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Institution

Emory University

EducationAtlanta, 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.


Papers
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Journal ArticleDOI
TL;DR: Although related to mental illness, positive mental health is a distinct indicator of mental well-being that is reliably assessed with the MHC-SF, and this article draws on data of the LISS panel of CentERdata, a representative panel for Longitudinal Internet Studies for the Social Sciences.
Abstract: There is a growing consensus that mental health is not merely the absence of mental illness, but it also includes the presence of positive feelings (emotional well-being) and positive functioning in individual life (psychological well-being) and community life (social well-being). We examined the structure, reliability, convergent validity, and discriminant validity of the Mental Health Continuum-Short Form (MHC-SF), a new self-report questionnaire for positive mental health assessment. We expected that the MHC-SF is reliable and valid, and that mental health and mental illness are 2 related but distinct continua. This article draws on data of the LISS panel of CentERdata, a representative panel for Longitudinal Internet Studies for the Social Sciences (N = 1,662). Results revealed high internal and moderate test-retest reliability. Confirmatory factor analysis (CFA) confirmed the 3-factor structure in emotional, psychological, and social well-being. These subscales correlated well with corresponding aspects of well-being and functioning, showing convergent validity. CFA supported the hypothesis of 2 separate yet related factors for mental health and mental illness, showing discriminant validity. Although related to mental illness, positive mental health is a distinct indicator of mental well-being that is reliably assessed with the MHC-SF

956 citations

Journal ArticleDOI
TL;DR: The involvement of oxidative damage in rotenone toxicity is demonstrated and antioxidant therapies for Parkinson's disease are supported, using three model systems of increasing complexity.
Abstract: Exposure of rats to the pesticide and complex I inhibitor rotenone reproduces features of Parkinson's disease, including selective nigrostriatal dopaminergic degeneration and alpha-synuclein-positive cytoplasmic inclusions (Betarbet et al., 2000; Sherer et al., 2003). Here, we examined mechanisms of rotenone toxicity using three model systems. In SK-N-MC human neuroblastoma cells, rotenone (10 nm to 1 microm) caused dose-dependent ATP depletion, oxidative damage, and death. To determine the molecular site of action of rotenone, cells were transfected with the rotenone-insensitive single-subunit NADH dehydrogenase of Saccharomyces cerevisiae (NDI1), which incorporates into the mammalian ETC and acts as a "replacement" for endogenous complex I. In response to rotenone, NDI1-transfected cells did not show mitochondrial impairment, oxidative damage, or death, demonstrating that these effects of rotenone were caused by specific interactions at complex I. Although rotenone caused modest ATP depletion, equivalent ATP loss induced by 2-deoxyglucose was without toxicity, arguing that bioenergetic defects were not responsible for cell death. In contrast, reducing oxidative damage with antioxidants, or by NDI1 transfection, blocked cell death. To determine the relevance of rotenone-induced oxidative damage to dopaminergic neuronal death, we used a chronic midbrain slice culture model. In this system, rotenone caused oxidative damage and dopaminergic neuronal loss, effects blocked by alpha-tocopherol. Finally, brains from rotenone-treated animals demonstrated oxidative damage, most notably in midbrain and olfactory bulb, dopaminergic regions affected by Parkinson's disease. These results, using three models of increasing complexity, demonstrate the involvement of oxidative damage in rotenone toxicity and support the evaluation of antioxidant therapies for Parkinson's disease.

956 citations

Journal ArticleDOI
Joseph Henrich1
TL;DR: It is explained how, in contrast to non-cultural species, the details of the authors' evolved cultural learning capacities create the conditions for the cultural evolution of prosociality, and how natural selection is likely to favor prosocial genes that would not be expected in a purely genetic approach.
Abstract: In constructing improved models of human behavior, both experimental and behavioral economists have increasingly turned to evolutionary theory for insights into human psychology and preferences. Unfortunately, the existing genetic evolutionary approaches can explain neither the degree of prosociality (altruism and altruistic punishment) observed in humans, nor the patterns of variation in these behaviors across different behavioral domains and social groups. Ongoing misunderstandings about why certain models work, what they predict, and what the place is of “group selection” in evolutionary theory have hampered the use of insights from biology and anthropology. This paper clarifies some of these issues and proposes an approach to the evolution of prosociality rooted in the interaction between cultural and genetic transmission. I explain how, in contrast to non-cultural species, the details of our evolved cultural learning capacities (e.g., imitative abilities) create the conditions for the cultural evolution of prosociality. By producing multiple behavioral equilibria, including group-beneficial equilibria, cultural evolution endogenously generates a mechanism of equilibrium selection that can favor prosociality. Finally, in the novel social environments left in the wake of these cultural evolutionary processes, natural selection is likely to favor prosocial genes that would not be expected in a purely genetic approach. © 2003 Published by Elsevier B.V.

954 citations

Journal ArticleDOI
TL;DR: Coenzyme Q10 appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.
Abstract: Background Parkinson disease (PD) is a degenerative neurological disorder for which no treatment has been shown to slow the progression. Objective To determine whether a range of dosages of coenzyme Q10is safe and well tolerated and could slow the functional decline in PD. Design Multicenter, randomized, parallel-group, placebo-controlled, double-blind, dosage-ranging trial. Setting Academic movement disorders clinics. Patients Eighty subjects with early PD who did not require treatment for their disability. Interventions Random assignment to placebo or coenzyme Q10at dosages of 300, 600, or 1200 mg/d. Main Outcome Measure The subjects underwent evaluation with the Unified Parkinson Disease Rating Scale (UPDRS) at the screening, baseline, and 1-, 4-, 8-, 12-, and 16-month visits. They were followed up for 16 months or until disability requiring treatment with levodopa had developed. The primary response variable was the change in the total score on the UPDRS from baseline to the last visit. Results The adjusted mean total UPDRS changes were +11.99 for the placebo group, +8.81 for the 300-mg/d group, +10.82 for the 600-mg/d group, and +6.69 for the 1200-mg/d group. ThePvalue for the primary analysis, a test for a linear trend between the dosage and the mean change in the total UPDRS score, was .09, which met our prespecified criteria for a positive trend for the trial. A prespecified, secondary analysis was the comparison of each treatment group with the placebo group, and the difference between the 1200-mg/d and placebo groups was significant (P= .04). Conclusions Coenzyme Q10was safe and well tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects assigned to coenzyme Q10than in those assigned to placebo, and the benefit was greatest in subjects receiving the highest dosage. Coenzyme Q10appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.

953 citations

Journal ArticleDOI
TL;DR: It is confirmed that stromal lymphocytic infiltration constitutes a robust prognostic factor in TNBCs and studies assessing outcomes and therapeutic efficacies should consider stratification for this parameter.
Abstract: Purpose Recent studies suggest that tumor-infiltrating lymphocytes (TILs) are associated with disease-free (DFS) and overall survival (OS) in operable triple-negative breast cancer (TNBC). We seek to validate the prognostic impact of TILs in primary TNBCs in two adjuvant phase III trials conducted by the Eastern Cooperative Oncology Group (ECOG). Patients and methods Full-face hematoxylin and eosin–stained sections of 506 tumors from ECOG trials E2197 and E1199 were evaluated for density of TILs in intraepithelial (iTILs) and stromal compartments (sTILs). Patient cases of TNBC from E2197 and E1199 were randomly selected based on availability of sections. For the primary end point of DFS, association with TIL scores was determined by fitting proportional hazards models stratified on study. Secondary end points were OS and distant recurrence–free interval (DRFI). Reporting recommendations for tumor marker prognostic studies criteria were followed, and all analyses were prespecified. Results The majority of 481 evaluable cancers had TILs (sTILs, 80%; iTILs, 15%). With a median follow-up of 10.6 years, higher sTIL scores were associated with better prognosis; for every 10% increase in sTILs, a 14% reduction of risk of recurrence or death (P = .02), 18% reduction of risk of distant recurrence (P = .04), and 19% reduction of risk of death (P = .01) were observed. Multivariable analysis confirmed sTILs to be an independent prognostic marker of DFS, DRFI, and OS. Conclusion In two national randomized clinical trials using contemporary adjuvant chemotherapy, we confirm that stromal lymphocytic infiltration constitutes a robust prognostic factor in TNBCs. Studies assessing outcomes and therapeutic efficacies should consider stratification for this parameter.

951 citations


Authors

Showing all 52622 results

NameH-indexPapersCitations
Younan Xia216943175757
Eric J. Topol1931373151025
Bernard Rosner1901162147661
Paul G. Richardson1831533155912
Peter W.F. Wilson181680139852
Dennis S. Charney179802122408
Joseph Biederman1791012117440
Kenneth C. Anderson1781138126072
David A. Weitz1781038114182
Lei Jiang1702244135205
William J. Sandborn1621317108564
Stephen J. Elledge162406112878
Ali H. Mokdad156634160599
Michael Tomasello15579793361
Don W. Cleveland15244484737
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023195
20221,124
20218,694
20208,001
20197,033
20186,326