4 results match your criteria: "University of Louisville and Louisville Veterans Affairs Medical Center[Affiliation]"
Divergent tumor necrosis factor receptor-related remodeling responses in heart failure: role of nuclear factor-kappaB and inflammatory activation.
Circulation
March 2009
Institute Institute of Molecular Cardiology, Department of Medicine, University of Louisville and Louisville Veterans Affairs Medical Center, Louisville, KY 40202, USA.
Article Synopsis
- Preclinical evidence indicated that blocking tumor necrosis factor-alpha (TNF) might help heart failure (HF), but clinical trials showed no benefits, leading researchers to explore the differing effects of TNF receptors TNFR1 and TNFR2 in HF.
- Mice lacking TNFR1 and TNFR2 showed improved survival and heart function compared to wild-type mice after heart failure was induced, with TNFR1 deficiency leading to better heart remodeling and TNFR2 deficiency resulting in worse outcomes.
- The study concluded that TNFR1 worsens inflammation and heart remodeling in HF while TNFR2 has protective effects, suggesting that targeting these receptors could be crucial for developing effective therapies.
Southern Society for Clinical Investigation Founders Medal recipient's address.
Am J Med Sci
October 2001
Department of Internal Medicine and James Graham Brown Cancer Center, University of Louisville and Louisville Veterans Affairs Medical Center, Kentucky 40202, USA.
Urinary incontinence among male veterans receiving care in primary care clinics.
Ann Intern Med
April 2000
Division of General Internal Medicine, University of Louisville and Louisville Veterans Affairs Medical Center, Kentucky 40292, USA.
Background: Male urinary incontinence is not a well-investigated subject.
Objective: To determine the prevalence and consequences of incontinence in men.
Design: Cross-sectional survey.
Glucose and glutamine gavage increase portal vein nitric oxide metabolite levels via adenosine A2b activation.
J Surg Res
June 1999
Center for Excellence in Applied Microcirculatory Research and Department of Surgery, University of Louisville and Louisville Veterans Affairs Medical Center, Louisville, Kentucky, 40206, USA.
Introduction: Postprandial intestinal hyperemia is a complex vascular response during nutrient absorption. Many mediators have been studied including enteric reflexes, GI hormones, and absorption-stimulated metabolic mediators such as pH and adenosine. We have shown that nitric oxide (NO) mediates premucosal arteriolar dilation during glucose absorption and that glucose-induced portal vein NO metabolite production requires adenosine A2b receptor activation.
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