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Institution

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: It has long been suggested that the adduction moment is the primary determinate of the distribution of load between the medial and lateral plateaus, but this is the first evidence of its relationship to the underlying bone distribution.

321 citations

Journal ArticleDOI
Michael D. Hill1, Mayank Goyal1, Bijoy K Menon1, Raul G. Nogueira2  +773 moreInstitutions (39)
TL;DR: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo, and this trial is registered with ClinicalTrials.gov, NCT02930018.

321 citations

Journal ArticleDOI
TL;DR: The evidence that age-related clinical syndromes are exacerbated by HIV is outlined, the ways in which HIV is similar, and dissimilar from natural aging are examined, and the validity of HIV as a model of premature aging is assessed.
Abstract: Background Antiretroviral therapy has reduced the incidence of adverse events and early mortality in HIV-infected persons. Despite these benefits, important comorbidities that increase with age (eg, diabetes, cardiovascular disease, cancer, liver disease, and neurocognitive impairment) are more prevalent in HIV-infected persons than in HIV-uninfected persons at every age, and geriatric syndromes such as falls and frailty occur earlier in HIV-infected persons. This raises a critical research question: Does HIV accelerate aging through pathways and mechanisms common to the aging process or is HIV simply an additional risk factor for a wide number of chronic conditions, thus accentuating aging? Methods Extensive literature review. Results The purpose of this review is to briefly outline the evidence that age-related clinical syndromes are exacerbated by HIV, examine the ways in which HIV is similar, and dissimilar from natural aging, and assess the validity of HIV as a model of premature aging. Specific biomarkers of aging are limited in HIV-infected hosts and impacted by antiretroviral therapy, and a high rate of modifiable life style confounders (eg, smoking, substance abuse, alcohol) and coinfections (eg, hepatitis) in HIV-infected participants. Conclusions There is a need for validated biomarkers of aging in the context of HIV. Despite these differences, welldesigned studies of HIV-infected participants are likely to provide new opportunities to better understand the mechanisms that lead to aging and age-related diseases.

321 citations

Journal ArticleDOI
TL;DR: What is known about fatigue in Parkinson's disease is reviewed, putting it into the context of fatigue in other disorders, and a program for developing better understanding and therapy is outlined.
Abstract: Fatigue is a common problem in Parkinson's disease (PD), often the most troubling of all symptoms. It is poorly understood, generally under-recognized, and has no known treatment. This article reviews what is known about the symptom, putting it into the context of fatigue in other disorders, and outlines a program for developing better understanding and therapy.

320 citations

Journal ArticleDOI
TL;DR: It is concluded that increased diastolic SR Ca2+ leak in HF may contribute to reductions in SR Ca 2+ content, but changes in NCX in this HF model have more impact on [Ca2+]SRT.
Abstract: Altered sarcoplasmic reticulum (SR) Ca2+-ATPase and Na+-Ca2+ exchange (NCX) function have been implicated in depressing SR Ca2+ content and contractile function in heart failure (HF). Enhanced diastolic ryanodine receptor (RyR) leak could also lower SR Ca2+ load in HF, but direct cellular measurements are lacking. In this study, we measure SR Ca2+ leak directly in intact isolated rabbit ventricular myocytes from a well-developed nonischemic HF model. Abrupt block of SR Ca2+ leak by tetracaine shifts Ca2+ from the cytosol to SR. The tetracaine-induced decline in [Ca2+]i and increase total SR Ca2+ load ([Ca2+]SRT) directly indicate the SR Ca2+ leak (before tetracaine). Diastolic SR Ca2+ leak increases with [Ca2+]SRT, and for any [Ca2+]SRT is greater in HF versus control. Mathematical modeling was used to compare the relative impact of alterations in SR Ca2+ leak, SR Ca2+-ATPase, and Na+-Ca2+ exchange on SR Ca2+ load in HF. We conclude that increased diastolic SR Ca2+ leak in HF may contribute to reductions in SR Ca2+ content, but changes in NCX in this HF model have more impact on [Ca2+]SRT.

320 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