Institution
Jewish Hospital
Healthcare•Cincinnati, Ohio, United States•
About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.
Topics: Antigen, Population, Pregnancy, Thrombophilia, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: This phase 1/2, single-arm, 2-stage, open-label study was designed to evaluate the safety and efficacy of brentuximab vedotin in combination with bendamustine for the treatment of pts with primary refractory disease or in first relapse.
61 citations
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TL;DR: Newer endoscopic technologies are an effective option to improve ADR and PDR and decrease AMR, particularly with mechanical NTDs, and no differences in operability and safety were found.
61 citations
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TL;DR: Complications of NOM of pediatric blunt hepatic injury are rare, but may include biloma, hepatic artery pseudoaneurysm, and necrotic gallbladder and the clinician must maintain a high index of suspicion for the development of complications.
Abstract: Background:Nonoperative management (NOM) of blunt hepatic injury is the standard of care in the hemodynamically stable pediatric patient, but it is not without pitfalls. The purpose of this study is to assess the incidence and types of complications associated with NOM in terms of diagnosis, managem
60 citations
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60 citations
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TL;DR: In a 29 year old white male with osteonecrosis of both hips and a shoulder, and in his family, basal and stimulated fibrinolytic activity was measured to determine whether low fibrinogen activator inhibitor activity might be heritable and etiologically associated with oste onecrosis.
Abstract: In a 29 year old white male with osteonecrosis of both hips and a shoulder, and in his family, we measured basal and stimulated (10 min cuff venous occlusion at 100 mgHg) fibrinolytic activity to determine whether low fibrinolytic activity might be heritable and etiologically associated with osteonecrosis. The proband's basal tPA-Fx was low, 0.08 IU/ml (normal 0.11-1.94), tPA-Ag was normal (11.6 ng/ml), plasminogen activator inhibitor activity (PAI-Fx) was very high, 119 U/ml (normal 3.5-27), as was his plasminogen activator inhibitor antigen (PAI-Ag), 202 ng/ml (normal 3.2-37.1). The proband's basal PAI-Fx (119) and PAI-Ag (202) were respectively 6 and 13 standard deviations greater than the mean PAI-Fx (17 +/- 15 U/ml) and the mean PAI-Ag (25 +/- 13 ng/ml) in 172 concomitantly studied hyperlipidemic men. Alpha-2 antiplasmin, fibrinogen, plasminogen and Lp(a) were normal. Despite lowering TG to 301 mg/dl, basal tPA-Fx remained low, 0.05; PAI-Fx and PAI-Ag remained very high (109 and 191). Following venous occlusion, stimulated tPA-Fx remained very low, 0.1 (normal 2.3-11.3), but tPA-Ag rose normally to 17 (normal 8.4-31.4); stimulated PAI-Fx and PAI-Ag were very high, 134 and 223, (normal PAI-Fx 3.6-24, PAI-Ag 12-96). Stimulated D-dimer was < the 10th percentile, 0.084 micrograms/ml. With such high PAI-Fx available to bind tPA, occlusion-stimulated tPA-Fx could not rise, and fibrinolysis could not be initiated. Neither diseases nor drugs could explain the high PAI-Fx and PAI-Ag, low tPA-Fx; or osteonecrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
60 citations
Authors
Showing all 3894 results
Name | H-index | Papers | Citations |
---|---|---|---|
John C. Morris | 183 | 1441 | 168413 |
David L. Kaplan | 177 | 1944 | 146082 |
Robert H. Purcell | 139 | 666 | 70366 |
Nancy J. Cox | 135 | 778 | 109195 |
Jennifer S. Haas | 128 | 840 | 71315 |
David A. Cheresh | 125 | 337 | 62252 |
John W. Kappler | 122 | 464 | 57541 |
Philippa Marrack | 120 | 416 | 54345 |
Arthur Weiss | 117 | 380 | 45703 |
Thomas J. Kipps | 114 | 748 | 63240 |
Michael Pollak | 114 | 663 | 57793 |
Peter M. Henson | 112 | 369 | 54246 |
Roberto Bolli | 111 | 528 | 44010 |
William D. Foulkes | 108 | 682 | 45013 |
David A. Lynch | 108 | 714 | 59678 |