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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 & 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.


Papers
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Journal ArticleDOI
TL;DR: The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar.
Abstract: Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake.

930 citations

Journal ArticleDOI
TL;DR: By better harnessing the immunizing functions of maturing dendritic cells, antibody-mediated antigen targeting via the DEC-205 receptor increases the efficiency of vaccination for T cell immunity, including systemic and mucosal resistance in disease models.
Abstract: The prevention and treatment of prevalent infectious diseases and tumors should benefit from improvements in the induction of antigen-specific T cell immunity. To assess the potential of antigen targeting to dendritic cells to improve immunity, we incorporated ovalbumin protein into a monoclonal antibody to the DEC-205 receptor, an endocytic receptor that is abundant on these cells in lymphoid tissues. Simultaneously, we injected agonistic α-CD40 antibody to mature the dendritic cells. We found that a single low dose of antibody-conjugated ovalbumin initiated immunity from the naive CD4+ and CD8+ T cell repertoire. Unexpectedly, the αDEC-205 antigen conjugates, given s.c., targeted to dendritic cells systemically and for long periods, and ovalbumin peptide was presented on MHC class I for 2 weeks. This was associated with stronger CD8+ T cell–mediated immunity relative to other forms of antigen delivery, even when the latter was given at a thousand times higher doses. In parallel, the mice showed enhanced resistance to an established rapidly growing tumor and to viral infection at a mucosal site. By better harnessing the immunizing functions of maturing dendritic cells, antibody-mediated antigen targeting via the DEC-205 receptor increases the efficiency of vaccination for T cell immunity, including systemic and mucosal resistance in disease models.

928 citations

Journal ArticleDOI
01 Jul 1990-Neuron
TL;DR: These immortalized cells will provide an invaluable model system for study of hypothalamic neurosecretory neurons that regulate reproduction and demonstrates the feasibility of immortalizing differentiated neurons by targeting tumorigenesis in transgenic mice to specific neurons of the CNS.

926 citations

Journal ArticleDOI
TL;DR: Dissemination of information about obesity genetics may have neither a beneficial nor a harmful impact on how overweight individuals perceive themselves, but some overweight individuals may be interested in receiving personalized genetic information.
Abstract: Background/Aims: Increasing public awareness of obesity genetics could have beneficial or harmful effects on overweight individuals. This study examined the impact of genetic information on weight-related cognitions as well as interest in personalized genetic information about obesity among overweight individuals. Methods: Online survey respondents (n = 655) were randomly assigned to read either genetic, gene-environment, or nongenetic obesity causal information. Fifty-two percent of the participants were female, 82.4% were White, 45% had an annual income of USD Results: Participants in the genetic and gene-environment conditions were more likely to believe genetics increase obesity risk than participants in the nongenetic condition (both p Conclusion: Dissemination of information about obesity genetics may have neither a beneficial nor a harmful impact on how overweight individuals perceive themselves. Some overweight individuals may be interested in receiving personalized genetic information. The actual effects of obesity genetic information being incorporated into public health messages and of personalized genetic information on obesity prevention and treatment interventions remain to be seen.

925 citations

Journal ArticleDOI
TL;DR: Three robust HCC subclasses are observed, each correlated with clinical parameters such as tumor size, extent of cellular differentiation, and serum alpha-fetoprotein levels, and it is indicated that S1 reflected aberrant activation of the WNT signaling pathway, S2 was characterized by proliferation as well as MYC and AKT activation, and S3 was associated with hepatocyte differentiation.
Abstract: Hepatocellular carcinoma (HCC) is a highly heterogeneous disease, and prior attempts to develop genomic-based classification for HCC have yielded highly divergent results, indicating difficulty in identifying unified molecular anatomy We performed a meta-analysis of gene expression profiles in data sets from eight independent patient cohorts across the world In addition, aiming to establish the real world applicability of a classification system, we profiled 118 formalin-fixed, paraffin-embedded tissues from an additional patient cohort A total of 603 patients were analyzed, representing the major etiologies of HCC (hepatitis B and C) collected from Western and Eastern countries We observed three robust HCC subclasses (termed S1, S2, and S3), each correlated with clinical parameters such as tumor size, extent of cellular differentiation, and serum α-fetoprotein levels An analysis of the components of the signatures indicated that S1 reflected aberrant activation of the WNT signaling pathway, S2 was characterized by proliferation as well as MYC and AKT activation, and S3 was associated with hepatocyte differentiation Functional studies indicated that the WNT pathway activation signature characteristic of S1 tumors was not simply the result of β-catenin mutation but rather was the result of transforming growth factor-β activation, thus representing a new mechanism of WNT pathway activation in HCC These experiments establish the first consensus classification framework for HCC based on gene expression profiles and highlight the power of integrating multiple data sets to define a robust molecular taxonomy of the disease [Cancer Res 2009;69(18):7385–92]

922 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
2022844
20217,117
20206,224
20195,200
20184,505