Institution
Emory University
Education•Atlanta, Georgia, United States•
About: Emory University is a education organization based out in Atlanta, Georgia, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 51959 authors who have published 122469 publications receiving 6010698 citations.
Topics: Population, Medicine, Cancer, Health care, Poison control
Papers published on a yearly basis
Papers
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Health Effects Institute1, University of British Columbia2, Health Canada3, St George's, University of London4, Institute for Health Metrics and Evaluation5, Sri Ramachandra University6, Utrecht University7, Public Health Foundation of India8, Auckland University of Technology9, United States Environmental Protection Agency10, University of Bath11, Fudan University12, University of Queensland13, Emory University14, Dalhousie University15, Queensland University of Technology16, Brigham Young University17, International Agency for Research on Cancer18
TL;DR: In this paper, the authors explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels, and estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using nonlinear exposure-response functions spanning the global range of exposure.
3,960 citations
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TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
Abstract: Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli.
3,942 citations
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Uppsala University1, Karolinska Institutet2, University of Glasgow3, University College London4, University of Oxford5, King's College London6, University of Exeter7, Black Dog Institute8, University of California, Irvine9, University of Cambridge10, Swansea University11, Guy's and St Thomas' NHS Foundation Trust12, UCL Institute of Child Health13, St George's, University of London14, Emory University15, University of Bristol16, Academy of Medical Sciences, United Kingdom17
TL;DR: There is an urgent need for research to address how mental health consequences for vulnerable groups can be mitigated under pandemic conditions, and on the impact of repeated media consumption and health messaging around COVID-19.
3,909 citations
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TL;DR: In this paper, the authors present a general strain theory of crime and delinquency that is capable of overcoming the criticisms of previous strain theories, and argue that strain has a central role to play in explanations of crime/delinquency, but that the theory has to be substantially revised to play this role.
Abstract: This paper presents a general strain theory of crime and delinquency that is capable of overcoming the criticisms of previous strain theories. In the first section, strain theory is distinguished from social control and differential association/social learning theory. In the second section, the three major types of strain are described: (1) strain as the actual or anticipated failure to achieve positively valued goals, (2) strain as the actual or anticipated removal of positively valued stimuli, and (3) strain as the actual or anticipated presentation of negatively valued stimuli. In the third section, guidelines for the measurement of strain are presented. And in the fourth section, the major adaptations to strain are described, and thcwe factors influencing the choice of delinquent versus nondelinquent adaptations are discussed. After dominating deviance research in the 196Os, strain theory came under heavy attack in the 1970s (Bernard, 1984; Cole, 1975), with several prominent researchers suggesting that the theory be abandoned (Hirschi, 1969; Kornhauser, 1978). Strain theory has survived those attacks, but its influence is much diminished (see Agnew, 1985a; Bernard, 1984; Farnworth and Leiber, 1989). In particular, variables derived from strain theory now play a very limited role in explanations of crime/delinquency. Several recent causal models of delinquency, in fact, either entirely exchde strain variables or assign them a small role (e.g., Elliott et al., 1985; Johnson, 1979; Massey and Krohn, 1986; Thornberry, 1987; Tonry et al., 1991). Causal models of crime/delinquency are dominated, instead, by variables derived from differential association/social learning theory and social control theory. This paper argues that strain theory has a central role to play in explanations of crime/delinquency, but that the theory has to be substantially revised to play this role. Most empirical studies of strain theory continue to rely on the strain models developed by Merton (1938), A. Cohen (1955), and Cloward and Ohlin (1960). In recent years, however, a wealth of research in several fields has questioned certain of the assumptions underlying those theories and pointed to new directions for the development of strain theory. Most notable in this area is the research on stress in medical sociology and psychology, on equity/justice in social psychology, and on aggression in psychology-particularly recent versions of frustration-aggression and social
3,854 citations
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TL;DR: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone, and as the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
Abstract: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO(.)) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension, hypercholesterolemia, diabetes, and cigarette smoking. Loss of NO(.) associated with these traditional risk factors may in part explain why they predispose to atherosclerosis. Among many enzymatic systems that are capable of producing ROS, xanthine oxidase, NADH/NADPH oxidase, and uncoupled endothelial nitric oxide synthase have been extensively studied in vascular cells. As the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
3,756 citations
Authors
Showing all 52622 results
Name | H-index | Papers | Citations |
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Younan Xia | 216 | 943 | 175757 |
Eric J. Topol | 193 | 1373 | 151025 |
Bernard Rosner | 190 | 1162 | 147661 |
Paul G. Richardson | 183 | 1533 | 155912 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Dennis S. Charney | 179 | 802 | 122408 |
Joseph Biederman | 179 | 1012 | 117440 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
David A. Weitz | 178 | 1038 | 114182 |
Lei Jiang | 170 | 2244 | 135205 |
William J. Sandborn | 162 | 1317 | 108564 |
Stephen J. Elledge | 162 | 406 | 112878 |
Ali H. Mokdad | 156 | 634 | 160599 |
Michael Tomasello | 155 | 797 | 93361 |
Don W. Cleveland | 152 | 444 | 84737 |