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Rush University Medical Center

HealthcareChicago, Illinois, United States
About: Rush University Medical Center is a healthcare organization based out in Chicago, Illinois, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 13915 authors who have published 29027 publications receiving 1379216 citations. The organization is also known as: Rush Presbyterian St. Luke's Medical Center.


Papers
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Journal ArticleDOI
TL;DR: The advances made toward understanding the basis of cancer immune evasion are discussed, the efficacy of various therapeutic measures and targets that have been developed or are being investigated to enhance tumor rejection are summarized and some natural agents and phytochemicals merit further study.

1,064 citations

Journal ArticleDOI
TL;DR: Study of lipopolysaccharide and cytokine levels in 97 patients with the sepsis syndrome found a positive correlation between high levels of plasma TNF- and mortality, and implicate T NF- as an important mediator in sepsi.
Abstract: Objective: To determine whether plasma tumor necrosis factor- (TNF-), interleukin-1 (IL-1 ), interleukin-6 (IL-6), and lipopolysaccharide are detectable in patients when they first present with the...

1,062 citations

Journal ArticleDOI
TL;DR: The objective of this work was to update previous EBM reviews on treatments for PD with a focus on non‐motor symptoms and found that most of the other interventions there is insufficient evidence to make adequate conclusions on their efficacy.
Abstract: The Movement Disorder Society (MDS) Task Force on Evidence-Based Medicine (EBM) Review of Treatments for Parkinson's Disease (PD) was first published in 2002 and was updated in 2005 to cover clinical trial data up to January 2004 with the focus on motor symptoms of PD. In this revised version the MDS task force decided it was necessary to extend the review to non-motor symptoms. The objective of this work was to update previous EBM reviews on treat- ments for PD with a focus on non-motor symptoms. Level-I (randomized controlled trial, RCT) reports of pharmacological and nonpharmacological interventions for the non-motor symptoms of PD, published as full

1,061 citations

Journal ArticleDOI
TL;DR: Dietary intake of n-3 polyunsaturated fatty acids and weekly consumption of fish may reduce the risk of incident Alzheimer disease.
Abstract: Background Dietary n-3 polyunsaturated fatty acids improve brain functioning in animal studies, but there is limited study of whether this type of fat protects against Alzheimer disease. Objective To examine whether fish consumption and intake of different types of n-3 fatty acids protect against Alzheimer disease. Design Prospective study conducted from 1993 through 2000, of a stratified random sample from a geographically defined community. Participants were followed up for an average of 3.9 years for the development of Alzheimer disease. Patients A total of 815 residents, aged 65 to 94 years, who were initially unaffected by Alzheimer disease and completed a dietary questionnaire on average 2.3 years before clinical evaluation of incident disease. Main Outcome Measure Incident Alzheimer disease diagnosed in a structured neurologic examination by means of standardized criteria. Results A total of 131 sample participants developed Alzheimer disease. Participants who consumed fish once per week or more had 60% less risk of Alzheimer disease compared with those who rarely or never ate fish (relative risk, 0.4; 95% confidence interval, 0.2-0.9) in a model adjusted for age and other risk factors. Total intake of n-3 polyunsaturated fatty acids was associated with reduced risk of Alzheimer disease, as was intake of docosahexaenoic acid (22:6n-3). Eicosapentaenoic acid (20:5n-3) was not associated with Alzheimer disease. The associations remained unchanged with additional adjustment for intakes of other dietary fats and of vitamin E and for cardiovascular conditions. Conclusion Dietary intake of n-3 fatty acids and weekly consumption of fish may reduce the risk of incident Alzheimer disease.

1,054 citations

Journal ArticleDOI
28 May 2003-JAMA
TL;DR: Excess risk for all strokes attributed to estrogen plus progestin appeared to be present in all subgroups of women examined, and excess risk of all stroke was apparent in all age groups, in all categories of baseline stroke risk, and in women with and without hypertension, prior history of cardiovascular disease, use of hormones, statins, or aspirin.
Abstract: ContextThe Women's Health Initiative (WHI) trial of estrogen plus progestin was stopped early because of adverse effects, including an increased risk of stroke in the estrogen plus progestin group.ObjectiveTo assess the effect of estrogen plus progestin on ischemic and hemorrhagic stroke and in subgroups, and to determine whether the effect of estrogen plus progestin was modified by baseline levels of blood biomarkers.DesignMulticenter double-blind, placebo-controlled, randomized clinical trial involving 16 608 women aged 50 through 79 years with an average follow-up of 5.6 years. Baseline levels of blood-based markers of inflammation, thrombosis, and lipid levels were measured in the first 140 centrally confirmed stroke cases and 513 controls.InterventionsParticipants received 0.625 mg/d of conjugated equine estrogen plus 2.5 mg/d of medroxyprogesterone acetate (n = 8506) or placebo (n = 8102).Main Outcome MeasuresOverall strokes and stroke subtype and severity were centrally adjudicated by stroke neurologists.ResultsOne hundred fifty-one patients (1.8%) in the estrogen plus progestin and 107 (1.3%) in the placebo groups had strokes. Overall 79.8% of strokes were ischemic. For combined ischemic and hemorrhagic strokes, the intention-to-treat hazard ratio (HR) for estrogen plus progestin vs placebo was 1.31 (95% confidence interval [CI], 1.02-1.68); with adjustment for adherence, the HR was 1.50 (95% CI, 1.08-2.08). The HR for ischemic stroke was 1.44 (95% CI, 1.09-1.90) and for hemorrhagic stroke, 0.82 (95% CI, 0.43-1.56). Point estimates of the HRs indicate that excess risk of all stroke was apparent in all age groups, in all categories of baseline stroke risk, and in women with and without hypertension, prior history of cardiovascular disease, use of hormones, statins, or aspirin. Other risk factors for stroke, including smoking, blood pressure, diabetes, lower use of vitamin C supplements, blood-based biomarkers of inflammation, higher white blood cell count, and higher hematocrit levels did not modify the effect of estrogen plus progestin on stroke risk.ConclusionsEstrogen plus progestin increases the risk of ischemic stroke in generally healthy postmenopausal women. Excess risk for all strokes attributed to estrogen plus progestin appeared to be present in all subgroups of women examined.

1,052 citations


Authors

Showing all 14032 results

NameH-indexPapersCitations
John Q. Trojanowski2261467213948
Virginia M.-Y. Lee194993148820
Luigi Ferrucci1931601181199
David A. Bennett1671142109844
Todd R. Golub164422201457
David Cella1561258106402
M.-Marsel Mesulam15055890772
John D. E. Gabrieli14248068254
David J. Kupfer141862102498
Clifford B. Saper13640672203
Pasi A. Jänne13668589488
Nikhil C. Munshi13490667349
Martin B. Keller13154165069
Michael E. Thase13192375995
Steven R. Simon129109080331
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202336
2022166
20212,147
20201,939
20191,708
20181,410