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
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TL;DR: The diverse procedures used to assess internalizing/externalizing problems pose challenges for clinical and research applications and recommendations are provided for using assessment instruments supported by published standardization, reliability, validity, and normative data to advance clinical services and research.
Abstract: Objective More than 75,000 articles have been published on internalizing and externalizing problems. To advance clinical and research applications of internalizing/externalizing concepts and data, our objectives were as follows: to provide an overview of recent research on internalizing/externalizing problems assessed at ages 1½ to 18 years; to identify issues raised by methods for assessing such problems; and to develop recommendations for more precise, consistent, informative, and productive assessment of such problems. Method A total of 4,870 peer-reviewed articles published from January 1, 2012 through December 31, 2014 were systematically reviewed and identified by the search terms "internalizing" or "externalizing," followed by detailed coding of 693 articles that reported use of measures meeting criteria for methodologically sound assessment of internalizing/externalizing problems. Results Many articles reported data based on measures that did not meet criteria for methodologically sound assessment of internalizing/externalizing problems. The 693 articles that used measures meeting criteria for methodological soundness and that qualified for detailed coding reported findings for 649,457 children living in 65 societies on all inhabited continents. Data were obtained from parents, teachers, children, clinicians, caregivers, and others. Samples included general population, clinical, school, at-risk, multicultural, welfare, and various ethnic/racial and socioeconomic groups. Many analytic methods were used to test associations of diverse variables with internalizing/externalizing problems. Conclusion The diverse procedures used to assess internalizing/externalizing problems pose challenges for clinical and research applications. To meet the challenges, recommendations are provided for using assessment instruments supported by published standardization, reliability, validity, and normative data to advance clinical services and research.
279 citations
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TL;DR: Results indicate that endothelial SK3 channels exert a profound, tonic, hyperpolarizing influence in resistance arteries and suggest that the level of SK3 channel expression in endothelial cells is a fundamental determinant of vascular tone and blood pressure.
Abstract: The endothelium is a critical regulator of vascular tone, and dysfunction of the endothelium contributes to numerous cardiovascular pathologies. Recent studies suggest that apamin-sensitive, small-conductance, Ca 2+ -activated K + channels may play an important role in active endothelium-dependent vasodilations, and expression of these channels may be altered in disease states characterized by vascular dysfunction. Here, we used a transgenic mouse (SK3 T/T ) in which SK3 expression levels can be manipulated with dietary doxycycline (DOX) to test the hypothesis that the level of expression of the SK subunit, SK3, in endothelial cells alters arterial function and blood pressure. SK3 protein was elevated in small mesenteric arteries from SK3 T/T mice compared with wild-type mice and was greatly suppressed by dietary DOX. SK3 was detected in the endothelium and not in the smooth muscle by immunohistochemistry. In whole-cell patch-clamp experiments, SK currents in endothelial cells from SK3 T/T mice were almost completely suppressed by dietary DOX. In intact arteries, SK3 channels contributed to sustained hyperpolarization of the endothelial membrane potential, which was communicated to the arterial smooth muscle. Pressure- and phenylephrine-induced constrictions of SK3 T/T arteries were substantially enhanced by treatment with apamin, suppression of SK3 expression with DOX, or removal of the endothelium. In addition, suppression of SK3 expression caused a pronounced and reversible elevation of blood pressure. These results indicate that endothelial SK3 channels exert a profound, tonic, hyperpolarizing influence in resistance arteries and suggest that the level of SK3 channel expression in endothelial cells is a fundamental determinant of vascular tone and blood pressure.
278 citations
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University of Florida1, University of Alaska Fairbanks2, University of Vermont3, Max Planck Society4, Bowdoin College5, CSIRO Marine and Atmospheric Research6, Florida State University7, Lund University8, Centre national de la recherche scientifique9, Idaho State University10, University of California11, United States Geological Survey12, Oak Ridge National Laboratory13, Stockholm University14, Argonne National Laboratory15, Lawrence Berkeley National Laboratory16, National Center for Atmospheric Research17, National Park Service18, Cooperative Institute for Research in Environmental Sciences19, University of Oxford20, University of Guelph21, Los Alamos National Laboratory22
TL;DR: In this article, the authors used a survey to quantify variability in the perception of the vulnerability of permafrost C to climate change and found that approximately 1700 Pg of soil carbon (C) are stored in the northern circumpolar permafure zone, more than twice as much C than in the atmosphere.
Abstract: Approximately 1700 Pg of soil carbon (C) are stored in the northern circumpolar permafrost zone, more than twice as much C than in the atmosphere. The overall amount, rate, and form of C released to the atmosphere in a warmer world will influence the strength of the permafrost C feedback to climate change. We used a survey to quantify variability in the perception of the vulnerability of permafrost C to climate change. Experts were asked to provide quantitative estimates of permafrost change in response to four scenarios of warming. For the highest warming scenario (RCP 8.5), experts hypothesized that C release from permafrost zone soils could be 19–45 Pg C by 2040, 162–288 Pg C by 2100, and 381–616 Pg C by 2300 in CO2 equivalent using 100-year CH4 global warming potential (GWP). These values become 50 % larger using 20-year CH4 GWP, with a third to a half of expected climate forcing coming from CH4 even though CH4 was only 2.3 % of the expected C release. Experts projected that two-thirds of this release could be avoided under the lowest warming scenario (RCP 2.6). These results highlight the potential risk from permafrost thaw and serve to frame a hypothesis about the magnitude of this feedback to climate change. However, the level of emissions proposed here are unlikely to overshadow the impact of fossil fuel burning, which will continue to be the main source of C emissions and climate forcing.
278 citations
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TL;DR: The shape of the menisci and the orientation of the collagen fibers are optimal for weight bearing and shock absorption and an attempt should be made to save viable meniscus when performing knee surgery.
278 citations
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TL;DR: The findings provide a mechanistic rationale for the paradoxical inability of asbestos to transform HM in vitro, elucidate and underscore the role of TNF-α in asbestos pathogenesis in humans, and identify potential molecular targets for anti-MM prevention and therapy.
Abstract: Asbestos is the main cause of human malignant mesothelioma (MM) In vivo, macrophages phagocytize asbestos and, in response, release TNF-alpha and other cytokines that contribute to carcinogenesis through unknown mechanisms In vitro, asbestos does not induce transformation of primary human mesothelial cells (HM); instead, asbestos is very cytotoxic to HM, causing extensive cell death This finding raised an apparent paradox: How can asbestos cause MM if HM exposed to asbestos die? We found that asbestos induced the secretion of TNF-alpha and the expression of TNF-alpha receptor I in HM Treatment of HM with TNF-alpha significantly reduced asbestos cytotoxicity Through numerous technical approaches, including chemical inhibitors and small interfering RNA strategies, we demonstrate that, in HM, TNF-alpha activates NF-kappaB and that NF-kappaB activation leads to HM survival and resistance to the cytotoxic effects of asbestos Our data show a critical role for TNF-alpha and NF-kappaB signaling in mediating HM responses to asbestos TNF-alpha signaling through NF-kappaB-dependent mechanisms increases the percent of HM that survives asbestos exposure, thus increasing the pool of asbestos-damaged HM that are susceptible to malignant transformation Cytogenetics supported this hypothesis, showing only rare, aberrant metaphases in HM exposed to asbestos and an increased mitotic rate with fewer irregular metaphases in HM exposed to both TNF-alpha and asbestos Our findings provide a mechanistic rationale for the paradoxical inability of asbestos to transform HM in vitro, elucidate and underscore the role of TNF-alpha in asbestos pathogenesis in humans, and identify potential molecular targets for anti-MM prevention and therapy
278 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 |