Institution
University of Arkansas for Medical Sciences
Education•Little Rock, Arkansas, United States•
About: University of Arkansas for Medical Sciences is a education organization based out in Little Rock, Arkansas, United States. It is known for research contribution in the topics: Population & Health care. The organization has 14077 authors who have published 26012 publications receiving 973592 citations. The organization is also known as: UAMS.
Topics: Population, Health care, Medicine, Poison control, Multiple myeloma
Papers published on a yearly basis
Papers
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TL;DR: Reassuringly, penicillins, erythromycins, and cephalosporins, although used commonly by pregnant women, were not associated with many birth defects, indicating a need for additional scrutiny.
Abstract: poplastic left heart syndrome (AOR=3.2; 95% CI, 1.37.6), coarctation of the aorta (AOR=2.7; 95% CI, 1.35.6), choanal atresia (AOR =8 .0; 95% CI, 2.7-23.5), transverse limb deficiency (AOR=2.5; 95% CI, 1.0-5.9), and diaphragmatic hernia (AOR=2.4; 95% CI, 1.1-5.4). Nitrofurantoins were associated with anophthalmia or microphthalmos (AOR=3.7; 95% CI, 1.1-12.2), hypoplastic left heart syndrome (AOR=4.2; 95% CI, 1.9-9.1), atrial septal defects (AOR=1.9; 95% CI, 1.1-3.4), and cleft lip with cleft palate (AOR=2.1; 95% CI, 1.2-3.9). Other antibacterial agents that showed associations included erythromycins (2 defects), penicillins (1 defect), cephalosporins (1 defect), and quinolones (1 defect). Conclusions: Reassuringly, penicillins, erythromycins, and cephalosporins, although used commonly by pregnant women, were not associated with many birth defects. Sulfonamides and nitrofurantoins were associated with several birth defects, indicating a need for additional scrutiny.
216 citations
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TL;DR: The FDRI results suggest that disregulation of iron metabolism occurs in PD and that this disregulation may differ in earlier- versus later-onset Parkinson's disease.
216 citations
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TL;DR: In vivo evidence is provided that GPIbα absolutely is required for recruitment of platelets to both exposed subendothelium and thrombi under arterial flow conditions and contributes to arterial thrombosis by important adhesion mechanisms independent of the binding to VWF.
Abstract: GPIbα binding to von Willebrand factor (VWF) exposed at a site of vascular injury is thought to be the first step in the formation of a hemostatic plug. However, our previous studies in VWF-deficient mice demonstrated delayed but not absent arterial thrombus formation, suggesting that, under these conditions, GPIbα may bind other ligands or that a receptor other than GPIbα can mediate platelet adhesion. Here, we studied thrombus formation in transgenic mice expressing GPIbα in which the extracellular domain was replaced by that of the human IL-4 receptor (IL4Rα/GPIbα-tg mice). Platelet adhesion to ferric chloride-treated mesenteric arterioles in IL4Rα/GPIbα-tg mice was virtually absent in contrast to avid adhesion in WT mice. As a consequence, arterial thrombus formation was inhibited completely in the mutant mice. Our studies further show that, when infused into WT recipient mice, IL4Rα/GPIbα-tg platelets or WT platelets lacking the 45-kDa N-terminal domain of GPIbα failed to incorporate into growing arterial thrombi, even if the platelets were activated before infusion. Surprisingly, platelets lacking β3 integrins, which are unable to form thrombi on their own, incorporated efficiently into WT thrombi. Our studies provide in vivo evidence that GPIbα absolutely is required for recruitment of platelets to both exposed subendothelium and thrombi under arterial flow conditions. Thus, GPIbα contributes to arterial thrombosis by important adhesion mechanisms independent of the binding to VWF.
216 citations
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TL;DR: Treatment of mice with a toxic dose of acetaminophen significantly increased hepatotoxicity at 4 h, as evidenced by histological necrosis in the centrilobular areas of the liver, and increased serum levels of alanine aminotransferase (ALT).
Abstract: Treatment of mice with a toxic dose of acetaminophen (300 mg/kg, ip) significantly increased hepatotoxicity at 4 h, as evidenced by histological necrosis in the centrilobular areas of the liver, and increased serum levels of alanine aminotransferase (ALT) (from 8 ± 1 IU/L in saline-treated mice to 3226 ± 892 IU/L in the acetaminophen-treated mice). Serum levels of nitrate plus nitrite (a marker of nitric oxide synthesis) were also increased from 62 ± 8 μM in saline-treated mice to 110 ± 14 μM in acetaminophen-treated mice (P < 0.05). Regression analysis of serum ALT levels to serum nitrate plus nitrite levels in individual mice revealed a positive, linear relationship between serum ALT levels and serum nitrate plus nitrite levels with a correlation coefficient of 0.9 (P < 0.05). The y intercept value (nitrate plus nitrite level) was 63 ± 15 μM. Immunohistochemical analysis of liver sections from acetaminophen-intoxicated mice using an anti-3-nitrotyrosine antibody indicated tyrosine nitration in the prote...
216 citations
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TL;DR: It is suggested that the initial oncogenic event for most MM tumors is a primary immunoglobulin translocation that dysregulatescyclin D1, cyclin D3, and other oncogenes to provide a proliferative stimulus to postgerminal center plasma cells.
215 citations
Authors
Showing all 14187 results
Name | H-index | Papers | Citations |
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Hagop M. Kantarjian | 204 | 3708 | 210208 |
Yusuke Nakamura | 179 | 2076 | 160313 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
David R. Williams | 178 | 2034 | 138789 |
Yang Yang | 171 | 2644 | 153049 |
John E. Morley | 154 | 1377 | 97021 |
Jeffrey L. Cummings | 148 | 833 | 116067 |
Hugh A. Sampson | 147 | 816 | 76492 |
Michael J. Keating | 140 | 1169 | 76353 |
Kristine Yaffe | 136 | 794 | 72250 |
Nancy J. Cox | 135 | 778 | 109195 |
Stephen W. Scherer | 135 | 685 | 85752 |
Nikhil C. Munshi | 134 | 906 | 67349 |
Siamon Gordon | 131 | 420 | 77948 |
Jian-Guo Bian | 128 | 1219 | 80964 |