Androgen receptor (AR) promotes clear cell renal cell carcinoma (ccRCC) migration and invasion via altering the circHIAT1/miR-195-5p/29a-3p/29c-3p/CDC42 signals.

Science.gov (United States)

Wang, Kefeng; Sun, Yin; Tao, Wei; Fei, Xiang; Chang, Chawnshang

2017-05-28

Increasing evidence has demonstrated that the androgen receptor (AR) plays important roles to promote the metastasis of clear cell renal cell carcinoma (ccRCC). The detailed mechanisms, especially how AR functions via altering the circular RNAs (circRNAs) remain unclear. Here we identified a new circRNA (named as circHIAT1) whose expression was lower in ccRCCs than adjacent normal tissues. Targeting AR could suppress ccRCC cell progression via increasing circHIAT1 expression. ChIP assay and luciferase assay demonstrated that AR suppressed circHIAT1 expression via regulating its host gene, Hippocampus Abundant Transcript 1 (HIAT1) expression at the transcriptional level. The consequences of AR-suppressed circHIAT1 resulted in deregulating miR-195-5p/29a-3p/29c-3p expressions, which increased CDC42 expression to enhance ccRCC cell migration and invasion. Increasing this newly identified signal via circHIAT1 suppressed AR-enhanced ccRCC cell migration and invasion. Together, these results suggested that circHIAT1 functioned as a metastatic inhibitor to suppress AR-enhanced ccRCC cell migration and invasion. Targeting this newly identified AR-circHIAT1-mediated miR-195-5p/29a-3p/29c-3p/CDC42 signals may help us develop potential new therapies to better suppress ccRCC metastasis. Copyright © 2017 Elsevier B.V. All rights reserved.

Boomerang deformity of cervical spinal cord migrating between split laminae after laminoplasty.

Science.gov (United States)

Kimura, S; Gomibuchi, F; Shimoda, H; Ikezawa, Y; Segawa, H; Kaneko, F; Uchiyama, S; Homma, T

2000-04-01

Patients with cervical compression myelopathy were studied to elucidate the mechanism underlying boomerang deformity, which results from the migration of the cervical spinal cord between split laminae after laminoplasty with median splitting of the spinous processes (boomerang sign). Thirty-nine cases, comprising 25 patients with cervical spondylotic myelopathy, 8 patients with ossification of the posterior longitudinal ligament, and 6 patients with cervical disc herniation with developmental canal stenosis, were examined. The clinical and radiological findings were retrospectively compared between patients with (B group, 8 cases) and without (C group, 31 cases) boomerang sign. Moderate increase of the grade of this deformity resulted in no clinical recovery, although there was no difference in clinical recovery between the two groups. Most boomerang signs developed at the C4/5 and/or C5/6 level, where maximal posterior movement of the spinal cord was achieved. Widths between lateral hinges and between split laminae in the B group were smaller than in the C group. Flatness of the spinal cord in the B group was more severe than in the C group. In conclusion, the boomerang sign was caused by posterior movement of the spinal cord, narrower enlargement of the spinal canal and flatness of the spinal cord.

miR-106a-5p inhibits the proliferation and migration of astrocytoma cells and promotes apoptosis by targeting FASTK.

Directory of Open Access Journals (Sweden)

Feng Zhi

Full Text Available Astrocytomas are common malignant intracranial tumors that comprise the majority of adult primary central nervous system tumors. MicroRNAs (miRNAs are small, non-coding RNAs (20-24 nucleotides that post-transcriptionally modulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. In our previous studies, we found that the downregulation of miR-106a-5p in astrocytomas is associated with poor prognosis. However, its specific gene target(s and underlying functional mechanism(s in astrocytomas remain unclear. In this study, we used mRNA microarray experiments to measure global mRNA expression in the presence of increased or decreased miR-106a-5p levels. We then performed bioinformatics analysis based on multiple target prediction algorithms to obtain candidate target genes that were further validated by computational predictions, western blot analysis, quantitative real-time PCR, and the luciferase reporter assay. Fas-activated serine/threonine kinase (FASTK was identified as a direct target of miR-106a-5p. In human astrocytomas, miR-106a-5p is downregulated and negatively associated with clinical staging, whereas FASTK is upregulated and positively associated with advanced clinical stages, at both the protein and mRNA levels. Furthermore, Kaplan-Meier analysis revealed that the reduced expression of miR-106a-5p or the increased expression of FASTK is significantly associated with poor survival outcome. These results further supported the finding that FASTK is a direct target gene of miR-106a-5p. Next, we explored the function of miR-106a-5p and FASTK during astrocytoma progression. Through gain-of-function and loss-of-function studies, we demonstrated that miR-106a-5p can significantly inhibit cell proliferation and migration and can promote cell apoptosis in vitro. The knockdown of FASTK induced similar effects on astrocytoma cells as those induced by the overexpression of miR-106a-5p. These

GSE1 negative regulation by miR-489-5p promotes breast cancer cell proliferation and invasion

International Nuclear Information System (INIS)

Chai, Peng; Tian, Jingzhong; Zhao, Deyin; Zhang, Hongyan; Cui, Jian; Ding, Keshuo; Liu, Bin

2016-01-01

Gse1 coiled-coil protein (GSE1), also known as KIAA0182, is a proline rich protein. However, the function of GSE1 is largely unknown. In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. Furthermore, GSE1 was identified as a direct target of miR-489-5p, which is significantly reduced in breast cancer tissues. In addition, forced expression of miR-489-5p suppressed breast cancer cells proliferation, migration and invasion. Moreover, depletion of GSE1 by siRNAs significantly abrogated the enhanced proliferation, migration and invasion of breast cancer cells consequent to miR-489-5p depletion. Taken together, these findings suggest that GSE1 may function as a novel oncogene in breast cancer and it can be regulated by miR-489-5p. - Highlights: • GSE1 is overexpressed in breast cancer and increased GSE1 expression predicts poor prognosis in breast cancer patients. • Knockdown of GSE1 inhibits breast cancer cell proliferation, migration and invasion. • GSE1 is a direct target of miR-489-5p. • Forced expression of miR-489-5p inhibits breast cancer cell proliferation, migration and invasion.

Discovering the miR-26a-5p Targetome in Prostate Cancer Cells

DEFF Research Database (Denmark)

Rizzo, Milena; Berti, Gabriele; Russo, Francesco

2017-01-01

Purpose. miR-26a-5p is a tumor suppressor (TS) miRNA often downregulated in several tumor tissues and tumor cell lines. In this work, we performed the re-expression of the miR-26a-5p in DU-145 prostate cancer cells to collect genes interacting with miR-26a-5p and analyzed their integration...... in the tumorigenesis related pathways. Methods. The transfection of DU-145 prostate cancer cells with miR-26a-5p was done using nucleofection. The biological effects induced by miR-26a-5p re-expression were detected with routine assays for cell proliferation, cell cycle, survival, apoptosis and cell migration. The mi...... to integrate target genes in KEGG pathways and Protein-Protein Interaction networks (PPINs) and modules were built. Results. miR-26a-5p exerted an anti-proliferative effect acting at several levels, by decreasing survival and migration and inducing both cell cycle block and apoptosis. The analysis of the mi...

miR-409-3p suppresses breast cancer cell growth and invasion by targeting Akt1

Energy Technology Data Exchange (ETDEWEB)

Zhang, Guoqiang [Department of Breast Surgery, Qilu Hospital, Shandong University, Jinan 250012 (China); Department of Thyroid and Breast Surgery, Hospital Affiliated to Binzhou Medical University, 661 Second Huanghe Street, Binzhou 256603 (China); Liu, Zengyan [Department of Hematology, Hospital Affiliated to Binzhou Medical University, 661 Second Huanghe Street, Binzhou 256603 (China); Xu, Hao [Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029 (China); Yang, Qifeng, E-mail: qifengy_sdu1@163.com [Department of Breast Surgery, Qilu Hospital, Shandong University, Jinan 250012 (China)

2016-01-08

Altered levels and functions of microRNAs (miRNAs) are correlated with carcinogenesis. While miR-409-3p has been shown to play important roles in several cancer types, its function in the context of breast cancer (BC) remains unknown. In this study, miR-409-3p was significantly downregulated in BC tissues and cell lines, compared with the corresponding control counterparts. Overexpression of miR-409-3p inhibited BC cell proliferation, migration and invasion in vitro and suppressed tumor growth in vivo. Notably, miR-409-3p induced downregulation of Akt1 protein through binding to its 3′ untranslated region (UTR). Conversely, restoring Akt1 expression rescued the suppressive effects of miR-409-3p. Our data collectively indicate that miR-409-3p functions as a tumor suppressor in BC through downregulating Akt1, supporting the targeting of the novel miR-409-3p/Akt1 axis as a potentially effective therapeutic approach for BC. - Highlights: • miR-409-3p inhibits proliferation, migration and invasion of BC cells. • miR-409-3p suppresses tumor growth in nude mice. • Akt1 is a direct downstream target of miR-409-3p. • Ectopic expression of Akt1 reverses the effects of miR-409-3p on cell proliferation, migration and invasion.

Radiological and migration results of the DURALOC(R)-cup after two years

International Nuclear Information System (INIS)

Juen, F.

2000-10-01

In 1997 a study was conduced concerning 69 consecutive patients, all of whom consisted of DURALOC(R) series 100 acetabular components. The clinical, radiological and migrational aspect of each component was investigated 2 and 4 years postoperatively. In addition to this, a further 92 cups were analyzed in an identical manner, again 2 years after implantation. This therefore equated to a total of 161 investigated cups after a follow up interval of 2 years. In 144 of these cases the cup was combined with a cementless hydroxyapatite coated Spotorno shaft, with the remaining 17 involving a cemented Link-shaft (Lubinus SP II). A 28 mm Biolox(R) ceramic head was constant in all cases. Clinical data for each cup was collected via completion of a standard examination form, while acetabular migration, both vertical and horizontal, was measured on serial radiographs by the computer assisted EBRA method. From analyses of collected data, it was clearly shown that the clinical results remained very good over the 2- and 4-year-periods however, from radiological evidence it was indicated that for the period 3-4 years postoperatively, an increasing amount of radiolucencies around the cups were apparent. There was clearly no correlation between clinical and migration results. From the data taken from 106 migration curves, the mean total migration over the initial two-year-period was calculated to be 0.88 mm. From analysis of a further 56 migration curves, the mean total migration within 4 years of implantation was assessed to be 1.23 mm, however a decreasing speed of migration over the final 2-year-period was indicated. Our results demonstrate that statements relating to migration results of particular cups are more accurate after four years. However, statements about mean migration values are possible after two years. A migration speed of 1 mm total migration within the first 2 years after operation was predictive for radiological loosening of the cup after four years (p=0

Lipid raft-mediated miR-3908 inhibition of migration of breast cancer cell line MCF-7 by regulating the interactions between AdipoR1 and Flotillin-1.

Science.gov (United States)

Li, Yuan; Shan, Fei; Chen, Jinglong

2017-03-21

The mechanisms of lipid raft regulation by microRNAs in breast cancer are not fully understood. This work focused on the evaluation and identification of miR-3908, which may be a potential biomarker related to the migration of breast cancer cells, and elucidates lipid-raft-regulating cell migration in breast cancer. To confirm the prediction that miR-3908 is matched with AdipoR1, we used 3'-UTR luciferase activity of AdipoR1 to assess this. Then, human breast cancer cell line MCF-7 was cultured in the absence or presence of the mimics or inhibitors of miR-3908, after which the biological functions of MCF-7 cells were analyzed. The protein expression of AdipoR1, AMPK, and SIRT-1 were examined. The interaction between AdipoR1 and Flotillin-1, or its effects on lipid rafts on regulating cell migration of MCF-7, was also investigated. AdipoR1 is a direct target of miR-3908. miR-3908 suppresses the expression of AdipoR1 and its downstream pathway genes, including AMPK, p-AMPK, and SIRT-1. miR-3908 enhances the process of breast cancer cell clonogenicity. miR-3908 exerts its effects on the proliferation and migration of MCF-7 cells, which are mediated by lipid rafts regulating AdipoR1's ability to bind Flotillin-1. miR-3908 is a crucial mediator of the migration process in breast cancer cells. Lipid rafts regulate the interactions between AdipoR1 and Flotillin-1 and then the migration process associated with miR-3908 in MCF-7 cells. Our findings suggest that targeting miR-3908 and the lipid raft, may be a promising strategy for the treatment and prevention of breast cancer.

Measurement of the mass splittings between the b bar bχb,J(1P) states

International Nuclear Information System (INIS)

Edwards, K.W.; Edwards, K.W.; Bellerive, A.; Bellerive, A.; Janicek, R.; Janicek, R.; MacFarlane, D.B.; MacFarlane, D.B.; Patel, P.M.; Patel, P.M.; Sadoff, A.J.; Ammar, R.; Baringer, P.; Bean, A.; Besson, D.; Coppage, D.; Darling, C.; Davis, R.; Kotov, S.; Kravchenko, I.; Kwak, N.; Zhou, L.; Anderson, S.; Kubota, Y.; Lee, S.J.; ONeill, J.J.; Poling, R.; Riehle, T.; Smith, A.; Alam, M.S.; Athar, S.B.; Ling, Z.; Mahmood, A.H.; Timm, S.; Wappler, F.; Anastassov, A.; Duboscq, J.E.; Fujino, D.; Gan, K.K.; Hart, T.; Honscheid, K.; Kagan, H.; Kass, R.; Lee, J.; Schwarthoff, H.; Spencer, M.B.; Sung, M.; Undrus, A.; Wolf, A.; Zoeller, M.M.; Richichi, S.J.; Severini, H.; Skubic, P.; Bishai, M.; Fast, J.; Hinson, J.W.; Menon, N.; Miller, D.H.; Shibata, E.I.; Shipsey, I.P.; Yurko, M.; Glenn, S.; Kwon, Y.; Lyon, A.L.; Roberts, S.; Thorndike, E.H.; Jessop, C.P.; Lingel, K.; Marsiske, H.; Perl, M.L.; Savinov, V.; Ugolini, D.; Zhou, X.; Coan, T.E.; Fadeyev, V.; Korolkov, I.; Maravin, Y.; Narsky, I.; Shelkov, V.; Staeck, J.; Stroynowski, R.; Volobouev, I.; Ye, J.; Artuso, M.; Azfar, F.; Efimov, A.; Goldberg, M.; He, D.; Kopp, S.; Moneti, G.C.; Mountain, R.; Schuh, S.; Skwarnicki, T.

1999-01-01

We present new measurements of photon energies and branching fractions for the radiative transitions Υ(2S)→γχ b(J=0,1,2) (1P). The masses of the χ b states are determined from the measured radiative photon energies. The ratio of mass splittings between the χ b substates, r≡(M J=2 -M J=1 )/(M J=1 -M J=0 ), with M the χ b mass, provides information on the nature of the b bar b confining potential. We find r(1P)=0.542±0.022±0.024. This value is somewhat lower than the previous world average, but more consistent with the theoretical expectation that r(1P) b (1P) states than for the χ b (2P) states. copyright 1999 The American Physical Society

Split Active Asteroid P/2016 J1 (PANSTARRS)

Science.gov (United States)

Hui, Man-To; Jewitt, David; Du, Xinnan

2017-10-01

We present a photometric and astrometric study of the split active asteroid P/2016 J1 (PANSTARRS). Separation occurred either in 2012 May to June, or 2010 April, with a separation speed Vsep = 0.70 ± 0.02 m s-1 for the former scenario and 0.83 ± 0.06 m s-1 for the latter. The two fragments (hereafter J1-A and J1-B) have similar, Sun-like colors that are comparable to the colors of primitive C- and G-type asteroids. With a nominal comet-like albedo, pR = 0.04, the effective, dust-contaminated cross sections are estimated to be 2.4 km2 (J1-A) and 0.5 km2 (J1-B). We estimate that the nucleus radii lie in the range 140 times of 2016 J1 are both short compared to the age of the solar system, raising the question of why this object still exists. We suggest that formerly buried ice became exposed at the surface, perhaps via a minor impact, and that sublimation torques then rapidly drove the body to breakup. Further disintegration events are anticipated owing to the rotational instability. Reference: Hui, M.-T., Jewitt, D. and Du, X., 2017. AJ, 153(4), p.141.

The distinct role of strand-specific miR-514b-3p and miR-514b-5p in colorectal cancer metastasis.

Science.gov (United States)

Ren, Lin-Lin; Yan, Ting-Ting; Shen, Chao-Qin; Tang, Jia-Yin; Kong, Xuan; Wang, Ying-Chao; Chen, Jinxian; Liu, Qiang; He, Jie; Zhong, Ming; Chen, Hao-Yan; Hong, Jie; Fang, Jing-Yuan

2018-06-07

The abnormal expression of microRNAs (miRNAs) in colorectal cancer (CRC) progression has been widely investigated. It was reported that the same hairpin RNA structure could generate mature products from each strand, termed 5p and 3p, which binds different target mRNAs. Here, we explored the expression, functions, and mechanisms of miR-514b-3p and miR-514b-5p in CRC cells and tissues. We found that miR-514b-3p was significantly down-regulated in CRC samples, and the ratio of miR-514b-3p/miR-514b-5p increased from advanced CRC, early CRC to matched normal colorectal tissues. Follow-up functional experiments illustrated that miR-514b-3p and miR-514b-5p had distinct effects through interacting with different target genes: MiR-514b-3p reduced CRC cell migration, invasion and drug resistance through increasing epithelial marker and decreasing mesenchymal marker expressions, conversely, miR-514b-5p exerted its pro-metastatic properties in CRC by promoting EMT progression. MiR-514b-3p overexpressing CRC cells developed tumors more slowly in mice compared with control cells, however, miR-514b-5p accelerated tumor metastasis. Overall, our data indicated that though miR-514b-3p and miR-514b-5p were transcribed from the same RNA hairpin, each microRNA has distinct effect on CRC metastasis.

TUG1 promotes osteosarcoma tumorigenesis by upregulating EZH2 expression via miR-144-3p.

Science.gov (United States)

Cao, Jiaqing; Han, Xinyou; Qi, Xin; Jin, Xiangyun; Li, Xiaolin

2017-10-01

lncRNA-TUG1 (Taurine upregulated 1) is up-regulated and highly correlated with poor prognosis and disease status in osteosarcoma. TUG1 knockdown inhibits osteosarcoma cell proliferation, migration and invasion, and promotes apoptosis. However, its mechanism of action has not been well addressed. Growing evidence documented that lncRNA works as competing endogenous (ce)RNAs to modulate the expression and biological functions of miRNA. As a putative combining target of TUG1, miR-144-3p has been associated with the progress of osteosarcoma. To verify whether TUG1 functions through regulating miR-144-3p, the expression levels of TUG1 and miR-144-3p in osteosarcoma tissues and cell lines were determined. TUG1 was upregulated in osteosarcoma tissues and cell lines, and negatively correlated with miR-144-3p. TUG1 knockdown induced miR-144-3p expression in MG63 and U2OS cell lines. Results from dual luciferase reporter assay, RNA-binding protein immuno-precipitation (RIP) and applied biotin-avidin pull-down system confirmed TUG1 regulated miR-144-3p expression through direct binding. EZH2, a verified target of miR-144-3p was upregulated in osteosarcoma tissues and negatively correlated with miR-144-3p. EZH2 was negatively regulated by miR-144-3p and positively regulated by TUG1. Gain-and loss-of-function experiments were performed to analyze the role of TUG1, miR-144-3p and EZH2 in the migration and EMT of osteosarcoma cells. EZH2 over-expression partly abolished TUG1 knockdown or miR-144-3p overexpression induced inhibition of migration and EMT in osteosarcoma cells. In addition, TUG1 knockdown represses the activation of Wnt/β-catenin pathway, which was reversed by EZH2 over-expression. The activator of Wnt/β-catenin pathway LiCl could partially block the TUG1-knockdown induced osteosarcoma cell migration and EMT inhibition. In conclusion, our results showed that TUG1 plays an important role in osteosarcoma development through miRNA-144-3p/EZH2/Wnt/β-catenin pathway.

R-Ras regulates migration through an interaction with filamin A in melanoma cells.

Directory of Open Access Journals (Sweden)

Joanna E Gawecka

2010-06-01

Full Text Available Changes in cell adhesion and migration in the tumor microenvironment are key in the initiation and progression of metastasis. R-Ras is one of several small GTPases that regulate cell adhesion and migration on the extracellular matrix, however the mechanism has not been completely elucidated. Using a yeast two-hybrid approach we sought to identify novel R-Ras binding proteins that might mediate its effects on integrins.We identified Filamin A (FLNa as a candidate interacting protein. FLNa is an actin-binding scaffold protein that also binds to integrin beta1, beta2 and beta7 tails and is associated with diverse cell processes including cell migration. Indeed, M2 melanoma cells require FLNa for motility. We further show that R-Ras and FLNa interact in co-immunoprecipitations and pull-down assays. Deletion of FLNa repeat 3 (FLNaDelta3 abrogated this interaction. In M2 melanoma cells active R-Ras co-localized with FLNa but did not co-localize with FLNa lacking repeat 3. Thus, activated R-Ras binds repeat 3 of FLNa. The functional consequence of this interaction was that active R-Ras and FLNa coordinately increased cell migration. In contrast, co-expression of R-Ras and FLNaDelta3 had a significantly reduced effect on migration. While there was enhancement of integrin activation and fibronectin matrix assembly, cell adhesion was not altered. Finally, siRNA knockdown of endogenous R-Ras impaired FLNa-dependent fibronectin matrix assembly.These data support a model in which R-Ras functionally associates with FLNa and thereby regulates integrin-dependent migration. Thus in melanoma cells R-Ras and FLNa may cooperatively promote metastasis by enhancing cell migration.

Fibronectin induces macrophage migration through a SFK-FAK/CSF-1R pathway.

Science.gov (United States)

Digiacomo, Graziana; Tusa, Ignazia; Bacci, Marina; Cipolleschi, Maria Grazia; Dello Sbarba, Persio; Rovida, Elisabetta

2017-07-04

Integrins, following binding to proteins of the extracellular matrix (ECM) including collagen, laminin and fibronectin (FN), are able to transduce molecular signals inside the cells and to regulate several biological functions such as migration, proliferation and differentiation. Besides activation of adaptor molecules and kinases, integrins transactivate Receptor Tyrosine Kinases (RTK). In particular, adhesion to the ECM may promote RTK activation in the absence of growth factors. The Colony-Stimulating Factor-1 Receptor (CSF-1R) is a RTK that supports the survival, proliferation, and motility of monocytes/macrophages, which are essential components of innate immunity and cancer development. Macrophage interaction with FN is recognized as an important aspect of host defense and wound repair. The aim of the present study was to investigate on a possible cross-talk between FN-elicited signals and CSF-1R in macrophages. FN induced migration in BAC1.2F5 and J774 murine macrophage cell lines and in human primary macrophages. Adhesion to FN determined phosphorylation of the Focal Adhesion Kinase (FAK) and Src Family Kinases (SFK) and activation of the SFK/FAK complex, as witnessed by paxillin phosphorylation. SFK activity was necessary for FAK activation and macrophage migration. Moreover, FN-induced migration was dependent on FAK in either murine macrophage cell lines or human primary macrophages. FN also induced FAK-dependent/ligand-independent CSF-1R phosphorylation, as well as the interaction between CSF-1R and β1. CSF-1R activity was necessary for FN-induced macrophage migration. Indeed, genetic or pharmacological inhibition of CSF-1R prevented FN-induced macrophage migration. Our results identified a new SFK-FAK/CSF-1R signaling pathway that mediates FN-induced migration of macrophages.

Comparison of X-ray photoelectron spectroscopy multiplet splitting of Cr 2p peaks from chromium tris(β-diketonates) with chemical effects

Energy Technology Data Exchange (ETDEWEB)

Liu, R.; Conradie, J.; Erasmus, E., E-mail: erasmuse@ufs.ac.za

2016-01-15

Graphical abstract: Synopsis and pictogram for Table of contents The Cr 2p{sub 3/2} peaks obtained from X-ray photoelectron spectra (XPS) of a series of chromium(III) β-diketonato complexes were fitted with calculated multiplet peaks. The ratio of the fac and mer isomers obtained from XPS compared very well with the Boltzmann calculated ratio. The electronegativity of the R-groups on the β-diketonato ligand influences the XPS peak positions. - Highlights: • β-diketonato complexes Cr(RCOCHCOR’){sub 3} • Cr 2p{sub 3/2} XPS peaks fitted with calculated multiplet peaks. • Different calculated multiplet peaks fit the Cr 2p{sub 3/2} peak for fac and mer isomers. • XPS peak positions influenced by the electronegativity of the R- and R'-group. - Abstract: X-ray photoelectron spectra (XPS) measurements of a series of chromium(III) β-diketonato complexes of the Cr 2p spectra was fitted with calculated multiplet peaks. The XPS of these Cr(III) complexes did not exhibit fine structure, however, well-defined line shapes could be fitted to the Cr 2p{sub 3/2} envelope. The splitting patterns obtained for the Cr(III) β-diketonato complexes compared well with the multiplet splitting predicted by Gupta and Sen for the free Cr(III) ion. The Cr(III) β-diketonato complexes containing unsymmetrically substituted β-diketonato ligands, which display both the fac and mer isomers, could be fitted with two sets of multiplets and were useful in determining the ratio between the fac and mer isomers, which was compared with the Boltzman calculated ratio obtained from density functional theory energies. The obtained binding energy of the first multiplet splitting peak of the Cr 2p{sub 3/2} envelope was found to be dependent on the combined Gordy group electronegativity of the R-groups substituted on the β-diketonato ligand (RCOCHCOR′){sup −}.

Vitamin D attenuates sphingosine-1-phosphate (S1P)-mediated inhibition of extravillous trophoblast migration.

Science.gov (United States)

Westwood, Melissa; Al-Saghir, Khiria; Finn-Sell, Sarah; Tan, Cherlyn; Cowley, Elizabeth; Berneau, Stéphane; Adlam, Daman; Johnstone, Edward D

2017-12-01

Failure of trophoblast invasion and remodelling of maternal blood vessels leads to the pregnancy complication pre-eclampsia (PE). In other systems, the sphingolipid, sphingosine-1-phosphate (S1P), controls cell migration therefore this study determined its effect on extravillous trophoblast (EVT) function. A transwell migration system was used to assess the behaviour of three trophoblast cell lines, Swan-71, SGHPL-4, and JEG3, and primary human trophoblasts in the presence or absence of S1P, S1P pathway inhibitors and 1,25(OH) 2 D 3 . QPCR and immunolocalisation were used to demonstrate EVT S1P receptor expression. EVTs express S1P receptors 1, 2 and 3. S1P inhibited EVT migration. This effect was abolished in the presence of the specific S1PR2 inhibitor, JTE-013 (p S1P alone) whereas treatment with the S1R1/3 inhibitor, FTY720, had no effect. In other cell types S1PR2 is regulated by vitamin D; here we found that treatment with 1,25(OH) 2 D 3 for 48 or 72 h reduces S1PR2 (4-fold; S1P did not inhibit the migration of cells exposed to 1,25(OH) 2 D 3 (p S1P receptor isoforms, S1P predominantly signals through S1PR2/Gα 12/13 to activate Rho and thereby acts as potent inhibitor of EVT migration. Importantly, expression of S1PR2, and therefore S1P function, can be down-regulated by vitamin D. Our data suggest that vitamin D deficiency, which is known to be associated with PE, may contribute to the impaired trophoblast migration that underlies this condition. Copyright © 2017 Elsevier Ltd. All rights reserved.

Split Active Asteroid P/2016 J1 (PANSTARRS)

Energy Technology Data Exchange (ETDEWEB)

Hui, Man-To; Jewitt, David [Department of Earth, Planetary, and Space Sciences, UCLA, 595 Charles Young Drive East, Box 951567, Los Angeles, CA 90095-1567 (United States); Du, Xinnan, E-mail: pachacoti@ucla.edu [Department of Physics and Astronomy, UCLA, 430 Portola Plaza, Box 951547, Los Angeles, CA 90095-1547 (United States)

2017-04-01

We present a photometric and astrometric study of the split active asteroid P/2016 J1 (PANSTARRS). The two components (hereafter J1-A and J1-B) separated either ∼1500 days (2012 May to June) or 2300 days (2010 April) prior to the current epoch, with a separation speed V {sub sep} = 0.70 ± 0.02 m s{sup −1} for the former scenario and 0.83 ± 0.06 m s{sup −1} for the latter. Keck photometry reveals that the two fragments have similar, Sun-like colors that are comparable to the colors of primitive C- and G-type asteroids. With a nominal comet-like albedo, p{sub R} = 0.04, the effective, dust-contaminated cross sections are estimated to be 2.4 km{sup 2} for J1-A and 0.5 km{sup 2} for J1-B. We estimate that the nucleus radii lie in the range 140 ≲  R {sub N} ≲ 900 m for J1-A and 40 ≲  R {sub N} ≲ 400 m for J1-B. A syndyne–synchrone simulation shows that both components have been active for 3–6 months, by ejecting dust grains at speeds ∼0.5 m s{sup −1} with rates ∼1 kg s{sup −1} for J1-A and 0.1 kg s{sup −1} for J1-B. In its present orbit, the rotational spin-up and devolatilization times of 2016 J1 are very small compared to the age of the solar system, raising the question of why this object still exists. We suggest that ice that was formerly buried within this asteroid became exposed at the surface, perhaps via a small impact, and that sublimation torques then rapidly drove it to breakup. Further disintegration events are anticipated owing to the rotational instability.

MiR-1254 inhibits proliferation, migration and invasion of human ...

African Journals Online (AJOL)

Thus, miR-1254 has promising potential for use in the treatment of brain tumour. Keywords: Brain tumour, Astrocytoma, miR-1254, Apoptosis, Cell migration ... colorectal cancer, adenocarcinoma carcinoma and lung cancer [6]. However, the expression profile of miR-1254 in brain tumour has not been investigated.

Overexpression of long intergenic noncoding RNA LINC00312 inhibits the invasion and migration of thyroid cancer cells by down-regulating microRNA-197-3p.

Science.gov (United States)

Liu, Kai; Huang, Wen; Yan, Dan-Qing; Luo, Qing; Min, Xiang

2017-08-31

The study evaluated the ability of long intergenic noncoding RNA LINC00312 (LINC00312) to influence the proliferation, invasion, and migration of thyroid cancer (TC) cells by regulating miRNA-197-3p. TC tissues and adjacent normal tissues were collected from 211 TC patients. K1 (papillary TC), SW579 (squamous TC), and 8505C (anaplastic TC) cell lines were assigned into a blank, negative control (NC), LINC00312 overexpression, miR-197-3p inhibitors, and LINC00312 overexpression + miR-197-3p mimics group. The expression of LINC00312, miR-197-3p , and p120 were measured using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed via CCK8 assay, cell invasion through the scratch test, and cell migration via Transwell assay. In comparison with adjacent normal tissues, the expression of LINC00312 is down-regulated and the expression of miR-197-3p is up-regulated in TC tissues. The dual luciferase reporter gene assay confirmed that P120 is a target of miR-197-3p The expression of LINC00312 and p120 was higher in the LINC00312 overexpression group than in the blank and NV groups. However, the expression of miR-197-3p was lower in the LINC00312 overexpression group than in the blank and NC groups. The miR-197-3p inhibitors group had a higher expression of miR-197-3p , but a lower expression of p120 than the blank and NC groups. The LINC00312 overexpression and miR-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and NC groups. These results indicate that a LINC00312 overexpression inhibits the proliferation, invasion, and migration of TC cells and that this can be achieved by down-regulating miR-197-3p . © 2017 The Author(s).

Mir-22-3p Inhibits Arterial Smooth Muscle Cell Proliferation and Migration and Neointimal Hyperplasia by Targeting HMGB1 in Arteriosclerosis Obliterans

Directory of Open Access Journals (Sweden)

Shui-chuan Huang

2017-08-01

Full Text Available Background: Aberrant vascular smooth muscle cell (VSMC proliferation and migration contribute to the development of vascular pathologies, such as atherosclerosis and post-angioplasty restenosis. The aim of this study was to determine whether miR-22-3p plays a role in regulating human artery vascular smooth muscle cell (HASMC function and neointima formation. Methods: Quantitative real-time PCR (qRT-PCR and fluorescence in situ hybridization (FISH were used to detect miR-22-3p expression in human arteries. Cell Counting Kit-8 (CCK-8 and EdU assays were performed to assess cell proliferation, and transwell and wound closure assays were performed to assess cell migration. Moreover, luciferase reporter assays were performed to identify the target genes of miR-22-3p. Finally, a rat carotid artery balloon-injury model was used to determine the role of miR-22-3p in neointima formation. Results: MiR-22-3p expression was downregulated in arteriosclerosis obliterans (ASO arteries compared with normal arteries, as well as in platelet-derived growth factor-BB (PDGF-BB-stimulated HASMCs compared with control cells. MiR-22-3p overexpression had anti-proliferative and anti-migratory effects and dual-luciferase assay showed that high mobility group box-1 (HMGB1 is a direct target of miR-22-3p in HASMCs. Furthermore, miR-22-3p expression was negatively correlated with HMGB1 expression in ASO tissue specimens. Finally, LV-miR-22-3p-mediated miR-22-3p upregulation significantly suppressed neointimal hyperplasia specifically by reducing HMGB1 expression in vivo. Conclusions: Our results indicate that miR-22-3p is a key molecule in regulating HASMC proliferation and migration by targeting HMGB1 and that miR-22-3p and HMGB1 may be therapeutic targets in the treatment of human ASO.

MiR-1254 inhibits proliferation, migration and invasion of human ...

African Journals Online (AJOL)

MiR-1254 inhibits proliferation, migration and invasion of human brain tumour cell lines. ... The transcripts were analysed by real-time polymerase chain reaction (RT-PCR) ... Over-expression of miR- 1254 also led to significant decrease in cell ...

Expression of MiR-9 promotes proliferation, migration and ...

African Journals Online (AJOL)

Purpose: To investigate the effect of miR-9 on the proliferation, differentiation and migration of human neural stem cells (NSCs). Methods: The expression of miR-9 was investigated by quantitative real-time polymerase chain reaction (RT-PCR). Cell proliferation was assessed by cell counting kit-8 (CCK8) assay, while cell ...

Migration og etnicitet

DEFF Research Database (Denmark)

Christiansen, Connie Carøe

2004-01-01

Migration og etnicitet er aktuelle og forbundne fænomener, idet migration øger berøringsfladerne mellem befolkningsgrupper. Etniciteter formes i takt med at grænser drages imellem disse grupper. Imod moderniserings-teoriernes forventning forsvandt etnicitet ikke som en traditionel eller oprindelig...... måde at skabe tilhørsforhold på; globalt set fremstår vor tid istedet som en "migrationens tidsalder", der tilsyneladende også er en tidsalder, hvor kulturelle særtræk, i form af etnicitet, udgør vigtige linjer, hvorefter grupper skilller sig ud fra hinanden. Både migration og etnicitet bringer fokus...... den finder sted i modtagerlandet, men nyere perspektiver på migration, som begreber om medborgerskab, transnationalisme og diaspora er eksponenter for, søger udover den nationalstatslige ramme og inddrager konsekvenserne af migrationen for afsenderlande....

Diagnostic and prognostic potential of serum miR-7, miR-16, miR-25, miR-93, miR-182, miR-376a and miR-429 in ovarian cancer patients.

Science.gov (United States)

Meng, Xiaodan; Joosse, Simon A; Müller, Volkmar; Trillsch, Fabian; Milde-Langosch, Karin; Mahner, Sven; Geffken, Maria; Pantel, Klaus; Schwarzenbach, Heidi

2015-11-03

Owing to late diagnosis in advanced disease stages, prognosis of patients with epithelial ovarian cancer (EOC) is poor. The quantification of deregulated levels of microRNAs could facilitate earlier diagnosis and improve prognosis of EOC. Seven microRNAs (miR-7, miR-16, miR-25, miR-93, miR-182, miR-376a and miR-429) were quantified in the serum of 180 EOC patients and 66 healthy women by TaqMan PCR microRNA assays. Median follow-up time was 21 months. The effects of miR-7 and miR-429 on apoptosis, cell proliferation, migration and invasion were investigated in two (EOC) cell lines. Serum levels of miR-25 (P=0.0001) and miR-93 (P=0.0001) were downregulated, whereas those of miR-7 (P=0.001) and miR-429 (P=0.0001) were upregulated in EOC patients compared with healthy women. The four microRNAs discriminated EOC patients from healthy women with a sensitivity of 93% and a specificity of 92%. The levels of miR-429 positively correlated with CA125 values (P=0.0001) and differed between FIGO I-II and III-IV stages (P=0.001). MiR-429 was an independent predictor of overall survival (P=0.011). Overexpressed miR-429 in SKOV3 cells led to suppression of cell migration (P=0.037) and invasion (P=0.011). Increased levels of miR-7 were associated with lymph node metastases (P=0.0001) and FIGO stages III-IV (P=0.0001). Overexpressed miR-7 in SKOV3 cells resulted in increased cell migration (P=0.001) and invasion (P=0.011). Additionally, the increased levels of miR-376a correlated with FIGO stages III-IV (P=0.02). Our data indicate the diagnostic potential of miR-7, miR-25, miR-93 and miR-429 in EOC and the prognostic potential of miR-429. This microRNA panel may be promising molecules to be targeted in the treatment of EOC.

MiR-138 promotes smooth muscle cells proliferation and migration in db/db mice through down-regulation of SIRT1

Energy Technology Data Exchange (ETDEWEB)

Xu, Juan [Department of Gynecology, Changzhou Maternity and Children Health Hospital, Changzhou, Jiangsu 213003 (China); Li, Li; Yun, Hui-fang [Department of Anesthesiology, Changzhou No. 2 People' s Hospital, Changzhou, Jiangsu 213003 (China); Han, Ye-shan, E-mail: yeshanhan123@163.com [Department of Anesthesiology, Changzhou No. 2 People' s Hospital, Changzhou, Jiangsu 213003 (China)

2015-08-07

Background: Diabetic vascular smooth muscle cells (VSMCs) exhibit significantly increased rates of proliferation and migration, which was the most common pathological change in atherosclerosis. In addition, the study about the role for miRNAs in the regulation of VSMC proliferation is just beginning to emerge and additional miRNAs involved in VSMC proliferation modulation should be identified. Methods: The expression of miR-138 and SIRT1 were examined in SMCs separated from db/db mice and in SMC lines C-12511 exposed to high glucose with qRT-PCR and western blot. The regulation of miR-138 on the expression of SMCs was detected with luciferase report assay. VSMCs proliferation and migration assays were performed to examine the effect of miR-138 inhibitor on VSMCs proliferation and migration. Results: We discovered that higher mRNA level of miR-138 and reduced expression of SIRT1 were observed in SMCs separated from db/db mice and in SMC lines C-12511. Moreover, luciferase report assay showed that the activity of SIRT1 3′-UTR was highly increased by miR-138 inhibitor and reduced by miR-138 mimic. In addition, we examined that the up-regulation of NF-κB induced by high glucose in SMCs was reversed by resveratrol and miR-138 inhibitor. MTT and migration assays showed that miR-138 inhibitor attenuated the proliferation and migration of smooth muscle cells. Conclusion: In this study, we revealed that miR-138 might promote proliferation and migration of SMC in db/db mice through suppressing the expression of SIRT1. - Highlights: • Higher mRNA level of miR-138 was observed in SMCs from db/db mice. • The mRNA and protein level of SIRT1 in SMCs from db/db mice were greatly reduced. • miR-138 could regulate the expression of SIRT1 in SMCs. • SIRT1 overexpression reversed the up-regulation of acetylized p65 and NF-κB induced by high glucose. • MiR-138 inhibitor reversed VSMCs proliferation and migration induced by high glucose.

Religion, migration og integration

DEFF Research Database (Denmark)

Borup, Jørn

2010-01-01

Sammenhængen mellem religion og integration har de sidste år været genstand for debat. Artiklen kommer ind på begreber og sammenhænge relateret til området (migration, diaspora, assimilation, etnicitet, kultur) og ser på religionens mulige rolle som negativ eller positiv ressource i integrationss......Sammenhængen mellem religion og integration har de sidste år været genstand for debat. Artiklen kommer ind på begreber og sammenhænge relateret til området (migration, diaspora, assimilation, etnicitet, kultur) og ser på religionens mulige rolle som negativ eller positiv ressource i...

Plasma-Assisted Synthesis of NiCoP for Efficient Overall Water Splitting

KAUST Repository

Liang, Hanfeng

2016-11-09

Efficient water splitting requires highly active, earth-abundant, and robust catalysts. Monometallic phosphides such as NiP have been shown to be active toward water splitting. Our theoretical analysis has suggested that their performance can be further enhanced by substitution with extrinsic metals, though very little work has been conducted in this area. Here we present for the first time a novel PH plasma-assisted approach to convert NiCo hydroxides into ternary NiCoP. The obtained NiCoP nanostructure supported on Ni foam shows superior catalytic activity toward the hydrogen evolution reaction (HER) with a low overpotential of 32 mV at 10 mA cm in alkaline media. Moreover, it is also capable of catalyzing the oxygen evolution reaction (OER) with high efficiency though the real active sites are surface oxides in situ formed during the catalysis. Specifically, a current density of 10 mA cm is achieved at overpotential of 280 mV. These overpotentials are among the best reported values for non-noble metal catalysts. Most importantly, when used as both the cathode and anode for overall water splitting, a current density of 10 mA cm is achieved at a cell voltage as low as 1.58 V, making NiCoP among the most efficient earth-abundant catalysts for water splitting. Moreover, our new synthetic approach can serve as a versatile route to synthesize various bimetallic or even more complex phosphides for various applications.

Sinomenine inhibits breast cancer cell invasion and migration by suppressing NF-κB activation mediated by IL-4/miR-324-5p/CUEDC2 axis

Energy Technology Data Exchange (ETDEWEB)

Song, Lingqin, E-mail: qinlingsongxa@163.com [Department of Oncology, The Second Affiliated Hospital, Medical School of Xi' an Jiaotong University, Xi' an 710004 (China); Liu, Di; Zhao, Yang [Department of Oncology, The Second Affiliated Hospital, Medical School of Xi' an Jiaotong University, Xi' an 710004 (China); He, Jianjun [Department of Surgical Oncology, The First Affiliated Hospital, Medical School of Xi' an Jiaotong University, Xi' an 710061 (China); Kang, Huafeng; Dai, Zhijun; Wang, Xijing; Zhang, Shuqun; Zan, Ying [Department of Oncology, The Second Affiliated Hospital, Medical School of Xi' an Jiaotong University, Xi' an 710004 (China)

2015-08-28

Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a vital transcription factor that regulates multiple important biological processes, including the epithelial–mesenchymal transition (EMT) and metastasis of breast cancer. Sinomenine is an isoquinoline well known for its remarkable curative effect on rheumatic and arthritic diseases and can induce apoptosis of several cancer cell types. Recently, sinomenine was reported as a tumor suppressor via inhibiting cell proliferation and inducing apoptosis. However, the role and mechanism of sinomenine in invasion and metastasis of breast cancer are largely unknown. Here, we report that sinomenine suppressed the invasion and migration of MDA-MB-231 and 4T1 breast cancer cells in a dose-dependent manner. We detected binding of NF-κB to the inhibitor of NF-κB (IκB) after the MDA-MB-231 cells were treated with 0.25, 0.5, and 1 mM sinomenine. Co-IP analysis revealed that sinomenine enhanced the binding of NF-κB and IκB in a dose-dependent manner, suggesting that sinomenine had an effect on inactivation of NF-κB. Western blotting and ELISA approaches indicated that the suppression effect was closely associated with the phosphorylation of IκB kinase (IKK) and its negative regulator CUEDC2. Sinomenine treatment decreased miR-324-5p expression, thus increased the level of its target gene CUEDC2, and then blocked the phosphorylation of IKK through altering the upstream axis. Finally, transfection of a miR-324-5p mimic inhibited the suppression of invasion and metastasis of MDA-MB-231 and 4T1 cell by sinomenine, providing evidence that sinomenine treatment suppressed breast cancer cell invasion and metastasis via regulation of the IL4/miR-324-5p/CUEDC2 axis. Our findings reveal a novel mechanism by which sinomenine suppresses cancer cell invasion and metastasis, i.e., blocking NF-κB activation. - Highlights: • Sinomenine reduced invasion and migration of MDA-MB-231 and 4T1 breast cancer cells. �

Sinomenine inhibits breast cancer cell invasion and migration by suppressing NF-κB activation mediated by IL-4/miR-324-5p/CUEDC2 axis

International Nuclear Information System (INIS)

Song, Lingqin; Liu, Di; Zhao, Yang; He, Jianjun; Kang, Huafeng; Dai, Zhijun; Wang, Xijing; Zhang, Shuqun; Zan, Ying

2015-01-01

Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a vital transcription factor that regulates multiple important biological processes, including the epithelial–mesenchymal transition (EMT) and metastasis of breast cancer. Sinomenine is an isoquinoline well known for its remarkable curative effect on rheumatic and arthritic diseases and can induce apoptosis of several cancer cell types. Recently, sinomenine was reported as a tumor suppressor via inhibiting cell proliferation and inducing apoptosis. However, the role and mechanism of sinomenine in invasion and metastasis of breast cancer are largely unknown. Here, we report that sinomenine suppressed the invasion and migration of MDA-MB-231 and 4T1 breast cancer cells in a dose-dependent manner. We detected binding of NF-κB to the inhibitor of NF-κB (IκB) after the MDA-MB-231 cells were treated with 0.25, 0.5, and 1 mM sinomenine. Co-IP analysis revealed that sinomenine enhanced the binding of NF-κB and IκB in a dose-dependent manner, suggesting that sinomenine had an effect on inactivation of NF-κB. Western blotting and ELISA approaches indicated that the suppression effect was closely associated with the phosphorylation of IκB kinase (IKK) and its negative regulator CUEDC2. Sinomenine treatment decreased miR-324-5p expression, thus increased the level of its target gene CUEDC2, and then blocked the phosphorylation of IKK through altering the upstream axis. Finally, transfection of a miR-324-5p mimic inhibited the suppression of invasion and metastasis of MDA-MB-231 and 4T1 cell by sinomenine, providing evidence that sinomenine treatment suppressed breast cancer cell invasion and metastasis via regulation of the IL4/miR-324-5p/CUEDC2 axis. Our findings reveal a novel mechanism by which sinomenine suppresses cancer cell invasion and metastasis, i.e., blocking NF-κB activation. - Highlights: • Sinomenine reduced invasion and migration of MDA-MB-231 and 4T1 breast cancer cells. �

miR-411-5p inhibits proliferation and metastasis of breast cancer cell via targeting GRB2

International Nuclear Information System (INIS)

Zhang, Yunda; Xu, Guoxing; Liu, Gang; Ye, Yongzhi; Zhang, Chuankai; Fan, Chuannan; Wang, Haibin; Cai, Huali; Xiao, Rui; Huang, Zhengjie; Luo, Qi

2016-01-01

miR-411-5p (previously called miR-411) is severely involved in human diseases, however, the relationship between miR-411-5p and breast cancer has not been investigated thoroughly. Here, we found that the expression of miR-411-5p was downregulated in breast cancer tissues compared with their matched adjacent non-neoplastic tissues. In addition, the expression of miR-411-5p was also lower in breast cancer cell lines in contrast with MCF-10A. Moreover, we investigated the target and mechanism of miR-411-5p in breast cancer using mimic and inhibitor, and demonstrated the involvement of GRB2 and Ras activation. Ectopic expression of miR-411-5p suppressed the breast cancer cell proliferation, migration and invasion while low expression of miR-411-5p exhibited the opposite effect. Furthermore, GRB2 was demonstrated to be significantly overexpressed in breast cancer tissues compared with normal tissues, and low expression of GRB2 had a longer overall survival compared with high expression of GRB2 in breast cancer. In general, our study shed light on the miR-411-5p related mechanism in the progression of breast cancer and, miR-411-5p/GRB2/Ras axis is potential to be molecular target for breast cancer therapy. - Highlights: • miR-411-5p is downregulated in breast cancer tissues and cell lines. • miR-411-5p inhibits breast cancer cells growth, migration and invasion in vitro. • GRB2 is a direct target of miR-411-5p in breast cancer. • GRB2 is overexpressed in breast cancer and associates with disease outcome. • miR-411-5p suppresses breast cancer progression though GRB2-SOS-Ras pathway.

miR-411-5p inhibits proliferation and metastasis of breast cancer cell via targeting GRB2

Energy Technology Data Exchange (ETDEWEB)

Zhang, Yunda [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361102 (China); Xu, Guoxing [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005 (China); Liu, Gang; Ye, Yongzhi [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); Zhang, Chuankai [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361102 (China); Fan, Chuannan [State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361102 (China); Wang, Haibin; Cai, Huali; Xiao, Rui [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005 (China); Huang, Zhengjie, E-mail: huangzhengjie@xmu.edu.cn [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005 (China); Luo, Qi, E-mail: luoqixmzsh@126.com [Department of Gastrointestinal Surgery, First Affiliated Hospital of Xiamen University, Xiamen 361003 (China); Department of Gastrointestinal Surgery, First Clinical Medical College of Fujian Medical University, Fuzhou 350005 (China)

2016-08-05

miR-411-5p (previously called miR-411) is severely involved in human diseases, however, the relationship between miR-411-5p and breast cancer has not been investigated thoroughly. Here, we found that the expression of miR-411-5p was downregulated in breast cancer tissues compared with their matched adjacent non-neoplastic tissues. In addition, the expression of miR-411-5p was also lower in breast cancer cell lines in contrast with MCF-10A. Moreover, we investigated the target and mechanism of miR-411-5p in breast cancer using mimic and inhibitor, and demonstrated the involvement of GRB2 and Ras activation. Ectopic expression of miR-411-5p suppressed the breast cancer cell proliferation, migration and invasion while low expression of miR-411-5p exhibited the opposite effect. Furthermore, GRB2 was demonstrated to be significantly overexpressed in breast cancer tissues compared with normal tissues, and low expression of GRB2 had a longer overall survival compared with high expression of GRB2 in breast cancer. In general, our study shed light on the miR-411-5p related mechanism in the progression of breast cancer and, miR-411-5p/GRB2/Ras axis is potential to be molecular target for breast cancer therapy. - Highlights: • miR-411-5p is downregulated in breast cancer tissues and cell lines. • miR-411-5p inhibits breast cancer cells growth, migration and invasion in vitro. • GRB2 is a direct target of miR-411-5p in breast cancer. • GRB2 is overexpressed in breast cancer and associates with disease outcome. • miR-411-5p suppresses breast cancer progression though GRB2-SOS-Ras pathway.

MiR-223 targeting MAFB suppresses proliferation and migration of nasopharyngeal carcinoma cells

International Nuclear Information System (INIS)

Yang, Wanyong; Lan, Xi; Li, Dongmin; Li, Tao; Lu, Shemin

2015-01-01

Mounting evidence suggests that miRNAs have major functions in tumor pathogenesis, and this study aimed to identify the candidate miRNA and investigate its role in nasopharyngeal carcinoma (NPC). MiRNA and mRNA expressions were screened by microarray assays. The cell proliferation, colony formation and migration ability were measured by MTT, soft agar and wound healing assays, respectively. The tumor growth suppression was evaluated by xenografting in nude mice. The plasma miR-223 levels in NPC patients were detected by TaqMan analysis. Real-time quantitative PCR and Western blotting were used to confirm miR-223 and MAFB expression levels. The targeting relationship between miR-223 and MAFB was verified using dual luciferase reporter assay. The miR-223 expression was decreased in CNE-1, CNE-2 cells as compared with NP69 cells, an immortalized human nasopharyngeal epithelial cell line, and its level also reduced in NPC patients’ plasma as compared with healthy controls. Exogenous expression of miR-223 in CNE-2 cells could inhibit cell proliferation both in vitro and in vivo. Extrogenous miR-223 in CNE-2 cells would decrease the ability of colony formation and migration. MAFB, a transcription factor of Maf family members, was identified as a target gene of miR-223. We found that migration and invasion abilities were inhibited by MAFB silencing. MiR-223 negatively regulates the growth and migration of NPC cells via reducing MAFB expression, and this finding provides a novel insight into understanding miR-223 regulation mechanism in nasopharyngeal carcinoma tumorigenesis

Spin-splitting in p-type Ge devices

Energy Technology Data Exchange (ETDEWEB)

Holmes, S. N., E-mail: s.holmes@crl.toshiba.co.uk; Newton, P. J.; Llandro, J.; Mansell, R.; Barnes, C. H. W. [Cavendish Laboratory, Department of Physics, University of Cambridge, J. J. Thomson Avenue, Cambridge CB3 0HE (United Kingdom); Morrison, C.; Myronov, M. [Department of Physics, University of Warwick, Coventry CV4 7AL (United Kingdom)

2016-08-28

Compressively strained Ge quantum well devices have a spin-splitting in applied magnetic field that is entirely consistent with a Zeeman effect in the heavy hole valence band. The spin orientation is determined by the biaxial strain in the quantum well with the relaxed SiGe buffer layers and is quantized in the growth direction perpendicular to the conducting channel. The measured spin-splitting in the resistivity ρ{sub xx} agrees with the predictions of the Zeeman Hamiltonian where the Shubnikov-deHaas effect exhibits a loss of even filling factor minima in the resistivity ρ{sub xx} with hole depletion from a gate field, increasing disorder or increasing temperature. There is no measurable Rashba spin-orbit coupling irrespective of the structural inversion asymmetry of the confining potential in low p-doped or undoped Ge quantum wells from a density of 6 × 10{sup 10} cm{sup −2} in depletion mode to 1.7 × 10{sup 11} cm{sup −2} in enhancement.

En fornemmelse for migration

DEFF Research Database (Denmark)

Schütze, Laura Maria

Afhandlingen undersøger, hvordan sted, museets rolle som aktør og religion er relevante for produktionen af migration på Immigrantmuseet (2012) og i Københavns Museums udstilling At blive københavner (2010). Afhandlingen er baseret på udstillingsanalyse samt interview med relevant museumsfagligt......, anvendes som virkemidler til at nuancere migration og distancere udstillingen fra den offentlige debat om indvandring. Afhandlingen peger på, at produktionen af den nyere danske historie på museum er præget af et fravær af religion. Det skyldes, at de museumsfaglige praksisser og traditioner afspejler en...... identiteter, som vi tager for givet: nationer, byer, kvinder - såvel som migration og religion. Afhandlingen argumenterer følgelig for, at museernes produktion af (materiel) religion er et særdeles relevant, men kun ringe udforsket, genstandsfelt for religionssociologien....

MiR-129-5p Inhibits Proliferation and Invasion of Chondrosarcoma Cells by Regulating SOX4/Wnt/β-Catenin Signaling Pathway.

Science.gov (United States)

Zhang, Peng; Li, Jifeng; Song, Yuze; Wang, Xiao

2017-01-01

Recently, microRNAs (miRNA) have been identified as novel regulators in Chondrosarcoma (CHS). This study was aimed to identify the roles of miR-129-5p-5p in regulation of SOX4 and Wnt/β-catenin signaling pathway, as well as cell proliferation and apoptosis in chondrosarcomas. Tissue samples were obtained from chondrosarcoma patients. Immunohistochemistry, real-time quantitative RT-PCR (RT-qPCR) and western blot analysis were performed to detect the expressions of miR-129-5p and SOX4. Luciferase assay was conducted to confirm that miR-129-5p directly targeted SOX4 mRNA. Manipulations of miR-129-5p and SOX4 expression were achieved through cell transfection. Cell proliferation, migration and apoptosis were evaluated by CCK-8 assay, colony forming assay, wound healing assay and flow cytometry in vitro. For in vivo experiment, the tumor xenograft model was established to evaluate the effects of miR-129-5p and SOX4 on chondrosarcomas. The expression of miR-129-5p was significantly down-regulated in chondrosarcoma tissues as well as cells in comparison with normal ones, while SOX4 was over-activated. Further studies suggested that miR-129-5p suppressed cell proliferation, migration and promoted apoptosis by inhibiting SOX4 and Wnt/β-catenin pathway. MiR-129-5p inhibits the Wnt/β-catenin signaling pathway by targeting SOX4 and further suppresses cell proliferation, migration and promotes apoptosis in chondrosarcomas. © 2017 The Author(s). Published by S. Karger AG, Basel.

The experimental investigation of refrigerant distribution and leaking characteristics of R290 in split type household air conditioner

International Nuclear Information System (INIS)

Tang, Weier; He, Guogeng; Cai, Dehua; Zhu, Yihao; Zhang, Aoni; Tian, Qiqi

2017-01-01

Highlights: • A new quasi-liquid nitrogen method (QLNM) was proposed and firstly applied in experiments. • The R290 distribution was investigated by QLNM and the results proved the validation. • A solenoid valve was proposed to install near the capillary in STHAC in order to reduce risk factor. • R290 leaking rate was firstly measured by QLNM before and after the installation a solenoid valve. - Abstract: As a high-profile replacement for R22 split type household air conditioner (STHAC), R290 has several advantages in terms of thermodynamic properties, environmental characteristics, and cost. However, the obvious shortcoming of R290 is its flammability, which has a potential fire risk to the building. At present, the most important measure to ensure the safety of a R290 STHAC is to limit the refrigerant charge by domestic and international standards. But in fact, when the leakage of R290 occur from a STHAC, the distribution of R290 in STHAC, and the leaking rate also will seriously affect the safety of an R290 STHAC. In this study, a new quasi-liquid nitrogen method (QLNM) has been proposed in order to investigate the refrigerant distribution in R290 STHACs and the leaking rate under various conditions, and the experiments have been conducted. The experimental results of distribution proved the validation of the QLNM and showed that a large portion of the refrigerant distributed in the condenser when the air conditioner is on running stage and the refrigerant will migrate from the condenser to the evaporator when the air conditioner is on closed stage. Based on this, the installation of a solenoid valve near the capillary has been proposed. The comparison of experimental results of R290 leaking rate before and after the installation of a solenoid valve showed it will obviously reduce the leaking rate and thereby improve the safety of the R290 STHACs.

miR-196a targets netrin 4 and regulates cell proliferation and migration of cervical cancer cells

International Nuclear Information System (INIS)

Zhang, Jie; Zheng, Fangxia; Yu, Gang; Yin, Yanhua; Lu, Qingyang

2013-01-01

Highlights: •miR-196a was overexpressed in cervical cancer tissue compared to normal tissue. •miR-196a expression elevated proliferation and migration of cervical cancer cells. •miR-196a inhibited NTN4 expression by binding 3′-UTR region of NTN4 mRNA. •NTN4 inversely correlated with miR-196a expression in cervical tissue and cell line. •NTN4 expression was low in cervical cancer tissue compared to normal tissue. -- Abstract: Recent research has uncovered tumor-suppressive and oncogenic potential of miR-196a in various tumors. However, the expression and mechanism of its function in cervical cancer remains unclear. In this study, we assess relative expression of miR-196a in cervical premalignant lesions, cervical cancer tissues, and four cancer cell lines using quantitative real-time PCR. CaSki and HeLa cells were treated with miR-196a inhibitors, mimics, or pCDNA/miR-196a to investigate the role of miR-196a in cancer cell proliferation and migration. We demonstrated that miR-196a was overexpressed in cervical intraepithelial neoplasia 2–3 and cervical cancer tissue. Moreover, its expression contributes to the proliferation and migration of cervical cancer cells, whereas inhibiting its expression led to a reduction in proliferation and migration. Five candidate targets of miR-196a chosen by computational prediction and Cervical Cancer Gene Database search were measured for their mRNA in both miR-196a-overexpressing and -depleted cancer cells. Only netrin 4 (NTN4) expression displayed an inverse association with miR-196a. Fluorescent reporter assays revealed that miR-196a inhibited NTN4 expression by targeting one binding site in the 3′-untranslated region (3′-UTR) of NTN4 mRNA. Furthermore, qPCR and Western blot assays verified NTN4 expression was downregulated in cervical cancer tissues compared to normal controls, and in vivo mRNA level of NTN4 inversely correlated with miR-196a expression. In summary, our findings provide new insights about the

MiR-200a enhances the migrations of A549 and SK-MES-1 cells by ...

Indian Academy of Sciences (India)

By a series of gain-of-function and loss-offunction studies, over-expression of miR-200a was indicated to enhance cells migration, and its knock-down inhibited migration of cells in NSCLC cell lines. Furthermore, miR-200a was identified to induce TSPAN1 expression which was related to migration. TSPAN1 was proved to ...

Loss of expression of miR-335 is implicated in hepatic stellate cell migration and activation

International Nuclear Information System (INIS)

Chen, Chao; Wu, Chao-Qun; Zhang, Zong-Qi; Yao, Ding-Kang; Zhu, Liang

2011-01-01

Activation and migration of resident stellate cells (HSCs) within the hepatic space of Disse play an important role in hepatic fibrosis, which accounts for the increased numbers of activated HSCs in areas of inflammation during hepatic fibrosis. Currently, microRNAs have been found to play essential roles in HSC differentiation, proliferation, apoptosis, fat accumulation and collagen production. However, little is known about microRNA mediated HSC activation and migration. In this study, the miRNA expression profiles of quiescent HSCs, partially activated HSCs and fully activated HSCs were compared in pairs. Gene ontology (GO) and GO-Map network analysis indicated that the activation of HSCs was regulated by microRNAs. Among them miR-335 was confirmed to be significantly reduced during HSC activation by qRT-PCR, and restoring expression of miR-335 inhibited HSC migration and reduced α-SMA and collagen type I. Previous study revealed that tenascin-C (TNC), an extracellular matrix glycoprotein involved in cell migration, might be a target of miR-335. Therefore, we further studied the TNC expression in miR-335 over-expressed HSCs. Our data showed that exogenous TNC could enhance HSC migration in vitro and miR-335 restoration resulted in a significant inhibition of TNC expression. These results demonstrated that miR-335 restoration inhibited HSC migration, at least in part, via downregulating the TNC expression.

Loss of expression of miR-335 is implicated in hepatic stellate cell migration and activation

Energy Technology Data Exchange (ETDEWEB)

Chen, Chao [Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, No.415 Fengyang Road, Shanghai 200003 (China); Wu, Chao-Qun [Genetics Institute, Fudan University, No. 220 Handan Road, Shanghai 200433 (China); Zhang, Zong-Qi [Department of Cardiology, No. 3 Hospital, Shanghai Jiao Tong University Medical school, No.280 Mohe Road, Shanghai 201900 (China); Yao, Ding-Kang; Zhu, Liang, E-mail: 15900611429@163.com [Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, No.415 Fengyang Road, Shanghai 200003 (China)

2011-07-15

Activation and migration of resident stellate cells (HSCs) within the hepatic space of Disse play an important role in hepatic fibrosis, which accounts for the increased numbers of activated HSCs in areas of inflammation during hepatic fibrosis. Currently, microRNAs have been found to play essential roles in HSC differentiation, proliferation, apoptosis, fat accumulation and collagen production. However, little is known about microRNA mediated HSC activation and migration. In this study, the miRNA expression profiles of quiescent HSCs, partially activated HSCs and fully activated HSCs were compared in pairs. Gene ontology (GO) and GO-Map network analysis indicated that the activation of HSCs was regulated by microRNAs. Among them miR-335 was confirmed to be significantly reduced during HSC activation by qRT-PCR, and restoring expression of miR-335 inhibited HSC migration and reduced {alpha}-SMA and collagen type I. Previous study revealed that tenascin-C (TNC), an extracellular matrix glycoprotein involved in cell migration, might be a target of miR-335. Therefore, we further studied the TNC expression in miR-335 over-expressed HSCs. Our data showed that exogenous TNC could enhance HSC migration in vitro and miR-335 restoration resulted in a significant inhibition of TNC expression. These results demonstrated that miR-335 restoration inhibited HSC migration, at least in part, via downregulating the TNC expression.

Hsa-miR-875-5p exerts tumor suppressor function through down-regulation of EGFR in colorectal carcinoma (CRC).

Science.gov (United States)

Zhang, Tiening; Cai, Xun; Li, Qi; Xue, Peng; Chen, Zhixiao; Dong, Xiao; Xue, Ying

2016-07-05

Hsa-miRNA-875-5p (miR-875-5p) has recently been discovered to have anticancer efficacy in different organs. However, the role of miR-875-5p on colorectal carcinoma (CRC) is still ambiguous. In this study, we investigated the role of miR-875-5p on the development of CRC. The results indicated that miR-875-5p was significantly down-regulated in primary tumor tissues and very low levels were found in CRC cell lines. Ectopic expression of miR-875-5p in CRC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4 and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-875-5p induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-875-5p inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene EGFR was revealed to be a putative target of miR-875-5p, which was inversely correlated with miR-875-5p expression in CRC. Taken together, our results demonstrated that miR-875-5p played a pivotal role on CRC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic EGFR.

Experimental Assessment of residential split type air-conditioning systems using alternative refrigerants to R-22 at high ambient temperatures

International Nuclear Information System (INIS)

Joudi, Khalid A.; Al-Amir, Qusay R.

2014-01-01

Highlights: • R290, R407C and R410A in residential split A/C units at high ambient. • 1 and 2 TR residential air conditioners with R22 alternatives at high ambient. • Residential split unit performance at ambients up to 55 °C with R22 alternatives. - Abstract: Steady state performance of residential air conditioning systems using R22 and alternatives R290, R407C, R410A, at high ambient temperatures, have been investigated experimentally. System performance parameters such as optimum refrigerant charge, coefficient of performance, cooling capacity, power consumption, pressure ratio, power per ton of refrigeration and TEWI environmental factor have been determined. All refrigerants were tested in the cooling mode operation under high ambient air temperatures, up to 55 °C, to determine their suitability. Two split type air conditioner of 1 and 2 TR capacities were used. A psychrometric test facility was constructed consisting of a conditioned cool compartment and an environmental duct serving the condenser. Air inside the conditioned compartment was maintained at 25 °C dry bulb and 19 °C wet bulb for all tests. In the environmental duct, the ambient air temperature was varied from 35 °C to 55 °C in 5 °C increments. The study showed that R290 is the better candidate to replace R22 under high ambient air temperatures. It has lower TEWI values and a better coefficient of performance than the other refrigerants tested. It is suitable as a drop-in refrigerant. R407C has the closest performance to R22, followed by R410A

MicroRNA-181a-5p Impedes IL-17-Induced Nonsmall Cell Lung Cancer Proliferation and Migration through Targeting VCAM-1

Directory of Open Access Journals (Sweden)

Yang Cao

2017-05-01

Full Text Available Aim: The contribution of the inflammatory mediator interleukin-17 (IL-17 in nonsmall cell lung cancer (NSCLC malignancy has been reported in the literature. MicroRNA-181a-5p (miR-181a-5p acts as a tumor suppressor which can regulate target gene at the posttranscriptional level. Our study aimed to investigate the interaction between IL-17 and miR-181a-5p in NSCLC. Methods: 35 patients with NSCLC and 24 COPD controls were selected and examined in our study. In vitro, H226 and H460 cell lines were exposed to different doses (20, 40, 60, and 80 ng/mL of IL-17 to examine the effect of IL-17 on miR-181a-5p and vascular cell adhesion molecule 1 (VCAM-1 expression. MiR-181 mimic and miR-181a-5p inhibitor were transfected to explore the regulation of VCAM-1 as well as tumor cell proliferation and migration. Results: miR-181a-5p expression was downregulated, and IL-17 and VCAM-1 expression was upregulated in NSCLC tissues. Furthermore, IL-17 decreased miR-181a-5p expression but increased VCAM-1 expression in H226 and H460 cells. MiR-181 regulated VCAM-1 expression through binding to 3’-UTR sequence. MiR-181 attenuated tumor cell proliferation and migration. IL-17 modulated miR-181a-5p expression through activating NF-κB but not Stat3. Conclusion: Taken together, our data show the regulation of VCAM-1 expression by miR-181a-5p under IL-17 exposure, predicting a potential way for counteracting cancer metastasis.

MiR-375 inhibits the hepatocyte growth factor-elicited migration of mesenchymal stem cells by downregulating Akt signaling.

Science.gov (United States)

He, Lihong; Wang, Xianyao; Kang, Naixin; Xu, Jianwei; Dai, Nan; Xu, Xiaojing; Zhang, Huanxiang

2018-04-01

The migration of mesenchymal stem cells (MSCs) is critical for their use in cell-based therapies. Accumulating evidence suggests that microRNAs are important regulators of MSC migration. Here, we report that the expression of miR-375 was downregulated in MSCs treated with hepatocyte growth factor (HGF), which strongly stimulates the migration of these cells. Overexpression of miR-375 decreased the transfilter migration and the migration velocity of MSCs triggered by HGF. In our efforts to determine the mechanism by which miR-375 affects MSC migration, we found that miR-375 significantly inhibited the activation of Akt by downregulating its phosphorylation at T308 and S473, but had no effect on the activity of mitogen-activated protein kinases. Further, we showed that 3'phosphoinositide-dependent protein kinase-1 (PDK1), an upstream kinase necessary for full activation of Akt, was negatively regulated by miR-375 at the protein level. Moreover, miR-375 suppressed the phosphorylation of focal adhesion kinase (FAK) and paxillin, two important regulators of focal adhesion (FA) assembly and turnover, and decreased the number of FAs at cell periphery. Taken together, our results demonstrate that miR-375 inhibits HGF-elicited migration of MSCs through downregulating the expression of PDK1 and suppressing the activation of Akt, as well as influencing the tyrosine phosphorylation of FAK and paxillin and FA periphery distribution.

Ascites promotes cell migration through the repression of miR-125b in ovarian cancer.

Science.gov (United States)

Yang, Lan; Zhang, Xiaoli; Ma, Yiming; Zhao, Xinhua; Li, Bin; Wang, Hongying

2017-08-01

Interactions between ovarian cancer cells and the surrounding tumor microenvironment are not well characterized. Here, we investigated the molecular mechanisms by which malignant ascites promote the metastasis of ovarian cancer. It was found that ovarian cancer ascites promoted ovarian cancer cell migration which was attenuated by either heat inactivation or antibody blockade of TGF-β. High level (at ng/ml level) of TGF-β was detected in the ascites. In addition, ascites repressed the expression of miRNA-125b in a TGF-β-dependent manner. Mimic of miR-125b blocked ascites-induced cell migration. Furthermore, Gab2 (a target gene of miR-125b) was elevated by ascites in a TGF-β-dependent manner. And forced expression of Gab2 reversed the inhibition of migration induced by miR-125b mimic. Most importantly, the expression of miR-125b and Gab2 mRNA was negatively correlated in ovarian cancer specimens. Taken together, our finding suggested that TGF-β in ascites promoted cancer cell migration through repression of miR-125b in ovarian cancer. This might provide a novel therapeutic target for ovarian cancer in the future.

LincRNA-p21 inhibits invasion and metastasis of hepatocellular carcinoma through miR-9/E-cadherin cascade signaling pathway molecular mechanism

Directory of Open Access Journals (Sweden)

Ding G

2017-06-01

Full Text Available Gangqiang Ding, Zhen Peng, Jia Shang, Yi Kang, Huibin Ning, Chongshan Mao Department of Infectious Diseases, People’s Hospital of Zhengzhou University, Henan Provincial People’s Hospital, Zhengzhou, China Abstract: In the previous study, it was found that long intergenic noncoding RNA-p21 (lincRNA-p21 was downregulated in hepatocellular carcinoma (HCC and lincRNA-p21 overexpression inhibited tumor invasion through inducing epithelial–mesenchymal transition. However, the underlying mechanism was not fully elaborated. In this study, lincRNA-p21 expression was measured in 12 paired HCC and nontumor adjacent normal tissues by ­quantitative real-time polymerase chain reaction. The effects of lincRNA-p21 on HCC cells were studied using lentivirus expressing lincRNA-p21 vector in vitro. The association between lincRNA-p21 level and miR-9 level was tested with the Spearman rank correlation. The effects of miR-9 on HCC cells were studied by using miR-9 inhibitor in vitro. Luciferase assay was used to validate the target of miR-9. The results showed that lincRNA-p21 was downregulated in human HCC tissues and cell lines. LincRNA-p21 overexpression significantly inhibited HCC cell migration and invasion in vitro. Besides, lincRNA-p21 negatively regulated miR-9 expression level, and miR-9 was upregulated in human HCC tissues and cells. MiR-9 knockdown inhibited HCC cell migration and invasion in vitro. Finally, the luciferase assay results showed that E-cadherin was a direct target of miR-9. The expression level of E-cadherin was found to be regulated by lincRNA-p21 and miR-9. Altogether, the results suggested that lincRNA-p21 inhibits migration and invasion of HCC cells through regulating miR-9-mediated E-cadherin cascade signaling pathway. Keywords: hepatocellular carcinoma, lincRNA-p21, miR-9, E-cadherin, epithelial–mesenchymal transition

P R Mirkute

Indian Academy of Sciences (India)

Home; Journals; Sadhana. P R Mirkute. Articles written in Sadhana. Volume 28 Issue 6 December 2003 pp 1019-1026. A third-order active-R filter with feedforward input signal · G N Shinde P B Patil P R Mirkute · More Details Abstract Fulltext PDF. A realization of voltage-mode transfer functions with feedforward input signal ...

Measurement of the Splitting Function in p p and Pb-Pb Collisions at √{sN N }=5.02 TeV

Science.gov (United States)

Sirunyan, A. M.; Tumasyan, A.; Adam, W.; Ambrogi, F.; Asilar, E.; Bergauer, T.; Brandstetter, J.; Brondolin, E.; Dragicevic, M.; Erö, J.; Flechl, M.; Friedl, M.; Frühwirth, R.; Ghete, V. M.; Grossmann, J.; Hrubec, J.; Jeitler, M.; König, A.; Krammer, N.; Krätschmer, I.; Liko, D.; Madlener, T.; Mikulec, I.; Pree, E.; Rad, N.; Rohringer, H.; Schieck, J.; Schöfbeck, R.; Spanring, M.; Spitzbart, D.; Waltenberger, W.; Wittmann, J.; Wulz, C.-E.; Zarucki, M.; Chekhovsky, V.; Mossolov, V.; Suarez Gonzalez, J.; De Wolf, E. A.; Di Croce, D.; Janssen, X.; Lauwers, J.; Van Haevermaet, H.; Van Mechelen, P.; Van Remortel, N.; Abu Zeid, S.; Blekman, F.; D'Hondt, J.; De Bruyn, I.; De Clercq, J.; Deroover, K.; Flouris, G.; Lontkovskyi, D.; Lowette, S.; Moortgat, S.; Moreels, L.; Python, Q.; Skovpen, K.; Tavernier, S.; Van Doninck, W.; Van Mulders, P.; Van Parijs, I.; Beghin, D.; Brun, H.; Clerbaux, B.; De Lentdecker, G.; Delannoy, H.; Dorney, B.; Fasanella, G.; Favart, L.; Goldouzian, R.; Grebenyuk, A.; Karapostoli, G.; Lenzi, T.; Luetic, J.; Maerschalk, T.; Marinov, A.; Randle-conde, A.; Seva, T.; Starling, E.; Vander Velde, C.; Vanlaer, P.; Vannerom, D.; Yonamine, R.; Zenoni, F.; Zhang, F.; Cimmino, A.; Cornelis, T.; Dobur, D.; Fagot, A.; Gul, M.; Khvastunov, I.; Poyraz, D.; Roskas, C.; Salva, S.; Tytgat, M.; Verbeke, W.; Zaganidis, N.; Bakhshiansohi, H.; Bondu, O.; Brochet, S.; Bruno, G.; Caputo, C.; Caudron, A.; David, P.; De Visscher, S.; Delaere, C.; Delcourt, M.; Francois, B.; Giammanco, A.; Komm, M.; Krintiras, G.; Lemaitre, V.; Magitteri, A.; Mertens, A.; Musich, M.; Piotrzkowski, K.; Quertenmont, L.; Saggio, A.; Vidal Marono, M.; Wertz, S.; Zobec, J.; Beliy, N.; Aldá Júnior, W. L.; Alves, F. L.; Alves, G. A.; Brito, L.; Correa Martins Junior, M.; Hensel, C.; Moraes, A.; Pol, M. E.; Rebello Teles, P.; Belchior Batista Das Chagas, E.; Carvalho, W.; Chinellato, J.; Coelho, E.; Da Costa, E. M.; Da Silveira, G. G.; De Jesus Damiao, D.; Fonseca De Souza, S.; Huertas Guativa, L. M.; Malbouisson, H.; Melo De Almeida, M.; Mora Herrera, C.; Mundim, L.; Nogima, H.; Sanchez Rosas, L. J.; Santoro, A.; Sznajder, A.; Thiel, M.; Tonelli Manganote, E. J.; Torres Da Silva De Araujo, F.; Vilela Pereira, A.; Ahuja, S.; Bernardes, C. A.; Tomei, T. R. Fernandez Perez; Gregores, E. M.; Mercadante, P. G.; Novaes, S. F.; Padula, Sandra S.; Romero Abad, D.; Ruiz Vargas, J. C.; Aleksandrov, A.; Hadjiiska, R.; Iaydjiev, P.; Misheva, M.; Rodozov, M.; Shopova, M.; Sultanov, G.; Dimitrov, A.; Glushkov, I.; Litov, L.; Pavlov, B.; Petkov, P.; Fang, W.; Gao, X.; Yuan, L.; Ahmad, M.; Bian, J. G.; Chen, G. M.; Chen, H. S.; Chen, M.; Chen, Y.; Jiang, C. H.; Leggat, D.; Liao, H.; Liu, Z.; Romeo, F.; Shaheen, S. M.; Spiezia, A.; Tao, J.; Wang, C.; Wang, Z.; Yazgan, E.; Zhang, H.; Zhang, S.; Zhao, J.; Ban, Y.; Chen, G.; Li, Q.; Liu, S.; Mao, Y.; Qian, S. J.; Wang, D.; Xu, Z.; Avila, C.; Cabrera, A.; Chaparro Sierra, L. F.; Florez, C.; González Hernández, C. F.; Ruiz Alvarez, J. D.; Courbon, B.; Godinovic, N.; Lelas, D.; Puljak, I.; Ribeiro Cipriano, P. M.; Sculac, T.; Antunovic, Z.; Kovac, M.; Brigljevic, V.; Ferencek, D.; Kadija, K.; Mesic, B.; Starodumov, A.; Susa, T.; Ather, M. W.; Attikis, A.; Mavromanolakis, G.; Mousa, J.; Nicolaou, C.; Ptochos, F.; Razis, P. A.; Rykaczewski, H.; Finger, M.; Finger, M.; Carrera Jarrin, E.; Abdelalim, A. A.; Mohammed, Y.; Salama, E.; Dewanjee, R. K.; Kadastik, M.; Perrini, L.; Raidal, M.; Tiko, A.; Veelken, C.; Eerola, P.; Kirschenmann, H.; Pekkanen, J.; Voutilainen, M.; Järvinen, T.; Karimäki, V.; Kinnunen, R.; Lampén, T.; Lassila-Perini, K.; Lehti, S.; Lindén, T.; Luukka, P.; Tuominen, E.; Tuominiemi, J.; Talvitie, J.; Tuuva, T.; Besancon, M.; Couderc, F.; Dejardin, M.; Denegri, D.; Faure, J. L.; Ferri, F.; Ganjour, S.; Ghosh, S.; Givernaud, A.; Gras, P.; Hamel de Monchenault, G.; Jarry, P.; Kucher, I.; Leloup, C.; Locci, E.; Machet, M.; Malcles, J.; Negro, G.; Rander, J.; Rosowsky, A.; Sahin, M. Ö.; Titov, M.; Abdulsalam, A.; Amendola, C.; Antropov, I.; Baffioni, S.; Beaudette, F.; Busson, P.; Cadamuro, L.; Charlot, C.; Granier de Cassagnac, R.; Jo, M.; Lisniak, S.; Lobanov, A.; Martin Blanco, J.; Nguyen, M.; Ochando, C.; Ortona, G.; Paganini, P.; Pigard, P.; Salerno, R.; Sauvan, J. B.; Sirois, Y.; Stahl Leiton, A. G.; Strebler, T.; Yilmaz, Y.; Zabi, A.; Zghiche, A.; Agram, J.-L.; Andrea, J.; Bloch, D.; Brom, J.-M.; Buttignol, M.; Chabert, E. C.; Chanon, N.; Collard, C.; Conte, E.; Coubez, X.; Fontaine, J.-C.; Gelé, D.; Goerlach, U.; Jansová, M.; Le Bihan, A.-C.; Tonon, N.; Van Hove, P.; Gadrat, S.; Beauceron, S.; Bernet, C.; Boudoul, G.; Chierici, R.; Contardo, D.; Depasse, P.; El Mamouni, H.; Fay, J.; Finco, L.; Gascon, S.; Gouzevitch, M.; Grenier, G.; Ille, B.; Lagarde, F.; Laktineh, I. B.; Lethuillier, M.; Mirabito, L.; Pequegnot, A. L.; Perries, S.; Popov, A.; Sordini, V.; Vander Donckt, M.; Viret, S.; Khvedelidze, A.; Tsamalaidze, Z.; Autermann, C.; Feld, L.; Kiesel, M. K.; Klein, K.; Lipinski, M.; Preuten, M.; Schomakers, C.; Schulz, J.; Zhukov, V.; Albert, A.; Dietz-Laursonn, E.; Duchardt, D.; Endres, M.; Erdmann, M.; Erdweg, S.; Esch, T.; Fischer, R.; Güth, A.; Hamer, M.; Hebbeker, T.; Heidemann, C.; Hoepfner, K.; Knutzen, S.; Merschmeyer, M.; Meyer, A.; Millet, P.; Mukherjee, S.; Pook, T.; Radziej, M.; Reithler, H.; Rieger, M.; Scheuch, F.; Teyssier, D.; Thüer, S.; Flügge, G.; Kargoll, B.; Kress, T.; Künsken, A.; Müller, T.; Nehrkorn, A.; Nowack, A.; Pistone, C.; Pooth, O.; Stahl, A.; Aldaya Martin, M.; Arndt, T.; Asawatangtrakuldee, C.; Beernaert, K.; Behnke, O.; Behrens, U.; Bermúdez Martínez, A.; Bin Anuar, A. A.; Borras, K.; Botta, V.; Campbell, A.; Connor, P.; Contreras-Campana, C.; Costanza, F.; Diez Pardos, C.; Eckerlin, G.; Eckstein, D.; Eichhorn, T.; Eren, E.; Gallo, E.; Garay Garcia, J.; Geiser, A.; Gizhko, A.; Grados Luyando, J. M.; Grohsjean, A.; Gunnellini, P.; Guthoff, M.; Harb, A.; Hauk, J.; Hempel, M.; Jung, H.; Kalogeropoulos, A.; Kasemann, M.; Keaveney, J.; Kleinwort, C.; Korol, I.; Krücker, D.; Lange, W.; Lelek, A.; Lenz, T.; Leonard, J.; Lipka, K.; Lohmann, W.; Mankel, R.; Melzer-Pellmann, I.-A.; Meyer, A. B.; Mittag, G.; Mnich, J.; Mussgiller, A.; Ntomari, E.; Pitzl, D.; Raspereza, A.; Roland, B.; Savitskyi, M.; Saxena, P.; Shevchenko, R.; Spannagel, S.; Stefaniuk, N.; Van Onsem, G. P.; Walsh, R.; Wen, Y.; Wichmann, K.; Wissing, C.; Zenaiev, O.; Aggleton, R.; Bein, S.; Blobel, V.; Centis Vignali, M.; Dreyer, T.; Garutti, E.; Gonzalez, D.; Haller, J.; Hinzmann, A.; Hoffmann, M.; Karavdina, A.; Klanner, R.; Kogler, R.; Kovalchuk, N.; Kurz, S.; Lapsien, T.; Marchesini, I.; Marconi, D.; Meyer, M.; Niedziela, M.; Nowatschin, D.; Pantaleo, F.; Peiffer, T.; Perieanu, A.; Scharf, C.; Schleper, P.; Schmidt, A.; Schumann, S.; Schwandt, J.; Sonneveld, J.; Stadie, H.; Steinbrück, G.; Stober, F. M.; Stöver, M.; Tholen, H.; Troendle, D.; Usai, E.; Vanelderen, L.; Vanhoefer, A.; Vormwald, B.; Akbiyik, M.; Barth, C.; Baur, S.; Butz, E.; Caspart, R.; Chwalek, T.; Colombo, F.; De Boer, W.; Dierlamm, A.; Freund, B.; Friese, R.; Giffels, M.; Haitz, D.; Harrendorf, M. A.; Hartmann, F.; Heindl, S. M.; Husemann, U.; Kassel, F.; Kudella, S.; Mildner, H.; Mozer, M. U.; Müller, Th.; Plagge, M.; Quast, G.; Rabbertz, K.; Schröder, M.; Shvetsov, I.; Sieber, G.; Simonis, H. J.; Ulrich, R.; Wayand, S.; Weber, M.; Weiler, T.; Williamson, S.; Wöhrmann, C.; Wolf, R.; Anagnostou, G.; Daskalakis, G.; Geralis, T.; Giakoumopoulou, V. A.; Kyriakis, A.; Loukas, D.; Topsis-Giotis, I.; Karathanasis, G.; Kesisoglou, S.; Panagiotou, A.; Saoulidou, N.; Kousouris, K.; Evangelou, I.; Foudas, C.; Kokkas, P.; Mallios, S.; Manthos, N.; Papadopoulos, I.; Paradas, E.; Strologas, J.; Triantis, F. A.; Csanad, M.; Filipovic, N.; Pasztor, G.; Surányi, O.; Veres, G. I.; Bencze, G.; Hajdu, C.; Horvath, D.; Hunyadi, Á.; Sikler, F.; Veszpremi, V.; Zsigmond, A. J.; Beni, N.; Czellar, S.; Karancsi, J.; Makovec, A.; Molnar, J.; Szillasi, Z.; Bartók, M.; Raics, P.; Trocsanyi, Z. L.; Ujvari, B.; Choudhury, S.; Komaragiri, J. R.; Bahinipati, S.; Bhowmik, S.; Mal, P.; Mandal, K.; Nayak, A.; Sahoo, D. K.; Sahoo, N.; Swain, S. K.; Bansal, S.; Beri, S. B.; Bhatnagar, V.; Chawla, R.; Dhingra, N.; Kalsi, A. K.; Kaur, A.; Kaur, M.; Kaur, S.; Kumar, R.; Kumari, P.; Mehta, A.; Singh, J. B.; Walia, G.; Kumar, Ashok; Shah, Aashaq; Bhardwaj, A.; Chauhan, S.; Choudhary, B. C.; Garg, R. B.; Keshri, S.; Kumar, A.; Malhotra, S.; Naimuddin, M.; Ranjan, K.; Sharma, R.; Bhardwaj, R.; Bhattacharya, R.; Bhattacharya, S.; Bhawandeep, U.; Dey, S.; Dutt, S.; Dutta, S.; Ghosh, S.; Majumdar, N.; Modak, A.; Mondal, K.; Mukhopadhyay, S.; Nandan, S.; Purohit, A.; Roy, A.; Roy, D.; Roy Chowdhury, S.; Sarkar, S.; Sharan, M.; Thakur, S.; Behera, P. K.; Chudasama, R.; Dutta, D.; Jha, V.; Kumar, V.; Mohanty, A. K.; Netrakanti, P. K.; Pant, L. M.; Shukla, P.; Topkar, A.; Aziz, T.; Dugad, S.; Mahakud, B.; Mitra, S.; Mohanty, G. B.; Sur, N.; Sutar, B.; Banerjee, S.; Bhattacharya, S.; Chatterjee, S.; Das, P.; Guchait, M.; Jain, Sa.; Kumar, S.; Maity, M.; Majumder, G.; Mazumdar, K.; Sarkar, T.; Wickramage, N.; Chauhan, S.; Dube, S.; Hegde, V.; Kapoor, A.; Kothekar, K.; Pandey, S.; Rane, A.; Sharma, S.; Chenarani, S.; Eskandari Tadavani, E.; Etesami, S. M.; Khakzad, M.; Mohammadi Najafabadi, M.; Naseri, M.; Paktinat Mehdiabadi, S.; Rezaei Hosseinabadi, F.; Safarzadeh, B.; Zeinali, M.; Felcini, M.; Grunewald, M.; Abbrescia, M.; Calabria, C.; Colaleo, A.; Creanza, D.; Cristella, L.; De Filippis, N.; De Palma, M.; Errico, F.; Fiore, L.; Iaselli, G.; Lezki, S.; Maggi, G.; Maggi, M.; Miniello, G.; My, S.; Nuzzo, S.; Pompili, A.; Pugliese, G.; Radogna, R.; Ranieri, A.; Selvaggi, G.; Sharma, A.; Silvestris, L.; Venditti, R.; Verwilligen, P.; Abbiendi, G.; Battilana, C.; Bonacorsi, D.; Borgonovi, L.; Braibant-Giacomelli, S.; Campanini, R.; Capiluppi, P.; Castro, A.; Cavallo, F. R.; Chhibra, S. S.; Codispoti, G.; Cuffiani, M.; Dallavalle, G. M.; Fabbri, F.; Fanfani, A.; Fasanella, D.; Giacomelli, P.; Grandi, C.; Guiducci, L.; Marcellini, S.; Masetti, G.; Montanari, A.; Navarria, F. L.; Perrotta, A.; Rossi, A. M.; Rovelli, T.; Siroli, G. P.; Tosi, N.; Albergo, S.; Costa, S.; Di Mattia, A.; Giordano, F.; Potenza, R.; Tricomi, A.; Tuve, C.; Barbagli, G.; Chatterjee, K.; Ciulli, V.; Civinini, C.; D'Alessandro, R.; Focardi, E.; Lenzi, P.; Meschini, M.; Paoletti, S.; Russo, L.; Sguazzoni, G.; Strom, D.; Viliani, L.; Benussi, L.; Bianco, S.; Fabbri, F.; Piccolo, D.; Primavera, F.; Calvelli, V.; Ferro, F.; Robutti, E.; Tosi, S.; Benaglia, A.; Brianza, L.; Brivio, F.; Ciriolo, V.; Dinardo, M. E.; Fiorendi, S.; Gennai, S.; Ghezzi, A.; Govoni, P.; Malberti, M.; Malvezzi, S.; Manzoni, R. A.; Menasce, D.; Moroni, L.; Paganoni, M.; Pauwels, K.; Pedrini, D.; Pigazzini, S.; Ragazzi, S.; Redaelli, N.; Tabarelli de Fatis, T.; Buontempo, S.; Cavallo, N.; Di Guida, S.; Fabozzi, F.; Fienga, F.; Iorio, A. O. M.; Khan, W. A.; Lista, L.; Meola, S.; Paolucci, P.; Sciacca, C.; Thyssen, F.; Azzi, P.; Bacchetta, N.; Benato, L.; Bisello, D.; Boletti, A.; Carlin, R.; Carvalho Antunes De Oliveira, A.; Checchia, P.; Dall'Osso, M.; De Castro Manzano, P.; Dorigo, T.; Dosselli, U.; Gozzelino, A.; Lacaprara, S.; Lujan, P.; Margoni, M.; Meneguzzo, A. T.; Montecassiano, F.; Pozzobon, N.; Ronchese, P.; Rossin, R.; Simonetto, F.; Torassa, E.; Zanetti, M.; Zotto, P.; Zumerle, G.; Braghieri, A.; Magnani, A.; Montagna, P.; Ratti, S. P.; Re, V.; Ressegotti, M.; Riccardi, C.; Salvini, P.; Vai, I.; Vitulo, P.; Alunni Solestizi, L.; Biasini, M.; Bilei, G. M.; Cecchi, C.; Ciangottini, D.; Fanò, L.; Lariccia, P.; Leonardi, R.; Manoni, E.; Mantovani, G.; Mariani, V.; Menichelli, M.; Rossi, A.; Santocchia, A.; Spiga, D.; Androsov, K.; Azzurri, P.; Bagliesi, G.; Boccali, T.; Borrello, L.; Castaldi, R.; Ciocci, M. A.; Dell'Orso, R.; Fedi, G.; Giannini, L.; Giassi, A.; Grippo, M. T.; Ligabue, F.; Lomtadze, T.; Manca, E.; Mandorli, G.; Martini, L.; Messineo, A.; Palla, F.; Rizzi, A.; Savoy-Navarro, A.; Spagnolo, P.; Tenchini, R.; Tonelli, G.; Venturi, A.; Verdini, P. G.; Barone, L.; Cavallari, F.; Cipriani, M.; Daci, N.; Del Re, D.; Di Marco, E.; Diemoz, M.; Gelli, S.; Longo, E.; Margaroli, F.; Marzocchi, B.; Meridiani, P.; Organtini, G.; Paramatti, R.; Preiato, F.; Rahatlou, S.; Rovelli, C.; Santanastasio, F.; Amapane, N.; Arcidiacono, R.; Argiro, S.; Arneodo, M.; Bartosik, N.; Bellan, R.; Biino, C.; Cartiglia, N.; Cenna, F.; Costa, M.; Covarelli, R.; Degano, A.; Demaria, N.; Kiani, B.; Mariotti, C.; Maselli, S.; Migliore, E.; Monaco, V.; Monteil, E.; Monteno, M.; Obertino, M. M.; Pacher, L.; Pastrone, N.; Pelliccioni, M.; Pinna Angioni, G. L.; Ravera, F.; Romero, A.; Ruspa, M.; Sacchi, R.; Shchelina, K.; Sola, V.; Solano, A.; Staiano, A.; Traczyk, P.; Belforte, S.; Casarsa, M.; Cossutti, F.; Della Ricca, G.; Zanetti, A.; Kim, D. H.; Kim, G. N.; Kim, M. S.; Lee, J.; Lee, S.; Lee, S. W.; Moon, C. S.; Oh, Y. D.; Sekmen, S.; Son, D. C.; Yang, Y. C.; Lee, A.; Kim, H.; Moon, D. H.; Oh, G.; Brochero Cifuentes, J. A.; Goh, J.; Kim, T. J.; Cho, S.; Choi, S.; Go, Y.; Gyun, D.; Ha, S.; Hong, B.; Jo, Y.; Kim, Y.; Lee, K.; Lee, K. S.; Lee, S.; Lim, J.; Park, S. K.; Roh, Y.; Almond, J.; Kim, J.; Kim, J. S.; Lee, H.; Lee, K.; Nam, K.; Oh, S. B.; Radburn-Smith, B. C.; Seo, S. h.; Yang, U. K.; Yoo, H. D.; Yu, G. B.; Choi, M.; Kim, H.; Kim, J. H.; Lee, J. S. H.; Park, I. C.; Choi, Y.; Hwang, C.; Lee, J.; Yu, I.; Dudenas, V.; Juodagalvis, A.; Vaitkus, J.; Ahmed, I.; Ibrahim, Z. A.; Md Ali, M. A. B.; Mohamad Idris, F.; Wan Abdullah, W. A. T.; Yusli, M. N.; Zolkapli, Z.; Reyes-Almanza, R.; Ramirez-Sanchez, G.; Duran-Osuna, M. C.; Castilla-Valdez, H.; De La Cruz-Burelo, E.; Heredia-De La Cruz, I.; Rabadan-Trejo, R. I.; Lopez-Fernandez, R.; Mejia Guisao, J.; Sanchez-Hernandez, A.; Carrillo Moreno, S.; Oropeza Barrera, C.; Vazquez Valencia, F.; Pedraza, I.; Salazar Ibarguen, H. A.; Uribe Estrada, C.; Morelos Pineda, A.; Krofcheck, D.; Butler, P. H.; Ahmad, A.; Ahmad, M.; Hassan, Q.; Hoorani, H. R.; Saddique, A.; Shah, M. A.; Shoaib, M.; Waqas, M.; Bialkowska, H.; Bluj, M.; Boimska, B.; Frueboes, T.; Górski, M.; Kazana, M.; Nawrocki, K.; Szleper, M.; Zalewski, P.; Bunkowski, K.; Byszuk, A.; Doroba, K.; Kalinowski, A.; Konecki, M.; Krolikowski, J.; Misiura, M.; Olszewski, M.; Pyskir, A.; Walczak, M.; Bargassa, P.; Beirão Da Cruz E Silva, C.; Di Francesco, A.; Faccioli, P.; Galinhas, B.; Gallinaro, M.; Hollar, J.; Leonardo, N.; Lloret Iglesias, L.; Nemallapudi, M. V.; Seixas, J.; Strong, G.; Toldaiev, O.; Vadruccio, D.; Varela, J.; Afanasiev, S.; Bunin, P.; Gavrilenko, M.; Golutvin, I.; Gorbunov, I.; Kamenev, A.; Karjavin, V.; Lanev, A.; Malakhov, A.; Matveev, V.; Palichik, V.; Perelygin, V.; Shmatov, S.; Shulha, S.; Skatchkov, N.; Smirnov, V.; Voytishin, N.; Zarubin, A.; Ivanov, Y.; Kim, V.; Kuznetsova, E.; Levchenko, P.; Murzin, V.; Oreshkin, V.; Smirnov, I.; Sulimov, V.; Uvarov, L.; Vavilov, S.; Vorobyev, A.; Andreev, Yu.; Dermenev, A.; Gninenko, S.; Golubev, N.; Karneyeu, A.; Kirsanov, M.; Krasnikov, N.; Pashenkov, A.; Tlisov, D.; Toropin, A.; Epshteyn, V.; Gavrilov, V.; Lychkovskaya, N.; Popov, V.; Pozdnyakov, I.; Safronov, G.; Spiridonov, A.; Stepennov, A.; Toms, M.; Vlasov, E.; Zhokin, A.; Aushev, T.; Bylinkin, A.; Chadeeva, M.; Markin, O.; Parygin, P.; Philippov, D.; Polikarpov, S.; Rusinov, V.; Andreev, V.; Azarkin, M.; Dremin, I.; Kirakosyan, M.; Terkulov, A.; Baskakov, A.; Belyaev, A.; Boos, E.; Demiyanov, A.; Ershov, A.; Gribushin, A.; Kodolova, O.; Korotkikh, V.; Lokhtin, I.; Miagkov, I.; Obraztsov, S.; Petrushanko, S.; Savrin, V.; Snigirev, A.; Vardanyan, I.; Blinov, V.; Skovpen, Y.; Shtol, D.; Azhgirey, I.; Bayshev, I.; Bitioukov, S.; Elumakhov, D.; Kachanov, V.; Kalinin, A.; Konstantinov, D.; Mandrik, P.; Petrov, V.; Ryutin, R.; Sobol, A.; Troshin, S.; Tyurin, N.; Uzunian, A.; Volkov, A.; Adzic, P.; Cirkovic, P.; Devetak, D.; Dordevic, M.; Milosevic, J.; Rekovic, V.; Alcaraz Maestre, J.; Barrio Luna, M.; Cerrada, M.; Colino, N.; De La Cruz, B.; Delgado Peris, A.; Escalante Del Valle, A.; Fernandez Bedoya, C.; Fernández Ramos, J. P.; Flix, J.; Fouz, M. C.; Gonzalez Lopez, O.; Goy Lopez, S.; Hernandez, J. M.; Josa, M. I.; Moran, D.; Pérez-Calero Yzquierdo, A.; Puerta Pelayo, J.; Quintario Olmeda, A.; Redondo, I.; Romero, L.; Soares, M. S.; Álvarez Fernández, A.; de Trocóniz, J. F.; Missiroli, M.; Cuevas, J.; Erice, C.; Fernandez Menendez, J.; Gonzalez Caballero, I.; González Fernández, J. R.; Palencia Cortezon, E.; Sanchez Cruz, S.; Vischia, P.; Vizan Garcia, J. M.; Cabrillo, I. J.; Calderon, A.; Chazin Quero, B.; Curras, E.; Duarte Campderros, J.; Fernandez, M.; Garcia-Ferrero, J.; Gomez, G.; Lopez Virto, A.; Marco, J.; Martinez Rivero, C.; Martinez Ruiz del Arbol, P.; Matorras, F.; Piedra Gomez, J.; Rodrigo, T.; Ruiz-Jimeno, A.; Scodellaro, L.; Trevisani, N.; Vila, I.; Vilar Cortabitarte, R.; Abbaneo, D.; Akgun, B.; Auffray, E.; Baillon, P.; Ball, A. H.; Barney, D.; Bianco, M.; Bloch, P.; Bocci, A.; Botta, C.; Camporesi, T.; Castello, R.; Cepeda, M.; Cerminara, G.; Chapon, E.; Chen, Y.; d'Enterria, D.; Dabrowski, A.; Daponte, V.; David, A.; De Gruttola, M.; De Roeck, A.; Deelen, N.; Dobson, M.; du Pree, T.; Dünser, M.; Dupont, N.; Elliott-Peisert, A.; Everaerts, P.; Fallavollita, F.; Franzoni, G.; Fulcher, J.; Funk, W.; Gigi, D.; Gilbert, A.; Gill, K.; Glege, F.; Gulhan, D.; Harris, P.; Hegeman, J.; Innocente, V.; Jafari, A.; Janot, P.; Karacheban, O.; Kieseler, J.; Knünz, V.; Kornmayer, A.; Kortelainen, M. J.; Krammer, M.; Lange, C.; Lecoq, P.; Lourenço, C.; Lucchini, M. T.; Malgeri, L.; Mannelli, M.; Martelli, A.; Meijers, F.; Merlin, J. A.; Mersi, S.; Meschi, E.; Milenovic, P.; Moortgat, F.; Mulders, M.; Neugebauer, H.; Ngadiuba, J.; Orfanelli, S.; Orsini, L.; Pape, L.; Perez, E.; Peruzzi, M.; Petrilli, A.; Petrucciani, G.; Pfeiffer, A.; Pierini, M.; Rabady, D.; Racz, A.; Reis, T.; Rolandi, G.; Rovere, M.; Sakulin, H.; Schäfer, C.; Schwick, C.; Seidel, M.; Selvaggi, M.; Sharma, A.; Silva, P.; Sphicas, P.; Stakia, A.; Steggemann, J.; Stoye, M.; Tosi, M.; Treille, D.; Triossi, A.; Tsirou, A.; Veckalns, V.; Verweij, M.; Zeuner, W. D.; Bertl, W.; Caminada, L.; Deiters, K.; Erdmann, W.; Horisberger, R.; Ingram, Q.; Kaestli, H. C.; Kotlinski, D.; Langenegger, U.; Rohe, T.; Wiederkehr, S. A.; Backhaus, M.; Bäni, L.; Berger, P.; Bianchini, L.; Casal, B.; Dissertori, G.; Dittmar, M.; Donegà, M.; Dorfer, C.; Grab, C.; Heidegger, C.; Hits, D.; Hoss, J.; Kasieczka, G.; Klijnsma, T.; Lustermann, W.; Mangano, B.; Marionneau, M.; Meinhard, M. T.; Meister, D.; Micheli, F.; Musella, P.; Nessi-Tedaldi, F.; Pandolfi, F.; Pata, J.; Pauss, F.; Perrin, G.; Perrozzi, L.; Quittnat, M.; Reichmann, M.; Sanz Becerra, D. A.; Schönenberger, M.; Shchutska, L.; Tavolaro, V. R.; Theofilatos, K.; Vesterbacka Olsson, M. L.; Wallny, R.; Zhu, D. H.; Aarrestad, T. K.; Amsler, C.; Canelli, M. F.; De Cosa, A.; Del Burgo, R.; Donato, S.; Galloni, C.; Hreus, T.; Kilminster, B.; Pinna, D.; Rauco, G.; Robmann, P.; Salerno, D.; Schweiger, K.; Seitz, C.; Takahashi, Y.; Zucchetta, A.; Candelise, V.; Doan, T. H.; Jain, Sh.; Khurana, R.; Kuo, C. M.; Lin, W.; Pozdnyakov, A.; Yu, S. S.; Kumar, Arun; Chang, P.; Chao, Y.; Chen, K. F.; Chen, P. H.; Fiori, F.; Hou, W.-S.; Hsiung, Y.; Liu, Y. F.; Lu, R.-S.; Paganis, E.; Psallidas, A.; Steen, A.; Tsai, J. f.; Asavapibhop, B.; Kovitanggoon, K.; Singh, G.; Srimanobhas, N.; Boran, F.; Cerci, S.; Damarseckin, S.; Demiroglu, Z. S.; Dozen, C.; Dumanoglu, I.; Girgis, S.; Gokbulut, G.; Guler, Y.; Hos, I.; Kangal, E. E.; Kara, O.; Kayis Topaksu, A.; Kiminsu, U.; Oglakci, M.; Onengut, G.; Ozdemir, K.; Sunar Cerci, D.; Tali, B.; Turkcapar, S.; Zorbakir, I. S.; Zorbilmez, C.; Bilin, B.; Karapinar, G.; Ocalan, K.; Yalvac, M.; Zeyrek, M.; Gülmez, E.; Kaya, M.; Kaya, O.; Tekten, S.; Yetkin, E. A.; Agaras, M. N.; Atay, S.; Cakir, A.; Cankocak, K.; Grynyov, B.; Levchuk, L.; Ball, F.; Beck, L.; Brooke, J. J.; Burns, D.; Clement, E.; Cussans, D.; Davignon, O.; Flacher, H.; Goldstein, J.; Heath, G. P.; Heath, H. F.; Jacob, J.; Kreczko, L.; Newbold, D. M.; Paramesvaran, S.; Sakuma, T.; Seif El Nasr-storey, S.; Smith, D.; Smith, V. J.; Belyaev, A.; Brew, C.; Brown, R. M.; Calligaris, L.; Cieri, D.; Cockerill, D. J. A.; Coughlan, J. A.; Harder, K.; Harper, S.; Olaiya, E.; Petyt, D.; Shepherd-Themistocleous, C. H.; Thea, A.; Tomalin, I. R.; Williams, T.; Auzinger, G.; Bainbridge, R.; Borg, J.; Breeze, S.; Buchmuller, O.; Bundock, A.; Casasso, S.; Citron, M.; Colling, D.; Corpe, L.; Dauncey, P.; Davies, G.; De Wit, A.; Della Negra, M.; Di Maria, R.; Elwood, A.; Haddad, Y.; Hall, G.; Iles, G.; James, T.; Lane, R.; Laner, C.; Lyons, L.; Magnan, A.-M.; Malik, S.; Mastrolorenzo, L.; Matsushita, T.; Nash, J.; Nikitenko, A.; Palladino, V.; Pesaresi, M.; Raymond, D. M.; Richards, A.; Rose, A.; Scott, E.; Seez, C.; Shtipliyski, A.; Summers, S.; Tapper, A.; Uchida, K.; Vazquez Acosta, M.; Virdee, T.; Wardle, N.; Winterbottom, D.; Wright, J.; Zenz, S. C.; Cole, J. E.; Hobson, P. R.; Khan, A.; Kyberd, P.; Reid, I. D.; Symonds, P.; Teodorescu, L.; Turner, M.; Zahid, S.; Borzou, A.; Call, K.; Dittmann, J.; Hatakeyama, K.; Liu, H.; Pastika, N.; Smith, C.; Bartek, R.; Dominguez, A.; Buccilli, A.; Cooper, S. I.; Henderson, C.; Rumerio, P.; West, C.; Arcaro, D.; Avetisyan, A.; Bose, T.; Gastler, D.; Rankin, D.; Richardson, C.; Rohlf, J.; Sulak, L.; Zou, D.; Benelli, G.; Cutts, D.; Garabedian, A.; Hadley, M.; Hakala, J.; Heintz, U.; Hogan, J. M.; Kwok, K. H. M.; Laird, E.; Landsberg, G.; Lee, J.; Mao, Z.; Narain, M.; Pazzini, J.; Piperov, S.; Sagir, S.; Syarif, R.; Yu, D.; Band, R.; Brainerd, C.; Burns, D.; Calderon De La Barca Sanchez, M.; Chertok, M.; Conway, J.; Conway, R.; Cox, P. T.; Erbacher, R.; Flores, C.; Funk, G.; Gardner, M.; Ko, W.; Lander, R.; Mclean, C.; Mulhearn, M.; Pellett, D.; Pilot, J.; Shalhout, S.; Shi, M.; Smith, J.; Stolp, D.; Tos, K.; Tripathi, M.; Wang, Z.; Bachtis, M.; Bravo, C.; Cousins, R.; Dasgupta, A.; Florent, A.; Hauser, J.; Ignatenko, M.; Mccoll, N.; Regnard, S.; Saltzberg, D.; Schnaible, C.; Valuev, V.; Bouvier, E.; Burt, K.; Clare, R.; Ellison, J.; Gary, J. W.; Ghiasi Shirazi, S. M. A.; Hanson, G.; Heilman, J.; Kennedy, E.; Lacroix, F.; Long, O. R.; Olmedo Negrete, M.; Paneva, M. I.; Si, W.; Wang, L.; Wei, H.; Wimpenny, S.; Yates, B. R.; Branson, J. G.; Cittolin, S.; Derdzinski, M.; Gerosa, R.; Gilbert, D.; Hashemi, B.; Holzner, A.; Klein, D.; Kole, G.; Krutelyov, V.; Letts, J.; Macneill, I.; Masciovecchio, M.; Olivito, D.; Padhi, S.; Pieri, M.; Sani, M.; Sharma, V.; Simon, S.; Tadel, M.; Vartak, A.; Wasserbaech, S.; Wood, J.; Würthwein, F.; Yagil, A.; Zevi Della Porta, G.; Amin, N.; Bhandari, R.; Bradmiller-Feld, J.; Campagnari, C.; Dishaw, A.; Dutta, V.; Franco Sevilla, M.; George, C.; Golf, F.; Gouskos, L.; Gran, J.; Heller, R.; Incandela, J.; Mullin, S. D.; Ovcharova, A.; Qu, H.; Richman, J.; Stuart, D.; Suarez, I.; Yoo, J.; Anderson, D.; Bendavid, J.; Bornheim, A.; Lawhorn, J. M.; Newman, H. B.; Nguyen, T.; Pena, C.; Spiropulu, M.; Vlimant, J. R.; Xie, S.; Zhang, Z.; Zhu, R. Y.; Andrews, M. B.; Ferguson, T.; Mudholkar, T.; Paulini, M.; Russ, J.; Sun, M.; Vogel, H.; Vorobiev, I.; Weinberg, M.; Cumalat, J. P.; Ford, W. T.; Jensen, F.; Johnson, A.; Krohn, M.; Leontsinis, S.; Mulholland, T.; Stenson, K.; Wagner, S. R.; Alexander, J.; Chaves, J.; Chu, J.; Dittmer, S.; Mcdermott, K.; Mirman, N.; Patterson, J. R.; Quach, D.; Rinkevicius, A.; Ryd, A.; Skinnari, L.; Soffi, L.; Tan, S. M.; Tao, Z.; Thom, J.; Tucker, J.; Wittich, P.; Zientek, M.; Abdullin, S.; Albrow, M.; Alyari, M.; Apollinari, G.; Apresyan, A.; Apyan, A.; Banerjee, S.; Bauerdick, L. A. T.; Beretvas, A.; Berryhill, J.; Bhat, P. C.; Bolla, G.; Burkett, K.; Butler, J. N.; Canepa, A.; Cerati, G. B.; Cheung, H. W. K.; Chlebana, F.; Cremonesi, M.; Duarte, J.; Elvira, V. D.; Freeman, J.; Gecse, Z.; Gottschalk, E.; Gray, L.; Green, D.; Grünendahl, S.; Gutsche, O.; Harris, R. M.; Hasegawa, S.; Hirschauer, J.; Hu, Z.; Jayatilaka, B.; Jindariani, S.; Johnson, M.; Joshi, U.; Klima, B.; Kreis, B.; Lammel, S.; Lincoln, D.; Lipton, R.; Liu, M.; Liu, T.; Lopes De Sá, R.; Lykken, J.; Maeshima, K.; Magini, N.; Marraffino, J. M.; Mason, D.; McBride, P.; Merkel, P.; Mrenna, S.; Nahn, S.; O'Dell, V.; Pedro, K.; Prokofyev, O.; Rakness, G.; Ristori, L.; Schneider, B.; Sexton-Kennedy, E.; Soha, A.; Spalding, W. J.; Spiegel, L.; Stoynev, S.; Strait, J.; Strobbe, N.; Taylor, L.; Tkaczyk, S.; Tran, N. V.; Uplegger, L.; Vaandering, E. W.; Vernieri, C.; Verzocchi, M.; Vidal, R.; Wang, M.; Weber, H. A.; Whitbeck, A.; Acosta, D.; Avery, P.; Bortignon, P.; Bourilkov, D.; Brinkerhoff, A.; Carnes, A.; Carver, M.; Curry, D.; Field, R. D.; Furic, I. K.; Gleyzer, S. V.; Joshi, B. M.; Konigsberg, J.; Korytov, A.; Kotov, K.; Ma, P.; Matchev, K.; Mei, H.; Mitselmakher, G.; Rank, D.; Shi, K.; Sperka, D.; Terentyev, N.; Thomas, L.; Wang, J.; Wang, S.; Yelton, J.; Joshi, Y. R.; Linn, S.; Markowitz, P.; Rodriguez, J. L.; Ackert, A.; Adams, T.; Askew, A.; Hagopian, S.; Hagopian, V.; Johnson, K. F.; Kolberg, T.; Martinez, G.; Perry, T.; Prosper, H.; Saha, A.; Santra, A.; Sharma, V.; Yohay, R.; Baarmand, M. M.; Bhopatkar, V.; Colafranceschi, S.; Hohlmann, M.; Noonan, D.; Roy, T.; Yumiceva, F.; Adams, M. R.; Apanasevich, L.; Berry, D.; Betts, R. R.; Cavanaugh, R.; Chen, X.; Evdokimov, O.; Gerber, C. E.; Hangal, D. A.; Hofman, D. J.; Jung, K.; Kamin, J.; Sandoval Gonzalez, I. D.; Tonjes, M. B.; Trauger, H.; Varelas, N.; Wang, H.; Wu, Z.; Zhang, J.; Bilki, B.; Clarida, W.; Dilsiz, K.; Durgut, S.; Gandrajula, R. P.; Haytmyradov, M.; Khristenko, V.; Merlo, J.-P.; Mermerkaya, H.; Mestvirishvili, A.; Moeller, A.; Nachtman, J.; Ogul, H.; Onel, Y.; Ozok, F.; Penzo, A.; Snyder, C.; Tiras, E.; Wetzel, J.; Yi, K.; Blumenfeld, B.; Cocoros, A.; Eminizer, N.; Fehling, D.; Feng, L.; Gritsan, A. V.; Maksimovic, P.; Roskes, J.; Sarica, U.; Swartz, M.; Xiao, M.; You, C.; Al-bataineh, A.; Baringer, P.; Bean, A.; Boren, S.; Bowen, J.; Castle, J.; Khalil, S.; Kropivnitskaya, A.; Majumder, D.; Mcbrayer, W.; Murray, M.; Royon, C.; Sanders, S.; Schmitz, E.; Tapia Takaki, J. D.; Wang, Q.; Ivanov, A.; Kaadze, K.; Maravin, Y.; Mohammadi, A.; Saini, L. K.; Skhirtladze, N.; Toda, S.; Rebassoo, F.; Wright, D.; Anelli, C.; Baden, A.; Baron, O.; Belloni, A.; Calvert, B.; Eno, S. C.; Feng, Y.; Ferraioli, C.; Hadley, N. J.; Jabeen, S.; Jeng, G. Y.; Kellogg, R. G.; Kunkle, J.; Mignerey, A. C.; Ricci-Tam, F.; Shin, Y. H.; Skuja, A.; Tonwar, S. C.; Abercrombie, D.; Allen, B.; Azzolini, V.; Barbieri, R.; Baty, A.; Bi, R.; Brandt, S.; Busza, W.; Cali, I. A.; D'Alfonso, M.; Demiragli, Z.; Gomez Ceballos, G.; Goncharov, M.; Hsu, D.; Hu, M.; Iiyama, Y.; Innocenti, G. M.; Klute, M.; Kovalskyi, D.; Lai, Y. S.; Lee, Y.-J.; Levin, A.; Luckey, P. D.; Maier, B.; Marini, A. C.; Mcginn, C.; Mironov, C.; Narayanan, S.; Niu, X.; Paus, C.; Roland, C.; Roland, G.; Salfeld-Nebgen, J.; Stephans, G. S. F.; Tatar, K.; Velicanu, D.; Wang, J.; Wang, T. W.; Wyslouch, B.; Benvenuti, A. C.; Chatterjee, R. M.; Evans, A.; Hansen, P.; Hiltbrand, J.; Kalafut, S.; Kubota, Y.; Lesko, Z.; Mans, J.; Nourbakhsh, S.; Ruckstuhl, N.; Rusack, R.; Turkewitz, J.; Wadud, M. A.; Acosta, J. G.; Oliveros, S.; Avdeeva, E.; Bloom, K.; Claes, D. R.; Fangmeier, C.; Gonzalez Suarez, R.; Kamalieddin, R.; Kravchenko, I.; Monroy, J.; Siado, J. E.; Snow, G. R.; Stieger, B.; Dolen, J.; Godshalk, A.; Harrington, C.; Iashvili, I.; Nguyen, D.; Parker, A.; Rappoccio, S.; Roozbahani, B.; Alverson, G.; Barberis, E.; Hortiangtham, A.; Massironi, A.; Morse, D. M.; Orimoto, T.; Teixeira De Lima, R.; Trocino, D.; Wood, D.; Bhattacharya, S.; Charaf, O.; Hahn, K. A.; Mucia, N.; Odell, N.; Pollack, B.; Schmitt, M. H.; Sung, K.; Trovato, M.; Velasco, M.; Dev, N.; Hildreth, M.; Hurtado Anampa, K.; Jessop, C.; Karmgard, D. J.; Kellams, N.; Lannon, K.; Loukas, N.; Marinelli, N.; Meng, F.; Mueller, C.; Musienko, Y.; Planer, M.; Reinsvold, A.; Ruchti, R.; Smith, G.; Taroni, S.; Wayne, M.; Wolf, M.; Woodard, A.; Alimena, J.; Antonelli, L.; Bylsma, B.; Durkin, L. S.; Flowers, S.; Francis, B.; Hart, A.; Hill, C.; Ji, W.; Liu, B.; Luo, W.; Puigh, D.; Winer, B. L.; Wulsin, H. W.; Cooperstein, S.; Driga, O.; Elmer, P.; Hardenbrook, J.; Hebda, P.; Higginbotham, S.; Lange, D.; Luo, J.; Marlow, D.; Mei, K.; Ojalvo, I.; Olsen, J.; Palmer, C.; Piroué, P.; Stickland, D.; Tully, C.; Malik, S.; Norberg, S.; Barker, A.; Barnes, V. E.; Das, S.; Folgueras, S.; Gutay, L.; Jha, M. K.; Jones, M.; Jung, A. W.; Khatiwada, A.; Miller, D. H.; Neumeister, N.; Peng, C. C.; Qiu, H.; Schulte, J. F.; Sun, J.; Wang, F.; Xie, W.; Cheng, T.; Parashar, N.; Stupak, J.; Adair, A.; Chen, Z.; Ecklund, K. M.; Freed, S.; Geurts, F. J. M.; Guilbaud, M.; Kilpatrick, M.; Li, W.; Michlin, B.; Northup, M.; Padley, B. P.; Roberts, J.; Rorie, J.; Shi, W.; Tu, Z.; Zabel, J.; Zhang, A.; Bodek, A.; de Barbaro, P.; Demina, R.; Duh, Y. t.; Ferbel, T.; Galanti, M.; Garcia-Bellido, A.; Han, J.; Hindrichs, O.; Khukhunaishvili, A.; Lo, K. H.; Tan, P.; Verzetti, M.; Ciesielski, R.; Goulianos, K.; Mesropian, C.; Agapitos, A.; Chou, J. P.; Gershtein, Y.; Gómez Espinosa, T. A.; Halkiadakis, E.; Heindl, M.; Hughes, E.; Kaplan, S.; Kunnawalkam Elayavalli, R.; Kyriacou, S.; Lath, A.; Montalvo, R.; Nash, K.; Osherson, M.; Saka, H.; Salur, S.; Schnetzer, S.; Sheffield, D.; Somalwar, S.; Stone, R.; Thomas, S.; Thomassen, P.; Walker, M.; Delannoy, A. G.; Foerster, M.; Heideman, J.; Riley, G.; Rose, K.; Spanier, S.; Thapa, K.; Bouhali, O.; Castaneda Hernandez, A.; Celik, A.; Dalchenko, M.; De Mattia, M.; Delgado, A.; Dildick, S.; Eusebi, R.; Gilmore, J.; Huang, T.; Kamon, T.; Mueller, R.; Pakhotin, Y.; Patel, R.; Perloff, A.; Perniè, L.; Rathjens, D.; Safonov, A.; Tatarinov, A.; Ulmer, K. A.; Akchurin, N.; Damgov, J.; De Guio, F.; Dudero, P. R.; Faulkner, J.; Gurpinar, E.; Kunori, S.; Lamichhane, K.; Lee, S. W.; Libeiro, T.; Mengke, T.; Muthumuni, S.; Peltola, T.; Undleeb, S.; Volobouev, I.; Wang, Z.; Greene, S.; Gurrola, A.; Janjam, R.; Johns, W.; Maguire, C.; Melo, A.; Ni, H.; Padeken, K.; Sheldon, P.; Tuo, S.; Velkovska, J.; Xu, Q.; Arenton, M. W.; Barria, P.; Cox, B.; Hirosky, R.; Joyce, M.; Ledovskoy, A.; Li, H.; Neu, C.; Sinthuprasith, T.; Wang, Y.; Wolfe, E.; Xia, F.; Harr, R.; Karchin, P. E.; Poudyal, N.; Sturdy, J.; Thapa, P.; Zaleski, S.; Brodski, M.; Buchanan, J.; Caillol, C.; Dasu, S.; Dodd, L.; Duric, S.; Gomber, B.; Grothe, M.; Herndon, M.; Hervé, A.; Hussain, U.; Klabbers, P.; Lanaro, A.; Levine, A.; Long, K.; Loveless, R.; Polese, G.; Ruggles, T.; Savin, A.; Smith, N.; Smith, W. H.; Taylor, D.; Woods, N.; CMS Collaboration

2018-04-01

Data from heavy ion collisions suggest that the evolution of a parton shower is modified by interactions with the color charges in the dense partonic medium created in these collisions, but it is not known where in the shower evolution the modifications occur. The momentum ratio of the two leading partons, resolved as subjets, provides information about the parton shower evolution. This substructure observable, known as the splitting function, reflects the process of a parton splitting into two other partons and has been measured for jets with transverse momentum between 140 and 500 GeV, in p p and PbPb collisions at a center-of-mass energy of 5.02 TeV per nucleon pair. In central PbPb collisions, the splitting function indicates a more unbalanced momentum ratio, compared to peripheral PbPb and p p collisions.. The measurements are compared to various predictions from event generators and analytical calculations.

MiR-200c suppresses the migration of retinoblastoma cells by reversing epithelial mesenchymal transition

Directory of Open Access Journals (Sweden)

Xiao-Lei Shao

2017-08-01

Full Text Available AIM: To analyze the relationship between clinical features and epithelial mesenchymal transition (EMT in retinoblastoma (RB, further to investigate whether miR-200c regulates the EMT and migration of RB cells. METHODS: Expression of EMT-related markers and tumor-related factors were detected by immuno-histochemistry analysis in RB tissue from 29 cases. Correlations between their expression and clinical characteristics were analyzed. The regulation effects of miR-200c on EMT-related markers, tumor-related factors were observed in mRNA level and protein level by real-time polymerase chain reaction (PCR and Western blot, respectively, in Y79 and Weri-rb1 cells. Its effects on migration force of these RB cell lines were also detected with Transwell test. RESULTS: Lower expression of E-cadherin was present in the cases with malignant prognosis. MiR-200c promoted the expression of E-cadherin and decreased the expression of Vimentin and N-cadherin in Y79 and Weri-rb1 cells. Migration force of RB cells could be inhibited by miR-200c. CONCLUSION: EMT might be associated with bad prognosis in RB. MiR-200c suppresses the migration of retinoblastomatous cells by reverse EMT.

miR-338-3p functions as a tumor suppressor in gastric cancer by targeting PTP1B.

Science.gov (United States)

Sun, Feng; Yu, Mengchao; Yu, Jing; Liu, Zhijian; Zhou, Xinyan; Liu, Yanqing; Ge, Xiaolong; Gao, Haidong; Li, Mei; Jiang, Xiaohong; Liu, Song; Chen, Xi; Guan, Wenxian

2018-05-09

Gastric cancer (GC) is one of the most common malignant tumors and peritoneal metastasis is the primary cause for advanced GC's mortality. Protein-tyrosine phosphatase 1B (PTP1B) functions as an oncogene and involves in carcinogenesis and cancer dissemination. However, the function and regulation of PTP1B in GC remain poorly understood. In this study, we found that PTP1B was upregulated in GC tissues and overexpression of PTP1B in vitro promoted cell migration and prevented apoptosis. Then, we predicted that PTP1B was a target of miR-338-3p and we revealed an inverse correlation between miR-338-3p levels and PTP1B protein levels in GC tissues. Next, we verified that PTP1B was inhibited by miR-338-3p via direct targeting to its 3'-untranslated regions. Moreover, overexpression of miR-338-3p in vitro attenuated GC cell migration and promoted apoptosis, and these effects could be partially reversed by reintroduction of PTP1B. Finally, we established an orthotopic xenograft model and a peritoneal dissemination model of GC to demonstrate that miR-338-3p restrained tumor growth and dissemination in vivo by targeting PTP1B. Taken together, our results highlight that PTP1B is an oncogene and is negatively regulated by miR-338-3p in GC, which may provide new insights into novel molecular therapeutic targets for GC.

Association of miR-548c-5p, miR-7-5p, miR-210-3p, miR-128-3p with recurrence in systemically untreated breast cancer

DEFF Research Database (Denmark)

Block, Ines; Burton, Mark; Sørensen, Kristina Pilekær

2018-01-01

. To validate their prognostic potential, we analyzed microRNA expression in an independent cohort (n = 110) using a pairmatched study design minimizing dependence of classical markers. The expression of hsa-miR-548c-5p was significantly associated with abridged disease-free survival (hazard ratio [HR]:1.96, p...... = 0.027). Contradicting published results, high hsa-miR516-3p expression was associated with favorable outcome (HR:0.29, p = 0.0068). The association is probably time-dependent indicating later relapse. Additionally, re-analysis of previously published expression data of two matching cohorts (n = 100......, n = 255) supports an association of hsa-miR-128-3p with shortened diseasefree survival (HR:2.48, p = 0.0033) and an upregulation of miR-7-5p (p = 0.0038; p = 0.039) and miR-210-3p (p = 0.031) in primary tumors of patients who experienced metastases. Further analysis may verify the prognostic...

Regulation of Glioma Cell Migration by Seri ne-Phosphorylated P3111

Directory of Open Access Journals (Sweden)

Wendy S. McDonough

2005-09-01

Full Text Available P311, an 8-kDa polypeptide, was previously shown to be highly expressed in invasive glioma cells. Here, we report the functional characteristics of P311 with regard to influencing glioma cell migration. P311 is constitutively serine-phosphorylated; decreased phosphorylation is observed in migration-activated glioma cells. The primary amino acid sequence of P311 indicates a putative serine phosphorylation site (S59 near the PEST domain. Site-directed mutagenesis of S59A retarded P311 degradation, induced glioma cell motility. In contrast, S59D mutation resulted in the rapid degradation of P311, reduced glioma cell migration. Coimmunoprecipitation coupled with matrixassisted laser desorption/ionization time-of-flight mass spectrometry analysis identified Filamin A as a binding partner of P311, immunofluorescence studies showed that both proteins colocalized at the cell periphery. Moreover, P311-induced cell migration was abrogated by inhibition of β1 integrin function using TACβ1A, a dominant-negative inhibitor of β1 integrin signaling, suggesting that P311 acts downstream of β1 signaling. Finally, overexpression of P311 or P311 S59A mutant protein activates Raci GTPase; small interfering RNA-mediated depletion of Raci suppresses P311-induced motility. Collectively, these results suggest a role for levels of P311 in regulating glioma motility, invasion through the reorganization of actin cytoskeleton at the cell periphery.

miR-625 suppresses cell proliferation and migration by targeting HMGA1 in breast cancer

Energy Technology Data Exchange (ETDEWEB)

Zhou, Wen-bin; Zhong, Cai-neng; Luo, Xun-peng; Zhang, Ya-yuan; Zhang, Gui-ying [Department of Breast Surgery, Second Clinical Medical College of Jinan University, Shenzhen People' s Hospital, Shenzhen, Guangdong Province (China); Zhou, Dong-xian, E-mail: 1072241978@qq.com [Department of Breast Surgery, Second Clinical Medical College of Jinan University, Shenzhen People' s Hospital, Shenzhen, Guangdong Province (China); Liu, Li-ping, E-mail: leoliping@aliyun.com [Department of Hepatobiliary and Pancreas Surgery, Second Clinical Medical College of Jinan University, Shenzhen People' s Hospital, Shenzhen, Guangdong Province (China)

2016-02-19

Dysregulation of microRNA contributes to the high incidence and mortality of breast cancer. Here, we show that miR-625 was frequently down-regulated in breast cancer. Decrease of miR-625 was closely associated with estrogen receptor (P = 0.004), human epidermal growth factor receptor 2 (P = 0.003) and clinical stage (P = 0.001). Kaplan–Meier and multivariate analyses indicated miR-625 as an independent factor for unfavorable prognosis (hazard ratio = 2.654, 95% confident interval: 1.300–5.382, P = 0.007). Re-expression of miR-625 impeded, whereas knockdown of miR-625 enhanced cell viabilities and migration abilities in breast cancer cells. HMGA1 was confirmed as a direct target of miR-625. The expressions of HMGA1 mRNA and protein were induced by miR-625 mimics, but reduced by miR-625 inhibitor. Re-introduction of HMGA1 in cells expressing miR-625 distinctly abrogated miR-625-mediated inhibition of cell growth. Taken together, our data demonstrate that miR-625 suppresses cell proliferation and migration by targeting HMGA1 and suggest miR-625 as a promising prognostic biomarker and a potential therapeutic target for breast cancer. - Highlights: • miR-625 expression was significantly decreased in breast cancer. • Decrease of miR-625 was associated with poor clinical outcomes and unfavorable overall survival. • miR-625 overexpression inhibits cell proliferation and migration in vitro. • miR-625 directly targets and suppresses the expression of HMGA1.

Downregulation of miR-200a-3p induced by hepatitis B Virus X (HBx) Protein promotes cell proliferation and invasion in HBV-infection-associated hepatocarcinoma.

Science.gov (United States)

Shi, Taiyang; Hua, Qinfang; Ma, Zhipeng; Lv, Qijun

2017-12-01

Hepatitis B Virus X (HBx) Protein encoded by HBV is believed to be the major player in the process of HBV-induced oncogenesis. Ectopic expression of miR-200a-3p was reported to be associated with diverse tumorigenesis. This study aimed to better understand the role of miR-200a-3p and its correlation with HBx in HBV-induced hepatocellular carcinoma (HCC). In this report, we examined the gene expression using quantitative RT-PCR and protein expression using Western blotting analysis. Cells were transfected with miR-200a-3p mimics or empty vector, and HBx-carrying vector or empty vector. Cell viability was tested using CCK-8 assay. Wound healing assay was performed to assess cell migration while Transwell assay was performed to evaluate cell invasion. miR-200a-3p was downregulated in HBV-positive tissue samples compared with HBV-negative tissue samples. This result was further confirmed with HBV-positive and - negative cell lines. HBx protein was overexpressed in HBV-positive cells where expression of miR-200a-3p was significantly suppressed. Increased cell viability, altered cell cycle progression, increased cell migration and invasion occurred in HBx-overexpressed cells compared to its controls. In forced expressed miR-200a-3p cells, cell viability, cell migration and invasion were significantly decreased, and cell cycle status was altered compared to its controls. Taken together, pathogenetic function of HBx is negatively correlated with miR-200a-3p in HBV-cased HCC through regulating cell viability, cell cycle arrest, cell migration and cell invasion. Copyright © 2017 Elsevier GmbH. All rights reserved.

P R Halmos

Indian Academy of Sciences (India)

Home; Journals; Resonance – Journal of Science Education. P R Halmos. Articles written in Resonance – Journal of Science Education. Volume 12 Issue 2 February 2007 pp 83-95 Classics. The Thrills of Abstraction · P R Halmos · More Details Fulltext PDF ...

IGF-1R Promotes Symmetric Self-Renewal and Migration of Alkaline Phosphatase+ Germ Stem Cells through HIF-2α-OCT4/CXCR4 Loop under Hypoxia

Directory of Open Access Journals (Sweden)

Yung-Che Kuo

2018-02-01

Full Text Available Summary: Hypoxia cooperates with endocrine signaling to maintain the symmetric self-renewal proliferation and migration of embryonic germline stem cells (GSCs. However, the lack of an appropriate in vitro cell model has dramatically hindered the understanding of the mechanism underlying this cooperation. Here, using a serum-free system, we demonstrated that hypoxia significantly induced the GSC mesenchymal transition, increased the expression levels of the pluripotent transcription factor OCT4 and migration-associated proteins (SDF-1, CXCR4, IGF-1, and IGF-1R, and activated the cellular expression and translocalization of the CXCR4-downstream proteins ARP3/pFAK. The underlying mechanism involved significant IGF-1/IGF-1R activation of OCT4/CXCR4 expression through HIF-2α regulation. Picropodophyllin-induced inhibition of IGF-1R phosphorylation significantly suppressed hypoxia-induced SDF-1/CXCR4 expression and cell migration. Furthermore, transactivation between IGF-1R and CXCR4 was involved. In summary, we demonstrated that niche hypoxia synergistically cooperates with its associated IGF-1R signaling to regulate the symmetric division (self-renewal proliferation and cell migration of alkaline phosphatase-positive GSCs through HIF-2α-OCT4/CXCR4 during embryogenesis. : In this article, Huang and colleagues demonstrate that niche hypoxia promotes symmetric self-renewal proliferation and migration of PGC-like CD49f+AP+GSCs through IGF-IR regulation. Using a serum-free culture system, the crosstalk between IGF-1R and CXCR4 signaling was discovered. This work demonstrated that embryonic hypoxia synergistically cooperated with IGF-1R signaling to regulate the symmetric self-renewal and migration of PGC-like GSCs through a HIF-2α–OCT4/CXCR4 loop. Keywords: hypoxia, niche, germline stem cells, self-renewal, migration, IGF-1R, HIF-2α, OCT4, SDF-1, CXCR4

[Migrations in Latin American countries. Characteristics of the pediatric population].

Science.gov (United States)

Vásquez-De Kartzow, Rodrigo; Castillo-Durán, Carlos; Lera M, Lydia

2015-01-01

Migration is a growing phenomenon among Latin American countries (LAC) as well as others; however, scarce information is available studying its impact on paediatric groups and its association with socioeconomic variables. To study the association among socioeconomic variables and the immigration rate of paediatric population in LAC. Official rates of migration of LAC were obtained from: International Organization for Migration, Pan American Health Organization, and United Nations Development Programme. Demographic and socioeconomic information was also obtained for: gross domestic product (GDP), human development index (HDI), Gini coefficient of inequality (GC), alphabetization rate for adults (AA), net migration rate (NMR), and immigration of childrenChile and Argentina. No association among NMR and GDP, HDI, GC, AA was found. A correlation of IM15 was found with: GC (r=0.668, P=.01), with GDP (r=-0.720; P=.01), AA (r=-0.755; P=.01) and with HDI (r=-0.799; P=.01). Rate of IM15 was lower in LA countries with advanced/medium development (GDP>median) vs those with low development (Fisher, P<.0001). There is a direct inverse association between GDP per capita, HDI, AA and GC and the proportion of each country IN15. We did not observe an association between NMR and HDI, AA, and GC. The health impact of these migrations should be analysed. Copyright © 2015. Publicado por Elsevier España, S.L.U.

Effect of miR-146a-5p on proliferation and metastasis of triple-negative breast cancer via regulation of SOX5.

Science.gov (United States)

Si, Chengshuai; Yu, Qiao; Yao, Yufeng

2018-05-01

MicroRNA (miR)-146a-5p functions as a tumor suppressor in various types of cancer. However, the role of miR-146a-5p in the development of triple-negative breast cancer (TNBC) is unclear. The present study aimed to investigate the role of miR-146a-5p in TNBC. The expression level of miR-146a-5p in TNBC tissues and cell lines was initially detected using reverse transcription-quantitative polymerase chain reaction. To predict the target gene of miR-146a-5p, TargetScan software was used and a dual luciferase assay was performed to verify the prediction. Furthermore, in order to explore the role of miR-146a-5p in TNBC, miR-146a-5p was overexpressed in TNBC cells using miR-146a-5p mimics. An MTT assay was performed to detect cell proliferation, and a Transwell assay was conducted to determine cell migration and invasion. Furthermore, western blotting was performed to measure associated protein expression. It was revealed that miR-146a-5p was downregulated in TNBC tissues and cell lines. SOX5 was indicated to be a target gene of miR-146a-5p and was upregulated in TNBC cells. Additionally, miR-146a-5p could inhibit TNBC cell proliferation, migration and invasion, repress the expression of mesenchymal markers (N-cadherin, vimentin and fibronectin) and increase epithelial marker (E-cadherin) expression. Furthermore, SOX5 overexpression eliminated the effects of miR-146a-5p mimics on TNBC cells. In conclusion, the data of the present study indicated that miR-146a-5p inhibits the proliferation and metastasis of TNBC cells by regulating SOX5.

P R Viswanath

Indian Academy of Sciences (India)

Home; Journals; Sadhana. P R Viswanath. Articles written in Sadhana. Volume 32 Issue 1-2 February-April 2007 pp 83-92. Some thoughts on separation control strategies · P R Viswanath · More Details Abstract Fulltext PDF. Separation control has received considerable emphasis in literature both owing to fundamental ...

R P Shukla

Indian Academy of Sciences (India)

Home; Journals; Sadhana. R P Shukla. Articles written in Sadhana. Volume 25 Issue 1 February 2000 pp 57-69. Design, fabrication and performance evaluation of a 22-channel direct reading atomic emission spectrometer using inductively coupled plasma as a source of excitation · R P Shukla S S Bhattacharya D V Udupa ...

miR-139 is up-regulated in osteoarthritis and inhibits chondrocyte proliferation and migration possibly via suppressing EIF4G2 and IGF1R

Energy Technology Data Exchange (ETDEWEB)

Hu, Weihua; Zhang, Weikai; Li, Feng; Guo, Fengjing; Chen, Anmin, E-mail: chenanmin6072@126.com

2016-05-27

Osteoarthritis (OA) is one of the most progressive articular cartilage erosions. microRNAs (miRNAs) play pivotal roles in OA modulation, but the role of miR-139 in OA remains elusive. This study aims to reveal the effects and possible mechanism of miR-139 in OA and chondrocytes. The levels of miR-139 and its possible targets eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) and insulin-like growth factor 1 receptor (IGF1R) were detected by qRT-PCR in the articular cartilages of 20 OA patients and 20 non-OA patients. Human chondrocyte CHON-001 cells were transfected with miR-139 mimic or inhibitor, as well as the siRNAs of EIF4G2 and IGF1R. Cell viability by MTT assay, proliferation by colony formation assay and migration by Transwell assay were performed. Results showed that miR-139 was up-regulated, while EIF4G2 and IGF1R mRNAs down-regulated in OA cartilages (P < 0.001), and negative correlations existed between the level of miR-139 and EIF4G2 or IGF1R. Overexpression of miR-139 in CHON-001 cells suppressed both mRNA and protein levels of EIF4G2 and IGF1R, and inhibited cell viability, colony formation number and cell migration, while miR-139 inhibitor induced the opposite effects. Knockdown of EIF4G2 or IGF1R in CHON-001 cells reversed the effects of miR-139 inhibitor on cell viability, colony formation and cell migration. These results indicate that miR-139 is capable of inhibiting chondrocyte proliferation and migration, thus being a possible therapeutic target for OA. The mechanism of miR-139 in chondrocytes may be related to its regulation on EIF4G2 and IGF1R.

La migration des hydrocarbures dans les bassins sédimentaires: aspects géologiques et géochimiques Migration of Hydrocarbons in Sedimentary Basins: Geological and Geochemical Aspects

OpenAIRE

Tissot B. P.

2006-01-01

La migration du pétrole vers les réservoirs et les pièges, et particulièrement son expulsion hors de la roche-mère où il s'est formé (migration primaire), est demeurée longtemps un des problèmes les plus mal connus de toute la géologie pétrolière. Le déplacement du pétrole et du gaz s'effectue en phase hydrocarbure séparée. L'eau, souvent considérée comme le véhicule du pétrole dans la migration, joue en fait un rôle négatif : il faut que la saturation en eau ait suffisamment diminué (par exp...

MiR-132 prohibits proliferation, invasion, migration, and metastasis in breast cancer by targeting HN1

Energy Technology Data Exchange (ETDEWEB)

Zhang, Zhan-Guo, E-mail: zhang_zhanguo@hotmail.com; Chen, Wei-Xun, E-mail: chenweixunclark@163.com; Wu, Yan-Hui, E-mail: wuyanhui84@126.com; Liang, Hui-Fang, E-mail: lianghuifang1997@126.com; Zhang, Bi-Xiang, E-mail: bixiangzhang@163.com

2014-11-07

Highlights: • MiR-132 is down-regulated in breast cancer tissues and cell lines. • MiR-132 directly regulates HN1 by binding its 3′ UTR. • MiR-132 shows regulatory role in proliferation, invasion, migration and metastasis. • HN1 is involved in miR-132-mediated cell behavior. • Aberrant HN1 is associated with worse overall survival of breast cancer patients. - Abstract: Accumulating evidence indicates that miRNAs play critical roles in tumorigenesis and cancer progression. This study aims to investigate the role and the underlying mechanism of miR-132 in breast cancer. Here, we report that miR-132 is significantly down-regulated in breast cancer tissues and cancer cell lines. Additional study identifies HN1 as a novel direct target of miR-132. MiR-132 down-regulates HN1 expression by binding to the 3′ UTR of HN1 transcript, thereby, suppressing multiple oncogenic traits such as cancer cell proliferation, invasion, migration and metastasis in vivo and in vitro. Overexpression of HN1 restores miR-132-suppressed malignancy. Importantly, higher HN1 expression is significantly associated with worse overall survival of breast cancer patients. Taken together, our data demonstrate a critical role of miR-132 in prohibiting cell proliferation, invasion, migration and metastasis in breast cancer through direct suppression of HN1, supporting the potential utility of miR-132 as a novel therapeutic strategy against breast cancer.

P R Deshmukh

Indian Academy of Sciences (India)

Home; Journals; Bulletin of Materials Science. P R Deshmukh. Articles written in Bulletin of Materials Science. Volume 34 Issue 6 October 2011 pp 1179-1183. Chemical synthesis and characterization of hydrous tin oxide (SnO2:H2O) thin films · S N Pusawale P R Deshmukh C D Lokhande · More Details Abstract Fulltext ...

P R Sengupta

Indian Academy of Sciences (India)

Home; Journals; Sadhana. P R Sengupta. Articles written in Sadhana. Volume 26 Issue 4 August 2001 pp 363-370. Surface waves in fibre-reinforced anisotropic elastic media · P R Sengupta Sisir Nath · More Details Abstract Fulltext PDF. The aim of this paper is to investigate surface waves in anisotropic fibre-reinforced ...

P R Sarma

Indian Academy of Sciences (India)

Home; Journals; Pramana – Journal of Physics. P R Sarma. Articles written in Pramana – Journal of Physics. Volume 67 Issue 3 September 2006 pp 477-486 Research Articles. Experimental study of the dependence of beam current on injection magnetic field in 6.4 GHz ECR ion source · G S Taki P R Sarma D K ...

IL-8 induces miR-424-5p expression and modulates SOCS2/STAT5 signaling pathway in oral squamous cell carcinoma.

Science.gov (United States)

Peng, Hsuan-Yu; Jiang, Shih-Sheng; Hsiao, Jenn-Ren; Hsiao, Michael; Hsu, Yuan-Ming; Wu, Guan-Hsun; Chang, Wei-Min; Chang, Jang-Yang; Jin, Shiow-Lian Catherine; Shiah, Shine-Gwo

2016-06-01

Suppressor of cytokine signaling (SOCS) proteins are negative feedback regulators of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Dysregulation of SOCS protein expression in cancers can be one of the mechanisms that maintain STAT activation, but this mechanism is still poorly understood in oral squamous cell carcinoma (OSCC). Here, we report that SOCS2 protein is significantly downregulated in OSCC patients and its levels are inversely correlated with miR-424-5p expression. We identified the SOCS2 protein, which modulates STAT5 activity, as a direct target of miR-424-5p. The miR-424-5p-induced STAT5 phosphorylation, matrix metalloproteinases (MMPs) expression, and cell migration and invasion were blocked by SOCS2 restoration, suggesting that miR-424-5p exhibits its oncogenic activity through negatively regulating SOCS2 levels. Furthermore, miR-424-5p expression could be induced by the cytokine IL-8 primarily through enhancing STAT5 transcriptional activity rather than NF-κB signaling. Antagomir-mediated inactivation of miR-424-5p prevented the IL-8-induced cell migration and invasion, indicating that miR-424-5p is required for IL-8-induced cellular invasiveness. Taken together, these data indicate that STAT5-dependent expression of miR-424-5p plays an important role in mediating IL-8/STAT5/SOCS2 feedback loop, and scavenging miR-424-5p function using antagomir may have therapeutic potential for the treatment of OSCC. Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.

IGF-1R Promotes Symmetric Self-Renewal and Migration of Alkaline Phosphatase+ Germ Stem Cells through HIF-2α-OCT4/CXCR4 Loop under Hypoxia.

Science.gov (United States)

Kuo, Yung-Che; Au, Heng-Kien; Hsu, Jue-Liang; Wang, Hsiao-Feng; Lee, Chiung-Ju; Peng, Syue-Wei; Lai, Ssu-Chuan; Wu, Yu-Chih; Ho, Hong-Nerng; Huang, Yen-Hua

2018-02-13

Hypoxia cooperates with endocrine signaling to maintain the symmetric self-renewal proliferation and migration of embryonic germline stem cells (GSCs). However, the lack of an appropriate in vitro cell model has dramatically hindered the understanding of the mechanism underlying this cooperation. Here, using a serum-free system, we demonstrated that hypoxia significantly induced the GSC mesenchymal transition, increased the expression levels of the pluripotent transcription factor OCT4 and migration-associated proteins (SDF-1, CXCR4, IGF-1, and IGF-1R), and activated the cellular expression and translocalization of the CXCR4-downstream proteins ARP3/pFAK. The underlying mechanism involved significant IGF-1/IGF-1R activation of OCT4/CXCR4 expression through HIF-2α regulation. Picropodophyllin-induced inhibition of IGF-1R phosphorylation significantly suppressed hypoxia-induced SDF-1/CXCR4 expression and cell migration. Furthermore, transactivation between IGF-1R and CXCR4 was involved. In summary, we demonstrated that niche hypoxia synergistically cooperates with its associated IGF-1R signaling to regulate the symmetric division (self-renewal proliferation) and cell migration of alkaline phosphatase-positive GSCs through HIF-2α-OCT4/CXCR4 during embryogenesis. Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.

DISINTEGRATING ASTEROID P/2013 R3

Energy Technology Data Exchange (ETDEWEB)

Jewitt, David; Li, Jing [Department of Earth, Planetary and Space Sciences, UCLA, 595 Charles Young Drive East, Los Angeles, CA 90095-1567 (United States); Agarwal, Jessica [Max Planck Institute for Solar System Research, Max-Planck-Str. 2, D-37191 Katlenburg-Lindau (Germany); Weaver, Harold [The Johns Hopkins University Applied Physics Laboratory, 11100 Johns Hopkins Road, Laurel, MD 20723 (United States); Mutchler, Max [Space Telescope Science Institute, 3700 San Martin Drive, Baltimore, MD 21218 (United States); Larson, Stephen, E-mail: jewitt@ucla.edu [Lunar and Planetary Laboratory, University of Arizona, 1629 E. University Boulevard, Tucson, AZ 85721-0092 (United States)

2014-03-20

Splitting of the nuclei of comets into multiple components has been frequently observed but, to date, no main-belt asteroid has been observed to break up. Using the Hubble Space Telescope, we find that main-belt asteroid P/2013 R3 consists of 10 or more distinct components, the largest up to 200 m in radius (assumed geometric albedo of 0.05) each of which produces a coma and comet-like dust tail. A diffuse debris cloud with total mass ∼2 × 10{sup 8} kg further envelopes the entire system. The velocity dispersion among the components, ΔV ∼ 0.2-0.5 m s{sup –1}, is comparable to the gravitational escape speeds of the largest members, while their extrapolated plane-of-sky motions suggest a break up between 2013 February and September. The broadband optical colors are those of a C-type asteroid. We find no spectral evidence for gaseous emission, placing model-dependent upper limits to the water production rate ≤1 kg s{sup –1}. Breakup may be due to a rotationally induced structural failure of the precursor body.

Determination of the spin orbit coupling and crystal field splitting in wurtzite InP by polarization resolved photoluminescence

Science.gov (United States)

Chauvin, Nicolas; Mavel, Amaury; Jaffal, Ali; Patriarche, Gilles; Gendry, Michel

2018-02-01

Excitation photoluminescence spectroscopy is usually used to extract the crystal field splitting (ΔCR) and spin orbit coupling (ΔSO) parameters of wurtzite (Wz) InP nanowires (NWs). However, the equations expressing the valence band splitting are symmetric with respect to these two parameters, and a choice ΔCR > ΔSO or ΔCR InP NWs grown on silicon. The experimental results combined with a theoretical model and finite difference time domain calculations allow us to conclude that ΔCR > ΔSO in Wz InP.

Kaempferol inhibits vascular smooth muscle cell migration by modulating BMP-mediated miR-21 expression.

Science.gov (United States)

Kim, Kwangho; Kim, Sunghwan; Moh, Sang Hyun; Kang, Hara

2015-09-01

Bioflavonoids are known to induce cardioprotective effects by inhibiting vascular smooth muscle cell (VSMC) proliferation and migration. Kaempferol has been shown to inhibit VSMC proliferation. However, little is known about the effect of kaempferol on VSMC migration and the underlying molecular mechanisms. Our studies provide the first evidence that kaempferol inhibits VSMC migration by modulating the BMP4 signaling pathway and microRNA expression levels. Kaempferol activates the BMP signaling pathway, induces miR-21 expression and downregulates DOCK4, 5, and 7, leading to inhibition of cell migration. Moreover, kaempferol antagonizes the PDGF-mediated pro-migratory effect. Therefore, our study uncovers a novel regulatory mechanism of VSMC migration by kaempferol and suggests that miRNA modulation by kaempferol is a potential therapy for cardiovascular diseases.

Lipopolysaccharide induces the migration of human dental pulp cells by up-regulating miR-146a.

Science.gov (United States)

Wang, Min-Ching; Hung, Pei-Shih; Tu, Hsi-Feng; Shih, Wen-Yu; Li, Wan-Chun; Chang, Kuo-Wei

2012-12-01

MicroRNAs are small noncoding RNAs that play crucial roles in regulating normal and pathologic functions. Bacterial lipopolysaccharide (LPS) is one of the key regulators of pulpal pathogenesis. This study investigated how LPS regulates microRNA expression and affects the phenotype of human dental pulp cells (DPCs). Primary DPCs were established and immortalized to achieve immortalized DPCs (I-DPCs). DPCs and I-DPCs were treated with LPS and examined to identify changes in microRNA expression, cell proliferation, and cell migration. Quantitative reverse-transcriptase polymerase chain reaction was used to detect changes in gene expression. Exogenous miR-146a expression was performed transfection with pre-mir-146a mimic. Knockdown of interleukin receptor-associated kinase (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) expression was performed by small interference oligonucleotide transfection. Western blot analysis was used to detect changes in the expression of the IRAK1 and TRAF6 proteins. The differentiation of DPCs was induced by osteogenic medium. I-DPCs had a higher level of human telomerase reverse transcriptase gene than the parental DPCs. Up-regulation of miR-146a expression and an increase in migration was induced by LPS treatment of DPCs and I-DPCs. Exogenous miR-146a expression increased the migration of DPCs and I-DPCs and down-regulated the expression of IRAK1 and TRAF6. Knockdown of IRAK1 and/or TRAF6 increased the migration of DPCs. The results suggested that LPS is able to increase the migration of DPCs by modulating the miR-146a-TRAF6/IRAK1 regulatory cascade. Copyright © 2012 American Association of Endodontists. All rights reserved.

miR-30a suppresses breast cancer cell proliferation and migration by targeting Eya2

International Nuclear Information System (INIS)

Fu, Jing; Xu, Xiaojie; Kang, Lei; Zhou, Liying; Wang, Shibin; Lu, Juming; Cheng, Long; Fan, Zhongyi; Yuan, Bin; Tian, Peirong; Zheng, Xiaofei; Yu, Chengze; Ye, Qinong; Lv, Zhaohui

2014-01-01

Highlights: • miR-30a represses Eya2 expression by binding to the 3′-untranslated region of Eya2. • The miR-30a/EYA2 axis regulates breast cancer cell proliferation and migration. • The miR-30a/EYA2 axis modulates G1/S cell cycle progression. • The miR-30a/EYA2 axis is dysregulated in breast cancer patients. - Abstract: Eye absent (Eya) proteins are involved in cell fate determination in a broad spectrum of cells and tissues. Aberrant expression of Eya2 has been documented in a variety of cancers and correlates with clinical outcome. However, whether microRNAs (miRNAs) can regulate Eya2 expression remains unknown. Here, we show that miR-30a represses Eya2 expression by binding to the 3′-untranslated region of Eya2. Overexpression of Eya2 in miR-30a-transfected breast cancer cells effectively rescued the inhibition of cell proliferation and migration caused by miR-30a. Knockdown of Eya2 by small-interfering RNA (siRNA) in breast cancer cells mimicked the effect induced by miR-30a and abolished the ability of miR-30a to regulate breast cancer cell proliferation and migration. The miR-30a/Eya2 axis could regulate G1/S cell cycle progression, accompanied by the modulation of expression of cell cycle-related proteins, including cyclin A, cyclin D1, cyclin E, and c-Myc. Moreover, miR-30a expression was downregulated in breast cancer patients, and negatively correlated with Eya2, which was upregulated in breast cancer patients. These data suggest that the miR-30a/Eya2 axis may play an important role in breast cancer development and progression and that miR-30a activation or Eya2 inhibition may be a useful strategy for cancer treatment

miR-199a-3p displays tumor suppressor functions in papillary thyroid carcinoma.

Science.gov (United States)

Minna, Emanuela; Romeo, Paola; De Cecco, Loris; Dugo, Matteo; Cassinelli, Giuliana; Pilotti, Silvana; Degl'Innocenti, Debora; Lanzi, Cinzia; Casalini, Patrizia; Pierotti, Marco A; Greco, Angela; Borrello, Maria Grazia

2014-05-15

Thyroid cancer incidence is rapidly increasing. Papillary Thyroid Carcinoma (PTC), the most frequent hystotype, usually displays good prognosis, but no effective therapeutic options are available for the fraction of progressive PTC patients. BRAF and RET/PTC are the most frequent driving genetic lesions identified in PTC. We developed two complementary in vitro models based on RET/PTC1 oncogene, starting from the hypothesis that miRNAs modulated by a driving PTC-oncogene are likely to have a role in thyroid neoplastic processes. Through this strategy, we identified a panel of deregulated miRNAs. Among these we focused on miR-199a-3p and showed its under-expression in PTC specimens and cell lines. We demonstrated that miR-199a-3p restoration in PTC cells reduces MET and mTOR protein levels, impairs migration and proliferation and, more interesting, induces lethality through an unusual form of cell death similar to methuosis, caused by macropinocytosis dysregulation. Silencing MET or mTOR, both involved in survival pathways, does not recapitulate miR-199a-3p-induced cell lethality, thus suggesting that the cooperative regulation of multiple gene targets is necessary. Integrated analysis of miR-199a-3p targets unveils interesting networks including HGF and macropinocytosis pathways. Overall our results indicate miR-199a-3p as a tumor suppressor miRNA in PTC.

MiR-142-3p Functions as a Potential Tumor Suppressor in Human Osteosarcoma by Targeting HMGA1

Directory of Open Access Journals (Sweden)

Guoxing Xu

2014-04-01

Full Text Available Background/Aims: Mounting evidence has shown that aberrant expression of miRNAs correlates with human cancers, and that miRNAs can function as tumor suppressors or oncogenes. Here, we investigated the role and mechanism of miR-142-3p in human osteosarcoma. Methods: We used quantitative real-time RT-PCR to measure the expression of miR-142-3p in human osteosarcoma cell lines and tissues. The roles of miR-142-3p in osteosarcoma development were studied using cultured HOS, MG63 and Saos-2 cells and tumor xenograft analyses in nude mice; their target genes were also investigated. Results: We found that miR-142-3p was significantly downregulated in osteosarcoma cell lines and clinical specimens. Overexpression of miR-142-3p suppressed osteosarcoma cell proliferation, migration and invasion, whereas miR-142-3p knockdown increased these parameters. The xenograft mouse model also revealed the suppressive effect of miR-142-3p on tumor growth. High mobility group AT-hook 1 (HMGA1 was identified as a target of miR-142-3p. Downregulation of HMGA1 induced effects on osteosarcoma cell lines similar to those induced by miR-142-3p. In contrast, restoration of HMGA1 abrogated the effects induced by miR-142-3p up-regulation. Conclusion: These results indicated that miR-142-3p may function as a tumor suppressor by targeting HMGA1 in osteosarcoma.

Exit Strategies: S1P Signaling and T Cell Migration.

Science.gov (United States)

Baeyens, Audrey; Fang, Victoria; Chen, Cynthia; Schwab, Susan R

2015-12-01

Whereas the role of sphingosine 1-phosphate receptor 1 (S1PR1) in T cell egress and the regulation of S1P gradients between lymphoid organs and circulatory fluids in homeostasis are increasingly well understood, much remains to be learned about S1P signaling and distribution during an immune response. Recent data suggest that the role of S1PR1 in directing cells from tissues into circulatory fluids is reprised again and again, particularly in guiding activated T cells from non-lymphoid tissues into lymphatics. Conversely, S1P receptor 2 (S1PR2), which antagonizes migration towards chemokines, confines cells within tissues. Here we review the current understanding of the roles of S1P signaling in activated T cell migration. In this context, we outline open questions, particularly regarding the shape of S1P gradients in different tissues in homeostasis and inflammation, and discuss recent strategies to measure S1P. Copyright © 2015 Elsevier Ltd. All rights reserved.

Study of ln s Physics in $\\bar{p}p$ Interactions at the Split Field Magnet

CERN Multimedia

2002-01-01

This experiment uses the Split Field Magnet detector to investigate the low p^t, ``ln~s'', type of interactions that dominate the @*p cross-section. Systematic comparisons will be made to pp interactions. \\\\ \\\\ Specific areas to be studied include elastic scattering in the regions 0.05 $<$ !t! $<$ 0.8 GeV|2 and 0.8 $<$ !t! $<$ 4.0 GeV|2, and the use of a minimum bias trigger to study topological cross-sections, inclusive spectra, and two-body correlations. Some specialized triggers, run simultaneously with the high t elastic scattering trigger, are being studied. Examples are a trigger requiring Cerenkov identification in a limited region of phase space, and a trigger to select diffractively produced events.

Upregulation of MiR-212 Inhibits Migration and Tumorigenicity and Inactivates Wnt/β-Catenin Signaling in Human Hepatocellular Carcinoma.

Science.gov (United States)

Jia, Pengbo; Wei, Guangbing; Zhou, Cancan; Gao, Qi; Wu, Yunhua; Sun, Xuejun; Li, Xuqi

2018-01-01

MicroRNAs are involved in hepatocellular carcinoma metastasis, a principal cause of hepatocellular carcinoma-related death in patients worldwide. MiR-212 is a microRNA that has been identified in several types of cancers and is postulated to influence cell signaling and subsequent malignant pathogenesis. Despite emerging reports suggesting that miR-212 plays a significant role in the onset, progression, and migration of these types of malignant tumors, its involvement in the development of hepatocellular carcinoma has not been fully elucidated. Quantitative reverse transcription polymerase chain reaction, wound healing, transwell migration and invasion assays, Western blotting, and xenograft tumor growth models were performed to test the expression levels and functions of miR-212 in hepatocellular carcinoma. Luciferase reporter assay, quantitative reverse transcription polymerase chain reaction, Western blotting, and immunohistochemistry were used to identify and verify the target of miR-212. In this study, we identify significant repression of miR-212 in hepatocellular carcinoma and demonstrate that overexpression of miR-212 inhibits the migration of hepatocellular carcinoma cells in vitro and in vivo. Furthermore, we identify forkhead box M1, whose expression is inversely related to that of miR-212, as a direct target of miR-212. Additionally, reexpression of forkhead box M1 rescues the miR-212-mediated inhibition of cell migration. We observed that inhibition of miR-212 activates forkhead box M1 but inhibits the Wnt/β-catenin pathway by suppressing Wnt, LEF-1, c-Myc, and nuclear β-catenin. Finally, in vivo studies confirmed the inhibitory effect of miR-212 on hepatocellular carcinoma growth. Our present findings indicate that miR-212 is a potential prognostic biomarker of hepatocellular carcinoma and that the miR-212/forkhead box M1 regulatory axis may represent a new therapeutic objective for hepatocellular carcinoma treatment.

Répercussions de la migration causée par les réformes agraires sur ...

International Development Research Centre (IDRC) Digital Library (Canada)

De récentes réformes agraires ont entraîné un phénomène unique de migration entre régions rurales dans le district de Chimanimani, au Zimbabwe. Les chercheurs vérifieront l'hypothèse selon laquelle les migrants sont fortement attirés par les ressources forestières dans les régions où ils s'établissent et verront s'il est ...

Downregulation of sphingosine 1-phosphate (S1P) receptor 1 by dexamethasone inhibits S1P-induced mesangial cell migration.

Science.gov (United States)

Koch, Alexander; Jäger, Manuel; Völzke, Anja; Grammatikos, Georgios; Zu Heringdorf, Dagmar Meyer; Huwiler, Andrea; Pfeilschifter, Josef

2015-06-01

Sphingosine 1-phosphate (S1P) is generated by sphingosine kinase (SK)-1 and -2 and acts mainly as an extracellular ligand at five specific receptors, denoted S1P1-5. After activation, S1P receptors regulate important processes in the progression of renal diseases, such as mesangial cell migration and survival. Previously, we showed that dexamethasone enhances SK-1 activity and S1P formation, which protected mesangial cells from stress-induced apoptosis. Here we demonstrate that dexamethasone treatment lowered S1P1 mRNA and protein expression levels in rat mesangial cells. This effect was abolished in the presence of the glucocorticoid receptor antagonist RU-486. In addition, in vivo studies showed that dexamethasone downregulated S1P1 expression in glomeruli isolated from mice treated with dexamethasone (10 mg/kg body weight). Functionally, we identified S1P1 as a key player mediating S1P-induced mesangial cell migration. We show that dexamethasone treatment significantly lowered S1P-induced migration of mesangial cells, which was again reversed in the presence of RU-486. In summary, we suggest that dexamethasone inhibits S1P-induced mesangial cell migration via downregulation of S1P1. Overall, these results demonstrate that dexamethasone has functional important effects on sphingolipid metabolism and action in renal mesangial cells.

P R Vasudeva Rao

Indian Academy of Sciences (India)

Home; Journals; Sadhana. P R Vasudeva Rao. Articles written in Sadhana. Volume 27 Issue 5 October 2002 pp 527-558. Development of fuels and structural materials for fast breeder reactors · Baldev Raj S L Mannan P R Vasudeva Rao M D Mathew · More Details Abstract Fulltext PDF. Fast breeder reactors (FBRs) are ...

P-R-R Study Technique, Group Counselling And Gender Influence ...

African Journals Online (AJOL)

Read-Recall (P-R-R) study technique and group counselling on the academic performance of senior secondary school students. The objectives of this study were to determine the effect of Group Counselling combined with P-R-R study ...

Hierarchically scaffolded CoP/CoP2 nanoparticles: controllable synthesis and their application as a well-matched bifunctional electrocatalyst for overall water splitting.

Science.gov (United States)

Li, Wan; Zhang, Shilin; Fan, Qining; Zhang, Fazhi; Xu, Sailong

2017-05-04

Transition metal phosphide (TMP) nanostructures have stimulated increasing interest for use in water splitting owing to their abundant natural sources and high activity for the hydrogen evolution reaction (HER) and oxygen evolution reaction (OER). Typically, the preparation of hierarchical TMPs involves the utilization of expensive or dangerous phosphorus sources, and, in particular, the understanding of topotactic transformations of the precursors to crystalline phases-which could be utilized to enhance electrocatalytic performance-remains very limited. We, herein, report a controllable preparation of CoP/CoP 2 nanoparticles well dispersed in flower-like Al 2 O 3 scaffolds (f-CoP/CoP 2 /Al 2 O 3 ) as a bifunctional electrocatalyst for the HER and OER via the phosphorization of a flower-like CoAl layered double hydroxide precursor. Characterization by in situ X-ray diffraction (XRD) monitored the topotactic transformation underlying the controllable formation of CoP/CoP 2 via tuning the phosphorization time. Electrocatalytic tests showed that an f-CoP/CoP 2 /Al 2 O 3 electrode exhibited a lower onset potential and higher electrocatalytic activity for the HER and OER in the same alkaline electrolyte than electrodes of flower-like and powdered CoP/Al 2 O 3 . The enhanced electrochemical performance was experimentally supported by measuring the electrochemically active surface area. The f-CoP/CoP 2 /Al 2 O 3 composite further generated a current density of 10 mA cm -2 at 1.65 V when used as a bifunctional catalyst for overall water splitting. Our results demonstrate that the preparation route based on the LDH precursor may provide an alternative for investigating diverse TMPs as bifunctional electrocatalysts for water splitting.

R N P Choudhary

Indian Academy of Sciences (India)

Home; Journals; Bulletin of Materials Science. R N P Choudhary. Articles written in Bulletin of Materials Science. Volume 23 Issue 4 August 2000 pp 239-241 Phase Transitions. Phase transitions in Na2TeO4 ceramics · N K Singh R N P Choudhary · More Details Abstract Fulltext PDF. Polycrystalline samples of NaTeO4 ...

The three-loop splitting functions P{sup (2)}{sub qg} and P{sup (2,N{sub F})}{sub gg}

Energy Technology Data Exchange (ETDEWEB)

Ablinger, J.; Schneider, C. [Johannes Kepler Univ., Linz (Austria). Research Inst. for Symbolic Computation (RISC); Behring, A. [Deutsches Elektronen-Synchrotron (DESY), Zeuthen (Germany); RWTH Aachen Univ. (Germany). Inst. fuer Theoretische Teilchenphysik und Kosmologie; Bluemlein, J.; Freitas, A. de [Deutsches Elektronen-Synchrotron (DESY), Zeuthen (Germany); Von Manteuffel, A. [Michigan State Univ., East Lansing, MI (United States). Dept. of Physics and Astronomy

2017-04-15

We calculate the unpolarized twist-2 three-loop splitting functions P{sup (2)}{sub qg}(x) and P{sup (2,N{sub F})}{sub gg}(x) and the associated anomalous dimensions using massive three-loop operator matrix elements. While we calculate P{sup (2,N{sub F})}{sub gg}(x) directly, P{sup (2)}{sub qg}(x) is computed from 1200 even moments, without any structural prejudice, using a hierarchy of recurrences obtained for the corresponding operator matrix element. The largest recurrence to be solved is of order 12 and degree 191. We confirm results in the foregoing literature.

LncRNA TUG1 serves an important role in hypoxia-induced myocardial cell injury by regulating the miR-145-5p-Binp3 axis

Science.gov (United States)

Wu, Zhongwei; Zhao, Shengji; Li, Chunfu; Liu, Chaoquan

2018-01-01

The aim of the present study was to investigate the function of long non-coding RNA TUG1 in hypoxia-induced myocardial cell injury and to explore the potential molecular mechanisms. The cardiomyocyte cell line H9c2 was cultured under hypoxic and normoxic conditions. TUG1 expression under hypoxic conditions was then detected. The effects of TUG1 overexpression on viability, apoptosis, migration and invasion were assayed. In addition, the microRNA (miR)-145-5p expression was detected. Following H9c2 cell transfection with miR-145-5p mimics, the H9c2 cell viability, apoptosis, migration and invasion were also detected. Additionally, the target gene of miR-145-5p was assayed by Luciferase reporter assay. The protein expressions of Wnt-3a, Wnt5a, and β-catenin in H9c2 cells under hypoxic conditions were also determined. The results revealed that hypoxia induced injury in H9c2 cells, including inhibiting cell viability, migration and invasion, and promoting cell apoptosis. Overexpression of TUG1 aggravated hypoxia-induced injury in H9c2 cells. In addition, miR-145-5p was negatively regulated by TUG1, and TUG1 overexpression aggravated hypoxia-induced injury via the downregulation of miR-145-5p. Furthermore, B-cell lymphoma 2 interacting protein 3 (Bnip3) was a target of miR-145-5p, and overexpression of Bnip3 aggravated hypoxia-induced cell injury by activating Wnt/β-catenin signaling pathways in H9c2 cells. In conclusion, overexpression of TUG1 aggravated hypoxia-induced injury in cardiomyocytes by regulating the miR-145-5p-Binp3 axis. Activation of the Wnt/β-catenin signaling pathway may be a key mechanism to mediate the role of TUG1 in regulating hypoxia-induced myocardial injury. TUG1 may be an effective diagnostic marker and therapeutic target for myocardial ischemia. PMID:29207102

Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.

Science.gov (United States)

Liu, Chibo; Pan, Chunqin; Cai, Yanqun; Wang, Haibao

2017-08-01

In our previous study, we found long noncoding RNA ZEB1-AS1 is upregulated and functions as an oncogene in osteosarcoma. MiR-200 family (miR-200s) functions as tumor suppressor via directly targeting ZEB1 in various cancers. In this study, we further investigate the potential interplay between ZEB1-AS1, miR-200s, and ZEB1 in osteosarcoma. Our results showed that ZEB1-AS1 functions as a molecular sponge for miR-200s and relieves the inhibition of ZEB1 caused by miR-200s. ZEB1-AS1 and miR-200s reciprocally negatively regulate each other. MiR-200s are downregulated in osteosarcoma tissues, and negatively correlated with ZEB1-AS1 and ZEB1 expression levels in osteosarcoma. Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1. The interplay between ZEB1-AS1 and miR-200s contributes to osteosarcoma cell proliferation and migration, and targeting this interplay could be a promising strategy for osteosarcoma treatment. J. Cell. Biochem. 118: 2250-2260, 2017. © 2017 Wiley Periodicals, Inc. © 2017 Wiley Periodicals, Inc.

Resistin promotes tumor metastasis by down-regulation of miR-519d through the AMPK/p38 signaling pathway in human chondrosarcoma cells

Science.gov (United States)

Huang, Ho-Ning; Hung, Chih-Hung; Hsu, Chin-Jung; Fong, Yi-Chin; Hsu, Horng-Chaung; Huang, Yuan-Li; Tang, Chih-Hsin

2015-01-01

Resistin is a recently discovered adipocyte-secreting adipokine, which may play a critical role in modulating cancer pathogenesis. Chondrosarcoma is a highly malignant tumor known to frequently metastasize; however, the role of resistin in the metastasis of human chondrosarcoma is largely unknown. Here, we found that the expression of resistin was higher in chondrosarcoma biopsy tissues than in normal cartilage. Moreover, treatment with resistin increased matrix metalloproteinase (MMP)-2 expression and promoted cell migration in human chondrosarcoma cells. Co-transfection with microRNA (miR)-519d mimic resulted in reversed resistin-mediated cell migration and MMP-2 expression. Additionally, AMP-activated protein kinase (AMPK) and p38 inhibitors or siRNAs reduced the resistin-increased cell migration and miR-519d suppression, and inhibition of resistin expression resulted in suppression of MMP-2 expression and lung metastasis in vivo. Taken together, our results indicate that resistin promotes chondrosarcoma metastasis and MMP-2 expression through activation of the AMPK/p38 signaling pathway and down-regulation of miR-519d expression. Therefore, resistin may represent a potential novel molecular therapeutic target in chondrosarcoma metastasis. PMID:25404641

Crystal electric field splitting of R{sup 3+}-ions in pure and Co- and Cu-doped RNi{sub 2}B{sub 2}C (R=Ho, Er, Tm)

Energy Technology Data Exchange (ETDEWEB)

Gasser, U.; Allenspach, P.; Henggeler, W.; Zolliker, M.; Furrer, A. [Paul Scherrer Inst. (PSI), Villigen (Switzerland)

1997-09-01

From the crystal-electric-field (CEF) splitting of the R{sup 3+}-ions, the CEF parameters of RNi{sub 2}B{sub 2}C (R=Ho, Er, Tm) were deduced. In order to get information about the influence of the variation of the density of states (DOS) at the Fermi level (E{sub F}), CEF spectroscopy measurements with Co- and Cu-doped ErNi{sub 2}B{sub 2}C-samples were performed. (author) 1 fig., 1 tab., 1 ref.

ISR split-field magnet

CERN Multimedia

CERN PhotoLab

1975-01-01

The experimental apparatus used at intersection 4 around the Split-Field Magnet by the CERN-Bologna Collaboration (experiment R406). The plastic scintillator telescopes are used for precise pulse-height and time-of-flight measurements.

Glutathione S-transferase P influences redox and migration pathways in bone marrow.

Directory of Open Access Journals (Sweden)

Jie Zhang

Full Text Available To interrogate why redox homeostasis and glutathione S-transferase P (GSTP are important in regulating bone marrow cell proliferation and migration, we isolated crude bone marrow, lineage negative and bone marrow derived-dendritic cells (BMDDCs from both wild type (WT and knockout (Gstp1/p2(-/- mice. Comparison of the two strains showed distinct thiol expression patterns. WT had higher baseline and reactive oxygen species-induced levels of S-glutathionylated proteins, some of which (sarco-endoplasmic reticulum Ca2(+-ATPase regulate Ca(2+ fluxes and subsequently influence proliferation and migration. Redox status is also a crucial determinant in the regulation of the chemokine system. CXCL12 chemotactic response was stronger in WT cells, with commensurate alterations in plasma membrane polarization/permeability and intracellular calcium fluxes; activities of the downstream kinases, ERK and Akt were also higher in WT. In addition, expression levels of the chemokine receptor CXCR4 and its associated phosphatase, SHP-2, were higher in WT. Inhibition of CXCR4 or SHP2 decreased the extent of CXCL12-induced migration in WT BMDDCs. The differential surface densities of CXCR4, SHP-2 and inositol trisphosphate receptor in WT and Gstp1/p2(-/- cells correlated with the differential CXCR4 functional activities, as measured by the extent of chemokine-induced directional migration and differences in intracellular signaling. These observed differences contribute to our understanding of how genetic ablation of GSTP causes different levels of myeloproliferation and migration [corrected

HIF-inducible miR-191 promotes migration in breast cancer through complex regulation of TGFβ-signaling in hypoxic microenvironment.

Science.gov (United States)

Nagpal, Neha; Ahmad, Hafiz M.; Chameettachal, Shibu; Sundar, Durai; Ghosh, Sourabh; Kulshreshtha, Ritu

2015-01-01

The molecular mechanisms of hypoxia induced breast cell migration remain incompletely understood. Our results show that hypoxia through hypoxia-inducible factor (HIF) brings about a time-dependent increase in the level of an oncogenic microRNA, miR-191 in various breast cancer cell lines. miR-191 enhances breast cancer aggressiveness by promoting cell proliferation, migration and survival under hypoxia. We further established that miR-191 is a critical regulator of transforming growth factor beta (TGFβ)-signaling and promotes cell migration by inducing TGFβ2 expression under hypoxia through direct binding and indirectly by regulating levels of a RNA binding protein, human antigen R (HuR). The levels of several TGFβ pathway genes (like VEGFA, SMAD3, CTGF and BMP4) were found to be higher in miR-191 overexpressing cells. Lastly, anti-miR-191 treatment given to breast tumor spheroids led to drastic reduction in spheroid tumor volume. This stands as a first report of identification of a microRNA mediator that links hypoxia and the TGFβ signaling pathways, both of which are involved in regulation of breast cancer metastasis. Together, our results show a critical role of miR-191 in hypoxia-induced cancer progression and suggest that miR-191 inhibition may offer a novel therapy for hypoxic breast tumors. PMID:25867965

R-parity violation, sneutrino mixing phenomena, and CP violation in p bar p→ν→l+l-+X

International Nuclear Information System (INIS)

Bar-Shalom, S.; Eilam, G.; Soni, A.

1999-01-01

The sneutrino resonance reactions p bar p→ν+X→l + l - +X, for l=e,μ,τ, in the MSSM without R-parity are considered. We perform a cross-section analysis and show that present limits on some products of R P couplings in the sneutrino sector can be significantly improved in future upgraded Fermilab Tevatron runs. Furthermore, we introduce CP-violating and CP-conserving τ-spin asymmetries which are generated already at the tree level in the reaction p bar p→ν+X→τ + τ - +X if there is ν μ -ν ampersand dbartil; μ mixing and that vanish in the SM. We find, for example, that for muon-sneutrino masses in the range 150 GeV approx-lt m ν μ approx-lt 450 GeV, these spin asymmetries reach ∼20 - 30% and ∼10% for mass splitting between the muon-sneutrino CP-odd and CP-even states at the level of Δm∼Γ and Δm∼Γ/4, respectively, where Γ is the ν μ width. Both the CP-violating and the CP-conserving spin asymmetries should be detectable in future Tevatron runs even for a heavy sneutrino with a mass approx-lt 500 GeV. If detected, such asymmetries being proportional to the mass splitting between the CP-even and CP-odd sneutrino states may serve as a strong indication for the existence of the sneutrino mixing phenomenon. copyright 1999 The American Physical Society

[Regulation of microRNA-199a on adhesion, migration and invasion ability of human endometrial stromal cells].

Science.gov (United States)

Dai, Lan; Gu, Li-ying; Zhu, Jie; Shi, Jun; Wang, Yao; Ji, Fang; Di, Wen

2011-11-01

To study the regulation of microRNA 199a (miR-199a) on adhesion, migration and invasion ability of human eutopic endometrial stromal cells (ESC) from patients with endometriosis. ESC were transfected with miR-199a mimics or negative control (NC) RNA by lipofectamine 2000. The adhesion, migration and invasion ability of ESC were detected by cell adhesion assay, scratch assay, cell migration assay and matrigel invasion assay, respectively. Luciferase reporter assay was used to evaluate whether IKKβ was the target gene of miR-199a. The expression of ikappa B kinase beta (IKKβ), inhibitory kappa B alpha (IκB-α), phospho-IκB-α(p-IκB-α) and nuclear factor-kappa B (NF-κB) protein were measured by western blot. (1) Adhesion potential: the adhesion inhibitory rates were (14 ± 4)% in miR-199a group and 0 in control group, which showed significant difference (P scratch assay, ESC transfected with miR-199a exhibited a lower scratch closure rate than that of controls. In migration and invasion assays, the migration and invasion ability of miR-199a group were significantly decreased compared with those of NC group [130 ± 31 vs. 247 ± 36 (P < 0.01); 63 ± 15 vs. 133 ± 17 (P < 0.01), respectively]. (3) The luciferase activity of miR-199a group was significantly lowered than that of control group [0.160 ± 0.006 vs. 0.383 ± 0.083 (P < 0.01)]. The protein levels of IKKβ, p-IκB-α, IκB-α and NF-κB of 0.350 ± 0.195, 0.443 ± 0.076, 1.970 ± 0.486 and 0.454 ± 0.147 in miR-199a group were significantly different compared with the NC group in which the protein levels were set at 1.000 (P < 0.01). miR-199a can inhibit the adhesion, migration and invasion of the ESC. IKKβ is the target gene of miR-199a in ESC. One of the mechanisms of the inhibition effect is probably that miR-199a inhibits the activation of NF-κB signaling pathway by targeting IKKβ gene.

Ang II-AT2R increases mesenchymal stem cell migration by signaling through the FAK and RhoA/Cdc42 pathways in vitro.

Science.gov (United States)

Xu, Xiu-Ping; He, Hong-Li; Hu, Shu-Ling; Han, Ji-Bin; Huang, Li-Li; Xu, Jing-Yuan; Xie, Jian-Feng; Liu, Ai-Ran; Yang, Yi; Qiu, Hai-Bo

2017-07-12

Mesenchymal stem cells (MSCs) migrate via the bloodstream to sites of injury and are possibly attracted by inflammatory factors. As a proinflammatory mediator, angiotensin II (Ang II) reportedly enhances the migration of various cell types by signaling via the Ang II receptor in vitro. However, few studies have focused on the effects of Ang II on MSC migration and the underlying mechanisms. Human bone marrow MSCs migration was measured using wound healing and Boyden chamber migration assays after treatments with different concentrations of Ang II, an AT1R antagonist (Losartan), and/or an AT2R antagonist (PD-123319). To exclude the effect of proliferation on MSC migration, we measured MSC proliferation after stimulation with the same concentration of Ang II. Additionally, we employed the focal adhesion kinase (FAK) inhibitor PF-573228, RhoA inhibitor C3 transferase, Rac1 inhibitor NSC23766, or Cdc42 inhibitor ML141 to investigate the role of cell adhesion proteins and the Rho-GTPase protein family (RhoA, Rac1, and Cdc42) in Ang II-mediated MSC migration. Cell adhesion proteins (FAK, Talin, and Vinculin) were detected by western blot analysis. The Rho-GTPase family protein activities were assessed by G-LISA and F-actin levels, which reflect actin cytoskeletal organization, were detected by using immunofluorescence. Human bone marrow MSCs constitutively expressed AT1R and AT2R. Additionally, Ang II increased MSC migration in an AT2R-dependent manner. Notably, Ang II-enhanced migration was not mediated by Ang II-mediated cell proliferation. Interestingly, Ang II-enhanced migration was mediated by FAK activation, which was critical for the formation of focal contacts, as evidenced by increased Talin and Vinculin expression. Moreover, RhoA and Cdc42 were activated by FAK to increase cytoskeletal organization, thus promoting cell contraction. Furthermore, FAK, Talin, and Vinculin activation and F-actin reorganization in response to Ang II were prevented by PD-123319 but

miR-346 and miR-582-3p-regulated EG-VEGF expression and trophoblast invasion via matrix metalloproteinases 2 and 9.

Science.gov (United States)

Su, Mei-Tsz; Tsai, Pei-Yin; Tsai, Hui-Ling; Chen, Yi-Chi; Kuo, Pao-Lin

2017-03-01

Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is an important regulator for embryo implantation and placental development, and is clinically associated with several obstetric disorders related to insufficient or inappropriate trophoblast invasion, such as recurrent abortion, preeclampsia, and intrauterine fetal growth restriction. This study was performed to identify the microRNAs targeting EG-VEGF, and evaluate the regulatory effect on trophoblast biology. miR-346 and miR-582-3p were initially identified via bioinformatic tools, and their specific binding sites on the EG-VEGF 3'UTR were further confirmed using dual luciferase and a co-transfection assays. miR-346 and miR-582-3p were demonstrated not only to suppress EG-VEGF expression, but also inhibit trophoblast invasion and migration in the JAR and HTR-8/SVneo cell lines. We further evaluated the effect of microRNAs in HTR-8/SVneo cells coexpressing EG-VEGF and miR-346 or miR-582-3p on matrix metalloproteinase (MMP 2 and MMP 9) and the tissue inhibitors of metalloproteinase (TIMP 1 and TIMP 2) using RT-PCR, western blotting and gelatin zymography. TIMP 1 and TIMP 2 were not affected by the two microRNAs, whereas the expressions and activities of MMP 2 and MMP 9 were significantly downregulated, which in turn inhibited the invasion ability of trophoblasts. In conclusion, miR-346 and miR-582-3p regulate EG-VEGF-induced trophoblast invasion through repressing MMP 2 and MMP 9, and may become novel diagnostic biomarkers or therapeutic targets for EG-VEGF-related obstetric disorders. © 2016 BioFactors, 43(2):210-219, 2017. © 2016 International Union of Biochemistry and Molecular Biology.

Overexpression of miR-206 suppresses glycolysis, proliferation and migration in breast cancer cells via PFKFB3 targeting

Energy Technology Data Exchange (ETDEWEB)

Ge, Xin; Lyu, Pengwei; Cao, Zhang; Li, Jingruo; Guo, Guangcheng; Xia, Wanjun; Gu, Yuanting, E-mail: zzyuantinggu@126.com

2015-08-07

miRNAs, sorting as non-coding RNAs, are differentially expressed in breast tumor and act as tumor promoters or suppressors. miR-206 could suppress the progression of breast cancer, the mechanism of which remains unclear. The study here was aimed to investigate the effect of miR-206 on human breast cancers. We found that miR-206 was down-regulated while one of its predicted targets, 6-Phosphofructo-2-kinase (PFKFB3) was up-regulated in human breast carcinomas. 17β-estradiol dose-dependently decreased miR-206 expression as well as enhanced PFKFB3 mRNA and protein expression in estrogen receptor α (ERα) positive breast cancer cells. Furthermore, we identified that miR-206 directly interacted with 3′-untranslated region (UTR) of PFKFB3 mRNA. miR-206 modulated PFKFB3 expression in MCF-7, T47D and SUM159 cells, which was influenced by 17β-estradiol depending on ERα expression. In addition, miR-206 overexpression impeded fructose-2,6-bisphosphate (F2,6BP) production, diminished lactate generation and reduced cell proliferation and migration in breast cancer cells. In conclusion, our study demonstrated that miR-206 regulated PFKFB3 expression in breast cancer cells, thereby stunting glycolysis, cell proliferation and migration. - Highlights: • miR-206 was down-regulated and PFKFB3 was up-regulated in human breast carcinomas. • 17β-estradiol regulated miR-206 and PFKFB3 expression in ERα+ cancer cells. • miR-206directly interacted with 3′-UTR of PFKFB3 mRNA. • miR-206 fructose-2,6-bisphosphate (F2,6BP) impeded production and lactate generation. • miR-206 reduced cell proliferation and migration in breast cancer cells.

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR).

Science.gov (United States)

Xiong, Yaoyao; Wang, Long; Li, Yuan; Chen, Minfeng; He, Wei; Qi, Lin

2017-01-01

Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA's target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells' proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3'UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation. © 2017 The Author(s). Published by S. Karger AG, Basel.

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR

Directory of Open Access Journals (Sweden)

Yaoyao Xiong

2017-08-01

Full Text Available Backgrounds/Aims: Long non-coding RNA (lncRNA X-inactive specific transcript (XIST is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

Effects of miR-424 on Proliferation and Migration Abilities in Non-small Cell Lung Cancer A549 Cells and Its Molecular Mechanism

Directory of Open Access Journals (Sweden)

Hongmin LI

2016-09-01

Full Text Available Background and objective The inhibitory ability of miR-424 on the proliferation of renal carcinoma cell and the migration and invasion of cancer cells has been widely explored and demonstrated. However, the effects of miR-424 on non-small cell lung cancer (NSCLC have not been systematically examined. In this study, detected the growth and invasion effect of miR-424 in NSCLC A549 cell. The migration and molecular mechanism of this cell are also detected. Methods NSCLC A549 cell was transfected with miR-424 and its inhibitor. After transfection, the proliferation ability of A549 cell was detectedby CCK8 assay. Then, the migration ability in A549 cell was detected by migration assays. Furthermore, the expression level of MMP2 and MMP9 in A549 was detected by Western blot and immune fluorescence. The 3'UTR of E2F6 was cloned into luciferase reporter vector and its enzymatic activitywas detected to verify whether miR-424 can target E2F6. The expression level of E2F6 in a549 cell after transfecing with miR-424 was detected by Western blot. Results After transfection of miR-424, the proliferation and migration abilities were remarkably decreased and the expression level of MMP-2 and MMP-9 were down-regulated in A549. Moreover, MiR-424 inhibited the enzymatic activity of luviferase reporter vector of E2F6. Specifically, the expression level of E2F6 was down-regulated in A549. Conclusion miR-424 can inhibit the proliferation and migration abilities of A549 by negatively regulating the expression of E2F6.

Checking the Adequacy of Fit of Models from Split-Plot Designs

DEFF Research Database (Denmark)

Almini, A. A.; Kulahci, Murat; Montgomery, D. C.

2009-01-01

models. In this article, we propose the computation of two R-2, R-2-adjusted, prediction error sums of squares (PRESS), and R-2-prediction statistics to measure the adequacy of fit for the WP and the SP submodels in a split-plot design. This is complemented with the graphical analysis of the two types......One of the main features that distinguish split-plot experiments from other experiments is that they involve two types of experimental errors: the whole-plot (WP) error and the subplot (SP) error. Taking this into consideration is very important when computing measures of adequacy of fit for split-plot...... of errors to check for any violation of the underlying assumptions and the adequacy of fit of split-plot models. Using examples, we show how computing two measures of model adequacy of fit for each split-plot design model is appropriate and useful as they reveal whether the correct WP and SP effects have...

miR-367 regulation of DOC-2/DAB2 interactive protein promotes proliferation, migration and invasion of osteosarcoma cells.

Science.gov (United States)

Cai, Wei; Jiang, Haitao; Yu, Yifan; Xu, Yong; Zuo, Wenshan; Wang, Shouguo; Su, Zhen

2017-11-01

Recently, miR-367 is reported to exert either oncogenic or tumor suppressive effects in human malignancies. Recent study reports that miR-367 is up-regulated in OS tissues and cell lines, and abrogates adriamycin-induced apoptosis. The clinical significance of miR-367 and its function in OS need further investigation. In our study, miR-367 expression in OS was markedly elevated compared with corresponding non-tumor tissues. High miR-367 expression was associated with malignant clinical features and poor prognosis of OS patients. In accordance, the levels of miR-367 were dramatically up-regulated in OS cells. Loss of miR-367 expression in Saos-2 cells obviously inhibited the proliferation, migration and invasion of cancer cells in vitro. Meanwhile, miR-367 restoration promoted these malignant behaviors of MG-63 cells. Mechanistically, miR-367 negatively regulated DOC-2/DAB2 interactive protein (DAB2IP) abundance in OS cells. Hereby, DAB2IP was recognized as a direct target gene of miR-367 in OS. DAB2IP mRNA level was down-regulated and inversely correlated with miR-367 expression in OS specimens. DAB2IP overexpression prohibited proliferation, migration and invasion in Saos-2 cells, while DAB2IP knockdown showed promoting effects on proliferation, migration and invasion of MG-63 cells. Furthermore, the role of miR-367 might be mediated by DAB2IP-regulated phosphorylation of ERK and AKT in OS cells. To conclude, miR-367 may function as a biomarker for prediction of prognosis and a target for OS therapy. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Role of MiR-3619-5p in β-Catenin-Mediated Non-Small Cell Lung Cancer Growth and Invasion

Directory of Open Access Journals (Sweden)

Xuecai Niu

2015-10-01

Full Text Available Background/Aims: The malignancy of non-small cell lung cancer (NSCLC is largely due to its fast growth and invasion. WNT/β-catenin signaling plays a critical role in regulating NSCLC carcinogenesis. Hence, suppression of β-catenin signal transduction in NSCLC cells may improve the therapeutic outcome. Methods: We analyzed the levels of β-catenin and miR-3619-5p in NSCLC specimens, compared to paired non-tumor normal lung tissue (NT. We did Bioinformatics analyses on the binding sites of 3'-UTR of β-catenin mRNA by miR-3619-5p. We modified the levels of miR-3619-5p in NSCLC cells and examined their effects on β-catenin levels, and on the growth and invasion of NSCLC cells in an MTT assay and a transwell cell migration assay, respectively. Results: NSCLC specimens had significant higher levels of β-catenin, and significantly lower levels of miR-3619-5p, compared to NT. The levels of β-catenin and miR-3619-5p were inversely correlated in NSCLC specimens. Bioinformatics analyses showed that miR-3619-5p bound to 3'-UTR of β-catenin mRNA in NSCLC cells to inhibit its translation. Overexpression of miR-3619-5p decreased β-catenin protein, while depletion of miR-3619-5p increased β-catenin protein in NSCLC cells, without altering β-catenin mRNA levels. Overexpression of miR-3619-5p in NSCLC cells inhibited cell growth and invasion, while depletion of miR-3619-5p in NSCLC lines increased cell growth and invasion. Conclusion: Our data demonstrate a previously unappreciated role for miR-3619-5p in suppression of β-catenin-mediated cancer growth and invasion in NSCLC cells, and highlight miR-3619-5p as a novel cancer suppressor in NSCLC.

SIRT1 mediates Sphk1/S1P-induced proliferation and migration of endothelial cells.

Science.gov (United States)

Gao, Zhan; Wang, Hua; Xiao, Feng-Jun; Shi, Xue-Feng; Zhang, Yi-Kun; Xu, Qin Qin; Zhang, Xiao-Yan; Ha, Xiao-Qin; Wang, Li-Sheng

2016-05-01

Angiogenesis is one of the most important components of embryonic organ formation and vessel growth after birth. Sphingosine kinase 1 (Sphk1) and S1P has been confirmed to participate in various cell signaling pathways and physiological processes including neovascularisation. However, the mechanisms that Sphk1/S1P regulates neovascularisation remain unclear. In this study, we elucidated that Sphk1/S1P upregulates sirtuin 1 (SIRT1), a NAD+ dependent deacetylases protease which exerts multiple cellular functions, to regulate the proliferation and migration of endothelial cells. By using CCK8 and Transwell assays, we demonstrated that Sphk1 and SIRT1 knockdown could significantly decrease proliferation and migration of HUVEC cells. Sphk1 inhibition results in SIRT1 downregulation which could be reversed by exogenous S1P in HUVEC cells. Treatment of HUVECs with S1P reverses the impaired proliferation and migration caused by SIRT1 knockdown. Furthermore, Sphk1 knockdown inhibits the phosphorylation of P38 MAPK, ERK and AKT. Treatment of HUVECs with PD98059, SB203580 and Wortmannin, which are the inhibitors of ERK, P38 MAPK and AKT respectively, resulted in decreased SIRT1 expression and reduced migration of HUVEC cells. Thus, we conclude that Sphk1/S1P induces SIRT1 upregulation through multiple pathways including P38 MAPK, ERK and AKT signals. This is the first report to disclose the existence and roles of Sphk1/S1P/SIRT1 axis in regulation of endothelial cell proliferation and migration, which may provide a theoretical basis for angiogenesis. Copyright © 2016. Published by Elsevier Ltd.

The genetic landscape of Equatorial Guinea and the origin and migration routes of the Y chromosome haplogroup R-V88

OpenAIRE

González, Miguel; Gomes, Verónica; López-Parra, Ana Maria; Amorim, António; Carracedo, Ángel; Sánchez-Diz, Paula; Arroyo-Pardo, Eduardo; Gusmão, Leonor

2012-01-01

Human Y chromosomes belonging to the haplogroup R1b1-P25, although very common in Europe, are usually rare in Africa. However, recently published studies have reported high frequencies of this haplogroup in the central-western region of the African continent and proposed that this represents a ‘back-to-Africa' migration during prehistoric times. To obtain a deeper insight into the history of these lineages, we characterised the paternal genetic background of a population in Equatorial Guinea,...

High brightness InP micropillars grown on silicon with Fermi level splitting larger than 1 eV.

Science.gov (United States)

Tran, Thai-Truong D; Sun, Hao; Ng, Kar Wei; Ren, Fan; Li, Kun; Lu, Fanglu; Yablonovitch, Eli; Chang-Hasnain, Constance J

2014-06-11

The growth of III-V nanowires on silicon is a promising approach for low-cost, large-scale III-V photovoltaics. However, performances of III-V nanowire solar cells have not yet been as good as their bulk counterparts, as nanostructured light absorbers are fundamentally challenged by enhanced minority carriers surface recombination rates. The resulting nonradiative losses lead to significant reductions in the external spontaneous emission quantum yield, which, in turn, manifest as penalties in the open-circuit voltage. In this work, calibrated photoluminescence measurements are utilized to construct equivalent voltage-current characteristics relating illumination intensities to Fermi level splitting ΔF inside InP microillars. Under 1 sun, we show that splitting can exceed ΔF ∼ 0.90 eV in undoped pillars. This value can be increased to values of ΔF ∼ 0.95 eV by cleaning pillar surfaces in acidic etchants. Pillars with nanotextured surfaces can yield splitting of ΔF ∼ 0.90 eV, even though they exhibit high densities of stacking faults. Finally, by introducing n-dopants, ΔF of 1.07 eV can be achieved due to a wider bandgap energy in n-doped wurzite InP, the higher brightness of doped materials, and the extraordinarily low surface recombination velocity of InP. This is the highest reported value for InP materials grown on a silicon substrate. These results provide further evidence that InP micropillars on silicon could be a promising material for low-cost, large-scale solar cells with high efficiency.

Giant Rashba spin splitting in Bi2Se3: Tl

KAUST Repository

Singh, Nirpendra

2014-07-25

First-principles calculations are employed to demonstrate a giant Rashba spin splitting in Bi2Se3:Tl. Biaxial tensile and compressive strain is used to tune the splitting by modifying the potential gradient. The band gap is found to increase under compression and decreases under tension, whereas the dependence of the Rashba spin splitting on the strain is the opposite. Large values of αR = 1.57 eV Å at the bottom of the conduction band (electrons) and αR = 3.34 eV Å at the top of the valence band (holes) are obtained without strain. These values can be further enhanced to αR = 1.83 eV Å and αR = 3.64 eV Å, respectively, by 2% tensile strain. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

-5p and -3p strands of miR-145 and miR-140 during mesenchymal stem cell chondrogenic differentiation.

Science.gov (United States)

Kenyon, Jonathan D; Sergeeva, Olga; Somoza, Rodrigo A; Li, Ming; Caplan, Arnold I; Khalil, Ahmad M; Lee, Zhenghong

2018-04-20

The chondrogenic differentiation of mesenchymal stem cells (MSCs) is mediated by transcription factors and small non-coding RNAs such as micro-RNAs (miRNAs). Each miRNA is initially transcribed as a long transcript, which matures to produce -5p and -3p strands. It is widely believed that the mature and functional miRNA from any given pre-miRNA, usually the -5p strand, is functional, while the opposing -3p strand is degraded. However, recent cartilage literature started to show functional -3p stands for a few miRNAs. This study aimed at examining both -5p and -3p strands of two key miRNAs miR-140 and miR-145 that are known to be involved in the chondrogenic differentiation of MSCs. The level (copy number) of both -5p and -3p strands of miR-145 and miR-140 along the timeline of MSC chondrogenic differentiation was determined by PCR. The gene expression profiles of several genes related to MSC chondrogenesis were compared with these miRNA profiles along the same timeline. While miR-145-3p is declining in step with miR-145-5p in pellet cultures during the process, the -3p strand is only 1% - 2% of the total miR-145 products. In contrast, the mature -3p and -5p products of miR-140 are found to increase with near equal molar expression throughout chondrogenic differentiation. Numerous genes are expressed by cartilage progenitor cells during development. One such target gene, Sox9 is a regulatory target of the dominant miR-145-5p, consistent with the data. Further experimental validations are warranted to confirm that ACAN, FOXO1 and RUNX3 as direct targets of miR-145-5p in the context of MSC chondrogenesis. Similarly, TRSP1 and ACAN are worth further validation as direct targets of miR-145-3p. For miR-140, SOX4 shall be further validated as a direct target of miR-140-5p while KLF4, PTHLH, and WNT5A can be validated as direct targets of miR-140-3p.

miR-1207-3p regulates the androgen receptor in prostate cancer via FNDC1/fibronectin

International Nuclear Information System (INIS)

Das, Dibash K.; Naidoo, Michelle; Ilboudo, Adeodat; Park, Jong Y.; Ali, Thahmina; Krampis, Konstantinos; Robinson, Brian D.; Osborne, Joseph R.; Ogunwobi, Olorunseun O.

2016-01-01

Prostate cancer (PCa) is frequently diagnosed in men, and dysregulation of microRNAs is characteristic of many cancers. MicroRNA-1207-3p is encoded at the non-protein coding gene locus PVT1 on the 8q24 human chromosomal region, an established PCa susceptibility locus. However, the role of microRNA-1207-3p in PCa is unclear. We discovered that microRNA-1207-3p is significantly underexpressed in PCa cell lines in comparison to normal prostate epithelial cells. Increased expression of microRNA-1207-3p in PCa cells significantly inhibits proliferation, migration, and induces apoptosis via direct molecular targeting of FNDC1, a protein which contains a conserved protein domain of fibronectin (FN1). FNDC1, FN1, and the androgen receptor (AR) are significantly overexpressed in PCa cell lines and human PCa, and positively correlate with aggressive PCa. Prostate tumor FN1 expression in patients that experienced PCa-specific death is significantly higher than in patients that remained alive. Furthermore, FNDC1, FN1 and AR are concomitantly overexpressed in metastatic PCa. Consequently, these studies have revealed a novel microRNA-1207-3p/FNDC1/FN1/AR regulatory pathway in PCa. - Graphical abstract: miR-1207-3p/FNDC1/FN1/AR is a novel regulatory pathway in prostate cancer. - Highlights: • Expression of microRNA-1207-3p is significantly lost in prostate cancer (PCa) cells. • MicroRNA-1207-3p regulates proliferation, apoptosis, and migration via direct molecular targeting of the 3′UTR of FNDC1. • MicroRNA-1207-3p regulates proliferation, apoptosis, and migration via direct molecular targeting of the 3′UTR of FNDC1. • FNDC1, FN1, and AR are concurrently overexpressed in metastatic PCa.

miR-1207-3p regulates the androgen receptor in prostate cancer via FNDC1/fibronectin

Energy Technology Data Exchange (ETDEWEB)

Das, Dibash K. [Department of Biological Sciences, Hunter College of The City University of New York, New York, NY 10065 (United States); The Graduate Center Departments of Biology and Biochemistry, The City University of New York, New York, NY 10016 (United States); Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY 10065 (United States); Naidoo, Michelle; Ilboudo, Adeodat [Department of Biological Sciences, Hunter College of The City University of New York, New York, NY 10065 (United States); Park, Jong Y. [Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida 33612 (United States); Ali, Thahmina [Department of Biological Sciences, Hunter College of The City University of New York, New York, NY 10065 (United States); Krampis, Konstantinos [Department of Biological Sciences, Hunter College of The City University of New York, New York, NY 10065 (United States); Department of Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medicine, Cornell University, New York, NY 10065 (United States); Robinson, Brian D. [Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, Cornell University, New York, NY 10065 (United States); Department of Urology, Weill Cornell Medicine, Cornell University, New York, NY 10065 (United States); Osborne, Joseph R. [Department of Radiology, Memorial Sloan Kettering Cancer Center, New York, NY 10065 (United States); Ogunwobi, Olorunseun O., E-mail: ogunwobi@genectr.hunter.cuny.edu [Department of Biological Sciences, Hunter College of The City University of New York, New York, NY 10065 (United States); The Graduate Center Departments of Biology and Biochemistry, The City University of New York, New York, NY 10016 (United States); Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY 10065 (United States)

2016-11-01

Prostate cancer (PCa) is frequently diagnosed in men, and dysregulation of microRNAs is characteristic of many cancers. MicroRNA-1207-3p is encoded at the non-protein coding gene locus PVT1 on the 8q24 human chromosomal region, an established PCa susceptibility locus. However, the role of microRNA-1207-3p in PCa is unclear. We discovered that microRNA-1207-3p is significantly underexpressed in PCa cell lines in comparison to normal prostate epithelial cells. Increased expression of microRNA-1207-3p in PCa cells significantly inhibits proliferation, migration, and induces apoptosis via direct molecular targeting of FNDC1, a protein which contains a conserved protein domain of fibronectin (FN1). FNDC1, FN1, and the androgen receptor (AR) are significantly overexpressed in PCa cell lines and human PCa, and positively correlate with aggressive PCa. Prostate tumor FN1 expression in patients that experienced PCa-specific death is significantly higher than in patients that remained alive. Furthermore, FNDC1, FN1 and AR are concomitantly overexpressed in metastatic PCa. Consequently, these studies have revealed a novel microRNA-1207-3p/FNDC1/FN1/AR regulatory pathway in PCa. - Graphical abstract: miR-1207-3p/FNDC1/FN1/AR is a novel regulatory pathway in prostate cancer. - Highlights: • Expression of microRNA-1207-3p is significantly lost in prostate cancer (PCa) cells. • MicroRNA-1207-3p regulates proliferation, apoptosis, and migration via direct molecular targeting of the 3′UTR of FNDC1. • MicroRNA-1207-3p regulates proliferation, apoptosis, and migration via direct molecular targeting of the 3′UTR of FNDC1. • FNDC1, FN1, and AR are concurrently overexpressed in metastatic PCa.

MiR-137 inhibited cell proliferation and migration of vascular smooth muscle cells via targeting IGFBP-5 and modulating the mTOR/STAT3 signaling.

Directory of Open Access Journals (Sweden)

Jin Pan

Full Text Available Abnormal proliferation of vascular smooth muscle cells (VSMCs contributes to the development of cardiovascular diseases. Studies have shown the great impact of microRNAs (miRNAs on the cell proliferation of VSMCs. This study examined the effects of miR-137 on the cell proliferation and migration of VSMCs and also explored the underlying molecular mechanisms. The mRNA and protein expression levels were determined by qRT-PCR and western blot assays, respectively. The CCK-8 assay, wound healing assay and transwell migration assay were performed to measure cell proliferation and migration of VSMCs. The miR-137-targeted 3'untranslated region of insulin-like growth factor-binding protein-5 (IGFBP-5 was confirmed by luciferase reporter assay. Platelet-derived growth factor-bb (PDGF-bb treatment enhanced cell proliferation and suppressed the expression of miR-137 in VSMCs. The gain-of-function and loss-of-function assays showed that overexpression of miR-137 suppressed the cell proliferation and migration, and also inhibited the expression of matrix genes of VSMCs; down-regulation of miR-137 had the opposite effects on VSMCs. Bioinformatics analysis and luciferase report assay results showed that IGFBP-5 was a direct target of miR-137, and miR-137 overexpression suppressed the IGFBP-5 expression and down-regulation of miR-137 increased the IGFBP-5 expression in VSMCs. PDGF-bb treatment also increased the IGFBP-5 mRNA expression. In addition, enforced expression of IGFBP-5 reversed the inhibitory effects of miR-137 on cell proliferation and migration of VSMCs. More importantly, overexpression of miR-137 also suppressed the activity of mTOR/STAT3 signaling in VSMCs. Taken together, the results suggest that miR-137 may suppress cell proliferation and migration of VSMCs via targeting IGFBP-5 and modulating mTOR/STAT3 signaling pathway.

miR-206 inhibits cell proliferation, migration, and invasion by targeting BAG3 in human cervical cancer.

Science.gov (United States)

Wang, Yingying; Tian, Yongjie

2018-01-02

miR-206 and bcl2-associated athanogene 3 (BAG3) have been suggested as important regulators in various cancer types. However, the biological role of miR-206 and BAG3 in cervical cancer (CC) remains unclear. Here, we investigated the expressions and mechanisms of miR-206 and BAG3 in cervical cancer using in vitro and in vivo assays. In the present study, miR-206 expression was expressed at a lower level in CC tissues and cells than adjacent normal tissues and NEEC cells. By contrast, BAG3 mRNA and protein were expressed at higher levels in CC tissues and cells. Furthermore, miR-206 overexpression repressed cell proliferation, migration and invasion in vitro, and the 3'-untranslated region (3'-UTR) of BAG3 was a direct target of miR-206. miR-206 overexpression also inhibited EGFR, Bcl-2 and MMP2/9 protein expression, but promoted Bax protein expression. Besides, BAG3 over-expression partially abrogated miR-206-inhibited cell proliferation and invasion, while BAG3 silencing enhanced miR206-mediated inhibition. In vivo assay revealed that miR-206 repressed tumor growth in nude mice xenograft model. In conclusion, miR-206 inhibits cell proliferation, migration, and invasion by targeting BAG3 in human cervical cancer. Thus, miR-206-BAG3 can be used as a useful target for cervical cancer.

High-Performance Rh ₂ P Electrocatalyst for Efficient Water Splitting

Energy Technology Data Exchange (ETDEWEB)

Duan, Haohong [Department; Chemistry; Li, Dongguo [Materials; Tang, Yan [Department; amp, Molecular; He, Yang [Department; Ji, Shufang [Department; Wang, Rongyue [Materials; Lv, Haifeng [Materials; Lopes, Pietro P. [Materials; Paulikas, Arvydas P. [Materials; Li, Haoyi [Department; amp, Molecular; Mao, Scott X. [Department; Wang, Chongmin [Environmental; Markovic, Nenad M. [Materials; Li, Jun [Department; amp, Molecular; Stamenkovic, Vojislav R. [Materials; Li, Yadong [Department

2017-04-05

The search for active, stable, and cost-efficient electrocatalysts for hydrogen production via water splitting could make a substantial impact on energy technologies that do not rely on fossil fuels. Here we report the synthesis of rhodium phosphide electrocatalyst with low metal loading in the form of nanocubes (NCs) dispersed in high-surface-area carbon (Rh2P/C) by a facile solvo-thermal approach. The Rh2P/C NCs exhibit remarkable performance for hydrogen evolution reaction and oxygen evolution reaction compared to Rh/C and Pt/C catalysts. The atomic structure of the Rh2P NCs was directly observed by annular dark-field scanning transmission electron microscopy, which revealed a phosphorus-rich outermost atomic layer. Combined experimental and computational studies suggest that surface phosphorus plays a crucial role in determining the robust catalyst properties.

Relationship between mandibular anatomy and the occurrence of a bad split upon sagittal split osteotomy.

Science.gov (United States)

Aarabi, Mohammadali; Tabrizi, Reza; Hekmat, Mina; Shahidi, Shoaleh; Puzesh, Ayatollah

2014-12-01

A bad split is a troublesome complication of the sagittal split osteotomy (SSO). The aim of this study was to evaluate the relation between the occurrence of a bad split and mandibular anatomy in SSO using cone-beam computed tomography. The authors designed a cohort retrospective study. Forty-eight patients (96 SSO sites) were studied. The buccolingual thickness of the retromandibular area (BLR), the buccolingual thickness of the ramus at the level of the lingula (BLTR), the height of the mandible from the alveolar crest to the inferior border of the mandible, (ACIB), the distance between the sigmoid notch and the inferior border of the mandible (SIBM), and the anteroposterior width of the ramus (APWR) were measured. The independent t test was applied to compare anatomic measurements between the group with and the group without bad splits. The receiver operating characteristic (ROC) test was used to find a cutoff point in anatomic size for various parts of the mandible related to the occurrence of bad splits. The mean SIBM was 47.05±6.33 mm in group 1 (with bad splits) versus 40.66±2.44 mm in group 2 (without bad splits; P=.01). The mean BLTR was 5.74±1.11 mm in group 1 versus 3.19±0.55 mm in group 2 (P=.04). The mean BLR was 14.98±2.78 mm in group 1 versus 11.21±1.29 mm in group 2 (P=.001). No statistically significant difference was found for APWR and ACIB between the 2 groups. The ROC test showed cutoff points of 10.17 mm for BLR, 36.69 mm for SIBM, and 4.06 mm for BLTR. This study showed that certain mandibular anatomic differences can increase the risk of a bad split during SSO surgery. Copyright © 2014 American Association of Oral and Maxillofacial Surgeons. Published by Elsevier Inc. All rights reserved.

Habitat split and the global decline of amphibians.

Science.gov (United States)

Becker, Carlos Guilherme; Fonseca, Carlos Roberto; Haddad, Célio Fernando Baptista; Batista, Rômulo Fernandes; Prado, Paulo Inácio

2007-12-14

The worldwide decline in amphibians has been attributed to several causes, especially habitat loss and disease. We identified a further factor, namely "habitat split"-defined as human-induced disconnection between habitats used by different life history stages of a species-which forces forest-associated amphibians with aquatic larvae to make risky breeding migrations between suitable aquatic and terrestrial habitats. In the Brazilian Atlantic Forest, we found that habitat split negatively affects the richness of species with aquatic larvae but not the richness of species with terrestrial development (the latter can complete their life cycle inside forest remnants). This mechanism helps to explain why species with aquatic larvae have the highest incidence of population decline. These findings reinforce the need for the conservation and restoration of riparian vegetation.

Instant migration from Windows Server 2008 and 2008 R2 to 2012 how-to

CERN Document Server

Sivarajan, Santhosh

2013-01-01

Presented in a hands-on reference manual style, with real-world scenarios to lead you through each process. This book is intended for Windows server administrators who are performing migrations from their existing Windows Server 2008 / 2008 R2 environment to Windows Server 2012. The reader must be familiar with Windows Server 2008.

MicroRNA-127-3p inhibits proliferation and invasion by targeting SETD8 in human osteosarcoma cells

International Nuclear Information System (INIS)

Zhang, Jun; Hou, Wengen; Chai, Mingxiang; Zhao, Hongxing; Jia, Jinling; Sun, Xiaohui; Zhao, Bin; Wang, Ran

2016-01-01

MicroRNAs (miRNAs) play an essential role in cancer development. Several studies have indicated that miRNAs mediate tumorigenesis processes, such as, inflammation, proliferation, apoptosis and invasion. In the present study, we focused on the influence of the miR-127-3p on the proliferation, migration and invasion of osteosarcoma (OS). MiR-127-3p was found at reduced levels in OS tissues and cell lines. Overexpression of miR-127-3p in the OS cell lines significantly inhibited the cell proliferation, migration and invasion; however, inhibition of miR-127-3p increased the proliferation, migration and invasion of OS in vitro. SETD8 was identified as a direct target of miR-127-3p, and SETD8 expression decreased post miR-127-3p overexpression, while SETD8 overexpression could reverse the potential influence of miR-127-3p on the migration and invasion of OS cells. MiR-127-3p is suggested to act mainly via the suppression of SETD8 expression. Overall, the results revealed that miR-127-3p acts as a tumor suppressor and that its down-regulation in cancer may contribute to OS progression and metastasis, suggesting that miR-127-3p could be a potential therapeutic target in the treatment of OS. - Highlights: • MiR-127-3p is decreased in osteosarcoma tissues and cell lines. • MiR-127-3p overexpression suppresses cell migration and invasion in MG63 and U2OS. • SETD8 overexpression abolishes the roles of miR-127-3p in osteosarcoma.

Spin-Rotation Hyperfine Splittings at Moderate to High J Values in Methanol

Science.gov (United States)

Xu, Li-Hong; Hougen, Jon T.; Belov, Sergey; Golubiatnikov, G. Yu; Lapinov, Alexander; Ilyushin, V.; Alekseev, E. A.; Mescheryakov, A. A.

2015-06-01

In this talk we present a possible explanation, based on torsionally mediated proton-spin-overall-rotation interaction operators, for the surprising observation in Nizhny Novgorod several years ago of doublets in some Lamb-dip sub-millimeter-wave transitions between torsion-rotation states of E symmetry in methanol. These observed doublet splittings, some as large as 70 kHz, were later confirmed by independent Lamb-dip measurements in Kharkov. In this talk we first show the observed J-dependence of the doublet splittings for two b-type Q branches (one from each laboratory), and then focus on our theoretical explanation. The latter involves three topics: (i) group theoretically allowed terms in the spin-rotation Hamiltonian, (ii) matrix elements of these terms between the degenerate components of torsion-rotation E states, calculated using wavefunctions from an earlier global fit of torsion-rotation transitions of methanol in the vt = 0, 1, and 2 states, and (iii) least-squares fits of coefficients of these terms to about 35 experimentally resolved doublet splittings in the quantum number ranges of K = -2 to +2, J = 13 to 34, and vt = 0. Rather pleasing residuals are obtained for these doublet splittings, and a number of narrow transitions, in which no doublet splitting could be detected, are also in agreement with predictions from the theory. Some remaining disagreements between experiment and the present theoretical explanation will be mentioned. G. Yu. Golubiatnikov, S. P. Belov, A. V. Lapinov, "CH_3OH Sub-Doppler Spectroscopy," (Paper MF04) and S.P. Belov, A.V. Burenin, G.Yu. Golubiatnikov, A.V. Lapinov, "What is the Nature of the Doublets in the E-Methanol Lamb-dip Spectra?" (Paper FB07), 68th International Symposium on Molecular Spectroscopy, Columbus, Ohio, June 2013. Li-Hong Xu, J. Fisher, R.M. Lees, H.Y. Shi, J.T. Hougen, J.C. Pearson, B.J. Drouin, G.A. Blake, R. Braakman, "Torsion-Rotation Global Analysis of the First Three Torsional States (vt = 0, 1, 2

Identification and expression analysis of miR-144-5p and miR-130b-5p in dairy cattle

Directory of Open Access Journals (Sweden)

Z. Li

2017-07-01

Full Text Available MicroRNAs (miRNAs can coordinate the main pathways involved in innate and adaptive immune responses by regulating gene expression. To explore the resistance to mastitis in cows, miR-144-5p and miR-130b-5p were identified in bovine mammary gland tissue and 14 potential target genes belonging to the chemokine signaling pathway, the arginine and proline metabolism pathway and the mRNA surveillance pathway were predicted. Subsequently, we estimated the relative expression of miR-144-5p and miR-130b-5p in cow mammary tissues by using stem-loop quantitative real-time polymerase chain reaction. The results showed that the relative expression of miR-144-5p and miR-130b-5p in the mastitis-infected mammary tissues (n = 5 was significantly downregulated 0.14-fold (p < 0. 01 and upregulated 3.34-fold (p < 0. 01, respectively, compared to healthy tissues (n = 5. Our findings reveal that miR-144-5p and miR-130b-5p may have important roles in resistance to mastitis in dairy cattle.

p53/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis.

Science.gov (United States)

Wang, Wei; Liu, Haijun; Dai, Xiaoniu; Fang, Shencun; Wang, Xingang; Zhang, Yingming; Yao, Honghong; Zhang, Xilong; Chao, Jie

2015-11-18

Phagocytosis of SiO2 into the lung causes an inflammatory cascade that results in fibroblast proliferation and migration, followed by fibrosis. Clinical evidence has indicated that the activation of alveolar macrophages by SiO2 produces rapid and sustained inflammation characterized by the generation of monocyte chemotactic protein 1, which, in turn, induces fibrosis. However, the details of events downstream of monocyte chemotactic protein 1 activity in pulmonary fibroblasts remain unclear. Here, to elucidate the role of p53 in fibrosis induced by silica, both the upstream molecular mechanisms and the functional effects on cell proliferation and migration were investigated. Experiments using primary cultured adult human pulmonary fibroblasts led to the following results: 1) SiO2 treatment resulted in a rapid and sustained increase in p53 and PUMA protein levels; 2) the MAPK and PI3K pathways were involved in the SiO2-induced alteration of p53 and PUMA expression; and 3) RNA interference targeting p53 and PUMA prevented the SiO2-induced increases in fibroblast activation and migration. Our study elucidated a link between SiO2-induced p53/PUMA expression in fibroblasts and cell migration, thereby providing novel insight into the potential use of p53/PUMA in the development of novel therapeutic strategies for silicosis treatment.

miR-130b-3p Modulates Epithelial-Mesenchymal Crosstalk in Lung Fibrosis by Targeting IGF-1.

Science.gov (United States)

Li, Shuhong; Geng, Jing; Xu, Xuefeng; Huang, Xiaoxi; Leng, Dong; Jiang, Dingyuan; Liang, Jiurong; Wang, Chen; Jiang, Dianhua; Dai, Huaping

2016-01-01

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and usually lethal fibrotic lung disease with largely unknown etiology and pathogenesis. Evidence suggests microRNAs (miRNA) contribute to pathogenesis of IPF. In this study, we sought to identify miRNA expression signatures and determine the role of miR-130b-3p in lung fibrosis. The miRNA expression profile of the lungs from patients with IPF and normal donors was determined by Affymetrix microarray, and transcriptome with Affymetrix array. The functions and signal pathways as well as miRNA-mRNA networks were established by bioinformatics analysis. Luciferase assays and ELISA were used to confirm the miRNA target gene. The effect of miRNA-transfected epithelium on fibroblast activities was assessed using a co-culture system. The fibroblast activities were determined by qRT-PCR, western blotting, Transwell and BrdU assays. Seven miRNAs were significantly decreased in IPF lungs, with miR-130b-3p being the highest in the miRNA-mRNA network. Insulin-like growth factor (IGF-1) was a target gene of miR-130b-3p in the epithelium. miR-130b-3p inhibition in the epithelium induced collagen I expression and enhanced the proliferation and migration ability of fibroblast in co-culture systems, which mimicked the functions of exogenous IGF-1 on fibroblasts. Neutralizing IGF-1 with an antibody significantly reduced the modulatory effects of miR-130b-3p inhibitor-transfected epithelium on the activation of fibroblasts. Our results show that miR-130b-3p was downregulated in IPF lungs. miR-130b-3p downregulation contributed to the activation of fibroblasts and the dysregulated epithelial-mesenchymal crosstalk by promoting IGF-1 secretion from lung epithelium, suggesting a key regulatory role for this miRNA in preventing lung fibrosis.

TUG1 promotes osteosarcoma tumorigenesis by upregulating EZH2 expression via miR-144-3p

OpenAIRE

Cao, Jiaqing; Han, Xinyou; Qi, Xin; Jin, Xiangyun; Li, Xiaolin

2017-01-01

lncRNA-TUG1 (Taurine upregulated 1) is up regulated and highly correlated with poor prognosis and disease status in osteosarcoma. TUG1 knockdown inhibits osteosarcoma cell proliferation, migration and invasion, and promotes apoptosis. However, its mechanism of action has not been well addressed. Growing evidence documented that lncRNA works as competing endogenous (ce)RNAs to modulate the expression and biological functions of miRNA. As a putative combining target of TUG1, miR-144-3p has been...

P R Dhal

Indian Academy of Sciences (India)

Home; Journals; Sadhana. P R Dhal. Articles written in Sadhana. Volume 37 Issue 2 April 2012 pp 223-240. Multi-objective parametric optimization of powder mixed electro-discharge machining using response surface methodology and non-dominated sorting genetic algorithm · Soumyakant Padhee Niharranjan Nayak S K ...

Split-plot designs for robotic serial dilution assays.

Science.gov (United States)

Buzas, Jeffrey S; Wager, Carrie G; Lansky, David M

2011-12-01

This article explores effective implementation of split-plot designs in serial dilution bioassay using robots. We show that the shortest path for a robot to fill plate wells for a split-plot design is equivalent to the shortest common supersequence problem in combinatorics. We develop an algorithm for finding the shortest common supersequence, provide an R implementation, and explore the distribution of the number of steps required to implement split-plot designs for bioassay through simulation. We also show how to construct collections of split plots that can be filled in a minimal number of steps, thereby demonstrating that split-plot designs can be implemented with nearly the same effort as strip-plot designs. Finally, we provide guidelines for modeling data that result from these designs. © 2011, The International Biometric Society.

Covert orienting in the split brain: Right hemisphere specialization for object-based attention.

Science.gov (United States)

Kingstone, Alan

2015-12-18

The present paper takes as its starting point Phil Bryden's long-standing interest in human attention and the role it can play in laterality effects. Past split-brain research has suggested that object-based attention is lateralized to the left hemisphere [e.g., Egly, R., Rafal, R. D., Driver, J., & Starreveld, Y. (1994). Covert orienting in the split brain reveals hemispheric specialization for object-based attention. Psychological Science, 5(6), 380-382]. The task used to isolate object-based attention in that previous work, however, has been found wanting [Vecera, S. P. (1994). Grouped locations and object-based attention: Comment on Egly, Driver, and Rafal (1994). Journal of Experimental Psychology: General, 123(3), 316-320]; and indeed, subsequent research with healthy participants using a different task has suggested that object-based attention is lateralized to the opposite right hemisphere (RH) [Valsangkar-Smyth, M. A., Donovan, C. L., Sinnett, S., Dawson, M. R., & Kingstone, A. (2004). Hemispheric performance in object-based attention. Psychonomic Bulletin & Review, 11(1), 84-91]. The present study tested the same split-brain as Egly, Rafal, et al. (1994) but used the object-based attention task introduced by Valsangkar-Smyth et al. (2004). The results confirm that object-based attention is lateralized to the RH. They also suggest that subcortical interhemispheric competition may occur and be dominated by the RH.

Splitting strings on integrable backgrounds

Energy Technology Data Exchange (ETDEWEB)

Vicedo, Benoit

2011-05-15

We use integrability to construct the general classical splitting string solution on R x S{sup 3}. Namely, given any incoming string solution satisfying a necessary self-intersection property at some given instant in time, we use the integrability of the worldsheet {sigma}-model to construct the pair of outgoing strings resulting from a split. The solution for each outgoing string is expressed recursively through a sequence of dressing transformations, the parameters of which are determined by the solutions to Birkhoff factorization problems in an appropriate real form of the loop group of SL{sub 2}(C). (orig.)

Demethylation-mediated miR-129-5p up-regulation inhibits malignant phenotype of osteogenic osteosarcoma by targeting Homo sapiens valosin-containing protein (VCP).

Science.gov (United States)

Long, Xin Hua; Zhou, Yun Fei; Peng, Ai Fen; Zhang, Zhi Hong; Chen, Xuan Yin; Chen, Wen Zhao; Liu, Jia Ming; Huang, Shan Hu; Liu, Zhi Li

2015-05-01

Previous studies demonstrated that increased Homo sapiens valosin-containing protein (VCP) may be involved in osteosarcoma (OS) metastasis. However, the underlying mechanism of VCP over-expression in OS remains unknown. In the present study, we found a significantly negative correlation between miR-129-5p and VCP protein expression in OS tissues with pulmonary metastasis (Spearman's rho, rs = -0.948). Bioinformatical prediction, Luciferase reporter assay, Western blot, and RT-PCR assays performed on OS cells indicated that VCP is a target of miR-129-5p. In addition, three CPG islands in the region of miR-129-5p promoter were detected by bioinformatical prediction, and significantly higher expression of miR-129-5p and lower methylation level of miR-129-2 gene in OS cells treated with 5-Aza-2'-deoxycytidine (a potent DNA demethylating agent) than in those untreated cells were observed. Furthermore, lower migratory and invasive ability was found in cells with elevated miR-129-5p than in those with decreased miR-129-5p. These findings indicated that increased miR-129-5p may be mediated by demethylation and inhibit OS cell migration and invasion by targeting VCP in OS, and targeting miR-129-5p/VCP signaling pathway may serve as a therapeutic strategy for OS management, although further studies will be necessary.

French Policies towards the Chinese in Vietnam Les politiques françaises envers les Chinois du Viêt Nam : études des migrations et des réponses du colonisateur

Directory of Open Access Journals (Sweden)

Ramses Amer

2010-07-01

Full Text Available This study examines the patterns of Chinese migration to and from Vietnam as well as the demographic changes relating to the Chinese residing in the country. It also outlines how the French authorities responded to the arrival of the Chinese and how they treated them. The focus is on the period of French control over the whole of Vietnam from 1883 to 1954. The French authorities did pay considerable attention to the Chinese migration to Vietnam. The policies of the French aimed at keeping a close surveillance on the Chinese. To administer the Chinese communities the French opted to maintain the system of indirect control introduced by the Vietnamese Emperors. During the period of French rule the Chinese population grew considerably. Chinese migration to and from Vietnam was influenced by the political evolution in China and by repercussions of international economic developments. Thus, the French authorities could influence the migrants when they arrived or departed, but the decision to migrate was primarily due to other factors.Cette étude examine les modèles de la migration chinoise à destination et en provenance du Viêt Nam de même que les changements démographiques concernant les Chinois résidant dans le pays. Elle précise également les réponses des autorités françaises à l’arrivée des Chinois et le traitement qui leur était réservé. Elle traite tout spécialement la période du contrôle français sur le Viêt Nam de 1883 à 1954. Car les autorités françaises ont porté un intérêt considérable à la migration des Chinois au Viêt Nam. La politique française consistait à surveiller de près les Chinois. Pour l’administration des communautés chinoises les Français ont choisi de conserver le système de contrôle indirect mis en place par les empereurs vietnamiens. La population chinoise connut une croissance considérable pendant la période française. La migration vers et depuis le Viêt Nam était influenc

La migration des hydrocarbures dans les bassins sédimentaires: aspects géologiques et géochimiques Migration of Hydrocarbons in Sedimentary Basins: Geological and Geochemical Aspects

Directory of Open Access Journals (Sweden)

Tissot B. P.

2006-11-01

Full Text Available La migration du pétrole vers les réservoirs et les pièges, et particulièrement son expulsion hors de la roche-mère où il s'est formé (migration primaire, est demeurée longtemps un des problèmes les plus mal connus de toute la géologie pétrolière. Le déplacement du pétrole et du gaz s'effectue en phase hydrocarbure séparée. L'eau, souvent considérée comme le véhicule du pétrole dans la migration, joue en fait un rôle négatif : il faut que la saturation en eau ait suffisamment diminué (par expulsion et que la saturation en hydrocarbures ait suffisamment augmenté (par génération à partir du kérogène pour que l'écoulement d'une phase hydrocarbure devienne possible. Le moteur de cette expulsion est le gradient de pression : l'élévation de la pression dans l'espace poreux des roches-mères résulte de trois causes (la charge sédimentaire, la genèse des hydrocarbures, et l'expansion thermique de l'eau. La microfissuration, qui survient quand la pression interne des fluides dépasse la résistance mécanique de la roche peut jouer un rôle important. Les observations dans les bassins sédimentaires de cas bien documentés sont encore trop rares. Il est, en particulier, difficile de calculer les réserves mobilisées à l'échelle d'un permis ou d'un bassin. La modélisation numérique de la migration, associée à celle de la genèse du pétrole et du gaz, offre des perspectives dans ce sens, mais elle demande encore des travaux complémentaires. Parmi les conséquences de la migration, on peut citer : la possibilité de corrélation huile/roche-mère, la teneur plus faible en produits lourds dans les réservoirs que dans les roches-mères et le rôle souvent joué par un déplacement où hydrocarbures liquides et gazeux forment une phase unique, qui migre en laissant progressivement derrière elle les fractions plus lourdes, par condensation rétrograde. Oil migration toward reservoirs and traps, and especially its

The genetic landscape of Equatorial Guinea and the origin and migration routes of the Y chromosome haplogroup R-V88.

Science.gov (United States)

González, Miguel; Gomes, Verónica; López-Parra, Ana Maria; Amorim, António; Carracedo, Angel; Sánchez-Diz, Paula; Arroyo-Pardo, Eduardo; Gusmão, Leonor

2013-03-01

Human Y chromosomes belonging to the haplogroup R1b1-P25, although very common in Europe, are usually rare in Africa. However, recently published studies have reported high frequencies of this haplogroup in the central-western region of the African continent and proposed that this represents a 'back-to-Africa' migration during prehistoric times. To obtain a deeper insight into the history of these lineages, we characterised the paternal genetic background of a population in Equatorial Guinea, a Central-West African country located near the region in which the highest frequencies of the R1b1 haplogroup in Africa have been found to date. In our sample, the large majority (78.6%) of the sequences belong to subclades in haplogroup E, which are the most frequent in Bantu groups. However, the frequency of the R1b1 haplogroup in our sample (17.0%) was higher than that previously observed for the majority of the African continent. Of these R1b1 samples, nine are defined by the V88 marker, which was recently discovered in Africa. As high microsatellite variance was found inside this haplogroup in Central-West Africa and a decrease in this variance was observed towards Northeast Africa, our findings do not support the previously hypothesised movement of Chadic-speaking people from the North across the Sahara as the explanation for these R1b1 lineages in Central-West Africa. The present findings are also compatible with an origin of the V88-derived allele in the Central-West Africa, and its presence in North Africa may be better explained as the result of a migration from the south during the mid-Holocene.

GPC1 Regulated by miR-96-5p, Rather than miR-182-5p, in Inhibition of Pancreatic Carcinoma Cell Proliferation

Directory of Open Access Journals (Sweden)

Chunlong Li

2014-04-01

Full Text Available To determine the relationships between miR-96-5p/-182-5p and GPC1 in pancreatic cancer (PC, we conducted the population and in vitro studies. We followed 38 pancreatic cancer patients, measured and compared the expression of miR-96-5p/-182-5p, GPC1, characteristics and patients’ survival time of different miR-96-5p/-182-5p expression levels in PC tissues. In an in vitro study, we investigated the proliferation, cycle and apotosis in cells transfected with mimics/inhibitors of the two miRNAs, and determine their effects on GPC1 by dual-luciferase assay. In the follow-up study, we found that the expressions of miR-96-5p/-182-5p were lower/higher in PC tissues; patients with lower/higher levels of miR-96-5p/-182-5p suffered poorer characteristics and decreased survival time. In the in vitro study, the expressions of miR-96-5p/-182-5p were different in cells. Proliferation of cells transfected with miR-96-5p mimics/inhibitors was lower/higher in Panc-1/BxPC-3; when transfected with miR-182-5p mimics/inhibitors, proliferation of cells were higher/lower in AsPC-1/Panc-1. In a cell cycle study, panc-1 cells transfected with miR-96-5p mimics was arrested at G0/G1; BxPC-3 cells transfected with miR-96-5p inhibitors showed a significantly decrease at G0/G1; AsPC-1 cells transfected with miR-182-5p mimics was arrested at S; Panc-1 cells transfected with miR-182-5p inhibitors showed a decrease at S. MiR-96-5p mimics increased the apoptosis rate in Panc-1 cells, and its inhibitors decreased the apoptosis rate in BxPC-3. Dual luciferase assay revealed that GPC1 was regulated by miR-96-5p, not -182-5p. We found that miR-96-5p/-182-5p as good markers for PC; miR-96-5p, rather than -182-5p, inhibits GPC1 to suppress proliferation of PC cells.

P R Umashankar

Indian Academy of Sciences (India)

Home; Journals; Bulletin of Materials Science. P R Umashankar. Articles written in Bulletin of Materials Science. Volume 25 Issue 2 April 2002 pp 141-154 Biomaterials. Bone growth response with porous hydroxyapatite granules in a critical sized lapine tibial-defect model · Annie John S Abiraman H K Varma T V Kumari ...

Ouabain affects cell migration via Na,K-ATPase-p130cas and via nucleus-centrosome association.

Directory of Open Access Journals (Sweden)

Young Ou

Full Text Available Na,K-ATPase is a membrane protein that catalyzes ATP to maintain transmembrane sodium and potassium gradients. In addition, Na,K-ATPase also acts as a signal-transducing receptor for cardiotonic steroids such as ouabain and activates a number of signalling pathways. Several studies report that ouabain affects cell migration. Here we used ouabain at concentrations far below those required to block Na,K-ATPase pump activity and show that it significantly reduced RPE cell migration through two mechanisms. It causes dephosphorylation of a 130 kD protein, which we identify as p130cas. Src is involved, because Src inhibitors, but not inhibitors of other kinases tested, caused a similar reduction in p130cas phosphorylation and ouabain increased the association of Na,K-ATPase and Src. Knockdown of p130cas by siRNA reduced cell migration. Unexpectedly, ouabain induced separation of nucleus and centrosome, also leading to a block in cell migration. Inhibitor and siRNA experiments show that this effect is mediated by ERK1,2. This is the first report showing that ouabain can regulate cell migration by affecting nucleus-centrosome association.

Engineered split in Pfu DNA polymerase fingers domain improves incorporation of nucleotide γ-phosphate derivative

Science.gov (United States)

Hansen, Connie J.; Wu, Lydia; Fox, Jeffrey D.; Arezi, Bahram; Hogrefe, Holly H.

2011-01-01

Using compartmentalized self-replication (CSR), we evolved a version of Pyrococcus furiosus (Pfu) DNA polymerase that tolerates modification of the γ-phosphate of an incoming nucleotide. A Q484R mutation in α-helix P of the fingers domain, coupled with an unintended translational termination-reinitiation (split) near the finger tip, dramatically improve incorporation of a bulky γ-phosphate-O-linker-dabcyl substituent. Whether synthesized by coupled translation from a bicistronic (−1 frameshift) clone, or reconstituted from separately expressed and purified fragments, split Pfu mutant behaves identically to wild-type DNA polymerase with respect to chromatographic behavior, steady-state kinetic parameters (for dCTP), and PCR performance. Although naturally-occurring splits have been identified previously in the finger tip region of T4 gp43 variants, this is the first time a split (in combination with a point mutation) has been shown to broaden substrate utilization. Moreover, this latest example of a split hyperthermophilic archaeal DNA polymerase further illustrates the modular nature of the Family B DNA polymerase structure. PMID:21062827

Engineered split in Pfu DNA polymerase fingers domain improves incorporation of nucleotide gamma-phosphate derivative.

Science.gov (United States)

Hansen, Connie J; Wu, Lydia; Fox, Jeffrey D; Arezi, Bahram; Hogrefe, Holly H

2011-03-01

Using compartmentalized self-replication (CSR), we evolved a version of Pyrococcus furiosus (Pfu) DNA polymerase that tolerates modification of the γ-phosphate of an incoming nucleotide. A Q484R mutation in α-helix P of the fingers domain, coupled with an unintended translational termination-reinitiation (split) near the finger tip, dramatically improve incorporation of a bulky γ-phosphate-O-linker-dabcyl substituent. Whether synthesized by coupled translation from a bicistronic (-1 frameshift) clone, or reconstituted from separately expressed and purified fragments, split Pfu mutant behaves identically to wild-type DNA polymerase with respect to chromatographic behavior, steady-state kinetic parameters (for dCTP), and PCR performance. Although naturally-occurring splits have been identified previously in the finger tip region of T4 gp43 variants, this is the first time a split (in combination with a point mutation) has been shown to broaden substrate utilization. Moreover, this latest example of a split hyperthermophilic archaeal DNA polymerase further illustrates the modular nature of the Family B DNA polymerase structure.

Recombinant rubistatin (r-Rub), an MVD disintegrin, inhibits cell migration and proliferation, and is a strong apoptotic inducer of the human melanoma cell line SK-Mel-28.

Science.gov (United States)

Carey, Clayton M; Bueno, Raymund; Gutierrez, Daniel A; Petro, Christopher; Lucena, Sara E; Sanchez, Elda E; Soto, Julio G

2012-02-01

Disintegrins are low molecular weight peptides isolated from viper venom. These peptides bind to integrin receptors using a conserved binding motif sequence containing an RGD or similar motif. As a consequence, disintegrins can inhibit platelet aggregation and inhibit cell migration, proliferation, and initiate apoptosis in cancer cell lines. Rubistatin is a MVD disintegrin cloned from a Crotalus ruber ruber venom gland. The biological activity of MVD disintegrins is poorly understood. Recombinant rubistatin (r-Rub) was cloned into a pET32b plasmid and expressed in reductase-deficient Escherichia coli. Expression was induced with IPTG and the resulting fusion peptide was affinity purified, followed by thrombin cleavage, and removal of vector coded sequences. r-Rub peptide inhibited ADP-induced platelet aggregation by 54% ± 6.38 in whole blood. We assessed the ability of r-Rub to initiate apoptosis in three human cancer cell lines. Cultures of SK-Mel-28, HeLA, and T24 cells were grown for 24 h with 2.5 μM r-Rub followed by Hoechst staining. Chromatin fragmentation was observed in treated SK-Mel-28, but not in T24 or HeLA cells. A TUNEL assay revealed that 51.55% ± 5.28 of SK-Mel-28 cells were apoptotic after 18 h of treatment with 3.5 μM of r-Rub. Cell migration and proliferation assays were performed in order to further characterize the biological effects of r-Rub on SK-Mel-28 cells. At 3 μM, r-Rub inhibited cell migration by 44.4% ± 0.5, while at 3.5 μM it was able to inhibit cell proliferation by 83% ± 6.0. Copyright © 2011 Elsevier Ltd. All rights reserved.

High-Performance Rh ₂ P Electrocatalyst for Efficient Water Splitting

Energy Technology Data Exchange (ETDEWEB)

Duan, Haohong; Li, Dongguo; Tang, Yan; He, Yang; Ji, Shufang; Wang, Rongyue; Lv, Haifeng; Lopes, Pietro P.; Paulikas, Arvydas P.; Li, Haoyi; Mao, Scott X.; Wang, Chongmin; Markovic, Nenad M.; Li, Jun; Stamenkovic, Vojislav R.; Li, Yadong

2017-04-05

Search for active, stable and cost-efficient electrocatalysts for hydrogen production via water splitting could make substantial impact to the energy technologies that do not rely on fossil fuels. Here we report the synthesis of rhodium phosphide electrocatalyst with low metal loading in the form of nanocubes (NCs) dispersed in high surface area carbon (Rh2P/C) by a facile solvo-thermal approach. The Rh2P/C NCs exhibit remarkable performance for hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) compared to Rh/C and Pt/C catalysts. The atomic structure of the rhodium phosphide nanocubes was directly observed by annular dark-field scanning transmission electron microscopy (ADF-STEM), which revealed phosphorous-rich outermost atomic layer. Combined experimental and computational studies suggest that surface phosphorous plays crucial role in determining the robust catalyst properties.

miR-654-5p Targets GRAP to Promote Proliferation, Metastasis, and Chemoresistance of Oral Squamous Cell Carcinoma Through Ras/MAPK Signaling.

Science.gov (United States)

Lu, Meng; Wang, Chengyong; Chen, Weihui; Mao, Chuanqing; Wang, Jin

2018-04-01

Oral squamous cell carcinoma (OSCC) is characterized by rapid local migration and invasion. This study was aimed at clarifying the effect of miR-654-5p on progression of OSCC. miR-654-5p promoted proliferation, metastasis, and chemoresistance of OSCC in vitro and in vivo. Consistently, miR-654-5p was upregulated in late-stage OSCC and was correlated with poor prognosis of OSCC patients. Furthermore, miR-654-5p was mechanistically verified to target Grb-2-related adaptor protein (GRAP), accompanied by the activation of Ras/MAPK signaling and the facilitation of epithelial-mesenchymal transition in OSCC cells. GRAP was downregulated in T1-2 stage versus T3-4 stage head and neck squamous cell carcinoma (HNSC) and was negatively correlated with tumor-node-metastases (TNM) stage in HNSC patients based on The Cancer Genome Atlas (TCGA) analysis. In addition, GRAP was positively correlated with good prognosis in HNSC patients. Our findings suggest that the miR-654-5p/GRAP/Ras/Erk signaling pathway in OSCC cells might contribute to the underlying mechanism through which miR-654-5p participates in the regulation of OSCC progression. miR-654-5p, as a potential biomarker for the clinical diagnosis and prognosis of OSCC, may be an effective anticancer target for the treatment of OSCC.

Interplay between long noncoding RNA ZEB1-AS1 and miR-101/ZEB1 axis regulates proliferation and migration of colorectal cancer cells.

Science.gov (United States)

Xiong, Wan-Cheng; Han, Na; Wu, Nan; Zhao, Ke-Lei; Han, Chen; Wang, Hui-Xin; Ping, Guan-Fang; Zheng, Peng-Fei; Feng, Hailong; Qin, Lei; He, Peng

2018-01-01

Long noncoding RNAs (lncRNAs) are dysregulated in many diseases. MicroRNA-101 (miR-101) functions as a tumor suppressor by directly targeting ZEB1 in various cancers. However, the potential mechanism of lncRNA ZEB1-AS1 and miR-101/ZEB1 axis in CRC remains unknown. In this study, we further investigated the potential interplay between miR-101/ZEB1 axis and lncRNA ZEB1-AS1 in colorectal cancer (CRC). Results showed that ZEB1-AS1 was upregulated in CRC tissues and cells. MiR-101 was downregulated in CRC tissues and negatively correlated with ZEB1-AS1 and ZEB1 expression levels in CRC. Functional experiments showed that, consistent with ZEB1-AS1 depletion, miR-101 overexpression and ZEB1 depletion inhibited the proliferation and migration of CRC cells. Overexpression of miR-101 partially abolished the effects of ZEB1-AS1 on the proliferation and migration of these cells. Moreover, combined ZEB1-AS1 depletion and miR-101 overexpression significantly inhibited cell proliferation and migration of the CRC cells. Hence, ZEB1-AS1 functioned as a molecular sponge for miR-101 and relieved the inhibition of ZEB1 caused by miR-101. This study revealed a novel regulatory mechanism between ZEB1-AS1 and miR-101/ZEB1 axis. The interplay between ZEB1-AS1 and miR-101/ZEB1 axis contributed to the proliferation and migration of CRC cells, and targeting this interplay could be a promising strategy for CRC treatment.

Mir-513a-3p contributes to the controlling of cellular migration processes in the A549 lung tumor cells by modulating integrin β-8 expression.

Science.gov (United States)

da Silveira, Marina Bonfogo; Lima, Kelvin Furtado; da Silva, Andrea Renata; Dos Santos, Robson Augusto Souza; Moraes, Karen C M

2017-12-04

Lung tumors are a frequent type of cancer in humans and a leading cause of death, and the late diagnostic contributes to high mortality rates. New therapeutic strategies are needed, and the heptapeptide angiotensin-(1-7) [ang-(1-7)] demonstrated the ability to control cancer growth rates and migration in vitro and in vivo. However, the possible use of the heptapeptide in clinical trials demands deeper analyses to elucidate molecular mechanisms of its effect in the target cells. In this study, we investigated relevant elements that control pro-inflammatory environment and cellular migration, focusing in the post-transcription mechanism using lung tumor cell line. In our cellular model, the microRNA-513a-3p was identified as a novel element targeting ITG-β8, thereby controlling the protein level and its molecular function in the controlling of migration and pro-inflammatory environment. These findings provide useful information for future studies, using miR-513a-3p as an innovative molecular tool to control lung tumor cell migration, which will support more effective clinical treatment of the patients with the widely used chemotherapeutic agents, increasing survival rates.

Embryo splitting

Directory of Open Access Journals (Sweden)

Karl Illmensee

2010-04-01

Full Text Available Mammalian embryo splitting has successfully been established in farm animals. Embryo splitting is safely and efficiently used for assisted reproduction in several livestock species. In the mouse, efficient embryo splitting as well as single blastomere cloning have been developed in this animal system. In nonhuman primates embryo splitting has resulted in several pregnancies. Human embryo splitting has been reported recently. Microsurgical embryo splitting under Institutional Review Board approval has been carried out to determine its efficiency for blastocyst development. Embryo splitting at the 6–8 cell stage provided a much higher developmental efficiency compared to splitting at the 2–5 cell stage. Embryo splitting may be advantageous for providing additional embryos to be cryopreserved and for patients with low response to hormonal stimulation in assisted reproduction programs. Social and ethical issues concerning embryo splitting are included regarding ethics committee guidelines. Prognostic perspectives are presented for human embryo splitting in reproductive medicine.

Bad splits in bilateral sagittal split osteotomy: systematic review and meta-analysis of reported risk factors.

Science.gov (United States)

Steenen, S A; van Wijk, A J; Becking, A G

2016-08-01

An unfavourable and unanticipated pattern of the bilateral sagittal split osteotomy (BSSO) is generally referred to as a 'bad split'. Patient factors predictive of a bad split reported in the literature are controversial. Suggested risk factors are reviewed in this article. A systematic review was undertaken, yielding a total of 30 studies published between 1971 and 2015 reporting the incidence of bad split and patient age, and/or surgical technique employed, and/or the presence of third molars. These included 22 retrospective cohort studies, six prospective cohort studies, one matched-pair analysis, and one case series. Spearman's rank correlation showed a statistically significant but weak correlation between increasing average age and increasing occurrence of bad splits in 18 studies (ρ=0.229; Pbad split among the different splitting techniques. A meta-analysis pooling the effect sizes of seven cohort studies showed no significant difference in the incidence of bad split between cohorts of patients with third molars present and concomitantly removed during surgery, and patients in whom third molars were removed at least 6 months preoperatively (odds ratio 1.16, 95% confidence interval 0.73-1.85, Z=0.64, P=0.52). In summary, there is no robust evidence to date to show that any risk factor influences the incidence of bad split. Copyright © 2016 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Measurement of the Shared Momentum Fraction zg using Jet Reconstruction in p + p and Au + Au Collisions with STAR

Science.gov (United States)

Kauder, K.; STAR Collaboration

2017-11-01

One key difference in current energy loss models lies in the treatment of the Altarelli-Parisi, AP, splitting functions. It has been shown that the shared momentum fraction, henceforth called Jet Splitting Functionzg as determined by the SoftDrop grooming process can be made a Sudakov-safe measurement of the symmetrized AP functions in p+p collisions. The STAR collaboration presents the first zg measurements at √{sNN} = 200 GeV in p+p and Au+Au collisions, where in Au+Au we use a set of di-jets with hard cores reconstructed with a 2 GeV/c constituent cut. For a jet resolution parameter of R = 0.4, these di-jet pairs were found to be significantly imbalanced with respect to p+p, yet regained balance when all soft constituents were included. We find that within uncertainties there are no signs of a modified Jet Splitting Function on trigger or recoil sides of this di-jet selection.

miR-148a suppresses cell invasion and migration in gastric cancer by targeting DNA methyltransferase 1.

Science.gov (United States)

Shi, Huaijie; Chen, Xiaojing; Jiang, Hao; Wang, Xujie; Yu, Hao; Sun, Pijiang; Sui, Xin

2018-04-01

Gastric cancer (GC) is the fourth most common malignant tumor globally. The highest incidence of GC is found in Eastern Asia, particularly in China. It is therefore imperative to further elucidate the molecular pathogenesis of GC in order to identify new biomarkers and targets for effective therapy. In the present study, we determined whether miR-148a was aberrantly downregulated in gastric cancer tissues and significantly correlated with aggressive clinicopathological characteristics in the MGC-803, HGC-27 and GES-1 cell lines using reverse transcription-quantitative PCR and western blot analysis. The cell lines were obtained from 60 patients who presented at our hospital between September 2010 and July 2015. The results showed that, miR-148a was aberrantly downregulated in GC tissues and its expression was relatively lower in the MGC-803 and HGC-27 GC cell lines than in the normal gastric epithelial cell line, GES-1. The clinicopathological analysis revealed that a decrease of miR-148a was significantly correlated with lymph-node metastasis (Pblot analysis. Furthermore, we found that the re-expression of DNMT1 reversed the inhibition of cell migration and invasion induced by miR-148a. Taken together, we demonstrated that miR-148a suppresses cell invasion and migration in gastric cancer by regulating DNMT1 expression. The miR-148a/DNMT1 axis may therefore be a new potential target for GC therapy.

Aryl hydrocarbon receptor–ligand axis mediates pulmonary fibroblast migration and differentiation through increased arachidonic acid metabolism

International Nuclear Information System (INIS)

Su, Hsiang-Han; Lin, Hsin-Ting; Suen, Jau-Ling; Sheu, Chau Chyun; Yokoyama, Kazunari K.; Huang, Shau-Ku; Cheng, Chih Mei

2016-01-01

Pulmonary fibroblast migration and differentiation are critical events in fibrogenesis; meanwhile, fibrosis characterizes the pathology of many respiratory diseases. The role of aryl hydrocarbon receptor (AhR), a unique cellular chemical sensor, has been suggested in tissue fibrosis, but the mechanisms through which the AhR-ligand axis influences the fibrotic process remain undefined. In this study, the potential impact of the AhR-ligand axis on pulmonary fibroblast migration and differentiation was analyzed using human primary lung fibroblasts HFL-1 and CCL-202 cells. Boyden chamber-based cell migration assay showed that activated AhR in HFL-1cells significantly enhanced cell migration in response to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), and a known AhR antagonist, CH223191, inhibited its migratory activity. Furthermore, the calcium mobilization and subsequent upregulated expression of arachidonic acid metabolizing enzymes, including cyclooxygenase2 (COX-2) and 5-lipoxygenase (5-LOX), were observed in TCDD-treated HFL-1 cells, concomitant with elevated levels of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) secretion. Also, significantly increased expression of α-smooth muscle actin α-SMA), a fibroblast differentiation marker, was also noted in TCDD-treated HFL-1 cells (p < 0.05), resulting in a dynamic change in cytoskeleton protein levels and an increase in the nuclear translocation of the myocardin-related transcription factor. Moreover, the enhanced levels of α-SMA expression and fibroblast migration induced by TCDD, PGE2 and LTB4 were abrogated by selective inhibitors for COX-2 and 5-LOX. Knockdown of AhR by siRNA Completely diminished intracellular calcium uptake and reduced α-SMA protein verified by promoter-reporter assays and chromatin immunoprecipitation. Taken together, our results suggested the importance of the AhR-ligand axis in fibroblast migration and differentiation through its capacity in enhancing arachidonic acid metabolism.

High-efficiency p-n junction oxide photoelectrodes for photoelectrochemical water splitting.

Science.gov (United States)

Liu, Zhifeng; Yan, Lu

2016-11-16

Development of all oxide p-n junctions makes a significant advancement in photoelectrode catalysis functional materials. In this article, we report the preparation of TiO 2 nanorod (NR)/Cu 2 O photoanodes via a simple hydrothermal method followed by an electrochemical deposition process. This facile synthesis route can simultaneously achieve uniform TiO 2 NR/Cu 2 O composite nanostructures and obtain varied amounts of Cu 2 O by controlling the deposition time. The photocurrent density of TiO 2 NR/Cu 2 O heterojunction photoanodes enhanced the photocatalytic activity with a photocurrent density of 5.25 mA cm -2 at 1.23 V versus RHE compared to pristine TiO 2 NR photoanodes under the same conditions. It is demonstrated that the presence of Cu 2 O has played an important role in expanding the spectral response region and reducing the photogenerated charge recombination rate. More importantly, the results provide new insights into the performance of all oxide p-n junctions as photoanodes for PEC water splitting.

Shear-wave splitting measurements – Problems and solutions

Czech Academy of Sciences Publication Activity Database

Vecsey, Luděk; Plomerová, Jaroslava; Babuška, Vladislav

2008-01-01

Roč. 462, č. 1-4 (2008), s. 178-196 ISSN 0040-1951 R&D Projects: GA AV ČR(CZ) KJB300120605; GA AV ČR IAA3012405; GA AV ČR IAA300120709 Institutional research plan: CEZ:AV0Z30120515 Keywords : seismic anisotropy * shear-wave splitting * comparison of cross- correlation * eigenvalue * transverse minimization methods Subject RIV: DC - Siesmology, Volcanology, Earth Structure Impact factor: 1.677, year: 2008

Upregulation of long non-coding RNA TUG1 promotes bladder cancer cell 5 proliferation, migration and invasion by inhibiting miR-29c.

Science.gov (United States)

Guo, Peng; Zhang, Guohui; Meng, Jialin; He, Qian; Li, Zhihui; Guan, Yawei

2018-01-10

Bladder cancer (BC) is one of the leading causes of cancer-related death in the word. Long non-coding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) plays an important role in the development and progression of numerous cancers, including BC. However, the exact role of TUG1 in modulating BC progression is still poorly known. In this study, we found that TUG1 was upregulated and microRNA-29c (miR-29c) was downregulated in BC tissues and cell lines. Overexpression of TUG1 promoted the cell proliferation of T24 and EJ cells, whereas TUG1 knockdown had the opposite effect. Upregulation of TUG1 obviously facilitated the migration and invasion of T24 and EJ cells. In contrast, TUG1 silencing repressed the migration and invasion of T24 and EJ cells. Furthermore, TUG1 knockdown markedly increased the expression of miR-29c in vitro. On the contrary, overexpression of TUG1 remarkably decreased the expression of miR-29c. Transfection with plasmids containing mutant TUG1 has no effect on the expression of miR-29c. There were direct interactions between miR-29c and the binding sites of TUG1. In addition, the inhibitory effects of small interfering RNA specific for TUG1 on BC cell proliferation, migration and invasion were reversed by downregulation of miR-29c. Collectively, our study strongly demonstrates that TUG1 promotes BC cell proliferation, migration and invasion by inhibiting miR-29c, suggesting that lncRNATUG1 may be a promising target for BC gene therapy.

Low grade inflammation inhibits VEGF induced HUVECs migration in p53 dependent manner

International Nuclear Information System (INIS)

Panta, Sushil; Yamakuchi, Munekazu; Shimizu, Toshiaki; Takenouchi, Kazunori; Oyama, Yoko; Koriyama, Toyoyasu; Kojo, Tsuyoshi; Hashiguchi, Teruto

2017-01-01

In the course of studying crosstalk between inflammation and angiogenesis, high doses of pro-inflammatory factors have been reported to induce apoptosis in cells. Under normal circumstances also the pro-inflammatory cytokines are being released in low doses and are actively involved in cell signaling pathways. We studied the effects of low grade inflammation in growth factor induced angiogenesis using tumor necrosis factor alfa (TNFα) and vascular endothelial growth factor A (VEGF) respectively. We found that low dose of TNFα can inhibit VEGF induced angiogenesis in human umbilical vein endothelial cells (HUVECs). Low dose of TNFα induces mild upregulation and moreover nuclear localization of tumor suppressor protein 53 (P53) which causes decrease in inhibitor of DNA binding-1 (Id1) expression and shuttling to the cytoplasm. In absence of Id1, HUVECs fail to upregulate β 3 -integrin and cell migration is decreased. Connecting low dose of TNFα induced p53 to β 3 -integrin through Id1, we present additional link in cross talk between inflammation and angiogenesis. - Highlights: • Low grade inflammation (low dose of TNF alfa) inhibits VEGF induced endothelial cells migration. • The low grade inflammation with VEGF treatment upregulates P53 to a nonlethal level. • P53 activation inhibits Id1 shuttling to the cytoplasm in endothelial cells. • Inhibition of Id1 resulted in downregulation of β 3 -integrin which cause decrease in cell migration. • Inflammation and angiogenesis might cross-talk by P53 – Id1 – β 3 -integrin pathway in endothelial cells.

Liraglutide attenuates the migration of retinal pericytes induced by advanced glycation end products.

Science.gov (United States)

Lin, Wen-Jian; Ma, Xue-Fei; Hao, Ming; Zhou, Huan-Ran; Yu, Xin-Yang; Shao, Ning; Gao, Xin-Yuan; Kuang, Hong-Yu

2018-07-01

Retinal pericyte migration represents a novel mechanism of pericyte loss in diabetic retinopathy (DR), which plays a crucial role in the early impairment of the blood-retinal barrier (BRB). Glucagon-like peptide-1 (GLP-1) has been shown to protect the diabetic retina in the early stage of DR; however, the relationship between GLP-1 and retinal pericytes has not been discussed. In this study, advanced glycation end products (AGEs) significantly increased the migration of primary bovine retinal pericytes without influencing cell viability. AGEs also significantly enhanced phosphatidylinositol 3-kinase (PI3K)/Akt activation, and changed the expressions of migration-related proteins, including phosphorylated focal adhesion kinase (p-FAK), matrix metalloproteinase (MMP)-2 and vinculin. PI3K inhibition significantly attenuated the AGEs-induced migration of retinal pericytes and reversed the overexpression of MMP-2. Glucagon-like peptide-1 receptor (Glp1r) was expressed in retinal pericytes, and liraglutide, a GLP-1 analog, significantly attenuated the migration of pericytes by Glp1r and reversed the changes in p-Akt/Akt, p-FAK/FAK, vinculin and MMP-2 levels induced by AGEs, indicating that the protective effect of liraglutide was associated with the PI3K/Akt pathway. These results provided new insights into the mechanism underlying retinal pericyte migration. The early use of liraglutide exerts a potential bebefical effect on regulating pericyte migration, which might contribute to mechanisms that maintain the integrity of vascular barrier and delay the development of DR. Copyright © 2018 Elsevier Inc. All rights reserved.

Androgen receptor regulated microRNA miR-182-5p promotes prostate cancer progression by targeting the ARRDC3/ITGB4 pathway

Energy Technology Data Exchange (ETDEWEB)

Yao, Jingjing [Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, 200433 (China); Xu, Chen [Research Center of Developmental Biology, Second Military Medical University, 800th Xiangyin Road, Shanghai, 200433 (China); Department of Orthopedics, Changzheng Hospital Affiliated to Second Military Medical University, 415th Feng Yang Road, Shanghai, 200003 (China); Fang, Ziyu; Li, Yaoming [Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, 200433 (China); Liu, Houqi; Wang, Yue [Research Center of Developmental Biology, Second Military Medical University, 800th Xiangyin Road, Shanghai, 200433 (China); Translational Medicine Center, Second Military Medical University, 800th Xiangyin Road, Shanghai, 200433 (China); Xu, Chuanliang [Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, 200433 (China); Sun, Yinghao, E-mail: sunyh@medmail.com.cn [Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, 200433 (China)

2016-05-20

Abstracts: MicroRNAs (miRNAs) are important endogenous gene regulators that play key roles in prostate cancer development and metastasis. However, specific miRNA expression patterns in prostate cancer tissues from Chinese patients remain largely unknown. In this study, we compared miRNA expression patterns in 65 pairs of prostate cancer and para-cancer tissues by RNA sequencing and found that miR-182-5p was the most up-regulated miRNA in prostate cancer tissues. The result was validated using realtime PCR in 18 pairs of prostate cancer and para-cancer tissues. In in vitro analysis, it was confirmed that miR-182-5p promotes prostate cancer cell proliferation, invasion and migration and inhibit apoptosis. In addition, the androgen receptor directly regulated the transcription of miR-182-5p, which could target to the 3′UTR of ARRDC3 mRNA and affect the expression of ARRDC3 and its downstream gene ITGB4. For the in vivo experiment, miR-182-5p overexpression also promoted the growth and progression of prostate cancer tumors. In this regard, we suggest that miR-182-5p may be a key androgen receptor-regulated factor that contributes to the development and metastasis of Chinese prostate cancers and may be a potential target for the early diagnosis and therapeutic studies of prostate cancer. -- Highlights: •miR-182-5p is the mostly up-regulated miRNA in Chinese prostate cancer. •miR-182-5p is regulated by androgen receptor. •miR-182-5p promotes prostate cancer progression. •miR-182-5p regulates ARRDC3/ITGB4 pathway.

Androgen receptor regulated microRNA miR-182-5p promotes prostate cancer progression by targeting the ARRDC3/ITGB4 pathway

International Nuclear Information System (INIS)

Yao, Jingjing; Xu, Chen; Fang, Ziyu; Li, Yaoming; Liu, Houqi; Wang, Yue; Xu, Chuanliang; Sun, Yinghao

2016-01-01

Abstracts: MicroRNAs (miRNAs) are important endogenous gene regulators that play key roles in prostate cancer development and metastasis. However, specific miRNA expression patterns in prostate cancer tissues from Chinese patients remain largely unknown. In this study, we compared miRNA expression patterns in 65 pairs of prostate cancer and para-cancer tissues by RNA sequencing and found that miR-182-5p was the most up-regulated miRNA in prostate cancer tissues. The result was validated using realtime PCR in 18 pairs of prostate cancer and para-cancer tissues. In in vitro analysis, it was confirmed that miR-182-5p promotes prostate cancer cell proliferation, invasion and migration and inhibit apoptosis. In addition, the androgen receptor directly regulated the transcription of miR-182-5p, which could target to the 3′UTR of ARRDC3 mRNA and affect the expression of ARRDC3 and its downstream gene ITGB4. For the in vivo experiment, miR-182-5p overexpression also promoted the growth and progression of prostate cancer tumors. In this regard, we suggest that miR-182-5p may be a key androgen receptor-regulated factor that contributes to the development and metastasis of Chinese prostate cancers and may be a potential target for the early diagnosis and therapeutic studies of prostate cancer. -- Highlights: •miR-182-5p is the mostly up-regulated miRNA in Chinese prostate cancer. •miR-182-5p is regulated by androgen receptor. •miR-182-5p promotes prostate cancer progression. •miR-182-5p regulates ARRDC3/ITGB4 pathway.

Atomic oxygen fine-structure splittings with tunable far-infrared spectroscopy

Science.gov (United States)

Zink, Lyndon R.; Evenson, Kenneth M.; Matsushima, Fusakazu; Nelis, Thomas; Robinson, Ruth L.

1991-01-01

Fine-structure splittings of atomic oxygen (O-16) in the ground state have been accurately measured using a tunable far-infrared spectrometer. The 3P0-3pl splitting is 2,060,069.09 (10) MHz, and the 3Pl-3P2 splitting is 4,744,777.49 (16) MHz. These frequencies are important for measuring atomic oxygen concentration in earth's atmosphere and the interstellar medium.

MIGRATION OF EXTRASOLAR PLANETS: EFFECTS FROM X-WIND ACCRETION DISKS

International Nuclear Information System (INIS)

Adams, Fred C.; Cai, Mike J.; Lizano, Susana

2009-01-01

Magnetic fields are dragged in from the interstellar medium during the gravitational collapse that forms star/disk systems. Consideration of mean field magnetohydrodynamics in these disks shows that magnetic effects produce sub-Keplerian rotation curves and truncate the inner disk. This Letter explores the ramifications of these predicted disk properties for the migration of extrasolar planets. Sub-Keplerian flow in gaseous disks drives a new migration mechanism for embedded planets and modifies the gap-opening processes for larger planets. This sub-Keplerian migration mechanism dominates over Type I migration for sufficiently small planets (m P ∼ + ) and/or close orbits (r ∼< 1 AU). Although the inclusion of sub-Keplerian torques shortens the total migration time by only a moderate amount, the mass accreted by migrating planetary cores is significantly reduced. Truncation of the inner disk edge (for typical system parameters) naturally explains final planetary orbits with periods P ∼ 4 days. Planets with shorter periods, P ∼ 2 days, can be explained by migration during FU-Orionis outbursts, when the mass accretion rate is high and the disk edge moves inward. Finally, the midplane density is greatly increased at the inner truncation point of the disk (the X-point); this enhancement, in conjunction with continuing flow of gas and solids through the region, supports the in situ formation of giant planets.

Crystal-field splittings in rare-earth-based hard magnets: An ab initio approach

Science.gov (United States)

Delange, Pascal; Biermann, Silke; Miyake, Takashi; Pourovskii, Leonid

2017-10-01

We apply the first-principles density functional theory + dynamical mean-field theory framework to evaluate the crystal-field splitting on rare-earth sites in hard magnetic intermetallics. An atomic (Hubbard-I) approximation is employed for local correlations on the rare-earth 4 f shell and self-consistency in the charge density is implemented. We reduce the density functional theory self-interaction contribution to the crystal-field splitting by properly averaging the 4 f charge density before recalculating the one-electron Kohn-Sham potential. Our approach is shown to reproduce the experimental crystal-field splitting in the prototypical rare-earth hard magnet SmCo5. Applying it to R Fe12 and R Fe12X hard magnets (R =Nd , Sm and X =N , Li), we obtain in particular a large positive value of the crystal-field parameter A20〈r2〉 in NdFe12N resulting in a strong out-of-plane anisotropy observed experimentally. The sign of A20〈r2〉 is predicted to be reversed by substituting N with Li, leading to a strong out-of-plane anisotropy in SmFe12Li . We discuss the origin of this strong impact of N and Li interstitials on the crystal-field splitting on rare-earth sites.

Estradiol agonists inhibit human LoVo colorectal-cancer cell proliferation and migration through p53.

Science.gov (United States)

Hsu, Hsi-Hsien; Kuo, Wei-Wen; Ju, Da-Tong; Yeh, Yu-Lan; Tu, Chuan-Chou; Tsai, Ying-Lan; Shen, Chia-Yao; Chang, Sheng-Huang; Chung, Li-Chin; Huang, Chih-Yang

2014-11-28

To investigate the effects of 17β-estradiol via estrogen receptors (ER) or direct administration of ER agonists on human colorectal cancer. LoVo cells were established from the Bioresource Collection and Research Center and cultured in phenol red-free DMEM (Sigma, United States). To investigate the effects of E2 and/or ER selective agonists on cellular proliferation, LoVo colorectal cells were treated with E2 or ER-selective agonists for 24 h and 48 h and subjected to the MTT (Sigma) assay to find the concentration. And investigate the effects of E2 and/or ER selective agonists on cell used western immunoblotting to find out the diversification of signaling pathways. In order to observe motility and migration the wound healing assay and a transwell chamber (Neuro Probe) plate were tased. For a quantitative measure, we counted the number of migrating cells to the wound area post-wounding for 24 h. We further examined the cellular migration-regulating factors urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA) and matrix metalloproteinase (MMP)-9 in human LoVo cells so gelatin zymography that we used and gelatinolytic activity was visualized by Coomassie blue staining. And these results are presented as means ± SE, and statistical comparisons were made using Student's t-test. The structure was first compared with E2 and ER agonists. We then treated the LoVo cells with E2 and ER agonists (10(-8) mol/L) for 24 h and 48 h and subsequently measured the cell viability using MTT assay. Our results showed that treatment with 17β-estradiol and/or ER agonists in human LoVo colorectal cancer cells activated p53 and then up-regulated p21 and p27 protein levels, subsequently inhibiting the downstream target gene, cyclin D1, which regulates cell proliferation. Taken together, our findings demonstrate the anti-tumorigenesis effects of 17β-estradiol and/or ER agonists and suggest that these compounds may prove to be a potential alternative

Gravitino dark matter in split supersymmetry with bilinear R-parity violation

Energy Technology Data Exchange (ETDEWEB)

Cottin, Giovanna [University of Cambridge, Cavendish Laboratory, Cambridge (United Kingdom); Diaz, Marco A. [Universidad Catolica de Chile, Instituto de Fisica, Santiago (Chile); Guzman, Maria Jose [Instituto de Astronomia y Fisica del Espacio, Buenos Aires (Argentina); Panes, Boris [Universidade de Sao Paulo, Instituto de Fisica, Sao Paulo, SP (Brazil)

2014-11-15

In Split-SUSY with BRpV we show that the Gravitino DM solution is consistent with experimental evidence as regards its relic density and life time. We arrive at this conclusion by performing a complete numerical and algebraic study of the parameter space, including constraints from the recently determined Higgs mass, updated neutrino physics, and BBN constraints on NLSP decays. The Higgs mass requires a relatively low Split-SUSY mass scale, which is naturally smaller than usual values for reheating temperature, allowing the use of the standard expression for the relic density. We include restrictions from neutrino physics with three generations, and we notice that the gravitino decay width depends on the atmospheric neutrino mass scale. We calculate the neutralino decay rate and find it consistent with BBN. We mention some implications on indirect DM searches. (orig.)

miR-486-3p, miR-139-5p, and miR-21 as Biomarkers for the Detection of Oral Tongue Squamous Cell Carcinoma

Directory of Open Access Journals (Sweden)

Zujian Chen

2017-01-01

Full Text Available Oral tongue squamous cell carcinoma (TSCC is a complex disease with extensive genetic and epigenetic defects, including microRNA deregulation. The aims of the present study were to test the feasibility of performing the microRNA profiling analysis on archived TSCC specimens and to assess the potential diagnostic utility of the identified microRNA biomarkers for the detection of TSCC. TaqMan array-based microRNA profiling analysis was performed on 10 archived TSCC samples and their matching normal tissues. A panel of 12 differentially expressed microRNAs was identified. Eight of these differentially expressed microRNAs were validated in an independent sample set. A random forest (RF classification model was built with miR-486-3p, miR-139-5p, and miR-21, and it was able to detect TSCC with a sensitivity of 100% and a specificity of 86.7% (overall error rate = 6.7%. As such, this study demonstrated the utility of the archived clinical specimens for microRNA biomarker discovery. The feasibility of using microRNA biomarkers (miR-486-3p, miR-139-5p, and miR-21 for the detection of TSCC was confirmed.

Facilitators and constraints at each stage of the migration decision process.

Science.gov (United States)

Kley, Stefanie

2017-10-01

Behavioural models of migration emphasize the importance of migration decision-making for the explanation of subsequent behaviour. But empirical migration research regularly finds considerable gaps between those who intend to migrate and those who actually realize their intention. This paper applies the Theory of Planned Behaviour, enriched by the Rubicon model, to test specific hypotheses about distinct effects of facilitators and constraints on specific stages of migration decision-making and behaviour. The data come from a tailor-made panel survey based on random samples of people drawn from two German cities in 2006-07. The results show that in conventional models the effects of facilitators and constraints on migration decision-making are likely to be underestimated. Splitting the process of migration decision-making into a pre-decisional and a pre-actional phase helps to avoid bias in the estimated effects of facilitators and constraints on both migration decision-making and migration behaviour.

Use of computed tomography assessed kidney length to predict split renal GFR in living kidney donors

Energy Technology Data Exchange (ETDEWEB)

Gaillard, Francois; Fournier, Catherine; Leon, Carine; Legendre, Christophe [Paris Descartes University, AP-HP, Hopital Necker-Enfants Malades, Renal Transplantation Department, Paris (France); Pavlov, Patrik [Linkoeping University, Linkoeping (Sweden); Tissier, Anne-Marie; Correas, Jean-Michel [Paris Descartes University, AP-HP, Hopital Necker-Enfants Malades, Radiology Department, Paris (France); Harache, Benoit; Hignette, Chantal; Weinmann, Pierre [Paris Descartes University, AP-HP, Hopital Europeen Georges Pompidou, Nuclear Medicine Department, Paris (France); Eladari, Dominique [Paris Descartes University, and INSERM, Unit 970, AP-HP, Hopital Europeen Georges Pompidou, Physiology Department, Paris (France); Timsit, Marc-Olivier; Mejean, Arnaud [Paris Descartes University, AP-HP, Hopital Europeen Georges Pompidou, Urology Department, Paris (France); Friedlander, Gerard; Courbebaisse, Marie [Paris Descartes University, and INSERM, Unit 1151, AP-HP, Hopital Europeen Georges Pompidou, Physiology Department, Paris (France); Houillier, Pascal [Paris Descartes University, INSERM, Unit umrs1138, and CNRS Unit erl8228, AP-HP, Hopital Europeen Georges Pompidou, Physiology Department, Paris (France)

2017-02-15

Screening of living kidney donors may require scintigraphy to split glomerular filtration rate (GFR). To determine the usefulness of computed tomography (CT) to split GFR, we compared scintigraphy-split GFR to CT-split GFR. We evaluated CT-split GFR as a screening test to detect scintigraphy-split GFR lower than 40 mL/min/1.73 m{sup 2}/kidney. This was a monocentric retrospective study on 346 potential living donors who had GFR measurement, renal scintigraphy, and CT. We predicted GFR for each kidney by splitting GFR using the following formula: Volume-split GFR for a given kidney = measured GFR*[volume of this kidney/(volume of this kidney + volume of the opposite kidney)]. The same formula was used for length-split GFR. We compared length- and volume-split GFR to scintigraphy-split GFR at donation and with a 4-year follow-up. A better correlation was observed between length-split GFR and scintigraphy-split GFR (r = 0.92) than between volume-split GFR and scintigraphy-split GFR (r = 0.89). A length-split GFR threshold of 45 mL/min/1.73 m{sup 2}/kidney had a sensitivity of 100 % and a specificity of 75 % to detect scintigraphy-split GFR less than 40 mL/min/1.73 m{sup 2}/kidney. Both techniques with their respective thresholds detected living donors with similar eGFR evolution during follow-up. Length-split GFR can be used to detect patients requiring scintigraphy. (orig.)

Use of computed tomography assessed kidney length to predict split renal GFR in living kidney donors

International Nuclear Information System (INIS)

Gaillard, Francois; Fournier, Catherine; Leon, Carine; Legendre, Christophe; Pavlov, Patrik; Tissier, Anne-Marie; Correas, Jean-Michel; Harache, Benoit; Hignette, Chantal; Weinmann, Pierre; Eladari, Dominique; Timsit, Marc-Olivier; Mejean, Arnaud; Friedlander, Gerard; Courbebaisse, Marie; Houillier, Pascal

2017-01-01

Screening of living kidney donors may require scintigraphy to split glomerular filtration rate (GFR). To determine the usefulness of computed tomography (CT) to split GFR, we compared scintigraphy-split GFR to CT-split GFR. We evaluated CT-split GFR as a screening test to detect scintigraphy-split GFR lower than 40 mL/min/1.73 m"2/kidney. This was a monocentric retrospective study on 346 potential living donors who had GFR measurement, renal scintigraphy, and CT. We predicted GFR for each kidney by splitting GFR using the following formula: Volume-split GFR for a given kidney = measured GFR*[volume of this kidney/(volume of this kidney + volume of the opposite kidney)]. The same formula was used for length-split GFR. We compared length- and volume-split GFR to scintigraphy-split GFR at donation and with a 4-year follow-up. A better correlation was observed between length-split GFR and scintigraphy-split GFR (r = 0.92) than between volume-split GFR and scintigraphy-split GFR (r = 0.89). A length-split GFR threshold of 45 mL/min/1.73 m"2/kidney had a sensitivity of 100 % and a specificity of 75 % to detect scintigraphy-split GFR less than 40 mL/min/1.73 m"2/kidney. Both techniques with their respective thresholds detected living donors with similar eGFR evolution during follow-up. Length-split GFR can be used to detect patients requiring scintigraphy. (orig.)

Iterative methods for 3D implicit finite-difference migration using the complex Padé approximation

International Nuclear Information System (INIS)

Costa, Carlos A N; Campos, Itamara S; Costa, Jessé C; Neto, Francisco A; Schleicher, Jörg; Novais, Amélia

2013-01-01

Conventional implementations of 3D finite-difference (FD) migration use splitting techniques to accelerate performance and save computational cost. However, such techniques are plagued with numerical anisotropy that jeopardises the correct positioning of dipping reflectors in the directions not used for the operator splitting. We implement 3D downward continuation FD migration without splitting using a complex Padé approximation. In this way, the numerical anisotropy is eliminated at the expense of a computationally more intensive solution of a large-band linear system. We compare the performance of the iterative stabilized biconjugate gradient (BICGSTAB) and that of the multifrontal massively parallel direct solver (MUMPS). It turns out that the use of the complex Padé approximation not only stabilizes the solution, but also acts as an effective preconditioner for the BICGSTAB algorithm, reducing the number of iterations as compared to the implementation using the real Padé expansion. As a consequence, the iterative BICGSTAB method is more efficient than the direct MUMPS method when solving a single term in the Padé expansion. The results of both algorithms, here evaluated by computing the migration impulse response in the SEG/EAGE salt model, are of comparable quality. (paper)

C3G knock-down enhances migration and invasion by increasing Rap1-mediated p38α activation, while it impairs tumor growth through p38α-independent mechanisms

Science.gov (United States)

Priego, Neibla; Arechederra, María; Sequera, Celia; Bragado, Paloma; Vázquez-Carballo, Ana; Gutiérrez-Uzquiza, Álvaro; Martín-Granado, Víctor; Ventura, Juan José; Kazanietz, Marcelo G.; Guerrero, Carmen; Porras, Almudena

2016-01-01

C3G, a Guanine nucleotide Exchange Factor (GEF) for Rap1 and R-Ras, has been shown to play important roles in development and cancer. Previous studies determined that C3G regulates cell death through down-regulation of p38α MAPK activity. Here, we found that C3G knock-down in MEFs and HCT116 cells promotes migration and invasion through Rap1-mediated p38α hyper-activation. These effects of C3G were inhibited by Rap1 knock-down or inactivation. The enhanced migration observed in C3G depleted HCT116 cells was associated with reduction in E-cadherin expression, internalization of ZO-1, actin cytoskeleton reorganization and decreased adhesion. We also found that matrix metalloproteases MMP2 and MMP9 are involved in the pro-invasive effect of C3G down-regulation. Additionally, our studies revealed that both C3G and p38α collaborate to promote growth of HCT116 cells in vitro and in vivo, possibly by enhancing cell survival. In fact, knocking-down C3G or p38α individually or together promoted cell death in vitro, although only the double C3G-p38α silencing was able to increase cell death within tumors. Notably, we found that the pro-tumorigenic function of C3G does not depend on p38α or Rap1 activation. Altogether, our studies uncover novel mechanisms by which C3G controls key aspects of tumorigenesis. PMID:27286263

Oncogenic S1P signalling in EBV-associated nasopharyngeal carcinoma activates AKT and promotes cell migration through S1P receptor 3.

Science.gov (United States)

Lee, Hui Min; Lo, Kwok-Wai; Wei, Wenbin; Tsao, Sai Wah; Chung, Grace Tin Yun; Ibrahim, Maha Hafez; Dawson, Christopher W; Murray, Paul G; Paterson, Ian C; Yap, Lee Fah

2017-05-01

Undifferentiated nasopharyngeal carcinoma (NPC) is a cancer with high metastatic potential that is consistently associated with Epstein-Barr virus (EBV) infection. In this study, we have investigated the functional contribution of sphingosine-1-phosphate (S1P) signalling to the pathogenesis of NPC. We show that EBV infection or ectopic expression of the EBV-encoded latent genes (EBNA1, LMP1, and LMP2A) can up-regulate sphingosine kinase 1 (SPHK1), the key enzyme that produces S1P, in NPC cell lines. Exogenous addition of S1P promotes the migration of NPC cells through the activation of AKT; shRNA knockdown of SPHK1 resulted in a reduction in the levels of activated AKT and inhibition of cell migration. We also show that S1P receptor 3 (S1PR3) mRNA is overexpressed in EBV-positive NPC patient-derived xenografts and a subset of primary NPC tissues, and that knockdown of S1PR3 suppressed the activation of AKT and the S1P-induced migration of NPC cells. Taken together, our data point to a central role for EBV in mediating the oncogenic effects of S1P in NPC and identify S1P signalling as a potential therapeutic target in this disease. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Sphingosine 1-Phosphate (S1P) Receptors 1 and 2 Coordinately Induce Mesenchymal Cell Migration through S1P Activation of Complementary Kinase Pathways*

Science.gov (United States)

Quint, Patrick; Ruan, Ming; Pederson, Larry; Kassem, Moustapha; Westendorf, Jennifer J.; Khosla, Sundeep; Oursler, Merry Jo

2013-01-01

Normal bone turnover requires tight coupling of bone resorption and bone formation to preserve bone quantity and structure. With aging and during several pathological conditions, this coupling breaks down, leading to either net bone loss or excess bone formation. To preserve or restore normal bone metabolism, it is crucial to determine the mechanisms by which osteoclasts and osteoblast precursors interact and contribute to coupling. We showed that osteoclasts produce the chemokine sphingosine 1-phosphate (S1P), which stimulates osteoblast migration. Thus, osteoclast-derived S1P may recruit osteoblasts to sites of bone resorption as an initial step in replacing lost bone. In this study we investigated the mechanisms by which S1P stimulates mesenchymal (skeletal) cell chemotaxis. S1P treatment of mesenchymal (skeletal) cells activated RhoA GTPase, but this small G protein did not contribute to migration. Rather, two S1P receptors, S1PR1 and S1PR2, coordinately promoted migration through activation of the JAK/STAT3 and FAK/PI3K/AKT signaling pathways, respectively. These data demonstrate that the chemokine S1P couples bone formation to bone resorption through activation of kinase signaling pathways. PMID:23300082

An automated cell-counting algorithm for fluorescently-stained cells in migration assays

Directory of Open Access Journals (Sweden)

Novielli Nicole M

2011-10-01

Full Text Available Abstract A cell-counting algorithm, developed in Matlab®, was created to efficiently count migrated fluorescently-stained cells on membranes from migration assays. At each concentration of cells used (10,000, and 100,000 cells, images were acquired at 2.5 ×, 5 ×, and 10 × objective magnifications. Automated cell counts strongly correlated to manual counts (r2 = 0.99, P

p120-catenin differentially regulates cell migration by Rho-dependent intracellular and secreted signals

DEFF Research Database (Denmark)

Epifano, Carolina; Megias, Diego; Perez-Moreno, Mirna

2014-01-01

The adherens junction protein p120-catenin is implicated in the regulation of cadherin stability, cell migration and inflammatory responses in mammalian epithelial tissues. How these events are coordinated to promote wound repair is not understood. We show that p120 catenin regulates the intrinsic...... migratory properties of primary mouse keratinocytes, but also influences the migratory behavior of neighboring cells by secreted signals. These events are rooted in the ability of p120-catenin to regulate RhoA GTPase activity, which leads to a two-tiered control of cell migration. One restrains cell...... motility via an increase in actin stress fibers, reduction in integrin turnover and an increase in the robustness of focal adhesions. The other is coupled to the secretion of inflammatory cytokines including interleukin-24, which causally enhances randomized cell movements. Taken together, our results...

Samtidskunst og migration

DEFF Research Database (Denmark)

Petersen, Anne Ring

2010-01-01

"Samtidskunst og migration. En oversigt over faglitteraturen" er en forskningsoversigt der gør status over hvad der hidtil er skrevet inden for det kunsthistoriske område om vor tids billedkunst og migration som politisk, socialt og kulturelt fænomen, primært i forbindelse med immigration til...

Split and delay photon correlation spectroscopy with a visible light

International Nuclear Information System (INIS)

Rasch, Marten

2016-04-01

The development and performance of a setup constructed with the aim for the split pulse photon correlation spectroscopy is presented in this thesis. The double pulse time structure is accomplished with help of an Acusto-Optic Modulator (AOM) crystal, which mimics the splitting and delaying of photon pulses. The setup provides double pulses and allows to control the pulse width and delay and to synchronize them into one camera exposure window. The performance of the setup was successfully verified in a proof of principle experiment with a model system of polystyrene particles following Brownian motion. The measured radius of particles obtained with from the split pulse experiment (R h =(2.567±0.097) μm) is in agreement with the particle size provided by the manufacturer (R=(2.26±0.08) μm). The achieved results show higher statistics compared to a standard Dynamic Light Scattering (DLS) measurement.

Source splitting via the point source method

International Nuclear Information System (INIS)

Potthast, Roland; Fazi, Filippo M; Nelson, Philip A

2010-01-01

We introduce a new algorithm for source identification and field splitting based on the point source method (Potthast 1998 A point-source method for inverse acoustic and electromagnetic obstacle scattering problems IMA J. Appl. Math. 61 119–40, Potthast R 1996 A fast new method to solve inverse scattering problems Inverse Problems 12 731–42). The task is to separate the sound fields u j , j = 1, ..., n of n element of N sound sources supported in different bounded domains G 1 , ..., G n in R 3 from measurements of the field on some microphone array—mathematically speaking from the knowledge of the sum of the fields u = u 1 + ... + u n on some open subset Λ of a plane. The main idea of the scheme is to calculate filter functions g 1 ,…, g n , n element of N, to construct u l for l = 1, ..., n from u| Λ in the form u l (x) = ∫ Λ g l,x (y)u(y)ds(y), l=1,... n. (1) We will provide the complete mathematical theory for the field splitting via the point source method. In particular, we describe uniqueness, solvability of the problem and convergence and stability of the algorithm. In the second part we describe the practical realization of the splitting for real data measurements carried out at the Institute for Sound and Vibration Research at Southampton, UK. A practical demonstration of the original recording and the splitting results for real data is available online

Multiplet mass splitting in a gravitational field

International Nuclear Information System (INIS)

Maia, M.D.

An expression for the mass splitting of particles belonging to the same spin multiplet defined in a space-time of general relativity is derived. The geometrical symmetry is a subgroup of SO(r,s), 9 >=r > 3, 5 >=s >=1, the mass operator being proportional to the second order Casimir operator of that subgroup. A brief analysis of the calculated values as compared to the experimental data is included. (Author) [pt

Novel Split Chest Tube Improves Post-Surgical Thoracic Drainage

Science.gov (United States)

Olivencia-Yurvati, Albert H; Cherry, Brandon H; Gurji, Hunaid A; White, Daniel W; Newton, J Tyler; Scott, Gary F; Hoxha, Besim; Gourlay, Terence; Mallet, Robert T

2014-01-01

Objective Conventional, separate mediastinal and pleural tubes are often inefficient at draining thoracic effusions. Description We developed a Y-shaped chest tube with split ends that divide within the thoracic cavity, permitting separate intrathoracic placement and requiring a single exit port. In this study, thoracic drainage by the split drain vs. that of separate drains was tested. Methods After sternotomy, pericardiotomy, and left pleurotomy, pigs were fitted with separate chest drains (n=10) or a split tube prototype (n=9) with internal openings positioned in the mediastinum and in the costo-diaphragmatic recess. Separate series of experiments were conducted to test drainage of D5W or 0.58 M sucrose, an aqueous solution with viscosity approximating that of plasma. One litre of fluid was infused into the thorax, and suction was applied at −20 cm H2O for 30 min. Results When D5W was infused, the split drain left a residual volume of 53 ± 99 ml (mean value ± SD) vs. 148 ± 120 for the separate drain (P=0.007), representing a drainage efficiency (i.e. drained vol/[drained + residual vol]) of 95 ± 10% vs. 86 ± 12% for the separate drains (P = 0.011). In the second series, the split drain evacuated more 0.58 M sucrose in the first minute (967 ± 129 ml) than the separate drains (680 ± 192 ml, Pdrain evacuated a similar volume of sucrose vs. the conventional drain (1089 ± 72 vs. 1056 ± 78 ml; P = 0.5). Residual volume tended to be lower (25 ± 10 vs. 62 ± 72 ml; P = 0.128) and drainage efficiency tended to be higher (98 ± 1 vs. 95 ± 6%; P = 0.111) with the split drain vs. conventional separate drains. Conclusion The split chest tube drained the thoracic cavity at least as effectively as conventional separate tubes. This new device could potentially alleviate postoperative complications. PMID:25478289

Novel Split Chest Tube Improves Post-Surgical Thoracic Drainage.

Science.gov (United States)

Olivencia-Yurvati, Albert H; Cherry, Brandon H; Gurji, Hunaid A; White, Daniel W; Newton, J Tyler; Scott, Gary F; Hoxha, Besim; Gourlay, Terence; Mallet, Robert T

2014-01-01

Conventional, separate mediastinal and pleural tubes are often inefficient at draining thoracic effusions. We developed a Y-shaped chest tube with split ends that divide within the thoracic cavity, permitting separate intrathoracic placement and requiring a single exit port. In this study, thoracic drainage by the split drain vs. that of separate drains was tested. After sternotomy, pericardiotomy, and left pleurotomy, pigs were fitted with separate chest drains (n=10) or a split tube prototype (n=9) with internal openings positioned in the mediastinum and in the costo-diaphragmatic recess. Separate series of experiments were conducted to test drainage of D5W or 0.58 M sucrose, an aqueous solution with viscosity approximating that of plasma. One litre of fluid was infused into the thorax, and suction was applied at -20 cm H2O for 30 min. When D5W was infused, the split drain left a residual volume of 53 ± 99 ml (mean value ± SD) vs. 148 ± 120 for the separate drain (P=0.007), representing a drainage efficiency (i.e. drained vol/[drained + residual vol]) of 95 ± 10% vs. 86 ± 12% for the separate drains (P = 0.011). In the second series, the split drain evacuated more 0.58 M sucrose in the first minute (967 ± 129 ml) than the separate drains (680 ± 192 ml, Pdrain evacuated a similar volume of sucrose vs. the conventional drain (1089 ± 72 vs. 1056 ± 78 ml; P = 0.5). Residual volume tended to be lower (25 ± 10 vs. 62 ± 72 ml; P = 0.128) and drainage efficiency tended to be higher (98 ± 1 vs. 95 ± 6%; P = 0.111) with the split drain vs. conventional separate drains. The split chest tube drained the thoracic cavity at least as effectively as conventional separate tubes. This new device could potentially alleviate postoperative complications.

Migration characteristics of cobalt-60 through sandy soil in high pH solution

International Nuclear Information System (INIS)

Ohnuki, Toshihiko

1992-01-01

Migration characteristics of 60 Co through sandy soil in high pH solution has been investigated by both column and batch techniques. The association of 60 Co with the sandy soil and its components were studied by sequential extraction techniques. The concentration profile of 60 Co in the sandy soil column was composed of two exponential curves showing that 60 Co would consist of immobile and mobile fractions. The immobile 60 Co was retained by the sandy soil and was distributed near the top. Though the mobile 60 Co was little sorbed by soil and migrated through the soil column, maximum concentration of 60 Co in the effluents decreased slightly with increasing path length of the soil column. The sequential extraction of 60 Co from the sandy soil and from its components showed that 60 Co was sorbed by both manganese oxide and clay minerals. And manganese oxide is one of the responsible soil components for the observed decrease in the maximum concentration of 60 Co in the effluents. Although the content of manganese oxide in the sandy soil was 0.13%, manganese oxide is the important component to prevent from the migration of 60 Co in the high pH solution. (author)

Fermi level splitting and thermionic current improvement in low-dimensional multi-quantum-well (MQW) p-i-n structures

International Nuclear Information System (INIS)

Varonides, Argyrios C.

2006-01-01

Photo-excitation and subsequent thermionic currents are essential components of photo-excited carrier transport in multi-quantum-well photovoltaic (hetero-PV) structures. p-i-n multi-quantum structures are useful probes for a better understanding of PV device properties. Illumination of the intrinsic region of p-i-n multi-structures causes carrier trapping in any of the quantum wells, and subsequent carrier recombination or thermal escape is possible. At the vicinity of a quantum well, we find that the (quasi) Fermi levels undergo an upward split by a small, but non-negligible, energy amount ΔE F in the order of 12 meV. We conclude this fact by comparing the photo-excited carriers trapped in a quantum well, under illumination, to the carrier concentrations under dark. Based on such a prediction, we subsequently relate thermionic current density dependence on Fermi level splitting, concluding that excess thermal currents may increase by a factor of the order of 2. We conclude that illumination causes (a) Fermi level separation and (b) an apparent increase in thermionic currents

MiR-181a-5p is downregulated in hepatocellular carcinoma and suppresses motility, invasion and branching-morphogenesis by directly targeting c-Met.

Science.gov (United States)

Korhan, Peyda; Erdal, Esra; Atabey, Neşe

2014-08-08

c-Met receptor tyrosine kinase has been regarded as a promising therapeutic target for hepatocellular carcinoma (HCC). Recently, microRNAs (miRNAs) have been shown as a novel mechanism to control c-Met expression in cancer. In this study, we investigate the potential contribution of miR-181a-5p dysregulation to the biology of c-Met overexpression in HCC. Herein, we found an inverse expression pattern between miR-181a-5p and c-Met expression in normal, cirrhotic and HCC liver tissues. Luciferase assay confirmed that miR-181a-5p binding to the 3'-UTR of c-Met downregulated the expression of c-Met in HCC cells. Overexpression of miR-181a-5p suppressed both HGF-independent and -dependent activation of c-Met and consequently diminished branching-morphogenesis and invasion. Combined treatment with miR-181a-5p and c-Met inhibitor led to a further inhibition of c-Met-driven cellular activities. Knockdown of miR-181a-5p promoted HGF-independent/-dependent signaling of c-Met and accelerated migration, invasion and branching-morphogenesis. In conclusion, our results demonstrated for the first time that c-Met is a functional target gene of miR-181a-5p and the loss of miR-181a-5p expression led to the activation of c-Met-mediated oncogenic signaling in hepatocarcinogenesis. These findings display a novel molecular mechanism of c-Met regulation in HCC and strategies to increase miR-181a5p level might be an alternative approach for the enhancement of the inhibitory effects of c-Met inhibitors. Copyright © 2014 Elsevier Inc. All rights reserved.

Job på særlige vilkår

DEFF Research Database (Denmark)

Holt, Helle; Sonnefeld Jørgensen, Martin; Hohnen, Pernille

Job på særlige vilkår afviger fra ordinære job ved, at der kan medfølge et offentligt løntilskud, at jobbet kan være midlertidigt, og/eller at arbejdstid, præstationskrav og løn er anderledes. Ordningerne er en del af regeringens aktive arbejdsmarkedspolitik for at skabe et rummeligt arbejdsmarked...... og dermed undgå, at personer med nedsat arbejdsevne havner i passiv forsørgelse. Denne rapport gennemgår den viden, der findes om job på særlige vilkår. Det gælder både viden om de personer, der er ansat i et job på særlige vilkår, om de virksomheder, der ansætter personer på særlige vilkår, og om...... det system, der visiterer personer til job på særlige vilkår....

LncRNA-AK131850 Sponges MiR-93-5p in Newborn and Mature Osteoclasts to Enhance the Secretion of Vascular Endothelial Growth Factor a Promoting Vasculogenesis of Endothelial Progenitor Cells

Directory of Open Access Journals (Sweden)

Hongyu Quan

2018-03-01

Full Text Available Background/Aims: In the process of bone development and remodeling, the vasculature is regarded as the communicative network between the bone and neighboring tissues. Recently, it has been reported that the processes of angiogenesis and osteogenesis are coupled temporally and spatially. However, few studies reported the relationship and relevant mechanism between osteoclastogenesis and vasculogenesis. Methods: Arraystar Mouse lncRNA microarray V3.0 was firstly used to analyze the differentially expressed lncRNA genes in osteoclast different stages during osteoclastogenesis. Cell counting kit 8 (CCK-8 analysis, quantitative real-time polymerase chain reaction (qRT-PCR analysis, migration and tube formation assays were used to detect impact of osteoclast different stages on the proliferation, differentiation, migration and tube formation of endothelial progenitor cells (EPCs, respectively. Finally, transfection of AK131850 shRNA, miR-93-5p mimic and miR-93-5p inhibitor, qRT-PCR, western blotting, enzyme-linked immunosorbent assay (ELISA, fluorescence in situ hybridization (FISH and luciferase reporter assay were carried out to dissect molecular mechanisms. Results: In this study, we found that newborn OCs (N-OC and mature OCs (M-OC during osteoclastogenesis significantly promoted proliferation, differentiation, migration and tube formation of endothelial progenitor cells (EPCs. Through lncRNA microarray and GO&pathway analysis, we found that AK131850 and co-expressed gene, vascular endothelial growth factor a (VEGFa, were significantly up-regulated in N-OC and M-OC. After inhibition of AK131850 the promoting effect of N-OC and M-OC on EPCs was reversed. Furthermore, we found that AK131850 directly competed miR-93-5p in N-OC and M-OC through sponge, thereby increasing VEGFa transcription, expression and secretion through derepressing of miR-93-5p on VEGFa. Conclusion: Our results provided the first finding that lncRNA-AK131850 sponged miR-93-5p in

L_p- and S_{p,q}^rB-discrepancy of (order 2) digital nets

OpenAIRE

Markhasin, Lev

2014-01-01

Dick proved that all order $2$ digital nets satisfy optimal upper bounds of the $L_2$-discrepancy. We give an alternative proof for this fact using Haar bases. Furthermore, we prove that all digital nets satisfy optimal upper bounds of the $S_{p,q}^r B$-discrepancy for a certain parameter range and enlarge that range for order $2$ digitals nets. $L_p$-, $S_{p,q}^r F$- and $S_p^r H$-discrepancy is considered as well.

Introducing an experimental split-cylinder to study flows with geophysical interest: First steps and first results

Science.gov (United States)

Rodriguez-Garcia, Jesus O.; Burguete, Javier

2017-11-01

A new experimental setup has been developed in order to study rotating flows. Our research is derived from the experiments carried out in our group relating to this kind of flows, and the setup is inspired by the simulations performed by Lopez & Gutierrez-Castillo using a split-cylinder flow. In their work they study the different bifurcations taking place into the flow, among others, finding inertial waves in different configurations of the movement of the split-cylinder. Our setup consists in a split-cylinder in which each half can move in co-rotation or in counter-rotation. Moreover, we can set the rotation velocity of each half independently in order to study these different configurations of the flow. The aspect ratio defined as Γ = H / R can be modified, where H is the internal length of the cylinder and R is its radius. With this setup, we study the flow developed inside the split-cylinder depending on the Reynolds number like the different symmetry-breaking that should appear according to Lopez & Gutierrez-Castillo. To obtain the experimental data we use both laser Doppler velocimetry (LDV) and particle image velocimetry (PIV) techniques. The firsts results got are in the co-rotation case rotating one half faster than the other. We acknowledge support from Spanish Government Grant FIS 2014-54101-P. Jesús O. Rodríguez-García acknowledge research Grant from Asociación de Amigos de la Universidad de Navarra.

SplitDist—Calculating Split-Distances for Sets of Trees

DEFF Research Database (Denmark)

Mailund, T

2004-01-01

We present a tool for comparing a set of input trees, calculating for each pair of trees the split-distances, i.e., the number of splits in one tree not present in the other.......We present a tool for comparing a set of input trees, calculating for each pair of trees the split-distances, i.e., the number of splits in one tree not present in the other....

Novel migrating mouse neural crest cell assay system utilizing P0-Cre/EGFP fluorescent time-lapse imaging

Directory of Open Access Journals (Sweden)

Kawakami Minoru

2011-11-01

Full Text Available Abstract Background Neural crest cells (NCCs are embryonic, multipotent stem cells. Their long-range and precision-guided migration is one of their most striking characteristics. We previously reported that P0-Cre/CAG-CAT-lacZ double-transgenic mice showed significant lacZ expression in tissues derived from NCCs. Results In this study, by embedding a P0-Cre/CAG-CAT-EGFP embryo at E9.5 in collagen gel inside a culture glass slide, we were able to keep the embryo developing ex vivo for more than 24 hours; this development was with enough NCC fluorescent signal intensity to enable single-cell resolution analysis, with the accompanying NCC migration potential intact and with the appropriate NCC response to the extracellular signal maintained. By implantation of beads with absorbed platelet-derived growth factor-AA (PDGF-AA, we demonstrated that PDGF-AA acts as an NCC-attractant in embryos. We also performed assays with NCCs isolated from P0-Cre/CAG-CAT-EGFP embryos on culture plates. The neuromediator 5-hydroxytryptamine (5-HT has been known to regulate NCC migration. We newly demonstrated that dopamine, in addition to 5-HT, stimulated NCC migration in vitro. Two NCC populations, with different axial levels of origins, showed unique distribution patterns regarding migration velocity and different dose-response patterns to both 5-HT and dopamine. Conclusions Although avian species predominated over the other species in the NCC study, our novel system should enable us to use mice to assay many different aspects of NCCs in embryos or on culture plates, such as migration, division, differentiation, and apoptosis.

R248Q mutation--Beyond p53-DNA binding.

Science.gov (United States)

Ng, Jeremy W K; Lama, Dilraj; Lukman, Suryani; Lane, David P; Verma, Chandra S; Sim, Adelene Y L

2015-12-01

R248 in the DNA binding domain (DBD) of p53 interacts directly with the minor groove of DNA. Earlier nuclear magnetic resonance (NMR) studies indicated that the R248Q mutation resulted in conformation changes in parts of DBD far from the mutation site. However, how information propagates from the mutation site to the rest of the DBD is still not well understood. We performed a series of all-atom molecular dynamics (MD) simulations to dissect sterics and charge effects of R248 on p53-DBD conformation: (i) wild-type p53 DBD; (ii) p53 DBD with an electrically neutral arginine side-chain; (iii) p53 DBD with R248A; (iv) p53 DBD with R248W; and (v) p53 DBD with R248Q. Our results agree well with experimental observations of global conformational changes induced by the R248Q mutation. Our simulations suggest that both charge- and sterics are important in the dynamics of the loop (L3) where the mutation resides. We show that helix 2 (H2) dynamics is altered as a result of a change in the hydrogen bonding partner of D281. In turn, neighboring L1 dynamics is altered: in mutants, L1 predominantly adopts the recessed conformation and is unable to interact with the major groove of DNA. We focused our attention the R248Q mutant that is commonly found in a wide range of cancer and observed changes at the zinc-binding pocket that might account for the dominant negative effects of R248Q. Furthermore, in our simulations, the S6/S7 turn was more frequently solvent exposed in R248Q, suggesting that there is a greater tendency of R248Q to partially unfold and possibly lead to an increased aggregation propensity. Finally, based on the observations made in our simulations, we propose strategies for the rescue of R248Q mutants. © 2015 Wiley Periodicals, Inc.

Stereotactic core needle breast biopsy marker migration: An analysis of factors contributing to immediate marker migration.

Science.gov (United States)

Jain, Ashali; Khalid, Maria; Qureshi, Muhammad M; Georgian-Smith, Dianne; Kaplan, Jonah A; Buch, Karen; Grinstaff, Mark W; Hirsch, Ariel E; Hines, Neely L; Anderson, Stephan W; Gallagher, Katherine M; Bates, David D B; Bloch, B Nicolas

2017-11-01

To evaluate breast biopsy marker migration in stereotactic core needle biopsy procedures and identify contributing factors. This retrospective study analyzed 268 stereotactic biopsy markers placed in 263 consecutive patients undergoing stereotactic biopsies using 9G vacuum-assisted devices from August 2010-July 2013. Mammograms were reviewed and factors contributing to marker migration were evaluated. Basic descriptive statistics were calculated and comparisons were performed based on radiographically-confirmed marker migration. Of the 268 placed stereotactic biopsy markers, 35 (13.1%) migrated ≥1 cm from their biopsy cavity. Range: 1-6 cm; mean (± SD): 2.35 ± 1.22 cm. Of the 35 migrated biopsy markers, 9 (25.7%) migrated ≥3.5 cm. Patient age, biopsy pathology, number of cores, and left versus right breast were not associated with migration status (P> 0.10). Global fatty breast density (P= 0.025) and biopsy in the inner region of breast (P = 0.031) were associated with marker migration. Superior biopsy approach (P= 0.025), locally heterogeneous breast density, and t-shaped biopsy markers (P= 0.035) were significant for no marker migration. Multiple factors were found to influence marker migration. An overall migration rate of 13% supports endeavors of research groups actively developing new biopsy marker designs for improved resistance to migration. • Breast biopsy marker migration is documented in 13% of 268 procedures. • Marker migration is affected by physical, biological, and pathological factors. • Breast density, marker shape, needle approach etc. affect migration. • Study demonstrates marker migration prevalence; marker design improvements are needed.

Expression of S1P metabolizing enzymes and receptors correlate with survival time and regulate cell migration in glioblastoma multiforme.

Science.gov (United States)

Bien-Möller, Sandra; Lange, Sandra; Holm, Tobias; Böhm, Andreas; Paland, Heiko; Küpper, Johannes; Herzog, Susann; Weitmann, Kerstin; Havemann, Christoph; Vogelgesang, Silke; Marx, Sascha; Hoffmann, Wolfgang; Schroeder, Henry W S; Rauch, Bernhard H

2016-03-15

A signaling molecule which is involved in proliferation and migration of malignant cells is the lipid mediator sphingosine-1-phosphate (S1P). There are hints for a potential role of S1P signaling in malignant brain tumors such as glioblastoma multiforme (GBM) which is characterized by a poor prognosis. Therefore, a comprehensive expression analysis of S1P receptors (S1P1-S1P5) and S1P metabolizing enzymes in human GBM (n = 117) compared to healthy brain (n = 10) was performed to evaluate their role for patient´s survival. Furthermore, influence of S1P receptor inhibition on proliferation and migration were studied in LN18 GBM cells. Compared to control brain, mRNA levels of S1P1, S1P2, S1P3 and S1P generating sphingosine kinase-1 were elevated in GBM. Kaplan-Meier analyses demonstrated an association between S1P1 and S1P2 with patient´s survival times. In vitro, an inhibitory effect of the SphK inhibitor SKI-II on viability of LN18 cells was shown. S1P itself had no effect on viability but stimulated LN18 migration which was blocked by inhibition of S1P1 and S1P2. The participation of S1P1 and S1P2 in LN18 migration was further supported by siRNA-mediated silencing of these receptors. Immunoblots and inhibition experiments suggest an involvement of the PI3-kinase/AKT1 pathway in the chemotactic effect of S1P in LN18 cells.In summary, our data argue for a role of S1P signaling in proliferation and migration of GBM cells. Individual components of the S1P pathway represent prognostic factors for patients with GBM. Perspectively, a selective modulation of S1P receptor subtypes could represent a therapeutic approach for GBM patients and requires further evaluation.

Comparison between 125IUdR and 51Cr as cell labels in investigations of tumor cell migration

DEFF Research Database (Denmark)

Basse, P; Hokland, P; Hokland, M

1991-01-01

YAC-1 tumor cells double-labeled with Na2[51Cr]O4 [51Cr] and [125I]iododeoxyuridine [125IUdR] were injected intravenously into Balb/c mice in order to investigate their migration and fate 0-4 h after the injection. Whereas the clearance of tumor cells from the lung tissue was similar as judged...

miR-24-3p/FGFR3 Signaling as a Novel Axis Is Involved in Epithelial-Mesenchymal Transition and Regulates Lung Adenocarcinoma Progression

Directory of Open Access Journals (Sweden)

Pengyu Jing

2018-01-01

Full Text Available Our previous studies showed that Fibroblast growth factor receptor 3 (FGFR3 contributed to cell growth in lung cancer. However, the correlation between FGFR3 and tumor progression, coupled with the underlying mechanisms, are not fully understood. The clinical significance of FGFR3 was determined in two cohorts of clinical samples (n=22, n=78. A panel of biochemical assays and functional experiments was utilized to elucidate the underlying mechanisms and effects of FGFR3 and miR-24-3p on lung adenocarcinoma progression. Upregulated FGFR3 expression indicated an adverse prognosis for lung adenocarcinoma individuals and promoted metastatic potential of lung adenocarcinoma cells. Owing to the direct regulation towards FGFR3, miR-24-3p could interfere with the potential of proliferation, migration, and invasion in lung adenocarcinoma, following variations of EMT-related protein expression. As a significant marker of EMT, E-cadherin was negatively correlated with FGFR3, of which ectopic overexpression could neutralize the antitumour effects of miR-24-3p and reverse its regulatory effects on EMT markers. Taken together, these findings define a novel insight into the miR-24-3p/FGFR3 signaling axis in regulating lung adenocarcinoma progression and suggest that targeting the miR-24-3p/FGFR3 axis could be an effective and efficient way to prevent tumor progression.

La double répétition

Directory of Open Access Journals (Sweden)

Guillaume Soulez

2011-04-01

Full Text Available Cet article défend l'idée que la sérialité, trop souvent étudiée d'un seul point de vue, repose en réalité sur une double répétition. On peut distinguer en effet la matrice d'une série de sa structure et envisager un autre modèle de la répétition, plus heuristique. On se propose alors de distinguer ces deux dimensions pour mieux penser leur fonctionnement (les règles de lecture et leur articulation productive (la production d'objets à la fois répétitifs et singuliers, de Columbo aux Soprano, en passant par Le Caméléon.This paper argues that serialization, too often considered through a single point of view, is actually based on a double repetition. One can distinguish the matrix of a series from its structure and consider an alternative model of repetition, more heuristic. It then proposes to distinguish these two dimensions in order to get a better understanding of the functioning (the rules of reading and the productive articulation of series (production of items both repetitive and unique, especially through the analysis of Columbo, The Sopranos and The Pretender.

MiR-203 controls proliferation, migration and invasive potential of prostate cancer cell lines

DEFF Research Database (Denmark)

Viticchiè, Giuditta; Lena, Anna Maria; Latina, Alessia

2011-01-01

Prostate cancers show a slow progression from a local lesion (primary tumor) to a metastatic and hormone-resistant phenotype. After an initial step of hyperplasia, in a high percentage of cases a neoplastic transformation event occurs that, less frequently, is followed by epithelial to mesenchymal...... cell lines compared to normal epithelial prostatic cells. Overexpression of miR-203 in brain or bone metastatic prostate cell lines (DU145 and PC3) is sufficient to induce a mesenchymal to epithelial transition with inhibition of cell proliferation, migration and invasiveness. We have identified CKAP2...

Assessment of Soft Tissue Changes by Cephalometry and Two-Dimensional Photogrammetry in Bilateral Sagittal Split Ramus Osteotomy Cases

Directory of Open Access Journals (Sweden)

Jan Rustemeyer

2011-07-01

Full Text Available Objectives: We aimed to compare the standard methods of cephalometry and two-dimensional photogrammetry, to evaluate the reliability and accuracy of both methods.Material and Methods: Twenty-six patients (mean age 25.5, standard deviation (SD 5.2 years with Class II relationship and 23 patients with Class III relationship (mean age 26.4, SD 4.7 years who had undergone bilateral sagittal split ramus osteotomy were selected, with a median follow-up of 8 months between pre- and postsurgical evaluation. Pre- and postsurgical cephalograms and lateral photograms were traced and changes were recorded.Results: Pre- and postsurgical measurements of hard tissue angles and distances revealed higher correlations with cephalometrically performed soft tissue measurements of facial convexity (Class II: N-PG, r = - 0.50, P = 0.047; Class III: ANB, r = 0.73, P = 0.005; NaPg , r = 0.71, P = 0.007; and labiomental angle (Class II: SNB, r = 0.72, P = 0.002; ANB, r = - 0.72, P = 0.002; N-B, r = - 0.68, P = 0.004; ANS-Gn, r = 0.71, P = 0.002; Class III: ANS-Gn, r = 0.65, P = 0.043 compared with two-dimensional photogrammetry. However, two-dimensional photogrammetry revealed higher correlation between lower lip length and cephalometrically assessed angular hard tissue changes (Class II: SNB, r = 0.98, P = 0.007; N-B, r = 0.89, P = 0.037; N-Pg, r = 0.90, P = 0.033; Class III: SNB, r = - 0.54, P = 0.060; NAPg, r = - 0.65, P = 0.041; N-Pg, r = 0.58, P = 0.039.Conclusions: Our findings suggest that cephalometry and two-dimensional photogrammetry offer the possibility to complement one another.

Assessment of Soft Tissue Changes by Cephalometry and Two-Dimensional Photogrammetry in Bilateral Sagittal Split Ramus Osteotomy Cases

Science.gov (United States)

Martin, Alice

2011-01-01

ABSTRACT Objectives We aimed to compare the standard methods of cephalometry and two-dimensional photogrammetry, to evaluate the reliability and accuracy of both methods. Material and Methods Twenty-six patients (mean age 25.5, standard deviation (SD) 5.2 years) with Class II relationship and 23 patients with Class III relationship (mean age 26.4, SD 4.7 years) who had undergone bilateral sagittal split ramus osteotomy were selected, with a median follow-up of 8 months between pre- and postsurgical evaluation. Pre- and postsurgical cephalograms and lateral photograms were traced and changes were recorded. Results Pre- and postsurgical measurements of hard tissue angles and distances revealed higher correlations with cephalometrically performed soft tissue measurements of facial convexity (Class II: N-PG, r = - 0.50, P = 0.047; Class III: ANB, r = 0.73, P = 0.005; NaPg , r = 0.71, P = 0.007;) and labiomental angle (Class II: SNB, r = 0.72, P = 0.002; ANB, r = - 0.72, P = 0.002; N-B, r = - 0.68, P = 0.004; ANS-Gn, r = 0.71, P = 0.002; Class III: ANS-Gn, r = 0.65, P = 0.043) compared with two-dimensional photogrammetry. However, two-dimensional photogrammetry revealed higher correlation between lower lip length and cephalometrically assessed angular hard tissue changes (Class II: SNB, r = 0.98, P = 0.007; N-B, r = 0.89, P = 0.037; N-Pg, r = 0.90, P = 0.033; Class III: SNB, r = - 0.54, P = 0.060; NAPg, r = - 0.65, P = 0.041; N-Pg, r = 0.58, P = 0.039). Conclusions Our findings suggest that cephalometry and two-dimensional photogrammetry offer the possibility to complement one another. PMID:24421994

Theoretical analysis of dislocation splittings in MoSi2

Czech Academy of Sciences Publication Activity Database

Paidar, Václav; Čák, Miroslav; Šob, Mojmír; Vitek, V.

2010-01-01

Roč. 240, - (2010), 012007/1/-012007/6/ ISSN 1742-6588 R&D Projects: GA AV ČR IAA100100920; GA MŠk OC09011; GA MŠk OC09014 Institutional research plan: CEZ:AV0Z20410507; CEZ:AV0Z10100520 Keywords : dislocation splitting * MoSi2 Subject RIV: BM - Solid Matter Physics ; Magnetism

Anaerobic p-coumarate degradation by Rhodopseudomonas palustris and identification of CouR, a MarR repressor protein that binds p-coumaroyl coenzyme A.

Science.gov (United States)

Hirakawa, Hidetada; Schaefer, Amy L; Greenberg, E Peter; Harwood, Caroline S

2012-04-01

The phenylpropanoid p-coumarate and structurally related aromatic compounds are produced in large amounts by green plants and are excellent carbon sources for many soil bacteria. Aerobic bacteria remove the acyl side chain from phenylpropanoids to leave an aromatic aldehyde, which then enters one of several possible central pathways of benzene ring degradation. We investigated the pathway for the anaerobic degradation of p-coumarate by the phototrophic bacterium Rhodopseudomonas palustris and found that it also follows this metabolic logic. We characterized enzymes for the conversion of p-coumarate to p-hydroxybenzaldehyde and acetyl coenzyme A (acetyl-CoA) encoded by the couAB operon. We also identified a MarR family transcriptional regulator that we named CouR. A couR mutant had elevated couAB expression. In addition, His-tagged CouR bound with high affinity to a DNA fragment encompassing the couAB promoter region, and binding was abrogated by the addition of nanomolar quantities of p-coumaroyl-CoA but not by p-coumarate. Footprinting demonstrated binding of CouR to an inverted repeat sequence that overlaps the -10 region of the couAB promoter. Our results provide evidence for binding of a CoA-modified aromatic compound by a MarR family member. Although the MarR family is widely distributed in bacteria and archaea and includes over 12,000 members, ligands have been identified for relatively few family members. Here we provide biochemical evidence for a new category of MarR ligand.

Reactions of R(2)P-P(SiMe(3))Li with [(R'(3)P)(2)PtCl(2)]. A general and efficient entry to phosphanylphosphinidene complexes of platinum. Syntheses and structures of [(eta(2)-P=(i)Pr(2))Pt(p-Tol(3)P)(2)], [(eta(2)-P=(t)Bu(2))Pt(p-Tol(3)P)(2)], [{eta(2)-P=(N(i)Pr(2))(2)}Pt(p-Tol(3)P)(2)] and [{(Et(2)PhP)(2)Pt}(2)P(2)].

Science.gov (United States)

Domańska-Babul, Wioleta; Chojnacki, Jaroslaw; Matern, Eberhard; Pikies, Jerzy

2009-01-07

The reactions of lithium derivatives of diphosphanes R(2)P-P(SiMe(3))Li (R = (t)Bu, (i)Pr, Et(2)N and (i)Pr(2)N) with [(R'(3)P)(2)PtCl(2)] (R'(3)P = Et(3)P, Et(2)PhP, EtPh(2)P and p-Tol(3)P) proceed in a facile manner to afford side-on bonded phosphanylphosphinidene complexes of platinum [(eta(2)-P=R(2))Pt(PR'(3))(2)]. The related reactions of Ph(2)P-P(SiMe(3))Li with [(R'(3)P)(2)PtCl(2)] did not yield [(eta(2)-P=PPh(2))Pt(PR'(3))(2)] and resulted mainly in the formation of [{(R'(3)P)(2)Pt}(2)P(2)], Ph(2)P-PLi-PPh(2), (Me(3)Si)(2)PLi and (Me(3)Si)(3)P. Crystallographic data are reported for the compounds [(eta(2)-P=R(2))Pt(p-Tol(3)P)(2)] (R = (t)Bu, (i)Pr, ((i)Pr(2)N)(2)P) and for [{(Et(2)PhP)(2)Pt}(2)P(2)].

p16(INK4a translation suppressed by miR-24.

Directory of Open Access Journals (Sweden)

Ashish Lal

2008-03-01

Full Text Available Expression of the tumor suppressor p16(INK4a increases during aging and replicative senescence.Here, we report that the microRNA miR-24 suppresses p16 expression in human diploid fibroblasts and cervical carcinoma cells. Increased p16 expression with replicative senescence was associated with decreased levels of miR-24, a microRNA that was predicted to associate with the p16 mRNA coding and 3'-untranslated regions. Ectopic miR-24 overexpression reduced p16 protein but not p16 mRNA levels. Conversely, introduction of antisense (AS-miR-24 blocked miR-24 expression and markedly enhanced p16 protein levels, p16 translation, and the production of EGFP-p16 reporter bearing the miR-24 target recognition sites.Together, our results suggest that miR-24 represses the initiation and elongation phases of p16 translation.

Targeting S1P in Inflammatory bowel disease: new avenues for modulating intestinal leukocyte migration.

Science.gov (United States)

Danese, Silvio; Furfaro, Federica; Vetrano, Stefania

2017-07-28

Sphingosine 1 phosphate (S1P) is a bioactive lipid mediator involved in the regulation of several cellular processes though the activation of a G protein-coupled receptor family known as the S1P receptors (S1PRs). Advances in the understanding of the biological activities mediated by S1PRs have sparked great interest in the S1P/S1PRs axes as new therapeutic targets for the modulation of several cellular processes. In particular, S1P/ S1PR1 axis has been identified as key regulator for the lymphocyte migration from lymph nodes. The blockade of this axis is emerging as a new therapeutic approach to control the aberrant leukocytes migration into the mucosa in inflammatory bowel disease (IBD). This review briefly summarizes the current evidence coming from clinical studies and discusses the future prospects of S1P inhibitors for treatment of inflammatory bowel disease. Copyright © 2017 European Crohn’s and Colitis Organisation (ECCO). Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Splitting of turbulent spot in transitional pipe flow

Science.gov (United States)

Wu, Xiaohua; Moin, Parviz; Adrian, Ronald J.

2017-11-01

Recent study (Wu et al., PNAS, 1509451112, 2015) demonstrated the feasibility and accuracy of direct computation of the Osborne Reynolds' pipe transition problem without the unphysical, axially periodic boundary condition. Here we use this approach to study the splitting of turbulent spot in transitional pipe flow, a feature first discovered by E.R. Lindgren (Arkiv Fysik 15, 1959). It has been widely believed that spot splitting is a mysterious stochastic process that has general implications on the lifetime and sustainability of wall turbulence. We address the following two questions: (1) What is the dynamics of turbulent spot splitting in pipe transition? Specifically, we look into any possible connection between the instantaneous strain rate field and the spot splitting. (2) How does the passive scalar field behave during the process of pipe spot splitting. In this study, the turbulent spot is introduced at the inlet plane through a sixty degree wide numerical wedge within which fully-developed turbulent profiles are assigned over a short time interval; and the simulation Reynolds numbers are 2400 for a 500 radii long pipe, and 2300 for a 1000 radii long pipe, respectively. Numerical dye is tagged on the imposed turbulent spot at the inlet. Splitting of the imposed turbulent spot is detected very easily. Preliminary analysis of the DNS results seems to suggest that turbulent spot slitting can be easily understood based on instantaneous strain rate field, and such spot splitting may not be relevant in external flows such as the flat-plate boundary layer.

Light Modulation and Water Splitting Enhancement Using a Composite Porous GaN Structure.

Science.gov (United States)

Yang, Chao; Xi, Xin; Yu, Zhiguo; Cao, Haicheng; Li, Jing; Lin, Shan; Ma, Zhanhong; Zhao, Lixia

2018-02-14

On the basis of the laterally porous GaN, we designed and fabricated a composite porous GaN structure with both well-ordered lateral and vertical holes. Compared to the plane GaN, the composite porous GaN structure with the combination of the vertical holes can help to reduce UV reflectance and increase the saturation photocurrent during water splitting by a factor of ∼4.5. Furthermore, we investigated the underlying mechanism for the enhancement of the water splitting performance using a finite-difference time-domain method. The results show that the well-ordered vertical holes can not only help to open the embedded pore channels to the electrolyte at both sides and reduce the migration distance of the gas bubbles during the water splitting reactions but also help to modulate the light field. Using this composite porous GaN structure, most of the incident light can be modulated and trapped into the nanoholes, and thus the electric fields localized in the lateral pores can increase dramatically as a result of the strong optical coupling. Our findings pave a new way to develop GaN photoelectrodes for highly efficient solar water splitting.

Migration of methyl and phenyl radicals, oxygen and sulphur atoms in certain diphenylthiophosphorane derivatives under electron impact

International Nuclear Information System (INIS)

Cauquis, G.; Divisia, B.; Ulrich, J.

The fragmentation of various diphenylthiophosphoranes (Ph 2 P(S)R) subjected to electron impact gives rise to rearrangements dependent on the nature of the radical R. Migrations of phenyl or methyl radicals from phosphorus towards sulphur were thus observed for R=Ph, CH 3 , CH 2 Ph and NH 2 . When an electrophilic centre is formed, during a fragmentation, on a carbon in the α-position of the diphenylthiophosphoranyl radical, migrations of sulphur atoms and phenyl radicals take place from the phosphorus towards the carbon. This is found to be the case with certain fragmentations of diazo 5 and 6 compounds [fr

Når fogeden banker på

DEFF Research Database (Denmark)

Høst, Anders; Boje-Kovacs, Bence; Laursen Stigaard, Dorte

Antallet af udsættelser har været stigende i en årrække, og i de senere år har politikerne vedtaget en række forebyggelsestiltag. Denne undersøgelse ser nærmere på årsager til og konsekvenser af, at lejere bliver udsat af deres bolig samt mulighederne for at forbygge udsættelser. Der bliver også ...

A splitting algorithm for directional regularization and sparsification

DEFF Research Database (Denmark)

Rakêt, Lars Lau; Nielsen, Mads

2012-01-01

We present a new split-type algorithm for the minimization of a p-harmonic energy with added data fidelity term. The half-quadratic splitting reduces the original problem to two straightforward problems, that can be minimized efficiently. The minimizers to the two sub-problems can typically...... be computed pointwise and are easily implemented on massively parallel processors. Furthermore the splitting method allows for the computation of solutions to a large number of more advanced directional regularization problems. In particular we are able to handle robust, non-convex data terms, and to define...

Theory of solvent effects on the hyperfine splitting constants in ESR spectra of free radicals

International Nuclear Information System (INIS)

Abe, T.; Tero-Kubota, S.; Ikegami, Y.

1982-01-01

An expression for the effects of solvation and hydrogen bonding on the hyperfine splitting constants of a free radical has been derived by obtaining π-electron spin densities of the radical in solution by perturbation theory. When no hydrogen bonding occurs between the radical and a solvent molecule, the splitting constant is approximately proportional to the Block and Walker parameter of theta(epsilon/sub r/) identical with 3 epsilon/sub r/ (ln epsilon/sub r/)/(epsilon/sub r/ ln epsilon/sub r/ - epsilon/sub r/ + 1) - 6/(ln epsilon/sub r/) - 2, where epsilon/sub r/ is the relative permittivity of the solvent. The expression is successfully applied to the di-tert-butyl nitroxide radical, the 1-methyl-4-(methoxycarbonyl)pyridinyl radical, and other free radicals. The effects of hydrogen bonding are discussed

Facile formation of 2D Co2P@Co3O4 microsheets through in-situ toptactic conversion and surface corrosion: Bifunctional electrocatalysts towards overall water splitting

Science.gov (United States)

Yao, Lihua; Zhang, Nan; Wang, Yin; Ni, Yuanman; Yan, Dongpeng; Hu, Changwen

2018-01-01

Exploring efficient non-precious electrocatalysts for both the hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) is crucial for many renewable energy conversion processes. In this work, we report that 2D Co2P@Co3O4 microsheets can be prepared through an in-situ toptactic conversion from single-crystal β-Co(OH)2 microplatelets, associated with a surface phosphatization and corrosion process. The resultant Co2P@Co3O4 2D hybrid materials can further serve as self-supported bifunctional catalytic electrodes to drive the overall water splitting for HER and OER simultaneously, with low overpotentials and high long-term stability. Furthermore, a water electrolyzer based on Co2P@Co3O4 hybrid as both anode and cathode is fabricated, which achieves 10 mA cm-2 current at only 1.57 V during water splitting process. Therefore, this work provides a facile strategy to obtain 2D Co2P-based micro/nanostructures, which act as low-cost and highly active electrocatalysts towards overall water splitting application.

MiR-146b-5p overexpression attenuates stemness and radioresistance of glioma stem cells by targeting HuR/lincRNA-p21/β-catenin pathway

Science.gov (United States)

Yang, Wei; Yu, Hongquan; Shen, Yueming; Liu, Yingying; Yang, Zhanshan; Sun, Ting

2016-01-01

A stem-like subpopulation existed in GBM cells, called glioma stem cells (GSCs), might contribute to cancer invasion, angiogenesis, immune evasion, and therapeutic resistance, providing a rationale to eliminate GSCs population and their supporting niche for successful GBM treatment. LincRNA-p21, a novel regulator of cell proliferation, apoptosis and DNA damage response, is found to be downregulated in several types of tumor. However, little is known about the role of lincRNA-p21 in stemness and radioresistance of GSCs and its regulating mechanisms. In this study, we found that lincRNA-p21 negatively regulated the expression and activity of β-catenin in GSCs. Downregulation of lincRNA-p21 in GSCs was resulted from upregulation of Hu antigen R (HuR) expression caused by miR-146b-5p downregulation. MiR-146b-5p overexpression increased apoptosis and radiosensitivity, decreased cell viability, neurosphere formation capacity and stem cell marker expression, and induced differentiation in GSCs. Moreover, knock-down lincRNA-p21 or HuR and β-catenin overexpression could rescue the phenotypic changes resulted from miR-146b-5p overexpression in GSCs. These findings suggest that targeting the miR-146b-5p/HuR/lincRNA-p21/β-catenin signaling pathway may be valuable therapeutic strategies against glioma. PMID:27166258

Clinical study of GFR and split renal GFR in evaluating the glomerular function in patients with type 2 diabetes

International Nuclear Information System (INIS)

Fu Hongliang; Li Jinsong; Li Jianing; Wu Jingchuan; Yang Shurong; Gu Zhenhui; Zou Renjian; Shi Haihong

2003-01-01

Objective: To assess glomerular filtration function in patients with type 2 diabetes by glomerular filtration rate (GFR) and split GFR, namely left GFR (LGFR) and right GFR (RGFR). Methods: Fifty-one patients with type 2 diabetes were classified by urine albumin analysis into three groups, normalalbuminuria group (NA), microalbuminuria group(MA) and macroalbuminuria group (MAA) . Twelve patients without diabetes were included into control group. 99 Tc m -DTPA renography was performed on all these cases. GFR and split GFR were calculated by Gates formula. Results: 1) GFR, LGFR and RGFR of NA group were lower than that of the control group. 2) GFR, LGFR and RGFR were significantly correlated with the urine albumin level (r=-0.457, -0.412, -0.424, respectively, P all < 0.01). 3) In all 51 cases, there were 5 cases whose GFR were normal while split GFR were abnormal. Conclusions: 1) GFR and split GFR measurement can detect the incipient damage of glomerular function more sensitively than urine albumin analysis and show the degree of the damage correctly. 2) Split GFR measurement can improve the evaluation of the glomerular function in type 2 diabetes patients

Water splitting and the band edge positions of TiO2

Czech Academy of Sciences Publication Activity Database

Deák, P.; Kullgren, J.; Aradi, B.; Frauenheim, T.; Kavan, Ladislav

2016-01-01

Roč. 199, MAY 2016 (2016), s. 27-34 ISSN 0013-4686 R&D Projects: GA ČR GA13-07724S Grant - others:COST(XE) CM1104 Institutional support: RVO:61388955 Keywords : water splitting * rutile * anatase Subject RIV: CG - Electrochemistry Impact factor: 4.798, year: 2016

Strong association between in-migration and HIV prevalence in urban sub-Saharan Africa.

Science.gov (United States)

Voeten, Hélène A C M; Vissers, Debby C J; Gregson, Simon; Zaba, Basia; White, Richard G; de Vlas, Sake J; Habbema, J Dik F

2010-04-01

Enormous variation exists in HIV prevalence between countries in sub-Saharan Africa. The contribution of migration to the spread of HIV has long been recognized, but its effect at the population level has never been assessed. In this ecological analysis, we explore how much variation in HIV prevalence in urban sub-Saharan Africa is explained by in-migration. We performed a linear regression to analyze the association between the proportion of recent in-migrants and HIV prevalence for men and women in urban areas, using 60 data points from 28 sub-Saharan African countries between 1987 and 2005. We found a strong association between recent in-migration and HIV prevalence for women (Pearson R = 57%, P Africa (R = 50%, P = 0.003). For both genders, the association was strongest between 1985 and 1994, slightly weaker between 1995 and 1999, and nonexistent as from 2000. The overall association for both men and women was not confounded by the developmental indicators GNI per capita, income inequalities, or adult literacy. Migration explains much of the variation in HIV spread in urban areas of sub-Saharan Africa, especially before the year 2000, after which HIV prevalences started to level off in many countries. Our findings suggest that migration is an important factor in the spread of HIV, especially in rapidly increasing epidemics. This may be of relevance to the current HIV epidemics in China and India.

CSF-1R as an inhibitor of apoptosis and promoter of proliferation, migration and invasion of canine mammary cancer cells

Science.gov (United States)

2013-01-01

Background Tumor-associated macrophages (TAMs) have high impact on the cancer development because they can facilitate matrix invasion, angiogenesis, and tumor cell motility. It gives cancer cells the capacity to invade normal tissues and metastasize. The signaling of colony-stimulating factor-1 receptor (CSF-1R) which is an important regulator of proliferation and differentiation of monocytes and macrophages regulates most of the tissue macrophages. However, CSF-1R is expressed also in breast epithelial tissue during some physiological stages i.g.: pregnancy and lactation. Its expression has been also detected in various cancers. Our previous study has showed the expression of CSF-1R in all examined canine mammary tumors. Moreover, it strongly correlated with grade of malignancy and ability to metastasis. This study was therefore designed to characterize the role of CSF-1R in canine mammary cancer cells proliferation, apoptosis, migration, and invasion. As far as we know, the study presented hereby is a pioneering experiment in this field of veterinary medicine. Results We showed that csf-1r silencing significantly increased apoptosis (Annexin V test), decreased proliferation (measured as Ki67 expression) and decreased migration (“wound healing” assay) of canine mammary cancer cells. Treatment of these cells with CSF-1 caused opposite effect. Moreover, csf-1r knock-down changed growth characteristics of highly invasive cell lines on Matrigel matrix, and significantly decreased the ability of these cells to invade matrix. CSF-1 treatment increased invasion of cancer cells. Conclusion The evidence of the expression and functional role of the CSF-1R in canine mammary cancer cells indicate that CSF-1R targeting may be a good therapeutic approach. PMID:23561040

Transcription factor FOXO1 promotes cell migration toward exogenous ATP via controlling P2Y1 receptor expression in lymphatic endothelial cells.

Science.gov (United States)

Niimi, Kenta; Ueda, Mizuha; Fukumoto, Moe; Kohara, Misaki; Sawano, Toshinori; Tsuchihashi, Ryo; Shibata, Satoshi; Inagaki, Shinobu; Furuyama, Tatsuo

2017-08-05

Sprouting migration of lymphatic endothelial cell (LEC) is a pivotal step in lymphangiogenic process. However, its molecular mechanism remains unclear including effective migratory attractants. Meanwhile, forkhead transcription factor FOXO1 highly expresses in LEC nuclei, but its significance in LEC migratory activity has not been researched. In this study, we investigated function of FOXO1 transcription factor associated with LEC migration toward exogenous ATP which has recently gathered attentions as a cell migratory attractant. The transwell membrane assay indicated that LECs migrated toward exogenous ATP, which was impaired by FOXO1 knockdown. RT-PCR analysis showed that P2Y1, a purinergic receptor, expression was markedly reduced by FOXO1 knockdown in LECs. Moreover, P2Y1 blockage impaired LEC migration toward exogenous ATP. Western blot analysis revealed that Akt phosphorylation contributed to FOXO1-dependent LEC migration toward exogenous ATP and its blockage affected LEC migratory activity. Furthermore, luciferase reporter assay and ChIP assay suggested that FOXO1 directly bound to a conserved binding site in P2RY1 promoter and regulated its activity. These results indicated that FOXO1 serves a pivotal role in LEC migration toward exogenous ATP via direct transcriptional regulation of P2Y1 receptor. Copyright © 2017 Elsevier Inc. All rights reserved.

pH sensing by lipids in membranes: The fundamentals of pH-driven migration, polarization and deformations of lipid bilayer assemblies.

Science.gov (United States)

Angelova, Miglena I; Bitbol, Anne-Florence; Seigneuret, Michel; Staneva, Galya; Kodama, Atsuji; Sakuma, Yuka; Kawakatsu, Toshihiro; Imai, Masayuki; Puff, Nicolas

2018-03-06

Most biological molecules contain acido-basic groups that modulate their structure and interactions. A consequence is that pH gradients, local heterogeneities and dynamic variations are used by cells and organisms to drive or regulate specific biological functions including energetic metabolism, vesicular traffic, migration and spatial patterning of tissues in development. While the direct or regulatory role of pH in protein function is well documented, the role of hydrogen and hydroxyl ions in modulating the properties of lipid assemblies such as bilayer membranes is only beginning to be understood. Here, we review approaches using artificial lipid vesicles that have been instrumental in providing an understanding of the influence of pH gradients and local variations on membrane vectorial motional processes: migration, membrane curvature effects promoting global or local deformations, crowding generation by segregative polarization processes. In the case of pH induced local deformations, an extensive theoretical framework is given and an application to a specific biological issue, namely the structure and stability of mitochondrial cristae, is described. This article is part of a Special Issue entitled: Emergence of Complex Behavior in Biomembranes edited by Marjorie Longo. Copyright © 2018 Elsevier B.V. All rights reserved.

Long Non-coding RNA LINC00339 Stimulates Glioma Vasculogenic Mimicry Formation by Regulating the miR-539-5p/TWIST1/MMPs Axis

Directory of Open Access Journals (Sweden)

Junqing Guo

2018-03-01

Full Text Available Glioma is recognized as a highly angiogenic malignant brain tumor. Vasculogenic mimicry (VM greatly restricts the therapeutic effect of anti-angiogenic tumor therapy for glioma patients. However, the molecular mechanisms of VM formation in glioma remain unclear. Here, we demonstrated that LINC00339 was upregulated in glioma tissue as well as in glioma cell lines. The expression of LINC00339 in glioma tissues was positively correlated with glioma VM formation. Knockdown of LINC00339 inhibited glioma cell proliferation, migration, invasion, and tube formation, meanwhile downregulating the expression of VM-related molecular MMP-2 and MMP-14. Furthermore, knockdown of LINC00339 significantly increased the expression of miR-539-5p. Both bioinformatics and luciferase reporter assay revealed that LINC00339 regulated the above effects via binding to miR-539-5p. Besides, overexpression of miR-539-5p resulted in decreased expression of TWIST1, a transcription factor known to play an oncogenic role in glioma and identified as a direct target of miR-539-5p. TWIST1 upregulated the promoter activities of MMP-2 and MMP-14. The in vivo study showed that nude mice carrying tumors with knockdown of LINC00339 and overexpression of miR-539-5p exhibited the smallest tumor volume through inhibiting VM formation. In conclusion, LINC00339 may be used as a novel therapeutic target for VM formation in glioma.

Rapid expansion and pseudo spectral implementation for reverse time migration in VTI media

KAUST Repository

Pestana, Reynam C

2012-04-24

In isotropic media, we use the scalar acoustic wave equation to perform reverse time migration (RTM) of the recorded pressure wavefield data. In anisotropic media, P- and SV-waves are coupled, and the elastic wave equation should be used for RTM. For computational efficiency, a pseudo-acoustic wave equation is often used. This may be solved using a coupled system of second-order partial differential equations. We solve these using a pseudo spectral method and the rapid expansion method (REM) for the explicit time marching. This method generates a degenerate SV-wave in addition to the P-wave arrivals of interest. To avoid this problem, the elastic wave equation for vertical transversely isotropic (VTI) media can be split into separate wave equations for P- and SV-waves. These separate wave equations are stable, and they can be effectively used to model and migrate seismic data in VTI media where |ε- δ| is small. The artifact for the SV-wave has also been removed. The independent pseudo-differential wave equations can be solved one for each mode using the pseudo spectral method for the spatial derivatives and the REM for the explicit time advance of the wavefield. We show numerically stable and high-resolution modeling and RTM results for the pure P-wave mode in VTI media. © 2012 Sinopec Geophysical Research Institute.

Rapid expansion and pseudo spectral implementation for reverse time migration in VTI media

KAUST Repository

Pestana, Reynam C; Ursin, Bjø rn; Stoffa, Paul L

2012-01-01

In isotropic media, we use the scalar acoustic wave equation to perform reverse time migration (RTM) of the recorded pressure wavefield data. In anisotropic media, P- and SV-waves are coupled, and the elastic wave equation should be used for RTM. For computational efficiency, a pseudo-acoustic wave equation is often used. This may be solved using a coupled system of second-order partial differential equations. We solve these using a pseudo spectral method and the rapid expansion method (REM) for the explicit time marching. This method generates a degenerate SV-wave in addition to the P-wave arrivals of interest. To avoid this problem, the elastic wave equation for vertical transversely isotropic (VTI) media can be split into separate wave equations for P- and SV-waves. These separate wave equations are stable, and they can be effectively used to model and migrate seismic data in VTI media where |ε- δ| is small. The artifact for the SV-wave has also been removed. The independent pseudo-differential wave equations can be solved one for each mode using the pseudo spectral method for the spatial derivatives and the REM for the explicit time advance of the wavefield. We show numerically stable and high-resolution modeling and RTM results for the pure P-wave mode in VTI media. © 2012 Sinopec Geophysical Research Institute.

The effect of pH on cell viability, cell migration, cell proliferation, wound closure, and wound reepithelialization

DEFF Research Database (Denmark)

Kruse, Carla R; Singh, Mansher; Targosinski, Stefan

2017-01-01

primary keratinocyte and fibroblast function in vitro and on wound healing in vivo. In vitro, primary human keratinocytes and fibroblasts were cultured in different levels of pH (5.5-12.5) and the effect on cell viability, proliferation, and migration was studied. A rat full-thickness wound model was used...... to investigate the effect of pH (5.5-9.5) on wound healing in vivo. The effect of pH on inflammation was monitored by measuring IL-1 α concentrations from wounds and cell cultures exposed to different pH environments. Our results showed that both skin cell types tolerated wide range of pH very well. They further...... demonstrated that both acidic and alkaline environments decelerated cell migration in comparison to neutral environments and interestingly alkaline conditions significantly enhanced cell proliferation. Results from the in vivo experiments indicated that a prolonged, strongly acidic wound environment prevents...

miR-342-3p suppresses hepatocellular carcinoma proliferation through inhibition of IGF-1R-mediated Warburg effect.

Science.gov (United States)

Liu, Wenpeng; Kang, Lei; Han, Juqiang; Wang, Yadong; Shen, Chuan; Yan, Zhifeng; Tai, Yanhong; Zhao, Caiyan

2018-01-01

Insulin-like growth factor-1 receptor (IGF-1R) is a well-studied oncogenic factor that promotes cell proliferation and energy metabolism and is overexpressed in numerous cancers including hepatocellular carcinoma (HCC). Aerobic glycolysis is a hallmark of cancer, and drugs targeting its regulators, including IGF-1R, are being developed. However, the mechanisms of IGF-1R inhibition and the physiological significance of the IGF-1R inhibitors in cancer cells are unclear. Cell proliferation was evaluated by cell counting Kit-8 and colony formation assay. Western blot and real-time PCR were accordingly used to detect the relevant proteins, miRNA and gene expression. Luciferase reporter assays were used to illustrate the interaction between miR-342-3p and IGF-1R. The effect of miR-342-3p on glycolysis was determined by glucose uptake, ATP concentration, lactate generation, extracellular acidification rate and oxygen consumption rate assays. In vivo, subcutaneous tumor formation assay and PET were performed in nude mice. In this study, we demonstrate that by directly targeting the 3'-UTR (3'-untranslated regions) of IGF-1R, microRNA-342-3p (miR-342-3p) suppresses IGF-1R-mediated PI3K/AKT/GLUT1 signaling pathway both in vitro and in vivo. Through suppression of IGF-1R, miR-342-3p dampens glycolysis by decreasing glucose uptake, lactate generation, ATP production, and extracellular acidification rate (ECAR), and increasing oxygen consumption rate (OCR) in hepatoma cells. Importantly, glycolysis regulated by miR-342-3p is critical for its regulating HCC growth both in vitro and in vivo. Our findings provide clues regarding the role of miR-342-3p as a tumor suppressor in liver cancer mainly through the inhibition of IGF-1R. Targeting IGF-1R by miR-342-3p could be a potential therapeutic strategy in liver cancer.

Rashba split surface states in BiTeBr

International Nuclear Information System (INIS)

Eremeev, S V; Rusinov, I P; Nechaev, I A; Chulkov, E V

2013-01-01

Within density functional theory, we study the bulk band structure and surface states of BiTeBr. We consider both ordered and disordered phases, which differ in atomic order in the Te–Br sublattice. On the basis of relativistic ab initio calculations, we show that the ordered BiTeBr is energetically preferable as compared with the disordered one. We demonstrate that both Te- and Br-terminated surfaces of the ordered BiTeBr hold surface states with a giant spin–orbit splitting. The Te-terminated surface-state spin splitting has Rashba-type behavior with the coupling parameter α R ∼ 2 eVÅ. (paper)

Nursery school at Vincennes: O.P.R.I. investigation

International Nuclear Information System (INIS)

Pasquier, J.L.; Fouquet, G.; Linden, G.

2001-01-01

After five children neoplasms at the nursery of Vincennes, the O.P.R.I. has realised two measurement campaigns during the year 2001. The track of a radioactive contamination, based on the private laboratory analysis has been denied by O.P.R.I. (N.C.)

p21-Activated kinase (PAK regulates cytoskeletal reorganization and directional migration in human neutrophils.

Directory of Open Access Journals (Sweden)

Asako Itakura

Full Text Available Neutrophils serve as a first line of defense in innate immunity owing in part to their ability to rapidly migrate towards chemotactic factors derived from invading pathogens. As a migratory function, neutrophil chemotaxis is regulated by the Rho family of small GTPases. However, the mechanisms by which Rho GTPases orchestrate cytoskeletal dynamics in migrating neutrophils remain ill-defined. In this study, we characterized the role of p21-activated kinase (PAK downstream of Rho GTPases in cytoskeletal remodeling and chemotactic processes of human neutrophils. We found that PAK activation occurred upon stimulation of neutrophils with f-Met-Leu-Phe (fMLP, and PAK accumulated at the actin-rich leading edge of stimulated neutrophils, suggesting a role for PAK in Rac-dependent actin remodeling. Treatment with the pharmacological PAK inhibitor, PF3758309, abrogated the integrity of RhoA-mediated actomyosin contractility and surface adhesion. Moreover, inhibition of PAK activity impaired neutrophil morphological polarization and directional migration under a gradient of fMLP, and was associated with dysregulated Ca(2+ signaling. These results suggest that PAK serves as an important effector of Rho-family GTPases in neutrophil cytoskeletal reorganization, and plays a key role in driving efficient directional migration of human neutrophils.

Nærvær i pædagogisk praksis

DEFF Research Database (Denmark)

Nærvær i pædagogisk praksis handler om, hvordan lærere og pædagoger kan arbejde med mindfulness i skole og daginstitution. Målet er at give inspiration til, hvordan man kan skabe et lærings- og udviklingsmiljø, som understøtter en praksis, hvor børn får erfaringer med at være til stede i sig selv......, ligesom de giver eksempler på nærværende kunst- og musikundervisning.   Den røde tråd er ønsket om at bistå barnet i at rumme sig selv og andre og en interesse for de muligheder, som øget nærvær kan give det enkelte barn og fællesskabet....

Clinical application of calculated split renal volume using computed tomography-based renal volumetry after partial nephrectomy: Correlation with technetium-99m dimercaptosuccinic acid renal scan data.

Science.gov (United States)

Lee, Chan Ho; Park, Young Joo; Ku, Ja Yoon; Ha, Hong Koo

2017-06-01

To evaluate the clinical application of computed tomography-based measurement of renal cortical volume and split renal volume as a single tool to assess the anatomy and renal function in patients with renal tumors before and after partial nephrectomy, and to compare the findings with technetium-99m dimercaptosuccinic acid renal scan. The data of 51 patients with a unilateral renal tumor managed by partial nephrectomy were retrospectively analyzed. The renal cortical volume of tumor-bearing and contralateral kidneys was measured using ImageJ software. Split estimated glomerular filtration rate and split renal volume calculated using this renal cortical volume were compared with the split renal function measured with technetium-99m dimercaptosuccinic acid renal scan. A strong correlation between split renal function and split renal volume of the tumor-bearing kidney was observed before and after surgery (r = 0.89, P volumetry had a strong correlation with the split renal function measured using technetium-99m dimercaptosuccinic acid renal scan. Computed tomography-based split renal volume measurement before and after partial nephrectomy can be used as a single modality for anatomical and functional assessment of the tumor-bearing kidney. © 2017 The Japanese Urological Association.

miR-34 and p53: New Insights into a Complex Functional Relationship.

Directory of Open Access Journals (Sweden)

Francisco Navarro

Full Text Available miR-34, a tumor suppressor miRNA family transcriptionally activated by p53, is considered a critical mediator of p53 function. However, knockout of the mouse miR-34 family has little or no effect on the p53 response. The relative contribution of different miR-34 family members to p53 function or how much p53 relies on miR-34 in human cells is unclear. Here we show that miR-34a has a complex effect on the p53 response in human cells. In HCT116 cells miR-34a overexpression enhances p53 transcriptional activity, but the closely related family members, miR-34b and miR-34c, even when over-expressed, have little effect. Both TP53 itself and MDM4, a strong p53 transactivation inhibitor, are direct targets of miR-34a. The genes regulated by miR-34a also include four other post-translational inhibitors of p53. miR-34a overexpression leads to variable effects on p53 levels in p53-sufficient human cancer cell lines. In HCT116, miR-34a overexpression increases p53 protein levels and stability. About a quarter of all mRNAs that participate in the human p53 network bind to biotinylated miR-34a, suggesting that many are direct miR-34a targets. However, only about a fifth of the mRNAs that bind to miR-34a also bind to miR-34b or miR-34c. Two human cell lines knocked out for miR-34a have unimpaired p53-mediated responses to genotoxic stress, like mouse cells. The complex positive and negative effects of miR-34 on the p53 network suggest that rather than simply promoting the p53 response, miR-34a might act at a systems level to stabilize the robustness of the p53 response to genotoxic stress.

Algebraic techniques for diagonalization of a split quaternion matrix in split quaternionic mechanics

International Nuclear Information System (INIS)

Jiang, Tongsong; Jiang, Ziwu; Zhang, Zhaozhong

2015-01-01

In the study of the relation between complexified classical and non-Hermitian quantum mechanics, physicists found that there are links to quaternionic and split quaternionic mechanics, and this leads to the possibility of employing algebraic techniques of split quaternions to tackle some problems in complexified classical and quantum mechanics. This paper, by means of real representation of a split quaternion matrix, studies the problem of diagonalization of a split quaternion matrix and gives algebraic techniques for diagonalization of split quaternion matrices in split quaternionic mechanics

Methylation of miR-145a-5p promoter mediates adipocytes differentiation

Energy Technology Data Exchange (ETDEWEB)

Du, Jingjing; Cheng, Xiao; Shen, Linyuan; Tan, Zhendong; Luo, Jia; Wu, Xiaoqian; Liu, Chendong [College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130 (China); Yang, Qiong [Department of Animal Husbandry and Veterinary Medicine, Chengdu Agricultural College, Chengdu 611100, Sichuan (China); Jiang, Yanzhi [College of Life and Science, Sichuan Agricultural University, Chengdu 611130 (China); Tang, Guoqing; Li, Xuewei [College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130 (China); Zhang, Shunhua, E-mail: zhangsh1919@163.com [College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130 (China); Zhu, Li, E-mail: zhuli7508@163.com [College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130 (China)

2016-06-17

MicroRNAs (miRNAs, miR) play important roles in adipocyte development. Recent studies showed that the expression of several miRNAs is closely related with promoter methylation. However, it is not known whether miRNA mediates adipocytes differentiation by means of DNA methylation. Here, we showed that miR-145a-5p was poorly expressed in adipose tissue from mice fed a high fat diet (HFD). Overexpression or inhibition of miR-145a-5p was unfavorable or beneficial, respectively, for adipogenesis, and these effects were achieved by regulating adipocyte-specific genes involved in lipogenic transcription, fatty acid synthesis, and fatty acid transportation. Particularly, we first suggested that miR-145a-5p mimics or inhibitors promoted or repressed adipocytes proliferation by regulating p53 and p21, which act as cell cycle regulating factors. Surprisingly, the miR-145a-5p-repressed adipocyte differentiation was enhanced or rescued when cells treated with 5-Aza-dC were transfected with miR-145a-5p mimics or inhibitors, respectively. These data indicated that, as a new mean to positively regulate adipocyte proliferation, the process of miR-145a-5p-inhibited adipogenesis may be regulated by DNA methylation. -- Highlights: •MiR-145a-5p promotes adipocytes proliferation. •MiR-145a-5p is negatively correlated with obesity. •MiR-145a-5p mediates adipocytes differentiation via regulating pathway related adipocytes differentiation. MiR-145a-5p mediating adipocytes differentiation was regulated by DNA methylation.

Na+, HCO3--cotransporter NBCn1 increases pHi gradients, filopodia, and migration of smooth muscle cells and promotes arterial remodelling.

Science.gov (United States)

Boedtkjer, Ebbe; Bentzon, Jacob F; Dam, Vibeke S; Aalkjaer, Christian

2016-08-01

Arterial remodelling can cause luminal narrowing and obstruct blood flow. We tested the hypothesis that cellular acid-base transport facilitates proliferation and migration of vascular smooth muscle cells (VSMCs) and enhances remodelling of conduit arteries. [Formula: see text]-cotransport via NBCn1 (Slc4a7) mediates net acid extrusion and controls steady-state intracellular pH (pHi) in VSMCs of mouse carotid arteries and primary aortic explants. Carotid arteries undergo hypertrophic inward remodelling in response to partial or complete ligation in vivo, but the increase in media area and thickness and reduction in lumen diameter are attenuated in arteries from NBCn1 knock-out compared with wild-type mice. With [Formula: see text] present, gradients for pHi (∼0.2 units magnitude) exist along the axis of VSMC migration in primary explants from wild-type but not NBCn1 knock-out mice. Knock-out or pharmacological inhibition of NBCn1 also reduces filopodia and lowers initial rates of VSMC migration after scratch-wound infliction. Interventions to reduce H(+)-buffer mobility (omission of [Formula: see text] or inhibition of carbonic anhydrases) re-establish axial pHi gradients, filopodia, and migration rates in explants from NBCn1 knock-out mice. The omission of [Formula: see text] also lowers global pHi and inhibits proliferation in primary explants. Under physiological conditions (i.e. with [Formula: see text] present), NBCn1-mediated [Formula: see text] uptake raises VSMC pHi and promotes filopodia, VSMC migration, and hypertrophic inward remodelling. We propose that axial pHi gradients enhance VSMC migration whereas global acidification inhibits VSMC proliferation and media hypertrophy after carotid artery ligation. These findings support a key role of acid-base transport, particularly via NBCn1, for development of occlusive artery disease. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please

Large Bandgap Semiconductors for Solar Water Splitting

DEFF Research Database (Denmark)

Malizia, Mauro

Photoelectrochemical water splitting represents an eco-friendly technology that could enable the production of hydrogen using water as reactant and solar energy as primary energy source. The exploitation of solar energy for the production of hydrogen would help modern society to reduce the reliance...... on fossil fuels as primary feedstock for hydrogen production and diminish the emission of greenhouse gases in the atmosphere, weakening the global warming phenomenon.The dissertation reports the development of GaP (gallium phosphide) photocathodes as a large bandgap semiconductor for photoelectrochemical...... water splitting devices having tandem design. The increase of the photovoltage produced by GaP under illumination was the main goal of this work. GaP has a bandgap of 2.25 eV and could in theory produce a photovoltage of approximately 1.7 V. Instead, the photovoltage produced by the semiconductor...

SOX9 regulates microRNA miR-202-5p/3p expression during mouse testis differentiation

DEFF Research Database (Denmark)

Wainwright, Elanor N; Jorgensen, Joan S; Kim, Youngha

2013-01-01

MicroRNAs are important regulators of developmental gene expression, but their contribution to fetal gonad development is not well understood. We have identified the evolutionarily conserved gonadal microRNAs miR-202-5p and miR-202-3p as having a potential role in regulating mouse embryonic gonad....... Expression of the primary transcript of miR-202-5p/3p remained low in XY gonads in a conditional Sox9-null mouse model, suggesting that pri-miR-202 transcription is downstream of SOX9, a transcription factor that is both necessary and sufficient for male sex determination. We identified the pri-miR-202...

Role of biogenic amines in the post-mortem migration of Anisakis pegreffii (Nematoda: Anisakidae Dujardin, 1845) larvae into fish fillets.

Science.gov (United States)

Šimat, Vida; Miletić, Jelena; Bogdanović, Tanja; Poljak, Vedran; Mladineo, Ivona

2015-12-02

Infective third-stage larvae (L3) of nematode Anisakis spp. have been recognized as one of the major food-borne threats in lightly processed fish products in Europe, particularly in the Mediterranean region. Therefore, the effect of different storage temperatures of fish on larval post-mortem migration from visceral cavity into fillets is an important parameter to take into account when evaluating the risk for consumer safety. The European anchovy (Engraulis encrasicolus) were caught during fishing season, a subsample of fillets was checked for the presence of Anisakis larvae at capture (mean abundance=0.07), and the rest was stored at four different temperatures (-18, 0, 4 and 22°C) in order to count migrating larvae and measure the production of biogenic amines over a period of time. Larvae were identified by morphological features and molecular tools. Post-mortem migration was observed in fillets stored at 0 and 4°C after three and five days, respectively, but not at 22 and -18°C. In case of storage at 22°C for two days, at the onset of putrefaction of the visceral organs, larvae migrated out of the visceral cavity towards the fish surface. Measured pH and biogenic amine profile during storage indicated that certain biochemical conditions trigger larval migration into fillets. Likewise, migration was observed at pH ~6.4 when sensory degradation of the fish was markedly visible. Although larval migration was delayed for approximately four days at a temperature of fillet was high and statistically significant at both 0 (r=0.998, p<0.01) and 4°C (r=0.946, p<0.05). Out of eight biogenic amines measured, cadaverine and putrescine levels correlated the most with the post-mortem migration at 4°C, while tyramine levels were significant at both temperatures. Copyright © 2015 Elsevier B.V. All rights reserved.

miR-342-3p suppresses hepatocellular carcinoma proliferation through inhibition of IGF-1R-mediated Warburg effect

Directory of Open Access Journals (Sweden)

Liu W

2018-03-01

Full Text Available Wenpeng Liu,1,* Lei Kang,2,* Juqiang Han,3 Yadong Wang,1 Chuan Shen,1 Zhifeng Yan,4 Yanhong Tai,5 Caiyan Zhao1 1Department of Infectious Diseases, Third Affiliated Hospital of Hebei Medical University, Shijiazhuang, China; 2Department of Nuclear Medicine, Peking University First Hospital, Beijing, China; 3Institute of Liver Disease, Beijing Military General Hospital, Beijing, China; 4Department of Gynecology and Obstetrics, PLA General Hospital, Beijing, China; 5Department of Pathology, Hospital of PLA, Beijing, China *These authors contributed equally to this work Background: Insulin-like growth factor-1 receptor (IGF-1R is a well-studied oncogenic factor that promotes cell proliferation and energy metabolism and is overexpressed in numerous cancers including hepatocellular carcinoma (HCC. Aerobic glycolysis is a hallmark of cancer, and drugs targeting its regulators, including IGF-1R, are being developed. However, the mechanisms of IGF-1R inhibition and the physiological significance of the IGF-1R inhibitors in cancer cells are unclear. Materials and methods: Cell proliferation was evaluated by cell counting Kit-8 and colony formation assay. Western blot and real-time PCR were accordingly used to detect the relevant proteins, miRNA and gene expression. Luciferase reporter assays were used to illustrate the interaction between miR-342-3p and IGF-1R. The effect of miR-342-3p on glycolysis was determined by glucose uptake, ATP concentration, lactate generation, extracellular acidification rate and oxygen consumption rate assays. In vivo, subcutaneous tumor formation assay and PET were performed in nude mice. Results: In this study, we demonstrate that by directly targeting the 3’-UTR (3’-untranslated regions of IGF-1R, microRNA-342-3p (miR-342-3p suppresses IGF-1R-mediated PI3K/AKT/GLUT1 signaling pathway both in vitro and in vivo. Through suppression of IGF-1R, miR-342-3p dampens glycolysis by decreasing glucose uptake, lactate generation

Energetics of formation and migration of self-interstitials and self-interstitial clusters in α-iron

International Nuclear Information System (INIS)

Wirth, B.D.; Odette, G.R.; California Univ., Santa Barbara, CA; Maroudas, D.; Lucas, G.E.; California Univ., Santa Barbara, CA

1997-01-01

Energetic primary recoil atoms from fast neutron irradiation generate both isolated point defects and clusters of vacancies and interstitials. Self-interstitial mobility as well as defect cluster stability and mobility play key roles in the subsequent fate of defects and, hence, in the overall microstructural evolution under irradiation. Self-interstitials and two, three and four-member self-interstitial clusters are highly mobile at low temperatures as observed in molecular-dynamics simulations and high mobility probably also extends to larger clusters. In this study, the morphology, energetics and mobility of self-interstitials and small self-interstitial clusters in α-iron are studied by molecular-statics and molecular-dynamics simulations using a Finnis-Sinclair many-body interatomic potential. Self-interstitial migration is found to be a two-step process consisting of a rotation out of the split-dumbbell configuration into the split-dumbbell configuration and translational jumps through the crowdion configuration before returning to the dumbbell configuration. Self-interstitial clusters of type split-interstitials assembled on adjacent {110} planes migrate along directions in an amoeba-like fashion by sequential local dissociation and re-association processes. (orig.)

The role of intraoperative positioning of the inferior alveolar nerve on postoperative paresthesia after bilateral sagittal split osteotomy of the mandible: prospective clinical study

Czech Academy of Sciences Publication Activity Database

Hanzelka, T.; Foltán, R.; Pavlíková, G.; Horká, E.; Šedý, Jiří

2011-01-01

Roč. 40, č. 9 (2011), s. 901-906 ISSN 0901-5027 R&D Projects: GA MŠk(CZ) LC554; GA ČR GAP304/10/0320 Grant - others:GA MŠk(CZ) 1M0538 Program:1M Institutional research plan: CEZ:AV0Z50390703 Keywords : orthognathic surgery * paresthesia * bilateral sagittal split osteotomy Subject RIV: FJ - Surgery incl. Transplants; FH - Neurology (UEM-P) Impact factor: 1.506, year: 2011

Semantics-Driven Migration of Java Programs: a Practical Experience

Directory of Open Access Journals (Sweden)

Artyom O. Aleksyuk

2017-01-01

Full Text Available The purpose of the study is to demonstrate the feasibility of automated code migration to a new set of programming libraries. Code migration is a common task in modern software projects. For example, it may arise when a project should be ported to a more secure or feature-rich library, a new platform or a new version of an already used library. The developed method and tool are based on the previously created by the authors a formalism for describing libraries semantics. The formalism specifies a library behaviour by using a system of extended finite state machines (EFSM. This paper outlines the metamodel designed to specify library descriptions and proposes an easy to use domainspecific language (DSL, which can be used to define models for particular libraries. The mentioned metamodel directly forms the code migration procedure. A process of migration is split into five steps, and each step is also described in the paper. The procedure uses an algorithm based on the breadth- first search extended for the needs of the migration task. Models and algorithms were implemented in the prototype of an automated code migration tool. The prototype was tested by both artificial code examples and a real-world open source project. The article describes the experiments performed, the difficulties that have arisen in the process of migration of test samples, and how they are solved in the proposed procedure. The results of experiments indicate that code migration can be successfully automated. 

Polarization Insensitivity in Double-Split Ring and Triple-Split Ring Terahertz Resonators

International Nuclear Information System (INIS)

Wu Qian-Nan; Lan Feng; Tang Xiao-Pin; Yang Zi-Qiang

2015-01-01

A modified double-split ring resonator and a modified triple-split ring resonator, which offer polarization-insensitive performance, are investigated, designed and fabricated. By displacing the two gaps of the conventional double-split ring resonator away from the center, the second resonant frequency for the 0° polarized wave and the resonant frequency for the 90° polarized wave become increasingly close to each other until they are finally identical. Theoretical and experimental results show that the modified double-split ring resonator and the modified triple-split ring resonator are insensitive to different polarized waves and show strong resonant frequency dips near 433 and 444 GHz, respectively. The results of this work suggest new opportunities for the investigation and design of polarization-dependent terahertz devices based on split ring resonators. (paper)

The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p

Directory of Open Access Journals (Sweden)

Haoyou Wang

2017-04-01

Full Text Available Background/Aims: Long non-coding RNAs (lncRNAs are key players in the development and progression of human cancers. The lncRNA XIST (X-inactive specific transcript has been shown to be upregulated in human non-small cell lung cancer (NSCLC; however, its role and molecular mechanisms in NSCLC cell progression remain unclear. Methods: qRT-PCR was conducted to assess the expression of XIST and miR-186. Cell proliferation was detected using MTT assay. Cell invasion and migration were evaluated using transwell assay. Cell cycle distribution and apoptosis rates were analyzed by flow cytometry. Luciferase reporter assay was used to identify the direct regulation of XIST and miR-186. A RNA immunoprecipitation was used to analyze whether XIST was associated with the RNA-induced silencing complex (RISC. Results: We confirmed that XIST was upregulated in NSCLC cell lines and tissues. Functionally, XIST knockdown inhibited cancer cell proliferation and invasion, and induced apoptosis in vitro, and suppressed subcutaneous tumor growth in vivo. Mechanistic investigations revealed a reciprocal repressive interaction between XIST and miR-186-5p. Furthermore, we showed that miR-186-5p has a binding site for XIST. Our data also indicated that XIST and miR-186-5p are likely in the same RNA induced silencing complex. Conclusion: Together, our data revealed that XIST knockdown confers suppressive function in NSCLC and XIST may be a novel therapeutic marker in this disease.

Nanocrystalline diamond on Si solar cells for direct photoelectrochemical water splitting

Czech Academy of Sciences Publication Activity Database

Ashcheulov, Petr; Kusko, M.; Fendrych, František; Poruba, A.; Taylor, Andrew; Jäger, Aleš; Fekete, Ladislav; Kraus, I.; Kratochvílová, Irena

2014-01-01

Roč. 211, č. 10 (2014), s. 2347-2352 ISSN 1862-6300 R&D Projects: GA ČR GA13-31783S; GA MŠk(CZ) LM2011026 EU Projects: European Commission(XE) 238201 - MATCON Institutional support: RVO:68378271 Keywords : boron-doped diamond * solar cell * heterostructure * water splitting Subject RIV: JI - Composite Materials Impact factor: 1.616, year: 2014

Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation, migration and invasion by depending on p53’s transcriptional activity

Energy Technology Data Exchange (ETDEWEB)

Sun, Lin [West Biostatistics and Cost-effectiveness Research Center, Medical Insurance Office, West China Hospital of Sichuan University, 610041, Sichuan (China); Li, Yu [Department of Anesthesiology, West China Hospital, Sichuan University, 610041, Sichuan (China); Yang, Bangxiang, E-mail: b19933009@qq.coom [Department of Pain Management, West China Hospital of Sichuan University, 610041, Sichuan (China)

2016-09-09

Long non-coding RNAs (lncRNAs) was found to play critical roles in tumorigenesis, hence, screen of tumor-related lncRNAs, identification of their biological roles is important for understanding the processes of tumorigenesis. In this study, we identified the expressing difference of several tumor-related lncRNAs in breast cancer samples and found that, MEG3, which is downregulated in non-small cell lung cancer (NSCLC) tumor tissues, is also downregulated in breast cancer samples compared with adjacent tissues. For figuring out the effect of MEG3 in breast cancer cells MCF7 and MB231, we overexpressed MEG3 in these cells, and found that it resulted the inhibition of proliferation, colony formation, migration and invasion capacities by enhancing p53’s transcriptional activity on its target genes, including p21, Maspin and KAI1. MEG3 presented similar effects in MB157, which is a p53-null breast cancer cell line, when functional p53 but not p53R273H mutant, which lacks transcriptional activity, was introduced. Surprisingly, overexpression of MEG3 activates p53’s transcriptional activity by decreasing MDM2’s transcription level, and thus stabilizes and accumulates P53. Taken together, our findings indicate that MEG3 is downregulated in breast cancer tissues and affects breast cancer cells’ malignant behaviors, which indicate MEG3 a potential therapeutic target for breast cancer. - Highlights: • MEG3 RNA is widely downregulated in breast tumor tissue. • MEG3 regulates P53 indirectly through transcriptional regulation of MDM2. • Under unstressed condition, MEG3-related P53 accumulation transcriptionally activates p53’s target genes. • MEG3 expression level tightly regulates proliferation, colony formation, migration and invasion in breast tumor cells.

Application of the operator splitting to the Maxwell equations with the source term

NARCIS (Netherlands)

Bochev, Mikhail A.; Faragó, I.; Horváth, R.

Motivated by numerical solution of the time-dependent Maxwell equations, we consider splitting methods for a linear system of differential equations $w'(t)=Aw(t)+f(t),$ $A\\in\\mathbb{R}^{n\\times n}$ split into two subproblems $w_1'(t)=A_1w_1(t)+f_1(t)$ and $w_2'(t)=A_2w_2(t)+f_2(t),$ $A=A_1+A_2,$

Quantitative analysis on electric dipole energy in Rashba band splitting.

Science.gov (United States)

Hong, Jisook; Rhim, Jun-Won; Kim, Changyoung; Ryong Park, Seung; Hoon Shim, Ji

2015-09-01

We report on quantitative comparison between the electric dipole energy and the Rashba band splitting in model systems of Bi and Sb triangular monolayers under a perpendicular electric field. We used both first-principles and tight binding calculations on p-orbitals with spin-orbit coupling. First-principles calculation shows Rashba band splitting in both systems. It also shows asymmetric charge distributions in the Rashba split bands which are induced by the orbital angular momentum. We calculated the electric dipole energies from coupling of the asymmetric charge distribution and external electric field, and compared it to the Rashba splitting. Remarkably, the total split energy is found to come mostly from the difference in the electric dipole energy for both Bi and Sb systems. A perturbative approach for long wave length limit starting from tight binding calculation also supports that the Rashba band splitting originates mostly from the electric dipole energy difference in the strong atomic spin-orbit coupling regime.

Extracellular acidification synergizes with PDGF to stimulate migration of mouse embryo fibroblasts through activation of p38MAPK with a PTX-sensitive manner

International Nuclear Information System (INIS)

An, Caiyan; Sato, Koichi; Wu, Taoya; Bao, Muqiri; Bao, Liang; Tobo, Masayuki; Damirin, Alatangaole

2015-01-01

The elucidation of the functional mechanisms of extracellular acidification stimulating intracellular signaling pathway is of great importance for developing new targets of treatment for solid tumors, and inflammatory disorders characterized by extracellular acidification. In the present study, we focus on the regulation of extracellular acidification on intracellular signaling pathways in mouse embryo fibroblasts (MEFs). We found extracellular acidification was at least partly involved in stimulating p38MAPK pathway through PTX-sensitive behavior to enhance cell migration in the presence or absence of platelet-derived growth factor (PDGF). Statistical analysis showed that the actions of extracellular acidic pH and PDGF on inducing enhancement of cell migration were not an additive effect. However, we also found extracellular acidic pH did inhibit the viability and proliferation of MEFs, suggesting that extracellular acidification stimulates cell migration probably through proton-sensing mechanisms within MEFs. Using OGR1-, GPR4-, and TDAG8-gene knock out technology, and real-time qPCR, we found known proton-sensing G protein-coupled receptors (GPCRs), transient receptor potential vanilloid subtype 1 (TRPV1), and acid-sensing ion channels (ASICs) were unlikely to be involved in the regulation of acidification on cell migration. In conclusion, our present study validates that extracellular acidification stimulates chemotactic migration of MEFs through activation of p38MAPK with a PTX-sensitive mechanism either by itself, or synergistically with PDGF, which was not regulated by the known proton-sensing GPCRs, TRPV1, or ASICs. Our results suggested that others proton-sensing GPCRs or ion channels might exist in MEFs, which mediates cell migration induced by extracellular acidification in the presence or absence of PDGF. - Highlights: • Acidic pH and PDGF synergize to stimulate MEFs migration via Gi/p38MAPK pathway. • Extracellular acidification inhibits the

Extracellular acidification synergizes with PDGF to stimulate migration of mouse embryo fibroblasts through activation of p38MAPK with a PTX-sensitive manner

Energy Technology Data Exchange (ETDEWEB)

An, Caiyan [Department of Biochemistry and Molecular Biology, College of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia (China); Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi (Japan); Clinical Medicine Research Center of the Affiliated Hospital, Inner Mongolia Medical University, Hohhot, Inner Mongolia (China); Sato, Koichi [Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi (Japan); Wu, Taoya; Bao, Muqiri; Bao, Liang [Department of Biochemistry and Molecular Biology, College of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia (China); Tobo, Masayuki [Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi (Japan); Damirin, Alatangaole, E-mail: bigaole@imu.edu.cn [Department of Biochemistry and Molecular Biology, College of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia (China)

2015-05-01

The elucidation of the functional mechanisms of extracellular acidification stimulating intracellular signaling pathway is of great importance for developing new targets of treatment for solid tumors, and inflammatory disorders characterized by extracellular acidification. In the present study, we focus on the regulation of extracellular acidification on intracellular signaling pathways in mouse embryo fibroblasts (MEFs). We found extracellular acidification was at least partly involved in stimulating p38MAPK pathway through PTX-sensitive behavior to enhance cell migration in the presence or absence of platelet-derived growth factor (PDGF). Statistical analysis showed that the actions of extracellular acidic pH and PDGF on inducing enhancement of cell migration were not an additive effect. However, we also found extracellular acidic pH did inhibit the viability and proliferation of MEFs, suggesting that extracellular acidification stimulates cell migration probably through proton-sensing mechanisms within MEFs. Using OGR1-, GPR4-, and TDAG8-gene knock out technology, and real-time qPCR, we found known proton-sensing G protein-coupled receptors (GPCRs), transient receptor potential vanilloid subtype 1 (TRPV1), and acid-sensing ion channels (ASICs) were unlikely to be involved in the regulation of acidification on cell migration. In conclusion, our present study validates that extracellular acidification stimulates chemotactic migration of MEFs through activation of p38MAPK with a PTX-sensitive mechanism either by itself, or synergistically with PDGF, which was not regulated by the known proton-sensing GPCRs, TRPV1, or ASICs. Our results suggested that others proton-sensing GPCRs or ion channels might exist in MEFs, which mediates cell migration induced by extracellular acidification in the presence or absence of PDGF. - Highlights: • Acidic pH and PDGF synergize to stimulate MEFs migration via Gi/p38MAPK pathway. • Extracellular acidification inhibits the

MicroRNA-144-3p suppresses gastric cancer progression by inhibiting epithelial-to-mesenchymal transition through targeting PBX3

International Nuclear Information System (INIS)

Li, Butian; Zhang, Shengping; Shen, Hao; Li, Chenglong

2017-01-01

MicroRNAs are aberrantly expressed in a wide variety of human cancers. The present study aims to elucidate the effects and molecular mechanisms of miR-144-3p that underlie gastric cancer (GC) development. It was observed that miR-144-3p expression was significantly decreased in GC tissues compared to that in paired non-tumor tissues; moreover, its expression was lower in tissues of advanced stage and larger tumor size, as well as in lymph node metastasis tissues compared to that in control groups. miR-144-3p expression was associated with depth of invasion (P = 0.030), tumor size (P = 0.047), lymph node metastasis (P = 0.047), and TNM stage (P = 0.048). Additionally, miR-144-3p significantly inhibited proliferation, migration, and invasion in GC cells. It also reduced F-actin expression and suppressed epithelial-to-mesenchymal transition (EMT) in GC cells. Furthermore, pre-leukemia transcription factor 3 (PBX3) was a direct target gene of miR-144-3p. PBX3 was overexpressed in GC tissues and promoted EMT in GC cells. The effects of miR-144-3p mimics or inhibitors on cell migration, invasion, and proliferation were reversed by PBX3 overexpression or downregulation respectively. These results suggest that miR-144-3p suppresses GC progression by inhibiting EMT through targeting PBX3. - Highlights: • miR-144-3p is downregulated in gastric cancer tissues and associated with malignant clinical factors. • miR-144-3p inhibits proliferation, migration, and invasion in gastric cancer cells. • PBX3 is a direct target of miR-144-3p and promotes EMT in gastric cancer. • miR-144-3p suppresses EMT in gastric cancer by regulating PBX3.

Bad splits in bilateral sagittal split osteotomy: systematic review of fracture patterns.

Science.gov (United States)

Steenen, S A; Becking, A G

2016-07-01

An unfavourable and unanticipated pattern of the mandibular sagittal split osteotomy is generally referred to as a 'bad split'. Few restorative techniques to manage the situation have been described. In this article, a classification of reported bad split pattern types is proposed and appropriate salvage procedures to manage the different types of undesired fracture are presented. A systematic review was undertaken, yielding a total of 33 studies published between 1971 and 2015. These reported a total of 458 cases of bad splits among 19,527 sagittal ramus osteotomies in 10,271 patients. The total reported incidence of bad split was 2.3% of sagittal splits. The most frequently encountered were buccal plate fractures of the proximal segment (types 1A-F) and lingual fractures of the distal segment (types 2A and 2B). Coronoid fractures (type 3) and condylar neck fractures (type 4) have seldom been reported. The various types of bad split may require different salvage approaches. Copyright © 2016 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Relationship between S. typhi R plasmid (pRST98) and macrophage apoptosis

International Nuclear Information System (INIS)

Song Guorong; Wu Shuyan; Li Yuanyuan; Lv Jie; Xu Yang; Huang Rui

2008-01-01

Objective: To study the relationship between S. typhi R plasmid (pR ST98 ) and macrophage apoptosis. Methods: pR ST98 was transferred into a less virulent strain of S. typhimurium for creating a transconjugant pR ST98 /RIA, the standard S. typhimurium virulence strain SR-11 was used as the positive control, and RIA as the negative one. Infection with murine macrophage J 774A.1 occurred separately under the same conditions. J 774A.1 apoptosis was detected by flow cytometry and TUNEL at 0, 2, 4, 6, 12, 24 hours respectively. Mitochondria membrane potential was detected by JC-1 staining method. Viable bacteria was detected by serial dilution at the same time and viable cells stained with Trypan blue were counted. Results: SR-11 results in a higher apoptosis in J 774A.1 than pR ST98 /RIA, and a combined pR ST98 /RIA higher than RIA (P pR ST98 /RIA>SR-11 (P ST98 could increase the macrophage apoptosis. (authors)

Splitting Strategy for Simulating Genetic Regulatory Networks

Directory of Open Access Journals (Sweden)

Xiong You

2014-01-01

Full Text Available The splitting approach is developed for the numerical simulation of genetic regulatory networks with a stable steady-state structure. The numerical results of the simulation of a one-gene network, a two-gene network, and a p53-mdm2 network show that the new splitting methods constructed in this paper are remarkably more effective and more suitable for long-term computation with large steps than the traditional general-purpose Runge-Kutta methods. The new methods have no restriction on the choice of stepsize due to their infinitely large stability regions.

circ-SHKBP1 Regulates the Angiogenesis of U87 Glioma-Exposed Endothelial Cells through miR-544a/FOXP1 and miR-379/FOXP2 Pathways

Directory of Open Access Journals (Sweden)

Qianru He

2018-03-01

Full Text Available Circular RNAs (circRNAs are a type of endogenous non-coding RNAs, which have been considered to mediate diverse tumorigenesis including angiogenesis. The present study aims to elucidate the potential role and molecular mechanism of circ-SHKBP1 in regulating the angiogenesis of U87 glioma-exposed endothelial cells (GECs. The expression of circ-SHKBP1, but not linear SHKBP1, was significantly upregulated in GECs compared with astrocyte-exposed endothelial cells (AECs. circ-SHKBP1 knockdown inhibited the viability, migration, and tube formation of GECs dramatically. The expressions of miR-379/miR-544a were downregulated in GECs, and circ-SHKBP1 functionally targeted miR-544a/miR-379 in an RNA-induced silencing complex (RISC manner. Dual-luciferase reporter assay demonstrated that forkhead box P1/P2 (FOXP1/FOXP2 were targets of miR-544a/miR-379. The expressions of FOXP1/FOXP2 were upregulated in GECs, and silencing of FOXP1/FOXP2 inhibited the viability, migration, and tube formation of GECs. Meanwhile, FOXP1/FOXP2 promoted angiogenic factor with G patch and FHA domains 1 (AGGF1 expression at the transcriptional level. Furthermore, knockdown of AGGF1 suppressed the viability, migration, and tube formation of GECs via phosphatidylinositol 3-kinase (PI3K/AKT and extracellular signal-regulated kinase (ERK1/2 pathways. Taken together, the present study demonstrated that circ-SHKBP1 regulated the angiogenesis of GECs through miR-544a/FOXP1 and miR-379/FOXP2 pathways, and these findings might provide a potential target and effective strategy for combined therapy of gliomas.

The metrics and correlates of physician migration from Africa

Directory of Open Access Journals (Sweden)

Arah Onyebuchi A

2007-05-01

Full Text Available Abstract Background Physician migration from poor to rich countries is considered an important contributor to the growing health workforce crisis in the developing world. This is particularly true for Africa. The perceived magnitude of such migration for each source country might, however, depend on the choice of metrics used in the analysis. This study examined the influence of choice of migration metrics on the rankings of African countries that suffered the most physician migration, and investigated the correlates of physician migration. Methods Ranking and correlational analyses were conducted on African physician migration data adjusted for bilateral net flows, and supplemented with developmental, economic and health system data. The setting was the 53 African birth countries of African-born physicians working in nine wealthier destination countries. Three metrics of physician migration were used: total number of physician émigrés; emigration fraction defined as the proportion of the potential physician pool working in destination countries; and physician migration density defined as the number of physician émigrés per 1000 population of the African source country. Results Rankings based on any of the migration metrics differed substantially from those based on the other two metrics. Although the emigration fraction and physician migration density metrics gave proportionality to the migration crisis, only the latter was consistently associated with source countries' workforce capacity, health, health spending, economic and development characteristics. As such, higher physician migration density was seen among African countries with relatively higher health workforce capacity (0.401 ≤ r ≤ 0.694, p ≤ 0.011, health status, health spending, and development. Conclusion The perceived magnitude of physician migration is sensitive to the choice of metrics. Complementing the emigration fraction, the physician migration density is a metric

IMPORTANT INFORMATION - Flagstaff Car-Park and Park-and-Ride (P+R)

CERN Document Server

GS Department

2011-01-01

As part of the new arrangements following the arrival of the tram-line at CERN, an Automatic Number-Plate Recognition (ANPR) system has been installed restricting access to the Flagstaff Car-park and the Park-and-Ride (P+R) zone according to the conditions set out below: Holders of a valid P+R user card may enter the car-park at all hours but may only park in the area specifically designated as the P+R zone. P+R user cards can be purchased from the Fondation des Parkings de Genève (http://www.ge.ch/parkings/abonnements.html)   Members of CERN personnel and of contractors' personnel, whatever their status, may freely access the Flagstaff Car-Park at all hours, as long as their vehicle is duly registered with CERN, but they may not use the P+R zone, which is reserved for holders of P+R user cards. Please check that your vehicle number-plates are properly registered via AdaMS (http://cern.ch/adams). If this is not the case, the following action must be taken: - for private or co...

miR-199a-5p Is upregulated during fibrogenic response to tissue injury and mediates TGFbeta-induced lung fibroblast activation by targeting caveolin-1.

Directory of Open Access Journals (Sweden)

Christian Lacks Lino Cardenas

Full Text Available As miRNAs are associated with normal cellular processes, deregulation of miRNAs is thought to play a causative role in many complex diseases. Nevertheless, the precise contribution of miRNAs in fibrotic lung diseases, especially the idiopathic form (IPF, remains poorly understood. Given the poor response rate of IPF patients to current therapy, new insights into the pathogenic mechanisms controlling lung fibroblasts activation, the key cell type driving the fibrogenic process, are essential to develop new therapeutic strategies for this devastating disease. To identify miRNAs with potential roles in lung fibrogenesis, we performed a genome-wide assessment of miRNA expression in lungs from two different mouse strains known for their distinct susceptibility to develop lung fibrosis after bleomycin exposure. This led to the identification of miR-199a-5p as the best miRNA candidate associated with bleomycin response. Importantly, miR-199a-5p pulmonary expression was also significantly increased in IPF patients (94 IPF versus 83 controls. In particular, levels of miR-199a-5p were selectively increased in myofibroblasts from injured mouse lungs and fibroblastic foci, a histologic feature associated with IPF. Therefore, miR-199a-5p profibrotic effects were further investigated in cultured lung fibroblasts: miR-199a-5p expression was induced upon TGFβ exposure, and ectopic expression of miR-199a-5p was sufficient to promote the pathogenic activation of pulmonary fibroblasts including proliferation, migration, invasion, and differentiation into myofibroblasts. In addition, we demonstrated that miR-199a-5p is a key effector of TGFβ signaling in lung fibroblasts by regulating CAV1, a critical mediator of pulmonary fibrosis. Remarkably, aberrant expression of miR-199a-5p was also found in unilateral ureteral obstruction mouse model of kidney fibrosis, as well as in both bile duct ligation and CCl4-induced mouse models of liver fibrosis, suggesting that

Altered regulation of miR-34a and miR-483-3p in alcoholic hepatitis and DDC fed mice.

Science.gov (United States)

Liu, Hui; French, Barbara A; Li, Jun; Tillman, Brittany; French, Samuel W

2015-12-01

MicroRNAs are small noncoding RNAs that negatively regulate gene expression by binding to the untranslated regions of their target mRNAs. Deregulation of miRNAs is shown to play pivotal roles in tumorigenesis and progression. Mallory-Denk Bodies (MDBs) are prevalent in various liver diseases including alcoholic hepatitis (AH) and are formed in mice livers by feeding DDC. By comparing AH livers where MDBs had formed with normal livers, there were significant changes of miR-34a and miR-483-3p by RNA sequencing (RNA-Seq) analyses. Real-time PCR further shows a 3- and 6-fold upregulation (respectively) of miR-34a in the AH livers and in the livers of DDC re-fed mice, while miR-483-3p was significantly downregulated in AH and DDC re-fed mice livers. This indicates that miR-34a and miR-483-3p may be crucial for liver MDB formation. P53 mRNA was found to be significantly downregulated both in the AH livers and in the livers of DDC re-fed mice, indicating that the upregulation of miR-34a is permitted by the decrease of p53 in AH since miR-34a is a main target of p53. Overexpression of miR-34a leads to an increase of p53 targets such as p27, which inhibits the cell cycle leading to cell cycle arrest. Importantly, BRCA1 is a target gene of miR-483-3p by RNA-Seq analyses and the downregulation of miR-483-3p may be the mechanism for liver MDB formation since the BRCA1 signal was markedly upregulated in AH livers. These results constitute a demonstration of the altered regulation of miR-34a and miR-483-3p in the livers of AH and mice fed DDC where MDBs formed, providing further insight into the mechanism of MDB formation mediated by miR-34a and miR-483-3p in AH. Copyright © 2015 Elsevier Inc. All rights reserved.

Market Structure and Stock Splits

OpenAIRE

David Michayluk; Paul Kofman

2001-01-01

Enhanced liquidity is one possible motivation for stock splits but empirical research frequently documents declines in liquidity following stock splits. Despite almost thirty years of inquiry, little is known about all the changes in a stock's trading activity following a stock split. We examine how liquidity measures change around more than 2,500 stock splits and find a pervasive decline in most measures. Large stock splits exhibit a more severe liquidity decline than small stock splits, esp...

miRNA-135a promotes breast cancer cell migration and invasion by targeting HOXA10

International Nuclear Information System (INIS)

Chen, Yating; Zhang, Hongwei; Ma, Duan; Zhang, Jin; Wang, Huijun; Zhao, Jiayi; Xu, Cheng; Du, Yingying; Luo, Xin; Zheng, Fengyun; Liu, Rui

2012-01-01

miRNAs are a group of small RNA molecules regulating target genes by inducing mRNA degradation or translational repression. Aberrant expression of miRNAs correlates with various cancers. Although miR-135a has been implicated in several other cancers, its role in breast cancer is unknown. HOXA10 however, is associated with multiple cancer types and was recently shown to induce p53 expression in breast cancer cells and reduce their invasive ability. Because HOXA10 is a confirmed miR-135a target in more than one tissue, we examined miR-135a levels in relation to breast cancer phenotypes to determine if miR-135a plays role in this cancer type. Expression levels of miR-135a in tissues and cells were determined by poly (A)-RT PCR. The effect of miR-135a on proliferation was evaluated by CCK8 assay, cell migration and invasion were evaluated by transwell migration and invasion assays, and target protein expression was determined by western blotting. GFP and luciferase reporter plasmids were constructed to confirm the action of miR-135a on downstream target genes including HOXA10. Results are reported as means ± S.D. and differences were tested for significance using 2-sided Student's t-test. Here we report that miR-135a was highly expressed in metastatic breast tumors. We found that the expression of miR-135a was required for the migration and invasion of breast cancer cells, but not their proliferation. HOXA10, which encodes a transcription factor required for embryonic development and is a metastasis suppressor in breast cancer, was shown to be a direct target of miR-135a in breast cancer cells. Our analysis showed that miR-135a suppressed the expression of HOXA10 both at the mRNA and protein level, and its ability to promote cellular migration and invasion was partially reversed by overexpression of HOXA10. In summary, our results indicate that miR-135a is an onco-miRNA that can promote breast cancer cell migration and invasion. HOXA10 is a target gene for miR

On the Numerical Behavior of Matrix Splitting Iteration Methods for Solving Linear Systems

Czech Academy of Sciences Publication Activity Database

Bai, Z.-Z.; Rozložník, Miroslav

2015-01-01

Roč. 53, č. 4 (2015), s. 1716-1737 ISSN 0036-1429 R&D Projects: GA ČR GA13-06684S Institutional support: RVO:67985807 Keywords : matrix splitting * stationary iteration method * backward error * rounding error analysis Subject RIV: BA - General Mathematics Impact factor: 1.899, year: 2015

Expression of MiR-9 promotes proliferation, migration and ...

African Journals Online (AJOL)

differentiation of human neural stem cells. Fei Zeng ... Keywords: Neural stem cells, MicroRNA, Mir-9, Migration, Differentiation, Proliferation ... Neural stem cells (NSCs) are basically ..... application of patient-specific pluripotent stem cells. J.

MicroRNA-139-5p affects cisplatin sensitivity in human nasopharyngeal carcinoma cells by regulating the epithelial-to-mesenchymal transition.

Science.gov (United States)

Shao, Qianqian; Zhang, Pei; Ma, Yingye; Lu, Zhaoyi; Meng, Jie; Li, Hui; Wang, Xiaoming; Chen, Deshang; Zhang, Mingjie; Han, Yaofeng; Liu, Hao; Ma, Shiyin

2018-04-30

Nasopharyngeal carcinoma (NPC) is a head and neck cancer associated with poor prognosis. Many studies have shown that the epithelial-to-mesenchymal transition (EMT) is important in cancer progression, metastasis, and chemotherapy resistance and that microRNAs (miRNAs) play a key role in chemotherapy resistance associated with EMT. The miRNA miR-139-5p is downregulated in many human cancers and is closely related to tumor progression. The aim of this study was to investigate the ability of miR-139-5p to influence the cisplatin resistance, apoptosis, invasion and migration in NPC cells through the regulation of the EMT. We investigated these processes in parental HNE1 and cisplatin-resistant HNE1/DDP cells transfected with miR-139-5p inhibitors and mimics, respectively. Our results suggest that the upregulation of miR-139-5p expression inhibits proliferation, invasion, migration and EMT in human NPC cells. In addition, we found that miR-139-5p expression levels and DDP-induced apoptosis positively correlate in NPC cells. In conclusion, our results demonstrate that miR-139-5p can regulate the migration, invasion and DDP resistance in human NPC by modulating the EMT. The regulation of miR-139-5p levels might be a new approach to reverse EMT and DDP resistance and counteract metastasis and chemotherapy resistance in human NPC. Copyright © 2018 Elsevier B.V. All rights reserved.

Iodine 125 seed migration after prostate brachytherapy: a study of 170 patients

International Nuclear Information System (INIS)

Chauveinc, L.; Osseili, A.; Rosenwald, J.C.; Cosset, J.M.; Flam, T.; Thiounn, N.; Savignoni, A.

2004-01-01

Purpose. To study the number of migrating seeds, the anatomical site of migration and possible predictive parameters of migration, after prostate cancer brachytherapy using a loose-seed (I125) implantation technique. Patients and methods. The charts of the 170 patients consecutively treated by the Institut Curie/Hospital Cochin/Hospital Necker Group between September 1, 2001 and August 31, 2002, were analysed. All seeds having migrated to the lungs and seen on the chest X-ray systematically performed at 2 months, have been recorded, as well as the seeds lost by the urines (after sieving) or in the sperm (condom). Results. Among 12,179 implanted seeds, 44 were found to have migrated (0.36%). Most of the migrating seeds (32/44; 73%), were found in the lungs. Overall, one or several seed migrations were observed in 35 patients (21% of the total number of patients in this series). In the majority of cases (77< r i. only one seed migrated. A significant relationship (P = 0.04) vs as found between the number of migrating seeds and the number of implanted ones (or with the prostate volume, but those two parameters were closely linked in our series). More specifically, a significant relationship (P = 0.02) could be demonstrated between the number of seeds implanted at the periphery of the prostate and the number of seeds migrating to the lungs. Conclusion. The percentage of migrating seeds observed in this series is low. actually one of the lowest found in the literature when using the loose-seed technique. There was no clinical consequences and the loss of-usually only one seed is very unlikely to alter the quality of the dose distribution. However, the predominance of pulmonary migrations in our series led us to slightly modify our implantation technique. We now try to avoid too 'peripheral' seed implantations, due to the risk of migration towards the peri-prostatic veins, and subsequently to the lungs. (author)

High-power pulsed plasma deposition of hematite photoanode for PEC water splitting

Czech Academy of Sciences Publication Activity Database

Kment, Š.; Hubička, Zdeněk; Krysa, J.; Olejníček, Jiří; Čada, Martin; Gregora, Ivan; Zlámal, M.; Brunclíková, Michaela; Remeš, Zdeněk; Liu, N.; Wang, L.; Kirchgeorg, R.; Lee, Ch.Y.; Schmuki, P.

2014-01-01

Roč. 230, Jul (2014), 8-14 ISSN 0920-5861 R&D Projects: GA ČR GAP108/12/2104; GA MŠk LH12043 Institutional support: RVO:68378271 Keywords : electrical properties * hematite * HiPIMS * hollow cathode plasma jet * photoelectrochemical water splitting * thin films Subject RIV: BL - Plasma and Gas Discharge Physics Impact factor: 3.893, year: 2014

Performance Optimization of Alternative Lower Global Warming Potential Refrigerants in Mini-Split Room Air Conditioners

Energy Technology Data Exchange (ETDEWEB)

Shen, Bo [ORNL; Abdelaziz, Omar [ORNL; Shrestha, Som S [ORNL

2017-01-01

Oak Ridge National laboratory (ORNL) recently conducted extensive laboratory, drop-in investigations for lower Global Warming Potential (GWP) refrigerants to replace R-22 and R-410A. ORNL studied propane, DR-3, ARM-20B, N-20B and R-444B as lower GWP refrigerant replacement for R-22 in a mini-split room air conditioner (RAC) originally designed for R-22; and, R-32, DR-55, ARM-71A, and L41-2, in a mini-split RAC designed for R-410A. We obtained laboratory testing results with very good energy balance and nominal measurement uncertainty. Drop-in studies are not enough to judge the overall performance of the alternative refrigerants since their thermodynamic and transport properties might favor different heat exchanger configurations, e.g. cross-flow, counter flow, etc. This study compares optimized performances of individual refrigerants using a physics-based system model tools. The DOE/ORNL Heat Pump Design Model (HPDM) was used to model the mini-split RACs by inputting detailed heat exchangers geometries, compressor displacement and efficiencies as well as other relevant system components. The RAC models were calibrated against the lab data for each individual refrigerant. The calibrated models were then used to conduct a design optimization for the cooling performance by varying the compressor displacement to match the required capacity, and changing the number of circuits, refrigerant flow direction, tube diameters, air flow rates in the condenser and evaporator at 100% and 50% cooling capacities. This paper compares the optimized performance results for all alternative refrigerants and highlights best candidates for R-22 and R-410A replacement.

Semiflexible polymer conformation, distribution and migration in microcapillary flows

Energy Technology Data Exchange (ETDEWEB)

Chelakkot, Raghunath; Gompper, Gerhard [Institut fuer Festkoerperforschung, Forschungszentrum Juelich, 52425 Juelich (Germany); Winkler, Roland G [Institute for Advanced Simulation, Forschungszentrum Juelich, 52425 Juelich (Germany)

2011-05-11

The flow behavior of a semiflexible polymer in microchannels is studied using multiparticle collision dynamics, a particle-based hydrodynamic simulation technique. Conformations, distributions, and radial cross-streamline migration are investigated for various bending rigidities, with persistence lengths L{sub p} in the range 0.5 {<=} L{sub p}/L{sub r} {<=} 30. The flow behavior is governed by the competition between a hydrodynamic lift force and steric repulsion from the wall, which lead to migration away from the wall, and a locally varying flow induced orientation, which drives the polymer away from the channel center and towards the wall. The different dependences of these effects on the polymer bending rigidity and the flow velocity results in a complex dynamical behavior. However, a generic effect is the appearance of a maximum in the monomer and the center-of-mass distributions, which occurs at the channel center for small flow velocities, but moves off-center at higher velocities.

Semiflexible polymer conformation, distribution and migration in microcapillary flows

International Nuclear Information System (INIS)

Chelakkot, Raghunath; Gompper, Gerhard; Winkler, Roland G

2011-01-01

The flow behavior of a semiflexible polymer in microchannels is studied using multiparticle collision dynamics, a particle-based hydrodynamic simulation technique. Conformations, distributions, and radial cross-streamline migration are investigated for various bending rigidities, with persistence lengths L p in the range 0.5 ≤ L p /L r ≤ 30. The flow behavior is governed by the competition between a hydrodynamic lift force and steric repulsion from the wall, which lead to migration away from the wall, and a locally varying flow induced orientation, which drives the polymer away from the channel center and towards the wall. The different dependences of these effects on the polymer bending rigidity and the flow velocity results in a complex dynamical behavior. However, a generic effect is the appearance of a maximum in the monomer and the center-of-mass distributions, which occurs at the channel center for small flow velocities, but moves off-center at higher velocities.

Neutral Higgs Sector of the MSSM without $R_{p}$

CERN Document Server

Davidson, Sacha; Rius, N

2000-01-01

We analyse the neutral scalar sector of the MSSM without R-parity. Our analysis is performed for a one-generation model in terms of ``basis-independent'' parameters, and includes one-loop corrections due to large yukawa couplings. We concentrate on the consequences of large $R_p$ violating masses in the soft sector, which mix the Higgses with the sleptons, because these are only constrained by their one-loop contributions to neutrino masses. We focus on the effect of $R_p$-violation on the Higgs mass and branching ratios. We find that the experimental lower bound on the lightest CP-even Higgs in this model can be lower than in the MSSM.

Upregulated expression of Nogo-A and NgR in an experimental model of focal microgyria regulates the migration, proliferation and self-renewal of subventricular zone neural progenitors

Energy Technology Data Exchange (ETDEWEB)

Yu, Sixun; Shu, Haifeng; Yang, Tao; Huang, Haidong [Department of Neurosurgery, General Hospital of the People' s Liberation Army Chengdu Military Region, Chengdu, Sichuan, 610083 (China); Li, Song [Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037 (China); Zhao, Ziyi [Central Laboratory, Teaching Hospital of Chengdu University of Traditional Chinese Medicine, 610075 (China); Kuang, Yongqin, E-mail: kuangyongqin@163.com [Department of Neurosurgery, General Hospital of the People' s Liberation Army Chengdu Military Region, Chengdu, Sichuan, 610083 (China)

2016-04-29

Nogo-A and its receptor (NgR) were first described as myelin-associated inhibitors of neuronal regeneration in response to injury. In recent years, knowledge about the important role of the Nogo-A protein in several neuronal pathologies has grown considerably. Here, we employed a neonatal cortex freeze-lesion (NFL) model in neonatal rats and measured the expression of Nogo-A and NgR in the resulting cerebrocortical microdysgenesis 5–75 days after freezing injury. We observed marked upregulation of Nogo-A and NgR in protein levels. Furthermore, the migration of neural precursor cells (NPCs) derived from the subventricular zone (SVZ) toward the sits of injury was perturbed by treatment of NgR antagonist peptide NEP1-40. In vitro analysis showed that the knockdown of NgR by lentivirus-delivered siRNA promoted in axonal regeneration and SVZ-derived neural stem cell/progenitor cell (SVZ-NPCs) adhesion and migration, findings which were similar to the effects of NEP1-40. Taken together, our results indicate an important role for NgR in regulating the physiological processes of SVZ-NPCs. The observation of upregulated Nogo-A/NgR in lesion sites in the NFL model suggest that the effects of the perturbed Nogo-A are a key feature during the development and/or the progression of cortical malformation. - Highlights: • NFL model is an accurate experimental reproduction of focal microgyria of FCD. • The increase of the Nogo-A Levels occurs in response to freeze-induced focal lesioning. • Nogo-A/NgR may play a critical role for in the pathologic progression of FCD. • Nogo-A is associated with the migration, proliferation and self-renewal of SVZ-NPCs.

Elevation of circulating miR-210-3p in high-altitude hypoxic environment

Directory of Open Access Journals (Sweden)

Yan eYan

2016-03-01

Full Text Available Background: The induction of miR-210-3p, a master hypoxamir, is a consistent feature of the hypoxic response in both normal and malignant cells. However, whether miR-210-3p acts as a circulating factor in response to a hypoxic environment remains unknown. The current study aimed to examine the effect of a high-altitude hypoxic environment on circulating miR-210-3p.Methods: We examined and compared the levels of miR-210-3p using TaqMan-based qRT-PCR in both peripheral blood cells and plasma from 84 ethnic Chinese Tibetans residing at 3560 m, 46 newly arrived migrant Han Chinese (Tibet Han and 82 Han Chinese residing at 8.9 m (Nanjing Han. Furthermore, we analyzed the correlations of miR-210-3p with hematological indices. Results: The relative concentrations of miR-210-3p to internal reference U6 in blood cells were significantly higher in the Tibet Han group (1.01±0.11, P<0.001 and in the Tibetan group (1.17±0.09, P<0.001 than in the Nanjing Han group (0.51±0.04. The absolute concentrations of plasma miR-210-3p were also markedly elevated in the Tibet Han group (503.54±42.95 fmol/L, P=0.004 and in the Tibetan group (557.78±39.84 fmol/L, P<0.001 compared to the Nanjing Han group (358.39±16.16 fmol/L. However, in both blood cells and plasma, miR-210-3p levels were not significantly different between the Tibet Han group and the Tibetan group (P=0.280, P=0.620, respectively. Plasma miR-210-3p concentrations were positively correlated with miR-210-3p levels in blood cells (r=0.192, P=0.005. Furthermore, miR-210-3p levels in both blood cells and plasma showed strong positive correlations with red blood cell counts and hemoglobin and hematocrit values. Conclusion: These data demonstrated, for the first time, that miR-210-3p might act as a circulating factor in response to hypoxic environments and could be associated with human adaptation to life at high altitudes.

MiR-338-3p regulates neuronal maturation and suppresses glioblastoma proliferation.

Directory of Open Access Journals (Sweden)

James R Howe

Full Text Available Neurogenesis is a highly-regulated process occurring in the dentate gyrus that has been linked to learning, memory, and antidepressant efficacy. MicroRNAs (miRNAs have been previously shown to play an important role in the regulation of neuronal development and neurogenesis in the dentate gyrus via modulation of gene expression. However, this mode of regulation is both incompletely described in the literature thus far and highly multifactorial. In this study, we designed sensors and detected relative levels of expression of 10 different miRNAs and found miR-338-3p was most highly expressed in the dentate gyrus. Comparison of miR-338-3p expression with neuronal markers of maturity indicates miR-338-3p is expressed most highly in the mature neuron. We also designed a viral "sponge" to knock down in vivo expression of miR-338-3p. When miR-338-3p is knocked down, neurons sprout multiple primary dendrites that branch off of the soma in a disorganized manner, cellular proliferation is upregulated, and neoplasms form spontaneously in vivo. Additionally, miR-338-3p overexpression in glioblastoma cell lines slows their proliferation in vitro. Further, low miR-338-3p expression is associated with increased mortality and disease progression in patients with glioblastoma. These data identify miR-338-3p as a clinically relevant tumor suppressor in glioblastoma.

R2P in the UN Security Council: Darfur, Libya and beyond

OpenAIRE

Gifkins, J

2016-01-01

It has been argued that consensus on the responsibility to protect (R2P) was lost in the UN Security Council as a result of the NATO-led intervention in Libya in 2011. This argument assumes that there was more agreement on R2P before the Libyan intervention than there was afterwards. Yet a close examination of the Security Council’s use of language on R2P shows the opposite: R2P was highly contentious within the Security Council prior to the Libyan intervention, and less so afterwards. Not on...

Hinder för utomhusundervisning med fokus på årskurs 4-6

OpenAIRE

Petersson, Essi; Carstensen, Linnea

2018-01-01

I den här studien har vi tagit fram de hinder som begränsar möjligheterna för utomhusundervisning för elever i grundskolan, med fokus på årskurs 4-6 och middle school. Syftet med studien var att synliggöra vilka hinder som kan stå i vägen för utomhusundervisning samt visa på behov av vidare forskning i området. Forskningsfrågan som vi har försökt svara på är: Vad utgör hinder för utomhusundervisning med elever i grundskolan, med fokus på årskurs 4-6 och middle school? Studien bygger på den pr...

Examination of post operative split lung function using quantitative xenon 133 (133Xe) inhalation scan

International Nuclear Information System (INIS)

Omote, Yoshiharu; Maeda, Tomio; Ikeda, Koichiro; Kubo, Yoshihiko

1992-01-01

133 Xe inhalation scan and ordinary lung function testing were performed three times in 34 patients undergoing pulmonary resection: before surgery, and one and six months postoperatively. Forced vital capacity (FVC) and forced expiratory volume in the first second (FEV 1.0 ) were used as spirometric parameters. From the 133 Xe inhalation scan, a split lung capacity (right to left, upper, middle and lower) and T1/2 (time required for half of the inhalation of 133 Xe gas to be expired) were calculated by computer and used as indices of split lung capacity and ventilation, respectively. The predicted postoperative lung functions were calculated using preoperative spirometric respiratory function and 133 Xe inhalation data according to the formula reported by Ali and associates. At sixth postoperative month, both predicted FVC (r=0.895, p 1.0 (r=0.897, p<0.001) correlated highly with those actually observed. These results appear to be very useful for preoperative evaluation of operative indications and the choice of surgical method. The ratios of observed to predicted lung capacity in the post operative state were examined by splitting the right and left lung and the means±S.D.(%) were 80.5±9.7% on the operated side and 119.2±11.7% on the opposite side one month after surgery. Six months after surgery, the corresponding figures were 111.0±5.6% and 96.7±16.4%. The post operative T1/2 values on the operated sides were about 2.4 times the preoperative values at one month after surgery but returned to the preoperative values by the six postoperative month. From these results, it can be said that respiratory functions after pulmonary resection are maintained primarily by compensatory lung function of opposite and operated sides at one and six months, respectively. These results also provide valuable information on postoperative respiratory care for patients who have undergone lung resection. (author)

MiR-9 is overexpressed in spontaneous canine osteosarcoma and promotes a metastatic phenotype including invasion and migration in osteoblasts and osteosarcoma cell lines.

Science.gov (United States)

Fenger, Joelle M; Roberts, Ryan D; Iwenofu, O Hans; Bear, Misty D; Zhang, Xiaoli; Couto, Jason I; Modiano, Jaime F; Kisseberth, William C; London, Cheryl A

2016-10-10

MicroRNAs (miRNAs) regulate the expression of networks of genes and their dysregulation is well documented in human malignancies; however, limited information exists regarding the impact of miRNAs on the development and progression of osteosarcoma (OS). Canine OS exhibits clinical and molecular features that closely resemble the corresponding human disease and it is considered a well-established spontaneous animal model to study OS biology. The purpose of this study was to investigate miRNA dysregulation in canine OS. We evaluated miRNA expression in primary canine OS tumors and normal canine osteoblast cells using the nanoString nCounter system. Quantitative PCR was used to validate the nanoString findings and to assess miR-9 expression in canine OS tumors, OS cell lines, and normal osteoblasts. Canine osteoblasts and OS cell lines were stably transduced with pre-miR-9 or anti-miR-9 lentiviral constructs to determine the consequences of miR-9 on cell proliferation, apoptosis, invasion and migration. Proteomic and gene expression profiling of normal canine osteoblasts with enforced miR-9 expression was performed using 2D-DIGE/tandem mass spectrometry and RNA sequencing and changes in protein and mRNA expression were validated with Western blotting and quantitative PCR. OS cell lines were transduced with gelsolin (GSN) shRNAs to investigate the impact of GSN knockdown on OS cell invasion. We identified a unique miRNA signature associated with primary canine OS and identified miR-9 as being significantly overexpressed in canine OS tumors and cell lines compared to normal osteoblasts. Additionally, high miR-9 expression was demonstrated in tumor-specific tissue obtained from primary OS tumors. In normal osteoblasts and OS cell lines transduced with miR-9 lentivirus, enhanced invasion and migration were observed, but miR-9 did not affect cell proliferation or apoptosis. Proteomic and transcriptional profiling of normal canine osteoblasts overexpressing miR-9 identified

Mechano-growth factor induces migration of rat mesenchymal stem cells by altering its mechanical properties and activating ERK pathway

Energy Technology Data Exchange (ETDEWEB)

Wu, Jiamin; Wu, Kewen; Lin, Feng; Luo, Qing; Yang, Li; Shi, Yisong [Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044 (China); Song, Guanbin, E-mail: song@cqu.edu.cn [Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044 (China); Sung, Kuo-Li Paul [Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044 (China); Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093-0412 (United States)

2013-11-08

Highlights: •MGF induced the migration of rat MSC in a concentration-dependent manner. •MGF enhanced the mechanical properties of rMSC in inducing its migration. •MGF activated the ERK 1/2 signaling pathway of rMSC in inducing its migration. •rMSC mechanics may synergy with ERK 1/2 pathway in MGF-induced rMSC migration. -- Abstract: Mechano-growth factor (MGF) generated by cells in response to mechanical stimulation has been identified as a mechano effector molecule, playing a key role in regulating mesenchymal stem cell (MSC) function, including proliferation and migration. However, the mechanism(s) underlying how MGF-induced MSC migration occurs is still unclear. In the present study, MGF motivated migration of rat MSCs (rMSCs) in a concentration-dependent manner and optimal concentration of MGF at 50 ng/mL (defined as MGF treatment in this paper) was demonstrated. Notably, enhancement of mechanical properties that is pertinent to cell migration, such as cell traction force and cell stiffness were found to respond to MGF treatment. Furthermore, MGF increased phosphorylation of extracellular signal-regulated kinase (ERK), ERK inhibitor (i.e., PD98059) suppressed ERK phosphorylation, and abolished MGF-induced rMSC migration were found, demonstrating that ERK is involved molecule for MGF-induced rMSC migration. These in vitro evidences of MGF-induced rMSC migration and its direct link to altering rMSC mechanics and activating the ERK pathway, uncover the underlying biomechanical and biological mechanisms of MGF-induced rMSC migration, which may help find MGF-based application of MSC in clinical therapeutics.

Splitting methods for split feasibility problems with application to Dantzig selectors

International Nuclear Information System (INIS)

He, Hongjin; Xu, Hong-Kun

2017-01-01

The split feasibility problem (SFP), which refers to the task of finding a point that belongs to a given nonempty, closed and convex set, and whose image under a bounded linear operator belongs to another given nonempty, closed and convex set, has promising applicability in modeling a wide range of inverse problems. Motivated by the increasingly data-driven regularization in the areas of signal/image processing and statistical learning, in this paper, we study the regularized split feasibility problem (RSFP), which provides a unified model for treating many real-world problems. By exploiting the split nature of the RSFP, we shall gainfully employ several efficient splitting methods to solve the model under consideration. A remarkable advantage of our methods lies in their easier subproblems in the sense that the resulting subproblems have closed-form representations or can be efficiently solved up to a high precision. As an interesting application, we apply the proposed algorithms for finding Dantzig selectors, in addition to demonstrating the effectiveness of the splitting methods through some computational results on synthetic and real medical data sets. (paper)

System effects in sample self-stacking CZE: Single analyte peak splitting of salt-containing samples

Czech Academy of Sciences Publication Activity Database

Malá, Zdeňka; Gebauer, Petr; Boček, Petr

2009-01-01

Roč. 30, č. 5 (2009), s. 866-874 ISSN 0173-0835 R&D Projects: GA ČR GA203/08/1536; GA AV ČR IAA400310609; GA AV ČR IAA400310703 Institutional research plan: CEZ:AV0Z40310501 Keywords : CZE * peak splitting * self-stacking Subject RIV: CB - Analytical Chemistry, Separation Impact factor: 3.077, year: 2009

Coded Splitting Tree Protocols

DEFF Research Database (Denmark)

Sørensen, Jesper Hemming; Stefanovic, Cedomir; Popovski, Petar

2013-01-01

This paper presents a novel approach to multiple access control called coded splitting tree protocol. The approach builds on the known tree splitting protocols, code structure and successive interference cancellation (SIC). Several instances of the tree splitting protocol are initiated, each...... instance is terminated prematurely and subsequently iterated. The combined set of leaves from all the tree instances can then be viewed as a graph code, which is decodable using belief propagation. The main design problem is determining the order of splitting, which enables successful decoding as early...

Multifunctional Binary Monolayers Ge xP y: Tunable Band Gap, Ferromagnetism, and Photocatalyst for Water Splitting.

Science.gov (United States)

Li, Pengfei; Zhang, Wei; Li, Dongdong; Liang, Changhao; Zeng, Xiao Cheng

2018-06-04

The most stable structures of two-dimensional Ge x P y and Ge x As y monolayers with different stoichiometries (e.g., GeP, GeP 2 , and GeP 3 ) are explored systematically through the combination of the particle-swarm optimization technique and density functional theory optimization. For GeP 3 , we show that the newly predicted most stable C2/ m structure is 0.16 eV/atom lower in energy than the state-of-the-art P3̅m1 structure reported previously ( Nano Lett. 2017, 17, 1833). The computed electronic band structures suggest that all the stable and metastable monolayers of Ge x P y are semiconductors with highly tunable band gaps under the biaxial strain, allowing strain engineering of their band gaps within nearly the whole visible-light range. More interestingly, the hole doping can convert the C2/ m GeP 3 monolayer from nonmagnetic to ferromagnetic because of its unique valence band structure. For the GeP 2 monolayer, the predicted most stable Pmc2 1 structure is a (quasi) direct-gap semiconductor that possesses a high electron mobility of ∼800 cm 2 V -1 s -1 along the k a direction, which is much higher than that of MoS 2 (∼200 cm 2 V -1 s -1 ). More importantly, the Pmc2 1 GeP 2 monolayer not only can serve as an n-type channel material in field-effect transistors but also can be an effective catalyst for splitting water.

miR-143 Activation Regulates Smooth Muscle and Endothelial Cell Crosstalk in Pulmonary Arterial Hypertension

Science.gov (United States)

Stevens, Hannah; Lu, Ruifang; Caudrillier, Axelle; McBride, Martin; McClure, John D; Grant, Jenny; Thomas, Matthew; Frid, Maria; Stenmark, Kurt; White, Kevin; Seto, Anita G.; Morrell, Nicholas W.; Bradshaw, Angela C; MacLean, Margaret R.; Baker, Andrew H.

2015-01-01

Rationale The pathogenesis of PAH remains unclear. The four microRNAs representing the miR-143 and miR-145 stem loops are genomically clustered. Objective To elucidate the transcriptional regulation of the miR-143/145 cluster, and the role of miR-143 in PAH. Methods and Results We identified the promoter region that regulates miR-143/145 miRNA expression in pulmonary artery smooth muscle cells (PASMCs). We mapped PAH-related signalling pathways, including estrogens receptor (ER), liver X factor/retinoic X receptor (LXR/RXR), TGF-β (Smads), and hypoxia (HRE) that regulated levels of all pri-miR stem loop transcription and resulting miRNA expression. We observed that miR-143-3p is selectively upregulated compared to miR-143-5p during PASMC migration. Modulation of miR-143 in PASMCs significantly altered cell migration and apoptosis. In addition, we found high abundance of miR-143-3p in PASMCs-derived exosomes. Using assays with pulmonary arterial endothelial cells (PAECs) we demonstrated a paracrine pro-migratory and pro-angiogenic effect of miR-143-3p enriched exosomes from PASMC. Quantitative PCR and in situ hybridisation showed elevated expression of miR-143 in calf models of PAH as well as in samples from PAH patients. Moreover, in contrast to our previous findings that had not supported a therapeutic role in vivo, we now demonstrate a protective role for miR-143 in experimental PH in vivo in miR-143−/− and antimiR143-3p-treated mice exposed to chronic hypoxia in both preventative and reversal settings. Conclusions miR-143-3p modulated both cellular and exosome-mediated responses in pulmonary vascular cells, while inhibition of miR-143-3p blocked experimental PH. Taken together these findings confirm an important role for the miR-143/145 cluster in PAH pathobiology. PMID:26311719

Hematopoietic stem cell migration and proliferation after Partial body irradiation

International Nuclear Information System (INIS)

Murata, Takashi; Utsumi, Makoto; Hotta, Tomomitsu; Yamada, Hideo

1983-01-01

Stem cell migration in hematopoietic recovery after partial body irradiation was investigated with special emphasis on the comparative roles of the bone marrow and the spleen. The number of CFU-S in circulation declined rapidly and reached zero within a day after irradiation, thereafter it increased gradually. This finding suggests the presence of two different phases of stem cell migration. One is a rapid migrating phase in which stem cells are released rapidly within a day after irradiation, and the other is a slow migrating phase. The result of split doses of local body irradiation experiments implicated a role for the spleen distinct from that of the bone marrow in the preferential distribution of stem cells early after irradiation. The cell kinetic study showed that the proliferation of CFU-S occurred actively in irradiated bone marrow and the spleens as compared to that in unirradiated control. But on Day 7 and on Day 10 after irradiation, the proliferation of CFU-S in shielded bone marrow did not occur as actively as those in irradiated areas. The results of our present studies suggest that the spleen is not only the storage pools of migrating stem cells but also the main site of active proliferation of CFU-S in the early period of hematopoietic regeneration. (author)

CHCHD10 mutations p.R15L and p.G66V cause motoneuron disease by haploinsufficiency.

Science.gov (United States)

Brockmann, Sarah J; Freischmidt, Axel; Oeckl, Patrick; Müller, Kathrin; Ponna, Srinivas K; Helferich, Anika M; Paone, Christoph; Reinders, Jörg; Kojer, Kerstin; Orth, Michael; Jokela, Manu; Auranen, Mari; Udd, Bjarne; Hermann, Andreas; Danzer, Karin M; Lichtner, Peter; Walther, Paul; Ludolph, Albert C; Andersen, Peter M; Otto, Markus; Kursula, Petri; Just, Steffen; Weishaupt, Jochen H

2018-02-15

Mutations in the mitochondrially located protein CHCHD10 cause motoneuron disease by an unknown mechanism. In this study, we investigate the mutations p.R15L and p.G66V in comparison to wild-type CHCHD10 and the non-pathogenic variant p.P34S in vitro, in patient cells as well as in the vertebrate in vivo model zebrafish. We demonstrate a reduction of CHCHD10 protein levels in p.R15L and p.G66V mutant patient cells to approximately 50%. Quantitative real-time PCR revealed that expression of CHCHD10 p.R15L, but not of CHCHD10 p.G66V, is already abrogated at the mRNA level. Altered secondary structure and rapid protein degradation are observed with regard to the CHCHD10 p.G66V mutant. In contrast, no significant differences in expression, degradation rate or secondary structure of non-pathogenic CHCHD10 p.P34S are detected when compared with wild-type protein. Knockdown of CHCHD10 expression in zebrafish to about 50% causes motoneuron pathology, abnormal myofibrillar structure and motility deficits in vivo. Thus, our data show that the CHCHD10 mutations p.R15L and p.G66V cause motoneuron disease primarily based on haploinsufficiency of CHCHD10. © The Author(s) 2018. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Identification of MPL R102P Mutation in Hereditary Thrombocytosis.

Science.gov (United States)

Bellanné-Chantelot, Christine; Mosca, Matthieu; Marty, Caroline; Favier, Rémi; Vainchenker, William; Plo, Isabelle

2017-01-01

The molecular basis of hereditary thrombocytosis is germline mutations affecting the thrombopoietin (TPO)/TPO receptor (MPL)/JAK2 signaling axis. Here, we report one family presenting two cases with a mild thrombocytosis. By sequencing JAK2 and MPL coding exons, we identified a germline MPL R102P heterozygous mutation in the proband and his daughter. Concomitantly, we detected high TPO levels in the serum of these two patients. The mutation was not found in three other unaffected cases from the family except in another proband's daughter who did not present thrombocytosis but had a high TPO level. The MPL R102P mutation was first described in congenital amegakaryocytic thrombocytopenia in a homozygous state with a loss-of-function activity. It was previously shown that MPL R102P was blocked in the endoplasmic reticulum without being able to translocate to the plasma membrane. Thus, this case report identifies for the first time that MPL R102P mutation can differently impact megakaryopoiesis: thrombocytosis or thrombocytopenia depending on the presence of the heterozygous or homozygous state, respectively. The paradoxical effect associated with heterozygous MPL R102P may be due to subnormal cell-surface expression of wild-type MPL in platelets inducing a defective TPO clearance. As a consequence, increased TPO levels may activate megakaryocyte progenitors that express a lower, but still sufficient level of MPL for the induction of proliferation.

Identification of MPL R102P Mutation in Hereditary Thrombocytosis

Directory of Open Access Journals (Sweden)

Christine Bellanné-Chantelot

2017-09-01

Full Text Available The molecular basis of hereditary thrombocytosis is germline mutations affecting the thrombopoietin (TPO/TPO receptor (MPL/JAK2 signaling axis. Here, we report one family presenting two cases with a mild thrombocytosis. By sequencing JAK2 and MPL coding exons, we identified a germline MPL R102P heterozygous mutation in the proband and his daughter. Concomitantly, we detected high TPO levels in the serum of these two patients. The mutation was not found in three other unaffected cases from the family except in another proband’s daughter who did not present thrombocytosis but had a high TPO level. The MPL R102P mutation was first described in congenital amegakaryocytic thrombocytopenia in a homozygous state with a loss-of-function activity. It was previously shown that MPL R102P was blocked in the endoplasmic reticulum without being able to translocate to the plasma membrane. Thus, this case report identifies for the first time that MPL R102P mutation can differently impact megakaryopoiesis: thrombocytosis or thrombocytopenia depending on the presence of the heterozygous or homozygous state, respectively. The paradoxical effect associated with heterozygous MPL R102P may be due to subnormal cell-surface expression of wild-type MPL in platelets inducing a defective TPO clearance. As a consequence, increased TPO levels may activate megakaryocyte progenitors that express a lower, but still sufficient level of MPL for the induction of proliferation.

Wedge-Splitting Test – Determination of Minimal Starting Notch Length for Various Cement Based Composites

Czech Academy of Sciences Publication Activity Database

Seitl, Stanislav; Klusák, Jan; Veselý, V.; Řoutil, L.

452-453, - (2011), s. 81-84 ISSN 1013-9826 R&D Projects: GA AV ČR KJB200410901; GA ČR GA103/08/0963 Institutional research plan: CEZ:AV0Z20410507 Keywords : wedge-splitting test, cementitious composites, quasi-brittle fracture, brittle fracture Subject RIV: JL - Materials Fatigue, Friction Mechanics www.scientific.net

Postirradiation examination of capsules P13R and P13S

International Nuclear Information System (INIS)

Scott, C.B.; Harmon, D.P.; Holzgraf, J.F.

1976-01-01

Capsules P13R and P13S were the seventh and eighth in a series of irradiation tests conducted under the ERDA-sponsored HTGR Fuels and Core Development Program. Reference type LHTGR fuel fabricated with a broad spectrum of property and process variables was irradiated to extreme temperature and fluence conditions. Postirradiation examination revealed that the bonded fuel rods exhibited good stability after irradiation to fast neutron fluences of 12.4 x 10 21 n/cm 2 (E greater than 0.18 MeV), which is 55 percent beyond the LHTGR peak design fast neutron fluence of 8.0 x 10 21 n/cm 2 . Thermal cycling to high temperatures did not adversely affect fuel rod integrity. Particle batches with coating designs representative of the design requirements envisioned for the LHTGR exhibited excellent irradiation performance. Ten batches of fissile and fertile particles were irradiated without coating failure to fast neutron exposures which exceeded the LHTGR peak design exposure by 35 to 52 percent. Capsules P13R and P13S were considered to be very successful qualification tests of LHTGR fuel components. These results provided a substantial data base for the LHTGR Fuel Product Specification and Performance Models used in HTGR core design studies, and demonstrated the excellent irradiation performance of reference LHTGR fuel to well beyond peak design exposures

Brain-derived neurotrophic factor promotes VEGF-C-dependent lymphangiogenesis by suppressing miR-624-3p in human chondrosarcoma cells.

Science.gov (United States)

Lin, Chih-Yang; Wang, Shih-Wei; Chen, Yen-Ling; Chou, Wen-Yi; Lin, Ting-Yi; Chen, Wei-Cheng; Yang, Chen-Yu; Liu, Shih-Chia; Hsieh, Chia-Chu; Fong, Yi-Chin; Wang, Po-Chuan; Tang, Chih-Hsin

2017-08-03

Chondrosarcoma is the second most common primary malignancy of bone, and one of the most difficult bone tumors to diagnose and treat. It is well known that increased levels of vascular endothelial growth factor-C (VEGF-C) promote active tumor lymphangiogenesis and lymphatic tumor spread to regional lymph nodes. Brain-derived neurotrophic factor (BDNF) is known to promote metastasis in human chondrosarcoma cells. Knowing more about the mechanism of BDNF in VEGF-C expression and lymphangiogenesis in human chondrosarcoma would improve our understanding as how to prevent chondrosarcoma angiogenesis and metastasis, which currently lacks effective adjuvant treatment. Here, we found that BDNF expression was at least 2.5-fold higher in the highly migratory JJ012(S10) cell line as compared with the primordial cell line (JJ012). In addition, VEGF-C expression and secretion was markedly increased in JJ012(S10) cells. Conditioned medium from JJ012(S10) cells significantly promoted migration and tube formation of human lymphatic endothelial cells (LECs), whereas knockdown of BDNF attenuated LEC migration and tube formation by suppressing VEGF-C production in JJ012(S10) cells. Mechanistic investigations indicated that BDNF facilitated VEGF-C-dependent lymphangiogenesis through the MEK/ERK/mTOR signaling pathway. We also showed that microRNA (miR)-624-3p expression was negatively regulated by BDNF via the MEK/ERK/mTOR cascade. Importantly, BDNF knockdown profoundly inhibited tumor-associated lymphangiogenesis in vivo. Further analyses identified that BDNF promoted tumor lymphangiogenesis by downregulating miR-624-3p in human chondrosarcoma tissues. In conclusion, this study is the first to reveal the mechanism underlying BDNF-induced lymphangiogenesis. We suggest that BDNF may serve as a promising therapeutic target for the restriction of VEGF-C-mediated tumor lymphangiogenesis and lymphatic metastasis.

Proton polarimetry using an Enge split-pole spectrograph

Energy Technology Data Exchange (ETDEWEB)

Moss, J M; Brown, D R; Cornelius, W D [Texas Agricultural and Mechanical Univ., College Station (USA). Cyclotron Inst.

1976-05-15

A high-efficiency (4 x 10/sup -5/ at A=0.4) high resolution (150 keV) polarimeter used in conjunction with an Enge split-pole spectrograph is described. This device permits for the first time polarization transfer studies in elastic scattering. Spectra are shown for /sup 11/B(p(pol),p(pol)')/sup 11/B (2.14 MeV)at Esub(p)=31 MeV.

Evaluation of Mandibular Anatomy Associated With Bad Splits in Sagittal Split Ramus Osteotomy of Mandible.

Science.gov (United States)

Wang, Tongyue; Han, Jeong Joon; Oh, Hee-Kyun; Park, Hong-Ju; Jung, Seunggon; Park, Yeong-Joon; Kook, Min-Suk

2016-07-01

This study aimed to identify risk factors associated with bad splits during sagittal split ramus osteotomy by using three-dimensional computed tomography. This study included 8 bad splits and 47 normal patients without bad splits. Mandibular anatomic parameters related to osteotomy line were measured. These included anteroposterior width of the ramus at level of lingula, distance between external oblique ridge and lingula, distance between sigmoid notch and inferior border of mandible, mandibular angle, distance between inferior outer surface of mandibular canal and inferior border of mandible under distal root of second molar (MCEM), buccolingual thickness of the ramus at level of lingula, and buccolingual thickness of the area just distal to first molar (BTM1) and second molar (BTM2). The incidence of bad splits in 625 sagittal split osteotomies was 1.28%. Compared with normal group, bad split group exhibited significantly thinner BTM2 and shorter sigmoid notch and inferior border of mandible (P bad splits. These anatomic data may help surgeons to choose the safest surgical techniques and best osteotomy sites.

S.P.Q.R. + Sicilia RoboCup 2005 Report

OpenAIRE

Iocchi , L; Nardi , D; Cherubini , Andrea; Marchetti , L; Ziparo , V.

2005-01-01

International audience; The Italian Robot Team SPQR+Sicilia is the result of a joint effort of two Italian research groups: S.P.Q.R. (Soccer Player Quadruped Robots, but also Senatus PopolusQue Romanus): the group of the Faculty of Engineering at University of Rome “La Sapienza” in Italy, that is involved in RoboCup competitions since 1998 in different leagues (Middle-size 1998-2002, Four-legged since 2001, Real-rescue-robots since 2003). The members of S.P.Q.R. are: Luca Iocchi (Team Leader)...

Splitting of the weak hypercharge quantum

Science.gov (United States)

Nielsen, H. B.; Brene, N.

1991-08-01

The ratio between the weak hypercharge quantum for particles having no coupling to the gauge bosons corresponding to the semi-simple component of the gauge group and the smallest hypercharge quantum for particles that do have such couplings is exceptionally large for the standard model, considering its rank. To compare groups with respect to this property we propose a quantity χ which depends on the rank of the group and the splitting ratio of the hypercharge(s) to be found in the group. The quantity χ has maximal value for the gauge group of the standard model. This suggests that the hypercharge splitting may play an important rôle either in the origin of the gauge symmetry at a fundamental scale or in some kind of selection mechanism at a scale perhaps nearer to the experimental scale. Such a selection mechanism might be what we have called confusion which removes groups with many (so-called generalized) automorphisms. The quantity χ tends to be large for groups with few generalized automorphisms.

Ancient wild reindeer pitfall trapping systems as indicators for former migration patterns and habitat use in the Dovre region, southern Norway

Directory of Open Access Journals (Sweden)

Per Jordhøy

2008-04-01

Full Text Available The distribution of ancient reindeer pitfall trap systems suggests an extensive regional migration of reindeer between seasonal pastures in parts of southern Norway. The migration routes were funnelled by natural barriers across a high, rolling mountain plateau. In the Dovre area, two pitfall trapping systems, totalling at least 1547 individual pitfalls, were identified and measured using a standard procedure and GPS to record location. Migrating reindeer typically cross over valleys between areas of higher ground and reindeer pitfall trap lines are therefore aligned along the valley, individually placed so that their long axis is perpendicular to the direction of the valleys. Pitfall trap systems for moose are also evident in the landscape. In contrast to reindeer, migrating moose mainly follow the line of the valley. Pitfall rows built for moose trapping are therefore placed mainly across the main direction of the valleys, and the individual pitfalls are also larger than those intended for reindeer. Migration and lichen utilization are important factors in reindeer adaption to limited food resources and existence in marginal mountain habitats. The trap systems and their ecological context support the hypothesis of ancient large-scale reindeer migration over the west-east Dovre axis between summer pastures and winter grazing land. This migration has ceased entirely because of increasing traffic on the north-south railway and highway and probably also because of reduced reindeer populations. Abstract in Norwegian / Sammendrag:Gamle fangstgropsystemer for rein som indikatorer for tidligere trekkmønster og habitatbruk i Dovreregionen, Sør-NorgeUtbredelse av fangstgropsystemer for rein tyder på at det har vært et regionalt trekkmønster mellom ulike sesongbeiter innen deler av Sør-Norge. Trekket har vært styrt av naturlige barrierer over et variert, bølgende fjellandskap. I dovreområdet er to store fangstgropsystemer på totalt minst 1547

The pH-sensing receptor OGR1 improves barrier function of epithelial cells and inhibits migration in an acidic environment.

Science.gov (United States)

de Vallière, Cheryl; Vidal, Solange; Clay, Ieuan; Jurisic, Giorgia; Tcymbarevich, Irina; Lang, Silvia; Ludwig, Marie-Gabrielle; Okoniewski, Michal; Eloranta, Jyrki J; Kullak-Ublick, Gerd A; Wagner, Carsten A; Rogler, Gerhard; Seuwen, Klaus

2015-09-15

The pH-sensing receptor ovarian cancer G protein-coupled receptor 1 (OGR1; GPR68) is expressed in the gut. Inflammatory bowel disease is typically associated with a decrease in local pH, which may lead to altered epithelial barrier function and subsequent gastrointestinal repair involving epithelial cell adhesion and migration. As the mechanisms underlying the response to pH changes are not well understood, we have investigated OGR1-mediated, pH-dependent signaling pathways in intestinal epithelial cells. Caco-2 cells stably overexpressing OGR1 were created and validated as tools to study OGR1 signaling. Barrier function, migration, and proliferation were measured using electric cell-substrate impedance-sensing technology. Localization of the tight junction proteins zonula occludens protein 1 and occludin and the rearrangement of cytoskeletal actin were examined by confocal microscopy. Paracellular permeability and protein and gene expression analysis using DNA microarrays were performed on filter-grown Caco-2 monolayers. We report that an acidic pH shift from pH 7.8 to 6.6 improved barrier function and stimulated reorganization of filamentous actin with prominent basal stress fiber formation. Cell migration and proliferation during in vitro wound healing were inhibited. Gene expression analysis revealed significant upregulation of genes related to cytoskeleton remodeling, cell adhesion, and growth factor signaling. We conclude that acidic extracellular pH can have a signaling function and impact the physiology of intestinal epithelial cells. The deconstruction of OGR1-dependent signaling may aid our understanding of mucosal inflammation mechanisms. Copyright © 2015 the American Physiological Society.

A calculation of the three-loop helicity-dependent splitting functions in QCD

International Nuclear Information System (INIS)

Vogt, A.

2014-05-01

We have calculated the complete matrix of three-loop helicity-difference ('polarized') splitting functions ΔP ik (2) (x), i,k=q,g, in massless perturbative QCD. In this note we briefly discuss some properties of the polarized splitting functions and our non-standard determination of the hitherto missing lower-row quantities ΔP gq (2) and ΔP gg (2) . The resulting next-to-next-to-leading order (NNLO) corrections to the evolution of polarized parton distributions are illustrated and found to be small even at rather large values of the strong coupling constant α s .

MIGRATION OF SMALL MOONS IN SATURN's RINGS

Energy Technology Data Exchange (ETDEWEB)

Bromley, Benjamin C. [Department of Physics and Astronomy, University of Utah, 115 S 1400 E, Rm 201, Salt Lake City, UT 84112 (United States); Kenyon, Scott J., E-mail: bromley@physics.utah.edu, E-mail: skenyon@cfa.harvard.edu [Smithsonian Astrophysical Observatory, 60 Garden Street, Cambridge, MA 02138 (United States)

2013-02-20

The motions of small moons through Saturn's rings provide excellent tests of radial migration models. In theory, torque exchange between these moons and ring particles leads to radial drift. We predict that moons with Hill radii r {sub H} {approx} 2-24 km should migrate through the A ring in 1000 yr. In this size range, moons orbiting in an empty gap or in a full ring eventually migrate at the same rate. Smaller moons or moonlets-such as the propellers-are trapped by diffusion of disk material into corotating orbits, creating inertial drag. Larger moons-such as Pan or Atlas-do not migrate because of their own inertia. Fast migration of 2-24 km moons should eliminate intermediate-size bodies from the A ring and may be responsible for the observed large-radius cutoff of r {sub H} {approx} 1-2 km in the size distribution of the A ring's propeller moonlets. Although the presence of Daphnis (r {sub H} Almost-Equal-To 5 km) inside the Keeler gap challenges this scenario, numerical simulations demonstrate that orbital resonances and stirring by distant, larger moons (e.g., Mimas) may be important factors. For Daphnis, stirring by distant moons seems the most promising mechanism to halt fast migration. Alternatively, Daphnis may be a recent addition to the ring that is settling into a low inclination orbit in {approx}10{sup 3} yr prior to a phase of rapid migration. We provide predictions of observational constraints required to discriminate among possible scenarios for Daphnis.

Clinical significance of miR-140-5p and miR-193b expression in patients with breast cancer and relationship to IGFBP5

Directory of Open Access Journals (Sweden)

Gökçe Güllü

2015-03-01

Full Text Available The functional role of IGFBP5 in breast cancer is complicated. Experimental and bioinformatics studies have shown that IGFBP5 is targeted by miR-140-5p and miR-193b, although this has not yet been proven in clinical samples. The aim of this study was to evaluate the expression of miR-140-5p and miR-193b in breast cancer and adjacent normal tissue and assess its correlation with IGFBP5 and the clinicopathological characteristics of the tumors. IGFBP5 protein expression was analyzed immunohistochemically and IGFBP5, miR-140 and miR-193b mRNA expression levels were analyzed with real-time RT-PCR. Tumor tissue had higher miR-140-5p expression than adjacent normal tissue (p = 0.015. Samples with no immunohistochemical staining for IGFBP5 showed increased miR-140-5p expression (p = 0.009. miR-140-5p expression was elevated in invasive ductal carcinomas (p = 0.002, whereas basal-like tumors had decreased expression of miR-140-5p compared to other tumors (p = 0.008. Lymph node-positive samples showed an approximately 13-fold increase in miR-140-5p expression compared to lymph node-negative tissue (p = 0.049. These findings suggest that miR-140-5p, but not miR-193b, could be an important determinant of IGFBP5 expression and clinical phenotype in breast cancer patients. Further studies are needed to clarify the expressional regulation of IGFBP5 by miR-140-5p.

MiR-9 is overexpressed in spontaneous canine osteosarcoma and promotes a metastatic phenotype including invasion and migration in osteoblasts and osteosarcoma cell lines

International Nuclear Information System (INIS)

Fenger, Joelle M.; Roberts, Ryan D.; Iwenofu, O. Hans; Bear, Misty D.; Zhang, Xiaoli; Couto, Jason I.; Modiano, Jaime F.; Kisseberth, William C.; London, Cheryl A.

2016-01-01

MicroRNAs (miRNAs) regulate the expression of networks of genes and their dysregulation is well documented in human malignancies; however, limited information exists regarding the impact of miRNAs on the development and progression of osteosarcoma (OS). Canine OS exhibits clinical and molecular features that closely resemble the corresponding human disease and it is considered a well-established spontaneous animal model to study OS biology. The purpose of this study was to investigate miRNA dysregulation in canine OS. We evaluated miRNA expression in primary canine OS tumors and normal canine osteoblast cells using the nanoString nCounter system. Quantitative PCR was used to validate the nanoString findings and to assess miR-9 expression in canine OS tumors, OS cell lines, and normal osteoblasts. Canine osteoblasts and OS cell lines were stably transduced with pre-miR-9 or anti-miR-9 lentiviral constructs to determine the consequences of miR-9 on cell proliferation, apoptosis, invasion and migration. Proteomic and gene expression profiling of normal canine osteoblasts with enforced miR-9 expression was performed using 2D-DIGE/tandem mass spectrometry and RNA sequencing and changes in protein and mRNA expression were validated with Western blotting and quantitative PCR. OS cell lines were transduced with gelsolin (GSN) shRNAs to investigate the impact of GSN knockdown on OS cell invasion. We identified a unique miRNA signature associated with primary canine OS and identified miR-9 as being significantly overexpressed in canine OS tumors and cell lines compared to normal osteoblasts. Additionally, high miR-9 expression was demonstrated in tumor-specific tissue obtained from primary OS tumors. In normal osteoblasts and OS cell lines transduced with miR-9 lentivirus, enhanced invasion and migration were observed, but miR-9 did not affect cell proliferation or apoptosis. Proteomic and transcriptional profiling of normal canine osteoblasts overexpressing miR-9 identified

Gold split-ring resonators (SRRs) as substrates for surface-enhanced raman scattering

KAUST Repository

Yue, Weisheng

2013-10-24

We used gold split ring resonators (SRRs) as substrates for surface-enhanced Raman scattering (SERS). The arrays of SRRs were fabricated by electron-beam lithography in combination with plasma etching. In the detection of rhodamine 6G (R6G) molecules, SERS enhancement factors of the order of 105 was achieved. This SERS enhancement increased as the size of the split gap decrease as a consequence of the matching between the resonance wavelength of the SRRs and the excitation wavelength of SERS. As the size of the split gap decreased, the localized surface plasmon resonance shifted to near the excitation wavelength and, thus, resulted in the increase in the electric field on the nanostructures. We used finite integration method (FIT) to simulate numerically the electromagnetic properties of the SRRs. The results of the simulation agreed well with our experimental observations. We anticipate this work will provide an approach to manipulate the SERS enhancement by modulating the size of split gap with SRRs without affecting the area and structural arrangement. © 2013 American Chemical Society.

Gold split-ring resonators (SRRs) as substrates for surface-enhanced raman scattering

KAUST Repository

Yue, Weisheng; Yang, Yang; Wang, Zhihong; Chen, Longqing; Wang, Xianbin

2013-01-01

We used gold split ring resonators (SRRs) as substrates for surface-enhanced Raman scattering (SERS). The arrays of SRRs were fabricated by electron-beam lithography in combination with plasma etching. In the detection of rhodamine 6G (R6G) molecules, SERS enhancement factors of the order of 105 was achieved. This SERS enhancement increased as the size of the split gap decrease as a consequence of the matching between the resonance wavelength of the SRRs and the excitation wavelength of SERS. As the size of the split gap decreased, the localized surface plasmon resonance shifted to near the excitation wavelength and, thus, resulted in the increase in the electric field on the nanostructures. We used finite integration method (FIT) to simulate numerically the electromagnetic properties of the SRRs. The results of the simulation agreed well with our experimental observations. We anticipate this work will provide an approach to manipulate the SERS enhancement by modulating the size of split gap with SRRs without affecting the area and structural arrangement. © 2013 American Chemical Society.

Differential Expression of MiR-106b-5p and MiR-200c-3p in Newly Diagnosed Versus Chronic Primary Immune Thrombocytopenia Patients Based on Systematic Analysis

Directory of Open Access Journals (Sweden)

Cheng Qian

2018-01-01

Full Text Available Background/Aims: MicroRNAs (miRNAs have been described to have important roles in primary immune thrombocytopenia (ITP. To gain additional understanding, we have now further evaluated the involvement of miRNAs in ITP. Methods: Microarray experiments were performed to examine the expression profiles of miRNAs and mRNAs in samples from subjects with newly diagnosed ITP (G1, chronic ITP (G2, and normal controls. The systematic Pipeline of Outlier MicroRNA Analysis framework was applied to identify key miRNAs expressed in the G1 and G2 samples. Quantitative PCR and receiver operator characteristic curves were used to confirm the performance of key miRNAs. Results: Compared with normal controls, 14 miRNAs (12 over-expressed and 2 under-expressed and 7 over-expressed miRNAs were identified as key in G1 and G2 samples, respectively. miR-106b-5p, miR-200c-3p, and miR-92a-3p exhibited significantly different expression profiles among the groups. In particular, miR-106b-5p and miR-200c-3p were expressed at higher levels in patients with ITP compared to the normal controls. Furthermore, these two miRNAs expressions were even higher in patients with chronic ITP. Conclusion: MiR-106b-5p and miR-200c-3p may represent valuable biomarkers of ITP, although further studies are needed to confirm and assess the value of these potential biomarkers at various stages of ITP.

The Split-Brain Phenomenon Revisited: A Single Conscious Agent with Split Perception.

Science.gov (United States)

Pinto, Yair; de Haan, Edward H F; Lamme, Victor A F

2017-11-01

The split-brain phenomenon is caused by the surgical severing of the corpus callosum, the main route of communication between the cerebral hemispheres. The classical view of this syndrome asserts that conscious unity is abolished. The left hemisphere consciously experiences and functions independently of the right hemisphere. This view is a cornerstone of current consciousness research. In this review, we first discuss the evidence for the classical view. We then propose an alternative, the 'conscious unity, split perception' model. This model asserts that a split brain produces one conscious agent who experiences two parallel, unintegrated streams of information. In addition to changing our view of the split-brain phenomenon, this new model also poses a serious challenge for current dominant theories of consciousness. Copyright © 2017 Elsevier Ltd. All rights reserved.

Hexachlorobenzene modulates the crosstalk between the aryl hydrocarbon receptor and transforming growth factor-β1 signaling, enhancing human breast cancer cell migration and invasion

International Nuclear Information System (INIS)

Miret, Noelia; Pontillo, Carolina; Ventura, Clara; Carozzo, Alejandro; Chiappini, Florencia

2016-01-01

Highlights: • HCB enhances TGF-β1 expression and activation levels in breast cancer cells. • HCB activates TGF-β1 pathways: Smad3, JNK and p38. • The HCB- induced migration and invasion involves TGF-β1 signaling pathways. • HCB modulates AhR levels and activation. • HCB enhances TGF-β1 mRNA expression in an AhR-dependent manner. - Abstract: Given the number of women affected by breast cancer, considerable interest has been raised in understanding the relationships between environmental chemicals and disease onset. Hexachlorobenzene (HCB) is a dioxin-like compound that is widely distributed in the environment and is a weak ligand of the aryl hydrocarbon receptor (AhR). We previously demonstrated that HCB acts as an endocrine disruptor capable of stimulating cell proliferation, migration, invasion, and metastasis in different breast cancer models. In addition, increasing evidence indicates that transforming growth factor-β1 (TGF-β1) can contribute to tumor maintenance and progression. In this context, this work investigated the effect of HCB (0.005, 0.05, 0.5, and 5 μM) on TGF-β1 signaling and AhR/TGF-β1 crosstalk in the human breast cancer cell line MDA-MB-231 and analyzed whether TGF-β1 pathways are involved in HCB-induced cell migration and invasion. RT-qPCR results indicated that HCB reduces AhR mRNA expression through TGF-β1 signaling but enhances TGF-β1 mRNA levels involving AhR signaling. Western blot analysis demonstrated that HCB could increase TGF-β1 protein levels and activation, as well as Smad3, JNK, and p38 phosphorylation. In addition, low and high doses of HCB were determined to exert differential effects on AhR protein levels, localization, and activation, with a high dose (5 μM) inducing AhR nuclear translocation and AhR-dependent CYP1A1 expression. These findings also revealed that c-Src and AhR are involved in HCB-mediated activation of Smad3. HCB enhances cell migration (scratch motility assay) and invasion (Transwell

Migration behavior of landfill leachate contaminants through alternative composite liners

Energy Technology Data Exchange (ETDEWEB)

Varank, Gamze, E-mail: gvarank@yildiz.edu.tr; Demir, Ahmet, E-mail: ahmetd@yildiz.edu.tr; Top, Selin, E-mail: stop@yildiz.edu.tr; Sekman, Elif, E-mail: esekman@yildiz.edu.tr; Akkaya, Ebru, E-mail: ekoca@yildiz.edu.tr; Yetilmezsoy, Kaan, E-mail: yetilmez@yildiz.edu.tr; Bilgili, M. Sinan, E-mail: mbilgili@yildiz.edu.tr

2011-08-01

Four identical pilot-scale landfill reactors with different alternative composite liners were simultaneously operated for a period of about 540 days to investigate and to simulate the migration behaviors of phenolic compounds (phenol, 2-CP, 2-MP, 3-MP, 4-MP, 2-NP, 4-NP, 2,4-DNP, 2,4-DCP, 2,6-DCP, 2,4,5-TCP, 2,4,6-TCP, 2,3,4,6-TeCP, PCP) and heavy metals (Pb, Cu, Zn, Cr, Cd, Ni) from landfill leachate to the groundwater. Alternative landfill liners of four reactors consist of R1: Compacted clay liner (10 cm + 10 cm, k = 10{sup -8} m/sn), R2: Geomembrane (2 mm HDPE) + compacted clay liner (10 cm + 10 cm, k = 10{sup -8} m/sn), R3: Geomembrane (2 mm HDPE) + compacted clay liner (10 cm, k = 10{sup -8} m/sn) + bentonite liner (2 cm) + compacted clay liner (10 cm, k = 10{sup -8} m/sn), and R4: Geomembrane (2 mm HDPE) + compacted clay liner (10 cm, k = 10{sup -8} m/sn) + zeolite liner (2 cm) + compacted clay liner (10 cm, k = 10{sup -8} m/sn). Wastes representing Istanbul municipal solid wastes were disposed in the reactors. To represent bioreactor landfills, reactors were operated by leachate recirculation. To monitor and control anaerobic degradation in the reactors, variations of conventional parameters (pH, alkalinity, chloride, conductivity, COD, TOC, TKN, ammonia and alcaly metals) were also investigated in landfill leachate samples. The results of this study showed that about 35-50% of migration of organic contaminants (phenolic compounds) and 55-100% of migration of inorganic contaminants (heavy metals) to the model groundwater could be effectively reduced with the use of bentonite and zeolite materials in landfill liner systems. Although leachate contaminants can reach to the groundwater in trace concentrations, findings of this study concluded that the release of these compounds from landfill leachate to the groundwater may potentially be of an important environmental concern based on the experimental findings. - Research highlights: {yields} Migration of

Air bubble migration is a random event post embryo transfer.

Science.gov (United States)

Confino, E; Zhang, J; Risquez, F

2007-06-01

Air bubble location following embryo transfer (ET) is the presumable placement spot of embryos. The purpose of this study was to document endometrial air bubble position and migration following embryo transfer. Multicenter prospective case study. Eighty-eight embryo transfers were performed under abdominal ultrasound guidance in two countries by two authors. A single or double air bubble was loaded with the embryos using a soft, coaxial, end opened catheters. The embryos were slowly injected 10-20 mm from the fundus. Air bubble position was recorded immediately, 30 minutes later and when the patient stood up. Bubble marker location analysis revealed a random distribution without visible gravity effect when the patients stood up. The bubble markers demonstrated splitting, moving in all directions and dispersion. Air bubbles move and split frequently post ET with the patient in the horizontal position, suggestive of active uterine contractions. Bubble migration analysis supports a rather random movement of the bubbles and possibly the embryos. Standing up changed somewhat bubble configuration and distribution in the uterine cavity. Gravity related bubble motion was uncommon, suggesting that horizontal rest post ET may not be necessary. This report challenges the common belief that a very accurate ultrasound guided embryo placement is mandatory. The very random bubble movement observed in this two-center study suggests that a large "window" of embryo placement maybe present.

Triadic split-merge sampler

Science.gov (United States)

van Rossum, Anne C.; Lin, Hai Xiang; Dubbeldam, Johan; van der Herik, H. Jaap

2018-04-01

In machine vision typical heuristic methods to extract parameterized objects out of raw data points are the Hough transform and RANSAC. Bayesian models carry the promise to optimally extract such parameterized objects given a correct definition of the model and the type of noise at hand. A category of solvers for Bayesian models are Markov chain Monte Carlo methods. Naive implementations of MCMC methods suffer from slow convergence in machine vision due to the complexity of the parameter space. Towards this blocked Gibbs and split-merge samplers have been developed that assign multiple data points to clusters at once. In this paper we introduce a new split-merge sampler, the triadic split-merge sampler, that perform steps between two and three randomly chosen clusters. This has two advantages. First, it reduces the asymmetry between the split and merge steps. Second, it is able to propose a new cluster that is composed out of data points from two different clusters. Both advantages speed up convergence which we demonstrate on a line extraction problem. We show that the triadic split-merge sampler outperforms the conventional split-merge sampler. Although this new MCMC sampler is demonstrated in this machine vision context, its application extend to the very general domain of statistical inference.

MiR-18a regulates the proliferation, migration and invasion of human glioblastoma cell by targeting neogenin

International Nuclear Information System (INIS)

Song, Yichen; Wang, Ping; Zhao, Wei; Yao, Yilong; Liu, Xiaobai; Ma, Jun; Xue, Yixue; Liu, Yunhui

2014-01-01

MiR-17-92 cluster has recently been reported as an oncogene in some tumors. However, the association of miR-18a, an important member of this cluster, with glioblastoma remains unknown. Therefore, this study aims to investigate the expression of miR-18a in glioblastoma and its role in biological behavior of U87 and U251 human glioblastoma cell lines. Quantitative RT-PCR results showed that miR-18a was highly expressed in glioblastoma tissues and U87 and U251 cell lines compared with that in human brain tissues and primary normal human astrocytes, and the expression levels were increased along with the rising pathological grades of glioblastoma. Neogenin was identified as the target gene of miR-18a by dual-luciferase reporter assays. RT-PCR and western blot results showed that its expression levels were decreased along with the rising pathological grades of glioblastoma. Inhibition of miR-18a expression was established by transfecting exogenous miR-18a inhibitor into U87 and U251 cells, and its effects on the biological behavior of glioblastoma cells were studied using CCK-8 assay, transwell assay and flow cytometry. Inhibition of miR-18a expression in U87 and U251 cells significantly up-regulated neogenin, and dramatically suppressed the abilities of cell proliferation, migration and invasion, induced cell cycle arrest and promoted cellular apoptosis. Collectively, these results suggest that miR-18a may regulate biological behavior of human glioblastoma cells by targeting neogenin, and miR-18a can serve as a potential target in the treatment of glioblastoma. - Highlights: • MiR-18a was highly expressed in glioblastoma tissues and U87 and U251 cell lines. • Neogenin was identified as the target gene of miR-18a. • Neogenin expressions were decreased along with the rising pathological grades of glioblastoma. • Inhibition of miR-18a suppressed biological behavior of glioma cells by up-regulating neogenin

MiR-18a regulates the proliferation, migration and invasion of human glioblastoma cell by targeting neogenin

Energy Technology Data Exchange (ETDEWEB)

Song, Yichen, E-mail: jeff200064017@163.com [Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004 (China); Wang, Ping, E-mail: pingwang8000@163.com [Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001 (China); Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001 (China); Zhao, Wei, E-mail: 15669746@qq.com [Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001 (China); Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001 (China); Yao, Yilong, E-mail: yaoyilong_322@163.com [Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004 (China); Liu, Xiaobai, E-mail: paganizonda1991@qq.com [The 96th Class, 7-year Program, China Medical University, Shenyang, Liaoning Province 110001 (China); Ma, Jun, E-mail: majun_724@163.com [Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001 (China); Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001 (China); Xue, Yixue, E-mail: xueyixue888@163.com [Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001 (China); Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001 (China); Liu, Yunhui, E-mail: liuyh@sj-hospital.org [Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004 (China)

2014-05-15

MiR-17-92 cluster has recently been reported as an oncogene in some tumors. However, the association of miR-18a, an important member of this cluster, with glioblastoma remains unknown. Therefore, this study aims to investigate the expression of miR-18a in glioblastoma and its role in biological behavior of U87 and U251 human glioblastoma cell lines. Quantitative RT-PCR results showed that miR-18a was highly expressed in glioblastoma tissues and U87 and U251 cell lines compared with that in human brain tissues and primary normal human astrocytes, and the expression levels were increased along with the rising pathological grades of glioblastoma. Neogenin was identified as the target gene of miR-18a by dual-luciferase reporter assays. RT-PCR and western blot results showed that its expression levels were decreased along with the rising pathological grades of glioblastoma. Inhibition of miR-18a expression was established by transfecting exogenous miR-18a inhibitor into U87 and U251 cells, and its effects on the biological behavior of glioblastoma cells were studied using CCK-8 assay, transwell assay and flow cytometry. Inhibition of miR-18a expression in U87 and U251 cells significantly up-regulated neogenin, and dramatically suppressed the abilities of cell proliferation, migration and invasion, induced cell cycle arrest and promoted cellular apoptosis. Collectively, these results suggest that miR-18a may regulate biological behavior of human glioblastoma cells by targeting neogenin, and miR-18a can serve as a potential target in the treatment of glioblastoma. - Highlights: • MiR-18a was highly expressed in glioblastoma tissues and U87 and U251 cell lines. • Neogenin was identified as the target gene of miR-18a. • Neogenin expressions were decreased along with the rising pathological grades of glioblastoma. • Inhibition of miR-18a suppressed biological behavior of glioma cells by up-regulating neogenin.

Tumor-suppressive function of miR-139-5p in esophageal squamous cell carcinoma.

Directory of Open Access Journals (Sweden)

Ran Liu

Full Text Available Recent studies have demonstrated the possible function of miR-139-5p in tumorigenesis. However, the exact mechanism of miR-139-5p in cancer remains unclear. In this study, the association of miR-139-5p expression with esophageal squamous cell carcinoma (ESCC was evaluated in 106 pairs of esophageal cancer and adjacent non-cancerous tissue from ESCC patients. The tumor suppressive features of miR-139-5p were measured by evaluating cell proliferation and cell cycle state, migratory activity and invasion capability, as well as apoptosis. Luciferase reporter assay and Western blot analysis were performed to determine the target gene regulated by miR-139-5p. The mRNA level of NR5A2, the target gene of miR-139-5p, was determined in ESCC patients. Results showed that reduced miR-139-5p level was associated with lymph node metastases of ESCC. MiR-139-5p was investigated to induce cell cycle arrest in the G0/G1 phase and to suppress the invasive capability of esophageal carcinoma cells by targeting the 3'UTR of oncogenic NR5A2. Cyclin E1 and MMP9 were confirmed to participate in cell cycle arrest and invasive suppression induced by NR5A2, respectively. Pearson correlation analysis further confirmed the significantly negative correlation between miR-139-5p and NR5A2 expression. The results suggest that miR-139-5p exerts a growth- and invasiveness-suppressing function in human ESCCs, which demonstrates that miR-139-5p is a potential biomarker for early diagnosis and prognosis and is a therapeutic target for ESCC.