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 & Cancer. 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, Cancer, Transplantation, Virus, Health care
Papers published on a yearly basis
Papers
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TL;DR: Comparisons of DNA methylation in eight diverse plant and animal genomes found that patterns of methylation are very similar in flowering plants with methylated cytosines detected in all sequence contexts, whereas CG methylation predominates in animals.
Abstract: Cytosine DNA methylation is a heritable epigenetic mark present in many eukaryotic organisms. Although DNA methylation likely has a conserved role in gene silencing, the levels and patterns of DNA methylation appear to vary drastically among different organisms. Here we used shotgun genomic bisulfite sequencing (BS-Seq) to compare DNA methylation in eight diverse plant and animal genomes. We found that patterns of methylation are very similar in flowering plants with methylated cytosines detected in all sequence contexts, whereas CG methylation predominates in animals. Vertebrates have methylation throughout the genome except for CpG islands. Gene body methylation is conserved with clear preference for exons in most organisms. Furthermore, genes appear to be the major target of methylation in Ciona and honey bee. Among the eight organisms, the green alga Chlamydomonas has the most unusual pattern of methylation, having non-CG methylation enriched in exons of genes rather than in repeats and transposons. In addition, the Dnmt1 cofactor Uhrf1 has a conserved function in maintaining CG methylation in both transposons and gene bodies in the mouse, Arabidopsis, and zebrafish genomes.
1,111 citations
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Baylor University Medical Center1, Tufts University2, Wake Forest University3, University of Pennsylvania4, Saint Louis University5, NorthShore University HealthSystem6, Icahn School of Medicine at Mount Sinai7, University of California, San Francisco8, University of Alabama at Birmingham9, Anacor Pharmaceuticals Inc.10, American Academy of Dermatology11
TL;DR: The classification of psoriasis; associated comorbidities including autoimmune diseases, cardiovascular risk, psychiatric/psychologic issues, and cancer risk; along with assessment tools for skin disease and quality-of-life issues; and the safety and efficacy of the biologic treatments used to treat patients with Psoriasis are discussed.
Abstract: Psoriasis is a common, chronic, inflammatory, multisystem disease with predominantly skin and joint manifestations affecting approximately 2% of the population. In this first of 5 sections of the guidelines of care for psoriasis, we discuss the classification of psoriasis; associated comorbidities including autoimmune diseases, cardiovascular risk, psychiatric/psychologic issues, and cancer risk; along with assessment tools for skin disease and quality-of-life issues. Finally, we will discuss the safety and efficacy of the biologic treatments used to treat patients with psoriasis.
1,103 citations
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TL;DR: In this article, the results of a genome-wide association study (GWAS) for educational attainment were reported, showing that single-nucleotide polymorphisms associated with educational attainment disproportionately occur in genomic regions regulating gene expression in the fetal brain.
Abstract: Educational attainment is strongly influenced by social and other environmental factors, but genetic factors are estimated to account for at least 20% of the variation across individuals. Here we report the results of a genome-wide association study (GWAS) for educational attainment that extends our earlier discovery sample of 101,069 individuals to 293,723 individuals, and a replication study in an independent sample of 111,349 individuals from the UK Biobank. We identify 74 genome-wide significant loci associated with the number of years of schooling completed. Single-nucleotide polymorphisms associated with educational attainment are disproportionately found in genomic regions regulating gene expression in the fetal brain. Candidate genes are preferentially expressed in neural tissue, especially during the prenatal period, and enriched for biological pathways involved in neural development. Our findings demonstrate that, even for a behavioural phenotype that is mostly environmentally determined, a well-powered GWAS identifies replicable associated genetic variants that suggest biologically relevant pathways. Because educational attainment is measured in large numbers of individuals, it will continue to be useful as a proxy phenotype in efforts to characterize the genetic influences of related phenotypes, including cognition and neuropsychiatric diseases.
1,102 citations
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University of Pittsburgh1, Veterans Health Administration2, University of Washington3, Emory University4, Baylor College of Medicine5, Icahn School of Medicine at Mount Sinai6, Yale University7, University of Maryland, Baltimore8, University of Vermont9, University of California, Los Angeles10, University of South Carolina11, National Institutes of Health12
TL;DR: Investigating whether HIV is associated with an increased risk of acute myocardial infarction after adjustment for all standard Framingham risk factors among a large cohort of HIV-positive and demographically and behaviorally similar uninfected veterans in care found infections with HIV are associated with a 50% increased risk beyond that explained by recognized risk factors.
Abstract: Importance Whether people infected with human immunodeficiency virus (HIV) are at an increased risk of acute myocardial infarction (AMI) compared with uninfected people is not clear. Without demographically and behaviorally similar uninfected comparators and without uniformly measured clinical data on risk factors and fatal and nonfatal AMI events, any potential association between HIV status and AMI may be confounded. Objective To investigate whether HIV is associated with an increased risk of AMI after adjustment for all standard Framingham risk factors among a large cohort of HIV-positive and demographically and behaviorally similar (ie, similar prevalence of smoking, alcohol, and cocaine use) uninfected veterans in care. Design and Setting Participants in the Veterans Aging Cohort Study Virtual Cohort from April 1, 2003, through December 31, 2009. Participants After eliminating those with baseline cardiovascular disease, we analyzed data on HIV status, age, sex, race/ethnicity, hypertension, diabetes mellitus, dyslipidemia, smoking, hepatitis C infection, body mass index, renal disease, anemia, substance use, CD4 cell count, HIV-1 RNA, antiretroviral therapy, and incidence of AMI. Main Outcome Measure Acute myocardial infarction. Results We analyzed data on 82 459 participants. During a median follow-up of 5.9 years, there were 871 AMI events. Across 3 decades of age, the mean (95% CI) AMI events per 1000 person-years was consistently and significantly higher for HIV-positive compared with uninfected veterans: for those aged 40 to 49 years, 2.0 (1.6-2.4) vs 1.5 (1.3-1.7); for those aged 50 to 59 years, 3.9 (3.3-4.5) vs 2.2 (1.9-2.5); and for those aged 60 to 69 years, 5.0 (3.8-6.7) vs 3.3 (2.6-4.2) (P Conclusions and Relevance Infection with HIV is associated with a 50% increased risk of AMI beyond that explained by recognized risk factors.
1,100 citations
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TL;DR: The sequence of a closely related amyloid cDNA, A4751, is distinguished from A4695 by the presence of a 168 base-pair sequence which adds 57 amino acids to, and removes one residue from, the predicted A4 695protein.
Abstract: The amyloid proteins isolated from neuritic plaques and the cerebrovasculature of Alzheimer's disease are self-aggregating moieties termed A4 protein1 and βprotein2,3, respectively. A putative A4 amyloid precursor (herein termed A4695) has been characterized by analysis of a human brain complementary DNA4. We report here the sequence of a closely related amyloid cDNA, A4751,distinguished from A4695 by the presence of a 168 base-pair (bp) sequence which adds 57 amino acids to, and removes one residue from, the predicted A4 695protein. The peptide predicted from this insert is very similar to the Kunitz family of serine proteinase inhibitors. The two A4-specific messenger RNAs are differentially expressed: in a limited survey, A4751 mRNA appears to be ubiquitous, whereas A4695 mRNA has a restricted pattern of expression which includes cells from neuronal tissue. These data may have significant implications for understanding amyloid deposition in Alzheimer's disease.
1,098 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 |