16 results match your criteria: "and Nashville Veterans Affairs Medical Center[Affiliation]"

Association of COPD With Risk for Pulmonary Infections Requiring Hospitalization in HIV-Infected Veterans.

J Acquir Immune Defic Syndr

November 2015

*Department of Medicine, University of Washington, Seattle, WA; †Veterans Affairs Connecticut Healthcare System, West Haven, CT; ‡Veterans Affairs Health Services Research and Development, Veterans Affairs Puget Sound Healthcare System, Seattle, WA; §Department of Medicine, Veterans Affairs Connecticut Healthcare System, West Haven, CT, and Department of Medicine, Yale University School of Medicine, New Haven, CT; ‖Department of Medicine and Veterans Affairs Pittsburgh Healthcare System, University of Pittsburgh School of Medicine, Pittsburgh, PA, and Hamad Medical Corporation, Doha, Qatar; ¶Department of Medicine, Veterans Affairs Greater Los Angeles Healthcare System and David Geffen School of Medicine at UCLA, Los Angeles, CA; #Division of General Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA; **Infectious Diseases Section, Michael E. DeBakey Veterans Affairs Medical Center and Department of Medicine, Baylor College of Medicine, Houston, Texas; ††Department of Medicine, Yale University School of Medicine, New Haven, CT; ‡‡Department of Medicine, Vanderbilt University School of Medicine and Nashville Veterans Affairs Medical Center, Nashville, TN; §§James J. Peters Veterans Affairs Medical Center, Department of Medicine, Bronx and Department of Medicine, Icahn School of Medicine at Mt. Sinai, New York, NY; ‖‖Department of Medicine, Atlanta Veterans Affairs Medical Center and Emory University School of Medicine, Atlanta, GA; ¶¶Department of Medicine, Washington DC Veterans Affairs Medical Center and George Washington University School of Medicine, Washington, DC; and ##Department of Medicine, University of California San Francisco, San Francisco, CA.

Background: Pulmonary infections remain more common in HIV-infected (HIV+) compared with uninfected individuals. The increase in chronic lung diseases among aging HIV+ individuals may contribute to this persistent risk. We sought to determine whether chronic obstructive pulmonary disease (COPD) is an independent risk factor for different pulmonary infections requiring hospitalization among HIV+ patients.

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HIV infection, cardiovascular disease risk factor profile, and risk for acute myocardial infarction.

J Acquir Immune Defic Syndr

February 2015

*Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA; Departments of †Biostatistics; ‡Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; §Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA; Department of Internal Medicine, Yale University School of Medicine, New Haven, CT; ‖Department of Medicine, VA Greater Los Angeles Healthcare System, Los Angeles, CA David Geffen School of Medicine at UCLA, Los Angeles, CA; ¶Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Los Angeles, CA; #VA Medical Center; Department of Medicine, Emory University School of Medicine, Atlanta, GA; **Infectious Disease Section, Department of Medicine, VA North Texas Health Care System, UT Southwestern Medical Center, Dallas, TX; ††Infectious Diseases Section, Michael E. DeBakey VA Medical Center; Baylor College of Medicine, Houston, TX; ‡‡Department of Medicine, University of Washington, Seattle, WA; §§VA Medical Center and George Washington University Medical Center, Washington, DC; ‖‖Department of Internal Medicine, The Mount Sinai Medical Center; Bronx Veterans Affairs Medical Center, NY; ¶¶Division of Cardiology, Department of Medicine, University of California, Los Angeles, CA. ##Department of Biostatistics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; ***VA Connecticut Healthcare System, West Haven, CT; †††VA Connecticut Healthcare System, West Haven, CT, and Section of General Medicine, Yale University School of Medicine, New Haven, CT; and ‡‡‡Vanderbilt University School of Medicine and Nashville Veterans Affairs Medical Center, Nashville TN.

Background: Traditional cardiovascular disease risk factors (CVDRFs) increase the risk of acute myocardial infarction (AMI) among HIV-infected (HIV+) participants. We assessed the association between HIV and incident AMI within CVDRF strata.

Methods: Cohort-81,322 participants (33% HIV+) without prevalent CVD from the Veterans Aging Cohort Study Virtual Cohort (prospective study of HIV+ and matched HIV- veterans) participated in this study.

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Objective: Ménétrier's disease (MD) is a rare hypertrophic gastropathy characterised by giant rugal folds, hypochlorhydria, protein loss and a classic constellation of symptoms (nausea, vomiting, abdominal pain and peripheral oedema). It is considered a clinical diagnosis that may at times be difficult to establish. Firm diagnostic criteria for MD are proposed by delineating the clinicopathological features that best differentiate MD from its mimics.

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Ménétrier disease and gastrointestinal stromal tumors (GISTs) are hyperproliferative disorders of the stomach caused by dysregulated receptor tyrosine kinases (RTKs). In Ménétrier disease, overexpression of TGF-alpha, a ligand for the RTK EGFR, results in selective expansion of surface mucous cells in the body and fundus of the stomach. In GISTs, somatic mutations of the genes encoding the RTK KIT (or PDGFRA in a minority of cases) result in constitutive kinase activity and neoplastic transformation of gut pacemaker cells (interstitial cells of Cajal).

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Role of inhaled human insulin in the management of Type 1 and 2 diabetes.

Expert Rev Endocrinol Metab

July 2006

b Department of Medicine, Vanderbilt University School of Medicine and Nashville Veterans Affairs Medical Center, 715 PRB, 2220, Pierce Avenue, Nashville, TN, 37232-6303, USA.

Inhaled human insulin (Exubera) has been approved by the FDA and other regulatory bodies for treatment in Type 1 and 2 diabetes in the USA. It is the first alternative to injectable insulin since the discovery of the insulin compound to treat diabetes. This article will review results of recent clinical studies that support the therapeutic efficacy and safety of inhalable insulin for use in patients with diabetes.

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To investigate the molecular mechanisms involved in the estrogen-dependent control of plasminogen activator inhibitor-1 (PAI-1) gene expression in vascular cells, we compared the transactivation properties of estrogen receptors (ERalpha and ERbeta) in regulating the activity of a human PAI-1 promoter reporter construct in transfected bovine aortic endothelial cells (BAECs). ERalpha increased PAI-1 promoter activity in BAECs by an estrogen-dependent mechanism, whereas ERbeta suppressed PAI-1 promoter activity by an estrogen-independent mechanism. The suppressive activity of ERbeta was dominant over the inductive activity of ERalpha.

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Article Synopsis
  • The study investigates the effects of DHEA-S on metabolic responses during repeated episodes of hypoglycemia in rats, as previous hypoglycemia and high cortisol levels were found to reduce these responses.
  • The experiment involved 40 male rats undergoing different conditions, including controls with euglycemia and hypoglycemia, and some receiving DHEA-S during these episodes.
  • Findings showed that DHEA-S administration helped maintain higher levels of norepinephrine, epinephrine, glucagon, and endogenous glucose production during hypoglycemia, indicating it may counteract the negative effects of prior hypoglycemia on metabolic responses.
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These studies examined the effects of hypoglycemia or exercise on leptin levels in 47 (23 women, 24 men) healthy (age 26+/-2 years, body mass index 23+/-0.5 kg.m(-2)) and type 1 diabetes mellitus (T1DM) subjects (age 29+/-2 years, body mass index 27+/-2 kg.

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Physiological levels of cortisol have been found to blunt neuroendocrine and metabolic responses to subsequent hypoglycemia in humans. The aim of this study was to determine whether cortisol acts directly on the brain to elicit this effect. A total of 41 conscious unrestrained Sprague-Dawley rats were studied during 2-day experiments.

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This study tested the hypothesis that estrogen is the mechanism responsible for the sexual dimorphism present in the neuroendocrine and metabolic responses to hypoglycemia. Postmenopausal women receiving (E2; n = 8) or not receiving (NO E2; n = 9) estrogen replacement were compared with age- and BMI-matched male subjects (n = 8) during a single-step 2-h hyperinsulinemic-hypoglycemic clamp. Plasma insulin (599 +/- 28 pmol/l) and glucose (2.

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Effect of morning exercise on counterregulatory responses to subsequent, afternoon exercise.

J Appl Physiol (1985)

July 2001

Departments of Medicine and Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, and Nashville Veterans Affairs Medical Center, Nashville, Tennessee 37232, USA.

The aim of this study was to determine whether a bout of morning exercise (EXE(1)) can alter neuroendocrine and metabolic responses to subsequent afternoon exercise (EXE(2)) and whether these changes follow a gender-specific pattern. Sixteen healthy volunteers (8 men and 8 women, age 27 +/- 1 yr, body mass index 23 +/- 1 kg/m(2), maximal O(2) uptake 31 +/- 2 ml x kg(-1) x min(-1)) were studied after an overnight fast. EXE(1) and EXE(2) each consisted of 90 min of cycling on a stationary bike at 48 +/- 2% of maximal O(2) uptake separated by 3 h.

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The role of thromboxane (Tx) in hyperacute rejection of pig lung by human blood was studied in an ex vivo model, wherein lungs from juvenile piglets were perfused with fresh heparinized human blood. In this model, hyperacute lung rejection was characterized by an abrupt rise in pulmonary vascular resistance (PVR; >1 cmH2O x ml(-1) x min) and prolific Tx elaboration (>15 ng/ml) within 5 min and loss of function within 10 min. Although papaverine significantly blunted the rise in PVR (<0.

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There is general agreement that prior hypoglycemia blunts subsequent hypoglycemic counterregulatory responses. However, there is considerable debate concerning the timing and number of prior hypoglycemic episodes required to cause this blunting effect. The aim of this study was to determine whether one episode of hypoglycemia could modify neuroendocrine, metabolic, and symptom responses to hypoglycemia induced 2 h later.

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p53-dependent acinar cell apoptosis triggers epithelial proliferation in duct-ligated murine pancreas.

Am J Physiol Gastrointest Liver Physiol

October 2000

Departments of Surgery and Cell Biology, The Vanderbilt-Ingram Cancer Center and Nashville Veterans Affairs Medical Center, Vanderbilt University, Nashville, Tennessee 37232-2736, USA.

The mechanisms linking acinar cell apoptosis and ductal epithelial proliferation remain unknown. To determine the relationship between these events, pancreatic duct ligation (PDL) was performed on p53(+/+) and p53(-/-) mice. In mice bearing a wild-type p53 allele, PDL resulted in upregulation of p53 protein in both acinar cells and proliferating duct-like epithelium.

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Urokinase-type plasminogen activator (uPA) binds to cells via a specific glycosylphosphatidylinositol-anchored receptor. Although occupancy of the uPA receptor (uPAR) has been shown to alter cellular function and to induce gene expression, the signaling mechanism has not been characterized. Urokinase induced an increase in the tyrosine phosphorylation of multiple proteins in bovine aortic endothelial cells.

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