Institution
Icahn School of Medicine at Mount Sinai
Education•New 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.
Topics: Population, Medicine, Cancer, Health care, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: The majority of cases in the SARS outbreak in the greater Toronto area were related to hospital exposure, and several features of the clinical presentation will be useful in raising the suspicion of SARS.
Abstract: ContextSevere acute respiratory syndrome (SARS) is an emerging infectious disease
that first manifested in humans in China in November 2002 and has subsequently
spread worldwide.ObjectivesTo describe the clinical characteristics and short-term outcomes of
SARS in the first large group of patients in North America; to describe how
these patients were treated and the variables associated with poor outcome.Design, Setting, and PatientsRetrospective case series involving 144 adult patients admitted to 10
academic and community hospitals in the greater Toronto, Ontario, area between
March 7 and April 10, 2003, with a diagnosis of suspected or probable SARS.
Patients were included if they had fever, a known exposure to SARS, and respiratory
symptoms or infiltrates observed on chest radiograph. Patients were excluded
if an alternative diagnosis was determined.Main Outcome MeasuresLocation of exposure to SARS; features of the history, physical examination,
and laboratory tests at admission to the hospital; and 21-day outcomes such
as death or intensive care unit (ICU) admission with or without mechanical
ventilation.ResultsOf the 144 patients, 111 (77%) were exposed to SARS in the hospital
setting. Features of the clinical examination most commonly found in these
patients at admission were self-reported fever (99%), documented elevated
temperature (85%), nonproductive cough (69%), myalgia (49%), and dyspnea (42%).
Common laboratory features included elevated lactate dehydrogenase (87%),
hypocalcemia (60%), and lymphopenia (54%). Only 2% of patients had rhinorrhea.
A total of 126 patients (88%) were treated with ribavirin, although its use
was associated with significant toxicity, including hemolysis (in 76%) and
decrease in hemoglobin of 2 g/dL (in 49%). Twenty-nine patients (20%) were
admitted to the ICU with or without mechanical ventilation, and 8 patients
died (21-day mortality, 6.5%; 95% confidence interval [CI], 1.9%-11.8%). Multivariable
analysis showed that the presence of diabetes (relative risk [RR], 3.1; 95%
CI, 1.4-7.2; P = .01) or other comorbid conditions
(RR, 2.5; 95% CI, 1.1-5.8; P = .03) were independently
associated with poor outcome (death, ICU admission, or mechanical ventilation).ConclusionsThe majority of cases in the SARS outbreak in the greater Toronto area
were related to hospital exposure. In the event that contact history becomes
unreliable, several features of the clinical presentation will be useful in
raising the suspicion of SARS. Although SARS is associated with significant
morbidity and mortality, especially in patients with diabetes or other comorbid
conditions, the vast majority (93.5%) of patients in our cohort survived.Published online May 6, 2003 (doi:10.1001/jama.289.21.JOC30885).
1,269 citations
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TL;DR: Exome sequencing analysis of 243 liver tumors identified mutational signatures associated with specific risk factors, mainly combined alcohol and tobacco consumption and exposure to aflatoxin B1, and defined the extensive landscape of altered genes and pathways in HCC.
Abstract: Genomic analyses promise to improve tumor characterization to optimize personalized treatment for patients with hepatocellular carcinoma (HCC). Exome sequencing analysis of 243 liver tumors identified mutational signatures associated with specific risk factors, mainly combined alcohol and tobacco consumption and exposure to aflatoxin B1. We identified 161 putative driver genes associated with 11 recurrently altered pathways. Associations of mutations defined 3 groups of genes related to risk factors and centered on CTNNB1 (alcohol), TP53 (hepatitis B virus, HBV) and AXIN1. Analyses according to tumor stage progression identified TERT promoter mutation as an early event, whereas FGF3, FGF4, FGF19 or CCND1 amplification and TP53 and CDKN2A alterations appeared at more advanced stages in aggressive tumors. In 28% of the tumors, we identified genetic alterations potentially targetable by US Food and Drug Administration (FDA)-approved drugs. In conclusion, we identified risk factor-specific mutational signatures and defined the extensive landscape of altered genes and pathways in HCC, which will be useful to design clinical trials for targeted therapy.
1,265 citations
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TL;DR: In this article, human blood CXCR5(+)CD4(+) T cells share functional properties with T follicular helper (Tfh) cells and appear to represent their circulating memory compartment.
1,263 citations
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TL;DR: The epidemiology, screening, and prevention of gastric cancer are reviewed, including its incidence, survival, mortality, and trends over time, and risk factors are characterized, both environmental and genetic.
Abstract: Less than a century ago, gastric cancer (GC) was the most common cancer in the United States and perhaps throughout the world. Despite its worldwide decline in incidence over the past century, GC remains a major killer across the globe. This article reviews the epidemiology, screening, and prevention of gastric cancer. We first discuss the descriptive epidemiology of GC, including its incidence, survival, and mortality, including trends over time. Next, we characterize the risk factors for gastric cancer, both environmental and genetic. Serological markers and histological precursor lesions of GC and early detection of GC of using these markers is reviewed. Finally, we discuss prevention strategies and provide suggestions for further research.
1,261 citations
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Cardiff University1, Harvard University2, Charité3, King's College London4, Broad Institute5, University of Adelaide6, Centre for Mental Health7, University of Queensland8, University of Münster9, University of Edinburgh10, QIMR Berghofer Medical Research Institute11, University of Vigo12, University of California, Los Angeles13, Icahn School of Medicine at Mount Sinai14, University of Oviedo15, Lundbeck16, Aarhus University17, University of Oslo18, Oslo University Hospital19, Statens Serum Institut20, University of Bergen21, Aarhus University Hospital22, University of Copenhagen23, University of Belgrade24, Tbilisi State Medical University25, deCODE genetics26, University of Verona27, Mental Health Services28, Eli Lilly and Company29, Martin Luther University of Halle-Wittenberg30, Ludwig Maximilian University of Munich31
TL;DR: A new genome-wide association study of schizophrenia is reported, and through meta-analysis with existing data and integrating genomic fine-mapping with brain expression and chromosome conformation data, 50 novel associated loci and 145 loci are identified.
Abstract: Schizophrenia is a debilitating psychiatric condition often associated with poor quality of life and decreased life expectancy. Lack of progress in improving treatment outcomes has been attributed to limited knowledge of the underlying biology, although large-scale genomic studies have begun to provide insights. We report a new genome-wide association study of schizophrenia (11,260 cases and 24,542 controls), and through meta-analysis with existing data we identify 50 novel associated loci and 145 loci in total. Through integrating genomic fine-mapping with brain expression and chromosome conformation data, we identify candidate causal genes within 33 loci. We also show for the first time that the common variant association signal is highly enriched among genes that are under strong selective pressures. These findings provide new insights into the biology and genetic architecture of schizophrenia, highlight the importance of mutation-intolerant genes and suggest a mechanism by which common risk variants persist in the population.
1,259 citations
Authors
Showing all 37948 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert Langer | 281 | 2324 | 326306 |
Shizuo Akira | 261 | 1308 | 320561 |
Gordon H. Guyatt | 231 | 1620 | 228631 |
Eugene Braunwald | 230 | 1711 | 264576 |
Bruce S. McEwen | 215 | 1163 | 200638 |
Robert J. Lefkowitz | 214 | 860 | 147995 |
Peter Libby | 211 | 932 | 182724 |
Mark J. Daly | 204 | 763 | 304452 |
Stuart H. Orkin | 186 | 715 | 112182 |
Paul G. Richardson | 183 | 1533 | 155912 |
Alan C. Evans | 183 | 866 | 134642 |
John C. Morris | 183 | 1441 | 168413 |
Paul M. Thompson | 183 | 2271 | 146736 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Bruce M. Psaty | 181 | 1205 | 138244 |