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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University of Minnesota1, Stony Brook University2, University of Notre Dame3, Macquarie University4, University of North Texas5, University at Buffalo6, University of Kentucky7, University of Vermont8, University of Toronto9, University of South Florida10, University of Maryland, Baltimore11, Southern Methodist University12, University of Hawaii13, College of William & Mary14, Ghent University15, University of Utah16, University of Michigan17, Columbia University18, University of Kansas19, Pennsylvania State University20, University of California, Davis21, Georgia State University22, University of Iowa23, University of Georgia24, Texas A&M University25, Oklahoma State University–Stillwater26, University of Groningen27, University of Liverpool28, Florida State University29, Uniformed Services University of the Health Sciences30, Maastricht University31, Bryn Mawr College32, Purdue University33, University of Otago34, University of Maryland, College Park35, University of Arizona36, University of New South Wales37, Northwestern University38, Emory University39, Oak Ridge National Laboratory40, University of Pittsburgh41, Vanderbilt University42
TL;DR: The aims and current foci of the HiTOP Consortium, a group of 70 investigators working together to study empirical classification of psychopathology, are described, which pertain to continued research on the empirical organization of psychopathological constructs; the connection between personality and psychopathology; the utility of empirically based psychopathology constructs in both research and the clinic.
308 citations
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University of California, Irvine1, Columbia University2, Ohio State University3, McGill University4, University of California, Los Angeles5, University at Buffalo6, New York University7, Icahn School of Medicine at Mount Sinai8, University of Vermont9, University of Illinois at Chicago10, McGill University Health Centre11, Duke University12, Brookhaven National Laboratory13
TL;DR: Stimulant-naïve school-age children with Combined type attention-deficit/hyperactivity disorder were, as a group, larger than expected from norms before treatment but show stimulant-related decreases in growth rates after initiation of treatment, which appeared to reach asymptotes within 3 years without evidence of growth rebound.
Abstract: Objective: To evaluate the hypothesis of stimulant medication effect on physical growth in the follow-up phase of the Multimodal Treatment Study of Children With ADHD. Method: Naturalistic subgroups were established based on patterns of treatment with stimulant medication at baseline, 14-, 24-, and 36-month assessments: not medicated ( n = 65), newly medicated ( n = 88), consistently medicated ( n = 70), and inconsistently medicated ( n = 147). Analysis of variance was used to evaluate effects of subgroup and assessment time on measures of relative size ( z scores) obtained from growth norms. Results: The subgroup × assessment time interaction was significant for z height ( p z weight ( p z scores significantly >0 at baseline. The newly medicated subgroup showed decreases in relative size that reached asymptotes by the 36-month assessment, when this group showed average growth of 2.0 cm and 2.7 kg less than the not medicated subgroup, which showed slight increases in relative size. Conclusions: Stimulant-naive school-age children with Combined type attention-deficit/hyperactivity disorder were, as a group, larger than expected from norms before treatment but show stimulant-related decreases in growth rates after initiation of treatment, which appeared to reach asymptotes within 3 years without evidence of growth rebound.
307 citations
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TL;DR: Using functional evidence from cardiac myocytes, and histological evidence from smooth muscle, it is explored whether Ca2+ channels, RyR channels, and KCa channels function as a coupled unit, through Ca2- and voltage, to regulate arterial smooth muscle membrane potential and vascular tone.
Abstract: Local calcium transients ('Ca2+ sparks') are thought to be elementary Ca2+ signals in heart, skeletal and smooth muscle cells. Ca2+ sparks result from the opening of a single, or the coordinated opening of many, tightly clustered ryanodine receptor (RyR) channels in the sarcoplasmic reticulum (SR). In arterial smooth muscle, Ca2+ sparks appear to be involved in opposing the tonic contraction of the blood vessel. Intravascular pressure causes a graded membrane potential depolarization to approximately -40 mV, an elevation of arterial wall [Ca2+]i and contraction ('myogenic tone') of arteries. Ca2+ sparks activate calcium-sensitive K+ (KCa) channels in the sarcolemmal membrane to cause membrane hyperpolarization, which opposes the pressure induced depolarization. Thus, inhibition of Ca2+ sparks by ryanodine, or of KCa channels by iberiotoxin, leads to membrane depolarization, activation of L-type voltage-gated Ca2+ channels, and vasoconstriction. Conversely, activation of Ca2+ sparks can lead to vasodilation through activation of KCa channels. Our recent work is aimed at studying the properties and roles of Ca2+ sparks in the regulation of arterial smooth muscle function. The modulation of Ca2+ spark frequency and amplitude by membrane potential, cyclic nucleotides and protein kinase C will be explored. The role of local Ca2+ entry through voltage-dependent Ca2+ channels in the regulation of Ca2+ spark properties will also be examined. Finally, using functional evidence from cardiac myocytes, and histological evidence from smooth muscle, we shall explore whether Ca2+ channels, RyR channels, and KCa channels function as a coupled unit, through Ca2+ and voltage, to regulate arterial smooth muscle membrane potential and vascular tone.
307 citations
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University of Vermont1, Bryn Mawr College2, University of Helsinki3, University of Southern Denmark4, Columbia University5, Babeș-Bolyai University6, University of Cologne7, Ankara University8, University of Barcelona9, Chuo University10, University of Missouri11, The Chinese University of Hong Kong12, Yonsei University13, University of Adelaide14, University of Zurich15, Medical University of Warsaw16, Mykolas Romeris University17, Erasmus University Medical Center18
TL;DR: Initial support for the taxonomic generalizability of the 8-syndrome model across very diverse societies, both genders, and 2 age groups is provided.
Abstract: As a basis for theories of psychopathology, clinical psychology and related disciplines need sound taxonomies that are generalizable across diverse populations. To test the generalizability of a statistically derived 8-syndrome taxonomic model for youth psychopathology, confirmatory factor analyses (CFAs) were performed on the Youth Self-Report (T. M. Achenbach & L. A. Rescorla, 2001) completed by 30,243 youths 11-18 years old from 23 societies. The 8-syndrome taxonomic model met criteria for good fit to the data from each society. This was consistent with findings for the parent-completed Child Behavior Checklist (Achenbach & Rescorla, 2001) and the teacher-completed Teacher's Report Form (Achenbach & Rescorla, 2001) from many societies. Separate CFAs by gender and age group supported the 8-syndrome model for boys and girls and for younger and older youths within individual societies. The findings provide initial support for the taxonomic generalizability of the 8-syndrome model across very diverse societies, both genders, and 2 age groups.
306 citations
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Northwestern University1, University of Chicago2, University of Oxford3, University of Warwick4, Hammersmith Hospital5, Broad Institute6, University of Utah7, National and Kapodistrian University of Athens8, Aristotle University of Thessaloniki9, Cedars-Sinai Medical Center10, Georgia Regents University11, Medical College of Wisconsin12, Texas Biomedical Research Institute13, Karolinska Institutet14, Pennsylvania State University15, University of Colorado Denver16, Duke University17, Stanford University18, University of Pennsylvania19, University of Alabama20, University of Texas Health Science Center at San Antonio21, University of Texas Southwestern Medical Center22, Baylor College of Medicine23, University of Vermont24, University of Michigan25, Wayne State University26, National Institutes of Health27, University of Pittsburgh28, University of California, San Francisco29, University of Virginia30, Yale University31, Virginia Commonwealth University32, Rutgers University33, State University of New York Upstate Medical University34, Carolinas Medical Center35
TL;DR: Common genetic susceptibility loci in European ancestry women for the National Institutes of Health PCOS phenotype are identified, which confers the highest risk for metabolic morbidities, as well as reproductive hormone levels, and implicate neuroendocrine changes in disease pathogenesis.
Abstract: Polycystic ovary syndrome (PCOS) is a common, highly heritable complex disorder of unknown aetiology characterized by hyperandrogenism, chronic anovulation and defects in glucose homeostasis. Increased luteinizing hormone relative to follicle-stimulating hormone secretion, insulin resistance and developmental exposure to androgens are hypothesized to play a causal role in PCOS. Here we map common genetic susceptibility loci in European ancestry women for the National Institutes of Health PCOS phenotype, which confers the highest risk for metabolic morbidities, as well as reproductive hormone levels. Three loci reach genome-wide significance in the case–control meta-analysis, two novel loci mapping to chr 8p32.1 and chr 11p14.1, and a chr 9q22.32 locus previously found in Chinese PCOS. The same chr 11p14.1 SNP, rs11031006, in the region of the follicle-stimulating hormone B polypeptide (FSHB) gene strongly associates with PCOS diagnosis and luteinizing hormone levels. These findings implicate neuroendocrine changes in disease pathogenesis.
306 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 |