Institution
Medical University of South Carolina
Education•Charleston, South Carolina, United States•
About: Medical University of South Carolina is a education organization based out in Charleston, South Carolina, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 23436 authors who have published 45440 publications receiving 1769397 citations. The organization is also known as: MUSC & Medical College of the State of South Carolina.
Topics: Population, Poison control, Medicine, Cancer, Stroke
Papers published on a yearly basis
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TL;DR: These results constitute the initial demonstration at the cellular level that adrenergic stimulation leads to cyclic AMP-mediated calcium overload of the cell, with a resultant decrease in synthetic activity and/or viability.
Abstract: BACKGROUNDTo delineate the mechanism(s) of catecholamine-mediated cardiac toxicity, we exposed cultures of adult cardiac muscle cells, or cardiocytes, to a broad range of norepinephrine concentrations.METHODS AND RESULTSNorepinephrine stimulation resulted in a concentration-dependent decrease in cardiocyte viability, as demonstrated by a significant decrease in viable rod-shaped cells and a significant release of creatine kinase from cells in norepinephrine-treated cultures. Norepinephrine-mediated cell toxicity was attenuated significantly by beta-adrenoceptor blockade and mimicked by selective stimulation of the beta-adrenoceptor, whereas the effects mediated by the alpha-adrenoceptor were relatively less apparent. When norepinephrine stimulation was examined in terms of cardiocyte anabolic activity, there was a concentration-dependent decrease in the incorporation of [3H]phenylalanine and [3H]uridine into cytoplasmic protein and nuclear RNA, respectively. The decrease in cytoplasmic labeling was largel...
858 citations
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TL;DR: The results demonstrate the importance of HA in mammalian embryogenesis and the pivotal role of Has2 during mammalian development and reveal a previously unrecognized pathway for cell migration and invasion that is HA-dependent and involves Ras activation.
Abstract: We identified hyaluronan synthase-2 (Has2) as a likely source of hyaluronan (HA) during embryonic development, and we used gene targeting to study its function in vivo. Has2(-/-) embryos lack HA, exhibit severe cardiac and vascular abnormalities, and die during midgestation (E9.5-10). Heart explants from Has2(-/-) embryos lack the characteristic transformation of cardiac endothelial cells into mesenchyme, an essential developmental event that depends on receptor-mediated intracellular signaling. This defect is reproduced by expression of a dominant-negative Ras in wild-type heart explants, and is reversed in Has2(-/-) explants by gene rescue, by administering exogenous HA, or by expressing activated Ras. Conversely, transformation in Has2(-/-) explants mediated by exogenous HA is inhibited by dominant-negative Ras. Collectively, our results demonstrate the importance of HA in mammalian embryogenesis and the pivotal role of Has2 during mammalian development. They also reveal a previously unrecognized pathway for cell migration and invasion that is HA-dependent and involves Ras activation.
856 citations
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University of Miami1, University of Duisburg-Essen2, McMaster University3, Boehringer Ingelheim4, Medical University of South Carolina5, Stanford University6, University of Nottingham7, National University of Singapore8, University of Coimbra9, University of Gothenburg10, University of Melbourne11, University of Illinois at Chicago12, University of Helsinki13, Fudan University14, University of British Columbia15, Sapienza University of Rome16, State University of New York System17, Seoul National University18
TL;DR: The trial did not meet the predefined criteria for noninferiority but showed similar rates of recurrent stroke with ASA-ERDP and with clopidogrel, and there is no evidence that either of the two treatments was superior to the other in the prevention of recurrent strokes.
Abstract: BACKGROUND: Recurrent stroke is a frequent, disabling event after ischemic stroke. This study compared the efficacy and safety of two antiplatelet regimens--aspirin plus extended-release dipyridamole (ASA-ERDP) versus clopidogrel. METHODS: In this double-blind, 2-by-2 factorial trial, we randomly assigned patients to receive 25 mg of aspirin plus 200 mg of extended-release dipyridamole twice daily or to receive 75 mg of clopidogrel daily. The primary outcome was first recurrence of stroke. The secondary outcome was a composite of stroke, myocardial infarction, or death from vascular causes. Sequential statistical testing of noninferiority (margin of 1.075), followed by superiority testing, was planned. RESULTS: A total of 20,332 patients were followed for a mean of 2.5 years. Recurrent stroke occurred in 916 patients (9.0%) receiving ASA-ERDP and in 898 patients (8.8%) receiving clopidogrel (hazard ratio, 1.01; 95% confidence interval [CI], 0.92 to 1.11). The secondary outcome occurred in 1333 patients (13.1%) in each group (hazard ratio for ASA-ERDP, 0.99; 95% CI, 0.92 to 1.07). There were more major hemorrhagic events among ASA-ERDP recipients (419 [4.1%]) than among clopidogrel recipients (365 [3.6%]) (hazard ratio, 1.15; 95% CI, 1.00 to 1.32), including intracranial hemorrhage (hazard ratio, 1.42; 95% CI, 1.11 to 1.83). The net risk of recurrent stroke or major hemorrhagic event was similar in the two groups (1194 ASA-ERDP recipients [11.7%], vs. 1156 clopidogrel recipients [11.4%]; hazard ratio, 1.03; 95% CI, 0.95 to 1.11). CONCLUSIONS: The trial did not meet the predefined criteria for noninferiority but showed similar rates of recurrent stroke with ASA-ERDP and with clopidogrel. There is no evidence that either of the two treatments was superior to the other in the prevention of recurrent stroke. (ClinicalTrials.gov number, NCT00153062.)
853 citations
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TL;DR: During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.
852 citations
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University of Cincinnati1, National Institutes of Health2, University of Toronto3, Medical University of South Carolina4, Niigata University5, Oregon Health & Science University6, Cleveland Clinic7, University of Florida8, University of Texas Health Science Center at Tyler9, University of Colorado Denver10, University of California, Los Angeles11, Harvard University12, Cincinnati Children's Hospital Medical Center13, Mayo Clinic14, University of South Florida15
TL;DR: In patients with LAM, sirolimus stabilized lung function, reduced serum VEGF-D levels, and was associated with a reduction in symptoms and improvement in quality of life.
Abstract: Background Lymphangioleiomyomatosis (LAM) is a progressive, cystic lung disease in women; it is associated with inappropriate activation of mammalian target of rapamycin (mTOR) signaling, which regulates cellular growth and lymphangiogenesis. Sirolimus (also called rapamycin) inhibits mTOR and has shown promise in phase 1–2 trials involving patients with LAM. Methods We conducted a two-stage trial of sirolimus involving 89 patients with LAM who had moderate lung impairment — a 12-month randomized, double-blind comparison of sirolimus with placebo, followed by a 12-month observation period. The primary end point was the difference between the groups in the rate of change (slope) in forced expiratory volume in 1 second (FEV1). Results During the treatment period, the FEV1 slope was −12±2 ml per month in the placebo group (43 patients) and 1±2 ml per month in the sirolimus group (46 patients) (P<0.001). The absolute between-group difference in the mean change in FEV1 during the treatment period was 153 ml, o...
851 citations
Authors
Showing all 23601 results
Name | H-index | Papers | Citations |
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Edward Giovannucci | 206 | 1671 | 179875 |
Ronald Klein | 194 | 1305 | 149140 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Yusuke Nakamura | 179 | 2076 | 160313 |
John J.V. McMurray | 178 | 1389 | 184502 |
Nora D. Volkow | 165 | 958 | 107463 |
L. Joseph Melton | 161 | 531 | 97861 |
Gregg C. Fonarow | 161 | 1676 | 126516 |
Michael Boehnke | 152 | 511 | 136681 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Deepak L. Bhatt | 149 | 1973 | 114652 |
Clifford R. Jack | 140 | 965 | 94814 |
Scott D. Solomon | 137 | 1145 | 103041 |
Karl Swedberg | 136 | 706 | 111214 |
Charles J. Yeo | 136 | 672 | 76424 |