MDD and 30 healthy controls matching in age, sex and education were investigated. Non-verbal learning and memory were measured by the Rey-Osterrieth-Complex-Figure-Test (RCFT). The RCFT provides measures of planning, organizational skills, perceptual and non-verbal memory functions. For assessing the mediating effects of organizational strategies, we used the Savage Organizational Score. Compared to healthy controls, participants with remitted MDD showed more deficits in their non-verbal memory function. Moreover, participants with remitted MDD demonstrated difficulties in organizing non-verbal information appropriately during learning. In contrast, no impairments regarding visual-spatial functions in remitted MDD were observed. Except for one patient, all the others were taking psychopharmacological medication. The neuropsychological function was solely investigated in the remitted phase of MDD. Individuals with MDD in remission showed persistent non-verbal memory impairments, modulated by a deficient use of organizational strategies during encoding. Therefore, our results strongly argue for additional therapeutic interventions in order to improve these remaining deficits in cognitive function. Copyright 2009 Elsevier B.V. All rights reserved.

In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring

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Zhengmeng Ye

2018-03-01

Full Text Available Background/Aims: Adverse environment in utero can modulate adult phenotypes including blood pressure. Fine particulate matter (PM2.5 exposure in utero causes hypertension in the offspring, but the exact mechanisms are not clear. Renal dopamine D1 receptor (D1R, regulated by G protein-coupled receptor kinase type 4 (GRK4, plays an important role in the regulation of renal sodium transport and blood pressure. In this present study, we determined if renal D1R dysfunction is involved in PM2.5–induced hypertension in the offspring. Methods: Pregnant Sprague–Dawley rats were given an oropharyngeal drip of PM2.5 (1.0 mg/kg at gestation day 8, 10, and 12. The blood pressure, 24-hour sodium excretion, and urine volume were measured in the offspring. The expression levels of GRK4 and D1R were determined by immunoblotting. The phosphorylation of D1R was investigated using immunoprecipitation. Plasma malondialdehyde and superoxide dismutase levels were also measured in the offspring. Results: As compared with saline-treated dams, offspring of PM2.5-treated dams had increased blood pressure, impaired sodium excretion, and reduced D1R-mediated natriuresis and diuresis, accompanied by decreased renal D1R expression and GRK4 expression. The impaired renal D1R function and increased GRK4 expression could be caused by increased reactive oxidative stress (ROS induced by PM2.5 exposure. Administration of tempol, a redox-cycling nitroxide, for 4 weeks in the offspring of PM2.5-treated dam normalized the decreased renal D1R expression and increased renal D1R phosphorylation and GRK4 expression. Furthermore, tempol normalized the increased renal expression of c-Myc, a transcription factor that regulates GRK4 expression. Conclusions: In utero exposure to PM2.5 increases ROS and GRK4 expression, impairs D1R-mediated sodium excretion, and increases blood pressure in the offspring. These studies suggest that normalization of D1R function may be a target for the

Modulation of sphingosine 1-phosphate (S1P) attenuates spatial learning and memory impairments in the valproic acid rat model of autism.

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Wu, Hongmei; Zhang, Quanzhi; Gao, Jingquan; Sun, Caihong; Wang, Jia; Xia, Wei; Cao, Yonggang; Hao, Yanqiu; Wu, Lijie

2018-03-01

Autism spectrum disorders (ASD) are a set of pervasive neurodevelopmental disorders that manifest in early childhood, and it is growing up to be a major cause of disability in children. However, the etiology and treatment of ASD are not well understood. In our previous study, we found that serum levels of sphingosine 1-phosphate (S1P) were increased significantly in children with autism, indicating that S1P levels may be involved in ASD. The objective of this study was to identify a link between increased levels of S1P and neurobehavioral changes in autism. We utilized a valproic acid (VPA) -induced rat model of autism to evaluate the levels of S1P and the expression of sphingosine kinase (SphK), a key enzyme for S1P production, in serum and hippocampal tissue. Furthermore, we assessed cognitive functional changes and histopathological and neurochemical alterations in VPA-exposed rats after SphK blockade to explore the possible link between increased levels of S1P and neurobehavioral changes in autism. We found that SphK2 and S1P are upregulated in hippocampal tissue from VPA-exposed rats, while pharmacological inhibition of SphK reduced S1P levels, attenuated spatial learning and memory impairments, increased the expression of phosphorylated CaMKII and CREB and autophagy-related proteins, inhibited cytochrome c release, decreased the expression of apoptosis related proteins, and protected against neuronal loss in the hippocampus. We have demonstrated that an increased level of SphK2/S1P is involved in the spatial learning and memory impairments of autism, and this signaling pathway represents a novel therapeutic target and direction for future studies.

Mutations affecting the SAND domain of DEAF1 cause intellectual disability with severe speech impairment and behavioral problems.

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Vulto-van Silfhout, Anneke T; Rajamanickam, Shivakumar; Jensik, Philip J; Vergult, Sarah; de Rocker, Nina; Newhall, Kathryn J; Raghavan, Ramya; Reardon, Sara N; Jarrett, Kelsey; McIntyre, Tara; Bulinski, Joseph; Ownby, Stacy L; Huggenvik, Jodi I; McKnight, G Stanley; Rose, Gregory M; Cai, Xiang; Willaert, Andy; Zweier, Christiane; Endele, Sabine; de Ligt, Joep; van Bon, Bregje W M; Lugtenberg, Dorien; de Vries, Petra F; Veltman, Joris A; van Bokhoven, Hans; Brunner, Han G; Rauch, Anita; de Brouwer, Arjan P M; Carvill, Gemma L; Hoischen, Alexander; Mefford, Heather C; Eichler, Evan E; Vissers, Lisenka E L M; Menten, Björn; Collard, Michael W; de Vries, Bert B A

2014-05-01

Recently, we identified in two individuals with intellectual disability (ID) different de novo mutations in DEAF1, which encodes a transcription factor with an important role in embryonic development. To ascertain whether these mutations in DEAF1 are causative for the ID phenotype, we performed targeted resequencing of DEAF1 in an additional cohort of over 2,300 individuals with unexplained ID and identified two additional individuals with de novo mutations in this gene. All four individuals had severe ID with severely affected speech development, and three showed severe behavioral problems. DEAF1 is highly expressed in the CNS, especially during early embryonic development. All four mutations were missense mutations affecting the SAND domain of DEAF1. Altered DEAF1 harboring any of the four amino acid changes showed impaired transcriptional regulation of the DEAF1 promoter. Moreover, behavioral studies in mice with a conditional knockout of Deaf1 in the brain showed memory deficits and increased anxiety-like behavior. Our results demonstrate that mutations in DEAF1 cause ID and behavioral problems, most likely as a result of impaired transcriptional regulation by DEAF1. Copyright © 2014 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.

Decreased systolic blood pressure is associated with increased risk of all-cause mortality in patients with type 2 diabetes and renal impairment: A nationwide longitudinal observational study of 27,732 patients based on the Swedish National Diabetes Register.

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Svensson, Maria K; Afghahi, Henri; Franzen, Stefan; Björk, Staffan; Gudbjörnsdottir, Soffia; Svensson, Ann-Marie; Eliasson, Björn

2017-05-01

Previous studies have shown a U-shaped relationship between systolic blood pressure and risk of all-cause of mortality in patients with type 2 diabetes and renal impairment. To evaluate the associations between time-updated systolic blood pressure and time-updated change in systolic blood pressure during the follow-up period and risk of all-cause mortality in patients with type 2 diabetes and renal impairment. A total of 27,732 patients with type 2 diabetes and renal impairment in the Swedish National Diabetes Register were followed for 4.7 years. Time-dependent Cox models were used to estimate risk of all-cause mortality. Time-updated mean systolic blood pressure is the average of the baseline and the reported post-baseline systolic blood pressures. A time-updated systolic blood pressure blood pressure > 10 mmHg between the last two observations was associated with higher risk of all-cause mortality (-10 to -25 mmHg; hazard ratio: 1.24, 95% confidence interval: 1.17-1.32). Both low systolic blood pressure and a decrease in systolic blood pressure during the follow-up are associated with a higher risk of all-cause mortality in patients with type 2 diabetes and renal impairment.

A population-based study of visual impairment among pre-school children in Beijing: the Beijing study of visual impairment in children.

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Lu, Qing; Zheng, Yuanyuan; Sun, Baochen; Cui, Tongtong; Congdon, Nathan; Hu, Ailian; Chen, Jianhua; Shi, Jiliang

2009-06-01

To evaluate the prevalence and causes of visual impairment among Chinese children aged 3 to 6 years in Beijing. Population-based prevalence survey. Presenting and pinhole visual acuity were tested using picture optotypes or, in children with pinhole vision children with pinhole vision children aged 3 to 6 years (95.3% of sample). Subjects with bilateral correctable low vision (presenting vision or= 6/18) numbered 57 (0.322%; 95% confidence interval [CI], 0.237% to 0.403%), while 14 (0.079%; 95% CI, 0.038% to 0.120%) had bilateral uncorrectable low vision (best-corrected vision of or= 3/60), and 5 subjects (0.028%; 95% CI, 0.004% to 0.054%) were bilaterally blind (best-corrected acuity visual impairment included: refractive error in 57 children (75%), hereditary factors (microphthalmos, congenital cataract, congenital motor nystagmus, albinism, and optic nerve disease) in 13 children (17.1 %), amblyopia in 3 children (3.95%), and cortical blindness in 1 child (1.3%). The cause of visual impairment could not be established in 2 (2.63%) children. The prevalence of visual impairment did not differ by gender, but correctable low vision was significantly (P children. The leading causes of visual impairment among Chinese preschool-aged children are refractive error and hereditary eye diseases. A higher prevalence of refractive error is already present among urban as compared with rural children in this preschool population.

Neurochemical characterization of the tree shrew dorsal striatum

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MATTHEW W RICE

2011-08-01

Full Text Available The striatum is a major component of the basal ganglia and is associated with motor and cognitive functions. Striatal pathologies have been linked to several disorders, including Huntington's, Tourette's syndrome, obsessive-compulsive disorders and schizophrenia. For the study of these striatal pathologies different animal models have been used, including rodents and non-human primates. Rodents lack on morphological complexity (for example, the lack of well defined caudate and putamen nuclei, which makes it difficult to translate data to the human paradigm. Primates, and especially higher primates, are the closest model to humans, but there are ever-increasing restrictions to the use of these animals for research. In our search for a non-primate animal model with a striatum that anatomically (and perhaps functionally can resemble that of humans, we turned our attention to the tree shrew. Evolutionary genetic studies have provided strong data supporting that the tree shrews (Scadentia are one of the closest groups to primates, although their brain anatomy has only been studied in detail for specific brain areas. Morphologically, the tree shrew striatum resembles the primate striatum with the presence of an internal capsule separating the caudate and putamen, but little is known about its neurochemical composition. Here we analyzed the expression of calcium-binding proteins, the presence and distribution of the striosome and matrix compartments (by the use of calbindin, tyrosine hydroxylase and acetylcholinesterase immunohistochemistry, and the GABAergic system by immunohistochemistry against glutamic acid decarboxylase and Golgi impregnation. In summary, our results show that when compared to primates, the tree shrew dorsal striatum presents striking similarities in the distribution of most of the markers studied, while presenting some marked divergences when compared to the rodent striatum.

Cerebral versus Ocular Visual Impairment: The Impact on Developmental Neuroplasticity.

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Martín, Maria B C; Santos-Lozano, Alejandro; Martín-Hernández, Juan; López-Miguel, Alberto; Maldonado, Miguel; Baladrón, Carlos; Bauer, Corinna M; Merabet, Lotfi B

2016-01-01

Cortical/cerebral visual impairment (CVI) is clinically defined as significant visual dysfunction caused by injury to visual pathways and structures occurring during early perinatal development. Depending on the location and extent of damage, children with CVI often present with a myriad of visual deficits including decreased visual acuity and impaired visual field function. Most striking, however, are impairments in visual processing and attention which have a significant impact on learning, development, and independence. Within the educational arena, current evidence suggests that strategies designed for individuals with ocular visual impairment are not effective in the case of CVI. We propose that this variance may be related to differences in compensatory neuroplasticity related to the type of visual impairment, as well as underlying alterations in brain structural connectivity. We discuss the etiology and nature of visual impairments related to CVI, and how advanced neuroimaging techniques (i.e., diffusion-based imaging) may help uncover differences between ocular and cerebral causes of visual dysfunction. Revealing these differences may help in developing future strategies for the education and rehabilitation of individuals living with visual impairment.

Behavioral and neurochemical effects of alpha lipoic acid associated with omega-3 in tardive dyskinesia induced by chronic haloperidol in rats.

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de Araújo, Dayane Pessoa; Camboim, Thaisa Gracielle Martins; Silva, Ana Patrícia Magalhães; Silva, Caio da Fonseca; de Sousa, Rebeca Canuto; Barbosa, Mabson Delâno Alves; Oliveira, Lucidio Clebeson; Cavalcanti, José Rodolfo Lopes de Paiva; Lucena, Eudes Euler de Souza; Guzen, Fausto Pierdoná

2017-07-01

Tardive dyskinesia (TD) is characterized by involuntary movements of the lower portion of the face being related to typical antipsychotic therapy. TD is associated with the oxidative imbalance in the basal ganglia. Lipoic acid (LA) and omega-3 (ω-3) are antioxidants acting as enzyme cofactors, regenerating antioxidant enzymes. This study aimed to investigate behavioral and neurochemical effects of supplementation with LA (100 mg/kg) and ω-3 (1 g/kg) in the treatment of TD induced by chronic use of haloperidol (HAL) (1 mg/kg) in rats. Wistar male rats were used, weighing between 180-200 g. The animals were treated chronically (31 days) with LA alone or associated with HAL or ω-3. Motor behavior was assessed by open-field test, the catalepsy test, and evaluation of orofacial dyskinesia. Oxidative stress was accessed by determination of lipid peroxidation and concentration of nitrite. LA and ω-3 alone or associated caused an improvement in motor performance by increasing locomotor activity in the open-field test and decreased the permanence time on the bar in the catalepsy test and decreased the orofacial dyskinesia. LA and ω-3 showed antioxidant effects, decreasing lipid peroxidation and nitrite levels. Thus, the use of LA associated with ω-3 reduced the extrapyramidal effects produced by chronic use of HAL.

Hepatitis B virus infection status and infertility causes in couples seeking fertility treatment-Indicator of impaired immune response?

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Lao, Terence T; Mak, Jennifer S M; Li, Tin-Chiu

2017-04-01

The relationship between hepatitis B (HBV) infection in infertile couples seeking in vitro fertilization (IVF) treatment and infertility causes is unknown. A total of 831 infertile couples attending our unit seeking IVF during January to December 2015 were recruited. HBV infection was found in 6.3% and 7.3% of female and male partners, respectively, and infection in one or both partners was associated with less primary infertility (44.2% vs 55.1%, P=.038). Infected female partners had increased tubal (69.2% vs 43.2%, Pinfertility, while infected male partners were associated with increased tubal (62.3% vs 43.4%, P=.004) causes and reduced endometriosis (62.3% vs 73.9%, P=.050). Our results suggest HBV infection in either partner was associated with tubal infertility. HBV infection in either partner probably increases the risk of pelvic infection in female partner through impaired immune response to sexually transmitted infections, with consequent tubal damage and infertility. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Neurochemical abnormalities in brains of renal failure patients treated by repeated hemodialysis.

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Perry, T L; Yong, V W; Kish, S J; Ito, M; Foulks, J G; Godolphin, W J; Sweeney, V P

1985-10-01

We examined autopsied brain from 10 patients with end-stage renal failure who had undergone repeated hemodialysis. Eight had classic symptoms, and two had suggestive symptoms of dialysis encephalopathy. Findings were compared with those in autopsied brain from control adults who had never been hemodialyzed. Mean gamma-aminobutyric acid (GABA) contents were significantly reduced in frontal and occipital cortex, cerebellar cortex, dentate nucleus, caudate nucleus, and medial-dorsal thalamus of the hemodialyzed patients, the reduction being greater than 40% in cerebral cortex and thalamus. Choline acetyltransferase activity was reduced by 25-35% in three cortical regions in the hemodialyzed patients. These two abnormalities were observed in the brain of each hemodialyzed patient, regardless of whether or not the patient died with unequivocal dialysis encephalopathy. Pyridoxal phosphate contents were substantially reduced in brains of the hemodialyzed patients, but metabolites of noradrenaline, 3,4-dihydroxyphenylethylamine (dopamine), and 5-hydroxytryptamine (serotonin) were present in normal amounts. Aluminum levels were abnormally high in frontal cortical gray matter in the hemodialyzed patients. Although this study does not clarify the role played by aluminum toxicity in the pathogenesis of dialysis encephalopathy, the abnormalities we found suggest the need for further neurochemical investigations in this disorder.

Biochemical and neurochemical effects in rats following Iow-level chronic moniliformin mycotoxin treatment

International Nuclear Information System (INIS)

Adam, Y.M.; Abdel-Kader, S.M.

2000-01-01

An investigation was conducted to study the biochemical and neurochemical effects of moniliformin mycotoxins in rats. Moniliformin was extracted from fusarium oxysporum and injected intraperitoneally to male albino rats at a dose level 225 magaa g/kg (1/220 LD 5 0) daily for three weeks. The results. The results revealed a decrease in body weight of treated animals, in addition to alteration in the weights of some selected organs. A significant increase of serum ALT, AST and ALP were observed, indicating changes in liver function. Kidney function of treated rats as determined by alteration creatinine and blood urea also was affected. On the other hand the data obtained revealed a dramatic decrease in brain acetylcholinesterase activity. In addition, moniliformin exhibited alteration in the total content of catecholamines, dopamine (DA), norepinephrine (NE), serotonine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), free inorganic phosphate (Pi) and gamma-aminobutyric acid (GABA) in rat brain of treated animals. Also, profound decline in serum testosterone level was observed. No pathological changes were detected. Hormonal assays were performed using radioimmunoassay techniques

Electrophysiology in visually impaired children

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Genderen, Maria Michielde van

2006-01-01

Inherited retinal disorders and posterior visual pathway abnormalities are important causes of visual impairment in children. Visual electrophysiology often is indispensable in diagnosing these conditions. This thesis shows the wide range of use of pediatric electro-ophthalmology, and demonstrates

Risks and benefits of antireflux operations in neurologically impaired children

NARCIS (Netherlands)

Borgstein, E. S.; Heij, H. A.; Beugelaar, J. D.; Ekkelkamp, S.; Vos, A.

1994-01-01

Gastro-oesophageal reflux (GER) in neurologically impaired children often causes feeding problems and complications of oesophagitis and is frequently resistant to medical treatment. Fifty neurologically impaired children underwent anterior gastropexy as anti-reflux operation, combined with

The relationship between separation anxiety and impairment

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Foley, Debra L; Rowe, Richard; Maes, Hermine; Silberg, Judy; Eaves, Lindon; Pickles, Andrew

2009-01-01

The goal of this study was to characterize the contemporaneous and prognostic relationship between symptoms of separation anxiety disorder (SAD) and associated functional impairment. The sample comprised n=2067 8–16 year-old twins from a community-based registry. Juvenile subjects and their parents completed a personal interview on two occasions, separated by an average follow-up period of 18 months, about the subject’s current history of SAD and associated functional impairment. Results showed that SAD symptoms typically caused very little impairment but demonstrated significant continuity over time. Older youth had significantly more persistent symptoms than younger children. Prior symptom level independently predicted future symptom level and diagnostic symptom threshold, with and without impairment. Neither diagnostic threshold nor severity of impairment independently predicted outcomes after taking account of prior symptom levels. The results indicate that impairment may index current treatment need but symptom levels provide the best information about severity and prognosis. PMID:17658718

Edaravone attenuates intracerebroventricular streptozotocin-induced cognitive impairment in rats.

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Reeta, K H; Singh, Devendra; Gupta, Yogendra K

2017-04-01

Alzheimer's disease is a major cause of dementia worldwide. Edaravone, a potent free radical scavenger, is reported to be neuroprotective. The present study was designed to investigate the effect of chronic edaravone administration on intracerebroventricular-streptozotocin (ICV-STZ) induced cognitive impairment in male Wistar rats. Cognitive impairment was developed by single ICV-STZ (3 mg/kg) injection bilaterally on day 1. Edaravone (1, 3 and 10 mg/kg, orally, once daily) was administered for 28 days. Morris water maze and passive avoidance tests were used to assess cognitive functions at baseline and on days 14 and 28. ICV-STZ caused cognitive impairment as evidenced by increased escape latency and decreased time spent in target quadrant in the Morris water maze test and reduced retention latency in the passive avoidance test. STZ caused increase in oxidative stress, cholinesterases, inflammatory cytokines and protein expression of ROCK-II and decrease in protein expression of ChAT. Edaravone ameliorated the STZ-induced cognitive impairment. STZ-induced increase in oxidative stress and increased levels of pro-inflammatory cytokines (TNF-α, IL-1β) were mitigated by edaravone. Edaravone also prevented STZ-induced increased protein expression of ROCK-II. Moreover, edaravone significantly prevented STZ-induced increased activity of cholinesterases in the cortex and hippocampus. The decreased expression of ChAT caused by STZ was brought towards normal by edaravone in the hippocampus. The results thus show that edaravone is protective against STZ-induced cognitive impairment, oxidative stress, cholinergic dysfunction and altered protein expressions. This study thus suggests the potential of edaravone as an adjuvant in the treatment of Alzheimer's disease. © 2017 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

Decreased numbers of progenitor cells but no response to antidepressant drugs in the hippocampus of elderly depressed patients

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Lucassen, P.J.; Stumpel, M.W.; Wang, Q.; Aronica, E.

2010-01-01

Imaging studies have consistently documented hippocampal volume reductions in depression. Although depressive disorders are traditionally considered to have a neurochemical basis, recent studies suggest that impairments of structural plasticity contribute to the volume reductions and the related

Rapid assessment of visual impairment in urban population of Delhi, India.

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Gupta, Noopur; Vashist, Praveen; Malhotra, Sumit; Senjam, Suraj Singh; Misra, Vasundhara; Bhardwaj, Amit

2015-01-01

To determine the prevalence, causes and associated demographic factors related to visual impairment amongst the urban population of New Delhi, India. A population-based, cross-sectional study was conducted in East Delhi district using cluster random sampling methodology. This Rapid Assessment of Visual Impairment (RAVI) survey involved examination of all individuals aged 40 years and above in 24 randomly selected clusters of the district. Visual acuity (VA) assessment and comprehensive ocular examination were done during the door-to-door survey. A questionnaire was used to collect personal and demographic information of the study population. Blindness and Visual Impairment was defined as presenting VA visual impairment. Of 2421 subjects enumerated, 2331 (96.3%) were available for ophthalmic examination. Among those examined, 49.3% were males. The prevalence of visual impairment (VI) in the study population, was 11.4% (95% C.I. 10.1, 12.7) and that of blindness was 1.2% (95% C.I. 0.8, 1.6). Uncorrected refractive error was the leading cause of VI accounting for 53.4% of all VI followed by cataract (33.8%). With multivariable logistic regression, the odds of having VI increased with age (OR = 24.6[95% C.I.: 14.9, 40.7]; p visual impairment is considerable in this region despite availability of adequate eye care facilities. Awareness generation and simple interventions like cataract surgery and provision of spectacles will help to eliminate the major causes of blindness and visual impairment in this region.

Cardiovascular mortality, all-cause mortality, and diabetes incidence after lifestyle intervention for people with impaired glucose tolerance in the Da Qing Diabetes Prevention Study: a 23-year follow-up study.

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Li, Guangwei; Zhang, Ping; Wang, Jinping; An, Yali; Gong, Qiuhong; Gregg, Edward W; Yang, Wenying; Zhang, Bo; Shuai, Ying; Hong, Jing; Engelgau, Michael M; Li, Hui; Roglic, Gojka; Hu, Yinghua; Bennett, Peter H

2014-06-01

Lifestyle interventions among people with impaired glucose tolerance reduce the incidence of diabetes, but their effect on all-cause and cardiovascular disease mortality is unclear. We assessed the long-term effect of lifestyle intervention on long-term outcomes among adults with impaired glucose tolerance who participated in the Da Qing Diabetes Prevention Study. The study was a cluster randomised trial in which 33 clinics in Da Qing, China-serving 577 adults with impaired glucose tolerance-were randomised (1:1:1:1) to a control group or lifestyle intervention groups (diet or exercise or both). Patients were enrolled in 1986 and the intervention phase lasted for 6 years. In 2009, we followed up participants to assess the primary outcomes of cardiovascular mortality, all-cause mortality, and incidence of diabetes in the intention-to-treat population. Of the 577 patients, 439 were assigned to the intervention group and 138 were assigned to the control group (one refused baseline examination). 542 (94%) of 576 participants had complete data for mortality and 568 (99%) contributed data to the analysis. 174 participants died during the 23 years of follow-up (121 in the intervention group vs 53 in the control group). Cumulative incidence of cardiovascular disease mortality was 11.9% (95% CI 8.8-15.0) in the intervention group versus 19.6% (12.9-26.3) in the control group (hazard ratio [HR] 0.59, 95% CI 0.36-0.96; p=0.033). All-cause mortality was 28.1% (95% CI 23.9-32.4) versus 38.4% (30.3-46.5; HR 0.71, 95% CI 0.51-0.99; p=0.049). Incidence of diabetes was 72.6% (68.4-76.8) versus 89.9% (84.9-94.9; HR 0.55, 95% CI 0.40-0.76; p=0.001). A 6-year lifestyle intervention programme for Chinese people with impaired glucose tolerance can reduce incidence of cardiovascular and all-cause mortality and diabetes. These findings emphasise the long-term clinical benefits of lifestyle intervention for patients with impaired glucose tolerance and provide further justification for

IMPAIRED MOBILITY OF VOCAL FOLDS - etiology and symptoms

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Karlo Pintarić

2015-06-01

Full Text Available Paresis or paralysis of one or both vocal cords affects some significant aspects of a human life: breathing, swallowing and speech. The major causes for reduced mobility or even immobility are innervation damage, less often fixation of vocal cord or impaired mobility of crycoarytenoid joint. An injury of the superior or/and inferior laryngeal nerve can be a consequence of different medical procedures, tumor growth, trauma, infection, neurological disorders, radiation exposure, toxic damage, impaired circulation of the area or it is idiopathic. The symptoms are different in the case of unilateral and bilateral paresis of the vocal folds. They also depend on the cause for the impaired mobility. In the patients with unilateral vocal fold paresis, hoarseness and aspiration during swallowing are the leading symptoms. In the bilateral vocal fold paralysis, dyspnea prevails. 

EPA Office of Water (OW): Nutrient, Sediment, and Pathogens Water Impairments

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U.S. Environmental Protection Agency — National dataset consisting of a snapshot of 303(d) Listed Impaired Waters combined with Impaired Waters with TMDLs whose parent cause is Nutrients, Sediments, and...

Audiometric Characteristics of a Dutch DFNA10 Family With Mid-Frequency Hearing Impairment

NARCIS (Netherlands)

Beelen, E. van; Oonk, A.M.M.; Leijendeckers, J.M.; Hoefsloot, E.H.; Pennings, R.J.E.; Feenstra, I.; Dieker, H.J.; Huygen, P.L.M.; Snik, A.F.M.; Kremer, H.; Kunst, H.P.M.

2016-01-01

OBJECTIVES: Mutations in EYA4 can cause nonsyndromic autosomal dominant sensorineural hearing impairment (DFNA10) or a syndromic variant with hearing impairment and dilated cardiomyopathy. A mutation in EYA4 was found in a Dutch family, causing DFNA10. This study is focused on characterizing the

Impairment of ceramide synthesis causes a novel progressive myoclonus epilepsy.

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Vanni, Nicola; Fruscione, Floriana; Ferlazzo, Edoardo; Striano, Pasquale; Robbiano, Angela; Traverso, Monica; Sander, Thomas; Falace, Antonio; Gazzerro, Elisabetta; Bramanti, Placido; Bielawski, Jacek; Fassio, Anna; Minetti, Carlo; Genton, Pierre; Zara, Federico

2014-08-01

Alterations of sphingolipid metabolism are implicated in the pathogenesis of many neurodegenerative disorders. We identified a homozygous nonsynonymous mutation in CERS1, the gene encoding ceramide synthase 1, in 4 siblings affected by a progressive disorder with myoclonic epilepsy and dementia. CerS1, a transmembrane protein of the endoplasmic reticulum (ER), catalyzes the biosynthesis of C18-ceramides. We demonstrated that the mutation decreases C18-ceramide levels. In addition, we showed that downregulation of CerS1 in a neuroblastoma cell line triggers ER stress response and induces proapoptotic pathways. This study demonstrates that impairment of ceramide biosynthesis underlies neurodegeneration in humans. © 2014 American Neurological Association.

Heterozygous Disruption of Autism susceptibility candidate 2 Causes Impaired Emotional Control and Cognitive Memory.

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Kei Hori

Full Text Available Mutations in the Autism susceptibility candidate 2 gene (AUTS2 have been associated with a broad range of psychiatric illnesses including autism spectrum disorders, intellectual disability and schizophrenia. We previously demonstrated that the cytoplasmic AUTS2 acts as an upstream factor for the Rho family small GTPase Rac1 and Cdc42 that regulate the cytoskeletal rearrangements in neural cells. Moreover, genetic ablation of the Auts2 gene in mice has resulted in defects in neuronal migration and neuritogenesis in the developing cerebral cortex caused by inactivation of Rac1-signaling pathway, suggesting that AUTS2 is required for neural development. In this study, we conducted a battery of behavioral analyses on Auts2 heterozygous mutant mice to examine the involvement of Auts2 in adult cognitive brain functions. Auts2-deficient mice displayed a decrease in exploratory behavior as well as lower anxiety-like behaviors in the absence of any motor dysfunction. Furthermore, the capability for novel object recognition and cued associative memory were impaired in Auts2 mutant mice. Social behavior and sensory motor gating functions were, however, normal in the mutant mice as assessed by the three-chamber test and prepulse inhibition test, respectively. Together, our findings indicate that AUTS2 is critical for the acquisition of neurocognitive function.

Prevalence and causes of blindness and visual impairment and their associated risk factors, in three tribal areas of Andhra Pradesh, India.

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Singh, Nakul; Eeda, Shiva Shankar; Gudapati, Bala Krishna; Reddy, Srinivasa; Kanade, Pushkar; Shantha, Ghanshyam Palamaner Subash; Rani, Padmaja Kumari; Chakrabarti, Subhabrata; Khanna, Rohit C

2014-01-01

To assess the prevalence of blindness and visual impairment (VI), their associated causes and underlying risk factors in three tribal areas of Andhra Pradesh, India and compare this data in conjunction with data from other countries with low and middle income settings. Using a validated Rapid Assessment of Avoidable Blindness methodology, a two stage sampling survey was performed in these areas involving probability proportionate to size sampling and compact segment sampling methods. Blindness, VI and severe visual impairment (SVI) were defined as per the WHO guidelines and Indian definitions. Based on a prior enumeration, 7281 (97.1%) subjects were enrolled (mean age = 61.0+/-7.9 years). Based on the presenting visual acuity (PVA), the prevalences of VI, SVI and blindness were 16.9% (95% CI: 15.7-18.1), 2.9% (95% CI: 2.5-3.4), and 2.3% (95% CI: 1.9-2.7), respectively. When based on the Pinhole corrected visual acuity (PCVA), the prevalences were lower in VI (6.2%, 95% CI: 5.4-6.9), SVI (1.5%, 95% CI: 1.2-1.9) and blindness (2.1%, 95% CI: 1.7-2.5). Refractive error was the major cause of VI (71.4%), whereas, cataract was the major cause of SVI and blindness (70.3%). Based on the PVA, the odds ratio (OR) of blindness increased in the age groups of 60-69 years (OR = 3.8, 95% CI: 2.8, 5.1), 70-79 years (OR = 10.6, 95% CI: 7.2, 15.5) and 80 years and above (OR = 30.7, 95% CI: 19.2, 49). The ORs were relatively higher in females (OR = 1.3, 95% CI: 1.0, 1.6) and illiterate subjects (OR = 4.3, 95% CI: 2.2, 8.5), but lower in those wearing glasses (OR = 0.2, 95% CI: 0.1, 0.4). This is perhaps the first study to assess the prevalence of blindness and VI in these tribal regions and the majority of the causes of blindness and SVI were avoidable (88.5%). These findings may be useful for planning eye care services in these underserved regions.

Synergistic effects of cognitive impairment on physical disability in all-cause mortality among men aged 80 years and over: Results from longitudinal older veterans study.

Directory of Open Access Journals (Sweden)

Wan-Chen Yu

is a major risk factor for all-cause mortality among men aged 80 years and older, and risk increased synergistically when cognitive impairment was present. Cognitive impairment alone without physical disability did not increase mortality risk in this population.

Synergistic effects of cognitive impairment on physical disability in all-cause mortality among men aged 80 years and over: Results from longitudinal older veterans study.

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Yu, Wan-Chen; Chou, Ming-Yueh; Peng, Li-Ning; Lin, Yu-Te; Liang, Chih-Kuang; Chen, Liang-Kung

2017-01-01

risk factor for all-cause mortality among men aged 80 years and older, and risk increased synergistically when cognitive impairment was present. Cognitive impairment alone without physical disability did not increase mortality risk in this population.

Acute lesions that impair affective empathy

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Oishi, Kenichi; Hsu, John; Lindquist, Martin; Gottesman, Rebecca F.; Jarso, Samson; Crainiceanu, Ciprian; Mori, Susumu

2013-01-01

Functional imaging studies of healthy participants and previous lesion studies have provided evidence that empathy involves dissociable cognitive functions that rely on at least partially distinct neural networks that can be individually impaired by brain damage. These studies converge in support of the proposal that affective empathy—making inferences about how another person feels—engages at least the following areas: prefrontal cortex, orbitofrontal gyrus, anterior insula, anterior cingulate cortex, temporal pole, amygdala and temporoparietal junction. We hypothesized that right-sided lesions to any one of these structures, except temporoparietal junction, would cause impaired affective empathy (whereas bilateral damage to temporoparietal junction would be required to disrupt empathy). We studied 27 patients with acute right hemisphere ischaemic stroke and 24 neurologically intact inpatients on a test of affective empathy. Acute impairment of affective empathy was associated with infarcts in the hypothesized network, particularly temporal pole and anterior insula. All patients with impaired affective empathy were also impaired in comprehension of affective prosody, but many patients with impairments in prosodic comprehension had spared affective empathy. Patients with impaired affective empathy were older, but showed no difference in performance on tests of hemispatial neglect, volume of infarct or sex distribution compared with patients with intact affective empathy. PMID:23824490

Behavioral and Neurochemical Effects of Alpha-Lipoic Acid in the Model of Parkinson’s Disease Induced by Unilateral Stereotaxic Injection of 6-Ohda in Rat

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Dayane Pessoa de Araújo

2013-01-01

Full Text Available This study aimed to investigate behavioral and neurochemical effects of α-lipoic acid (100 mg/kg or 200 mg/kg alone or associated with L-DOPA using an animal model of Parkinson’s disease induced by stereotaxic injection of 6-hydroxydopamine (6-OHDA in rat striatum. Motor behavior was assessed by monitoring body rotations induced by apomorphine, open field test and cylinder test. Oxidative stress was accessed by determination of lipid peroxidation using the TBARS method, concentration of nitrite and evaluation of catalase activity. α-Lipoic acid decreased body rotations induced by apomorphine, as well as caused an improvement in motor performance by increasing locomotor activity in the open field test and use of contralateral paw (in the opposite side of the lesion produced by 6-OHDA at cylinder test. α-lipoic acid showed antioxidant effects, decreasing lipid peroxidation and nitrite levels and interacting with antioxidant system by decreasing of endogenous catalase activity. Therefore, α-lipoic acid prevented the damage induced by 6-OHDA or by chronic use of L-DOPA in dopaminergic neurons, suggesting that α-lipoic could be a new therapeutic target for Parkinson's disease prevention and treatment.

Neurochemical binding profiles of novel indole and benzofuran MDMA analogues.

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Shimshoni, Jakob A; Winkler, Ilan; Golan, Ezekiel; Nutt, David

2017-01-01

3,4-Methylenedioxy-N-methylamphetamine (MDMA) has been shown to be effective in the treatment of post-traumatic stress disorder (PTSD) in numerous clinical trials. In the present study, we have characterized the neurochemical binding profiles of three MDMA-benzofuran analogues (1-(benzofuran-5-yl)-propan-2-amine, 5-APB; 1-(benzofuran-6-yl)-N-methylpropan-2-amine, 6-MAPB; 1-(benzofuran-5-yl)-N-methylpropan-2-amine, 5-MAPB) and one MDMA-indole analogue (1-(1H-indol-5-yl)-2-methylamino-propan-1-ol, 5-IT). These compounds were screened as potential second-generation anti-PTSD drugs, against a battery of human and non-human receptors, transporters, and enzymes, and their potencies as 5-HT 2 receptor agonist and monoamine uptake inhibitors determined. All MDMA analogues displayed high binding affinities for 5-HT 2a,b,c and NE α2 receptors, as well as significant 5-HT, DA, and NE uptake inhibition. 5-APB revealed significant agonist activity at the 5-HT 2a,b,c receptors, while 6-MAPB, 5-MAPB, and 5-IT exhibited significant agonist activity at the 5-HT 2c receptor. There was a lack of correlation between the results of functional uptake and the monoamine transporter binding assay. MDMA analogues emerged as potent and selective monoamine oxidase A inhibitors. Based on 6-MAPB favorable pharmacological profile, it was further subjected to IC 50 determination for monoamine transporters. Overall, all MDMA analogues displayed higher monoamine receptor/transporter binding affinities and agonist activity at the 5-HT 2a,c receptors as compared to MDMA.

Neurochemical Evidence of Potential Neurotoxicity After Prophylactic Cranial Irradiation

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Kalm, Marie, E-mail: marie.kalm@neuro.gu.se [Department of Clinical Neuroscience and Rehabilitation, Insitute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Abel, Edvard [Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Wasling, Pontus [Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Nyman, Jan [Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Hietala, Max Albert [Department of Neurology, Karolinska University Hospital, Stockholm (Sweden); Bremell, Daniel; Hagberg, Lars [Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Elam, Mikael [Department of Clinical Neuroscience and Rehabilitation, Insitute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Blennow, Kaj [Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal (Sweden); Björk-Eriksson, Thomas [Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg (Sweden); Zetterberg, Henrik [Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal (Sweden); UCL Institute of Neurology, London (United Kingdom)

2014-07-01

Purpose: To examine whether cerebrospinal fluid biomarkers for neuroaxonal damage, neuroglial activation, and amyloid β–related processes could characterize the neurochemical response to cranial radiation. Methods and Materials: Before prophylactic cranial irradiation (PCI) of patients with small cell lung cancer, each patient underwent magnetic resonance imaging of the brain, lumbar puncture, and Mini-Mental State Examination of cognitive function. These examinations were repeated at approximately 3 and 12 months after radiation. Results: The major findings were as follows. (1) Cerebrospinal fluid markers for neuronal and neuroglial injury were elevated during the subacute phase after PCI. Neurofilament and T-tau increased 120% and 50%, respectively, after PCI (P<.05). The same was seen for the neuroglial markers YKL-40 and glial fibrillary acidic protein, which increased 144% and 106%, respectively, after PCI (P<.05). (2) The levels of secreted amyloid precursor protein-α and -β were reduced 44% and 46%, respectively, 3 months after PCI, and the levels continued to decrease as long as 1 year after treatment (P<.05). (3) Mini-Mental State Examination did not reveal any cognitive decline, indicating that a more sensitive test should be used in future studies. Conclusion: In conclusion, we were able to detect radiation therapy–induced changes in several markers reflecting neuronal injury, inflammatory/astroglial activation, and altered amyloid precursor protein/amyloid β metabolism, despite the low number of patients and quite moderate radiation doses (20-30 Gy). These changes are hypothesis generating and could potentially be used to assess the individual risk of developing long-term symptoms of chronic encephalopathy after PCI. This has to be evaluated in large studies with extended clinical follow-up and more detailed neurocognitive assessments.

Neurochemical Evidence of Potential Neurotoxicity After Prophylactic Cranial Irradiation

International Nuclear Information System (INIS)

Kalm, Marie; Abel, Edvard; Wasling, Pontus; Nyman, Jan; Hietala, Max Albert; Bremell, Daniel; Hagberg, Lars; Elam, Mikael; Blennow, Kaj; Björk-Eriksson, Thomas; Zetterberg, Henrik

2014-01-01

Purpose: To examine whether cerebrospinal fluid biomarkers for neuroaxonal damage, neuroglial activation, and amyloid β–related processes could characterize the neurochemical response to cranial radiation. Methods and Materials: Before prophylactic cranial irradiation (PCI) of patients with small cell lung cancer, each patient underwent magnetic resonance imaging of the brain, lumbar puncture, and Mini-Mental State Examination of cognitive function. These examinations were repeated at approximately 3 and 12 months after radiation. Results: The major findings were as follows. (1) Cerebrospinal fluid markers for neuronal and neuroglial injury were elevated during the subacute phase after PCI. Neurofilament and T-tau increased 120% and 50%, respectively, after PCI (P<.05). The same was seen for the neuroglial markers YKL-40 and glial fibrillary acidic protein, which increased 144% and 106%, respectively, after PCI (P<.05). (2) The levels of secreted amyloid precursor protein-α and -β were reduced 44% and 46%, respectively, 3 months after PCI, and the levels continued to decrease as long as 1 year after treatment (P<.05). (3) Mini-Mental State Examination did not reveal any cognitive decline, indicating that a more sensitive test should be used in future studies. Conclusion: In conclusion, we were able to detect radiation therapy–induced changes in several markers reflecting neuronal injury, inflammatory/astroglial activation, and altered amyloid precursor protein/amyloid β metabolism, despite the low number of patients and quite moderate radiation doses (20-30 Gy). These changes are hypothesis generating and could potentially be used to assess the individual risk of developing long-term symptoms of chronic encephalopathy after PCI. This has to be evaluated in large studies with extended clinical follow-up and more detailed neurocognitive assessments

[Visual impairment and blindness in children in a Malawian school for the blind].

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Schulze Schwering, M; Nyrenda, M; Spitzer, M S; Kalua, K

2013-08-01

The aim of this study was to determine the anatomic sites of severe visual impairment and blindness in children in an integrated school for the blind in Malawi, and to compare the results with those of previous Malawian blind school studies. Children attending an integrated school for the blind in Malawi were examined in September 2011 using the standard WHO/PBL eye examination record for children with blindness and low vision. Visual acuity [VA] of the better eye was classified using the standardised WHO reporting form. Fifty-five pupils aged 6 to 19 years were examined, 39 (71 %) males, and 16 (29 %) females. Thirty eight (69%) were blind [BL], 8 (15 %) were severely visually impaired [SVI], 8 (15 %) visually impaired [VI], and 1 (1.8 %) was not visually impaired [NVI]. The major anatomic sites of visual loss were optic nerve (16 %) and retina (16 %), followed by lens/cataract (15 %), cornea (11 %) and lesions of the whole globe (11 %), uveal pathologies (6 %) and cortical blindness (2 %). The exact aetiology of VI or BL could not be determined in most children. Albinism accounted for 13 % (7/55) of the visual impairments. 24 % of the cases were considered to be potentially avoidable: refractive amblyopia among pseudophakic patients and corneal scaring. Optic atrophy, retinal diseases (mostly albinism) and cataracts were the major causes of severe visual impairment and blindness in children in an integrated school for the blind in Malawi. Corneal scarring was now the fourth cause of visual impairment, compared to being the commonest cause 35 years ago. Congenital cataract and its postoperative outcome were the commonest remedial causes of visual impairment. Georg Thieme Verlag KG Stuttgart · New York.

Cause of impaired carbohydrate metabolism in hyperthyroidism

International Nuclear Information System (INIS)

Foeldes, J.; Megyesi, K.; Koranyi, L.

1984-01-01

Hyperthyroidism (HT) affects glucose metabolism in various ways. The role of insulin, glucagon and growth-hormone (GH) was determined. After glucose loading the insulin response is weaker in HT than in euthyroid subjects. Enhanced degradation of insulin has been reported. It is suggested that in HT the serum insulin concentration declines at a slightly accelerated rate. In HT the deranged carbohydrate metabolism might be a consequence of altered tissue sensitivity to insulin. To elucidate this problem insulin receptors on erythrocytes obtained from hyperthyroid women were investigated. The maximal specific binding of 125 I-insulin to RBC of hyperthyroid patients was decreased and the analysis refers to a decreased receptor concentration in RBC. The nature of glucagon secretion and its influence on glucose metabolism in HT was investigated. The basal plasma glucagon is elevated in hyperthyroid patients. The suppression of glucagon secretion induced by an oral glucose loading was of significantly lesser degree in hyperthyroid patients than in controls. Applying the erythrocyte receptor assay a decreased specific binding of 125 I-glucagon to RBC of hyperthyroid patients has been found and data indicate a significantly less glucagon receptor concentration in thyrotoxicosis. Physiological elevations of serum GH levels led to a significant impairment of glucose metabolism. Beside the GH-RH and somatostatin, the dopaminergic neurotransmitter system participates in the regulation of GH secretion too. It has been demonstrated that after administration of the dopamine agonist l-dopa the GH response was weaker in HT than in controls. This indicates that in thyrotoxicosis the GH secretion can not be stimulated in such a degree as in euthyroidism. (author)

Cause of impaired carbohydrate metabolism in hyperthyroidism

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Foeldes, J.; Megyesi, K.; Koranyi, L. (Semmelweis Orvostudomanyi Egyetem, Budapest (Hungary))

1984-01-01

Hyperthyroidism (HT) affects glucose metabolism in various ways. The role of insulin, glucagon and growth-hormone (GH) was determined. After glucose loading the insulin response is weaker in HT than in euthyroid subjects. Enhanced degradation of insulin has been reported. It is suggested that in HT the serum insulin concentration declines at a slightly accelerated rate. In HT the deranged carbohydrate metabolism might be a consequence of altered tissue sensitivity to insulin. To elucidate this problem insulin receptors on erythrocytes obtained from hyperthyroid women were investigated. The maximal specific binding of /sup 125/I-insulin to RBC of hyperthyroid patients was decreased and the analysis refers to a decreased receptor concentration in RBC. The nature of glucagon secretion and its influence on glucose metabolism in HT was investigated. The basal plasma glucagon is elevated in hyperthyroid patients. The suppression of glucagon secretion induced by an oral glucose loading was of significantly lesser degree in hyperthyroid patients than in controls. Applying the erythrocyte receptor assay a decreased specific binding of /sup 125/I-glucagon to RBC of hyperthyroid patients has been found and data indicate a significantly less glucagon receptor concentration in thyrotoxicosis. Physiological elevations of serum GH levels led to a significant impairment of glucose metabolism. Beside the GH-RH and somatostatin, the dopaminergic neurotransmitter system participates in the regulation of GH secretion too. It has been demonstrated that after administration of the dopamine agonist l-dopa the GH response was weaker in HT than in controls. This indicates that in thyrotoxicosis the GH secretion can not be stimulated in such a degree as in euthyroidism.

One Minute of Marijuana Secondhand Smoke Exposure Substantially Impairs Vascular Endothelial Function.

Science.gov (United States)

Wang, Xiaoyin; Derakhshandeh, Ronak; Liu, Jiangtao; Narayan, Shilpa; Nabavizadeh, Pooneh; Le, Stephenie; Danforth, Olivia M; Pinnamaneni, Kranthi; Rodriguez, Hilda J; Luu, Emmy; Sievers, Richard E; Schick, Suzaynn F; Glantz, Stanton A; Springer, Matthew L

2016-07-27

Despite public awareness that tobacco secondhand smoke (SHS) is harmful, many people still assume that marijuana SHS is benign. Debates about whether smoke-free laws should include marijuana are becoming increasingly widespread as marijuana is legalized and the cannabis industry grows. Lack of evidence for marijuana SHS causing acute cardiovascular harm is frequently mistaken for evidence that it is harmless, despite chemical and physical similarity between marijuana and tobacco smoke. We investigated whether brief exposure to marijuana SHS causes acute vascular endothelial dysfunction. We measured endothelial function as femoral artery flow-mediated dilation (FMD) in rats before and after exposure to marijuana SHS at levels similar to real-world tobacco SHS conditions. One minute of exposure to marijuana SHS impaired FMD to a comparable extent as impairment from equal concentrations of tobacco SHS, but recovery was considerably slower for marijuana. Exposure to marijuana SHS directly caused cannabinoid-independent vasodilation that subsided within 25 minutes, whereas FMD remained impaired for at least 90 minutes. Impairment occurred even when marijuana lacked cannabinoids and rolling paper was omitted. Endothelium-independent vasodilation by nitroglycerin administration was not impaired. FMD was not impaired by exposure to chamber air. One minute of exposure to marijuana SHS substantially impairs endothelial function in rats for at least 90 minutes, considerably longer than comparable impairment by tobacco SHS. Impairment of FMD does not require cannabinoids, nicotine, or rolling paper smoke. Our findings in rats suggest that SHS can exert similar adverse cardiovascular effects regardless of whether it is from tobacco or marijuana. © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

Research advances in indicators for early diagnosis of liver cirrhosis patients with renal impairment

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LU Lifang

2016-09-01

Full Text Available The liver is closely associated with the kidney, and liver injury in various stages can cause various kidney diseases to varying degrees, which further lead to renal impairment. Such renal impairment in the early stage is often functional and can be reversed by drugs, otherwise it can progress to hepatorenal syndrome, cause acute renal failure, and even threaten human life. The indicators such as serum creatinine and urea nitrogen have a limited effect in the early diagnosis of renal impairment and cannot be used for early monitoring and diagnosis of liver cirrhosis patients with renal impairment. Therefore, early monitoring of liver cirrhosis patients with renal impairment has always been a hot topic in this field. This article summarizes the research advances in the indicators for early diagnosis of renal impairment.

Effect of Somatosensory Impairments on Balance Control

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Alireza Hassanpour

2012-10-01

Full Text Available Background and Aim: The somatosensory system is one of the most effective systems in balance control. It consists of peripheral and central components. Knowing the role of these components in balance control assists the developing of effective rehabilitation protocols. In some diseases peripheral components and in others central components are impaired. This paper reviews the effect of impairment of peripheral and central components of the somatosensory system on balance control.Methods: In this study publication about somatosensory impairments from 1983 through 2011 in PubMed, Scopus, ProQuest, Google Scholar, Iran Medex, Iran Doc and Magiran were reviewed. Medical subject headings terms and keywords related to balance, somatosensory, somatosensory loss, and sensory integration/processing were used to perform the searches.Conclusion: Somatosensory impairments either with peripheral or central origin, can cause problems in balance control. However, these problems are not considered in some patients. In these impairments, balance training is recommended to be used alongside other routine treatments in the patients' rehabilitation programs.

Modulatory effect of cilostazol on tramadol-induced behavioral and neurochemical alterations in rats challenged across the forced swim despair test

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Noha M. Gamil

2016-06-01

Full Text Available Pain-associated depression is encountered clinically in some cases such as cancer, chronic neuropathy, and after operations. Tramadol is an opioid analgesic drug that may modulate monoaminergic neurotransmission by inhibition of noradrenaline and serotonin reuptake that may contribute to its antidepressant-like effects. Clinically, tramadol is used either alone or in combination with other NSAIDs in the treatment of cases associated with pain and depression, e.g. low back pain, spinal cord injury, and post-operative pain management. However, tramadol monotherapy as an antidepressant is impeded by severe adverse effects including seizures and serotonin syndrome. Interestingly, phosphodiesterase-III inhibitors demonstrated novel promising antidepressant effects. Among which, cilostazol was reported to attenuate depression in post-stroke cases, geriatrics and patients undergoing carotid artery stenting. Therefore, this study was carried out to investigate the possible antidepressant-like effects of tramadol and/or cilostazol on the behavioral level in experimental animals, and to examine the neurochemical and biochemical effects of tramadol, cilostazol and their combination in rats, in order to explore the probable mechanisms of action underlying their effects. To achieve our target, male albino mice and rats were randomly allocated into five groups and administered either vehicle for control, fluoxetine (20 mg/kg, p.o., tramadol HCl (20 mg/kg, p.o., cilostazol (100 mg/kg, p.o., or combination of both tramadol and cilostazol. At day 14, mice and rats were challenged in the tail suspension test and forced swim test, respectively. Rats were sacrificed and brains were isolated for determination of brain monoamines, MDA, NO, SOD, and TNF-α. The current results showed that concurrent administration of cilostazol to tramadol-treated animals modulated depression on the behavioral level, and showed ameliorative neurochemical and biochemical effects

[Clinical characteristics in Parkinson's disease patients with cognitive impairment and effects of cognitive impairment on sleep].

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Gong, Yan; Xiong, Kang-ping; Mao, Cheng-jie; Huang, Juan-ying; Hu, Wei-dong; Han, Fei; Chen, Rui; Liu, Chun-feng

2013-09-03

To analyze the clinical characteristics, correlation factors and clinical heterogeneities in Parkinson's disease (PD) patients with cognitive impairment and identify whether cognitive impairment could influence the aspect of sleep. A total of 130 PD outpatients and inpatients of sleep center at our hospital were eligible for participation. According to Montreal cognitive assessment (MOCA), they were divided into cognitive normal group (MOCA ≥ 26) (n = 51) and cognitive impairment group (MOCA cognitive impairment (MOCA cognitive impairment, the PD patients with cognitive impairment had significantly higher score of HAMD (10 ± 7 vs 7 ± 4), increased incidence of hallucinations (40.50% vs 19.60%) and REM behavior disorders (RBD) (63.29% vs 39.21%), significantly higher H-Y stage [2.5(2.0-3.0) vs 2.0 (2.0-2.5)] , United Kingdom Parkinson Disease Society (UPDRS) part III (22 ± 10 vs 19 ± 10) and levodopa-equivalent daily dose (LED) (511 ± 302vs 380 ± 272) (all P 0.05). Non-conditional Logistic regression analysis showed that PD duration, score of HAMD and H-Y stage were the major influencing factors of cognition. On PSG, significantly decreased sleep efficiency (57% ± 21% vs 66% ± 17%), higher percentage of non-REM sleep stage 1 (NREMS1) (37% ± 21% vs 27% ± 13%), lower percentage of NREMS2 (40% ± 17% vs 46% ± 13%) and REM sleep (39% ± 28% vs 54% ± 36%) were found for PD patients with cognitive impairment (all P cognitive impairment have more severe disease and partial nonmotor symptoms. And the severity of disease and depression is closely associated with cognitive impairment. Cognitive impairment may also affect sleep to cause decreased sleep efficiency and severe sleep structure disorder.

Hippocampal neurochemical changes in senescent mice induced with chronic injection of D-galactose and NaNO₂: an in vitro high-resolution NMR spectroscopy study at 9.4T.

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Yan Lin

Full Text Available Proton magnetic resonance spectroscopy (¹H-MRS has been used to provide useful information about the neurochemical changes reflecting early pathological alterations in Alzheimer's disease (AD brain. In this study, we have longitudinally measured the hippocampal neurochemical profile in vitro in senescent mice induced with chronic injection of D-Galactose and NaNO₂, at different time point from day 30 to day 70 with a 10-day interval. Pathological brain alterations induced by D-Galactose and NaNO₂ were monitored through hematoxylin and eosin (HE staining, Congo red staining and bielschowsky silver staining, and the cognition deficits were assessed via Morris Water Maze (MWM test. This D-galactose and NaNO₂ treated mouse model, characterized by an early-onset memory dysfunction, a robust neuronal loss, amyloid plaques and neurofibrillary tangles in hippocampal subdivision, well mimics a prodromal Alzheimer's phenotype. Consistent with previously published in vivo ¹H MRS findings in human AD patients and AD transgenic mice, our in vitro ¹H MRS on the perchloric acid extractions of hippocampus in senescent mice observed significant decreases of N-acetylaspartate (NAA and Glutamate (Glu but an increase in Myo-inositol (mIns. Elevated mIns occurred prior to the reduction of NAA and Glu during the progression of aging. In addition, changes in mIns, NAA and Glu were found to precede pathological abnormalities. Overall, our in vitro findings in senescent mice validated the concept that hippocampal neurochemical alternations preceded the pathological changes of the brain, and could serve as potential markers of AD progression. Reductions of NAA and Glu can be interpreted in terms of neuronal degeneration and dysfunctions in glutamatergic activity that may contribute to the pathophysiological mechanisms underlying AD. Elevated mIns might be related to glial activation. Further experiments are needed to explore the potential value of mIns in the

GRM7 variants confer susceptibility to age-related hearing impairment

DEFF Research Database (Denmark)

Friedman, Rick A; Van Laer, Lut; Huentelman, Matthew J

2009-01-01

Age-related hearing impairment (ARHI), or presbycusis, is the most prevalent sensory impairment in the elderly. ARHI is a complex disease caused by an interaction between environmental and genetic factors. Here we describe the results of the first whole genome association study for ARHI. The stud...

Post-stroke cognitive impairment: epidemiology, mechanisms and management

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Sun, Jia-Hao

2014-01-01

Post-stroke cognitive impairment occurs frequently in the patients with stroke. The prevalence of post-stroke cognitive impairment ranges from 20% to 80%, which varies for the difference between the countries, the races, and the diagnostic criteria. The risk of post-stroke cognitive impairment is related to both the demographic factors like age, education and occupation and vascular factors. The underlying mechanisms of post-stroke cognitive impairment are not known in detail. However, the neuroanatomical lesions caused by the stroke on strategic areas such as the hippocampus and the white matter lesions (WMLs), the cerebral microbleeds (CMBs) due to the small cerebrovascular diseases and the mixed AD with stroke, alone or in combination, contribute to the pathogenesis of post-stroke cognitive impairment. The treatment of post-stroke cognitive impairment may benefit not only from the anti-dementia drugs, but also the manage measures on cerebrovascular diseases. In this review, we will describe the epidemiological features and the mechanisms of post-stroke cognitive impairment, and discuss the promising management strategies for these patients. PMID:25333055

COPA mutations impair ER-Golgi transport causing hereditary autoimmune-mediated lung disease and arthritis

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Watkin, Levi B.; Jessen, Birthe; Wiszniewski, Wojciech; Vece, Timothy; Jan, Max; Sha, Youbao; Thamsen, Maike; Santos-Cortez, Regie L. P.; Lee, Kwanghyuk; Gambin, Tomasz; Forbes, Lisa; Law, Christopher S.; Stray-Petersen, Asbjørg; Cheng, Mickie H.; Mace, Emily M.; Anderson, Mark S.; Liu, Dongfang; Tang, Ling Fung; Nicholas, Sarah K.; Nahmod, Karen; Makedonas, George; Canter, Debra; Kwok, Pui-Yan; Hicks, John; Jones, Kirk D.; Penney, Samantha; Jhangiani, Shalini N.; Rosenblum, Michael D.; Dell, Sharon D.; Waterfield, Michael R.; Papa, Feroz R.; Muzny, Donna M.; Zaitlen, Noah; Leal, Suzanne M.; Gonzaga-Jauregui, Claudia; Boerwinkle, Eric; Eissa, N. Tony; Gibbs, Richard A.; Lupski, James R.; Orange, Jordan S.; Shum, Anthony K.

2015-01-01

Advances in genomics have allowed unbiased genetic studies of human disease with unexpected insights into the molecular mechanisms of cellular immunity and autoimmunity1. We performed whole exome sequencing (WES) and targeted sequencing in patients with an apparent Mendelian syndrome of autoimmune disease characterized by high-titer autoantibodies, inflammatory arthritis and interstitial lung disease (ILD). In five families, we identified four unique deleterious variants in the Coatomer subunit alpha (COPA) gene all located within the same functional domain. We hypothesized that mutant COPA leads to a defect in intracellular transport mediated by coat protein complex I (COPI)2–4. We show that COPA variants impair binding of proteins targeted for retrograde Golgi to ER transport and demonstrate that expression of mutant COPA leads to ER stress and the upregulation of Th17 priming cytokines. Consistent with this pattern of cytokine expression, patients demonstrated a significant skewing of CD4+ T cells toward a T helper 17 (Th17) phenotype, an effector T cell population implicated in autoimmunity5,6. Our findings uncover an unexpected molecular link between a vesicular transport protein and a syndrome of autoimmunity manifested by lung and joint disease. These findings provide a unique opportunity to understand how alterations in cellular homeostasis caused by a defect in the intracellular trafficking pathway leads to the generation of human autoimmune disease. PMID:25894502

45 CFR 1308.17 - Eligibility criteria: Other impairments.

Science.gov (United States)

2010-10-01

... classified as deaf-blind, whose concomitant hearing and visual impairments cause such severe communication... areas: physical development, cognitive development, communication development, social or emotional...

Epinephrine and glucose modulate training-related CREB phosphorylation in old rats: relationships to age-related memory impairments.

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Morris, Ken A; Gold, Paul E

2013-02-01

Epinephrine enhances memory in young adult rats, in part, by increasing blood glucose levels needed to modulate memory. In old rats, epinephrine is deficient at raising blood glucose levels and thus is only moderately effective at enhancing memory. In contrast, systemic glucose injections improve memory in old rats, with resulting memory performance equal to that of young rats. The diminished response of glucose to training in old rats may blunt downstream neurochemical and molecular mechanisms needed to upregulate memory processes. In the first experiment, young adult and old rats were trained on an inhibitory avoidance task with immediate post-training injections of aCSF or glucose into the dorsal hippocampus. Old rats had significant memory impairments compared to young rats 7 days after training. Intrahippocampal injections of glucose reversed age-related deficits, improving memory scores in old rats to values seen in young rats. A second experiment examined age-related changes in activation of the transcription factor CREB, which is widely implicated in memory formation and may act downstream of hormonal and metabolic signals. Activation was assessed in response to training with systemic injections of epinephrine and glucose at doses known to enhance memory. Young adult and old rats were trained on inhibitory avoidance with immediate post-training systemic injections of saline, epinephrine, or glucose. After training, old rats had significant impairments in CREB phosphorylation in area CA1 and the dentate gyrus region of the hippocampus, and in the basolateral and lateral amygdala. Epinephrine and glucose attenuated age-related deficits in CREB phosphorylation, but were more effective in the amygdala and hippocampus, respectively. Together, these results support the view that age-related changes in blood glucose responses to epinephrine contribute to memory impairments, which may be related to alterations in regional patterns of CREB phosphorylation. Copyright

A High-Fat Diet Causes Impairment in Hippocampal Memory and Sex-Dependent Alterations in Peripheral Metabolism

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Erica L. Underwood

2016-01-01

Full Text Available While high-fat diets are associated with rising incidence of obesity/type-2 diabetes and can induce metabolic and cognitive deficits, sex-dependent comparisons are rarely systematically made. Effects of exclusive consumption of a high-fat diet (HFD on systemic metabolism and on behavioral measures of hippocampal-dependent memory were compared in young male and female LE rats. Littermates were fed from weaning either a HFD or a control diet (CD for 12 wk prior to testing. Sex-different effects of the HFD were observed in classic metabolic signs associated with type-2 diabetes. Males fed the HFD became obese, and had elevated fasted blood glucose levels, elevated corticosterone, and impaired glucose-tolerance, while females on the HFD exhibited only elevated corticosterone. Regardless of peripheral metabolism alteration, rats of both sexes fed the HFD were equally impaired in a spatial object recognition memory task associated with impaired hippocampal function. While the metabolic changes reported here have been characterized previously in males, the set of diet-induced effects observed here in females are novel. Impaired memory can have significant cognitive consequences, over the short-term and over the lifespan. A significant need exists for comparative research into sex-dependent differences underlying obesity and metabolic syndromes relating systemic, cognitive, and neural plasticity mechanisms.

Investigación neuroquímica cerebral y aplicación preventiva para la reducción de los índices de criminalidad/Neurochemical brain research and it’s preventive application to reduce the crime statistics

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Osvaldo Tieghi (Argentina

2014-01-01

Full Text Available Investigación neuroquímica cerebral y aplicación preventiva para la reducción de los índices de criminalidad Neurochemical brain research and it’s preventive application to reduce the crime statistics

[National survey of blindness and avoidable visual impairment in Argentina, 2013].

Science.gov (United States)

Barrenechea, Rosario; de la Fuente, Inés; Plaza, Roberto Gustavo; Flores, Nadia; Segovia, Lía; Villagómez, Zaida; Camarero, Esteban Elián; Zepeda-Romero, Luz Consuelo; Lansingh, Van C; Limburg, Hans; Silva, Juan Carlos

2015-01-01

Determine the prevalence of blindness and avoidable visual impairment in Argentina, its causes, the coverage of cataract surgery, and the barriers that hinder access to these services. Cross-sectional population study conducted between May and November 2013 using the standard methodology for rapid assessment of avoidable blindness (RAAB), with a random cluster sampling of 50 people aged 50 years or more, -representative of the entire country. Participants' visual acuity (VA) was measured and the lens and posterior pole were examined by direct ophthalmoscopy. An assessment was made of the causes of having VA blindness was 0.7% (confidence interval of 95%: 0.4-1.0%). Unoperated cataract was the main cause of blindness and severe visual impairment (44.0% and 71.1%, respectively), while the main cause of moderate visual impairment was uncorrected refractive errors (77.8%). Coverage of cataract surgery was of 97.1%, and 82.0% of operated eyes achieved VA ≥ 20/60. The main barriers to receiving this treatment were fear of the surgical procedure or of a poor result (34.9%), the cost (30.2%), and not having access to the treatment (16.3%). There is a low prevalence of blindness in the studied population and cataract is the main cause of blindness and severe visual impairment. Efforts should continue to extend coverage of cataract surgery, enhance preoperative evaluation, improve calculations of the intraocular lenses that patients need, and correct post-operative refractive errors with greater precision.

Epidemiology, aetiology and management of visual impairment in children.

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Solebo, Ameenat Lola; Rahi, Jugnoo

2014-04-01

An estimated 19 million of the world's children are visually impaired, while 1.4 million are blind. Using the UK as a model for high income countries, from a population-based incidence study, the annual cumulative incidence of severe visual impairment/blindness (SVL/BL) is estimated to be 6/10 000 by age 15 years, with the incidence being highest in the first year of life. The population of visually impaired children within high, middle and lower income countries differ considerably between and within countries. The numerous and mainly uncommon disorders which can cause impaired vision result in heterogeneous population which includes a substantial proportion (for SVI/BL, the majority) of children with additional systemic disorders or impairments whose needs differ substantially from those with isolated vision impairment. Paediatricians and other paediatric professionals have a key role in early detection and multidisciplinary management to minimise the impact of visual impairment (VI) in childhood.

Putting theory of mind in its place: psychological explanations of the socio-emotional-communicative impairments in autistic spectrum disorder.

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Boucher, Jill

2012-05-01

In this review, the history of the theory of mind (ToM) theory of autistic spectrum disorder (ASD) is outlined (in which ToM is indexed by success on false belief tasks), and the explanatory power and psychological causes of impaired ToM in ASD are critically discussed. It is concluded that impaired ToM by itself has only limited explanatory power, but that explorations of the psychological precursors of impaired ToM have been fruitful in increasing understanding of mindreading impairments in ASD (where 'mindreading' refers those abilities that underlie triadic interaction as well as ToM). It is argued that early explanations of impaired mindreading are untenable for various reasons, but that impairments of dyadic interaction in ASD that could lead to impaired ability to represent others' mental states may be the critical psychological cause, or causes, of impaired ToM. The complexity of causal routes to impaired ToM is emphasized.

Measuring and managing cognitive impairment in HIV.

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Nightingale, Sam; Winston, Alan

2017-06-01

: Cognitive impairment remains a frequently reported complaint in HIV-positive patients despite virologically suppressive antiretroviral therapy. Rates of cognitive impairment in antiretroviral treated HIV-positive cohorts vary and strongly depend on definitions utilized.The underlying pathogenesis is likely to be multifactorial and includes immune activation, neuroinflammation, antiretroviral neurotoxicity, the presence of noninfectious comorbidities such as vascular disease and depression and patient lifestyle factors such as recreational drug use.Contributing factors to cognitive impairment may change over time with ageing HIV-positive populations. Cerebrovascular disease and neurodegenerative causes of cognitive impairment may become more common with advancing age; how these factors interact with HIV-associated cognitive impairment is not yet known.Cerebrospinal fluid HIV RNA escape may occur in up to 10% of patients undergoing lumbar puncture clinically and can be associated with compartmentalized and resistant virus.Changes in antiretroviral therapy in patients with cognitive impairment should be based on current and historic resistance profiles of cerebrospinal fluid and plasma virus, or on potential antiretroviral drug neurotoxicity. Whether and how antiretroviral therapy should be changed in the absence of these factors is not known and requires study in adequately powered randomized trials in carefully selected clinical cohorts.

Agmatine for combined treatment of epilepsy, depression and cognitive impairment in chronic epileptic animals.

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Singh, Tanveer; Bagga, Neetu; Kaur, Anureet; Kaur, Navjot; Gawande, Dinesh Yugraj; Goel, Rajesh Kumar

2017-08-01

Epilepsy is fourth most common neurological disorders associated with depression and cognitive deficits. As per present scenario, none of the antiseizure drugs have been reported successful to have ameliorative effect on epilepsy associated depression and cognitive deficits. Thus, the study was envisioned to assess an ameliorative potential of agmatine on epilepsy and its efficacy and safety for management of associated depression and cognitive deficits. The animals were made epileptic employing pentylenetetrazole (35mg/kg i.p. every 48±2h) kindling model of epilepsy and subsequently were treated with vehicle, valproic acid (300mg/kg/day i.p.) and agmatine (2.5, 5, and 10mg/kg)/day/i.p. for 15days. Except naïve, all the groups were challenged with same pentylenetetrazole dose as employed during kindling on days 5, 10, and 15 to evaluate seizure severity. Two hours after seizure severity test, tail suspension test and passive shock avoidance paradigm was employed to evaluate depression and cognitive behavior respectively. Results suggested that epileptic animals were significantly associated with depression and cognitive impairment. Chronic valproate treatment significantly reduced seizure severity, but was found unable to mitigate depression and cognitive deficits. However, agmatine treatment dose dependently ameliorated seizure severity as well as associated depression and cognitive deficits. On 15th day, animals were euthanized and pertinent neurochemical estimations were carried out in cortical and hippocampal areas of the mice brain. Thus, study concluded that agmatine ameliorated seizure severity, depression and cognitive impairment in epileptic animals, possibly via restoring glutamate-GABA neurotransmission and serotonin synthesis with decreased nitrosative stress. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Hearing impairment after childhood bacterial meningitis dependent on etiology in Luanda, Angola.

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Karppinen, Mariia; Pelkonen, Tuula; Roine, Irmeli; Cruzeiro, Manuel Leite; Peltola, Heikki; Pitkäranta, Anne

2015-11-01

Childhood bacterial meningitis (BM) damages hearing, but the potential of different agents to cause impairment in developing countries is poorly understood. We compared the extent of hearing impairment in BM caused by Haemophilus influenzae type b (Hib), Streptococcus pneumoniae or Neisseria meningitidis among children aged 2 months to 13 years in Luanda, Angola. Hearing of 685 ears of 351 (78%) survivors among 723 enrolled patients was tested by brainstem-evoked response audiometry on day 7 of hospitalization. The causative agent was sought by cerebrospinal fluid culture, PCR or the latex-agglutination test. Altogether, 45 (12%) of the survivors were deaf (threshold >80 dB), and 20 (6%) had a threshold of 80 dB. The incidence of any kind of hearing loss, with ≥60 dB, was 34% with Hib, 30% with S. pneumoniae, 19% with N. meningitidis and 33% with other bacteria. Examining all ears combined and using the ≥60 dB threshold, the agents showed dissimilar harm (P=0.005), Hib being the most frequent and N. meningitidis the most infrequent cause. Compared to other agents, S. pneumoniae more often caused deafness (P=0.025) and hearing impairment at ≥60 dB (P=0.017) in infants, whereas this level of hearing loss in older survivors was most commonly caused by Hib (P=0.031). BM among children in Angola is often followed by hearing impairment, but the risk depends on the agent. S. pneumoniae is a major problem among infants, whereas Hib is mainly a risk beyond 12 months. N. meningitidis impairs hearing less frequently. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Neurochemical Metabolomics Reveals Disruption to Sphingolipid Metabolism Following Chronic Haloperidol Administration.

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McClay, Joseph L; Vunck, Sarah A; Batman, Angela M; Crowley, James J; Vann, Robert E; Beardsley, Patrick M; van den Oord, Edwin J

2015-09-01

Haloperidol is an effective antipsychotic drug for treatment of schizophrenia, but prolonged use can lead to debilitating side effects. To better understand the effects of long-term administration, we measured global metabolic changes in mouse brain following 3 mg/kg/day haloperidol for 28 days. These conditions lead to movement-related side effects in mice akin to those observed in patients after prolonged use. Brain tissue was collected following microwave tissue fixation to arrest metabolism and extracted metabolites were assessed using both liquid and gas chromatography mass spectrometry (MS). Over 300 unique compounds were identified across MS platforms. Haloperidol was found to be present in all test samples and not in controls, indicating experimental validity. Twenty-one compounds differed significantly between test and control groups at the p < 0.05 level. Top compounds were robust to analytical method, also being identified via partial least squares discriminant analysis. Four compounds (sphinganine, N-acetylornithine, leucine and adenosine diphosphate) survived correction for multiple testing in a non-parametric analysis using false discovery rate threshold < 0.1. Pathway analysis of nominally significant compounds (p < 0.05) revealed significant findings for sphingolipid metabolism (p = 0.015) and protein biosynthesis (p = 0.024). Altered sphingolipid metabolism is suggestive of disruptions to myelin. This interpretation is supported by our observation of elevated N-acetyl-aspartyl-glutamate in the haloperidol-treated mice (p = 0.004), a marker previously associated with demyelination. This study further demonstrates the utility of murine neurochemical metabolomics as a method to advance understanding of CNS drug effects.

Visual Impairment Registry of Patients from North Kolkata, Eastern India: A Hospital-based Study.

Science.gov (United States)

Bandyopadhyay, Sabyasachi; Bandyopadhyay, Samir Kumar; Biswas, Jaya; Saha Dutta Chowdhury, Mita; Dey, Asim Kumar; Chakrabarti, Asim

2018-01-01

To study the demographic profile, severity and causes of visual impairment among registered patients in a tertiary care hospital in north Kolkata, eastern India, and to assess the magnitude of under-registration in that population. This is a retrospective analytical study. A review of all visually impaired patients registered at our tertiary care hospital during a ten-year period from January 2005 to December 2014, which is entitled for certification of people of north Kolkata, eastern India (with a population denominator of 1.1 million), was performed. Overall, 2472 eyes of 1236 patients were analyzed in terms of demographic characteristics, cause of visual impairment, and percentage of visual disability as per the guidelines established by the government of India. Male patients (844, 68.28%; 95% confidence interval [CI], 65.69-70.87) registered more often than female patients (392; 31.72%, P = 0.0004). The registration rate for visual impairment was 11.24 per 100,000 per annum; this is not the true incidence rate, as both new patients and those visiting for renewal of certification were included in the study. Optic atrophy was the most common cause of visual impairment (384 eyes, 15.53%; 95% CI, 14.1-16.96). Commonest cause of visual impairment was optic atrophy followed by microphthalmos. Under-registration is a prevalent problem as the registration system is voluntary rather than mandatory, and female patients are more likely to be unregistered in this area.

Altered Neurochemical Ingredient of Hippocampus in Patients with Bipolar Depression

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Murad Atmaca

2012-01-01

Full Text Available Background. In a number of investigations, hippocampal neurochemicals were evaluated in the patients with bipolar disorder who were on their first episode or euthymic periods. However, we did not meet any investigation in which only patients with bipolar depression were examined. As a consequence, the objective of the present study was to examine both sides of hippocampus of patients with bipolar disorder in depressive episode and healthy controls using 1H-MRS. Methods. Thirteen patients with DSM-IV bipolar I disorder, most recent episode depressed, were recruited from the Department of Psychiatry at Firat University School of Medicine. We also studied 13 healthy comparison subjects who were without any DSM-IV Axis I disorders recruited from the hospital staff. The patients and controls underwent proton magnetic resonance spectroscopy (1H-MRS of their hippocampus. NAA, CHO, and CRE values were measured. Results. No significant effect of diagnosis was observed for NAA/CRE ratio. For the NAA/CHO ratio, the ANCOVA with age, gender, and whole brain volume as covariates revealed that the patients with bipolar depression had significantly lower ratio compared to healthy control subjects for right and for left side. As for the CHO/CRE ratio, the difference was statistically significant for right side, with an effect diagnosis of F = 4.763, P = 0.038, and was very nearly significant for left side, with an effect diagnosis of F = 3.732, P = 0.064. Conclusions. We found that the patients with bipolar depression had lower NAA/CHO and higher CHO/CRE ratios compared to those of healthy control subjects. The findings of the present study also suggest that there may be a degenerative process concerning the hippocampus morphology in the patients with bipolar depression.

A national survey of musculoskeletal impairment in Rwanda: prevalence, causes and service implications.

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Oluwarantimi Atijosan

Full Text Available BACKGROUND: Accurate information on the prevalence and causes of musculoskeletal impairment (MSI is lacking in low income countries. We present a new survey methodology that is based on sound epidemiological principles and is linked to the World Health Organisation's International Classification of Functioning. METHODS: Clusters were selected with probability proportionate to size. Households were selected within clusters through compact segment sampling. 105 clusters of 80 people (all ages were included. All participants were screened for MSI by a physiotherapist and medical assistant. Possible cases plus a random sample of 10% of non-MSI cases were examined further to ascertain diagnosis, aetiology, quality of life, and treatment needs. FINDINGS: 6757 of 8368 enumerated individuals (80.8% were screened. There were 352 cases, giving an overall prevalence for MSI of 5.2%. (95% CI 4.5-5.9 The prevalence of MSI increased with age and was similar in men and women. Extrapolating these estimates, there are approximately 488,000 MSI diagnoses in Rwanda. Only 8.2% of MSI cases were severe, while the majority were moderate (43.7% or mild (46.3%. Diagnostic categories comprised 11.5% congenital, 31.3% trauma, 3.8% infection, 9.0% neurological, and 44.4% non-traumatic non infective acquired. The most common individual diagnoses were joint disease (13.3%, angular limb deformity (9.7% and fracture mal- and non-union (7.2%. 96% of all cases required further treatment. INTERPRETATION: This survey demonstrates a large burden of MSI in Rwanda, which is mostly untreated. The survey methodology will be useful in other low income countries, to assist with planning services and monitoring trends.

Visual impairment in children and adolescents in Norway.

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Haugen, Olav H; Bredrup, Cecilie; Rødahl, Eyvind

2016-06-01

BACKGROUND Due to failures in reporting and poor data security, the Norwegian Registry of Blindness was closed down in 1995. Since that time, no registration of visual impairment has taken place in Norway. All the other Nordic countries have registries for children and adolescents with visual impairment. The purpose of this study was to survey visual impairments and their causes in children and adolescents, and to assess the need for an ophthalmic registry.MATERIAL AND METHOD Data were collected via the county teaching centres for the visually impaired in the period from 2005 - 2010 on children and adolescents aged less than 20 years with impaired vision (n = 628). This was conducted as a point prevalence study as of 1 January 2004. Visual function, ophthalmological diagnosis, systemic diagnosis and additional functional impairments were recorded.RESULTS Approximately two-thirds of children and adolescents with visual impairment had reduced vision, while one-third were blind. The three largest diagnostic groups were neuro-ophthalmic diseases (37 %), retinal diseases (19 %) and conditions affecting the eyeball in general (14 %). The prevalence of additional functional impairments was high, at 53 %, most often in the form of motor problems or cognitive impairments.INTERPRETATION The results of the study correspond well with similar investigations in the other Nordic countries. Our study shows that the registries associated with teaching for the visually impaired are inadequate in terms of medical data, and this underlines the need for an ophthalmic registry of children and adolescents with visual impairment.

Obstructive sleep apnea and cognitive impairment: Addressing the blood–brain barrier

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Lim, Diane C.; Pack, Allan I.

2013-01-01

SUMMARY Increasing data support a connection between obstructive sleep apnea (OSA) and cognitive impairment but a causal link has yet to be established. Although neuronal loss has been linked to cognitive impairment, emerging theories propose that changes in synaptic plasticity can cause cognitive impairment. Studies demonstrate that disruption to the blood–brain barrier (BBB), which is uniquely structured to tightly maintain homeostasis inside the brain, leads to changes in the brain’s microenvironment and affects synaptic plasticity. Cyclical intermittent hypoxia is a stressor that could disrupt the BBB via molecular responses already known to occur in either OSA patients or animal models of intermittent hypoxia. However, we do not yet know if or how intermittent hypoxia can cause cognitive impairment by mechanisms operating at the BBB. Therefore, we propose that initially, adaptive homeostatic responses at the BBB occur in response to increased oxygen and nutrient demand, specifically through regulation of influx and efflux BBB transporters that alter microvessel permeability. We further hypothesize that although these responses are initially adaptive, these changes in BBB transporters can have long-term consequences that disrupt the brain’s microenvironment and alter synaptic plasticity leading to cognitive impairment. PMID:23541562

Vascular cognitive impairment in Pemphigus vulgaris: a case report

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José Ibiapina Siqueira- Neto

Full Text Available ABSTRACT Pemphigus vulgaris is a systemic auto-immune medical condition that mainly manifests with changes in skin and vasculopathy. This is a case report of a 69-year-old male with confirmed histopathologic diagnosis of Pemphigus vulgaris presenting ulterior Cognitive Impairment, mostly in executive function. The patient was treated using steroids, immunomodulatory therapy, fluoxetine and galantamine. Neuropsychological testing and magnetic resonance (MRI were performed. This is the first report of correlational cognitive impairment with Pemphigus vulgaris in the literature. Physicians should be aware of vascular causes for cognitive impairment in patients presenting auto-immune conditions.

Processing of spatial sounds in the impaired auditory system

DEFF Research Database (Denmark)

Arweiler, Iris

with an intelligibility-weighted “efficiency factor” which revealed that the spectral characteristics of the ER’s caused the reduced benefit. Hearing-impaired listeners were able to utilize the ER energy as effectively as normal-hearing listeners, most likely because binaural processing was not required...... implications for speech perception models and the development of compensation strategies in future generations of hearing instruments.......Understanding speech in complex acoustic environments presents a challenge for most hearing-impaired listeners. In conditions where normal-hearing listeners effortlessly utilize spatial cues to improve speech intelligibility, hearing-impaired listeners often struggle. In this thesis, the influence...

Vision Impairment and Ocular Morbidity in a Refugee Population in Malawi.

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Kaphle, Dinesh; Gyawali, Rajendra; Kandel, Himal; Reading, Angela; Msosa, Joseph Matiya

2016-02-01

To provide screening services and obtain information on the eye health status and distribution of visual impairments in a refugee population of the sole refugee camp in Malawi. A general eye screening at Dzaleka refugee settlement camp was organized in November 2012. Final-year optometry students conducted detailed optometry examinations, including visual acuity (VA) assessment for near and distance, retinoscopy, and subjective refraction in cases with distance VA less than 6/12 or near VA less than N8, anterior and posterior segment evaluation. Their findings were then verified by an optometrist. The World Health Organization definition of vision impairment was followed, and the cause of vision impairment was determined at the end of each examination. Where possible, participants requiring refractive correction were provided spectacles free of cost. Of a total 635 participants examined, around one-half were male with 61% in the 16 to 49 years age group. The overall prevalence of presenting blindness, severe vision impairment, and vision impairment were 1.3% (95% confidence interval [95% CI], 0.5 to 2.4), 0.5% (95% CI, 0.0 to 1.1), and 3.6% (95% CI, 2.3 to 5.2), respectively. Overall vision impairment (VA vision impairment, and vision impairment were cataracts, refractive errors, and corneal opacities, respectively; and more than 90% of the overall vision impairment was avoidable. Refractive errors and presbyopia were the most common morbidity, present in more than two-thirds of the participants examined. Only 5% of all the participants ever had a previous eye examination. The prevalence and causes of blindness and vision impairment in a refugee population are comparable with those of the general population. Lack of basic eye care services in the health center for refugees is a major concern. The health care facility in the settlement camp needs to be upgraded to provide comprehensive eye care including refractive care services.

Annual incidences of visual impairment during 10-year period in Mie prefecture, Japan.

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Ikesugi, Kengo; Ichio, Takako; Tsukitome, Hideyuki; Kondo, Mineo

2017-07-01

To determine the annual incidence of visual impairment in a Japanese population during a 10-year period. We examined the physical disability certificates issued yearly between 2004 and 2013 in Mie prefecture, Japan. During this period 2468 visually impaired people were registered under the newly defined Act on Welfare of the Physically Disabled Persons' criteria. The age, sex distribution, and causes of visual impairment were determined from the certificates. The major causes of visual impairment during the ten-year period were glaucoma (23.3%), diabetic retinopathy (17.3%), retinitis pigmentosa (12.2%), macular degeneration (9.0%), chorioretinal degeneration or high myopia (7.4%), optic atrophy (5.8%), stroke or brain tumor (5.4%) and cataracts (3.7%). The incidence of glaucoma was significantly higher throughout the period (2004-2013), and that of diabetic retinopathy was lower between 2007 and 2013. The incidence of retinitis pigmentosa did not change significantly during the 10-year period. The incidence of macular degeneration tended to increase between 2004 and 2007, but it decreased significantly between 2007 and 2013. The results indicate that in Japan, the rates of the major causes of visual impairment altered in the most recent 10-year period reflecting the recent changes in the social background and advances in ocular and systemic treatment.

2-Phenylethylamine, a constituent of chocolate and wine, causes mitochondrial complex-I inhibition, generation of hydroxyl radicals and depletion of striatal biogenic amines leading to psycho-motor dysfunctions in Balb/c mice.

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Sengupta, T; Mohanakumar, K P

2010-11-01

Behavioral and neurochemical effects of chronic administration of high doses of 2-phenylethylamine (PEA; 25-75 mg/kg, i.p. for up to 7 days) have been investigated in Balb/c mice. Depression and anxiety, as demonstrated respectively by increased floating time in forced swim test, and reduction in number of entries and the time spent in the open arms in an elevated plus maze were observed in these animals. General motor disabilities in terms of akinesia, catalepsy and decreased swimming ability were also observed in these animals. Acute and sub-acute administration of PEA caused significant, dose-dependent depletion of striatal dopamine, and its metabolites levels. PEA caused dose-dependent generation of hydroxyl radicals in vitro in Fenton's reaction in test tubes, in isolated mitochondrial fraction, and in vivo in the striatum of mice. A significant inhibition of NADH-ubiquinone oxidoreductase (complex-I; EC: 1.6.5.3) activity suggests the inhibition in oxidative phosphorylation in the mitochondria resulting in hydroxyl radical generation. Nissl staining and TH immnunohistochemistry in brain sections failed to show any morphological aberrations in dopaminergic neurons or nerve terminals. Long-term over-consumption of PEA containing food items could be a neurological risk factor having significant pathological relevance to disease conditions such as depression or motor dysfunction. However, per-oral administration of higher doses of PEA (75-125 mg/kg; 7 days) failed to cause such overt neurochemical effects in rats, which suggested safe consumption of food items rich in this trace amine by normal population. Copyright © 2010 Elsevier Ltd. All rights reserved.

Prevalence of Refractive Error and Visual Impairment among Rural ...

African Journals Online (AJOL)

Refractive error was the major cause of visual impairment accounting for 54% of all causes in the study group. No child was found wearing ... So, large scale community level screening for refractive error should be conducted and integrated with regular school eye screening programs. Effective strategies need to be devised ...

Long-lasting spatial learning and memory impairments caused by chronic cerebral hypoperfusion associate with a dynamic change of HCN1/HCN2 expression in hippocampal CA1 region.

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Luo, Pan; Lu, Yun; Li, Changjun; Zhou, Mei; Chen, Cheng; Lu, Qing; Xu, Xulin; He, Zhi; Guo, Lianjun

2015-09-01

Chronic cerebral hypoperfusion (CCH) causes learning and memory impairments and increases the risk of Alzheimer disease (AD) and vascular dementia (VD) through several biologically plausible pathways, yet the mechanisms underlying the disease process remained unclear particularly in a temporal manner. We performed permanent bilateral occlusion of the common carotid arteries (two-vessel occlusion, 2VO) to induce CCH. To determine whether hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are altered at different stages of cognitive impairment caused by CCH, adult male SD rats were randomly distributed into sham-operated 4, 8 and 12weeks group, 2VO 4, 8 and 12weeks group. Learning and memory performance were evaluated with Morris water maze (MWM) and long-term potentiation (LTP) was used to address the underlying synaptic mechanisms. Expression of NeuN, HCN1 and HCN2 in hippocampal CA1, DG and CA3 areas was quantified by immunohistochemistry and western blotting. Our data showed that CCH induced a remarkable spatial learning and memory deficits in rats of 2VO 4, 8, and 12weeks group although neuronal loss only occurred after 4weeks of 2VO surgery in CA1. In addition, a significant reduction of HCN1 surface expression in CA1 was observed in the group that suffered 4weeks ischemia but neither 8 nor 12weeks. However, HCN2 surface expression in CA1 increased throughout the ischemia time-scales (4, 8 and 12w). Our findings indicate spatial learning and memory deficits in the CCH model are associated with disturbed HCN1 and HCN2 surface expression in hippocampal CA1. The altered patterns of both HCN1 and HCN2 surface expression may be implicated in the early stage (4w) of spatial learning and memory impairments; and the stable and long-lasting impairments of spatial learning and memory may partially attribute to the up-regulated HCN2 surface expression. Copyright © 2015 Elsevier Inc. All rights reserved.

Arterial stiffness and cognitive impairment.

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Li, Xiaoxuan; Lyu, Peiyuan; Ren, Yanyan; An, Jin; Dong, Yanhong

2017-09-15

damages the cerebral microcirculation, which causes various phenomena associated with cerebral small vessel diseases (CSVDs), such as white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and lacunar infarctions (LIs). The mechanisms underlying the relationship between arterial stiffness and cognitive impairment may also be associated with reductions in white matter and gray matter integrity, medial temporal lobe atrophy and Aβ protein deposition. Engaging in more frequent physical exercise; increasing flavonoid and long-chain n-3 polyunsaturated fatty acid consumption; increasing tea, nitrite, dietary calcium and vitamin D intake; losing weight and taking medications intended to improve insulin sensitivity; quitting smoking; and using antihypertensive drugs and statins are early interventions and lifestyle changes that may be effective in preventing arterial stiffness and thus preventing cognitive impairment. Arterial stiffness is a sensitive predictor of cognitive impairment, and arterial stiffness severity has the potential to serve as an indicator used to facilitate treatments designed to prevent or delay the onset and progression of dementia in elderly individuals. Early treatment of arterial stiffness is beneficial and recommended. Copyright © 2017 Elsevier B.V. All rights reserved.

Effects of melatonin on aluminium-induced neurobehavioral and neurochemical changes in aging rats.

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Allagui, M S; Feriani, A; Saoudi, M; Badraoui, R; Bouoni, Z; Nciri, R; Murat, J C; Elfeki, A

2014-08-01

This study aimed to investigate the potential protective effects of melatonin (Mel) against aluminium-induced neurodegenerative changes in aging Wistar rats (24-28months old). Herein, aluminium chloride (AlCl3) (50mg/kg BW/day) was administered by gavage, and melatonin (Mel) was co-administered to a group of Al-treated rats by an intra-peritoneal injection at a daily dose of 10mg/kg BW for four months. The findings revealed that aluminium administration induced a significant decrease in body weight associated with marked mortality for the old group of rats, which was more pronounced in old Al-treated rats. Behavioural alterations were assessed by 'open fields', 'elevated plus maze' and 'Radial 8-arms maze' tests. The results demonstrated that Mel co-administration alleviated neurobehavioral changes in both old and old Al-treated rats. Melatonin was noted to play a good neuroprotective role, reducing lipid peroxidation (TBARs), and enhancing enzymatic (SOD, CAT and GPx) activities in the brain organs of old control and old Al-treated rats. Mel treatment also reversed the decrease of AChE activity in the brain tissues, which was confirmed by histological sections. Overall, the results showed that Mel administration can induce beneficial effects for the treatment of Al-induced neurobehavioral and neurochemical changes in the central nervous system (CNS). Copyright © 2014 Elsevier Ltd. All rights reserved.

Social Inequality and Visual Impairment in Older People.

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Whillans, Jennifer; Nazroo, James

2018-03-02

Visual impairment is the leading cause of age-related disability, but the social patterning of loss of vision in older people has received little attention. This study's objective was to assess the association between social position and onset of visual impairment, to empirically evidence health inequalities in later life. Visual impairment was measured in 2 ways: self-reporting fair vision or worse (moderate) and self-reporting poor vision or blindness (severe). Correspondingly, 2 samples were drawn from the English Longitudinal Study on Ageing (ELSA). First, 7,483 respondents who had good vision or better at Wave 1; second, 8,487 respondents who had fair vision or better at Wave 1. Survival techniques were used. Cox proportional hazards models showed wealth and subjective social status (SSS) were significant risk factors associated with the onset of visual impairment. The risk of onset of moderate visual impairment was significantly higher for the lowest and second lowest wealth quintiles, whereas the risk of onset of severe visual impairment was significantly higher for the lowest, second, and even middle wealth quintiles, compared with the highest wealth quintile. Independently, lower SSS was associated with increased risk of onset of visual impairment (both measures), particularly so for those placing themselves on the lowest rungs of the social ladder. The high costs of visual impairment are disproportionately felt by the worst off elderly. Both low wealth and low SSS significantly increase the risk of onset of visual impairment.

Role of Neurochemicals in the Interaction between the Microbiota and the Immune and the Nervous System of the Host Organism.

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Oleskin, Alexander V; Shenderov, Boris A; Rogovsky, Vladimir S

2017-09-01

This work is concerned with the role of evolutionary conserved substances, neurotransmitters, and neurohormones, within the complex framework of the microbial consortium-immune system-nervous system axis in the human or animal organism. Although the operation of each of these systems per se is relatively well understood, their combined effects on the host organism still await further research. Drawing on recent research on host-produced and microbial low-molecular-weight neurochemicals such as biogenic amines, amino acids, and short-chain fatty acids (SCFAs), we suggest that these mediators form a part of a universal neurochemical "language." It mediates the whole gamut of harmonious and disharmonious interactions between (a) the intestinal microbial consortium, (b) local and systemic immune cells, and (c) the central and peripheral nervous system. Importantly, the ongoing microbiota-host interactivity is bidirectional. We present evidence that a large number of microbially produced low-molecular-weight compounds are identical or homologous to mediators that are synthesized by immune or nervous cells and, therefore, can bind to the corresponding host receptors. In addition, microbial cells specifically respond to host-produced neuromediators/neurohormones because they have adapted to them during the course of many millions of years of microbiota-host coevolution. We emphasize that the terms "microbiota" and "microbial consortium" are to be used in the broadest sense, so as to include, apart from bacteria, also eukaryotic microorganisms. These are exemplified by the mycobiota whose role in the microbial consortium-immune system-nervous system axis researchers are only beginning to elucidate. In light of the above, it is imperative to reform the current strategies of using probiotic microorganisms and their metabolites for treating and preventing dysbiosis-related diseases. The review demonstrates, in the example of novel probiotics (psychobiotics), that many target

Identifying and characterising cerebral visual impairment in children: a review.

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Philip, Swetha Sara; Dutton, Gordon N

2014-05-01

Cerebral visual impairment (CVI) comprises visual malfunction due to retro-chiasmal visual and visual association pathway pathology. This can be isolated or accompany anterior visual pathway dysfunction. It is a major cause of low vision in children in the developed and developing world due to increasing survival in paediatric and neonatal care. CVI can present in many combinations and degrees. There are multiple causes and it is common in children with cerebral palsy. CVI can be identified easily, if a structured approach to history-taking is employed. This review describes the features of CVI and describes practical management strategies aimed at helping affected children. A literature review was undertaken using 'Medline' and 'Pubmed'. Search terms included cerebral visual impairment, cortical visual impairment, dorsal stream dysfunction and visual function in cerebral palsy. © 2014 The Authors. Clinical and Experimental Optometry © 2014 Optometrists Association Australia.

Quality of life in patients with visual impairment in Ibadan: a clinical study in primary care.

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Adigun, Kehinde; Oluleye, Tunji S; Ladipo, Modupe Ma; Olowookere, Samuel Anu

2014-01-01

Visual function is important for optimal orientation in functional and social life, and has an effect on physical and emotional well-being. Visual impairment, therefore, leads to restrictions in all aspects of daily living and is related to quality of life. The aim of this study was to provide information on the causes of visual impairment in patients presenting to their family physician, the spectrum of impairment, and its impact on quality of life for these patients. This descriptive cross-sectional study of 375 adult patients with ocular symptoms was performed in the general outpatient department of the University College Hospital, Ibadan, from July to September, 2009. After checking their presenting visual acuity, the patients were interviewed using the Vision-Related Quality of Life questionnaire to determine the impact of visual impairment on their quality of life. Ophthalmic examinations were performed to determine the causes of visual impairment. The results were analyzed using proportions and percentages. The main causes of visual impairment were cataracts (58.7%), refractive error (19.4%), and glaucoma (2.9%). Visual impairment was found to be associated with advancing age, low education, and unemployment (Pvisual function (64.2%) and social interaction (50.9%). Quality of life was found to be related to the degree of visual impairment, ie, blind patients reported poor quality of life (41.4%) when compared with those having low vision (8.6%) or near normal vision (2.4%, Pvisual impairment. Family physicians need to identify these visually impaired patients early and make timely referrals.

Brain injury impairs working memory and prefrontal circuit function

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Colin James Smith

2015-11-01

Full Text Available More than 2.5 million Americans suffer a traumatic brain injury (TBI each year. Even mild to moderate traumatic brain injury causes long-lasting neurological effects. Despite its prevalence, no therapy currently exists to treat the underlying cause of cognitive impairment suffered by TBI patients. Following lateral fluid percussion injury (LFPI, the most widely used experimental model of TBI, we investigated alterations in working memory and excitatory/inhibitory synaptic balance in the prefrontal cortex. LFPI impaired working memory as assessed with a T-maze behavioral task. Field excitatory postsynaptic potentials recorded in the prefrontal cortex were reduced in slices derived from brain-injured mice. Spontaneous and miniature excitatory postsynaptic currents onto layer 2/3 neurons were more frequent in slices derived from LFPI mice while inhibitory currents onto layer 2/3 neurons were smaller after LFPI. Additionally, an increase in action potential threshold and concomitant decrease in firing rate was observed in layer 2/3 neurons in slices from injured animals. Conversely, no differences in excitatory or inhibitory synaptic transmission onto layer 5 neurons were observed; however, layer 5 neurons demonstrated a decrease in input resistance and action potential duration after LFPI. These results demonstrate synaptic and intrinsic alterations in prefrontal circuitry that may underlie working memory impairment caused by TBI.

Narcissistic personality disorder: relations with distress and functional impairment.

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Miller, Joshua D; Campbell, W Keith; Pilkonis, Paul A

2007-01-01

This study examined the construct validity of narcissistic personality disorder (NPD) by examining the relations between NPD and measures of psychologic distress and functional impairment both concurrently and prospectively across 2 samples. In particular, the goal was to address whether NPD typically "meets" criterion C of the DSM-IV definition of Personality Disorder, which requires that the symptoms lead to clinically significant distress or impairment in functioning. Sample 1 (n = 152) was composed of individuals receiving psychiatric treatment, whereas sample 2 (n = 151) was composed of both psychiatric patients (46%) and individuals from the community. Narcissistic personality disorder was linked to ratings of depression, anxiety, and several measures of impairment both concurrently and at 6-month follow-up. However, the relations between NPD and psychologic distress were (a) small, especially in concurrent measurements, and (b) largely mediated by impaired functioning. Narcissistic personality disorder was most strongly related to causing pain and suffering to others, and this relationship was significant even when other Cluster B personality disorders were controlled. These findings suggest that NPD is a maladaptive personality style which primarily causes dysfunction and distress in interpersonal domains. The behavior of narcissistic individuals ultimately leads to problems and distress for the narcissistic individuals and for those with whom they interact.

A methodology for the characterization and diagnosis of cognitive impairments-Application to specific language impairment.

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Oliva, Jesús; Serrano, J Ignacio; del Castillo, M Dolores; Iglesias, Angel

2014-06-01

The diagnosis of mental disorders is in most cases very difficult because of the high heterogeneity and overlap between associated cognitive impairments. Furthermore, early and individualized diagnosis is crucial. In this paper, we propose a methodology to support the individualized characterization and diagnosis of cognitive impairments. The methodology can also be used as a test platform for existing theories on the causes of the impairments. We use computational cognitive modeling to gather information on the cognitive mechanisms underlying normal and impaired behavior. We then use this information to feed machine-learning algorithms to individually characterize the impairment and to differentiate between normal and impaired behavior. We apply the methodology to the particular case of specific language impairment (SLI) in Spanish-speaking children. The proposed methodology begins by defining a task in which normal and individuals with impairment present behavioral differences. Next we build a computational cognitive model of that task and individualize it: we build a cognitive model for each participant and optimize its parameter values to fit the behavior of each participant. Finally, we use the optimized parameter values to feed different machine learning algorithms. The methodology was applied to an existing database of 48 Spanish-speaking children (24 normal and 24 SLI children) using clustering techniques for the characterization, and different classifier techniques for the diagnosis. The characterization results show three well-differentiated groups that can be associated with the three main theories on SLI. Using a leave-one-subject-out testing methodology, all the classifiers except the DT produced sensitivity, specificity and area under curve values above 90%, reaching 100% in some cases. The results show that our methodology is able to find relevant information on the underlying cognitive mechanisms and to use it appropriately to provide better

Analysis of refractive error in visual impairment among residents aged 40 years and above in Dongguan City

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Shu-Hui Chen

2015-06-01

Full Text Available AIM: To investigate the prevalence rate of visual impairment caused by refractive error among residents aged 40 years and above, and the influence factors of vision correction. METHODS: We conducted an epidemiological survey of diabetes and diabetic retinopathy among residents aged 40 and above in Guangdong Province, Hengli Town, Dongguan City from 2011 to 2012. At the same time, according to World Health Organization(WHO, according to the daily life vision, 0.05≤visual ability RESULTS: The prevalence rate of visual impairment was 7.90%(707/8 952. The prevalence rate of visual impairment caused by refractive error was 5.57%(499/8 952, accounted for visual impairment of 70.58%(499/707. The prevalence rate of correction of refractive error among visual impairment was 5.36%(480/8 952, accounting for visual impairment of 67.89%(480/707. The prevalence rate of visual impairment uncorrected was 0.21%(19/8 952, accounting for visual impairment of 2.69%(19/707. By χ2 test, with the increase of age, the rate of visual impairment caused by refractive error was significantly decreased(PPP>0.05. The rate of visual impairment can be corrected decreases with age, from 92.1% to 49.1%, there was a statistically significant difference(PPP>0.05. CONCLUSION: Through the development of refractive error correction of positive, can make the daily life of visual impairment in about 2/3 of patients improve eyesight and improve the quality of life of residents.

Impairment of brain endothelial glucose transporter by methamphetamine causes blood-brain barrier dysfunction

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Murrin L Charles

2011-03-01

Full Text Available Abstract Background Methamphetamine (METH, an addictive psycho-stimulant drug with euphoric effect is known to cause neurotoxicity due to oxidative stress, dopamine accumulation and glial cell activation. Here we hypothesized that METH-induced interference of glucose uptake and transport at the endothelium can disrupt the energy requirement of the blood-brain barrier (BBB function and integrity. We undertake this study because there is no report of METH effects on glucose uptake and transport across the blood-brain barrier (BBB to date. Results In this study, we demonstrate that METH-induced disruption of glucose uptake by endothelium lead to BBB dysfunction. Our data indicate that a low concentration of METH (20 μM increased the expression of glucose transporter protein-1 (GLUT1 in primary human brain endothelial cell (hBEC, main component of BBB without affecting the glucose uptake. A high concentration of 200 μM of METH decreased both the glucose uptake and GLUT1 protein levels in hBEC culture. Transcription process appeared to regulate the changes in METH-induced GLUT1 expression. METH-induced decrease in GLUT1 protein level was associated with reduction in BBB tight junction protein occludin and zonula occludens-1. Functional assessment of the trans-endothelial electrical resistance of the cell monolayers and permeability of dye tracers in animal model validated the pharmacokinetics and molecular findings that inhibition of glucose uptake by GLUT1 inhibitor cytochalasin B (CB aggravated the METH-induced disruption of the BBB integrity. Application of acetyl-L-carnitine suppressed the effects of METH on glucose uptake and BBB function. Conclusion Our findings suggest that impairment of GLUT1 at the brain endothelium by METH may contribute to energy-associated disruption of tight junction assembly and loss of BBB integrity.

Magnitude and Causes of Low Vision Disability (Moderate and Severe Visual Impairment among Students of Al-Noor Institute for the Blind in Al-Hassa, Saudi Arabia; A case series

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Fahad Al-Wadani

2012-02-01

Full Text Available Objectives: This study aimed to estimate the magnitude and causes of low vision disability (severe visual impairment [SVI] and moderate visual impairment [MVI] among students at Al-Noor Institute for the Blind (NIB in Al-Hassa, Saudi Arabia in 2006. Methods: An optometrist conducted refraction of 122 eyes of the 61 students (27 boys and 34 girls with MVI (vision <6/18 to 6/60 and SVI (vision <6/60 to 3/60. Ophthalmologists examined the anterior and posterior segments, and analysed the outcomes of additional investigations to finalise the diagnosis. The results were categorised as ‘preventable’, ‘treatable’ and ‘not amenable to treatment’. The low vision care was also reviewed. Results: In 12 (9.8% eyes, visual acuity was ≥6/18 and in 28 (23% eyes, it was <3/60. MVI and SVI were found in 82 eyes (67.2%. Hereditary retinal disorders were found in 68 (55.7% eyes. Although refractive errors were found in 112 (91.8% eyes, isolated refractive error was found in only 9 students. Congenital glaucoma and cataract were responsible for visual impairment in 16 (13.1% and 9 (7.4% eyes. These students were prescribed optical and non-optical low vision aids. Conclusion: Retinal disease was the main cause of SVI and MVI in our series. Some students at Al-Noor Institute for the Blind have curable low vision conditions. Rehabilitation of low vision disability should be different from that offered to the absolutely blind.

Phonological working memory and auditory processing speed in children with specific language impairment

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Fatemeh Haresabadi

2015-02-01

Full Text Available Background and Aim: Specific language impairment (SLI, one variety of developmental language disorder, has attracted much interest in recent decades. Much research has been conducted to discover why some children have a specific language impairment. So far, research has failed to identify a reason for this linguistic deficiency. Some researchers believe language disorder causes defects in phonological working memory and affects auditory processing speed. Therefore, this study reviews the results of research investigating these two factors in children with specific language impairment.Recent Findings: Studies have shown that children with specific language impairment face constraints in phonological working memory capacity. Memory deficit is one possible cause of linguistic disorder in children with specific language impairment. However, in these children, disorder in information processing speed is observed, especially regarding the auditory aspect.Conclusion: Much more research is required to adequately explain the relationship between phonological working memory and auditory processing speed with language. However, given the role of phonological working memory and auditory processing speed in language acquisition, a focus should be placed on phonological working memory capacity and auditory processing speed in the assessment and treatment of children with a specific language impairment.

Characteristics of childhood uveitis leading to visual impairment and blindness in the Netherlands.

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Hettinga, Ymkje M; Verhagen, Fleurieke H; van Genderen, Maria; de Boer, Joke H

2014-12-01

To investigate the clinical characteristics of childhood uveitis leading to visual impairment or blindness. In this descriptive study, we reviewed data from the medical records of 58 children with visual impairment or blindness due to childhood uveitis, which were seen at an institute for visually impaired patients (Bartiméus) between January 1981 and December 2012, in a retrospective, cross-sectional manner. Thirty-two of the 58 children (55%) were visually impaired and 26 (45%) were legally blind. Uveitis was posterior in 76% of all cases. Infectious uveitis represented 74% of all cases, of which 86% was congenital. Five patients (9%) had uveitis related to a systemic disease, and ten patients (17%) had idiopathic uveitis. There was a decrease in infectious causes over the last decades (p = 0.04) and an increase in idiopathic uveitis (p children with posterior uveitis remained constant. There was an overall decrease in the number of children with uveitis referred to Bartiméus. The number of ocular complications at the time of intake was higher in children with acquired disease compared with congenital diseases (p children with non-infectious uveitis compared with infectious uveitis (p = 0.04). Most comorbidities that were noted were seen in children with infectious uveitis. Most patients suffering from visual impairment or blindness due to childhood uveitis had posterior and/or infectious uveitis, mostly congenital. There is a shift in causes which shows a decrease in infectious causes and an increase in idiopathic causes. © 2014 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

[Amblyopia. Epidemiology, causes and risk factors].

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Elflein, H M

2016-04-01

Amblyopia is the main cause for mostly monocular, impaired vision in childhood. Treatment and prevention of amblyopia is only effective during childhood. Ophthalmological screening of children does not yet exist in Germany. The prevalence of amblyopia in Germany is 5.6%, which is higher than in reports from studies in Australia; however, the prevalence of amblyopia is not comparable in these studies due to different definitions of amblyopia and the inclusion/exclusion criteria of the study cohorts. At present it is unknown at what age ophthalmological screening should be carried out to prevent amblyopia and the appropriate frequency of screening examinations. Amblyopia is a disorder of the visual cortex that is due to suppression and deprivation of one eye leading to unilateral visual impairment. Approximately 50% of cases of amblyopia are caused by anisometropia, 25% by strabismus and in every sixth person by a combination of both. Other causes, such as unilateral congenital cataracts are relatively rare. A variety of factors, such as ocular pathologies, premature birth, familial disposition and general diseases are associated with an increased risk for amblyopia.

External ear anomalies and hearing impairment in Noonan Syndrome.

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van Trier, Dorothée C; van Nierop, Josephine; Draaisma, Jos M Th; van der Burgt, Ineke; Kunst, Henricus; Croonen, Ellen A; Admiraal, Ronald J C

2015-06-01

This is the first cohort in which hearing impairment and external ear anomalies in Noonan Syndrome are described extensively. Retrospective analysis of the otorhinolaryngological and clinical genetic data from 97 Noonan Syndrome (NS) patients. Forty-four NS patients were seen by an otorhinolaryngologist for the analysis of hearing impairment. In our cohort 80 of the 97 patients were genetically tested. In 71 of these mutations were found: in 48 patients a mutation in PTPN11, in 10 patients in SOS1, in 5 patients in SHOC2, in 5 patients in RAF1, in 1 patient in MAP2K2, in 1 patient in KRAS and in 1 patient in A2ML1. External ear anomalies were reported in 75 NS patients (77%). In 69 patients the ears were low-set, 28 patients had posteriorly rotated ears, 14 patients showed protruding ears and 18 had thickened helices. Hearing impairment was detected in 34 NS patients. Nine patients had sensorineural hearing impairment, two a permanent conductive hearing impairment, two other patients had mixed hearing impairment and 20 patients had conductive hearing impairment in the past, caused by otitis media with effusion. Their temporary conductive hearing impairment resolved between the ages of 2 and 18 years. Sensorineural hearing impairment varied between mild high-frequency hearing impairment and profound (uni- and bilateral) hearing impairment and was progressive in three patients. Four NS patients received cochlear implants for their severe sensorineural hearing impairment. The cohort is small for genotype-phenotype correlations, but sensorineural hearing impairment, especially the bilateral severe hearing impairment, was only seen in patients with a PTPN11 mutation. NS is characterized by dysmorphic external ear anomalies and both sensorineural and conductive hearing impairment. Audiological examinations are recommended in all patients with Noonan Syndrome. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Laser Frequency Noise in Coherent Optical Systems: Spectral Regimes and Impairments.

Science.gov (United States)

Kakkar, Aditya; Rodrigo Navarro, Jaime; Schatz, Richard; Pang, Xiaodan; Ozolins, Oskars; Udalcovs, Aleksejs; Louchet, Hadrien; Popov, Sergei; Jacobsen, Gunnar

2017-04-12

Coherent communication networks are based on the ability to use multiple dimensions of the lightwave together with electrical domain compensation of transmission impairments. Electrical-domain dispersion compensation (EDC) provides many advantages such as network flexibility and enhanced fiber nonlinearity tolerance, but makes the system more susceptible to laser frequency noise (FN), e.g. to the local oscillator FN in systems with post-reception EDC. Although this problem has been extensively studied, statistically, for links assuming lasers with white-FN, many questions remain unanswered. Particularly, the influence of a realistic non-white FN-spectrum due to e.g., the presence of 1/f-flicker and carrier induced noise remains elusive and a statistical analysis becomes insufficient. Here we provide an experimentally validated theory for coherent optical links with lasers having general non-white FN-spectrum and EDC. The fundamental reason of the increased susceptibility is shown to be FN-induced symbol displacement that causes timing jitter and/or inter/intra symbol interference. We establish that different regimes of the laser FN-spectrum cause a different set of impairments. The influence of the impairments due to some regimes can be reduced by optimizing the corresponding mitigation algorithms, while other regimes cause irretrievable impairments. Theoretical boundaries of these regimes and corresponding criteria applicable to system/laser design are provided.

Emotion-induced impairments in speeded word recognition tasks.

Science.gov (United States)

Zeelenberg, René; Bocanegra, Bruno R; Pecher, Diane

2011-01-01

Recent studies show that emotional stimuli impair the identification of subsequently presented, briefly flashed stimuli. In the present study, we investigated whether emotional distractors (primes) impaired target processing when presentation of the target stimulus was not impoverished. In lexical decision, animacy decision, rhyme decision, and nonword naming, targets were presented in such a manner that they were clearly visible (i.e., targets were not masked and presented until participants responded). In all tasks taboo-sexual distractors caused a slowdown in responding to the subsequent neutral target. Our results indicate that the detrimental effects of emotional distractors are not confined to paradigms in which visibility of the target is limited. Moreover, impairments were obtained even when semantic processing of stimuli was not required.

Δ9-THC-caused synaptic and memory impairments are mediated through COX-2 signaling

Science.gov (United States)

Yang, Hongwei; Tang, Ya-ping; Sun, Hao; Song, Yunping; Chen, Chu

2013-01-01

SUMMARY Marijuana has been used for thousands of years as a treatment for medical conditions. However, untoward side effects limit its medical value. Here we show that synaptic and cognitive impairments following repeated exposure to Δ9-tetrahydrocannabinol (Δ9-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids, in the brain. COX-2 induction by Δ9-THC is mediated via CB1 receptor-coupled G-protein βγ subunits. Pharmacological or genetic inhibition of COX-2 blocks down-regulation and internalization of glutamate receptor subunits and alterations of the dendritic spine density of hippocampal neurons induced by repeated Δ9-THC exposures. Ablation of COX-2 also eliminates Δ9-THC-impaired hippocampal long-term synaptic plasticity, spatial, and fear memories. Importantly, the beneficial effects of decreasing β-amyloid plaques and neurodegeneration by Δ9-THC in Alzheimer’s disease animals are retained in the presence of COX-2 inhibition. These results suggest that the applicability of medical marijuana would be broadened by concurrent inhibition of COX-2. PMID:24267894

Nuclear SREBP-1a causes loss of pancreatic β-cells and impaired insulin secretion

International Nuclear Information System (INIS)

Iwasaki, Yuko; Iwasaki, Hitoshi; Yatoh, Shigeru; Ishikawa, Mayumi; Kato, Toyonori; Matsuzaka, Takashi; Nakagawa, Yoshimi; Yahagi, Naoya; Kobayashi, Kazuto; Takahashi, Akimitsu; Suzuki, Hiroaki; Yamada, Nobuhiro; Shimano, Hitoshi

2009-01-01

Transgenic mice expressing nuclear sterol regulatory element-binding protein-1a under the control of the insulin promoter were generated to determine the role of SREBP-1a in pancreatic β-cells. Only low expressors could be established, which exhibited mild hyperglycemia, impaired glucose tolerance, and reduced plasma insulin levels compared to C57BL/6 controls. The islets isolated from the transgenic mice were fewer and smaller, and had decreased insulin content and unaltered glucagon staining. Both glucose- and potassium-stimulated insulin secretions were decreased. The transgenic islets consistently expressed genes for fatty acids and cholesterol synthesis, resulting in accumulation of triglycerides but not cholesterol. PDX-1, ΒΕΤΑ2, MafA, and IRS-2 were suppressed, partially explaining the loss and dysfunction of β-cell mass. The transgenic mice on a high fat/high sucrose diet still exhibited impaired insulin secretion and continuous β-cell growth defect. Therefore, nuclear SREBP-1a, even at a low level, strongly disrupts β-cell mass and function.

Does my older cancer patient have cognitive impairment?

Science.gov (United States)

Snaedal, Jon

2018-05-01

Cancer and impaired cognition are both frequent conditions in old age and consequently coexist to certain degree. The prevalence of impaired cognition increases sharply after the age of 65 and the more advanced form of cognitive impairment; dementia, is exceeding 30% by the age of 85years. Adequate cognition is crucial for understanding important facts and for giving consent for intervention. There are many different stages of cognitive impairment, ranging from subjective cognitive impairment to severe dementia. The mildest stages of cognitive impairment are sometimes reversible but in more severe stages, there is brain damage of some kind, most frequently caused by neurodegenerative disorder such as Alzheimer's disease. Therefore, some kind of evaluation of cognition should be offered to all older individuals with cancer and in need for intervention. In this evaluation, information should also be sought from a close relative. In the earlier stages of cognitive impairment, the individual usually retains ability to give consent and understands information given but in later stages of dementia, a surrogate decision maker is needed. In milder stages of dementia, an individual evaluation is needed for decision of capability for consent. A specific diagnosis of a disorder such as Alzheimer's disease does not in itself preclude the individual from giving consent, the degree of cognitive impairment, impaired judgement and poor insight are more decisive in this regard. It is also important to know the difference of delirium, most often a time limited condition and dementia that usually is progressive. Copyright © 2017 Elsevier Inc. All rights reserved.

Age-Related Sensory Impairments and Risk of Cognitive Impairment

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Fischer, Mary E; Cruickshanks, Karen J.; Schubert, Carla R; Pinto, Alex A; Carlsson, Cynthia M; Klein, Barbara EK; Klein, Ronald; Tweed, Ted S.

2016-01-01

Background/Objectives To evaluate the associations of sensory impairments with the 10-year risk of cognitive impairment. Previous work has primarily focused on the relationship between a single sensory system and cognition. Design The Epidemiology of Hearing Loss Study (EHLS) is a longitudinal, population-based study of aging in the Beaver Dam, WI community. Baseline examinations were conducted in 1993 and follow-up exams have been conducted every 5 years. Setting General community Participants EHLS members without cognitive impairment at EHLS-2 (1998–2000). There were 1,884 participants (mean age = 66.7 years) with complete EHLS-2 sensory data and follow-up information. Measurements Cognitive impairment was a Mini-Mental State Examination score of impairment was a pure-tone average of hearing thresholds (0.5, 1, 2 and 4 kHz) of > 25 decibel Hearing Level in either ear. Visual impairment was Pelli-Robson contrast sensitivity of impairment was a San Diego Odor Identification Test score of impairment were independently associated with cognitive impairment risk [Hearing: Hazard Ratio (HR) = 1.90, 95% Confidence Interval (C.I.) = 1.11, 3.26; Vision: HR = 2.05, 95% C.I. = 1.24, 3.38; Olfaction: HR = 3.92, 95% C.I. = 2.45, 6.26]. However, 85% with hearing impairment, 81% with visual impairment, and 76% with olfactory impairment did not develop cognitive impairment during follow-up. Conclusion The relationship between sensory impairment and cognitive impairment was not unique to one sensory system suggesting sensorineural health may be a marker of brain aging. The development of a combined sensorineurocognitive measure may be useful in uncovering mechanisms of healthy brain aging. PMID:27611845

Acute Treatment with T-Type Calcium Channel Enhancer SAK3 Reduces Cognitive Impairments Caused by Methimazole-Induced Hypothyroidism Via Activation of Cholinergic Signaling.

Science.gov (United States)

Husain, Noreen; Yabuki, Yasushi; Shinoda, Yasuharu; Fukunaga, Kohji

2018-01-01

Hypothyroidism is a common disorder that is associated with psychological disturbances such as dementia, depression, and psychomotor disorders. We recently found that chronic treatment with the T-type calcium channel enhancer SAK3 prevents the cholinergic neurodegeneration induced by a single intraperitoneal (i.p.) injection of methimazole (MMI; 75 mg/kg), thereby improving cognition. Here, we evaluated the acute effect of SAK3 on cognitive impairments and its mechanism of action following the induction of hypothyroidism. Hypothyroidism was induced by 2 injections of MMI (75 mg/kg, i.p.) administered once per week. Four weeks after the final MMI treatment, MMI-treated mice showed reduced serum thyroxine (T4) levels and cognitive impairments without depression-like behaviors. Although acute SAK3 (1.0 mg/kg, p.o.) administration failed to ameliorate the decreased T4 levels and histochemical destruction of the glomerular structure, acute SAK3 (1.0 mg/kg, p.o.) administration significantly reduced cognitive impairments in MMI-treated mice. Importantly, the α7 nicotinic acetylcholine receptor (nAChR)-selective inhibitor methyllycaconitine (MLA; 12 mg/kg, i.p.) and T-type calcium channel-specific blocker NNC 55-0396 (25 mg/kg, i.p.) antagonized the acute effect of SAK3 on memory deficits in MMI-treated mice. We also confirmed that acute SAK3 administration does not rescue reduced olfactory marker protein or choline acetyltransferase immunoreactivity levels in the olfactory bulb or medial septum. Taken together, these results suggest that SAK3 has the ability to improve the cognitive decline caused by hypothyroidism directly through activation of nAChR signaling and T-type calcium channels. © 2018 S. Karger AG, Basel.

Behavioral symptoms related to cognitive impairment.

Science.gov (United States)

Dillon, Carol; Serrano, Cecilia M; Castro, Diego; Leguizamón, Patricio Perez; Heisecke, Silvina L; Taragano, Fernando E

2013-01-01

Neuropsychiatric symptoms (NPS) are core features of Alzheimer's disease and related dementias. On one hand, behavioral symptoms in patients with mild cognitive impairment (MCI) can indicate an increased risk of progressing to dementia. On the other hand, mild behavioral impairment (MBI) in patients who usually have normal cognition indicates an increased risk of developing dementia. Whatever the cause, all dementias carry a high rate of NPI. These symptoms can be observed at any stage of the disease, may fluctuate over its course, are a leading cause of stress and overload for caregivers, and increase rates of hospitalization and early institutionalization for patients with dementia. The clinician should be able to promptly recognize NPI through the use of instruments capable of measuring their frequency and severity to support diagnosis, and to help monitor the treatment of behavioral symptoms. The aims of this review are to describe and update the construct 'MBI' and to revise the reported NPS related to prodromal stages of dementia (MCI and MBI) and dementia stages of Alzheimer's disease and frontotemporal lobar degeneration.

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease.

Science.gov (United States)

Edelstyn, Nicola M J; John, Christopher M; Shepherd, Thomas A; Drakeford, Justine L; Clark-Carter, David; Ellis, Simon J; Mayes, Andrew R

2015-10-01

Medicated, non-dementing mild-to-moderate Parkinson's disease (PD) patients usually show recall/recollection impairments but have only occasionally shown familiarity impairments. We aimed to assess two explanations of this pattern of impairment. Recollection typically improves when effortful planning of encoding and retrieval processing is engaged. This depends on prefrontally-dependent executive processes, which are often disrupted in PD. Relative to an unguided encoding and retrieval of words condition (C1), giving suitable guidance at encoding alone (C2) or at encoding and retrieval (C3) should, if executive processes are disrupted, improve PD recollection more than control recollection and perhaps raise it to normal levels. Familiarity, being a relatively automatic kind of memory, whether impaired or intact, should be unaffected by guidance. According to the second explanation, PD deficits are amnesia-like and caused by medial temporal lobe dysfunction and although poorer recollection, which is caused by hippocampal disruption, may be improved by guidance, it should not improve more than control recollection. Familiarity impairment will also occur if the perirhinal cortex is disrupted, but will be unimproved by guidance. Without guidance, recollection/recall was impaired in thirty PD patients relative to twenty-two healthy controls and remained relatively equally impaired when full guidance was provided (C1 vs C3), both groups improving to broadly the same extent. Although impaired, and markedly less so than recollection, familiarity was not improved by guidance in both groups. The patients showed elevated rates of subclinical depressive symptoms, which weakly correlated with recall/recollection in all three conditions. PD executive function was also deficient and correlated with unguided/C1 recollection only. Our results are consistent with a major cause of the patients' recall/recollection impairments being hippocampal disruption, probably exacerbated by

Behavioral symptoms related to cognitive impairment

Directory of Open Access Journals (Sweden)

Dillon C

2013-09-01

Full Text Available Carol Dillon,1 Cecilia M Serrano,1 Diego Castro,1 Patricio Perez Leguizamón,1 Silvina L Heisecke,1,2 Fernando E Taragano1 1CEMIC (Centro de Educación Médica e Investigaciones Clínicas University Institute, 2CONICET (Consejo Nacional de Investigaciones Cientificas y Técnicas, Buenos Aires, Argentina Abstract: Neuropsychiatric symptoms (NPS are core features of Alzheimer's disease and related dementias. On one hand, behavioral symptoms in patients with mild cognitive impairment (MCI can indicate an increased risk of progressing to dementia. On the other hand, mild behavioral impairment (MBI in patients who usually have normal cognition indicates an increased risk of developing dementia. Whatever the cause, all dementias carry a high rate of NPI. These symptoms can be observed at any stage of the disease, may fluctuate over its course, are a leading cause of stress and overload for caregivers, and increase rates of hospitalization and early institutionalization for patients with dementia. The clinician should be able to promptly recognize NPI through the use of instruments capable of measuring their frequency and severity to support diagnosis, and to help monitor the treatment of behavioral symptoms. The aims of this review are to describe and update the construct ‘MBI’ and to revise the reported NPS related to prodromal stages of dementia (MCI and MBI and dementia stages of Alzheimer’s disease and frontotemporal lobar degeneration. Keywords: behavioral or neuropsychiatric symptoms, cognitive impairment, dementia

Audiometric Characteristics of a Dutch DFNA10 Family With Mid-Frequency Hearing Impairment.

Science.gov (United States)

van Beelen, Eline; Oonk, Anne M M; Leijendeckers, Joop M; Hoefsloot, Elisabeth H; Pennings, Ronald J E; Feenstra, Ilse; Dieker, Hendrik-Jan; Huygen, Patrick L M; Snik, Ad F M; Kremer, Hannie; Kunst, Henricus P M

2016-01-01

Mutations in EYA4 can cause nonsyndromic autosomal dominant sensorineural hearing impairment (DFNA10) or a syndromic variant with hearing impairment and dilated cardiomyopathy. A mutation in EYA4 was found in a Dutch family, causing DFNA10. This study is focused on characterizing the hearing impairment in this family. Whole exome sequencing was performed in the proband. In addition, peripheral blood samples were collected from 23 family members, and segregation analyses were performed. All participants underwent otorhinolaryngological examinations and pure-tone audiometry, and 12 participants underwent speech audiometry. In addition, an extended set of audiometric measurements was performed in five family members to evaluate the functional status of the cochlea. Vestibular testing was performed in three family members. Two individuals underwent echocardiography to evaluate the nonsyndromic phenotype. The authors present a Dutch family with a truncating mutation in EYA4 causing a mid-frequency hearing impairment. This mutation (c.464del) leads to a frameshift and a premature stop codon (p.Pro155fsX). This mutation is the most N-terminal mutation in EYA4 found to date. In addition, a missense mutation, predicted to be deleterious, was found in EYA4 in two family members. Echocardiography in two family members revealed no signs of dilated cardiomyopathy. Results of caloric and velocity step tests in three family members showed no abnormalities. Hearing impairment was found to be symmetric and progressive, beginning as a mid-frequency hearing impairment in childhood and developing into a high-frequency, moderate hearing impairment later in life. Furthermore, an extended set of audiometric measurements was performed in five family members. The results were comparable to those obtained in patients with other sensory types of hearing impairments, such as patients with Usher syndrome type IIA and presbyacusis, and not to those obtained in patients with (cochlear

Blindness and severe visual impairment in pupils at schools for the blind in Burundi.

Science.gov (United States)

Ruhagaze, Patrick; Njuguna, Kahaki Kimani Margaret; Kandeke, Lévi; Courtright, Paul

2013-01-01

To determine the causes of childhood blindness and severe visual impairment in pupils attending schools for the blind in Burundi in order to assist planning for services in the country. All pupils attending three schools for the blind in Burundi were examined. A modified WHO/PBL eye examination record form for children with blindness and low vision was used to record the findings. Data was analyzed for those who became blind or severely visually impaired before the age of 16 years. Overall, 117 pupils who became visually impaired before 16 years of age were examined. Of these, 109 (93.2%) were blind or severely visually impaired. The major anatomical cause of blindness or severe visual impairment was cornea pathology/phthisis (23.9%), followed by lens pathology (18.3%), uveal lesions (14.7%) and optic nerve lesions (11.9%). In the majority of pupils with blindness or severe visual impairment, the underlying etiology of visual loss was unknown (74.3%). More than half of the pupils with lens related blindness had not had surgery; among those who had surgery, outcomes were generally poor. The causes identified indicate the importance of continuing preventive public health strategies, as well as the development of specialist pediatric ophthalmic services in the management of childhood blindness in Burundi. The geographic distribution of pupils at the schools for the blind indicates a need for community-based programs to identify and refer children in need of services.

Research Review: Structural Language in Autistic Spectrum Disorder--Characteristics and Causes

Science.gov (United States)

Boucher, Jill

2012-01-01

Background: Structural language anomalies or impairments in autistic spectrum disorder (ASD) are theoretically and practically important, although underrecognised as such. This review aims to highlight the ubiquitousness of structural language anomalies and impairments in ASD, and to stimulate investigation of their immediate causes and…

Progressively Disrupted Brain Functional Connectivity Network in Subcortical Ischemic Vascular Cognitive Impairment Patients.

Science.gov (United States)

Sang, Linqiong; Chen, Lin; Wang, Li; Zhang, Jingna; Zhang, Ye; Li, Pengyue; Li, Chuanming; Qiu, Mingguo

2018-01-01

Cognitive impairment caused by subcortical ischemic vascular disease (SIVD) has been elucidated by many neuroimaging studies. However, little is known regarding the changes in brain functional connectivity networks in relation to the severity of cognitive impairment in SIVD. In the present study, 20 subcortical ischemic vascular cognitive impairment no dementia patients (SIVCIND) and 20 dementia patients (SIVaD) were enrolled; additionally, 19 normal controls were recruited. Each participant underwent a resting-state functional MRI scan. Whole-brain functional networks were analyzed with graph theory and network-based statistics (NBS) to study the functional organization of networks and find alterations in functional connectivity among brain regions. After adjustments for age, gender, and duration of formal education, there were significant group differences for two network functional organization indices, global efficiency and local efficiency, which decreased (NC > SIVCIND > SIVaD) as cognitive impairment worsened. Between-group differences in functional connectivity (NBS corrected, p  impairment worsened, with an increased number of decreased connections between brain regions. We also observed more reductions in nodal efficiency in the prefrontal and temporal cortices for SIVaD than for SIVCIND. These findings indicated a progressively disrupted pattern of the brain functional connectivity network with increased cognitive impairment and showed promise for the development of reliable biomarkers of network metric changes related to cognitive impairment caused by SIVD.

Effects of Social Cognitive Impairment on Speech Disorder in Schizophrenia

OpenAIRE

Docherty, Nancy M.; McCleery, Amanda; Divilbiss, Marielle; Schumann, Emily B.; Moe, Aubrey; Shakeel, Mohammed K.

2012-01-01

Disordered speech in schizophrenia impairs social functioning because it impedes communication with others. Treatment approaches targeting this symptom have been limited by an incomplete understanding of its causes. This study examined the process underpinnings of speech disorder, assessed in terms of communication failure. Contributions of impairments in 2 social cognitive abilities, emotion perception and theory of mind (ToM), to speech disorder were assessed in 63 patients with schizophren...

Metabolic Profiling of Impaired Cognitive Function in Patients Receiving Dialysis

OpenAIRE

Kurella Tamura, Manjula; Chertow, Glenn M.; Depner, Thomas A.; Nissenson, Allen R.; Schiller, Brigitte; Mehta, Ravindra L.; Liu, Sai; Sirich, Tammy L.

2016-01-01

Retention of uremic metabolites is a proposed cause of cognitive impairment in patients with ESRD. We used metabolic profiling to identify and validate uremic metabolites associated with impairment in executive function in two cohorts of patients receiving maintenance dialysis. We performed metabolic profiling using liquid chromatography/mass spectrometry applied to predialysis plasma samples from a discovery cohort of 141 patients and an independent replication cohort of 180 patients partici...

Neurochemical changes in the pericalcarine cortex in congenital blindness attributable to bilateral anophthalmia.

Science.gov (United States)

Coullon, Gaelle S L; Emir, Uzay E; Fine, Ione; Watkins, Kate E; Bridge, Holly

2015-09-01

Congenital blindness leads to large-scale functional and structural reorganization in the occipital cortex, but relatively little is known about the neurochemical changes underlying this cross-modal plasticity. To investigate the effect of complete and early visual deafferentation on the concentration of metabolites in the pericalcarine cortex, (1)H magnetic resonance spectroscopy was performed in 14 sighted subjects and 5 subjects with bilateral anophthalmia, a condition in which both eyes fail to develop. In the pericalcarine cortex, where primary visual cortex is normally located, the proportion of gray matter was significantly greater, and levels of choline, glutamate, glutamine, myo-inositol, and total creatine were elevated in anophthalmic relative to sighted subjects. Anophthalmia had no effect on the structure or neurochemistry of a sensorimotor cortex control region. More gray matter, combined with high levels of choline and myo-inositol, resembles the profile of the cortex at birth and suggests that the lack of visual input from the eyes might have delayed or arrested the maturation of this cortical region. High levels of choline and glutamate/glutamine are consistent with enhanced excitatory circuits in the anophthalmic occipital cortex, which could reflect a shift toward enhanced plasticity or sensitivity that could in turn mediate or unmask cross-modal responses. Finally, it is possible that the change in function of the occipital cortex results in biochemical profiles that resemble those of auditory, language, or somatosensory cortex. Copyright © 2015 the American Physiological Society.

Size-dependent impairment of cognition in mice caused by the injection of gold nanoparticles

International Nuclear Information System (INIS)

Chen, Yu-Shiun; Hong, Meng-Yeng; Huang, G Steve; Hung, Yao-Ching; Lin, Li-Wei; Liau, Ian

2010-01-01

We explored the size-dependent impairment of cognition in mice caused by the injection of gold nanoparticles (GNPs). GNPs of 17 and 37 nm in diameter were injected intraperitoneally into BALB/c mice at doses ranging from 0.5 to 14.6 mg kg -1 . ICP-MS was performed on brain tissue collected 1, 14 and 21 days after the injection. A passive-avoidance test was performed on day 21. Monoamine levels were determined on day 21. The microscopic distribution of GNPs in the hippocampus was examined using coherent anti-Stokes Raman scattering (CARS) microscopy and transmission electron microscopy (TEM). The results indicated that 17 nm GNPs passed through the blood-brain barrier more rapidly than 37 nm GNPs. Treatment with 17 nm GNPs decreased the latency time, which was comparable to the effect of scopolamine treatment, while 37 nm GNPs showed no significant effect. Dopamine levels and serotonin levels in the brain were significantly altered by the injection of 17 and 37 nm GNPs. GNPs affected dopaminergic and serotonergic neurons. CARS microscopy indicated that 17 nm GNPs entered the Cornu Ammonis (CA) region of the hippocampus, while 37 nm GNPs were excluded from the CA region. TEM verified the presence of 17 nm GNPs in the cytoplasm of pyramidal cells. In this study, we showed that the ability of GNPs to damage cognition in mice was size-dependent and associated with the ability of the particles to invade the hippocampus. The dosage and duration of the treatment should be taken into account if GNPs are used in the future as vehicles to carry therapeutic agents into the brain.

Size-dependent impairment of cognition in mice caused by the injection of gold nanoparticles

Energy Technology Data Exchange (ETDEWEB)

Chen, Yu-Shiun; Hong, Meng-Yeng; Huang, G Steve [Institute of Nanotechnology, Department of Materials Science and Engineering, National Chiao Tung University, 1001 University Road, Hsinchu 300, Taiwan (China); Hung, Yao-Ching [Section of Gynecologic Oncology, Department of Obstetrics and Gynecology, China Medical University and Hospital, 91 Hsueh Shih Road, Taichung 404, Taiwan (China); Lin, Li-Wei [School of Chinese Medicine for Post-Baccalaureate, I-Shou University, 8 Yida Road, Yanchao Township, Kaohsiung Country 82445, Taiwan (China); Liau, Ian, E-mail: gstevehuang@mail.nctu.edu.tw [Department of Applied Chemistry, National Chiao Tung University, 1001 University Road, Hsinchu 300, Taiwan (China)

2010-12-03

We explored the size-dependent impairment of cognition in mice caused by the injection of gold nanoparticles (GNPs). GNPs of 17 and 37 nm in diameter were injected intraperitoneally into BALB/c mice at doses ranging from 0.5 to 14.6 mg kg{sup -1}. ICP-MS was performed on brain tissue collected 1, 14 and 21 days after the injection. A passive-avoidance test was performed on day 21. Monoamine levels were determined on day 21. The microscopic distribution of GNPs in the hippocampus was examined using coherent anti-Stokes Raman scattering (CARS) microscopy and transmission electron microscopy (TEM). The results indicated that 17 nm GNPs passed through the blood-brain barrier more rapidly than 37 nm GNPs. Treatment with 17 nm GNPs decreased the latency time, which was comparable to the effect of scopolamine treatment, while 37 nm GNPs showed no significant effect. Dopamine levels and serotonin levels in the brain were significantly altered by the injection of 17 and 37 nm GNPs. GNPs affected dopaminergic and serotonergic neurons. CARS microscopy indicated that 17 nm GNPs entered the Cornu Ammonis (CA) region of the hippocampus, while 37 nm GNPs were excluded from the CA region. TEM verified the presence of 17 nm GNPs in the cytoplasm of pyramidal cells. In this study, we showed that the ability of GNPs to damage cognition in mice was size-dependent and associated with the ability of the particles to invade the hippocampus. The dosage and duration of the treatment should be taken into account if GNPs are used in the future as vehicles to carry therapeutic agents into the brain.

Overview of a public health approach to pediatric hearing impairment in the Pacific Islands.

Science.gov (United States)

Kaspar, Annette; Kei, Joseph; Driscoll, Carlie; Swanepoel, De Wet; Goulios, Helen

2016-07-01

Childhood hearing impairment is a significant cause of disability in developing countries. Otitis media and meningitis are leading infectious causes of preventable hearing loss in children. It is estimated that the Pacific Islands have among the greatest global burden of childhood hearing impairment due to infectious causes, and yet there is currently very little in the research literature on pediatric hearing disorders in this region. (1) To review existing research literature on pediatric hearing impairment in the Pacific Islands, and (2) to present a public health approach to the development and improvement of childhood hearing services in the Pacific Islands. The primary tool was a comprehensive literature review. MEDLINE and ScienceDirect databases were searched for relevant journal articles. There was no limit on the date of publication. Any article reporting on hearing impairment in the Pacific Region was included. A total of 23 journal articles were found that satisfied the above inclusion criteria. The limited information available in the literature suggests that otitis media and vaccine-preventable infections are a significant cause of avoidable childhood hearing impairment in the Pacific Islands. Pediatric audiology services are limited in this region. Further research is required to develop effective public health programs that should reduce the burden of preventable childhood hearing loss in the Pacific Islands. There is limited information in the research literature on pediatric hearing impairment and audiology services in the Pacific Islands. Epidemiological data based on the WHO Ear and Hearing Disorders Survey Protocol are urgently needed, and the development of audiology services within the existing public and primary health care framework should reduce the burden of preventable hearing loss in the Pacific Islands. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Tetrahydrobiopterin in antenatal brain hypoxia-ischemia-induced motor impairments and cerebral palsy.

Science.gov (United States)

Vasquez-Vivar, Jeannette; Shi, Zhongjie; Luo, Kehuan; Thirugnanam, Karthikeyan; Tan, Sidhartha

2017-10-01

Antenatal brain hypoxia-ischemia, which occurs in cerebral palsy, is considered a significant cause of motor impairments in children. The mechanisms by which antenatal hypoxia-ischemia causes brain injury and motor deficits still need to be elucidated. Tetrahydrobiopterin is an important enzyme cofactor that is necessary to produce neurotransmitters and to maintain the redox status of the brain. A genetic deficiency of this cofactor from mutations of biosynthetic or recycling enzymes is a well-recognized factor in the development of childhood neurological disorders characterized by motor impairments, developmental delay, and encephalopathy. Experimental hypoxia-ischemia causes a decline in the availability of tetrahydrobiopterin in the immature brain. This decline coincides with the loss of brain function, suggesting this occurrence contributes to neuronal dysfunction and motor impairments. One possible mechanism linking tetrahydrobiopterin deficiency, hypoxia-ischemia, and neuronal injury is oxidative injury. Evidence of the central role of the developmental biology of tetrahydrobiopterin in response to hypoxic ischemic brain injury, especially the development of motor deficits, is discussed. Copyright © 2017. Published by Elsevier B.V.

Δ9-THC-caused synaptic and memory impairments are mediated through COX-2 signaling.

Science.gov (United States)

Chen, Rongqing; Zhang, Jian; Fan, Ni; Teng, Zhao-Qian; Wu, Yan; Yang, Hongwei; Tang, Ya-Ping; Sun, Hao; Song, Yunping; Chen, Chu

2013-11-21

Marijuana has been used for thousands of years as a treatment for medical conditions. However, untoward side effects limit its medical value. Here, we show that synaptic and cognitive impairments following repeated exposure to Δ(9)-tetrahydrocannabinol (Δ(9)-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids in the brain. COX-2 induction by Δ(9)-THC is mediated via CB1 receptor-coupled G protein βγ subunits. Pharmacological or genetic inhibition of COX-2 blocks downregulation and internalization of glutamate receptor subunits and alterations of the dendritic spine density of hippocampal neurons induced by repeated Δ(9)-THC exposures. Ablation of COX-2 also eliminates Δ(9)-THC-impaired hippocampal long-term synaptic plasticity, working, and fear memories. Importantly, the beneficial effects of decreasing β-amyloid plaques and neurodegeneration by Δ(9)-THC in Alzheimer's disease animals are retained in the presence of COX-2 inhibition. These results suggest that the applicability of medical marijuana would be broadened by concurrent inhibition of COX-2. Copyright © 2013 Elsevier Inc. All rights reserved.

Chronic marijuana smoke exposure in the rhesus monkey. IV: Neurochemical effects and comparison to acute and chronic exposure to delta-9-tetrahydrocannabinol (THC) in rats.

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Ali, S F; Newport, G D; Scallet, A C; Paule, M G; Bailey, J R; Slikker, W

1991-11-01

THC is the major psychoactive constituent of marijuana and is known to produce psychopharmacological effects in humans. These studies were designed to determine whether acute or chronic exposure to marijuana smoke or THC produces in vitro or in vivo neurochemical alterations in rat or monkey brain. For the in vitro study, THC was added (1-100 nM) to membranes prepared from different regions of the rat brain and muscarinic cholinergic (MCh) receptor binding was measured. For the acute in vivo study, rats were injected IP with vehicle, 1, 3, 10, or 30 mg THC/kg and sacrificed 2 h later. For the chronic study, rats were gavaged with vehicle or 10 or 20 mg THC/kg daily, 5 days/week for 90 days and sacrificed either 24 h or 2 months later. Rhesus monkeys were exposed to the smoke of a single 2.6% THC cigarette once a day, 2 or 7 days a week for 1 year. Approximately 7 months after the last exposure, animals were sacrificed by overdose with pentobarbital for neurochemical analyses. In vitro exposure to THC produced a dose-dependent inhibition of MCh receptor binding in several brain areas. This inhibition of MCh receptor binding, however, was also observed with two other nonpsychoactive derivatives of marijuana, cannabidiol and cannabinol. In the rat in vivo study, we found no significant changes in MCh or other neurotransmitter receptor binding in hippocampus, frontal cortex or caudate nucleus after acute or chronic exposure to THC. In the monkey brain, we found no alterations in the concentration of neurotransmitters in caudate nucleus, frontal cortex, hypothalamus or brain stem.(ABSTRACT TRUNCATED AT 250 WORDS)

Impact of Psychopathy on Moral Judgments about Causing Fear and Physical Harm.

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Elise M Cardinale

Full Text Available Psychopathy is a personality variable associated with persistent immoral behaviors. Despite this, attempts to link moral reasoning deficits to psychopathic traits have yielded mixed results with many findings supporting intact moral reasoning in individuals with psychopathic traits. Abundant evidence shows that psychopathy impairs responses to others' emotional distress. However, most studies of morality and psychopathy focus on judgments about causing others physical harm. Results of such studies may be inconsistent because physical harm is an imperfect proxy for emotional distress. No previous paradigm has explicitly separated judgments about physical harm and emotional distress and assessed how psychopathy affects each type of judgment. In three studies we found that psychopathy impairs judgments about causing others emotional distress (specifically fear but minimally affects judgments about causing physical harm and that judgments about causing fear predict instrumental aggression in psychopathy. These findings are consistent with reports linking psychopathy to insensitivity to others' fear, and suggest that sensitivity to others' fear may play a fundamental role in the types of moral decision-making impaired by psychopathy.

Inhibition of hippocampal aromatization impairs spatial memory performance in a male songbird.

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Bailey, David J; Ma, Chunqi; Soma, Kiran K; Saldanha, Colin J

2013-12-01

Recent studies have revealed the presence and regulation of aromatase at the vertebrate synapse, and identified a critical role played by presynaptic estradiol synthesis in the electrophysiological response to auditory and other social cues. However, if and how synaptic aromatization affects behavior remains to be directly tested. We have exploited 3 characteristics of the zebra finch hippocampus (HP) to test the role of synaptocrine estradiol provision on spatial memory function. Although the zebra finch HP contains abundant aromatase transcripts and enzyme activity, immunocytochemical studies reveal widespread pre- and postsynaptic, but sparse to undetectable somal, localization of this enzyme. Further, the superficial location of the avian HP makes possible the more exclusive manipulation of its neurochemical characteristics without perturbation of the neuropil and the resultant induction of astroglial aromatase. Last, as in other vertebrates, the HP is critical for spatial memory performance in this species. Here we report that local inhibition of hippocampal aromatization impairs spatial memory performance in an ecologically valid food-finding task. Local aromatase inhibition also resulted in lower levels of estradiol in the HP, but not in adjacent brain areas, and was achieved without the induction of astroglial aromatase. The observed decrement in acquisition and subsequent memory performance as a consequence of lowered aromatization was similar to that achieved by lesioning this locus. Thus, hippocampal aromatization, much of which is achieved at the synapse in this species, is critical for spatial memory performance.

A Cross-sectional Study of Prevalence and Etiology of Childhood Visual Impairment in Auckland, New Zealand.

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Chong, Chee Foong; McGhee, Charles N J; Dai, Shuan

2014-01-01

Childhood visual impairment has significant individual and socioeconomic costs with global differences in etiology and prevalence. This study aimed to determine prevalence, etiology, and avoidable causes of childhood visual impairment in New Zealand. Retrospective data analysis from a national referral center, the Blind and Low Vision Education Network New Zealand, Auckland. The World Health Organization Program for Prevention of Blindness eye examination records for visually impaired children, 16 years or younger, registered with the Auckland Visual Resource Centre, were included. Data analyzed included demographics, etiology, visual acuity, visual fields, educational setting, and rehabilitation plan. Charts of 340 children were examined, of which 267 children (144 blind, 123 low vision) were included in the analysis, whereas the remaining 73 charts of children with no visual impairment were excluded. The calculated prevalence of blindness and low vision was 0.05% and 0.04%, respectively, in the Auckland region. Principal causes of blindness affecting 91 children (63.9%) were cerebral visual impairment in 61 children (42.4%), optic nerve atrophy in 18 children (12.5%), and retinal dystrophy in 13 children (9.0%). The main potentially avoidable causes of blindness in 27 children (19%) were neonatal trauma, asphyxia in 9 children (33%), and nonaccidental injury 6 children (22%). This first report of prevalence for childhood blindness and low vision in New Zealand is similar to data from Established Market Economy countries. The leading causes of blindness are also comparable to other high-income countries; however, proportions of avoidable causes differ significantly.

Syngeneic B16F10 Melanoma Causes Cachexia and Impaired Skeletal Muscle Strength and Locomotor Activity in Mice

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Fabrício A. Voltarelli

2017-09-01

Full Text Available Muscle wasting has been emerging as one of the principal components of cancer cachexia, leading to progressive impairment of work capacity. Despite early stages melanomas rarely promotes weight loss, the appearance of metastatic and/or solid tumor melanoma can leads to cachexia development. Here, we investigated the B16F10 tumor-induced cachexia and its contribution to muscle strength and locomotor-like activity impairment. C57BL/6 mice were subcutaneously injected with 5 × 104 B16F10 melanoma cells or PBS as a Sham negative control. Tumor growth was monitored during a period of 28 days. Compared to Sham mice, tumor group depicts a loss of skeletal muscle, as well as significantly reduced muscle grip strength and epididymal fat mass. This data are in agreement with mild to severe catabolic host response promoted by elevated serum tumor necrosis factor-alpha (TNF-α, interleukin-6 (IL-6 and lactate dehydrogenase (LDH activity. Tumor implantation has also compromised general locomotor activity and decreased exploratory behavior. Likewise, muscle loss, and elevated inflammatory interleukin were associated to muscle strength loss and locomotor activity impairment. In conclusion, our data demonstrated that subcutaneous B16F10 melanoma tumor-driven catabolic state in response to a pro-inflammatory environment that is associated with impaired skeletal muscle strength and decreased locomotor activity in tumor-bearing mice.

Protective effect of rutin on cognitive impairment caused by phenytoin

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Dubey, Shagun; Ganeshpurkar, Aditya; Bansal, Divya; Dubey, Nazneen

2015-01-01

Objective: To study the effect of the co-administration of phenytoin (PHT) and rutin in comparison with PHT and piracetam (PIM) on seizure control, cognitive, and motor functions in mice. Materials and Methods: Increasing current electroshock seizure (ICES) test was used to evaluate the effect of the co-administration of PHT and PIM on convulsions. Cognitive functions in mice were assessed by a spontaneous alternation in behavior on a plus maze while motor functions were screened using rolling roller apparatus and by counting the number of arms entries on a plus maze. Brain acetyl-cholinesterase (AChE) activity was also estimated. Statistical Analysis: The expression of data was done as mean ± standard error of the mean. The normally distributed data were subjected to one-way ANOVA followed by Dunnett's test. P < 0.05 was considered significant. Results: The study showed that rutin when co-administered with PHT, significantly reversed PHT-induced reduction in spontaneous alternation without altering the efficacy of PHT against ICES, in both acute and chronic studies. Further, it also reversed PHT-induced increase in AChE activity. Conclusion: Rutin alleviated the PHT-induced cognitive impairment without compromising its antiepileptic efficacy. PMID:26729954

[Efficacy observation on electroacupuncture in the treatment of oculomotor impairment caused by ophthalmic nerve injury].

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Ji, Xiao-Jie; Zhou, Ling-Yun; Si, Cheng-Qing; Guo, Qing; Feng, Guang-Zhong; Gang, Bao-Zhi

2013-11-01

To observe the difference in the clinical efficacy on oculomotor impairment between electroacupuncture and acupuncture and explore the best therapeutic method in the treatment of this disease. Sixty cases of oculomotor impairment were randomized into an electroacupuncture group and an acupuncture group, 30 cases in each one. In the electroacupuncture group, the points were selected on extraocular muscles, the internal needling technique in the eye was used in combination of electroacupuncture therapy. In the acupuncture group, the points and needling technique were same as the electroacupuncture group, but without electric stimulation applied. The treatment was given 5 times a week, 15 treatments made one session. After 3 sessions of treatment, the clinical efficacy, palpebral fissure size, pupil size, oculomotor range and the recovery in diplopia were compared before and after treatment in the two groups. In the electroacupuncture group, the palpebral fissure size was (9.79+/-2.65)mm and the eyeball shifting distance was (18.12+/-1. 30)mm, which were hig-her than (8.23+/-2.74)mm and (16.71+/-1. 44)mm respectively in the acupuncture group. In the electroacupuncture group, the pupil diameter was (0. 44 +/-0. 42)mm, which was less than (0. 72 +/- 0. 53)mm in the acupuncture group, indicating the significant difference (all Pelectroacupuncture group, which was better than 36.67% (11/30) and 83. 333 (25/30) in the acupuncture group separately, indicating the significant difference (all PElectroacupuncture presents the obvious advantages in the treatment of oculomotor impairment, characterized as quick and high effect, short duration of treatment and remarkable improvements in clinical symptoms, there are important significance for the improvement of survival quality of patients.

Minocycline protects against lipopolysaccharide-induced cognitive impairment in mice.

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Hou, Yue; Xie, Guanbo; Liu, Xia; Li, Guoxun; Jia, Congcong; Xu, Jinghua; Wang, Bing

2016-03-01

The role of glial cells, especially microglia and astrocytes, in neuroinflammation and cognition has been studied intensively. Lipopolysaccharide (LPS), a commonly used inducer of neuroinflammation, can cause cognitive impairment. Minocycline is known to possess potent neuroprotective activity, but its effect on LPS-induced cognitive impairment is unknown. This study aims to investigate the effects of minocycline on LPS-induced cognitive impairment and glial cell activation in mice. Behavioral tests were conducted for cognitive function, immunohistochemistry for microglial and astrocyte response, and quantitative PCR for mRNA expression of proinflammatory cytokines. Minocycline significantly reversed the decreased spontaneous alternation induced by intrahippocampal administration of LPS in the Y-maze task. In the Morris water maze place navigation test, minocycline decreased the escape latency and distance traveled compared to LPS-treated mice. In the probe test, minocycline-treated mice spent more time in the target quadrant and crossed the platform area more frequently than animals in the LPS-treated group. Minocycline produced a significant decrease in the number of Iba-1- and GFAP-positive hippocampal cells compared to the LPS-treated group. Minocycline-treated mice had significantly reduced hippocampal TNF-α and IL-1β mRNA levels compared with LPS-treated animals. Minocycline caused a significant increase in hippocampal BDNF expression compared to the LPS-treated group. Minocycline can attenuate LPS-induced cognitive impairments in mice. This effect may be associated with its action to suppress the activation of microglia and astrocytes and to normalize BDNF expression. Since neuroinflammatory processes and cognitive impairments are implicated in neurodegenerative disorders, minocycline may be a promising candidate for treating such diseases.

Inhibition of mTOR improves the impairment of acidification in autophagic vesicles caused by hepatic steatosis

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Nakadera, Eisuke; Yamashina, Shunhei; Izumi, Kousuke; Inami, Yoshihiro; Sato, Toshifumi; Fukushima, Hirofumi; Kon, Kazuyoshi; Ikejima, Kenichi; Ueno, Takashi; Watanabe, Sumio

2016-01-01

Recent investigations revealed that dysfunction of autophagy involved in the progression of chronic liver diseases such as alcoholic and nonalcoholic steatohepatitis and hepatocellular neoplasia. Previously, it was reported that hepatic steatosis disturbs autophagic proteolysis via suppression of both autophagic induction and lysosomal function. Here, we demonstrate that autophagic acidification was altered by a decrease in lysosomal proton pump vacuolar-ATPase (V-ATPase) in steatohepatitis. The number of autophagic vesicles was increased in hepatocytes from obese KKAy mice as compared to control. Similarly, autophagic membrane protein LC3-II and lysosomal protein LAMP-2 expression were enhanced in KKAy mice liver. Nevertheless, both phospho-mTOR and p62 expression were augmented in KKAy mice liver. More than 70% of autophagosomes were stained by LysoTracker Red (LTR) in hepatocytes from control mice; however, the percentage of acidic autolysosomes was decreased in hepatocytes from KKAy mice significantly (40.1 ± 3.48%). Both protein and RNA level of V-ATPase subunits ATP6v1a, ATP6v1b, ATP6v1d in isolated lysosomes were suppressed in KKAy mice as compared to control. Interestingly, incubation with mTOR inhibitor rapamycin increased in the rate of LTR-positive autolysosomes in hepatocytes from KKAy mice and suppressed p62 accumulation in the liver from KKAy mice which correlated to an increase in the V-ATPase subunits expression. These results indicate that down-regulation of V-ATPase due to hepatic steatosis causes autophagic dysfunction via disruption of lysosomal and autophagic acidification. Moreover, activation of mTOR plays a pivotal role on dysregulation of lysosomal and autophagic acidification by modulation of V-ATPase expression and could therefore be a useful therapeutic target to ameliorate dysfunction of autophagy in NAFLD. - Highlights: • Hepatic steatosis causes accumulation of autophagic vesicles in hepatocytes. • Hepatic steatosis disturbs

Inhibition of mTOR improves the impairment of acidification in autophagic vesicles caused by hepatic steatosis

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Nakadera, Eisuke [Department of Gastroenterology, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421 (Japan); Yamashina, Shunhei, E-mail: syamashi@juntendo.ac.jp [Department of Gastroenterology, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421 (Japan); Izumi, Kousuke; Inami, Yoshihiro; Sato, Toshifumi; Fukushima, Hirofumi; Kon, Kazuyoshi; Ikejima, Kenichi [Department of Gastroenterology, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421 (Japan); Ueno, Takashi [Division of Proteomics and Biomolecular Science, Juntendo University, School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421 (Japan); Watanabe, Sumio [Department of Gastroenterology, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421 (Japan)

2016-01-22

Recent investigations revealed that dysfunction of autophagy involved in the progression of chronic liver diseases such as alcoholic and nonalcoholic steatohepatitis and hepatocellular neoplasia. Previously, it was reported that hepatic steatosis disturbs autophagic proteolysis via suppression of both autophagic induction and lysosomal function. Here, we demonstrate that autophagic acidification was altered by a decrease in lysosomal proton pump vacuolar-ATPase (V-ATPase) in steatohepatitis. The number of autophagic vesicles was increased in hepatocytes from obese KKAy mice as compared to control. Similarly, autophagic membrane protein LC3-II and lysosomal protein LAMP-2 expression were enhanced in KKAy mice liver. Nevertheless, both phospho-mTOR and p62 expression were augmented in KKAy mice liver. More than 70% of autophagosomes were stained by LysoTracker Red (LTR) in hepatocytes from control mice; however, the percentage of acidic autolysosomes was decreased in hepatocytes from KKAy mice significantly (40.1 ± 3.48%). Both protein and RNA level of V-ATPase subunits ATP6v1a, ATP6v1b, ATP6v1d in isolated lysosomes were suppressed in KKAy mice as compared to control. Interestingly, incubation with mTOR inhibitor rapamycin increased in the rate of LTR-positive autolysosomes in hepatocytes from KKAy mice and suppressed p62 accumulation in the liver from KKAy mice which correlated to an increase in the V-ATPase subunits expression. These results indicate that down-regulation of V-ATPase due to hepatic steatosis causes autophagic dysfunction via disruption of lysosomal and autophagic acidification. Moreover, activation of mTOR plays a pivotal role on dysregulation of lysosomal and autophagic acidification by modulation of V-ATPase expression and could therefore be a useful therapeutic target to ameliorate dysfunction of autophagy in NAFLD. - Highlights: • Hepatic steatosis causes accumulation of autophagic vesicles in hepatocytes. • Hepatic steatosis disturbs

Chronic copper exposure causes spatial memory impairment, selective loss of hippocampal synaptic proteins, and activation of PKR/eIF2α pathway in mice.

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Ma, Quan; Ying, Ming; Sui, Xiaojing; Zhang, Huimin; Huang, Haiyan; Yang, Linqing; Huang, Xinfeng; Zhuang, Zhixiong; Liu, Jianjun; Yang, Xifei

2015-01-01

Copper is an essential element for human growth and development; however, excessive intake of copper could contribute to neurotoxicity. Here we show that chronic exposure to copper in drinking water impaired spatial memory with simultaneous selective loss of hippocampal pre-synaptic protein synapsin 1, and post-synaptic density protein (PSD)-93/95 in mice. Copper exposure was shown to elevate the levels of nitrotyrosine and 8-hydroxydeoxyguanosine (8-OHdG) in hippocampus, two markers of oxidative stress. Concurrently, we also found that copper exposure activated double stranded RNA-dependent protein kinase (PKR) as evidenced by increased ratio of phosphorylated PKR at Thr451 and total PKR and increased the phosphorylation of its downstream signaling molecule eukaryotic initiation factor 2α (eIF2α) at Ser51 in hippocampus. Consistent with activation of PKR/eIF2α signaling pathway which was shown to mediate synaptic deficit and cognitive impairment, the levels of activating transcription factor 4 (ATF-4), a downstream signaling molecule of eIF2α and a repressor of CREB-mediated gene expression, were significantly increased, while the activity of cAMP response elements binding protein (CREB) was inactivated as suggested by decreased phosphorylation of CREB at Ser133 by copper exposure. In addition, the expression of the pro-apoptotic target molecule C/EBP homology protein (CHOP) of ATF-4 was upregulated and hippocampal neuronal apoptosis was induced by copper exposure. Taken together, we propose that chronic copper exposure might cause spatial memory impairment, selective loss of synaptic proteins, and neuronal apoptosis through the mechanisms involving activation of PKR/eIF2α signaling pathway.

Prevalence and causes of visual impairment in Asian and non-Hispanic white preschool children: Multi-ethnic Pediatric Eye Disease Study.

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Tarczy-Hornoch, Kristina; Cotter, Susan A; Borchert, Mark; McKean-Cowdin, Roberta; Lin, Jesse; Wen, Ge; Kim, Jeniffer; Varma, Rohit

2013-06-01

To determine the prevalence and causes of decreased visual acuity (VA). Population-based cross-sectional study. Multi-ethnic sample of children 30 to 72 months of age identified in Los Angeles. All eligible children underwent a comprehensive ophthalmic evaluation including monocular VA testing, cover testing, cycloplegic autorefraction, fundus evaluation, and VA retesting with refractive correction. Decreased VA was defined as presenting or best-measured VA worse than 20/50 in children 30 to 47 months of age and worse than 20/40 for children 48 months of age and older. The prevalence and causes of decreased VA were determined, for both presenting and best-measured VA, in the better-seeing and the worse-seeing eyes. Prevalence and causes of decreased vision. Presenting VA was assessed in 1840 children and best-measured VA was assessed in 1886 children. Presenting VA was decreased in the worse eye of 4.2% of Asian children and of 3.6% of non-Hispanic white (NHW) children. Close to one-fourth of these cases had no identifiable cause, and 81% of these resolved on retesting. Decreased presenting VA in the worse eye with an identifiable ophthalmic cause was present in 3.4% of Asian children and in 2.6% of NHW children. Decreased presenting VA attributable to simple refractive error (myopia ≥ 0.5 diopters [D]; hyperopia ≥ 3.0 D; astigmatism ≥ 2.0 D or ≥ 1.5 D for children older than 36 months) was present in the worse eye of 2.3% of Asian children and of 1.4% of NHW children and in the better eye of 0.5% of Asian children and of 0.3% of NHW children. Decreased best-measured VA attributable to a cause was present in the worse eye of 1.2% of both Asian children and NHW children and in the better eye of 0.2% of Asian and of 0.3% of NHW children. Amblyopia related to refractive error was the most common cause, and was 10 times as common as ocular disease. Severe visual impairment was rare. Seventy percent of all decreased VA in Asian and NHW preschool children and

The comparison of stress and marital satisfaction status of parents of hearing-impaired and normal children

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Karim Gharashi

2013-03-01

Full Text Available Background and Aim: Stress is the source of many problems in human-kind lives and threatens people's life constantly. Having hearing-impaired child, not only causes stress in parents, but also affects their marital satisfaction. The purpose of this study was comparing the stress and marital satisfaction status between the normal and hearing-impaired children's parents.Methods: This was a causal-comparative study. Eighty parents of normal children and 80 parents of hearing-impaired children were chosen from rehabilitation centers and kindergartens in city of Tabriz, Iran by available and clustering sampling method. All parents were asked to complete the Friedrich's source of stress and Enrich marital satisfaction questionnaires.Results: Parents of hearing-impaired children endure more stress than the normal hearing ones (p<0.001. The marital satisfaction of hearing-impaired children's parents was lower than the parents of normal hearing children, too (p<0.001.Conclusion: Having a hearing-impaired child causes stress and threatens the levels of marital satisfaction. This requires much more attention and a distinct planning for parents of handicap children to reduce their stress.

How aging affects sleep-dependent memory consolidation?

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Caroline eHarand

2012-02-01

Full Text Available Sleep plays multiple functions among which energy conservation or recuperative processes. Besides, growing evidence indicate that sleep plays also a major role in memory consolidation, a process by which recently acquired and labile memory traces are progressively strengthened into more permanent and/or enhanced forms. Indeed, memories are not stored as they were initially encoded but rather undergo a gradual reorganization process, which is favoured by the neurochemical environment and the electrophysiological activity observed during sleep. Two putative, probably not exclusive, models (hippocampo-neocortical dialogue and synaptic homeostasis hypothesis have been proposed to explain the beneficial effect of sleep on memory processes. It is worth noting that all data gathered until now emerged from studies conducted in young subjects. The investigation of the relationships between sleep and memory in older adults has sparked off little interest until recently. Though, aging is characterized by memory impairment, changes in sleep architecture, as well as brain and neurochemical alterations. All these elements suggest that sleep-dependent memory consolidation may be impaired or occurs differently in older adults.Here, we give an overview of the mechanisms governing sleep-dependent memory consolidation, and the crucial points of this complex process that may dysfunction and result in impaired memory consolidation in aging.

Social neuroscience and theory of mind.

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Westby, Carol E

2014-01-01

The role of theory of mind (ToM) in autism spectrum disorders and other communication impairments has been an active area of research in the last 30 years. Advances in neuroimaging in the last 10 years have led to the rise of the field of social neuroscience, which has markedly increased the understanding of the neurophysiological/neuroanatomical and neurochemical nature of ToM functioning and deficits in typically developing individuals and in children and adults with a variety of social and communication impairments. The goal of this paper is to (a) describe the current concepts of ToM based on neuroscience research, and (b) present a framework for the dimensions of ToM that have been identified, which can be used to guide assessment and intervention for persons with deficits in ToM that affect social interactions. This article presents neuroscience research that has documented the neurophysiological/neuroanatomical bases for cognitive and affective ToM and interpersonal and intrapersonal ToM as well as neurochemical and epigenetic influences on ToM. This information provides an important framework for assessing ToM deficits in persons with social and communication impairments and developing interventions that target the specific dimensions of ToM deficits. © 2014 S. Karger AG, Basel.

Renal Impairment and Prognosis of Patients with Atrial Fibrillation Undergoing Coronary Intervention - The AFCAS Trial.

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Heli M Lahtela

Full Text Available Renal impairment is a well-known risk factor for cardiovascular complications, but the effect of different stages of renal impairment on thrombotic/thromboembolic and bleeding complications in patients with atrial fibrillation (AF undergoing percutaneous coronary intervention (PCI remains largely unknown. We sought to evaluate the incidence and clinical impact of four stages of renal impairment in patients with AF undergoing PCI.We assessed renal function by estimated glomerular filtration rate (eGFR and outcomes in 781 AF patients undergoing PCI by using the data from a prospective European multicenter registry. End-points included all-cause mortality, major adverse cardiac and cerebrovascular events (MACCE and bleeding events at 12 months.A total of 195 (25% patients had normal renal function (eGFR ≥90 mL/min, 290 (37% mild renal impairment (eGFR 60-89, 263 (34% moderate renal impairment (eGFR 30-59 and 33 (4% severe renal impairment (eGFR <30. Degree of renal impairment remained an independent predictor of mortality and MACCE in an adjusted a Cox regression model. Even patients with mild renal impairment had a higher risk of all-cause mortality (HR 2.25, 95%CI 1.02-4.98, p=0.04 and borderline risk for MACCE (HR 1.56, 95%CI 0.98- 2.50, p=0.06 compared to those with normal renal function.Renal impairment is common in patients with AF undergoing PCI and even mild renal impairment has an adverse prognostic effect in these patients requiring multiple antithrombotic medications.

Stroke survivors' views and experiences on impact of visual impairment.

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Rowe, Fiona J

2017-09-01

We sought to determine stroke survivors' views on impact of stroke-related visual impairment to quality of life. Stroke survivors with visual impairment, more than 1 year post stroke onset, were recruited. Semistructured biographical narrative interviews were audio-recorded and transcribed verbatim. A thematic approach to analysis of the qualitative data was adopted. Transcripts were systematically coded using NVivo10 software. Thirty-five stroke survivors were interviewed across the UK: 16 females, 19 males; aged 20-75 years at stroke onset. Five qualitative themes emerged: "Formal care," "Symptoms and self," "Adaptations," "Daily life," and "Information." Where visual problems existed, they were often not immediately recognized as part of the stroke syndrome and attributed to other causes such as migraine. Many participants did not receive early vision assessment or treatment for their visual problems. Visual problems included visual field loss, double vision, and perceptual problems. Impact of visual problems included loss in confidence, being a burden to others, increased collisions/accidents, and fear of falling. They made many self-identified adaptations to compensate for visual problems: magnifiers, large print, increased lighting, use of white sticks. There was a consistent lack of support and provision of information about visual problems. Poststroke visual impairment causes considerable impact to daily life which could be substantially improved by simple measures including early formal visual assessment, management and advice on adaptive strategies and self-management options. Improved education about poststroke visual impairment for the public and clinicians could aid earlier diagnosis of visual impairments.

Retinopathy of prematurity as a major cause of severe visual impairment and blindness in children in schools for the blind in Guadalajara city, Mexico.

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Zepeda-Romero, L C; Barrera-de-Leon, J C; Camacho-Choza, C; Gonzalez Bernal, C; Camarena-Garcia, E; Diaz-Alatorre, C; Gutierrez-Padilla, J A; Gilbert, C

2011-11-01

To determine the causes of blindness in students attending schools for the blind in Guadalajara city, Mexico and to assess the availability of screening for retinopathy of prematurity (ROP) in local neonatal intensive care units. Information on causes of blindness was obtained by interview with parents and teachers, review of records and examination. Causes of visual loss in children with a distance visual acuity of blind) were determined and classified according to the WHO's classification system for children. Of 153 children in the two participating schools, 144 were severely visual impaired or blind. Their ages ranged from 4 months to 15 years and 58% were female. ROP was the most common cause of visual loss (34.7%), followed by optic nerve lesions (17.4%) and glaucoma (14.6%). 25/59 (42.3%) children aged 0-4 years were blind from ROP compared with 6/32 (18.8%) children aged 10-15 years. 78% of children blind from ROP had psychomotor delay and less than half (46%) had not received treatment for ROP. All five privately funded neonatal intensive care units in the city regularly screen for ROP compared with only four of the 12 units in the public sector. ROP is the leading cause of blindness in children in Mexico despite national guidelines being in place. Health policies promoting primary prevention through improved neonatal care need to be implemented. Advocacy is required so that the time ophthalmologists spend screening and treating ROP is included in their job description and hence salaried.

Intermittent hypoxia from obstructive sleep apnea may cause neuronal impairment and dysfunction in central nervous system: the potential roles played by microglia

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Yang Q

2013-08-01

Full Text Available Qingchan Yang,1,* Yan Wang,2,* Jing Feng,2 Jie Cao,2 Baoyuan Chen2 1Graduate School of Tianjin Medical University, 2Respiratory Department, Tianjin Medical University General Hospital, Tianjin, People's Republic of China *These authors contributed equally to this work Abstract: Obstructive sleep apnea (OSA is a common condition characterized by repetitive episodes of complete (apnea or partial (hypopnea obstruction of the upper airway during sleep, resulting in oxygen desaturation and arousal from sleep. Intermittent hypoxia (IH resulting from OSA may cause structural neuron damage and dysfunction in the central nervous system (CNS. Clinically, it manifests as neurocognitive and behavioral deficits with oxidative stress and inflammatory impairment as its pathophysiological basis, which are mediated by microglia at the cellular level. Microglia are dominant proinflammatory cells in the CNS. They induce CNS oxidative stress and inflammation, mainly through mitochondria, reduced nicotinamide adenine dinucleotide phosphate oxidase, and the release of excitatory toxic neurotransmitters. The balance between neurotoxic versus protective and anti- versus proinflammatory microglial factors might determine the final roles of microglia after IH exposure from OSA. Microglia inflammatory impairments will continue and cascade persistently upon activation, ultimately resulting in clinically significant neuron damage and dysfunction in the CNS. In this review article, we summarize the mechanisms of structural neuron damage in the CNS and its concomitant dysfunction due to IH from OSA, and the potential roles played by microglia in this process. Keywords: intermittent hypoxia, obstructive sleep apnea, microglia, inflammation, apoptosis

Impaired Cognition in Rats with Cortical Dysplasia: Additional Impact of Early-Life Seizures

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Lucas, Marcella M.; Lenck-Santini, Pierre-Pascal; Holmes, Gregory L.; Scott, Rod C.

2011-01-01

One of the most common and serious co-morbidities in patients with epilepsy is cognitive impairment. While early-life seizures are considered a major cause for cognitive impairment, it is not known whether it is the seizures, the underlying neurological substrate or a combination that has the largest impact on eventual learning and memory. Teasing…

Causes, Prevention and Correction of Impaired Posture in Children of Primary School Age

Directory of Open Access Journals (Sweden)

В. А. Щирба

2016-09-01

Full Text Available Research Objective. The objective of our research was to provide theoretical substantiation and implement corrective gymnastics in practice for the purposes of prevention and correction of faults in schoolchildren’s posture. The main means for shaping the correct posture, preventing and correcting faults in posture are callisthenic routine and special corrective exercises. Research methods: anamnesis, somatoscopy, clinical and mathematical methods. Research results. The medical examination revealed that only six of 60 pupils had normal correctly shaped posture, which accounts for 10%. The posture of the other 90% of the pupils was impaired. The most common faults were: asymmetrical pectoral girdle and shoulder blades, stooping posture. The examination revealed 19 pupils with scoliotic posture, which accounts for 44 %. The posture of 24 pupils, or 40%, was hyperkyphotic and stooping. In other words, the posture of 84% of the pupils was scoliotic or hyperkyphotic. The rest of the pupils had flat and kypholordic posture. It is worth mentioning that some of the pupils examined had more serious disorders of their musculoskeletal system, namely: organic disorders, such as spinal disorders in the sagittal plane — the scoliosis types excluded from the study. Significantly, the first main reason of posture disorders is weakness of the pectoral muscle sling. Conclusions. The principal means of prevention and correction of impaired posture are using special physical exercises designed to create a muscular corpus and correct particular faults in posture. We therefore developed sets of exercises intended to correct posture defects and proposed them to the physical education teacher and class teachers.

Repeated mild traumatic brain injury can cause acute neurologic impairment without overt structural damage in juvenile rats.

Directory of Open Access Journals (Sweden)

Alicia Meconi

Full Text Available Repeated concussion is becoming increasingly recognized as a serious public health concern around the world. Moreover, there is a greater awareness amongst health professionals of the potential for repeated pediatric concussions to detrimentally alter the structure and function of the developing brain. To better study this issue, we developed an awake closed head injury (ACHI model that enabled repeated concussions to be performed reliably and reproducibly in juvenile rats. A neurological assessment protocol (NAP score was generated immediately after each ACHI to help quantify the cumulative effects of repeated injury on level of consciousness, and basic motor and reflexive capacity. Here we show that we can produce a repeated ACHI (4 impacts in two days in both male and female juvenile rats without significant mortality or pain. We show that both single and repeated injuries produce acute neurological deficits resembling clinical concussion symptoms that can be quantified using the NAP score. Behavioural analyses indicate repeated ACHI acutely impaired spatial memory in the Barnes maze, and an interesting sex effect was revealed as memory impairment correlated moderately with poorer NAP score performance in a subset of females. These cognitive impairments occurred in the absence of motor impairments on the Rotarod, or emotional changes in the open field and elevated plus mazes. Cresyl violet histology and structural magnetic resonance imaging (MRI indicated that repeated ACHI did not produce significant structural damage. MRI also confirmed there was no volumetric loss in the cortex, hippocampus, or corpus callosum of animals at 1 or 7 days post-ACHI. Together these data indicate that the ACHI model can provide a reliable, high throughput means to study the effects of concussions in juvenile rats.

Chronic constipation causing obstructive nephropathy in a delayed toddler.

LENUS (Irish Health Repository)

Barrett, Michael Joseph

2012-01-01

Chronic constipation causing obstructive nephropathy is very rare in children. However, it can cause urinary tract obstruction with acute impairment of renal function with a need for emergent disimpaction. The authors discuss a 2 years 4 months old child who presented to our emergency department with acute renal failure due to faecal impaction.

Protective effects of Curcuma longa against neurobehavioral and neurochemical damage caused by cerium chloride in mice.

Science.gov (United States)

Kadri, Yamina; Nciri, Riadh; Brahmi, Noura; Saidi, Saber; Harrath, Abdel Halim; Alwasel, Saleh; Aldahmash, Waleed; El Feki, Abdelfatteh; Allagui, Mohamed Salah

2018-05-07

Cerium chloride (CeCl 3 ) is considered an environmental pollutant and a potent neurotoxic agent. Medicinal plants have many bioactive compounds that provide protection against damage caused by such pollutants. Curcuma longa is a bioactive compound-rich plant with very important antioxidant properties. To study the preventive and healing effects of Curcuma longa on cerium-damaged mouse brains, we intraperitoneally injected cerium chloride (CeCl 3 , 20 mg/kg BW) along with Curcuma longa extract, administrated by gavage (100 mg/kg BW), into mice for 60 days. We then examined mouse behavior, brain tissue damage, and brain oxidative stress parameters. Our results revealed a significant modification in the behavior of the CeCl 3 -treated mice. In addition, CeCl 3 induced a significant increment in lipid peroxidation, carbonyl protein (PCO), and advanced oxidation protein product levels, as well as a significant reduction in superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Acetylcholinesterase (AChE) activity remarkably increased in the brain of CeCl 3 -treated mice. Histopathological observations confirmed these results. Curcuma longa attenuated CeCl 3 -induced oxidative stress and increased the activities of antioxidant enzymes. It also decreased AChE activity in the CeCl 3 -damaged mouse brain that was confirmed by histopathology. In conclusion, this study suggests that Curcuma longa has a neuroprotective effect against CeCl 3 -induced damage in the brain.

Systemic Metabolic Impairment and Lung Injury Following Acrolein Inhalation

Science.gov (United States)

A single ozone exposure causes pulmonary injury and systemic metabolic alterations through neuronal and hypothalamus pituitary adrenal axis activation. Metabolically impaired Goto Kakizaki (GK) rats with non-obese type-2 diabetes are more sensitive to ozone induced changes than h...

Loss of Mitochondrial Function Impairs Lysosomes.

Science.gov (United States)

Demers-Lamarche, Julie; Guillebaud, Gérald; Tlili, Mouna; Todkar, Kiran; Bélanger, Noémie; Grondin, Martine; Nguyen, Angela P; Michel, Jennifer; Germain, Marc

2016-05-06

Alterations in mitochondrial function, as observed in neurodegenerative diseases, lead to disrupted energy metabolism and production of damaging reactive oxygen species. Here, we demonstrate that mitochondrial dysfunction also disrupts the structure and function of lysosomes, the main degradation and recycling organelle. Specifically, inhibition of mitochondrial function, following deletion of the mitochondrial protein AIF, OPA1, or PINK1, as well as chemical inhibition of the electron transport chain, impaired lysosomal activity and caused the appearance of large lysosomal vacuoles. Importantly, our results show that lysosomal impairment is dependent on reactive oxygen species. Given that alterations in both mitochondrial function and lysosomal activity are key features of neurodegenerative diseases, this work provides important insights into the etiology of neurodegenerative diseases. © 2016 by The American Society for Biochemistry and Molecular Biology, Inc.

Monogenic and chromosomal causes of isolated speech and language impairment.

Science.gov (United States)

Barnett, C P; van Bon, B W M

2015-11-01

The importance of a precise molecular diagnosis for children with intellectual disability, autism spectrum disorder and epilepsy has become widely accepted and genetic testing is an integral part of the diagnostic evaluation of these children. In contrast, children with an isolated speech or language disorder are not often genetically evaluated, despite recent evidence supporting a role for genetic factors in the aetiology of these disorders. Several chromosomal copy number variants and single gene disorders associated with abnormalities of speech and language have been identified. Individuals without a precise genetic diagnosis will not receive optimal management including interventions such as early testosterone replacement in Klinefelter syndrome, otorhinolaryngological and audiometric evaluation in 22q11.2 deletion syndrome, cardiovascular surveillance in 7q11.23 duplications and early dietary management to prevent obesity in proximal 16p11.2 deletions. This review summarises the clinical features, aetiology and management options of known chromosomal and single gene disorders that are associated with speech and language pathology in the setting of normal or only mildly impaired cognitive function. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

A framework for communication between visually impaired, hearing impaired and speech impaired using arduino

Science.gov (United States)

Sujatha, R.; Khandelwa, Prakhar; Gupta, Anusha; Anand, Nayan

2017-11-01

A long time ago our society accepted the notion of treating people with disabilities not as unviable and disabled but as differently-abled, recognizing their skills beyond their disabilities. The next step has to be taken by our scientific community, that is, to normalize lives of the people with disabilities and make it so as if they are no different to us. The primary step in this direction would be to normalize communication between people. People with an impaired speech or impaired vision or impaired hearing face difficulties while having a casual conversation with others. Any form of communication feels so strenuous that the impaired end up communicating just the important information and avoid a casual conversation. To normalize conversation between the impaired we need a simple and compact device which facilitates the conversation by providing the information in the desired form.

20 CFR 416.998 - If you become disabled by another impairment(s).

Science.gov (United States)

2010-04-01

... 20 Employees' Benefits 2 2010-04-01 2010-04-01 false If you become disabled by another impairment... Disability Or Blindness § 416.998 If you become disabled by another impairment(s). If a new severe impairment(s) begins in or before the month in which your last impairment(s) ends, we will find that your...

20 CFR 404.1598 - If you become disabled by another impairment(s).

Science.gov (United States)

2010-04-01

... 20 Employees' Benefits 2 2010-04-01 2010-04-01 false If you become disabled by another impairment... Disability § 404.1598 If you become disabled by another impairment(s). If a new severe impairment(s) begins in or before the month in which your last impairment(s) ends, we will find that your disability is...

Cataract after total body irradiation and bone marrow transplantation degree of visual impairment

International Nuclear Information System (INIS)

Kempen-Harteveld, M. Loes van; Struikmans, Henk; Kal, Henk B.; Tweel, Ingeborg van der; Mourits, Maarten P.; Verdonck, Leo F.; Schipper, Jan; Battermann, Jan J.

2002-01-01

Purpose: To assess the degree of visual impairment as a result of cataract formation after total body irradiation (TBI) for bone marrow transplantation. Methods and Materials: The data from 93 patients who received TBI in 1 or 2 fractions as a part of their conditioning regimen for bone marrow transplantation were analyzed with respect to the degree of visual impairment as a result of cataract formation. The probability to develop severe visual impairment (SVI) was determined for all patients, and the degree of visual impairment was assessed for 56 patients with stabilized cataract, using three categories: no, mild, or severe. Results: For all 93 patients, the probability of developing a cataract causing SVI was 0.44. For allogeneic patients, it was 0.33 without and 0.71 with steroid treatment (p<0.001). All SVI-free probability curves reached a plateau distinct from the cataract-free curves. Apparently, cataracts developing late in the follow-up period rarely cause SVI. Of the patients with stabilized cataract, 32% had no visual impairment, 16% had mild, and 52% severe impairment. No or mild visual impairment was present in 61% of all patients with stable cataract and no steroid treatment compared with only 13% of the patients treated with steroids (p=0.035). Conclusion: SVI occurs in only some of the patients (52%) with stable cataract after TBI for bone marrow transplantation in 1 or 2 fractions. Steroid treatment markedly increases the probability of developing visual problems as result of a cataract after TBI

Effect Considering of Mild and Moderate Visual and Auditory Impairment on the Activities of Daily Living and Balance Performance in the Elderly

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Mina Hosseini

2010-01-01

Conclusion: Even mild and moderate auditory impairment can cause disability in the basic ADL. If mild and moderate auditory impairment exist simultaneously with visual impairment, the person had balance disability. Auditory impairment didn't have any effect on balance.

A combination of two truncating mutations in USH2A causes more severe and progressive hearing impairment in Usher syndrome type IIa

DEFF Research Database (Denmark)

Hartel, Bas P.; Lofgren, Maria; Huygen, Patrick L. M.

2016-01-01

Objectives Usher syndrome is an inherited disorder that is characterized by hearing impairment (HI), retinitis pigmentosa, and in some cases vestibular dysfunction. Usher syndrome type IIa is caused by mutations in USH2A. HI in these patients is highly heterogeneous and the present study evaluates...... the effects of different types of USH2A mutations on the audiometric phenotype. Data from two large centres of expertise on Usher Syndrome in the Netherlands and Sweden were combined in order to create a large combined sample of patients to identify possible genotype-phenotype correlations. Design...... A retrospective study on HI in 110 patients (65 Dutch and 45 Swedish) genetically diagnosed with Usher syndrome type IIa. We used methods especially designed for characterizing and testing differences in audiological phenotype between patient subgroups. These methods included Age Related Typical Audiograms (ARTA...

Fertility impairment in radiotherapy

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Marta Biedka

2016-02-01

Full Text Available Infertility as a result of antineoplastic therapy is becoming a very important issue due to the growing incidence of neoplastic diseases. Routinely applied antineoplastic treatments and the illness itself lead to fertility disorders. Therapeutic methods used in antineoplastic treatment may cause fertility impairment or sterilization due to permanent damage to reproductive cells. The risk of sterilization depends on the patient’s sex, age during therapy, type of neoplasm, radiation dose and treatment area. It is known that chemotherapy and radiotherapy can lead to fertility impairment and the combination of these two gives an additive effect. The aim of this article is to raise the issue of infertility in these patients. It is of growing importance due to the increase in the number of children and young adults who underwent radiotherapy in the past. The progress in antineoplastic therapy improves treatment results, but at the same time requires a deeper look at existential needs of the patient. Reproductive function is an integral element of self-esteem and should be taken into account during therapy planning.

Hemodynamic causes of exercise intolerance in Fontan patients

DEFF Research Database (Denmark)

Hebert, Anders; Jensen, Annette S; Mikkelsen, Ulla Ramer

2014-01-01

BACKGROUND: Exercise intolerance is frequent among Fontan patients and an important determinant for quality of life. This study investigated the hemodynamic causes of impaired exercise capacity in Fontan patients with particular focus on the influence of stroke volume index (SVI) and heart rate (HR...... patients and controls respectively. CONCLUSION: SVI decreased significantly in Fontan patients near the end of maximal effort exercise. The low SVI at maximal exercise was the most important hemodynamic factor limiting exercise capacity in Fontan patients, whereas chronotropic impairment had a smaller...

Can cardiac surgery cause hypopituitarism?

Science.gov (United States)

Francis, Flverly; Burger, Ines; Poll, Eva Maria; Reineke, Andrea; Strasburger, Christian J; Dohmen, Guido; Gilsbach, Joachim M; Kreitschmann-Andermahr, Ilonka

2012-03-01

Apoplexy of pituitary adenomas with subsequent hypopituitarism is a rare but well recognized complication following cardiac surgery. The nature of cardiac on-pump surgery provides a risk of damage to the pituitary because the vascular supply of the pituitary is not included in the cerebral autoregulation. Thus, pituitary tissue may exhibit an increased susceptibility to hypoperfusion, ischemia or intraoperative embolism. After on-pump procedures, patients often present with physical and psychosocial impairments which resemble symptoms of hypopituitarism. Therefore, we analyzed whether on-pump cardiac surgery may cause pituitary dysfunction also in the absence of pre-existing pituitary disease. Twenty-five patients were examined 3-12 months after on-pump cardiac surgery. Basal hormone levels for all four anterior pituitary hormone axes were measured and a short synacthen test and a growth hormone releasing hormone plus arginine (GHRH-ARG)-test were performed. Quality of life (QoL), depression, subjective distress for a specific life event, sleep quality and fatigue were assessed by means of self-rating questionnaires. Hormonal alterations were only slight and no signs of anterior hypopituitarism were found except for an insufficient growth hormone rise in two overweight patients in the GHRH-ARG-test. Psychosocial impairment was pronounced, including symptoms of moderate to severe depression in 9, reduced mental QoL in 8, dysfunctional coping in 6 and pronounced sleep disturbances in 16 patients. Hormone levels did not correlate with psychosocial impairment. On-pump cardiac surgery did not cause relevant hypopituitarism in our sample of patients and does not serve to explain the psychosocial symptoms of these patients.

Does visual impairment lead to additional disability in adults with intellectual disabilities?

Science.gov (United States)

Evenhuis, H M; Sjoukes, L; Koot, H M; Kooijman, A C

2009-01-01

This study addresses the question to what extent visual impairment leads to additional disability in adults with intellectual disabilities (ID). In a multi-centre cross-sectional study of 269 adults with mild to profound ID, social and behavioural functioning was assessed with observant-based questionnaires, prior to expert assessment of visual function. With linear regression analysis the percentage of variance, explained by levels of visual function, was calculated for the total population and per ID level. A total of 107/269 participants were visually impaired or blind (WHO criteria). On top of the decrease by ID visual impairment significantly decreased daily living skills, communication & language, recognition/communication. Visual impairment did not cause more self-absorbed and withdrawn behaviour or anxiety. Peculiar looking habits correlated with visual impairment and not with ID. In the groups with moderate and severe ID this effect seems stronger than in the group with profound ID. Although ID alone impairs daily functioning, visual impairment diminishes the daily functioning even more. Timely detection and treatment or rehabilitation of visual impairment may positively influence daily functioning, language development, initiative and persistence, social skills, communication skills and insecure movement.

¹H MRS characterization of neurochemical profiles in orthotopic mouse models of human brain tumors.

Science.gov (United States)

Hulsey, Keith M; Mashimo, Tomoyuki; Banerjee, Abhishek; Soesbe, Todd C; Spence, Jeffrey S; Vemireddy, Vamsidhara; Maher, Elizabeth A; Bachoo, Robert M; Choi, Changho

2015-01-01

Glioblastoma (GBM), the most common primary brain tumor, is resistant to currently available treatments. The development of mouse models of human GBM has provided a tool for studying mechanisms involved in tumor initiation and growth as well as a platform for preclinical investigation of new drugs. In this study we used (1) H MR spectroscopy to study the neurochemical profile of a human orthotopic tumor (HOT) mouse model of human GBM. The goal of this study was to evaluate differences in metabolite concentrations in the GBM HOT mice when compared with normal mouse brain in order to determine if MRS could reliably differentiate tumor from normal brain. A TE =19 ms PRESS sequence at 9.4 T was used for measuring metabolite levels in 12 GBM mice and 8 healthy mice. Levels for 12 metabolites and for lipids/macromolecules at 0.9 ppm and at 1.3 ppm were reliably detected in all mouse spectra. The tumors had significantly lower concentrations of total creatine, GABA, glutamate, total N-acetylaspartate, aspartate, lipids/macromolecules at 0.9 ppm, and lipids/macromolecules at 1.3 ppm than did the brains of normal mice. The concentrations of glycine and lactate, however, were significantly higher in tumors than in normal brain. Copyright © 2014 John Wiley & Sons, Ltd.

Causes and Treatment of Insomnia among Adolescents.

Science.gov (United States)

Morrison, Jack R.; And Others

1985-01-01

As much as 13 percent of the adolescent population may suffer from chronic insomnia, which can impair the victim's daily existence and affect personal life, school performance, and school attendance. The prevalence of adolescent insomnia, and its cause, diagnosis, and treatment are examined. (Author/CB)

20 CFR 220.184 - If the annuitant becomes disabled by another impairment(s).

Science.gov (United States)

2010-04-01

... impairment(s). 220.184 Section 220.184 Employees' Benefits RAILROAD RETIREMENT BOARD REGULATIONS UNDER THE... Activity or Medical Improvement § 220.184 If the annuitant becomes disabled by another impairment(s). If a new severe impairment(s) begins in or before the month in which the last impairment(s) ends, the Board...

Δ9-THC-Caused Synaptic and Memory Impairments Are Mediated through COX-2 Signaling

OpenAIRE

Chen, Rongqing; Zhang, Jian; Fan, Ni; Teng, Zhao-qian; Wu, Yan; Yang, Hongwei; Tang, Ya-ping; Sun, Hao; Song, Yunping; Chen, Chu

2013-01-01

Marijuana has been used for thousands of years as a treatment for medical conditions. However, untoward side effects limit its medical value. Here we show that synaptic and cognitive impairments following repeated exposure to Δ9-tetrahydrocannabinol (Δ9-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids, in the brain. COX-2 induction by Δ9-THC is mediated via CB1 receptor-coupled G-protein βγ subunits. Pharmaco...

A functional approach to cerebral visual impairments in very preterm/very-low-birth-weight children

NARCIS (Netherlands)

Geldof, C.J.A.; van Wassenaer-Leemhuis, A.G.; Dik, M.; Kok, J.H.; Oosterlaan, J.

2015-01-01

Background:Cerebral visual impairment (CVI) is a major cause of visual impairment, with very preterm birth/very low birth weight (VP/VLBW) being a major risk factor. There is no generally accepted definition of CVI. This study aims to investigate the usefulness of an empirically-based functional

Homozygous disruption of PDZD7 by reciprocal translocation in a consanguineous family: a new member of the Usher syndrome protein interactome causing congenital hearing impairment.

Science.gov (United States)

Schneider, Eberhard; Märker, Tina; Daser, Angelika; Frey-Mahn, Gabriele; Beyer, Vera; Farcas, Ruxandra; Schneider-Rätzke, Brigitte; Kohlschmidt, Nicolai; Grossmann, Bärbel; Bauss, Katharina; Napiontek, Ulrike; Keilmann, Annerose; Bartsch, Oliver; Zechner, Ulrich; Wolfrum, Uwe; Haaf, Thomas

2009-02-15

A homozygous reciprocal translocation, 46,XY,t(10;11),t(10;11), was detected in a boy with non-syndromic congenital sensorineural hearing impairment. Both parents and their four other children were heterozygous translocation carriers, 46,XX,t(10;11) and 46,XY,t(10;11), respectively. Fluorescence in situ hybridization of region-specific clones to patient chromosomes was used to localize the breakpoints within bacterial artificial chromosome (BAC) RP11-108L7 on chromosome 10q24.3 and within BAC CTD-2527F12 on chromosome 11q23.3. Junction fragments were cloned by vector ligation and sequenced. The chromosome 10 breakpoint was identified within the PDZ domain containing 7 (PDZD7) gene, disrupting the open reading frame of transcript PDZD7-C (without PDZ domain) and the 5'-untranslated region of transcript PDZD7-D (with one PDZ and two prolin-rich domains). The chromosome 11 breakpoint was localized in an intergenic segment. Reverse transcriptase-polymerase chain reaction analysis revealed PDZD7 expression in the human inner ear. A murine Pdzd7 transcript that is most similar in structure to human PDZD7-D is known to be expressed in the adult inner ear and retina. PDZD7 shares sequence homology with the PDZ domain-containing genes, USH1C (harmonin) and DFNB31 (whirlin). Allelic mutations in harmonin and whirlin can cause both Usher syndrome (USH1C and USH2D, respectively) and congenital hearing impairment (DFNB18 and DFNB31, respectively). Protein-protein interaction assays revealed the integration of PDZD7 in the protein network related to the human Usher syndrome. Collectively, our data provide strong evidence that PDZD7 is a new autosomal-recessive deafness-causing gene and also a prime candidate gene for Usher syndrome.

Cognitive, emotional and behavioral impairments following traumatic brain injury and the neuro-radiological diagnosis

International Nuclear Information System (INIS)

Shinoda, Jun; Asano, Yoshitaka

2011-01-01

Definition and diagnostic criteria in Japan of a high order brain functional impairment are explained and recent findings of the useful imaging for the criteria are discussed. The criteria of cognitive, emotional and behavioral impairments following brain injury (BI) defined by Ministry of Health, Labour and Welfare (MHLW) and National Rehabilitation Center for Persons with Disabilities contain 4 items of major symptoms, test findings, exclusion criteria and diagnosis. The criteria contain parts of diseases F04, F06 and F7 in ICD (International Classification of Diseases) 10, and conceivably correspond to such Western terms as the neuropsychological impairment, neurobehavioral impairment, cognitive disability and post-concussion syndrome. Head trauma is the major cause of BI and in the second item (test findings) of the diagnostic criteria above, imaging confirmation of the organic BI (mainly diffuse) is essential. For imaging technology of chronic diffuse injury, discussed are on findings of the structural MRI, diffusion tensor imaging (DTI), functional MRI; 18 F-fluorodeoxyglucose-positron emission tomography (FDG-PET); and single photon emission computed tomography (SPECT) with 99m Tc-ethyl-cysteinate dimmer and 123 I-iomazenil. Based on those findings, it is thought that the impairment of the high order brain functions by diffuse injury is caused by the dysfunction of the primarily injured region and by its consequent disorder of cingulated gyrus and frontal anterior medial region through disturbance of cerebral nerve transmission and control. It is also suggested that a part of the blast related mild traumatic BI in US ex-servicemen is caused by the light diffuse BI, which can only be identified by the fractional anisotropy-statistical parametric mapping image in DTI. Number of patients with the high order brain functional impairment is estimated to be about 300,000 in Japan, but only 1/3 of those are actually diagnosed to be of the disease. (T.T.)

Acute Hemolysis Caused by Incidental Trichlorfon Exposure

Directory of Open Access Journals (Sweden)

Ming-Ling Wu

2009-04-01

Full Text Available Trichlorfon (o-o-dimethyl-2,2,2-trichloro-hydroxyethylphosphate, an organophosphate, has a moderately potent anti-cholinesterase activity. Organophosphate poisoning is well known for its characteristic symptoms and signs, but acute hemolysis caused by trichlorfon is rarely reported. We present a patient who developed acute hemolysis and renal function impairment after percutaneous trichlorfon exposure. A 54-year-old man applied trichlorfon powder to his dog to kill its parasites. Half an hour later, the dog was suspected to die of cholinergic crisis and the patient felt abdominal cramping pain. Later, he developed severe nausea, vomiting, chills, high fever, and cold sweat. Laboratory work-up disclosed a picture of acute hemolysis, jaundice, renal function impairment and leukocytosis. However, there were no clinical features of acute cholinergic syndrome except gastrointestinal symptoms, and blood cholinesterase activities were also normal. He eventually had a full recovery. Trichlorfon should be added to the toxins known to cause acute hemolysis.

A functional approach to cerebral visual impairments in very preterm/very-low-birth-weight children

NARCIS (Netherlands)

Geldof, Christiaan J. A.; van Wassenaer-Leemhuis, Aleid G.; Dik, Marjolein; Kok, Joke H.; Oosterlaan, Jaap

2015-01-01

Cerebral visual impairment (CVI) is a major cause of visual impairment, with very preterm birth/very low birth weight (VP/VLBW) being a major risk factor. There is no generally accepted definition of CVI. This study aims to investigate the usefulness of an empirically-based functional definition of

Effects of social cognitive impairment on speech disorder in schizophrenia.

Science.gov (United States)

Docherty, Nancy M; McCleery, Amanda; Divilbiss, Marielle; Schumann, Emily B; Moe, Aubrey; Shakeel, Mohammed K

2013-05-01

Disordered speech in schizophrenia impairs social functioning because it impedes communication with others. Treatment approaches targeting this symptom have been limited by an incomplete understanding of its causes. This study examined the process underpinnings of speech disorder, assessed in terms of communication failure. Contributions of impairments in 2 social cognitive abilities, emotion perception and theory of mind (ToM), to speech disorder were assessed in 63 patients with schizophrenia or schizoaffective disorder and 21 nonpsychiatric participants, after controlling for the effects of verbal intelligence and impairments in basic language-related neurocognitive abilities. After removal of the effects of the neurocognitive variables, impairments in emotion perception and ToM each explained additional variance in speech disorder in the patients but not the controls. The neurocognitive and social cognitive variables, taken together, explained 51% of the variance in speech disorder in the patients. Schizophrenic disordered speech may be less a concomitant of "positive" psychotic process than of illness-related limitations in neurocognitive and social cognitive functioning.

Hypothyroidism presenting as reversible renal impairment: an interesting case report.

Science.gov (United States)

Vikrant, Sanjay; Chander, Subhash; Kumar, Satish; Gupta, Dalip

2013-10-01

We describe an interesting case of reversible renal impairment secondary to hypothyroidism. A 57-years-old man was referred from peripheral institution for evaluation of elevated serum creatinine. He had vague complaints of weakness, lethargy and muscle ache but no urinary symptoms. He was found to have hypothyroidism, and thyroid hormone replacement therapy (THRT) was started which resulted in reversal of the renal dysfunction. There was marked improvement in estimated glomerular filtration rate. 99mTc DTPA renal scans done before and after THRT suggested hypothyroidism responsible for this reversible renal impairment. Several studies have described the pathophysiology of diminished renal function in hypothyroidism. Few studies or case reports have shown total amelioration of renal impairment as seen in our patient. The etiology is presumed to be multifactorial, in which hemodynamic effects and a direct effect of thyroid hormone on the kidney play an important role. We suggest that patients with renal impairment of unknown cause have thyroid function tests undertaken as part of routine investigation.

Impaired receptivity and decidualization in DHEA-induced PCOS mice.

Science.gov (United States)

Li, Shu-Yun; Song, Zhuo; Song, Min-Jie; Qin, Jia-Wen; Zhao, Meng-Long; Yang, Zeng-Ming

2016-12-07

Polycystic ovary syndrome (PCOS), a complex endocrine disorder, is a leading cause of female infertility. An obvious reason for infertility in PCOS women is anovulation. However, success rate with high quality embryos selected by assisted reproduction techniques in PCOS patients still remain low with a high rate of early clinical pregnancy loss, suggesting a problem in uterine receptivity. Using a dehydroepiandrosterone-induced mouse model of PCOS, some potential causes of decreased fertility in PCOS patients were explored. In our study, ovulation problem also causes sterility in PCOS mice. After blastocysts from normal mice are transferred into uterine lumen of pseudopregnant PCOS mice, the rate of embryo implantation was reduced. In PCOS mouse uteri, the implantation-related genes are also dysregulated. Additionally, artificial decidualization is severely impaired in PCOS mice. The serum estrogen level is significantly higher in PCOS mice than vehicle control. The high level of estrogen and potentially impaired LIF-STAT3 pathway may lead to embryo implantation failure in PCOS mice. Although there are many studies about effects of PCOS on endometrium, both embryo transfer and artificial decidualization are applied to exclude the effects from ovulation and embryos in our study.

Reduction of the cholesterol sensor SCAP in the brains of mice causes impaired synaptic transmission and altered cognitive function.

Directory of Open Access Journals (Sweden)

Ryo Suzuki

Full Text Available The sterol sensor SCAP is a key regulator of SREBP-2, the major transcription factor controlling cholesterol synthesis. Recently, we showed that there is a global down-regulation of cholesterol synthetic genes, as well as SREBP-2, in the brains of diabetic mice, leading to a reduction of cholesterol synthesis. We now show that in mouse models of type 1 and type 2 diabetes, this is, in part, the result of a decrease of SCAP. Homozygous disruption of the Scap gene in the brains of mice causes perinatal lethality associated with microcephaly and gliosis. Mice with haploinsufficiency of Scap in the brain show a 60% reduction of SCAP protein and ~30% reduction in brain cholesterol synthesis, similar to what is observed in diabetic mice. This results in impaired synaptic transmission, as measured by decreased paired pulse facilitation and long-term potentiation, and is associated with behavioral and cognitive changes. Thus, reduction of SCAP and the consequent suppression of cholesterol synthesis in the brain may play an important role in the increased rates of cognitive decline and Alzheimer disease observed in diabetic states.

Involvement of microglia activation in the lead induced long-term potentiation impairment.

Directory of Open Access Journals (Sweden)

Ming-Chao Liu

Full Text Available Exposure of Lead (Pb, a known neurotoxicant, can impair spatial learning and memory probably via impairing the hippocampal long-term potentiation (LTP as well as hippocampal neuronal injury. Activation of hippocampal microglia also impairs spatial learning and memory. Thus, we raised the hypothesis that activation of microglia is involved in the Pb exposure induced hippocampal LTP impairment and neuronal injury. To test this hypothesis and clarify its underlying mechanisms, we investigated the Pb-exposure on the microglia activation, cytokine release, hippocampal LTP level as well as neuronal injury in in vivo or in vitro model. The changes of these parameters were also observed after pretreatment with minocycline, a microglia activation inhibitor. Long-term low dose Pb exposure (100 ppm for 8 weeks caused significant reduction of LTP in acute slice preparations, meanwhile, such treatment also significantly increased hippocampal microglia activation as well as neuronal injury. In vitro Pb-exposure also induced significantly increase of microglia activation, up-regulate the release of cytokines including tumor necrosis factor-alpha (TNF-α, interleukin-1β (IL-1β and inducible nitric oxide synthase (iNOS in microglia culture alone as well as neuronal injury in the co-culture with hippocampal neurons. Inhibiting the microglia activation with minocycline significantly reversed the above-mentioned Pb-exposure induced changes. Our results showed that Pb can cause microglia activation, which can up-regulate the level of IL-1β, TNF-α and iNOS, these proinflammatory factors may cause hippocampal neuronal injury as well as LTP deficits.

Inhalation exposure to white spirit causes region-dependent alterations in the levels of glial fibrillary acidic protein

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Lam, Henrik Rye; Ladefoged, Ole; østergaard, G.

2000-01-01

Enhanced expression of glial fibrillary acidic protein (GFAP) is known to be associated with toxicant-induced gliosis, a homotypic response of the central nervous system to neural injury. A variety of neurochemical and neurophysiological effects have been observed in experimental animals exposed ...

Chronic Stress Impairs Prefrontal Cortex-Dependent Response Inhibition and Spatial Working Memory

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Mika, Agnieszka; Mazur, Gabriel J.; Hoffman, Ann N.; Talboom, Joshua S.; Bimonte-Nelson, Heather A.; Sanabria, Federico; Conrad, Cheryl D.

2012-01-01

Chronic stress leads to neurochemical and structural alterations in the prefrontal cortex (PFC) that correspond to deficits in PFC-mediated behaviors. The present study examined the effects of chronic restraint stress on response inhibition (using a response-withholding task, fixed-minimum interval schedule of reinforcement, or FMI), and working memory (using a radial arm water maze, RAWM). Adult male Sprague Dawley rats were first trained on the RAWM and subsequently trained on FMI. Following acquisition of FMI, rats were assigned to a restraint stress (6h/d/28d in wire mesh restrainers) or control condition. Immediately after chronic stress, rats were tested on FMI and subsequently on RAWM. FMI results suggest that chronic stress reduces response inhibition capacity and motivation to initiate the task on selective conditions when food reward was not obtained on the preceding trial. RAWM results suggest that chronic stress produces transient deficits in working memory without altering previously consolidated reference memory. Behavioral measures from FMI failed to correlate with metrics from RAWM except for one in which changes in FMI timing precision negatively correlated with changes in RAWM working memory errors for the controls, a finding that was not observed following chronic stress. Fisher’s r to z transformation revealed no significant differences between control and stress with correlation coefficients. These findings are the first to show that chronic stress impairs both response inhibition and working memory, two behaviors that have never been direct compared within the same animals following chronic stress, using FMI, an appetitive task, and RAWM, a non-appetitive task. PMID:22905921

Single prolonged stress impairs social and object novelty recognition in rats.

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Eagle, Andrew L; Fitzpatrick, Chris J; Perrine, Shane A

2013-11-01

Posttraumatic stress disorder (PTSD) results from exposure to a traumatic event and manifests as re-experiencing, arousal, avoidance, and negative cognition/mood symptoms. Avoidant symptoms, as well as the newly defined negative cognitions/mood, are a serious complication leading to diminished interest in once important or positive activities, such as social interaction; however, the basis of these symptoms remains poorly understood. PTSD patients also exhibit impaired object and social recognition, which may underlie the avoidance and symptoms of negative cognition, such as social estrangement or diminished interest in activities. Previous studies have demonstrated that single prolonged stress (SPS), models PTSD phenotypes, including impairments in learning and memory. Therefore, it was hypothesized that SPS would impair social and object recognition memory. Male Sprague Dawley rats were exposed to SPS then tested in the social choice test (SCT) or novel object recognition test (NOR). These tests measure recognition of novelty over familiarity, a natural preference of rodents. Results show that SPS impaired preference for both social and object novelty. In addition, SPS impairment in social recognition may be caused by impaired behavioral flexibility, or an inability to shift behavior during the SCT. These results demonstrate that traumatic stress can impair social and object recognition memory, which may underlie certain avoidant symptoms or negative cognition in PTSD and be related to impaired behavioral flexibility. Copyright © 2013 Elsevier B.V. All rights reserved.

Psychopathology among a sample of hearing impaired adolescents.

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Mosaku, Kolawole; Akinpelu, Victoria; Ogunniyi, Grace

2015-12-01

Hearing impairment is a recognized cause of emotional and psychological disturbances worldwide, however little is known about this condition in Nigeria. The aim of this study is to compare the prevalence of psychopathology between hearing impaired adolescents and healthy adolescents. Students attending two special schools for the hearing impaired were assessed for psychopathology with the help of a trained signer and their teacher, using the International Classification of Diseases Diagnostic Criteria (ICD 10). Fifty two hearing impaired students and 52 age and sex matched controls from the same school were also interviewed using the same instrument. The mean age of the hearing impaired students was 16 (sd=3.8), while for the controls the mean age was 16 (sd=2.5). Psychopathology was present in 10 (19%) of the hearing impaired adolescents compared to 2 (4%) among the control group, this difference was statistically significant (χ(2)=4.62 p=0.03). The most common diagnosis was generalized anxiety disorder 4 (8%), followed by depression 2 (4%). Years spent in school (t=4.81, p=0.001), primary guardian (χ(2)=18.3, p=0.001) and mean income of guardian (t=7.10, p=0.001) were all significantly different between the two groups. Psychopathology is relatively common in this population. Proper assessment and treatment should be made available for this population group. A limitation to this study is communication difficulty which made only a third party assessment possible; this may affect the generalizability of the findings. Copyright © 2015 Elsevier B.V. All rights reserved.

DJ-1 KNOCK-DOWN IMPAIRS ASTROCYTE MITOCHONDRIAL FUNCTION

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LARSEN, N. J.; AMBROSI, G.; MULLETT, S. J.; BERMAN, S. B.; HINKLE, D. A.

2012-01-01

Mitochondrial dysfunction has long been implicated in the pathogenesis of Parkinson’s disease (PD). PD brain tissues show evidence for mitochondrial respiratory chain Complex I deficiency. Pharmacological inhibitors of Complex I, such as rotenone, cause experimental parkinsonism. The cytoprotective protein DJ-1, whose deletion is sufficient to cause genetic PD, is also known to have mitochondria-stabilizing properties. We have previously shown that DJ-1 is over-expressed in PD astrocytes, and that DJ-1 deficiency impairs the capacity of astrocytes to protect co-cultured neurons against rotenone. Since DJ-1 modulated, astrocyte-mediated neuroprotection against rotenone may depend upon proper astrocytic mitochondrial functioning, we hypothesized that DJ-1 deficiency would impair astrocyte mitochondrial motility, fission/fusion dynamics, membrane potential maintenance, and respiration, both at baseline and as an enhancement of rotenone-induced mitochondrial dysfunction. In astrocyte-enriched cultures, we observed that DJ-1 knock-down reduced mitochondrial motility primarily in the cellular processes of both untreated and rotenone treated cells. In these same cultures, DJ-1 knock-down did not appreciably affect mitochondrial fission, fusion, or respiration, but did enhance rotenone-induced reductions in the mitochondrial membrane potential. In neuron–astrocyte co-cultures, astrocytic DJ-1 knock-down reduced astrocyte process mitochondrial motility in untreated cells, but this effect was not maintained in the presence of rotenone. In the same co-cultures, astrocytic DJ-1 knock-down significantly reduced mitochondrial fusion in the astrocyte cell bodies, but not the processes, under the same conditions of rotenone treatment in which DJ-1 deficiency is known to impair astrocyte-mediated neuroprotection. Our studies therefore demonstrated the following new findings: (i) DJ-1 deficiency can impair astrocyte mitochondrial physiology at multiple levels, (ii) astrocyte

[Detection of auditory impairment in the offsprings caused by drug treatment of the dams].

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Kameyama, T; Nabeshima, T; Itoh, J

1982-12-01

To study the auditory impairment induced by prenatal administration of aminoglycosides in the offspring, the shuttle box method to measure the auditory threshold of rats (Kameyama et al., Folia pharmacol. japon. 77, 15, 1981) was employed. Four groups of pregnant rats were administered 200 mg/kg kanamycin sulfate (KM), 200 mg/kg dihydrostreptomycin sulfate (DHSM), 100 mg/kg neomycin sulfate (NM), or 1 ml/kg saline intramuscularly from the 10th to the 19th day of pregnancy. The auditory threshold of the offspring could be measured by the shuttle box method in about 90% of the live born rats at the age of 100 days. The auditory thresholds of the groups were as follows (mean +/- S.E.): saline group, 53.8 +/- 0.6 dB (N = 36); KM group, 63.8 +/- 1.1 dB (N = 34); DHSM group, 60.0 +/- 1.2 dB (N = 29); NM group, 62.4 +/- 1.2 dB (N = 24). Auditory thresholds of drug-treated groups were significantly higher than that of the saline group. However, no increase in the auditory threshold of the mother rat was detected after treatment with aminoglycosides. In addition, the experimental procedure of the shuttle box method is very easy, and the auditory threshold of a large number of rats could be measured in a short period. These findings suggest that this method is a very useful one for screening for auditory impairment induced by prenatal drug treatment in rat offspring.

Neural correlates of alerting and orienting impairment in multiple sclerosis patients.

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Vázquez-Marrufo, Manuel; Galvao-Carmona, Alejandro; González-Rosa, Javier J; Hidalgo-Muñoz, Antonio R; Borges, Mónica; Ruiz-Peña, Juan Luis; Izquierdo, Guillermo

2014-01-01

A considerable percentage of multiple sclerosis patients have attentional impairment, but understanding its neurophysiological basis remains a challenge. The Attention Network Test allows 3 attentional networks to be studied. Previous behavioural studies using this test have shown that the alerting network is impaired in multiple sclerosis. The aim of this study was to identify neurophysiological indexes of the attention impairment in relapsing-remitting multiple sclerosis patients using this test. After general slowing had been removed in patients group to isolate the effects of each condition, some behavioral differences between them were obtained. About Contingent Negative Variation, a statistically significant decrement were found in the amplitude for Central and Spatial Cue Conditions for patient group (pmultiple sclerosis. P1 and N1 delayed latencies are evidence of the demyelination process that causes impairment in the first steps of the visual sensory processing. Lastly, P3 amplitude shows a general decrease for the pathological group probably indexing a more central impairment. These results suggest that the Attention Network Test give evidence of multiple levels of attention impairment, which could help in the assessment and treatment of relapsing-remitting multiple sclerosis patients.

Abeta(1-42) injection causes memory impairment, lowered cortical and serum BDNF levels, and decreased hippocampal 5-HT(2A) levels

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Christensen, R; Marcussen, Anders Bue; Wörtwein, Gitta

2008-01-01

was used to monitor Abeta(1-42) induced memory impairment. Memory impairment was seen 22 days after injection of Abeta(1-42) in the experimental group and until termination of the experiments. In the Abeta(1-42) injected animals we saw an abolished increase in serum BDNF levels that was accompanied...... by significant lower BDNF levels in frontal cortex and by an 8.5% reduction in hippocampal 5-HT(2A) receptor levels. A tendency towards lowered cortical 5-HT(2A) was also observed. These results indicate that the Abeta(1-42) associated memory deficit is associated with an impaired BDNF regulation, which...

Inability to produce a model of dialysis encephalopathy in the rat by aluminum administration.

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Perry, T L; Yong, V W; Godolphin, W J; Sutter, M; Hansen, S; Kish, S J; Foulks, J G; Ito, M

1987-04-01

We attempted to produce a rat model of brain aluminum toxicity in order to explore whether or not aluminum accumulation produces the neurochemical changes observed in brains of patients who die with dialysis encephalopathy. Daily subcutaneous injection of Al(OH)3 caused marked elevation of serum aluminum concentrations, but did not increase brain aluminum contents, either in rats with normal renal function, or in rats with unilateral or 5/6 nephrectomies. LiCl pretreatment, which has been reported to cause irreversible renal failure, did not impair renal function nor aid in achieving elevated brain aluminum contents. No reductions in brain contents of gamma-aminobutyric acid (GABA) or in glutamic acid decarboxylase (GAD, E.C.4.1.1.15) and choline acetyltransferase (ChAT, E.C.2.3.1.6) activities were observed in aluminum-treated rats. We conclude that the rat is not a suitable laboratory animal to explore the role of aluminum toxicity in causing the GABA and ChAT deficits present in brains of hemodialyzed human patients.

A mutation in the glutamate-rich region of RNA-binding motif protein 20 causes dilated cardiomyopathy through missplicing of titin and impaired Frank-Starling mechanism

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Beqqali, Abdelaziz; Bollen, I. A. E.; Rasmussen, T. B.

2016-01-01

Mutations in the RS-domain of RNA-binding motif protein 20 (RBM20) have recently been identified to segregate with aggressive forms of familial dilated cardiomyopathy (DCM). Loss of RBM20 in rats results in missplicing of the sarcomeric gene titin (TTN). The functional and physiological consequen......Mutations in the RS-domain of RNA-binding motif protein 20 (RBM20) have recently been identified to segregate with aggressive forms of familial dilated cardiomyopathy (DCM). Loss of RBM20 in rats results in missplicing of the sarcomeric gene titin (TTN). The functional and physiological...... consequences of RBM20 mutations outside the mutational hotspot of RBM20 have not been explored to date. In this study, we investigated the pathomechanism of DCM caused by a novel RBM20 mutation in human cardiomyocytes. We identified a family with DCM carrying a mutation (RBM20(E913K/+)) in a glutamate...... to the early onset, and malignant course of DCM caused by RBM20 mutations. Altogether, our results demonstrate that heterozygous loss of RBM20 suffices to profoundly impair myocyte biomechanics by its disturbance of TTN splicing....

Sound localization in noise in hearing-impaired listeners.

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Lorenzi, C; Gatehouse, S; Lever, C

1999-06-01

The present study assesses the ability of four listeners with high-frequency, bilateral symmetrical sensorineural hearing loss to localize and detect a broadband click train in the frontal-horizontal plane, in quiet and in the presence of a white noise. The speaker array and stimuli are identical to those described by Lorenzi et al. (in press). The results show that: (1) localization performance is only slightly poorer in hearing-impaired listeners than in normal-hearing listeners when noise is at 0 deg azimuth, (2) localization performance begins to decrease at higher signal-to-noise ratios for hearing-impaired listeners than for normal-hearing listeners when noise is at +/- 90 deg azimuth, and (3) the performance of hearing-impaired listeners is less consistent when noise is at +/- 90 deg azimuth than at 0 deg azimuth. The effects of a high-frequency hearing loss were also studied by measuring the ability of normal-hearing listeners to localize the low-pass filtered version of the clicks. The data reproduce the effects of noise on three out of the four hearing-impaired listeners when noise is at 0 deg azimuth. They reproduce the effects of noise on only two out of the four hearing-impaired listeners when noise is at +/- 90 deg azimuth. The additional effects of a low-frequency hearing loss were investigated by attenuating the low-pass filtered clicks and the noise by 20 dB. The results show that attenuation does not strongly affect localization accuracy for normal-hearing listeners. Measurements of the clicks' detectability indicate that the hearing-impaired listeners who show the poorest localization accuracy also show the poorest ability to detect the clicks. The inaudibility of high frequencies, "distortions," and reduced detectability of the signal are assumed to have caused the poorer-than-normal localization accuracy for hearing-impaired listeners.

Postpartum estrogen withdrawal impairs hippocampal neurogenesis and causes depression- and anxiety-like behaviors in mice.

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Zhang, Zhuan; Hong, Juan; Zhang, Suyun; Zhang, Tingting; Sha, Sha; Yang, Rong; Qian, Yanning; Chen, Ling

2016-04-01

Postpartum estrogen withdrawal is known to be a particularly vulnerable time for depressive symptoms. Ovariectomized adult mice (OVX-mice) treated with hormone-simulated pregnancy (HSP mice) followed by a subsequent estradiol benzoate (EB) withdrawal (EW mice) exhibited depression- and anxiety-like behaviors, as assessed by forced swim, tail suspension and elevated plus-maze, while HSP mice, OVX mice or EB-treated OVX mice (OVX/EB mice) did not. The survival and neurite growth of newborn neurons in hippocampal dentate gyrus were examined on day 5 after EW. Compared with controls, the numbers of 28-day-old BrdU(+) and BrdU(+)/NeuN(+) cells were increased in HSP mice but significantly decreased in EW mice; the numbers of 10-day-old BrdU(+) cells were increased in HSP mice and OVX/EB mice; and the density of DCX(+) fibers was reduced in EW mice and OVX mice. The phosphorylation of hippocampal NMDA receptor (NMDAr) NR2B subunit or Src was increased in HSP mice but decreased in EW mice. NMDAr agonist NMDA prevented the loss of 28-day-old BrdU(+) cells and the depression- and anxiety-like behaviors in EW mice. NR2B inhibitor Ro25-6981 or Src inhibitor dasatinib caused depression- and anxiety-like behaviors in HSP mice with the reduction of 28-day-old BrdU(+) cells. The hippocampal BDNF levels were reduced in EW mice and OVX mice. TrkB receptor inhibitor K252a reduced the density of DCX(+) fibers in HSP mice without the reduction of 28-day-old BrdU(+) cells, or the production of affective disorder. Collectively, these results indicate that postpartum estrogen withdrawal impairs hippocampal neurogenesis in mice that show depression- and anxiety-like behaviors. Copyright © 2016 Elsevier Ltd. All rights reserved.

High passage MIN6 cells have impaired insulin secretion with impaired glucose and lipid oxidation.

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Kim Cheng

Full Text Available Type 2 diabetes is a metabolic disorder characterized by the inability of beta-cells to secrete enough insulin to maintain glucose homeostasis. MIN6 cells secrete insulin in response to glucose and other secretagogues, but high passage (HP MIN6 cells lose their ability to secrete insulin in response to glucose. We hypothesized that metabolism of glucose and lipids were defective in HP MIN6 cells causing impaired glucose stimulated insulin secretion (GSIS. HP MIN6 cells had no first phase and impaired second phase GSIS indicative of global functional impairment. This was coupled with a markedly reduced ATP content at basal and glucose stimulated states. Glucose uptake and oxidation were higher at basal glucose but ATP content failed to increase with glucose. HP MIN6 cells had decreased basal lipid oxidation. This was accompanied by reduced expressions of Glut1, Gck, Pfk, Srebp1c, Ucp2, Sirt3, Nampt. MIN6 cells represent an important model of beta cells which, as passage numbers increased lost first phase but retained partial second phase GSIS, similar to patients early in type 2 diabetes onset. We believe a number of gene expression changes occurred to produce this defect, with emphasis on Sirt3 and Nampt, two genes that have been implicated in maintenance of glucose homeostasis.

Type 2 diabetes mellitus and exercise impairment.

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Reusch, Jane E B; Bridenstine, Mark; Regensteiner, Judith G

2013-03-01

Limitations in physical fitness, a consistent finding in individuals with both type I and type 2 diabetes mellitus, correlate strongly with cardiovascular and all-cause mortality. These limitations may significantly contribute to the persistent excess cardiovascular mortality affecting this group. Exercise impairments in VO2 peak and VO2 kinetics manifest early on in diabetes, even with good glycemic control and in the absence of clinically apparent complications. Subclinical cardiac dysfunction is often present but does not fully explain the observed defect in exercise capacity in persons with diabetes. In part, the cardiac limitations are secondary to decreased perfusion with exercise challenge. This is a reversible defect. Similarly, in the skeletal muscle, impairments in nutritive blood flow correlate with slowed (or inefficient) exercise kinetics and decreased exercise capacity. Several correlations highlight the likelihood of endothelial-specific impairments as mediators of exercise dysfunction in diabetes, including insulin resistance, endothelial dysfunction, decreased myocardial perfusion, slowed tissue hemoglobin oxygen saturation, and impairment in mitochondrial function. Both exercise training and therapies targeted at improving insulin sensitivity and endothelial function improve physical fitness in subjects with type 2 diabetes. Optimization of exercise functions in people with diabetes has implications for diabetes prevention and reductions in mortality risk. Understanding the molecular details of endothelial dysfunction in diabetes may provide specific therapeutic targets for the remediation of this defect. Rat models to test this hypothesis are under study.

Prevalence of Physical Impairment Among the Elderlly Persons of the Tehran City in 1385

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Afsoon Nodehi Moghadam

2007-01-01

Full Text Available Objectives: Musculoskeletal pain is common in elderly people with prevalence range from 10% to 71%. Musculoskeletal pain is found to be a strong risk factor for disability in elderly woman. The purpose of this study is to examine the prevalence of physical impairment of elderly people. Methods & Materials: A physiotherapist has evaluated elderly persons files in four physiotherapy centers during 1384-85. Results: Knee osteoarthritis and low back pain respectively were the most common causes of physical impairment in elderly women. Prevalence of knee osteoarthritis is increasing. This increase is likely due to several factors: advancing age of population, increasing injuries and rapidly advancing rates of obesity. Age–related change of intervertebral disks, decreased back muscle strength and decreased bone mineral density may lead to low back pain. Conclusion: Knee osteoarthritis and low back pain are the most commom causes of physical impairment.

Neurotoxicity of developmental hypothyroxinemia and hypothyroidism in rats: Impairments of long-term potentiation are mediated by phosphatidylinositol 3-kinase signaling pathway

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Wang, Yi; Wei, Wei; Wang, Yuan; Dong, Jing; Song, Binbin; Min, Hui [Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang (China); Teng, Weiping, E-mail: twpendocrine@yahoo.com.cn [Liaoning Provincial Key Laboratory of Endocrine Diseases, the First Hospital of China Medical University, Shenyang (China); Chen, Jie, E-mail: chenjie@mail.cmu.edu.cn [Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang (China)

2013-09-01

Neurotoxicity of iodine deficiency-induced hypothyroidism during developmental period results in serious impairments of brain function, such as learning and memory. These impairments are largely irreversible, and the underlying mechanisms remain unclear. In addition to hypothyroidism, iodine deficiency may cause hypothyroxinemia, a relatively subtle form of thyroid hormone deficiency. Neurotoxicity of developmental hypothyroxinemia also potentially impairs learning and memory. However, more direct evidence of the associations between developmental hypothyroxinemia and impairments of learning and memory should be provided, and the underlying mechanisms remain to be elucidated. Thus, in the present study, we investigated the effects of developmental hypothyroxinemia and hypothyroidism on long-term potentiation (LTP), a widely accepted cellular model of learning and memory, in the hippocampal CA1 region. The activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway – a pathway closely associated with synaptic plasticity and learning and memory – was also investigated. Wistar rats were treated with iodine deficient diet or methimazole (MMZ) to induce developmental hypothyroxinemia or hypothyroidism. The results showed that developmental hypothyroxinemia caused by mild iodine deficiency and developmental hypothyroidism caused by severe iodine deficiency or MMZ significantly reduced the field-excitatory postsynaptic potential (f-EPSP) slope and the population spike (PS) amplitude. Decreased activation of the PI3K signaling pathway was also observed in rats subjected to developmental hypothyroxinemia or hypothyroidism. Our results may support the hypothesis that neurotoxicity of both developmental hypothyroxinemia and hypothyroidism causes damages to learning and memory. Our results also suggest that decreased activation of the PI3K signaling pathway may contribute to impairments of LTP caused by neurotoxicity of both developmental hypothyroxinemia and

Neurotoxicity of developmental hypothyroxinemia and hypothyroidism in rats: Impairments of long-term potentiation are mediated by phosphatidylinositol 3-kinase signaling pathway

International Nuclear Information System (INIS)

Wang, Yi; Wei, Wei; Wang, Yuan; Dong, Jing; Song, Binbin; Min, Hui; Teng, Weiping; Chen, Jie

2013-01-01

Neurotoxicity of iodine deficiency-induced hypothyroidism during developmental period results in serious impairments of brain function, such as learning and memory. These impairments are largely irreversible, and the underlying mechanisms remain unclear. In addition to hypothyroidism, iodine deficiency may cause hypothyroxinemia, a relatively subtle form of thyroid hormone deficiency. Neurotoxicity of developmental hypothyroxinemia also potentially impairs learning and memory. However, more direct evidence of the associations between developmental hypothyroxinemia and impairments of learning and memory should be provided, and the underlying mechanisms remain to be elucidated. Thus, in the present study, we investigated the effects of developmental hypothyroxinemia and hypothyroidism on long-term potentiation (LTP), a widely accepted cellular model of learning and memory, in the hippocampal CA1 region. The activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway – a pathway closely associated with synaptic plasticity and learning and memory – was also investigated. Wistar rats were treated with iodine deficient diet or methimazole (MMZ) to induce developmental hypothyroxinemia or hypothyroidism. The results showed that developmental hypothyroxinemia caused by mild iodine deficiency and developmental hypothyroidism caused by severe iodine deficiency or MMZ significantly reduced the field-excitatory postsynaptic potential (f-EPSP) slope and the population spike (PS) amplitude. Decreased activation of the PI3K signaling pathway was also observed in rats subjected to developmental hypothyroxinemia or hypothyroidism. Our results may support the hypothesis that neurotoxicity of both developmental hypothyroxinemia and hypothyroidism causes damages to learning and memory. Our results also suggest that decreased activation of the PI3K signaling pathway may contribute to impairments of LTP caused by neurotoxicity of both developmental hypothyroxinemia and

The psychological and neurochemical mechanisms of drug memory reconsolidation: implications for the treatment of addiction.

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Milton, Amy L; Everitt, Barry J

2010-06-01

Memory reconsolidation is the process by which memories, destabilised at retrieval, require restabilisation to persist in the brain. It has been demonstrated that even old, well-established memories require reconsolidation following retrieval; therefore, memory reconsolidation could potentially be exploited to disrupt, or even erase, aberrant memories that underlie psychiatric disorders, thereby providing a novel therapeutic target. Drug addiction is one such disorder; it is both chronic and relapsing, and one prominent risk factor for a relapse episode is the presentation of environmental cues that have previously been associated with drugs of abuse. This 'cue-induced relapse' can be accounted for in psychological terms by reinforcing memories of the pavlovian association between the cue and the drug, which can thus influence behaviour through at least three psychologically and neurobiologically dissociable mechanisms: conditioned reinforcement, conditioned approach and conditioned motivation. As each of these psychological processes could contribute to the resumption of drug-seeking following abstinence, it is important to develop treatments that can reduce drug-seeking re-established via influences on each or all of these pavlovian processes, in order to minimise the risk of a subsequent relapse. Investigation of the memory reconsolidation mechanisms of the memories underlying conditioned reinforcement, conditioned approach and conditioned motivation indicate that they depend upon different neurochemical systems, including the glutamatergic and adrenergic systems within limbic corticostriatal circuitry. We also discuss here the subsequent translation to the clinic of this preclinical work.

A Rare Case of Intermittent Claudication Associated with Impaired Arterial Vasodilation

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J. J. Posthuma

2017-01-01

Full Text Available Exercise-related intermittent claudication is marked by reduced blood flow to extremities caused by either stenosis or impaired vascular function. Although intermittent claudication is common in the elderly, it rarely occurs in the young and middle-aged individuals. Here, we report a case of exercise-related claudication in a 41-year-old woman, in the absence of overt vascular pathology. Using a series of imaging and functional tests, we established that her complaints were due to impaired arterial vasodilation, possibly due to a defect in nitrous oxide-mediated dilation. The symptoms were reversible upon administration of a calcium antagonist, showing reversibility of the vascular impairment. Identification of reversible vascular “stiffness” merits consideration in young and otherwise healthy subjects with claudication of unknown origin.

Identification of Two Disease-causing Genes TJP2 and GJB2 in a Chinese Family with Unconditional Autosomal Dominant Nonsyndromic Hereditary Hearing Impairment

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Hong-Yang Wang

2015-01-01

Full Text Available Background: There are more than 300 genetic loci that have been found to be related to hereditary hearing impairment (HHI, including 92 causative genes for nonsyndromic hearing loss, among which 34 genes are related to autosomal dominant nonsyndromic HHI (ADNSHHI. Traditional linkage analysis and candidate gene sequencing are not effective at detecting the ADNSHHI, especially for the unconditional families that may have more than one pathogenic cause. This study identified two disease-causing genes TJP2 and GJB2 in a Chinese family with unconditional ADNSHHI. Methods: To decipher the genetic code of a Chinese family (family 686 with ADNSHHI, different gene screening techniques have been performed, including linkage analysis, candidate genes screening, high-throughput sequencing and Sanger sequencing. These techniques were done on samples obtained from this family over a period of 10 years. Results: We identified a pathogenic missense mutation, c. 2081G>A (p.G694E, in TJP2, a gene that plays a crucial role in apoptosis and age-related hearing loss (ARHL. The mutation was co-segregated in this pedigree in all, but not in the two patients who presented with different phenotypes from the other affected family members. In one of the two patients, we confirmed that the compound heterozygosity for p.Y136FNx01 and p.G45E in the GJB2 gene may account for the phenotype shown in this patient. Conclusions: We identified the co-occurrence of two genetic causes in family 686. The possible disease-causing missense mutation of TJP2 in family 686 presents an opportunity for further investigation into ARHL. It is necessary to combine various genes screening methods, especially for some unconventional cases.

7,8-dihydroxyflavone, a TrkB receptor agonist, blocks long-term spatial memory impairment caused by immobilization stress in rats.

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Andero, Raül; Daviu, Núria; Escorihuela, Rosa Maria; Nadal, Roser; Armario, Antonio

2012-03-01

Post-traumatic stress disorder (PTSD) patients show cognitive deficits, but it is unclear whether these are a consequence of the pathology or a pre-existing factor of vulnerability to PTSD. Animal models may help to demonstrate whether or not exposure to certain stressors can actually induce long-lasting (LL; days) impairment of hippocampus-dependent memory tasks and to characterize neurobiological mechanisms. Adult male rats were exposed to 2-h immobilization on boards (IMO), a severe stressor, and spatial learning in the Morris water maze (MWM) was studied days later. Exposure to IMO did not modify learning or short-term memory in the MWM when learning started 3 or 9 days after IMO, but stressed rats did show impaired long-term memory at both times, in accordance with the severity of the stressor. New treatments to prevent PTSD symptoms are needed. Thus, considering the potential protective role of brain-derived neurotrophic factor (BDNF) on hippocampal function, 7,8-dihydroxyflavone (7,8-DHF), a recently characterized agonist of the BDNF receptor TrkB, was given before or after IMO in additional experiments. Again, exposure to IMO resulted in LL deficit in long-term memory, and such impairment was prevented by the administration of 7,8-DHF either 2 h prior IMO or 8 h after the termination of IMO. The finding that IMO-induced impairment of spatial memory was prevented by pharmacological potentiation of TrkB pathway with 7,8-DHF even when the drug was given 8 h after IMO suggests that IMO-induced impairment is likely to be a LL process that is strongly dependent on the integrity of the BDNF-TrkB system and is susceptible to poststress therapeutic interventions. 7,8-DHF may represent a new therapeutic approach for early treatment of subjects who have suffered traumatic experiences. Copyright © 2010 Wiley Periodicals, Inc.

The prevalence of visual impairment and blindness in underserved rural areas: a crucial issue for future.

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Hashemi, H; Yekta, A; Jafarzadehpur, E; Doostdar, A; Ostadimoghaddam, H; Khabazkhoob, M

2017-08-01

PurposeTo determine the prevalence of visual impairment and blindness in underserved Iranian villages and to identify the most common cause of visual impairment and blindness.Patients and methodsMultistage cluster sampling was used to select the participants who were then invited to undergo complete examinations. Optometric examinations including visual acuity, and refraction were performed for all individuals. Ophthalmic examinations included slit-lamp biomicroscopy and ophthalmoscopy. Visual impairment was determined according to the definitions of the WHO and presenting vision.ResultsOf 3851 selected individuals, 3314 (86.5%) participated in the study. After using the exclusion criteria, the present report was prepared based on the data of 3095 participants. The mean age of the participants was 37.6±20.7 years (3-93 years). The prevalence of visual impairment and blindness was 6.43% (95% confidence interval (CI): 3.71-9.14) and 1.18% (95% CI: 0.56-1.79), respectively. The prevalence of visual impairment varied from 0.75% in participants aged less than 5 years to 38.36% in individuals above the age of 70 years. Uncorrected refractive errors and cataract were the first and second leading causes of visual impairment; moreover, cataract and refractive errors were responsible for 35.90 and 20.51% of the cases of blindness, respectively.ConclusionThe prevalence of visual impairment was markedly high in this study. Lack of access to health services was the main reason for the high prevalence of visual impairment in this study. Cataract and refractive errors are responsible for 80% of visual impairments which can be due to poverty in underserved villages.

Risk Factors for Visual Impairment in an Uninsured Population and the Impact of the Affordable Care Act.

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Guo, Weixia; Woodward, Maria A; Heisler, Michele; Blachley, Taylor; Corneail, Leah; Cederna, Jean; Kaplan, Ariane D; Newman Casey, Paula Anne

2016-01-01

To assess risk factors for visual impairment in a high-risk population of people: those without medical insurance. Secondarily, we assessed risk factors for remaining uninsured after implementation of the Affordable Care Act (ACA) and evaluated whether the ACA changed demand for local safety net ophthalmology clinic services one year after its implementation. In a retrospective cohort study of patients who attended a community-academic partnership free ophthalmology clinic in Southeastern, Michigan between September 2012 - March 2015, we assessed the prevalence of presenting with visual impairment, the most common causes of presenting with visual impairment and used logistic regression to assess socio-demographic risk factors for visual impairment. We assessed the initial impact of the ACA on clinic utilization. We also analyzed risk factors for remaining uninsured one year after implementation of the ACA private insurance marketplace and Medicaid expansion in the state of Michigan. Among 335 patients, one-fifth (22%) presented with visual impairment; refractive error was the leading cause for presenting with visual impairment. Unemployment was the single significant risk factor for presenting with visual impairment after adjusting for multiple confounding factors (OR = 3.05, 95% CI 1.19-7.87, p=0.01). There was no difference in proportion of visual impairment or type of vision-threatening disease between the insured and uninsured (p=0.26). Seventy six percent of patients remained uninsured one year after ACA implementation. Patients who were white, spoke English as a first language and were US Citizens were more likely to gain insurance coverage through the ACA in our population (p≤ 0.01). There was a non-significant decline in the mean number of patient treated per clinic (52 to 43) before and after ACA implementation (p=0.69). Refractive error was a leading cause for presenting with visual impairment in this vulnerable population, and being unemployed

Prevalence of refractive error and visual impairment among rural school-age children of Goro District, Gurage Zone, Ethiopia.

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Kedir, Jafer; Girma, Abonesh

2014-10-01

Refractive error is one of the major causes of blindness and visual impairment in children; but community based studies are scarce especially in rural parts of Ethiopia. So, this study aims to assess the prevalence of refractive error and its magnitude as a cause of visual impairment among school-age children of rural community. This community-based cross-sectional descriptive study was conducted from March 1 to April 30, 2009 in rural villages of Goro district of Gurage Zone, found south west of Addis Ababa, the capital of Ethiopia. A multistage cluster sampling method was used with simple random selection of representative villages in the district. Chi-Square and t-tests were used in the data analysis. A total of 570 school-age children (age 7-15) were evaluated, 54% boys and 46% girls. The prevalence of refractive error was 3.5% (myopia 2.6% and hyperopia 0.9%). Refractive error was the major cause of visual impairment accounting for 54% of all causes in the study group. No child was found wearing corrective spectacles during the study period. Refractive error was the commonest cause of visual impairment in children of the district, but no measures were taken to reduce the burden in the community. So, large scale community level screening for refractive error should be conducted and integrated with regular school eye screening programs. Effective strategies need to be devised to provide low cost corrective spectacles in the rural community.

Common Variable Immunodeficiency Caused by FANC Mutations.

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Sekinaka, Yujin; Mitsuiki, Noriko; Imai, Kohsuke; Yabe, Miharu; Yabe, Hiromasa; Mitsui-Sekinaka, Kanako; Honma, Kenichi; Takagi, Masatoshi; Arai, Ayako; Yoshida, Kenichi; Okuno, Yusuke; Shiraishi, Yuichi; Chiba, Kenichi; Tanaka, Hiroko; Miyano, Satoru; Muramatsu, Hideki; Kojima, Seiji; Hira, Asuka; Takata, Minoru; Ohara, Osamu; Ogawa, Seishi; Morio, Tomohiro; Nonoyama, Shigeaki

2017-07-01

Common variable immunodeficiency (CVID) is the most common adult-onset primary antibody deficiency disease due to various causative genes. Several genes, which are known to be the cause of different diseases, have recently been reported as the cause of CVID in patients by performing whole exome sequencing (WES) analysis. Here, we found FANC gene mutations as a cause of adult-onset CVID in two patients. B cells were absent and CD4 + T cells were skewed toward CD45RO + memory T cells. T-cell receptor excision circles (TRECs) and signal joint kappa-deleting recombination excision circles (sjKRECs) were undetectable in both patients. Both patients had no anemia, neutropenia, or thrombocytopenia. Using WES, we identified compound heterozygous mutations of FANCE in one patient and homozygous mutation of FANCA in another patient. The impaired function of FANC protein complex was confirmed by a monoubiquitination assay and by chromosome fragility test. We then performed several immunological evaluations including quantitative lymphocyte analysis and TRECs/sjKRECs analysis for 32 individuals with Fanconi anemia (FA). In total, 22 FA patients (68.8%) were found to have immunological abnormalities, suggesting that such immunological findings may be common in FA patients. These data indicate that FANC mutations are involved in impaired lymphogenesis probably by the accumulation of DNA replication stress, leading to CVID. It is important to diagnose FA because it drastically changes clinical management. We propose that FANC mutations can cause isolated immunodeficiency in addition to bone marrow failure and malignancy.

Impaired heat shock response in cells expressing full-length polyglutamine-expanded huntingtin.

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Sidhartha M Chafekar

Full Text Available The molecular mechanisms by which polyglutamine (polyQ-expanded huntingtin (Htt causes neurodegeneration in Huntington's disease (HD remain unclear. The malfunction of cellular proteostasis has been suggested as central in HD pathogenesis and also as a target of therapeutic interventions for the treatment of HD. We present results that offer a previously unexplored perspective regarding impaired proteostasis in HD. We find that, under non-stress conditions, the proteostatic capacity of cells expressing full length polyQ-expanded Htt is adequate. Yet, under stress conditions, the presence of polyQ-expanded Htt impairs the heat shock response, a key component of cellular proteostasis. This impaired heat shock response results in a reduced capacity to withstand the damage caused by cellular stress. We demonstrate that in cells expressing polyQ-expanded Htt the levels of heat shock transcription factor 1 (HSF1 are reduced, and, as a consequence, these cells have an impaired a heat shock response. Also, we found reduced HSF1 and HSP70 levels in the striata of HD knock-in mice when compared to wild-type mice. Our results suggests that full length, non-aggregated polyQ-expanded Htt blocks the effective induction of the heat shock response under stress conditions and may thus trigger the accumulation of cellular damage during the course of HD pathogenesis.

Hearing Impairment Among Noise-Exposed Workers - United States, 2003-2012.

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Masterson, Elizabeth A; Bushnell, P Timothy; Themann, Christa L; Morata, Thais C

2016-04-22

Hearing loss is the third most common chronic physical condition in the United States, and is more prevalent than diabetes or cancer (1). Occupational hearing loss, primarily caused by high noise exposure, is the most common U.S. work-related illness (2). Approximately 22 million U.S. workers are exposed to hazardous occupational noise (3). CDC compared the prevalence of hearing impairment within nine U.S. industry sectors using 1,413,789 noise-exposed worker audiograms from CDC's National Institute for Occupational Safety and Health (NIOSH) Occupational Hearing Loss Surveillance Project (4). CDC estimated the prevalence at six hearing impairment levels, measured in the better ear, and the impact on quality of life expressed as annual disability-adjusted life years (DALYs), as defined by the 2013 Global Burden of Disease (GBD) Study (5). The mining sector had the highest prevalence of workers with any hearing impairment, and with moderate or worse impairment, followed by the construction and manufacturing sectors. Hearing loss prevention, and early detection and intervention to avoid additional hearing loss, are critical to preserve worker quality of life.

Tinnitus-provoking salicylate treatment triggers social impairments in mice.

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Guitton, Matthieu J

2009-09-01

Tinnitus (perception of sound in silence) strongly affects the quality of life of sufferers. Tinnitus sufferers and their relatives frequently complain about major social impairments. However, it is not known whether this impairment directly results from the occurrence of tinnitus or is the indirect expression of a preexisting psychological vulnerability. Using the well-characterized animal model of salicylate-induced tinnitus, we investigate in mice whether the occurrence of tinnitus can trigger social impairments. Experiments were performed on 32 male Balb/C mice. Tinnitus was induced in mice using salicylate treatment. Social behavior was assessed in experimental and control animals using social interaction paradigm. Interaction time, number of social events, and number of nonsocial events were assessed in all animals. We demonstrate for the first time that treatment known to induce tinnitus triggers complex social impairments in mice. While salicylate-treated animals present a massive decrease in their overall social interactions compared to control untreated animals, they also display a paradoxal increase in the number of conspecific followings. Tinnitus can thus trigger a complex set of modifications of behavior, which will not only find their expression at the individual level, but also at the social level. Our results suggest that tinnitus can directly be a cause of psychosocial impairment in human and have strong implications for the clinical management of tinnitus sufferers.

Acute Liver Failure Due to Regorafenib May Be Caused by Impaired Liver Blood Flow: A Case Report.

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Akamine, Takaki; Ando, Koji; Oki, Eiji; Saeki, Hiroshi; Nakashima, Yuichiro; Imamura, Y U; Ohgaki, Kippei; Maehara, Yoshihiko

2015-07-01

Regorafenib has been approved for treatment of patients with unresectable or recurrent gastrointestinal stromal tumors resistant to imatinib or sunitinib. However, regorafenib has severe side-effects, including acute liver failure. We describe the case of a patient with multiple liver metastases of a small intestinal stromal tumor who experienced acute liver failure while being treated with regorafenib. A 50-year-old patient with an unresectable small intestinal stromal tumor resistant to prior treatment with imatinib and sunitinib was started on regorafenib, but experienced acute liver failure 10 days later. Plasma exchange and steroid pulse treatment improved her liver function. During liver failure, abdominal ultrasonography showed to-and-fro flow in the portal vein. Lactate dehydrogenase concentration was markedly elevated to 1633 U/l. These findings indicate that liver failure in this patient was due to impaired liver blood flow. Regorafenib may impair liver blood flow, inducing acute liver failure. Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.

IMPAIRMENT IN SHORT-TERM BUT ENHANCED LONG-TERM SYNAPTIC POTENTIATION AND ERK ACTIVATION IN ADULT HIPPOCAMPAL AREA CA1 FOLLOWING DEVELOPMENTAL HYPOTHYROIDISM.

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The EPA must evaluate the risk of exposure of the developing brain to chemicals with the potential to disrupt thyroid hormone homeostasis. The existing literature identifies morphological and neurochemical indices of severe neonatal hypothyroidism in the early postnatal period i...

Cerebral visual impairment and intellectual disability caused by PGAP1 variants.

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Bosch, Daniëlle G M; Boonstra, F Nienke; Kinoshita, Taroh; Jhangiani, Shalini; de Ligt, Joep; Cremers, Frans P M; Lupski, James R; Murakami, Yoshiko; de Vries, Bert B A

2015-12-01

Homozygous variants in PGAP1 (post-GPI attachment to proteins 1) have recently been identified in two families with developmental delay, seizures and/or spasticity. PGAP1 is a member of the glycosylphosphatidylinositol anchor biosynthesis and remodeling pathway and defects in this pathway are a subclass of congenital disorders of glycosylation. Here we performed whole-exome sequencing in an individual with cerebral visual impairment (CVI), intellectual disability (ID), and factor XII deficiency and revealed compound heterozygous variants in PGAP1, c.274_276del (p.(Pro92del)) and c.921_925del (p.(Lys308Asnfs*25)). Subsequently, PGAP1-deficient Chinese hamster ovary (CHO)-cell lines were transfected with either mutant or wild-type constructs and their sensitivity to phosphatidylinositol-specific phospholipase C (PI-PLC) treatment was measured. The mutant constructs could not rescue the PGAP1-deficient CHO cell lines resistance to PI-PLC treatment. In addition, lymphoblastoid cell lines (LCLs) of the affected individual showed no sensitivity to PI-PLC treatment, whereas the LCLs of the heterozygous carrier parents were partially resistant. In conclusion, we report novel PGAP1 variants in a boy with CVI and ID and a proven functional loss of PGAP1 and show, to our knowledge, for the first time this genetic association with CVI.

Visual impairment from uveitis in a reference hospital of Southeast Brazil: a retrospective review over a twenty years period.

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Silva, Luci Meire Pereira da; Muccioli, Cristina; Oliveira, Filipe de; Arantes, Tiago Eugênio; Gonzaga, Lucas Renó; Nakanami, Célia Regina

2013-01-01

To identify the frequency and causes of uveitis leading to visual impairment in patients referred to the Low Vision Service - Department of Ophthalmology - UNIFESP, over a twenty years period. In a retrospective study, medical records of 5,461 patients were reviewed. Data from the first clinical evaluation at the Low Vision Service were collected, patient's age, gender and cause of visual impairment were analyzed. Patients with uveitis had their chart reviewed for anatomical classification and clinical diagnosis. The mean age of the patients referred to the Low Vision Service was 42.86 years and the mean age of patients with uveitis diagnosis was 25.51 years. Retinal disorders were the most common cause of visual impairment (N=2,835 patients; 51.9%) followed by uveitis (862 patients, 15.7%). Uveitis was posterior in 792 patients (91.9% of uveitis) and toxoplasmosis was the most common diagnosis (765 patients, 88.7%). In our study, uveitis represents the second cause of visual impairment in patients referred for visual rehabilitation and toxoplasmic retinochoroiditis was the most common clinical diagnosis. It affects a young working age population with a relevant social and economic impact, but the early diagnosis and treatment can improve the quality of life of these patients.

Blindness and Visual Impairment Profile and Rapid Assessment of Avoidable Blindness in South East Asia: Analysis of New Data. 2017 APAO Holmes Lecture.

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Das, Taraprasad

2018-03-13

The International Agency for Prevention of Blindness (IAPB) South East Asia region (SEAR) that consists of 11 countries contains 26% of the world's population (1,761,000,000). In this region 12 million are blind and 78.5 million are visually impaired. This amounts to 30% of global blindness and 32% of global visual impairment. Rapid assessment of avoidable blindness (RAAB) survey analysis. RAAB, either a repeat or a first time survey, was completed in 8 countries in this decade (2010 onwards). These include Bangladesh, Bhutan, India, Indonesia, Maldives, Sri Lanka, Thailand, and Timor Leste. Cataract is the principal cause of blindness and severe visual impairment in all countries. Refractive error is the principal cause of moderate visual impairment in 4 countries: Bangladesh, India, Maldives, and Sri Lanka; cataract continues to be the principal cause of moderate visual impairment in 4 other countries: Bhutan, Indonesia, Thailand, and Timor Leste. Outcome of cataract surgery is suboptimal in the Maldives and Timor Leste. Rigorous focus is necessary to improve cataract surgery outcomes and correction of refractive error without neglecting the quality of care. At the same time allowances must be made for care of the emerging causes of visual impairment and blindness such as glaucoma and posterior segment disorders, particularly diabetic retinopathy. Copyright 2018 Asia-Pacific Academy of Ophthalmology.

Rescue of cAMP response element-binding protein signaling reversed spatial memory retention impairments induced by subanesthetic dose of propofol.

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Zhang, Hao; Zhang, Shao-Bo; Zhang, Qing-Qing; Liu, Meng; He, Xing-Ying; Zou, Zui; Sun, Hai-Jing; You, Zhen-Dong; Shi, Xue-Yin

2013-07-01

The intravenous anesthetic propofol caused episodic memory impairments in human. We hypothesized propofol caused episodic-like spatial memory retention but not acquisition impairments in rats and rescuing cAMP response element-binding protein (CREB) signaling using selective type IV phosphodiesterase (PDEIV) inhibitor rolipram reversed these effects. Male Sprague-Dawley rats were randomized into four groups: control; propofol (25 mg/kg, intraperitoneal); rolipram; and rolipram + propofol (pretreatment of rolipram 25 min before propofol, 0.3 mg/kg, intraperitoneal). Sedation and motor coordination were evaluated 5, 15, and 25 min after propofol injection. Invisible Morris water maze (MWM) acquisition and probe test (memory retention) were performed 5 min and 24 h after propofol injection. Visible MWM training was simultaneously performed to resist nonspatial effects. Hippocampal CREB signaling was detected 5 min, 50 min, and 24 h after propofol administration. Rolipram did not change propofol-induced anesthetic/sedative states or impair motor skills. No difference was found on the latency to the platform during the visible MWM. Propofol impaired spatial memory retention but not acquisition. Rolipram reversed propofol-induced spatial memory impairments and suppression on cAMP levels, CaMKIIα and CREB phosphorylation, brain-derived neurotropic factor (BDNF) and Arc protein expression. Propofol caused spatial memory retention impairments but not acquisition inability possibly by inhibiting CREB signaling. © 2013 John Wiley & Sons Ltd.

Functional impairment and hospital readmission in Medicare seniors.

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Greysen, S Ryan; Stijacic Cenzer, Irena; Auerbach, Andrew D; Covinsky, Kenneth E

2015-04-01

ADL (OR, 1.08; 95% CI, 0.96-1.21), 16.5% with dependency in 1 to 2 ADLs (OR, 1.26; 95% CI, 1.11-1.44), and 18.2% with dependency in 3 or more ADLs (OR, 1.42; 95% CI, 1.20-1.69). Subanalysis restricted to patients admitted with conditions targeted by Medicare (ie, heart failure, myocardial infarction, and pneumonia) revealed a parallel trend with larger effects for the most impaired (16.9% readmission rate for no impairment vs 25.7% for dependency in 3 or more ADLs [OR, 1.70; 95% CI, 1.04-2.78]). Functional impairment is associated with increased risk of 30-day all-cause hospital readmission in Medicare seniors, especially those admitted for heart failure, myocardial infarction, or pneumonia. Functional impairment may be an important but underaddressed factor in preventing readmissions for Medicare seniors.

Prevalence of Visual Impairment and Refractive Errors in Children of South Sinai, Egypt.

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Yamamah, Gamal Abdel Naser; Talaat Abdel Alim, Ahmed Ahmed; Mostafa, Yehia Salah El Din; Ahmed, Rania Ahmed Abdel Salam; Mohammed, Asmaa Mahmoud; Mahmoud, Asmaa Mohammed

2015-01-01

To assess the prevalence and causes of visual impairment in children of South Sinai, and to evaluate outcomes of rehabilitation programs. Population-based, cross-sectional analysis of 2070 healthy school children screened for visual impairment from 2009 through 2010 in cities of South Sinai and their surrounding Bedouin settlements. Visual acuity (VA) was tested using Snellen charts followed by cycloplegic autorefractometry for cases with presenting VA ≤ 6/9. Appropriate eyeglasses were prescribed and VA re-evaluated. This study included 1047 boys and 1023 girls, mean age 10.7 ± 3.1 years. Visual impairment (uncorrected VA ≤ 6/9) was detected in 29.4% of children, while 2.0% had moderate-severe visual impairment (uncorrected VA ≤ 6/24). There were statistically significant differences in prevalence of visual impairment between the studied cities (p visual impairment was significantly higher among girls (p children showed significantly lower prevalences of visual impairment. Only age was a reliable predictor of visual impairment (odds ratio 0.94, p children who received spectacles (p children had some form of visual impairment, 90.32% of which comprised refractive errors (mainly astigmatism) which were significantly corrected with eyeglasses. VA screening and correction of refractive errors are of the utmost importance for ensuring better visual outcomes and improved school performance.

Central Nervous Insulin Signaling in Sleep-Associated Memory Formation and Neuroendocrine Regulation

OpenAIRE

Feld, Gordon B; Wilhem, Ines; Benedict, Christian; Rüdel, Benjamin; Klameth, Corinna; Born, Jan; Hallschmid, Manfred

2016-01-01

The neurochemical underpinnings of sleep's contribution to the establishment and maintenance of memory traces are largely unexplored. Considering that intranasal insulin administration to the CNS improves memory functions in healthy and memory-impaired humans, we tested whether brain insulin signaling and sleep interact to enhance memory consolidation in healthy participants. We investigated the effect of intranasal insulin on sleep-associated neurophysiological and neuroendocrine parameters ...

Chronically impaired autoregulation of cerebral blood flow in long-term diabetics

DEFF Research Database (Denmark)

Bentsen, N; Larsen, B; Lassen, N A

1975-01-01

Using the arteriovenous oxygen difference method autoregulation of cerebral blood flow (CBF) was tested in 16 long-term diabetics and eight control patients. Blood pressure was raised by angiotensin infusion and lowered by trimethaphan camsylate infusion, in some cases combined with head-up tilting...... of the patient. Regression analysis was carried out on the results in order to quantify autoregulatory capacity. In the control patients CBF did not vary with moderate blood pressure variations, indicating normal autoregulation. In four of the 16 diabetic patients CBF showed significant pressure dependency......, indicating impaired autoregulation. The cause of impaired autoregulation in some long-term diabetics is believed to be diffuse or multifocal dysfunction of cerebral arterioles due to diabetic vascular disease. Other conditions with impaired autoregulation are discussed and compared with that seen in long...

Prevalence and causes of low vision and blindness in Baotou

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Zhang, Guisen; Li, Yan; Teng, Xuelong; Wu, Qiang; Gong, Hui; Ren, Fengmei; Guo, Yuxia; Liu, Lei; Zhang, Han

2016-01-01

Abstract The aim of this study was to investigate the prevalence and causes of low vision and blindness in Baotou, Inner Mongolia. A cross-sectional study was carried out. Multistage sampling was used to select samples. The visual acuity was estimated using LogMAR and corrected by pinhole as best-corrected visual acuity. There were 7000 samples selected and 5770 subjects included in this investigation. The overall bilateral prevalence rates of low vision and blindness were 3.66% (95% CI: 3.17–4.14) and 0.99% (95% CI: 0.73–1.24), respectively. The prevalence of bilateral low vision, blindness, and visual impairment increased with age and decreased with education level. The main leading cause of low vision and blindness was cataract. Diabetic retinopathy and age-related macular degeneration were found to be the second leading causes of blindness in Baotou. The low vision and blindness were more prevalent in elderly people and subjects with low education level in Baotou. Cataract was the main cause for visual impairment and more attention should be paid to fundus diseases. In order to prevent blindness, much more eye care programs should be established. PMID:27631267

Memory Impairment in Children with Language Impairment

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Baird, Gillian; Dworzynski, Katharina; Slonims, Vicky; Simonoff, Emily

2010-01-01

Aim: The aim of this study was to assess whether any memory impairment co-occurring with language impairment is global, affecting both verbal and visual domains, or domain specific. Method: Visual and verbal memory, learning, and processing speed were assessed in children aged 6 years to 16 years 11 months (mean 9y 9m, SD 2y 6mo) with current,…

Individual behavioral and neurochemical markers of unadapted decision-making processes in healthy inbred mice.

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Pittaras, Elsa; Callebert, Jacques; Chennaoui, Mounir; Rabat, Arnaud; Granon, Sylvie

2016-12-01

One of the hallmarks of decision-making processes is the inter-individual variability between healthy subjects. These behavioral patterns could constitute risk factors for the development of psychiatric disorders. Therefore, finding predictive markers of safe or risky decision-making is an important challenge for psychiatry research. We set up a mouse gambling task (MGT)-adapted from the human Iowa gambling task with uncertain contingencies between response and outcome that furthermore enables the emergence of inter-individual differences. Mice (n = 54) were further individually characterized for locomotive, emotional and cognitive behavior. Individual basal rates of monoamines and brain activation after the MGT were assessed in brain regions related to reward, emotion or cognition. In a large healthy mice population, 44 % showed a balanced strategy with limited risk-taking and flexible choices, 29 % showed a safe but rigid strategy, while 27 % adopted risky behavior. Risky mice took also more risks in other apparatus behavioral devices and were less sensitive to reward. No difference existed between groups regarding anxiety, working memory, locomotion and impulsivity. Safe/rigid mice exhibited a hypoactivation of prefrontal subareas, a high level of serotonin in the orbitofrontal cortex combined with a low level of dopamine in the putamen that predicted the emergence of rigid behavior. By contrast, high levels of dopamine, serotonin and noradrenalin in the hippocampus predicted the emergence of more exploratory and risky behaviors. The coping of C57bl/6J mice in MGT enables the determination of extreme patterns of choices either safe/rigid or risky/flexible, related to specific neurochemical and behavioral markers.

Communication Impairments in Patients with Right Hemisphere Damage

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Abusamra, Valeria

2009-06-01

Full Text Available Right brain damages can manifest deficits of communicative skills, which sometimes cause an important inability.The communication impairments following a right hemisphere damage are distinct from those in aphasia and may affect discursive, lexico-semantic, pragmatic, and prosodic components of communication. It is calculated that this troubles affect almost a 50% of this patients.However, these impairments have essentially been studied separately and their possible coexistence in a same individual is still unknown. Moreover, the clinical profiles of communication impairments following a right hemisphere damage, including their correlation with underlying cognitive deficits, are still unreported. The goal of this article is to offer an overview of the verbal communication deficits that can be found in right-hemisphere-damaged individuals. These deficits can interfere, at different levels, with prosody, the semantic processing of words and discourse and pragmatic abilities. In spite of the incapability that they produce, communicational impairments in right brain damaged are usually neglected. Probably, the sub-diagnostic is due to the lack of an appropriate classification or to the absent of adequate assessment tools. In fact, patients with right brain damages might present harsh communicational deficits but perform correctly on aphasia tests because the last ones are not designed to detect this kind of deficit but left brain damaged impairments. Increasing our knowledge about the role of the right-hemisphere in verbal communication will have major theoretical and clinical impacts; it could facilitate the diagnosis of right brain patients in the clinical circle and it will help to lay the foundations to elaborate methods and strategies of intervention.

Sensation of stasis is poorly correlated with impaired esophageal bolus transport

NARCIS (Netherlands)

Bogte, A.; Bredenoord, A. J.; Oors, J.; Siersema, P. D.; Smout, A. J. P. M.

2014-01-01

It is common belief that symptoms of patients with non-obstructive dysphagia are the result of impaired bolus clearance in the esophagus, usually caused by esophageal motility disorders. We therefore investigated the relationship between transit of swallowed boluses and the symptom dysphagia. Twenty

Protective effect of gallic acid in experimental model of ketamine-induced psychosis: possible behaviour, biochemical, neurochemical and cellular alterations.

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Yadav, Monu; Jindal, Deepak Kumar; Dhingra, Mamta Sachdeva; Kumar, Anil; Parle, Milind; Dhingra, Sameer

2018-04-01

Gallic acid has been reported to possess a number of psychopharmacological activities. These activities are attributed to the antioxidant potential due to the presence of phenolic moeity. The present study was carried out to investigate the protective effects of gallic acid in an experimental model of ketamine-induced psychosis in mice. Ketamine (50 mg/kg, i.p.) was used to induce stereotyped psychotic behavioural symptoms in mice. Behavioural studies (locomotor activity, stereotype behaviour, immobility duration and memory retention) were carried out to investigate the protective of gallic acid on ketamine-induced psychotic symptoms, followed by biochemical and neurochemical changes and cellular alterations in the brain. Chronic treatment with gallic acid for 15 consecutive days significantly attenuated stereotyped behavioural symptoms in mice. Biochemical estimations revealed that gallic acid reduced the lipid peroxidation and restored the total brain proteins. Furthermore, gallic acid remarkably reduced the dopamine levels, AChE activity and inflammatory surge (serum TNF-α), and increased the levels of GABA and increased glutathione in mice. The study revealed that gallic acid could ameliorate psychotic symptoms and biochemical changes in mice, indicating protective effects in psychosis.

Right unilateral electroconvulsive therapy does not cause more cognitive impairment than pharmacologic treatment in treatment-resistant bipolar depression: A 6-month randomized controlled trial follow-up study.

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Bjoerke-Bertheussen, Jeanette; Schoeyen, Helle; Andreassen, Ole A; Malt, Ulrik F; Oedegaard, Ketil J; Morken, Gunnar; Sundet, Kjetil; Vaaler, Arne E; Auestad, Bjoern; Kessler, Ute

2017-12-21

Electroconvulsive therapy is an effective treatment for bipolar depression, but there are concerns about whether it causes long-term neurocognitive impairment. In this multicenter randomized controlled trial, in-patients with treatment-resistant bipolar depression were randomized to either algorithm-based pharmacologic treatment or right unilateral electroconvulsive therapy. After the 6-week treatment period, all of the patients received maintenance pharmacotherapy as recommended by their clinician guided by a relevant treatment algorithm. Patients were assessed at baseline and at 6 months. Neurocognitive functions were assessed using the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery, and autobiographical memory consistency was assessed using the Autobiographical Memory Interview-Short Form. Seventy-three patients entered the trial, of whom 51 and 26 completed neurocognitive assessments at baseline and 6 months, respectively. The MATRICS Consensus Cognitive Battery composite score improved by 4.1 points in both groups (P = .042) from baseline to 6 months (from 40.8 to 44.9 and from 41.9 to 46.0 in the algorithm-based pharmacologic treatment and electroconvulsive therapy groups, respectively). The Autobiographical Memory Interview-Short Form consistency scores were reduced in both groups (72.3% vs 64.3% in the algorithm-based pharmacologic treatment and electroconvulsive therapy groups, respectively; P = .085). This study did not find that right unilateral electroconvulsive therapy caused long-term impairment in neurocognitive functions compared to algorithm-based pharmacologic treatment in bipolar depression as measured using standard neuropsychological tests, but due to the low number of patients in the study the results should be interpreted with caution. ClinicalTrials.gov: NCT00664976. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Visual Impairments, "Including Blindness." NICHCY Disability Fact Sheet #13

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National Dissemination Center for Children with Disabilities, 2012

2012-01-01

Vision is one of the five senses. Being able to see gives tremendous access to learning about the world around--people's faces and the subtleties of expression, what different things look like and how big they are, and the physical environments, including approaching hazards. When a child has a visual impairment, it is cause for immediate…

Visual impairment in children with congenital Zika syndrome.

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Ventura, Liana O; Ventura, Camila V; Lawrence, Linda; van der Linden, Vanessa; van der Linden, Ana; Gois, Adriana L; Cavalcanti, Milena M; Barros, Eveline A; Dias, Natalia C; Berrocal, Audina M; Miller, Marilyn T

2017-08-01

To describe the visual impairment associated with ocular and neurological abnormalities in a cohort of children with congenital Zika syndrome (CZS). This cross-sectional study included infants with microcephaly born in Pernambuco, Brazil, from May to December 2015. Immunoglobulin M antibody capture enzyme-linked immunosorbent assay for the Zika virus on the cerebrospinal fluid samples was positive for all infants. Clinical evaluation consisted of comprehensive ophthalmologic examination including visual acuity, visual function assessment, visual developmental milestone, neurologic examination, and neuroimaging. A total of 32 infants (18 males [56%]) were included. Mean age at examination was 5.7 ± 0.9 months (range, 4-7 months). Visual function and visual developmental milestone could not be tested in 1 child (3%). Visual impairment was detected in 32 infants (100%). Retinal and/or optic nerve findings were observed in 14 patients (44%). There was no statistical difference between the patients with ocular findings and those without (P = 0.180). All patients (100%) demonstrated neurological and neuroimaging abnormalities; 3 (9%) presented with late-onset of microcephaly. Children with CZS demonstrated visual impairment regardless of retina and/or optic nerve abnormalities. This finding suggests that cortical/cerebral visual impairment may be the most common cause of blindness identified in children with CZS. Copyright © 2017 American Association for Pediatric Ophthalmology and Strabismus. Published by Elsevier Inc. All rights reserved.

Reduced somatosensory impairment by piezosurgery during orthognathic surgery of the mandible.

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Brockmeyer, Phillipp; Hahn, Wolfram; Fenge, Stefan; Moser, Norman; Schliephake, Henning; Gruber, Rudolf Matthias

2015-09-01

This clinical trial aimed to test the hypothesis that piezosurgery causes reduced nerval irritations and, thus, reduced somatosensory impairment when used in orthognathic surgery of the mandible. To this end, 37 consecutive patients with Angle Class II and III malocclusion were treated using bilateral sagittal split osteotomies (BSSO) of the mandible. In a split mouth design, randomized one side of the mandible was operated using a conventional saw, while a piezosurgery device was used on the contralateral side. In order to test the individual qualities of somatosensory function, quantitative sensory testings (QSTs) were performed 1 month, 6 months and 1 year after surgery. A comparison of the data using a two-way analysis of variance (ANOVA) revealed a significant reduction in postoperative impairment in warm detection threshold (WDT) (P = 0.046), a decreased dynamic mechanical allodynia (ALL) (P = 0.002) and a decreased vibration detection threshold (VDT) (P = 0.030) on the piezosurgery side of the mandible as opposed to the conventionally operated control side. In the remaining QSTs, minor deviations from the preoperative baseline conditions and a more rapid regression could be observed. Piezosurgery caused reduced somatosensory impairment and a faster recovery of somatosensory functions in the present investigation.

Leading causes of certification for blindness and partial sight in England & Wales

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Wormald Richard

2006-03-01

Full Text Available Abstract Background Prevention of visual impairment is an international priority agreed at the World Health Assembly of 2002- yet many countries lack contemporary data about incidence and causes from which priorities for prevention, treatment and management can be identified. Methods Registration as blind or partially-sighted in England and Wales is voluntary and is initiated by certification by a consultant ophthalmologist. From all certificates completed during the year April 1999 to March 2000, the main cause of visual loss was ascertained where possible and here we present information on the leading causes observed and comment on changes in the three leading causes since the last analysis conducted for 1990–1991 data. Results 13788 people were certified as blind, 19107 were certified as partially sighted. The majority of certifications were in the older age groups. The most commonly recorded main cause of certifications for both blindness (57.2 % and partial sight (56 % was degeneration of the macula and posterior pole which largely comprises age-related macular degeneration. Glaucoma and diabetic retinopathy were the next most commonly recorded main causes. Overall, the age specific incidence of all three leading causes has increased since 1990–1991 – with changes in diabetic retinopathy being the most marked – particularly in the over 65's where figures have more than doubled. Conclusion The numbers of individuals per 100,000 population being certified blind or partially sighted due to the three leading causes – AMD, diabetic retinopathy and glaucoma have increased since 1990. This may to some extent be explained by improved ascertainment. The process of registration for severe visual impairment in England and Wales is currently undergoing review. Efforts must be made to ensure that routine collection of data on causes of severe visual impairment is continued, particularly in this age of improved technology, to allow such trends

Prevalence of Visual Impairment among 4- to 6-years-old Children in Khon Kaen City Municipality, Thailand.

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Wongwai, Phanthipha; Anupongongarch, Pacharapan; Suwannaraj, Sirinya; Asawaphureekorn, Somkiat

2016-08-01

To evaluate the prevalence of visual impairment of children aged four to six years in Khon Kaen City Municipality, Thailand. The visual acuity test was performed on 1,286 children in kindergarten schools located in Khon Kaen Municipality. The first test of visual acuity was done by trained teachers and the second test by the pediatric ophthalmologist. The prevalence of visual impairment of both tests was recorded including sensitivity, specificity, likelihood ratio, and predictive value of the test by teachers. The causes of visual impairment were also recorded. There were 39 children with visual impairment from the test by the teacher and 12 children from the test by the ophthalmologist. Myopia is the single cause of visual impairment. Mean spherical equivalence is 1.375 diopters (SD = 0.53). Median spherical equivalence is 1.375 diopters (minimum = 0.5, maximum =4). The detection of visual impairment by trained teachers had a sensitivity of 1.00 (95% CI 0.76-1.00), specificity of 0.98 (95% CI 0.97-0.99), likelihood ratio for a positive test 44.58 (95% CI 30.32-65.54), likelihood ratio for a negative test 0.04 (95% CI 0.003-0.60), positive predictive value of 0.31 (95% CI 0.19-0.47), and negative predictive value of 1.00 (95% CI 0.99-1.00). The prevalence of visual impairment among children aged four to six year old is 0.9%. Trained teachers can be examiners for screening purpose.

Causes of childhood blindness in the northeastern states of India

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Bhattacharjee Harsha

2008-01-01

Full Text Available Background: The northeastern region (NER of India is geographically isolated and ethno-culturally different from the rest of the country. There is lacuna regarding the data on causes of blindness and severe visual impairment in children from this region. Aim: To determine the causes of severe visual impairment and blindness amongst children from schools for the blind in the four states of NER of India. Design and Setting: Survey of children attending special education schools for the blind in the NER. Materials and Methods: Blind and severely visually impaired children (best corrected visual acuity < 20/200 in the better eye, aged up to 16 years underwent visual acuity estimation, external ocular examination, retinoscopy and fundoscopy. Refraction and low vision workup was done where indicated. World Health Organization′s reporting form was used to code anatomical and etiological causes of visual loss. Statistical Analysis: Microsoft Excel Windows software with SPSS. Results: A total of 376 students were examined of whom 258 fulfilled the eligibility criteria. The major anatomical causes of visual loss amongst the 258 were congenital anomalies (anophthalmos, microphthalmos 93 (36.1%; corneal conditions (scarring, vitamin A deficiency 94 (36.7%; cataract or aphakia 28 (10.9%, retinal disorders 15 (5.8% and optic atrophy 14 (5.3%. Nearly half of the children were blind from conditions which were either preventable or treatable (48.5%. Conclusion: Nearly half the childhood blindness in the NER states of India is avoidable and Vitamin A deficiency forms an important component unlike other Indian states. More research and multisectorial effort is needed to tackle congenital anomalies.

Enrichment of MCI and early Alzheimer's disease treatment trials using neurochemical and imaging candidate biomarkers.

LENUS (Irish Health Repository)

Hampel, H

2012-02-01

In the earliest clinical stages of Alzheimer\\'s Disease (AD), when symptoms are mild, clinical diagnosis will still be difficult. AD related molecular mechanisms precede symptoms. Biological markers can serve as early diagnostic indicators, as markers of preclinical pathological change, e.g. underlying mechanisms of action (MoA). Hypothesis based candidates are derived from structural and functional neuroimaging as well as from cerebrospinal fluid (CSF) and plasma. Unbiased exploratory approaches e.g. proteome analysis or rater independent fully automated imaging post-processing methods yield novel candidates. Recent progress in the validation of core feasible imaging and neurochemical biomarkers for functions such as early detection, classification, progression and prediction of AD is summarized. Single core feasible biomarkers can already be used to enrich populations at risk for AD and may be further enhanced using distinct combinations. Some biomarkers are currently in the process of implementation as primary or secondary outcome variables into regulatory guideline documents, e.g. regarding phase II in drug development programs as outcome measures in proof of concept or dose finding studies. There are specific biomarkers available depending on the hypothesized mechanism of action of a medicinal product, e.g. impact on the amyloidogenic cascade or on tauhyperphosphorylation. Ongoing large-scale international controlled multi-center trials will provide further validation of selected core feasible imaging and CSF biomarker candidates as outcome measures in early AD for use in phase III clinical efficacy trials. There is a need of rigorous co-development of biological trait- and statemarker candidates facilitated through planned synergistic collaboration between academic, industrial and regulatory partners.

The association between disability and cognitive impairment in an elderly Tanzanian population

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Catherine L. Dotchin

2015-03-01

Full Text Available Cognitive impairment is thought to be a major cause of disability worldwide, though data from sub-Saharan Africa (SSA are sparse. This study aimed to investigate the association between cognitive impairment and disability in a cohort of community-dwelling older adults living in Tanzania. The study cohort of 296 people aged 70 years and over was recruited as part of a dementia prevalence study. Subjects were diagnosed as having dementia or mild cognitive impairment according to the DSM-IV criteria. Disability level was assessed according to the WHO Disability Assessment Schedule, version 2.0 (WHODAS. A higher WHODAS score indicates greater disability. The median WHODAS in the background population was 25.0; in those with dementia and in those with mild cognitive impairment, 72 of 78 (92.3% and 41 of 46 (89.1%, respectively, had a WHODAS score above this level. The presence of dementia, mild cognitive impairment, hearing impairment, being unable to walk without an aid and not having attended school were independent predictors of having a WHODAS score above 25.0, though age and gender were not. In summary, cognitive impairment is a significant predictor of disability in elderly Tanzanians. Screening for early signs of cognitive decline would allow management strategies to be put in place that may reduce the associated disability burden.

Blood alcohol analysis alone versus comprehensive toxicological analysis - Systematic investigation of missed co-ingested other drugs in suspected alcohol-impaired drivers.

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Steuer, Andrea E; Eisenbeiss, Lisa; Kraemer, Thomas

2016-10-01

Driving under the influence of alcohol and/or drugs (DUID) is a safety issue of increasing public concern. When a police officer has reasonable grounds to classify a driver as impaired, he may arrange for a blood sample to be taken. In many countries, alcohol analysis only is ordered if impairment is suspected to be exclusively due to alcohol while comprehensive toxicological screening will be performed if additional suspicion for other illegal drugs of abuse (DoA) or medicinal drugs is on hand. The aim of the present study was firstly to evaluate whether signs of impairment can be differentiated to be caused by alcohol alone or a combination of alcohol and other driving-impairing drugs and secondly to which extent additional drugs are missed in suspected alcohol-impaired drivers. A total of 293 DUID cases (negative n=41; alcohol positive only, n=131; alcohol+active drug positive, n=121) analyzed in 2015 in the Canton of Zurich were evaluated for their documented impairment symptoms by translating these into a severity score and comparing them applying principle component analysis (PCA). Additional 500 cases suspected for alcohol-impaired driving only were reanalyzed using comprehensive LC-MS/MS screening methods covering about 1500 compounds. Drugs detected were classified for severity of driving impairment using the classification system established in the DRUID study of the European Commission. As partly expected from the pharmacological and toxicological point of view, PCA analysis revealed no differences between signs of impairment caused by alcohol alone and those caused by alcohol plus at least one active drug. Breaking it down to different blood alcohol concentration ranges, only between 0.3 and 0.5g/kg trends could be observed in terms of more severe impairment for combined alcohol and drug intake. In the 500 blood samples retrospectively analyzed in this study, a total of 330 additional drugs could be detected; in some cases up to 9 co-ingested ones. In

Prevalence of visual impairment and blindness in Upper Egypt: a gender-based perspective.

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Mousa, Ahmed; Courtright, Paul; Kazanjian, Arminee; Bassett, Ken

2014-06-01

To estimate the prevalence, causes of and risk factors for vision loss in Upper Egypt. In this cross-sectional study, four villages in Upper Egypt were randomly selected; within these four villages, households were randomly selected and within the selected households all residents aged ≥ 40 years were enumerated and enrolled. Door-to-door eye examinations of household members were conducted. Data on relevant demographic and socioeconomic characteristics were collected. The prevalence and causes of vision loss and associated risk factors were assessed. Sex differences in prevalence and determinants were also evaluated. The prevalence of best eye presenting visual impairment, severe visual impairment, and blindness were 23.9%, 6.4%, and 9.3% respectively. The prevalence of blindness among women significantly exceeded that among men (11.8% vs. 5.4%, respectively, p = 0.021). The prevalence of cataract was 22.9% (higher in women, 26.5% than men 17.2%, p = 0.018). The prevalence of trachomatous trichiasis was 9.7% (higher among women, 12.5%, than men, 5.4%, p = 0.012). The principal causes of blindness were cataract (60%), uncorrected refractive errors (16%) and corneal opacities (12%). Age, sex, family size, illiteracy, unemployment, water source and sanitation methods and living conditions were the major risk factors for vision loss. The prevalence of visual impairment remains high in Egypt, particularly among women. Risk factors for blindness may differ between men and women. There is a need for qualitative investigations to better understand the causes behind the excess in prevalence of blindness among women.

Subchronic steroid administration induces long lasting changes in neurochemical and behavioral response to cocaine in rats.

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Kailanto, Sanna; Kankaanpää, Aino; Seppälä, Timo

2011-11-01

The abuse of anabolic androgenic steroids (AASs), such as nandrolone, is not only a problem in the world of sports but is associated with the polydrug use of non-athletes. Among other adverse effects, AAS abuse has been associated with long term or even persistent psychiatric problems. We have previously found that nandrolone decanoate treatment could produce prolonged changes in rats' brain reward circuits associated to drug dependence. The aim in this study was to evaluate whether AAS-induced neurochemical and behavioral changes are reversible. The increases in extracellular dopamine (DA) and serotonin (5-HT) concentration, as well as stereotyped behavior and locomotor activity (LMA) evoked by cocaine were attenuated by pretreatment with nandrolone. The recovery period, which was needed for the DA system to return back to the basic level, was fairly long compared to the dosing period of the steroid. In the 5-HT system, the time that system needed to return back to the basal level, was even longer than in the DA system. The attenuation was still seen though there were no detectable traces of nandrolone in the blood samples. Given that accumbal outflow of DA and 5-HT, as well as LMA and stereotyped behavior are all related to reward of stimulant drugs, this study suggests that nandrolone decanoate has significant, long-lasting but reversible effects on the rewarding properties of cocaine. Copyright © 2011 Elsevier Ltd. All rights reserved.

Improving dementia care: The role of screening and detection of cognitive impairment

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Borson, Soo; Frank, Lori; Bayley, Peter J.; Boustani, Malaz; Dean, Marge; Lin, Pei-Jung; McCarten, J. Riley; Morris, John C.; Salmon, David P.; Schmitt, Frederick A.; Stefanacci, Richard G.; Mendiondo, Marta S.; Peschin, Susan; Hall, Eric J.; Fillit, Howard; Ashford, J. Wesson

2014-01-01

The value of screening for cognitive impairment, including dementia and Alzheimer's disease, has been debated for decades. Recent research on causes of and treatments for cognitive impairment has converged to challenge previous thinking about screening for cognitive impairment. Consequently, changes have occurred in health care policies and priorities, including the establishment of the annual wellness visit, which requires detection of any cognitive impairment for Medicare enrollees. In response to these changes, the Alzheimer's Foundation of America and the Alzheimer's Drug Discovery Foundation convened a workgroup to review evidence for screening implementation and to evaluate the implications of routine dementia detection for health care redesign. The primary domains reviewed were consideration of the benefits, harms, and impact of cognitive screening on health care quality. In conference, the workgroup developed 10 recommendations for realizing the national policy goals of early detection as the first step in improving clinical care and ensuring proactive, patient-centered management of dementia. PMID:23375564

Experiences of vision impairment in Papua New Guinea: implications for blindness prevention programs.

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Burnett, Anthea; Yashadhana, Aryati; Cabrera Aguas, Maria; Hanni, Yvonne; Yu, Mitasha

2016-01-01

A person's capability to access services and achieve good eye health is influenced by their behaviours, perceptions, beliefs and experiences. As evidence from Papua New Guinea (PNG) about people's lived experience with vision impairment is limited, the purpose of the present study was to better understand the beliefs, perceptions and emotional responses to vision impairment in PNG. A qualitative study, using both purposive and convenience sampling, was undertaken to explore common beliefs and perceptions about vision impairment, as well as the emotional responses to vision impairment. In-depth interviews were undertaken with 51 adults from five provinces representing culturally and geographically diverse regions of PNG. Grounded theory was used to elicit key themes from interview data. Participants described activities of everyday life impacted by vision impairment and the related worry, sadness and social exclusion. Common beliefs about the causes of vision impairment were environmental stressors (sun, dust, dirt and smoke), ageing and sorcery. Findings provide insight into the unique social context in PNG and identify a number of programmatic and policy implications, such as the need for preventative eye health information and services, addressing persisting beliefs in sorcery when developing health information packages, and the importance of coordinating with counselling and well-being services for people experiencing vision impairment.

Visual Impairment

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Different Patterns of Theory of Mind Impairment in Mild Cognitive Impairment.

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Moreau, Noémie; Rauzy, Stéphane; Bonnefoi, Bernadette; Renié, Laurent; Martinez-Almoyna, Laurent; Viallet, François; Champagne-Lavau, Maud

2015-01-01

Theory of Mind refers to the ability to infer other’s mental states, their beliefs, intentions, or knowledge. To date, only two studies have reported the presence of Theory of Mind impairment in mild cognitive impairment (MCI). In the present study,we evaluated 20 MCI patients and compared them with 25 healthy control participants using two Theory of Mind tasks. The first task was a false belief paradigm as frequently used in the literature, and the second one was a referential communication task,assessing Theory of Mind in a real situation of interaction and which had never been used before in this population. The results showed that MCI patients presented difficulties inferring another person’s beliefs about reality and attributing knowledge to them in a situation of real-life interaction. Two different patterns of Theory of Mind emerged among the patients. In comparison with the control group, some MCI patients demonstrated impairment only in the interaction task and presented isolated episodicmemory impairment, while others were impaired in both Theory of Mind tasks and presented cognitive impairment impacting both episodic memory and executive functioning. Theory of Mind is thus altered in the very early stages of cognitive impairment even in real social interaction, which could impact precociously relationships in daily life.

The association between cardiorespiratory fitness and risk of all-cause mortality among women with impaired fasting glucose or undiagnosed diabetes mellitus.

Science.gov (United States)

Lyerly, G William; Sui, Xuemei; Lavie, Carl J; Church, Timothy S; Hand, Gregory A; Blair, Steven N

2009-09-01

To evaluate the independent and joint associations among cardiorespiratory fitness (CRF), body mass index, and risk of mortality from any cause among women with impaired fasting glucose (IFG) or undiagnosed diabetes mellitus (DM). Female patients (N=3044; mean age, 47.4 years) with IFG or undiagnosed DM completed a maximal exercise treadmill test (between January 26, 1971, and March 21, 2001). The women had no history of a cardiovascular disease event or diagnosed DM at baseline. Cardiorespiratory fitness was defined categorically as low (bottom 20%), moderate (middle 40%), or high (upper 40%) according to previously published Aerobics Center Longitudinal Study guidelines. Body mass index was calculated as the weight in kilograms divided by the height in meters squared (kg/m(2)). During a 16-year follow-up period, 171 deaths occurred. There was an inverse association between CRF and all-cause mortality risk. Women with moderate or high CRF were at lower risk of mortality (moderate CRF, 35% lower; high CRF, 36% lower; P(trend)=.03) than those with low CRF. An exercise capacity lower than 7 metabolic equivalents was associated with a 1.5-fold higher risk of death than an exercise capacity of 9 metabolic equivalents or higher (P(trend)=.05). The multivariate adjusted hazard ratios (HRs), including adjustments for CRF, were higher for heavier patients than for patients of normal weight (overweight patients: HR, 0.86; 95% confidence interval, 0.57-1.30; obese patients: HR, 1.19; 95% confidence interval, 0.70-2.03; P(trend)=.84). Combined analyses showed that women who were overweight or obese and unfit (low CRF) were at more than twice the risk of death than women who were of normal weight and fit (moderate or high CRF). Cardiorespiratory fitness, not body mass index, is a significant predictor of all-cause mortality among women with IFG or undiagnosed DM. Assessing CRF levels provides important prognostic information independent of traditional risk factors.

KCNQ channels regulate age-related memory impairment.

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Sonia Cavaliere

Full Text Available In humans KCNQ2/3 heteromeric channels form an M-current that acts as a brake on neuronal excitability, with mutations causing a form of epilepsy. The M-current has been shown to be a key regulator of neuronal plasticity underlying associative memory and ethanol response in mammals. Previous work has shown that many of the molecules and plasticity mechanisms underlying changes in alcohol behaviour and addiction are shared with those of memory. We show that the single KCNQ channel in Drosophila (dKCNQ when mutated show decrements in associative short- and long-term memory, with KCNQ function in the mushroom body α/βneurons being required for short-term memory. Ethanol disrupts memory in wildtype flies, but not in a KCNQ null mutant background suggesting KCNQ maybe a direct target of ethanol, the blockade of which interferes with the plasticity machinery required for memory formation. We show that as in humans, Drosophila display age-related memory impairment with the KCNQ mutant memory defect mimicking the effect of age on memory. Expression of KCNQ normally decreases in aging brains and KCNQ overexpression in the mushroom body neurons of KCNQ mutants restores age-related memory impairment. Therefore KCNQ is a central plasticity molecule that regulates age dependent memory impairment.

[Is olfactory function impaired in moderate height?].

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Kühn, M; Welsch, H; Zahnert, T; Hummel, Thomas

2009-09-01

The human sense of smell seems to be influenced by the surrounding barometric pressure. These factors appear to be especially important during flights, for example, in order to recognize the smell of fire etc. Thus, questions are whether pilots or passengers exhibit an impaired smell sensitivity when tested at moderate heights, or, whether changes in humidity would affect the sense of smell. Using climate chambers, odor discrimination and butanol odor thresholds were tested in 77 healthy normosmic volunteers (5 female, 72 male; aged 25+/-8 years from 18 up to 53 years) under hypobaric (2 700+/-20 m, 20 degrees C+/-1 K, rh=50+/-5%) and hyperbaric, (10+/-0.5 m (2 bar)) and different humidity conditions (30 vs. 80%, 20 degrees C+/-1 K, normobaric). During all conditions cognitive performance was tested. Among other effects, olfactory sensitivity was impaired at threshold, but not suprathreshold level, in a hypobaric compared to a hyperbaric milieu, and thresholds were lower in humid, compared to relatively dry conditions. In conclusion, environmental conditions modulate the sense of smell, and may, consecutively, influence results from olfactory tests. During flight hypobaric conditions, mild hypoxia and dry air may cause impaired sensitivity of smell. Georg Thieme Verlag KG Stuttgart * New York.

Cognitive Impairment in Infratentorial Strokes

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Melek Kandemir

2009-12-01

Full Text Available OBJECTIVE: Beginning in the mid-1980s, with anatomical, behavioral, and neuropsychological evidence, it was suggested that the role of the cerebellum extends beyond a purely motor domain. A series of articles were published reviewing the potential role of the cerebellum in cognition. Both of these functions are supported by connections of dentate nucleus and frontal cortex through the thalamus. The cognitive profile of isolated subtentorial and cerebellar infarcts is related to the involved frontal circuit (especially executive functions. In this study, we aimed to demonstrate the cognitive profile of cerebellar and subtentorial infarcts. METHODS: Nineteen patients with infratentorial infarcts and 19 neurologically healthy individuals as a control group were included in this study. Neuropsychometric test battery was employed in both of the groups. RESULTS: Age, sex, education, clinical syndrome, and localization had no effect on the cognitive test performances. Performance on the California Verbal Learning Test, a verbal memory test, was worse in the patient group. Patients had difficulties in recognizing the items of the Rey-Osterrieth Complex Figure Test, and spent significantly more time to complete the trail making test part B. The patient group also demonstrated lower performance level in the verbal fluency test when compared to the control group. CONCLUSION: The cognitive impairment pattern of the verbal and visual memory tests and impairment determined on the verbal fluency test and the trail making tests may imply frontal impairment. Our results support the knowledge that cerebellar or brainstem strokes cause mild frontal type cognitive syndrome by damaging cerebello-ponto-thalamo-cortical pathways

Theory of Mind in Bipolar Disorder, with Comparison to the Impairments Observed in Schizophrenia

OpenAIRE

Mitchell, Rachel L. C.; Young, Allan H.

2016-01-01

Our ability to make sense of information on the potential intentions and dispositions of others is of paramount importance for understanding their communicative intent, and for judging what an appropriate reaction might be. Thus, anything that impinges on this ability has the potential to cause significant social impairment, and compromise an individual’s level of functioning. Both bipolar disorder and schizophrenia are known to feature theory of mind impairment. We conducted a theoretical re...

SU-F-I-68: Longitudinal Neurochemical Changes On Rat Prefrontal Cortex of Single Prolonged Stress Model by Using Proton Magnetic Resonance Spectroscopy at 9.4T

International Nuclear Information System (INIS)

Lim, S-I; Yoo, C-H; Song, K-H; Choe, B-Y; Woo, D-C

2016-01-01

Purpose: Single prolonged stress (SPS) is an animal model of posttraumatic stress disorder (PTSD). However, it has not been known how PTSD develops from the first exposure to traumatic events and neurochemical differences between acute/single stress and PTSD-triggering stress. Therefore, the object of this study is to determine time-dependent neurochemical changes in prefrontal cortex (PFC) of rats using in vivo proton magnetic resonance spectroscopy (1H-MRS). Methods: Male Sprague-Dawley rats (n=14; body weight=200–220g) were used. The SPS protocol was used in this study. Rats were restrained for 2h and then immediately forced to swim for 20min in water (20–24 Celsius). After a 15-min recuperation period, rats were exposed to ether (using a desiccator) until general anesthesia occurred (<5min). In vivo proton MRS was performed 30min before the SPS (Base), approximately 10min after the SPS (D+0), 3 (D+3) and 7 (D+7) days after SPS to investigate time-dependent changes on metabolites levels in the PFC. Acquisition of in vivo MRS spectra and MRI was conducted at the four time points using 9.4 T Agilent Scanner. Concentration of metabolites was quantified by LCModel. Results: Statistical significance was analyzed using one-way ANOVA with post hoc Tukey HSD tests to assess the metabolite changes in the PFC. The SPS resulted in significant stress-induced differences for 7 days in glutamine (F(3,52)=6.750, P=0.001), choline-containing compounds (F(3,52)=16.442, P=0.000), glutamine/glutamate concentrations (F(3,52)=7.352, P=0.000). Conclusion: PTSD in human is associated with decreased neuronal activity in the PFC. In this study, SPS altered total choline, glutamine levels but not NAA levels in the PFC of the rats. Therefore, for the three stressors and quiescent period of seven days, SPS attenuated excitatory tone and membrane turnover but did not affect neural integrity in the PFC.

The Gastric Ganglion of Octopus vulgaris: Preliminary Characterization of Gene- and Putative Neurochemical-Complexity, and the Effect of Aggregata octopiana Digestive Tract Infection on Gene Expression

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Elena Baldascino

2017-12-01

Full Text Available The gastric ganglion is the largest visceral ganglion in cephalopods. It is connected to the brain and is implicated in regulation of digestive tract functions. Here we have investigated the neurochemical complexity (through in silico gene expression analysis and immunohistochemistry of the gastric ganglion in Octopus vulgaris and tested whether the expression of a selected number of genes was influenced by the magnitude of digestive tract parasitic infection by Aggregata octopiana. Novel evidence was obtained for putative peptide and non-peptide neurotransmitters in the gastric ganglion: cephalotocin, corticotrophin releasing factor, FMRFamide, gamma amino butyric acid, 5-hydroxytryptamine, molluscan insulin-related peptide 3, peptide PRQFV-amide, and tachykinin–related peptide. Receptors for cholecystokininA and cholecystokininB, and orexin2 were also identified in this context for the first time. We report evidence for acetylcholine, dopamine, noradrenaline, octopamine, small cardioactive peptide related peptide, and receptors for cephalotocin and octopressin, confirming previous publications. The effects of Aggregata observed here extend those previously described by showing effects on the gastric ganglion; in animals with a higher level of infection, genes implicated in inflammation (NFκB, fascin, serpinB10 and the toll-like 3 receptor increased their relative expression, but TNF-α gene expression was lower as was expression of other genes implicated in oxidative stress (i.e., superoxide dismutase, peroxiredoxin 6, and glutathione peroxidase. Elevated Aggregata levels in the octopuses corresponded to an increase in the expression of the cholecystokininA receptor and the small cardioactive peptide-related peptide. In contrast, we observed decreased relative expression of cephalotocin, dopamine β-hydroxylase, peptide PRQFV-amide, and tachykinin-related peptide genes. A discussion is provided on (i potential roles of the various molecules

The Gastric Ganglion of Octopus vulgaris: Preliminary Characterization of Gene- and Putative Neurochemical-Complexity, and the Effect of Aggregata octopiana Digestive Tract Infection on Gene Expression

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Baldascino, Elena; Di Cristina, Giulia; Tedesco, Perla; Hobbs, Carl; Shaw, Tanya J.; Ponte, Giovanna; Andrews, Paul L. R.

2017-01-01

The gastric ganglion is the largest visceral ganglion in cephalopods. It is connected to the brain and is implicated in regulation of digestive tract functions. Here we have investigated the neurochemical complexity (through in silico gene expression analysis and immunohistochemistry) of the gastric ganglion in Octopus vulgaris and tested whether the expression of a selected number of genes was influenced by the magnitude of digestive tract parasitic infection by Aggregata octopiana. Novel evidence was obtained for putative peptide and non-peptide neurotransmitters in the gastric ganglion: cephalotocin, corticotrophin releasing factor, FMRFamide, gamma amino butyric acid, 5-hydroxytryptamine, molluscan insulin-related peptide 3, peptide PRQFV-amide, and tachykinin–related peptide. Receptors for cholecystokininA and cholecystokininB, and orexin2 were also identified in this context for the first time. We report evidence for acetylcholine, dopamine, noradrenaline, octopamine, small cardioactive peptide related peptide, and receptors for cephalotocin and octopressin, confirming previous publications. The effects of Aggregata observed here extend those previously described by showing effects on the gastric ganglion; in animals with a higher level of infection, genes implicated in inflammation (NFκB, fascin, serpinB10 and the toll-like 3 receptor) increased their relative expression, but TNF-α gene expression was lower as was expression of other genes implicated in oxidative stress (i.e., superoxide dismutase, peroxiredoxin 6, and glutathione peroxidase). Elevated Aggregata levels in the octopuses corresponded to an increase in the expression of the cholecystokininA receptor and the small cardioactive peptide-related peptide. In contrast, we observed decreased relative expression of cephalotocin, dopamine β-hydroxylase, peptide PRQFV-amide, and tachykinin-related peptide genes. A discussion is provided on (i) potential roles of the various molecules in food intake

SU-F-I-68: Longitudinal Neurochemical Changes On Rat Prefrontal Cortex of Single Prolonged Stress Model by Using Proton Magnetic Resonance Spectroscopy at 9.4T

Energy Technology Data Exchange (ETDEWEB)

Lim, S-I; Yoo, C-H [Department of Biomedical Engineering, and Research Institute of Biomedical Engineering, The Catholic University of Korea College of Medicine, Seoul, Seoul (Korea, Republic of); Asan Institute for Life Sciences, Asan Medical Center, Seoul, Seoul (Korea, Republic of); Song, K-H; Choe, B-Y [Department of Biomedical Engineering, and Research Institute of Biomedical Engineering, The Catholic University of Korea College of Medicine, Seoul, Seoul (Korea, Republic of); Woo, D-C [Asan Institute for Life Sciences, Asan Medical Center, Seoul, Seoul (Korea, Republic of)

2016-06-15

Purpose: Single prolonged stress (SPS) is an animal model of posttraumatic stress disorder (PTSD). However, it has not been known how PTSD develops from the first exposure to traumatic events and neurochemical differences between acute/single stress and PTSD-triggering stress. Therefore, the object of this study is to determine time-dependent neurochemical changes in prefrontal cortex (PFC) of rats using in vivo proton magnetic resonance spectroscopy (1H-MRS). Methods: Male Sprague-Dawley rats (n=14; body weight=200–220g) were used. The SPS protocol was used in this study. Rats were restrained for 2h and then immediately forced to swim for 20min in water (20–24 Celsius). After a 15-min recuperation period, rats were exposed to ether (using a desiccator) until general anesthesia occurred (<5min). In vivo proton MRS was performed 30min before the SPS (Base), approximately 10min after the SPS (D+0), 3 (D+3) and 7 (D+7) days after SPS to investigate time-dependent changes on metabolites levels in the PFC. Acquisition of in vivo MRS spectra and MRI was conducted at the four time points using 9.4 T Agilent Scanner. Concentration of metabolites was quantified by LCModel. Results: Statistical significance was analyzed using one-way ANOVA with post hoc Tukey HSD tests to assess the metabolite changes in the PFC. The SPS resulted in significant stress-induced differences for 7 days in glutamine (F(3,52)=6.750, P=0.001), choline-containing compounds (F(3,52)=16.442, P=0.000), glutamine/glutamate concentrations (F(3,52)=7.352, P=0.000). Conclusion: PTSD in human is associated with decreased neuronal activity in the PFC. In this study, SPS altered total choline, glutamine levels but not NAA levels in the PFC of the rats. Therefore, for the three stressors and quiescent period of seven days, SPS attenuated excitatory tone and membrane turnover but did not affect neural integrity in the PFC.

Long-term impairment of social memory in the rat after social defeat is not restored by desglycinamide-vasopressin

NARCIS (Netherlands)

Reijmers, L.G.J.E.; Hoekstra, K.; Burbach, J.P.H.; Ree, van J.M.; Spruijt, B.M.

2001-01-01

Repeated social defeat followed by individual housing caused a long-term impairment of social memory in male rats. Social memory, as assessed in the social discrimination test using an intertrial interval of 3 min, was impaired for at least 8 weeks after the social defeat experience. Since social

Otorhinolaryngological causes of proptosis and their sequelae in an ...

African Journals Online (AJOL)

The major causes of proptosis were due to malignancy (66%) followed by infections and cystic lesions in equal proportions. Half of the subjects who developed visual impairment had improvement in vision and improved facial symmetry after appropriate treatments were instituted. Cases of strabismus were also corrected.

Neuromuscular Impairments Are Associated With Impaired Head and Trunk Stability During Gait in Parkinson Fallers.

Science.gov (United States)

Cole, Michael H; Naughton, Geraldine A; Silburn, Peter A

2017-01-01

Background The trunk plays a critical role in attenuating movement-related forces that threaten to challenge the body's postural control system. For people with Parkinson's disease (PD), disease progression often leads to dopamine-resistant axial symptoms, which impair trunk control and increase falls risk. Objective This prospective study aimed to evaluate the relationship between impaired trunk muscle function, segmental coordination, and future falls in people with PD. Methods Seventy-nine PD patients and 82 age-matched controls completed clinical assessments and questionnaires to establish their medical history, symptom severity, balance confidence, and falls history. Gait characteristics and trunk muscle activity were assessed using 3-dimensional motion analysis and surface electromyography. The incidence, cause, and consequence of any falls experienced over the next 12 months were recorded and indicated that 48 PD and 29 control participants fell at least once during this time. Results PD fallers had greater peak and baseline lumbar multifidus (LMF) and thoracic erector spinae (TES) activations than control fallers and nonfallers. Analysis of covariance indicated that the higher LMF activity was attributable to the stooped posture adopted by PD fallers, but TES activity was independent of medication use, symptom severity, and trunk orientation. Furthermore, greater LMF and TES baseline activity contributed to increasing lateral head, trunk, and pelvis movements in PD fallers but not nonfallers or controls. Conclusions The results provide evidence of neuromuscular deficits for PD fallers that are independent of medications, symptom severity, and posture and contribute to impaired head, trunk, and pelvis control associated with falls in this population. © The Author(s) 2016.

Muscle enzyme release does not predict muscle function impairment after triathlon.

Science.gov (United States)

Margaritis, I; Tessier, F; Verdera, F; Bermon, S; Marconnet, P

1999-06-01

We sought to determine the effects of a long distance triathlon (4 km swim, 120 km bike-ride, and 30 km run) on the four-day kinetics of the biochemical markers of muscle damage, and whether they were quantitatively linked with muscle function impairment and soreness. Data were collected from 2 days before until 4 days after the completion of the race. Twelve triathletes performed the triathlon and five did not. Maximal voluntary contraction (MVC), muscle soreness (DOMS) and total serum CK, CK-MB, LDH, AST and ALT activities were assessed. Significant changes after triathlon completion were found for all muscle damage indirect markers over time (p triathlon. Long distance triathlon race caused muscle damage, but extent, as well as muscle recovery cannot be evaluated by the magnitude of changes in serum enzyme activities. Muscle enzyme release cannot be used to predict the magnitude of the muscle function impairment caused by muscle damage.

Cellular dynamical mechanisms for encoding the time and place of events along spatiotemporal trajectories in episodic memory

OpenAIRE

Hasselmo, Michael E.; Giocomo, Lisa M.; Yoshida, Motoharu

2009-01-01

Understanding the mechanisms of episodic memory requires linking behavioural data and lesion effects to data on the dynamics of cellular membrane potentials and population interactions within these brain regions. Linking behavior to specific membrane channels and neurochemicals has implications for therapeutic applications. Lesions of the hippocampus, entorhinal cortex and subcortical nuclei impair episodic memory function in humans and animals, and unit recording data from these regions in b...

Organochlorine pollutants in grey seal (Halichoerus grypus) pups and their impact on plasma thyroid hormone and vitamin A concentrations

OpenAIRE

Sørmo, Eugen Gravningen

2005-01-01

Studies on laboratory animals suggest that developing and newborn mammals are more vulnerable than the adults with respect to the harmful effects of organochlorine (OC) pollutants such polychlorinated biphenyls (PCBs) and OC pesticides (Brouwer et al. 1995; 1998a; Colborn 2004). These effects include neurobiological and neurochemical effects, reproductive effects, reduced brain and circulatory thyroid hormone levels, impaired immune functions and vitamin A homeostasis (Brouwer et al. 1995; Co...

Clinical-pathologic correlations in vascular cognitive impairment and dementia.

Science.gov (United States)

Flanagan, Margaret; Larson, Eric B; Latimer, Caitlin S; Cholerton, Brenna; Crane, Paul K; Montine, Kathleen S; White, Lon R; Keene, C Dirk; Montine, Thomas J

2016-05-01

The most common causes of cognitive impairment and dementia are Alzheimer's disease (AD) and vascular brain injury (VBI), either independently, in combination, or in conjunction with other neurodegenerative disorders. The contribution of VBI to cognitive impairment and dementia, particularly in the context of AD pathology, has been examined extensively yet remains difficult to characterize due to conflicting results. Describing the relative contribution and mechanisms of VBI in dementia is important because of the profound impact of dementia on individuals, caregivers, families, and society, particularly the stability of health care systems with the rapidly increasing age of our population. Here we discuss relationships between pathologic processes of VBI and clinical expression of dementia, specific subtypes of VBI including microvascular brain injury, and what is currently known regarding contributions of VBI to the development and pathogenesis of the dementia syndrome. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock. Copyright © 2015 Elsevier B.V. All rights reserved.

20 CFR 220.102 - Non-severe impairment(s), defined.

Science.gov (United States)

2010-04-01