Institution
University of South Florida
Education•Tampa, Florida, United States•
About: University of South Florida is a education organization based out in Tampa, Florida, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 34231 authors who have published 72644 publications receiving 2538044 citations. The organization is also known as: USF.
Topics: Population, Poison control, Cancer, Health care, Mental health
Papers published on a yearly basis
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Erica Sodergren1, George M. Weinstock1, Eric H. Davidson2, R. Andrew Cameron2 +243 more•Institutions (51)
TL;DR: The sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus is reported, a model for developmental and systems biology and yields insights into the evolution of deuterostomes.
Abstract: We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus, a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.
1,059 citations
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Nova Southeastern University1, University of Colorado Denver2, University of South Florida3, Yale University4, University of Texas Southwestern Medical Center5, Pennsylvania State University6, University of California, Los Angeles7, University of Washington8, Johns Hopkins University9, Duke University10, Northwestern University11
TL;DR: These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American Col- lege of Allergen,Asthma & immunology (ACAAI); and the Joint Council of All allergy, asthma, and Immunology.
Abstract: These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American Col- lege of Allergy, Asthma & Immunology (ACAAI); and the Joint Council of Allergy, Asthma & Immunology. The American Academy of Allergy, Asthma & Immunology and the American College of Allergy, Asthma & Immunology have jointly accepted responsibility for establishing ''Allergen immunotherapy: A practice parameter third update.'' This is a complete and com- prehensive document at the current time. The medical environ- ment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individ- ual, including those who served on the Joint Task Force, is authorizedtoprovideanofficial AAAAIorACAAIinterpretation ofthesepracticeparameters.Anyrequestforinformationaboutor an interpretation of these practice parameters by the AAAAI or the ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma & Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion. A current list of published practice parameters of the Joint Task Force on Practice ParametersforAllergyandImmunologycanbefoundinTableE1 in this article's Online Repository at www.jacionline.org. Disclosure ofpotentialconflictofinterest:L.Coxisaconsultant forGenentech/Novartis, Hollister-Stier, and Stallergenes; is a speaker for Novartis; has received research support from Stallergenes; is on the Board of Directors for the American Board of Allergy and Immunology; and is on the US Food and Drug Administration (FDA)'s Allergenic Product Advisory Committee. H. Nelson is a consultant for Merck and Planet Biopharmaceuticals, is a Data and Safety Monitoring Board member of DBV Technologies, and has received research support from ALK-AbellM. Nelson has re- ceivedresearchsupportfromtheDepartmentofDefense,isaspeakerfortheAmerican College of Allergy, Asthma & Immunology (ACAAI), and is a member of the FDA's AdvisoryCommitteeonAllergicProducts.R.Weberisonthespeakers'bureauforAs- traZeneca and Genentech, has received research support from Novartis and Glaxo- SmithKline, and is Committee Chair of the ACAAI. D. I. Bernstein is a consultant and on the advisory board for ALK America, is on the advisory board for Merck, and has received research support from Merck and Schering-Plough. J. Blessing- Moore is a speaker for Merck-Schering/AstraZeneca, Novartis, TEVA, and Meda Alcon and has received research support from Meda. D. A. Khan is a speaker for As- traZeneca and Merck, has received research support from the Vanberg Family Foun- dation and the Sellars Family Foundation, is Conjoint Board Review Chair for the ACAAI,andisapastpresidentoftheTexasAllergy,AsthmaandImmunologySociety. D. M. Lang is a speaker and consultant for GlaxoSmithKline; is a speaker for Astra- Zeneca, Merck, TEVA, Sanofi-Aventis, and Genentech/Novartis; and has received re- search support from Genentech/Novartis. R. A. Nicklas is a fellow for the ACAAI. J. Oppenheimer is a consultant and has provided lectures for AstraZeneca, Merck, and GlaxoSmithKline; and has received research support from AstraZeneca, Merck, Glax- oSmithKline, and Genentech. J. M. Portnoy is a speaker for Phadia, Merck, and CSL Behring; hasreceived researchsupportfromtheUSDepartment ofHousingandUrban Development;andisa board memberof theACAAI board of regents.S.L. Spector has received research support from Genentech, GlaxoSmithKline, Schering-Plough, Aventis, Novartis, Pharmaxis, Boehringer Ingelheim, AstraZeneca, Johnson & John- son, Xyzal, Alcon, Centocor, Sepracor, UCB, Amgen, Capnia, and IVAX. S. Tilles isaspeakerforAlcon; isontheadvisoryboard forALK,Ista,Merck,andStallergenes; has received research support from Alcon, Amgen, Amphastar, Astellas, Boehringer Ingelheim,Ception,Genentech,Icagen, MAP Pharma, MEDA, Merck, Novartis, Rox- ane, and Sepracor; is Associate Editor of Allergy Watchand Annals of Allergy; and is a task force member for the Joint Task Force for Practice Parameters. D. Wallace is a speaker and advisor for Alcon, is a speaker for Merck and Sanofi-Aventis, and is President-Elect of the ACAAI. The rest of the authors have declared that they have no conflict of interest.
1,055 citations
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TL;DR: It is concluded that PS1 is subject to endoproteolytic processing in vivo, and in brains of transgenic mice expressing human PS1, approximately 17 kDa and approximately 27 kDa PS1 derivatives accumulate to saturable levels, and at approximately 1:1 stoichiometry, independent of transgene-derived mRNA.
1,055 citations
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TL;DR: A Wner-grained analysis of the relationship between counterproductive work behavior and antecedents was conducted with the Wve-subscales (abuse toward others, production deviance, sabotage, theft, and withdrawal) taken from the 45-item Counterproductive Work Behavior Checklist, a measure that has been used in a number of prior studies as discussed by the authors.
1,054 citations
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TL;DR: In vivo models show that MDSCs directly disrupt the binding of specific peptide–major histocompatibility complex dimers to CD8-expressing T cells through nitration of tyrosines in a T-cell receptor (TCR)-CD8 complex, identifying a previously unknown mechanism of T- cell tolerance in cancer.
Abstract: Antigen-specific CD8+ T-cell tolerance, induced by myeloid-derived suppressor cells (MDSCs), is one of the main mechanisms of tumor escape. Using in vivo models, we show here that MDSCs directly disrupt the binding of specific peptide–major histocompatibility complex (pMHC) dimers to CD8-expressing T cells through nitration of tyrosines in a T-cell receptor (TCR)-CD8 complex. This process makes CD8-expressing T cells unable to bind pMHC and to respond to the specific peptide, although they retain their ability to respond to nonspecific stimulation. Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact. Molecular modeling suggests specific sites of nitration that might affect the conformational flexibility of TCR-CD8 and its interaction with pMHC. These data identify a previously unknown mechanism of T-cell tolerance in cancer that is also pertinent to many pathological conditions associated with accumulation of MDSCs.
1,049 citations
Authors
Showing all 34549 results
Name | H-index | Papers | Citations |
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David J. Hunter | 213 | 1836 | 207050 |
Aaron R. Folsom | 181 | 1118 | 134044 |
John Hardy | 177 | 1178 | 171694 |
David Cella | 156 | 1258 | 106402 |
Arul M. Chinnaiyan | 154 | 723 | 109538 |
Andrew D. Hamilton | 151 | 1334 | 105439 |
Charles B. Nemeroff | 149 | 979 | 90426 |
C. Ronald Kahn | 144 | 525 | 79809 |
Alexander Belyaev | 142 | 1895 | 100796 |
Tasuku Honjo | 141 | 712 | 88428 |
Weihong Tan | 140 | 892 | 67151 |
Alison Goate | 136 | 721 | 85846 |
Peter Kraft | 135 | 821 | 82116 |
Xiaodong Wang | 135 | 1573 | 117552 |
Lars Klareskog | 131 | 697 | 63281 |