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Institution

Icahn School of Medicine at Mount Sinai

EducationNew York, New York, United States
About: Icahn School of Medicine at Mount Sinai is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 37488 authors who have published 76057 publications receiving 3704104 citations. The organization is also known as: Mount Sinai School of Medicine.


Papers
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Journal ArticleDOI
TL;DR: It is believed that abstinence-only education programs, as defined by federal funding requirements, are morally problematic, by withholding information and promoting questionable and inaccurate opinions.

548 citations

Journal ArticleDOI
TL;DR: Treatment of noncomplex obstructive coronary artery disease with anEverolimus-eluting bioresorbable vascular scaffold, as compared with an everolimus -eluting cobalt-chromium stent, was within the prespecified margin for noninferiority with respect to target-lesion failure at 1 year.
Abstract: BACKGROUND In patients with coronary artery disease who receive metallic drug-eluting coronary stents, adverse events such as late target-lesion failure may be related in part to the persistent presence of the metallic stent frame in the coronary-vessel wall. Bioresorbable vascular scaffolds have been developed to attempt to improve longterm outcomes. METHODS In this large, multicenter, randomized trial, 2008 patients with stable or unstable angina were randomly assigned in a 2:1 ratio to receive an everolimus-eluting bioresorbable vascular (Absorb) scaffold (1322 patients) or an everolimus-eluting cobalt–chromium (Xience) stent (686 patients). The primary end point, which was tested for both noninferiority (margin, 4.5 percentage points for the risk difference) and superiority, was target-lesion failure (cardiac death, target-vessel myocardial infarction, or ischemia-driven target-lesion revascularization) at 1 year. RESULTS Target-lesion failure at 1 year occurred in 7.8% of patients in the Absorb group and in 6.1% of patients in the Xience group (difference, 1.7 percentage points; 95% confidence interval, −0.5 to 3.9; P = 0.007 for noninferiority and P = 0.16 for superiority). There was no significant difference between the Absorb group and the Xience group in rates of cardiac death (0.6% and 0.1%, respectively; P = 0.29), targetvessel myocardial infarction (6.0% and 4.6%, respectively; P = 0.18), or ischemiadriven target-lesion revascularization (3.0% and 2.5%, respectively; P = 0.50). Device thrombosis within 1 year occurred in 1.5% of patients in the Absorb group and in 0.7% of patients in the Xience group (P = 0.13). CONCLUSIONS In this large-scale, randomized trial, treatment of noncomplex obstructive coronary artery disease with an everolimus-eluting bioresorbable vascular scaffold, as compared with an everolimus-eluting cobalt–chromium stent, was within the prespecified margin for noninferiority with respect to target-lesion failure at 1 year. (Funded by Abbott Vascular; ABSORB III ClinicalTrials.gov number, NCT01751906.)

548 citations

Journal ArticleDOI
05 Oct 2006-Nature
TL;DR: It is found that mice infected with a virus containing all eight genes from the pandemic virus showed marked activation of pro-inflammatory and cell-death pathways by 24 h after infection that remained unabated until death on day 5, in contrast with smaller host immune responses as measured at the genomic level.
Abstract: The influenza pandemic of 1918-19 was responsible for about 50 million deaths worldwide. Modern histopathological analysis of autopsy samples from human influenza cases from 1918 revealed significant damage to the lungs with acute, focal bronchitis and alveolitis associated with massive pulmonary oedema, haemorrhage and rapid destruction of the respiratory epithelium. The contribution of the host immune response leading to this severe pathology remains largely unknown. Here we show, in a comprehensive analysis of the global host response induced by the 1918 influenza virus, that mice infected with the reconstructed 1918 influenza virus displayed an increased and accelerated activation of host immune response genes associated with severe pulmonary pathology. We found that mice infected with a virus containing all eight genes from the pandemic virus showed marked activation of pro-inflammatory and cell-death pathways by 24 h after infection that remained unabated until death on day 5. This was in contrast with smaller host immune responses as measured at the genomic level, accompanied by less severe disease pathology and delays in death in mice infected with influenza viruses containing only subsets of 1918 genes. The results indicate a cooperative interaction between the 1918 influenza genes and show that study of the virulence of the 1918 influenza virus requires the use of the fully reconstructed virus. With recent concerns about the introduction of highly pathogenic avian influenza viruses into humans and their potential to cause a worldwide pandemic with disastrous health and economic consequences, a comprehensive understanding of the global host response to the 1918 virus is crucial. Moreover, understanding the contribution of host immune responses to virulent influenza virus infections is an important starting point for the identification of prognostic indicators and the development of novel antiviral therapies.

548 citations

Journal ArticleDOI
15 Apr 2011-Cell
TL;DR: It is shown that WD repeat domain 5 (Wdr5), a core member of the mammalian Trithorax (trxG) complex, positively correlates with the undifferentiated state and is a regulator of ES cell self-renewal.

547 citations


Authors

Showing all 37948 results

NameH-indexPapersCitations
Robert Langer2812324326306
Shizuo Akira2611308320561
Gordon H. Guyatt2311620228631
Eugene Braunwald2301711264576
Bruce S. McEwen2151163200638
Robert J. Lefkowitz214860147995
Peter Libby211932182724
Mark J. Daly204763304452
Stuart H. Orkin186715112182
Paul G. Richardson1831533155912
Alan C. Evans183866134642
John C. Morris1831441168413
Paul M. Thompson1832271146736
Tadamitsu Kishimoto1811067130860
Bruce M. Psaty1811205138244
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023157
2022845
20217,117
20206,224
20195,200
20184,505