Institution
Wake Forest University
Education•Winston-Salem, North Carolina, United States•
About: Wake Forest University is a education organization based out in Winston-Salem, North Carolina, United States. It is known for research contribution in the topics: Population & Diabetes mellitus. The organization has 21499 authors who have published 48731 publications receiving 2246027 citations. The organization is also known as: Wake Forest College.
Topics: Population, Diabetes mellitus, Cancer, Medicine, Blood pressure
Papers published on a yearly basis
Papers
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University of Kentucky1, Dartmouth College2, Washington University in St. Louis3, Wake Forest University4, Anschutz Medical Campus5, Oregon Health & Science University6, Society of Thoracic Surgeons7, Yeshiva University8, Stanford University9, University of Toronto10, Englewood Hospital and Medical Center11, Duke University12, University of Pittsburgh13, Flinders University14, Harvard University15
TL;DR: Much has changed since the previously published 2007 STS blood management guidelines and this document contains new and revised recommendations.
1,090 citations
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University of Florida1, University of Maryland, Baltimore2, Wake Forest University3, University of South Carolina4, Pennington Biomedical Research Center5, United States Department of Agriculture6, Yale University7, Veterans Health Administration8, University of California, San Diego9, Stanford University10, Northwestern University11, University of Pittsburgh12
TL;DR: The findings suggest mobility benefit from a structured, moderate-intensity physical activity program compared with a health education program reduced major mobility disability over 2.6 years among older adults at risk for disability.
Abstract: Importance In older adults reduced mobility is common and is an independent risk factor for morbidity, hospitalization, disability, and mortality. Limited evidence suggests that physical activity may help prevent mobility disability; however, there are no definitive clinical trials examining whether physical activity prevents or delays mobility disability. Objective To test the hypothesis that a long-term structured physical activity program is more effective than a health education program (also referred to as a successful aging program) in reducing the risk of major mobility disability. Design, Setting, and Participants The Lifestyle Interventions and Independence for Elders (LIFE) study was a multicenter, randomized trial that enrolled participants between February 2010 and December 2011, who participated for an average of 2.6 years. Follow-up ended in December 2013. Outcome assessors were blinded to the intervention assignment. Participants were recruited from urban, suburban, and rural communities at 8 centers throughout the United States. We randomized a volunteer sample of 1635 sedentary men and women aged 70 to 89 years who had physical limitations, defined as a score on the Short Physical Performance Battery of 9 or below, but were able to walk 400 m. Interventions Participants were randomized to a structured, moderate-intensity physical activity program (n = 818) conducted in a center (twice/wk) and at home (3-4 times/wk) that included aerobic, resistance, and flexibility training activities or to a health education program (n = 817) consisting of workshops on topics relevant to older adults and upper extremity stretching exercises. Main Outcomes and Measures The primary outcome was major mobility disability objectively defined by loss of ability to walk 400 m. Results Incident major mobility disability occurred in 30.1% (246 participants) of the physical activity group and 35.5% (290 participants) of the health education group (hazard ratio [HR], 0.82 [95% CI, 0.69-0.98], P = .03). Persistent mobility disability was experienced by 120 participants (14.7%) in the physical activity group and 162 participants (19.8%) in the health education group (HR, 0.72 [95% CI, 0.57-0.91]; P = .006). Serious adverse events were reported by 404 participants (49.4%) in the physical activity group and 373 participants (45.7%) in the health education group (risk ratio, 1.08 [95% CI, 0.98-1.20]). Conclusions and Relevance A structured, moderate-intensity physical activity program compared with a health education program reduced major mobility disability over 2.6 years among older adults at risk for disability. These findings suggest mobility benefit from such a program in vulnerable older adults. Trial Registration clinicaltrials.gov Identifier:NCT01072500
1,089 citations
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TL;DR: Intensive glycemic control and intensive combination treatment of dyslipidemia, but not intensive blood-pressure control, reduced the rate of progression of diabetic retinopathy.
Abstract: BACKGROUND We investigated whether intensive glycemic control, combination therapy for dyslipidemia, and intensive blood-pressure control would limit the progression of diabetic retinopathy in persons with type 2 diabetes. Previous data suggest that these systemic factors may be important in the development and progression of diabetic retinopathy. METHODS In a randomized trial, we enrolled 10,251 participants with type 2 diabetes who were at high risk for cardiovascular disease to receive either intensive or standard treatment for glycemia (target glycated hemoglobin level, <6.0% or 7.0 to 7.9%, respectively) and also for dyslipidemia (160 mg daily of fenofibrate plus simvastatin or placebo plus simvastatin) or for systolic blood-pressure control (target, <120 or <140 mm Hg). A subgroup of 2856 participants was evaluated for the effects of these interventions at 4 years on the progression of diabetic retinopathy by 3 or more steps on the Early Treatment Diabetic Retinopathy Study Severity Scale (as assessed from seven-field stereoscopic fundus photographs, with 17 possible steps and a higher number of steps indicating greater severity) or the development of diabetic retinopathy necessitating laser photocoagulation or vitrectomy. RESULTS At 4 years, the rates of progression of diabetic retinopathy were 7.3% with intensive glycemia treatment, versus 10.4% with standard therapy (adjusted odds ratio, 0.67; 95% confidence interval [CI], 0.51 to 0.87; P=0.003); 6.5% with fenofibrate for intensive dyslipidemia therapy, versus 10.2% with placebo (adjusted odds ratio, 0.60; 95% CI, 0.42 to 0.87; P=0.006); and 10.4% with intensive blood-pressure therapy, versus 8.8% with standard therapy (adjusted odds ratio, 1.23; 95% CI, 0.84 to 1.79; P=0.29). CONCLUSIONS Intensive glycemic control and intensive combination treatment of dyslipidemia, but not intensive blood-pressure control, reduced the rate of progression of diabetic retinopathy. (Funded by the National Heart, Lung, and Blood Institute and others; ClinicalTrials.gov numbers, NCT00000620 for the ACCORD study and NCT00542178 for the ACCORD Eye study.)
1,084 citations
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Karol Estrada1, Unnur Styrkarsdottir, Evangelos Evangelou2, Yi-Hsiang Hsu3 +187 more•Institutions (69)
TL;DR: Light is shed on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility and within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways.
Abstract: Bone mineral density (BMD) is the most widely used predictor of fracture risk. We performed the largest meta-analysis to date on lumbar spine and femoral neck BMD, including 17 genome-wide association studies and 32,961 individuals of European and east Asian ancestry. We tested the top BMD-associated markers for replication in 50,933 independent subjects and for association with risk of low-trauma fracture in 31,016 individuals with a history of fracture (cases) and 102,444 controls. We identified 56 loci (32 new) associated with BMD at genome-wide significance (P < 5 × 10(-8)). Several of these factors cluster within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways. However, we also discovered loci that were localized to genes not known to have a role in bone biology. Fourteen BMD-associated loci were also associated with fracture risk (P < 5 × 10(-4), Bonferroni corrected), of which six reached P < 5 × 10(-8), including at 18p11.21 (FAM210A), 7q21.3 (SLC25A13), 11q13.2 (LRP5), 4q22.1 (MEPE), 2p16.2 (SPTBN1) and 10q21.1 (DKK1). These findings shed light on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility.
1,076 citations
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TL;DR: Low-dose diuretics are the most effective first-line treatment for preventing the occurrence of cardiovascular disease morbidity and mortality and future trials should use low-doseDiuretics as the standard for clinically useful comparisons.
Abstract: ContextEstablishing relative benefit or harm from specific antihypertensive
agents is limited by the complex array of studies that compare treatments.
Network meta-analysis combines direct and indirect evidence to better define
risk or benefit.ObjectiveTo summarize the available clinical trial evidence concerning the safety
and efficacy of various antihypertensive therapies used as first-line agents
and evaluated in terms of major cardiovascular disease end points and all-cause
mortality.Data Sources and Study SelectionWe used previous meta-analyses, MEDLINE searches, and journal reviews
from January 1995 through December 2002. We identified long-term randomized
controlled trials that assessed major cardiovascular disease end points as
an outcome. Eligible studies included both those with placebo-treated or untreated
controls and those with actively treated controls.Data ExtractionNetwork meta-analysis was used to combine direct within-trial between-drug
comparisons with indirect evidence from the other trials. The indirect comparisons,
which preserve the within-trial randomized findings, were constructed from
trials that had one treatment in common.Data SynthesisData were combined from 42 clinical trials that included 192 478
patients randomized to 7 major treatment strategies, including placebo. For
all outcomes, low-dose diuretics were superior to placebo: coronary heart
disease (CHD; RR, 0.79; 95% confidence interval [CI], 0.69-0.92); congestive
heart failure (CHF; RR, 0.51; 95% CI, 0.42-0.62); stroke (RR, 0.71; 0.63-0.81);
cardiovascular disease events (RR, 0.76; 95% CI, 0.69-0.83); cardiovascular
disease mortality (RR, 0.81; 95% CI, 0.73-0.92); and total mortality (RR,
0.90; 95% CI, 0.84-0.96). None of the first-line treatment strategies–β-blockers,
angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers (CCBs), α-blockers,
and angiotensin receptor blockers–was significantly better than low-dose
diuretics for any outcome. Compared with CCBs, low-dose diuretics were associated
with reduced risks of cardiovascular disease events (RR, 0.94; 95% CI, 0.89-1.00)
and CHF (RR, 0.74; 95% CI, 0.67-0.81). Compared with ACE inhibitors, low-dose
diuretics were associated with reduced risks of CHF (RR, 0.88; 95% CI, 0.80-0.96),
cardiovascular disease events (RR, 0.94; 95% CI, 0.89-1.00), and stroke (RR,
0.86; 0.77-0.97). Compared with β-blockers, low-dose diuretics were associated
with a reduced risk of cardiovascular disease events (RR, 0.89; 95% CI, 0.80-0.98).
Compared with α-blockers, low-dose diuretics were associated with reduced
risks of CHF (RR, 0.51; 95% CI, 0.43-0.60) and cardiovascular disease events
(RR, 0.84; 95% CI, 0.75-0.93). Blood pressure changes were similar between
comparison treatments.ConclusionsLow-dose diuretics are the most effective first-line treatment for preventing
the occurrence of cardiovascular disease morbidity and mortality. Clinical
practice and treatment guidelines should reflect this evidence, and future
trials should use low-dose diuretics as the standard for clinically useful
comparisons.
1,074 citations
Authors
Showing all 21721 results
Name | H-index | Papers | Citations |
---|---|---|---|
Salim Yusuf | 231 | 1439 | 252912 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
David J. Hunter | 213 | 1836 | 207050 |
Ronald Klein | 194 | 1305 | 149140 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Russel J. Reiter | 169 | 1646 | 121010 |
David R. Jacobs | 165 | 1262 | 113892 |
Barbara E.K. Klein | 160 | 856 | 93319 |
Christopher J. O'Donnell | 159 | 869 | 126278 |
Steven R. Cummings | 158 | 579 | 104007 |
David Cella | 156 | 1258 | 106402 |
Jack M. Guralnik | 148 | 453 | 83701 |