Institution
University of Virginia
Education•Charlottesville, Virginia, United States•
About: University of Virginia is a education organization based out in Charlottesville, Virginia, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 52543 authors who have published 113268 publications receiving 5220506 citations. The organization is also known as: U of V & UVa.
Topics: Population, Poison control, Galaxy, Context (language use), Medicine
Papers published on a yearly basis
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TL;DR: The many uses of data on biological variation in clinical chemistry are reviewed, including setting analytical goals, deciding the significance of changes in serial results from an individual, evaluating the utility of conventional population-based reference values in patient management, and other applications.
Abstract: Most clinical chemical analytes vary in a random manner around a homeostatic set point. Replicate analyses of a series of specimens collected from a group of subjects allows estimation of analytical, within and between subject components of variation. The preferred experimental procedures and statistical methods for evaluation of data and analysis of variance are described; a detailed example is provided in the Appendix. The many uses of data on biological variation in clinical chemistry are reviewed, including setting analytical goals, deciding the significance of changes in serial results from an individual, evaluating the utility of conventional population-based reference values in patient management, and other applications.
814 citations
French Institute of Health and Medical Research1, Pierre-and-Marie-Curie University2, San Antonio Military Medical Center3, University of Antwerp4, Paris Diderot University5, University of Melbourne6, Catholic University of Leuven7, University of Angers8, Duke University9, University of Virginia10, Radboud University Nijmegen11, Newcastle University12, university of lille13, Virginia Commonwealth University14, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico15, Semmelweis University16
TL;DR: A post-hoc analysis of data from trial of patients with NASH showed that elafibranor (120 mg/d for 1 year) resolved NASH without fibrosis worsening, based on a modified definition, in the intention-to-treat analysis and in patients with moderate or severe NASH.
813 citations
Genentech1, University of Gothenburg2, Royal Children's Hospital3, Eli Lilly and Company4, Aarhus University5, Boston Children's Hospital6, University of North Carolina at Chapel Hill7, University of Southern California8, Hokkaido University9, University of Turin10, Stanford University11, Garvan Institute of Medical Research12, Novo Nordisk13, National Scientific and Technical Research Council14, Ferring Pharmaceuticals15, Pfizer16, Food and Drug Administration17, University of Bern18, Emory University19, University of Tübingen20, Medical Research Council21, Oregon Health & Science University22, University of Tennessee Health Science Center23, Yeshiva University24, University of Pisa25, Royal London Hospital26, Ludwig Maximilian University of Munich27, University of Virginia28, Kaplan Medical Center29
810 citations
Paris Descartes University1, Institut Gustave Roussy2, Mount Sinai Hospital3, University of Texas Southwestern Medical Center4, University of Kiel5, Thomas Jefferson University6, Seconda Università degli Studi di Napoli7, University of Toronto8, University of Massachusetts Medical School9, Louisiana State University10, Ghent University11, Flanders Institute for Biotechnology12, Queen Mary University of London13, Cancer Research UK14, Roswell Park Cancer Institute15, Karolinska Institutet16, University of Freiburg17, University of California, San Francisco18, Buck Institute for Research on Aging19, Université Paris-Saclay20, French Institute of Health and Medical Research21, University College London22, University of Rome Tor Vergata23, Northwestern University24, Memorial Sloan Kettering Cancer Center25, National Institutes of Health26, Technion – Israel Institute of Technology27, Johns Hopkins University28, University of Chieti-Pescara29, University of Ulm30, Genentech31, New York University32, Pennsylvania State University33, University of Salento34, Yale University35, Goethe University Frankfurt36, University of Burgundy37, Pasteur Institute38, University of Strasbourg39, University of Zurich40, University of Tokyo41, Technische Universität München42, University of Bern43, University of Michigan44, Medical Research Council45, University of Adelaide46, University of South Australia47, Medical University of South Carolina48, University of Texas at Dallas49, Howard Hughes Medical Institute50, St. John's University51, University of Oviedo52, University of Graz53, Istituto Superiore di Sanità54, Katholieke Universiteit Leuven55, Trinity College, Dublin56, University of Geneva57, University of Amsterdam58, Stony Brook University59, University of Washington60, University of Ferrara61, Royal College of Surgeons in Ireland62, La Trobe University63, University of Buenos Aires64, University of Virginia65, University of Padua66, University of Lisbon67, University of Cambridge68, University of Würzburg69, Soochow University (Suzhou)70, Columbia University71, University of Glasgow72, Foundation for Research & Technology – Hellas73, University of Crete74, Innsbruck Medical University75, Carlos III Health Institute76, Rutgers University77, University of Minnesota78, Harvard University79, City University of New York80, Moscow State University81
TL;DR: The Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
Abstract: Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
809 citations
809 citations
Authors
Showing all 53083 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Joan Massagué | 189 | 408 | 149951 |
| Michael Rutter | 188 | 676 | 151592 |
| Gordon B. Mills | 187 | 1273 | 186451 |
| Ralph Weissleder | 184 | 1160 | 142508 |
| Gonçalo R. Abecasis | 179 | 595 | 230323 |
| Jie Zhang | 178 | 4857 | 221720 |
| John R. Yates | 177 | 1036 | 129029 |
| John A. Rogers | 177 | 1341 | 127390 |
| Bradley Cox | 169 | 2150 | 156200 |
| Mika Kivimäki | 166 | 1515 | 141468 |
| Hongfang Liu | 166 | 2356 | 156290 |
| Carl W. Cotman | 165 | 809 | 105323 |
| Ralph A. DeFronzo | 160 | 759 | 132993 |
| Elio Riboli | 158 | 1136 | 110499 |
| Dan R. Littman | 157 | 426 | 107164 |