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Institution

Vanderbilt University

EducationNashville, Tennessee, United States
About: Vanderbilt University is a education organization based out in Nashville, Tennessee, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 45066 authors who have published 106528 publications receiving 5435039 citations. The organization is also known as: Vandy.


Papers
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Journal ArticleDOI
TL;DR: Evidence is provided that Gr+CD11b+ cells of immune origin induced by tumors directly contribute to tumor growth and vascularization by producing MMP9 and differentiating into ECs.

1,084 citations

Journal ArticleDOI
01 Oct 1999-Science
TL;DR: This article showed that matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.
Abstract: Precursors of α-defensin peptides require activation for bactericidal activity. In mouse small intestine, matrilysin colocalized with α-defensins (cryptdins) in Paneth cell granules, and in vitro it cleaved the pro segment from cryptdin precursors. Matrilysin-deficient (MAT−/−) mice lacked mature cryptdins and accumulated precursor molecules. Intestinal peptide preparations from MAT−/− mice had decreased antimicrobial activity. Orally administered bacteria survived in greater numbers and were more virulent in MAT−/− mice than in MAT+/+ mice. Thus, matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.

1,081 citations

Journal ArticleDOI
TL;DR: In this article, reference groups are used as a source of brand associations, which can be linked to one's mental representation of self to meet self-verification or self-enhancement goals.
Abstract: The set of associations consumers have about a brand is an important component of brand equity. This paper focuses on reference groups as a source of brand associations, which can be linked to one's mental representation of self to meet self-verification or self-enhancement goals. We conceptualize this linkage at an aggregate level in terms of self-brand connections, i.e., the extent to which individuals have incorporated a brand into their self-concept. Two studies show that brands used by member groups and aspiration groups can become connected to consumers' mental representation of self as they use these brands to define and create their self-concepts. Results from Experiment 1 show that the degree to which member group and aspiration group usage influences individual self-brand connections is contingent upon the degree to which the individual belongs to a member group or wishes to belong to an aspiration group. Experiment 2 finds that for individuals with self-enhancement goals, aspiration group brand use has a greater impact on self-brand connections; for individuals with self-verification goals, on the other hand, member group use has a greater impact.

1,081 citations

Journal ArticleDOI
TL;DR: This approach requires a dual process: 1) routine developmental surveillance and screening specifically for autism to be performed on all children to first identify those atrisk for any type of atypical development, and to identify those specifically at risk for autism.
Abstract: Autism is a common disorder of childhood, affecting 1 in 500 children. Yet, it often remains unrecognized and undiagnosed until or after late preschool age because appropriate tools for routine developmental screening and screening specifically for autism have not been available. Early identification of children with autism and intensive, early intervention during the toddler and preschool years improves outcome for most young children with autism. This practice parameter reviews the available empirical evidence and gives specific recommendations for the identification of children with autism. This approach requires a dual process: 1) routine developmental surveillance and screening specifically for autism to be performed on all children to first identify those at risk for any type of atypical development, and to identify those specifically at risk for autism; and 2) to diagnose and evaluate autism, to differentiate autism from other developmental disorders.

1,077 citations

Journal ArticleDOI
10 Apr 2008-Nature
TL;DR: Ex vivo T cells from subjects with HIES failed to produce IL-17, but not IL-2, tumour-necrosis factor or interferon-γ, on mitogenic stimulation with staphylococcal enterotoxin B or on antigenic stimulation with Candida albicans or streptokinase, which is consistent with a crucial role for STAT3 signalling in the generation of TH17 cells.
Abstract: The autosomal dominant hyper-IgE syndrome (HIES, 'Job's syndrome') is characterized by recurrent and often severe pulmonary infections, pneumatoceles, eczema, staphylococcal abscesses, mucocutaneous candidiasis, and abnormalities of bone and connective tissue. Mutations presumed to underlie HIES have recently been identified in stat3, the gene encoding STAT3 (signal transducer and activator of transcription 3) (refs 3, 4). Although impaired production of interferon-gamma and tumour-necrosis factor by T cells, diminished memory T-cell populations, decreased delayed-type-hypersensitivity responses and decreased in vitro lymphoproliferation in response to specific antigens have variably been described, specific immunological abnormalities that can explain the unique susceptibility to particular infections seen in HIES have not yet been defined. Here we show that interleukin (IL)-17 production by T cells is absent in HIES individuals. We observed that ex vivo T cells from subjects with HIES failed to produce IL-17, but not IL-2, tumour-necrosis factor or interferon-gamma, on mitogenic stimulation with staphylococcal enterotoxin B or on antigenic stimulation with Candida albicans or streptokinase. Purified naive T cells were unable to differentiate into IL-17-producing (T(H)17) T helper cells in vitro and had lower expression of retinoid-related orphan receptor (ROR)-gammat, which is consistent with a crucial role for STAT3 signalling in the generation of T(H)17 cells. T(H)17 cells have emerged as an important subset of helper T cells that are believed to be critical in the clearance of fungal and extracellular bacterial infections. Thus, our data suggest that the inability to produce T(H)17 cells is a mechanism underlying the susceptibility to the recurrent infections commonly seen in HIES.

1,077 citations


Authors

Showing all 45403 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Meir J. Stampfer2771414283776
John Q. Trojanowski2261467213948
Robert M. Califf1961561167961
Matthew Meyerson194553243726
Scott M. Grundy187841231821
Tony Hunter175593124726
David R. Jacobs1651262113892
Donald E. Ingber164610100682
L. Joseph Melton16153197861
Ralph A. DeFronzo160759132993
David W. Bates1591239116698
Charles N. Serhan15872884810
David Cella1561258106402
Jay Hauser1552145132683
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023141
2022540
20215,134
20205,232
20194,883
20184,649