Institution
Wayne State University
Education•Detroit, Michigan, United States•
About: Wayne State University is a education organization based out in Detroit, Michigan, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 42801 authors who have published 82738 publications receiving 3083713 citations. The organization is also known as: WSU & Wayne University.
Topics: Population, Cancer, Poison control, Pregnancy, Medicine
Papers published on a yearly basis
Papers
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TL;DR: The value of community participation in health is reviewed and a detailed examination of the challenges facing its implementation and sustainability are provided.
Abstract: This article which examines the notion of community participation and identifies its most pressing challenges opens by noting that the concept of community participation was a foundation of the World Health Organizations strategy to achieve health for all by the year 2000. Next the article reviews the reputed benefits of community participation and the most significant problems with conceptualization and evaluation. Finally examples are given of obstacles to community participation that arise from failure to ensure that the predisposing conditions are met; the diverse nature of communities themselves; the nature of participation; and the relationship of community participation to empowerment and health promotion. It is concluded that community participation must be internalized by a community in order to be effective and sustainable. Continued study of community participation will be necessary because new problems will continue to arise and communities are mutable. The potential of this important strategy for achieving "health for all" will be maximized by continued experimentation and increased sharing of experiments.
404 citations
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TL;DR: It is shown that PER2 directly and specifically represses PPARγ, a nuclear receptor critical in adipogenesis, insulin sensitivity, and inflammatory response, and that lack of PER2 results in enhanced adipocyte differentiation of cultured fibroblasts.
403 citations
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University of Cambridge1, University of Bristol2, Wayne State University3, Copenhagen University Hospital4, University of Copenhagen5, Innsbruck Medical University6, University of Glasgow7, Leiden University Medical Center8, Leiden University9, Utrecht University10, National Institute for Health Research11, University of Pennsylvania12, Wellcome Trust Sanger Institute13
TL;DR: The association of genetically predicted Lp(a) concentration with CHD risk appeared to be independent of changes in LDL-C level owing to genetic variants that mimic the relationship of statins, PCSK9 inhibitors, and ezetimibe withCHD risk.
Abstract: Importance Human genetic studies have indicated that plasma lipoprotein(a) (Lp[a]) is causally associated with the risk of coronary heart disease (CHD), but randomized trials of several therapies that reduce Lp(a) levels by 25% to 35% have not provided any evidence that lowering Lp(a) level reduces CHD risk. Objective To estimate the magnitude of the change in plasma Lp(a) levels needed to have the same evidence of an association with CHD risk as a 38.67-mg/dL (ie, 1-mmol/L) change in low-density lipoprotein cholesterol (LDL-C) level, a change that has been shown to produce a clinically meaningful reduction in the risk of CHD. Design, Setting, and Participants A mendelian randomization analysis was conducted using individual participant data from 5 studies and with external validation using summarized data from 48 studies. Population-based prospective cohort and case-control studies featured 20 793 individuals with CHD and 27 540 controls with individual participant data, whereas summarized data included 62 240 patients with CHD and 127 299 controls. Data were analyzed from November 2016 to March 2018. Exposures GeneticLPA score and plasma Lp(a) mass concentration. Main Outcomes and Measures Coronary heart disease. Results Of the included study participants, 53% were men, all were of white European ancestry, and the mean age was 57.5 years. The association of genetically predicted Lp(a) with CHD risk was linearly proportional to the absolute change in Lp(a) concentration. A 10-mg/dL lower genetically predicted Lp(a) concentration was associated with a 5.8% lower CHD risk (odds ratio [OR], 0.942; 95% CI, 0.933-0.951;P = 3 × 10−37), whereas a 10-mg/dL lower genetically predicted LDL-C level estimated using an LDL-C genetic score was associated with a 14.5% lower CHD risk (OR, 0.855; 95% CI, 0.818-0.893;P = 2 × 10−12). Thus, a 101.5-mg/dL change (95% CI, 71.0-137.0) in Lp(a) concentration had the same association with CHD risk as a 38.67-mg/dL change in LDL-C level. The association of genetically predicted Lp(a) concentration with CHD risk appeared to be independent of changes in LDL-C level owing to genetic variants that mimic the relationship of statins, PCSK9 inhibitors, and ezetimibe with CHD risk. Conclusions and Relevance The clinical benefit of lowering Lp(a) is likely to be proportional to the absolute reduction in Lp(a) concentration. Large absolute reductions in Lp(a) of approximately 100 mg/dL may be required to produce a clinically meaningful reduction in the risk of CHD similar in magnitude to what can be achieved by lowering LDL-C level by 38.67 mg/dL (ie, 1 mmol/L).
403 citations
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TL;DR: In this article, the authors reconstructed hadrons in 0.15 4 4 GeV/c collisions with pp and Au+Au at the radical (s{sub NN}) = 200 GeV and the associated multiplicity and p{sub perpendicular} magnitude sum were found to increase from pp to central Au+AU collisions.
Abstract: Charged hadrons in 0.15 4 GeV/c are reconstructed in pp and Au+Au collisions at {radical}(s{sub NN})=200 GeV. The associated multiplicity and p{sub perpendicular} magnitude sum are found to increase from pp to central Au+Au collisions. The associated p{sub perpendicular} distributions, while similar in shape on the nearside, are significantly softened on the awayside in central Au+Au relative to pp and not much harder than that of inclusive hadrons. The results, consistent with jet quenching, suggest that the awayside fragments approach equilibration with the medium traversed.
403 citations
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TL;DR: Frentinib demonstrated activity in patients with advanced PRCC with a manageable toxicity profile and a high response rate in patientsWith germline MET mutations, the presence of a germlineMET mutation was highly predictive of a response.
Abstract: Purpose Foretinib is an oral multikinase inhibitor targeting MET, VEGF, RON, AXL, and TIE-2 receptors. Activating mutations or amplifications in MET have been described in patients with papillary renal cell carcinoma (PRCC). We aimed to evaluate the efficacy and safety of foretinib in patients with PRCC. Patients and Methods Patients were enrolled onto the study in two cohorts with different dosing schedules of foretinib: cohort A, 240 mg once per day on days 1 through 5 every 14 days (intermittent arm); cohort B, 80 mg daily (daily dosing arm). Patients were stratified on the basis of MET pathway activation (germline or somatic MET mutation, MET [7q31] amplification, or gain of chromosome 7). The primary end point was overall response rate (ORR). Results Overall, 74 patients were enrolled, with 37 in each dosing cohort. ORR by Response Evaluation Criteria in Solid Tumors (RECIST) 1.0 was 13.5%, median progression-free survival was 9.3 months, and median overall survival was not reached. The presence of a...
402 citations
Authors
Showing all 43073 results
Name | H-index | Papers | Citations |
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Robert Langer | 281 | 2324 | 326306 |
Eugene Braunwald | 230 | 1711 | 264576 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Anil K. Jain | 183 | 1016 | 192151 |
Richard A. Gibbs | 172 | 889 | 249708 |
Bradley Cox | 169 | 2150 | 156200 |
Jun Wang | 166 | 1093 | 141621 |
David Altshuler | 162 | 345 | 201782 |
Elliott M. Antman | 161 | 716 | 179462 |
Jovan Milosevic | 152 | 1433 | 106802 |
Roberto Romero | 151 | 1516 | 108321 |
Kypros H. Nicolaides | 147 | 1302 | 87091 |
John F. Hartwig | 145 | 714 | 66472 |
Charles Maguire | 142 | 1197 | 95026 |
Mingshui Chen | 141 | 1543 | 125369 |