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Institution

University of Vermont

EducationBurlington, 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.


Papers
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Journal ArticleDOI
TL;DR: None of the activities appear to have a requirement for Ca-2-+, and hence would not seem to be involved with active Ca- 2-+ transport in the typical manner, and the concept that the Mg-2+-ATPase and pyrophosphatase activities of matrix vesicles stem from one enzyme, namely, alkaline phosphatase is consistent.

279 citations

Journal ArticleDOI
TL;DR: This article presents high-yield information on the above-mentioned aspects of CI-AKI, primarily based on results of randomised controlled trials, meta-analyses, systematic reviews and international consensus guidelines.
Abstract: Contrast medium-induced acute kidney injury (CI-AKI) is a predominant cause of hospital-acquired renal insufficiency. With an increasing number of contrast medium-enhanced radiological procedures being performed in a rapidly increasing ageing population in the Western world, it is imperative that more attention is given to understand the aetiology of CI-AKI to devise novel diagnostic methods and to formulate effective prophylactic and therapeutic regimens to reduce its incidence and its associated morbidity and mortality. This article presents high-yield information on the above-mentioned aspects of CI-AKI, primarily based on results of randomised controlled trials, meta-analyses, systematic reviews and international consensus guidelines.

279 citations

Journal ArticleDOI
TL;DR: This review summarizes what is currently known about the time course and extent of the remodeling process, and how local vs. systemic factors influence its genesis, and focuses on upstream maternal vessels rather than spiral artery changes.
Abstract: Remodeling of the maternal uterine vasculature during pregnancy is a unique cardiovascular process that occurs in the adult and results in significant structural and functional changes in large and small arteries and veins, and in the creation of the placenta--a new fetomaternal vascular organ. This expansive, hypertrophic process results in increases in both lumen circumference and length, and is effected through a combination of tissue and cellular hypertrophy, endothelial and vascular smooth muscle hyperplasia, and matrix remodeling. This review summarizes what is currently known about the time course and extent of the remodeling process, and how local vs. systemic factors influence its genesis. The main focus is on upstream maternal vessels rather than spiral artery changes, although the latter are considered from the overall hemodynamic perspective. We also consider some of the underlying mechanisms and provide a hypothetical scenario that integrates our current knowledge. Abrogation of this adaptive vascular process is associated with several human gestational pathologies such as preeclampsia and intrauterine growth restriction (IUGR), which not only raise the risk of infant mortality and morbidity but are also a significant source of maternal mortality and susceptibility to cardiovascular and other diseases for both mother and neonate later in life.

279 citations

Journal ArticleDOI
TL;DR: In this article, a stochastic random chemistry (RC) algorithm is proposed to identify large collections of multiple (n-k) contingencies that initiate large cascading failures in a simulated power system.
Abstract: This paper describes a stochastic “Random Chemistry” (RC) algorithm to identify large collections of multiple (n-k) contingencies that initiate large cascading failures in a simulated power system. The method requires only O(log (n)) simulations per contingency identified, which is orders of magnitude faster than random search of this combinatorial space. We applied the method to a model of cascading failure in a power network with n=2896 branches and identify 148243 unique, minimal n-k branch contingencies (2 ≤ k ≤ 5) that cause large cascades, many of which would be missed by using pre-contingency flows, linearized line outage distribution factors, or performance indices as screening factors. Within each n-k collection, the frequency with which individual branches appear follows a power-law (or nearly so) distribution, indicating that a relatively small number of components contribute disproportionately to system vulnerability. The paper discusses various ways that RC generated collections of dangerous contingencies could be used in power systems planning and operations.

279 citations

Journal ArticleDOI
TL;DR: Insight gained from studies indicates that cFLIP and caspase-8 form a heterodimer that ultimately links T-cell-receptor signalling to activation of nuclear factor-κB through a complex that includes B-cell lymphoma 10 (BCL-10), mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1) and receptor-interacting protein 1 (RIP1).
Abstract: Cellular caspase-8 (FLICE)-like inhibitory protein (cFLIP) was originally identified as an inhibitor of death-receptor signalling through competition with caspase-8 for recruitment to FAS-associated via death domain (FADD). More recently, it has been determined that both cFLIP and caspase-8 are required for the survival and proliferation of T cells following T-cell-receptor stimulation. This paradoxical finding launched new investigations of how these molecules might connect with signalling pathways that link to cell survival and growth following antigen-receptor activation. As discussed in this Review, insight gained from these studies indicates that cFLIP and caspase-8 form a heterodimer that ultimately links T-cell-receptor signalling to activation of nuclear factor-kappaB through a complex that includes B-cell lymphoma 10 (BCL-10), mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1) and receptor-interacting protein 1 (RIP1).

279 citations


Authors

Showing all 17727 results

NameH-indexPapersCitations
Albert Hofman2672530321405
Ralph B. D'Agostino2261287229636
George Davey Smith2242540248373
Stephen V. Faraone1881427140298
Valentin Fuster1791462185164
Dennis J. Selkoe177607145825
Anders Björklund16576984268
Alfred L. Goldberg15647488296
Christopher P. Cannon1511118108906
Debbie A Lawlor1471114101123
Roger J. Davis147498103478
Andrew S. Levey144600156845
Jonathan G. Seidman13756389782
Yu Huang136149289209
Christine E. Seidman13451967895
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202359
2022177
20211,840
20201,762
20191,653
20181,569