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Institution

New York University

EducationNew York, New York, United States
About: New York University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 72380 authors who have published 165545 publications receiving 8334030 citations. The organization is also known as: NYU & University of the City of New York.


Papers
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Journal ArticleDOI
TL;DR: Understanding the host–microbial interactions that lead to neoplasia will improve cancer-targeted therapeutics and diagnostics, and provide mechanistic insights into other malignancies that arise within the context of microbially initiated inflammatory states.
Abstract: Although gastric adenocarcinoma is associated with the presence of Helicobacter pylori in the stomach, only a small fraction of colonized individuals develop this common malignancy. H. pylori strain and host genotypes probably influence the risk of carcinogenesis by differentially affecting host inflammatory responses and epithelial-cell physiology. Understanding the host-microbial interactions that lead to neoplasia will improve cancer-targeted therapeutics and diagnostics, and provide mechanistic insights into other malignancies that arise within the context of microbially initiated inflammatory states.

1,719 citations

Journal ArticleDOI
TL;DR: The International Standards Booklet for Neurological and Functional Classification of Spinal Cord Injury (ISBWC) as mentioned in this paper is a standard for the classification of spinal cord injury. But it is not a classification of neurological disorders.
Abstract: The International Standards Booklet for Neurological and Functional Classification of Spinal Cord Injury

1,709 citations

Journal ArticleDOI
08 May 2008-Nature
TL;DR: In this article, the authors demonstrate that, together with pro-inflammatory cytokines, TGF-beta orchestrates T helper cells that produce IL-17 (T(H)17 cells) in a concentration-dependent manner.
Abstract: T helper cells that produce IL-17 (T(H)17 cells) promote autoimmunity in mice and have been implicated in the pathogenesis of human inflammatory diseases. At mucosal surfaces, T(H)17 cells are thought to protect the host from infection, whereas regulatory T (T(reg)) cells control immune responses and inflammation triggered by the resident microflora. Differentiation of both cell types requires transforming growth factor-beta (TGF-beta), but depends on distinct transcription factors: RORgammat (encoded by Rorc(gammat)) for T(H)17 cells and Foxp3 for T(reg) cells. How TGF-beta regulates the differentiation of T cells with opposing activities has been perplexing. Here we demonstrate that, together with pro-inflammatory cytokines, TGF-beta orchestrates T(H)17 cell differentiation in a concentration-dependent manner. At low concentrations, TGF-beta synergizes with interleukin (IL)-6 and IL-21 (refs 9-11) to promote IL-23 receptor (Il23r) expression, favouring T(H)17 cell differentiation. High concentrations of TGF-beta repress IL23r expression and favour Foxp3+ T(reg) cells. RORgammat and Foxp3 are co-expressed in naive CD4+ T cells exposed to TGF-beta and in a subset of T cells in the small intestinal lamina propria of the mouse. In vitro, TGF-beta-induced Foxp3 inhibits RORgammat function, at least in part through their interaction. Accordingly, lamina propria T cells that co-express both transcription factors produce less IL-17 (also known as IL-17a) than those that express RORgammat alone. IL-6, IL-21 and IL-23 relieve Foxp3-mediated inhibition of RORgammat, thereby promoting T(H)17 cell differentiation. Therefore, the decision of antigen-stimulated cells to differentiate into either T(H)17 or T(reg) cells depends on the cytokine-regulated balance of RORgammat and Foxp3.

1,696 citations

Journal ArticleDOI
TL;DR: If the Brazilian health system is to overcome the challenges with which it is presently faced, strengthened political support is needed so that financing can be restructured and the roles of both the public and private sector can be redefined.

1,689 citations

Journal ArticleDOI
TL;DR: Several key insights of the group engagement model are reviewed, relating these insights to important trends in psychological research on justice, and implications of the model for the future of procedural justice research are discussed.
Abstract: The group engagement model expands the insights of the group-value model of procedural justice and the relational model of authority into an explanation for why procedural justice shapes cooperation in groups, organizations, and societies. It hypothesizes that procedures are important because they shape people's social identity within groups, and social identity in turn influences attitudes, values, and behaviors. The model further hypothesizes that resource judgments exercise their influence indirectly by shaping social identity. This social identity mediation hypothesis explains why people focus on procedural justice, and in particular on procedural elements related to the quality of their interpersonal treatment, because those elements carry the most social identity-relevant information. In this article, we review several key insights of the group engagement model, relate these insights to important trends in psychological research on justice, and discuss implications of the model for the future of procedural justice research.

1,688 citations


Authors

Showing all 73237 results

NameH-indexPapersCitations
Rob Knight2011061253207
Virginia M.-Y. Lee194993148820
Frank E. Speizer193636135891
Stephen V. Faraone1881427140298
Eric R. Kandel184603113560
Andrei Shleifer171514271880
Eliezer Masliah170982127818
Roderick T. Bronson169679107702
Timothy A. Springer167669122421
Alvaro Pascual-Leone16596998251
Nora D. Volkow165958107463
Dennis R. Burton16468390959
Charles N. Serhan15872884810
Giacomo Bruno1581687124368
Tomas Hökfelt158103395979
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023245
20221,205
20218,761
20209,108
20198,417
20187,680