Institution
University of Vermont
Education•Burlington, Vermont, United States•
About: University of Vermont is a education organization based out in Burlington, Vermont, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 17592 authors who have published 38251 publications receiving 1609874 citations. The organization is also known as: UVM & University of Vermont and State Agricultural College.
Topics: Population, Poison control, Breast cancer, Myosin, Anxiety
Papers published on a yearly basis
Papers
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TL;DR: It is proposed that frequency and amplitude modulation of Ca(2+) sparks by contractile and relaxant agents is an important mechanism to regulate smooth muscle function.
Abstract: Local intracellular Ca(2+) transients, termed Ca(2+) sparks, are caused by the coordinated opening of a cluster of ryanodine-sensitive Ca(2+) release channels in the sarcoplasmic reticulum of smooth muscle cells. Ca(2+) sparks are activated by Ca(2+) entry through dihydropyridine-sensitive voltage-dependent Ca(2+) channels, although the precise mechanisms of communication of Ca(2+) entry to Ca(2+) spark activation are not clear in smooth muscle. Ca(2+) sparks act as a positive-feedback element to increase smooth muscle contractility, directly by contributing to the global cytoplasmic Ca(2+) concentration ([Ca(2+)]) and indirectly by increasing Ca(2+) entry through membrane potential depolarization, caused by activation of Ca(2+) spark-activated Cl(-) channels. Ca(2+) sparks also have a profound negative-feedback effect on contractility by decreasing Ca(2+) entry through membrane potential hyperpolarization, caused by activation of large-conductance, Ca(2+)-sensitive K(+) channels. In this review, the roles of Ca(2+) sparks in positive- and negative-feedback regulation of smooth muscle function are explored. We also propose that frequency and amplitude modulation of Ca(2+) sparks by contractile and relaxant agents is an important mechanism to regulate smooth muscle function.
616 citations
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TL;DR: It is likely that knowledge gained on how inflammation affects health in HIV disease could have implications for the understanding of other chronic inflammatory diseases and the biology of aging.
616 citations
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TL;DR: This paper used existing theory and research on general stress and coping responses to describe responses to stigma-related stressors and discuss the adaptiveness of these responses, including emotional, cognitive, biological, and behavioral responses.
Abstract: Stigmatized people have a vast array of responses to stressors resulting from their devalued social status, including emotional, cognitive, biological, and behavioral responses. This article uses existing theory and research on general stress and coping responses to describe responses to stigma-related stressors and to discuss the adaptiveness of these responses.
616 citations
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TL;DR: It is demonstrated that NO and a membrane-permeable analogue of cGMP can activate KCa channels in on-cell patches approximately twofold and cG MP-PK, in the presence of ATP andcGMP added directly to the intracellular surface of inside-out patches, increases channel activity by approximately eightfold.
Abstract: Guanosine-3',5'-cyclic monophosphate (cGMP)-dependent protein kinase (cGMP-PK) plays a central role in the mediation of the vasodilator response to nitric oxide (NO) and other nitrovasodilators. It is unclear whether cGMP-PK affects calcium-activated potassium channels (KCa channels) or any other type of ion channel in smooth muscle. We provide here the first direct evidence that cGMP-PK can activate KCa channels in arterial smooth muscle cells. We demonstrate that NO and a membrane-permeable analogue of cGMP can activate KCa channels in on-cell patches approximately twofold. Furthermore, cGMP-PK, in the presence of ATP and cGMP added directly to the intracellular surface of inside-out patches, increases channel activity by approximately eightfold. These results suggest that cGMP-PK-mediated activation of KCa channels may contribute to the actions of NO and other nitrovasodilators.
613 citations
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TL;DR: Tumor cell lines with acquired resistance to the antineoplastic agent cis-diamminedichloroplatinum(II) overexpressed metallothionein and demonstrated cross-resistance to alkylating agents such as chlorambucil and melphalan.
Abstract: Resistance to antineoplastic agents is the major obstacle to curative therapy of cancer. Tumor cell lines with acquired resistance to the antineoplastic agent cis-diamminedichloroplatinum(II) overexpressed metallothionein and demonstrated cross-resistance to alkylating agents such as chlorambucil and melphalan. Human carcinoma cells that maintained high levels of metallothionein because of chronic exposure to heavy metals were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil. Furthermore, cells transfected with bovine papilloma virus expression vectors containing DNA encoding human metallothionein-IIA were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil but not to 5-fluorouracil or vincristine. Thus, overexpression of metallothionein represents one mechanism of resistance to a subset of clinically important anticancer drugs.
613 citations
Authors
Showing all 17727 results
Name | H-index | Papers | Citations |
---|---|---|---|
Albert Hofman | 267 | 2530 | 321405 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
George Davey Smith | 224 | 2540 | 248373 |
Stephen V. Faraone | 188 | 1427 | 140298 |
Valentin Fuster | 179 | 1462 | 185164 |
Dennis J. Selkoe | 177 | 607 | 145825 |
Anders Björklund | 165 | 769 | 84268 |
Alfred L. Goldberg | 156 | 474 | 88296 |
Christopher P. Cannon | 151 | 1118 | 108906 |
Debbie A Lawlor | 147 | 1114 | 101123 |
Roger J. Davis | 147 | 498 | 103478 |
Andrew S. Levey | 144 | 600 | 156845 |
Jonathan G. Seidman | 137 | 563 | 89782 |
Yu Huang | 136 | 1492 | 89209 |
Christine E. Seidman | 134 | 519 | 67895 |