Institution
Virginia Commonwealth University
Education•Richmond, Virginia, United States•
About: Virginia Commonwealth University is a education organization based out in Richmond, Virginia, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 23822 authors who have published 49587 publications receiving 1787046 citations. The organization is also known as: VCU.
Topics: Population, Poison control, Health care, Anxiety, Mental health
Papers published on a yearly basis
Papers
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TL;DR: The results show that the pore size of a scaffold is a more critical regulator of the BMMΦ polarization compared to the fiber diameter, and shows a potential role for MyD88 in regulating M1 B MMΦ signaling on the large vs. small fiber/pore size PDO scaffold.
346 citations
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TL;DR: In this paper, the authors investigate whether current economic activities in Korea can explain stock market returns by using a cointegration test and a Granger causality test from a vector error correction model.
346 citations
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TL;DR: A genome-wide association scan for schizophrenia in an Ashkenazi Jewish population using DNA pooling found a female-specific association with rs7341475, a SNP in the fourth intron of the reelin (RELN) gene, with a significant gene-sex effect.
Abstract: Schizophrenia is a complex mental disease, which includes symptoms of delusions, hallucinations, disorganized speech, aberrant behavior, lack of emotional expression, diminished motivation, and social withdrawal. The cause of schizophrenia is unknown, but there is extensive evidence that genetics play a significant role in its aetiology. We studied the genetic basis of schizophrenia by analyzing around 500,000 genetic variants distributed across the whole human genome in DNA from schizophrenic patients and controls. We analyzed separately the DNA from men and women, and identified a genetic variant that increases the risk of developing schizophrenia in women only. The genetic variant is estimated to increase the risk of schizophrenia for women carrying the risk variant by 1.4-fold. The genetic variant is in a gene called reelin, which is known to play a part in brain development. However, it is still unclear how this genetic variant predisposes to schizophrenia nor why it is specific to women only.
345 citations
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TL;DR: KU-60019 inhibits the DNA damage response, reduces AKT phosphorylation and prosurvival signaling, inhibits migration and invasion, and effectively radiosensitizes human glioma cells.
Abstract: Ataxia telangiectasia (A-T) mutated (ATM) is critical for cell cycle checkpoints and DNA repair. Thus, specific small molecule inhibitors targeting ATM could perhaps be developed into efficient radiosensitizers. Recently, a specific inhibitor of the ATM kinase, KU-55933, was shown to radiosensitize human cancer cells. Herein, we report on an improved analogue of KU-55933 (KU-60019) with K i and IC 50 values half of those of KU-55933. KU-60019 is 10-fold more effective than KU-55933 at blocking radiation-induced phosphorylation of key ATM targets in human glioma cells. As expected, KU-60019 is a highly effective radiosensitizer of human glioma cells. A-T fibroblasts were not radiosensitized by KU-60019, strongly suggesting that the ATM kinase is specifically targeted. Furthermore, KU-60019 reduced basal S473 AKT phosphorylation, suggesting that the ATM kinase might regulate a protein phosphatase acting on AKT. In line with this finding, the effect of KU-60019 on AKT phosphorylation was countered by low levels of okadaic acid, a phosphatase inhibitor, and A-T cells were impaired in S473 AKT phosphorylation in response to radiation and insulin and unresponsive to KU-60019. We also show that KU-60019 inhibits glioma cell migration and invasion in vitro , suggesting that glioma growth and motility might be controlled by ATM via AKT. Inhibitors of MEK and AKT did not further radiosensitize cells treated with KU-60019, supporting the idea that KU-60019 interferes with prosurvival signaling separate from its radiosensitizing properties. Altogether, KU-60019 inhibits the DNA damage response, reduces AKT phosphorylation and prosurvival signaling, inhibits migration and invasion, and effectively radiosensitizes human glioma cells. [Mol Cancer Ther 2009;8(10):2894–902]
345 citations
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TL;DR: A diet-induced animal model of non-alcoholic fatty liver disease (DIAMOND) that recapitulates the key physiological, metabolic, histologic, transcriptomic and cell-signaling changes seen in humans with progressive NASH is described.
345 citations
Authors
Showing all 24085 results
Name | H-index | Papers | Citations |
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Ronald C. Kessler | 274 | 1332 | 328983 |
Carlo M. Croce | 198 | 1135 | 189007 |
Nicholas G. Martin | 192 | 1770 | 161952 |
Michael Rutter | 188 | 676 | 151592 |
Kenneth S. Kendler | 177 | 1327 | 142251 |
Bernhard O. Palsson | 147 | 831 | 85051 |
Thomas J. Smith | 140 | 1775 | 113919 |
Ming T. Tsuang | 140 | 885 | 73865 |
Patrick F. Sullivan | 133 | 594 | 92298 |
Martin B. Keller | 131 | 541 | 65069 |
Michael E. Thase | 131 | 923 | 75995 |
Benjamin F. Cravatt | 131 | 666 | 61932 |
Jian Zhou | 128 | 3007 | 91402 |
Rena R. Wing | 128 | 649 | 67360 |
Linda R. Watkins | 127 | 519 | 56454 |