36 results match your criteria: "UK M.R.W.; University of Adelaide[Affiliation]"
Neutrophil Extracellular Traps Promote Angiogenesis: Evidence From Vascular Pathology in Pulmonary Hypertension.
Arterioscler Thromb Vasc Biol
October 2016
From the Department of Medicine, Centre for Pharmacology and Therapeutics (L.A., V.A.-S., L.D., A.J.A., M.R.W., B.W.-S.) and Centre for Haematology (T.M.K.), Experimental Medicine, Imperial College London, United Kingdom; and Pulmonary Vascular Diseases Unit, Papworth Hospital NHS Foundation Trust, Papworth Everard Cambridge, United Kingdom (J.P.-Z., M.S., C.H., M.T.).
Objective: Inflammation and dysregulated angiogenesis are features of endothelial dysfunction in pulmonary hypertension. Neutrophil extracellular traps (NETs), produced by dying neutrophils, contribute to pathogenesis of numerous vascular disorders but their role in pulmonary hypertension has not been studied. We sought evidence of (NETs) formation in pulmonary hypertension and investigated the effect of NETs on endothelial function.
View Article and Find Full Text PDFAllopurinol and Cardiovascular Outcomes in Adults With Hypertension.
Hypertension
March 2016
From the Institute of Cardiovascular and Medical Sciences, School of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom (R.L.M., M.R.W., P.H., S.P., A.F.D., R.M.T., J.D.); and Charité - Universitätsmedizin Berlin, Berlin, Germany (J.S.).
Allopurinol lowers blood pressure in adolescents and has other vasoprotective effects. Whether similar benefits occur in older individuals remains unclear. We hypothesized that allopurinol is associated with improved cardiovascular outcomes in older adults with hypertension.
View Article and Find Full Text PDFGenome-Wide Association Analysis of Young-Onset Stroke Identifies a Locus on Chromosome 10q25 Near HABP2.
Stroke
February 2016
From the Veterans Affairs Maryland Health Care System, Baltimore, MD (Y.-C.C., S.J.K., J.W.C., B.D.M.); University of Maryland School of Medicine, Baltimore (Y.-C.C., H.X., S.J.K., J.W.C., J.R.O., B.D.M.); The University of Gothenburg, Gothenburg, Sweden (T.M.S., C.J.); University of Rostock, Rostock, Germany (A.-K.G., A. Rolfs); University of Nottingham Malaysia Campus, Selangor Darul Ehsa, Malaysia (W.K.H.); University of Cambridge, Cambridge, UK (M.T., J.D., S.B., H.S.M., S.D., D.S.); Institut Pasteur de Lille, F-59000 Lille, France (P.A.); University of Newcastle, Australia (E.G.H.); Ludwig-Maximilians-Universität, Munich, Germany (R.M., K.S., M.D.); Wellcome Trust Sanger Institute, Cambridge, UK (J.D.); Center for Non-Communicable Diseases, Karachi, Pakistan (A. Rasheed, D.S.); University of Pennsylvania (W.Z., D.S.); Basel University Hospital, Switzerland (S.E.); Heidelberg University Hospital, Germany (C.G.-G.); Centre d'Étude du Polymorphisme Humain, Paris, France (Y.K.); RIKEN Center for Integrative Medical Sciences, Yokohama, Japan (Y.K.); National Genotyping Center, Evry, France (M.L.); Genome Quebec, McGill University, Montreal, Canada (M.L.); Lille University Hospital, France (D.L., S.D.); KU Leuven - University of Leuven, Leuven, Belgium (V.T.); Vesalius Research Center, VIB, Leuven, Belgium (V.T.); University Hospitals Leuven, Leuven, Belgium (V.T.); Helsinki University Central Hospital, Helsinki, Finland (T.M.M., T.T.); Università degli Studi di Brescia, Brescia, Italy (A. Pezzini); Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy (E.A.P., G.B.B.); University of Lund, Sweden (B.N.); University of Oxford, John Radcliffe Hospital (P.M.R.); University of Edinburgh, Edinburgh, UK (C.S.); Jagiellonian University Medical College, Krakow, Poland (A.S.); Lund University, Lund, Sweden (A.L.); Skåne University Hospital, Lund, Sweden (A.L.); University of Glasgow, Glasgow, UK (M.R.W.); University of Adelaide, Australia (J.J.); Mount Sinai Hos
Background And Purpose: Although a genetic contribution to ischemic stroke is well recognized, only a handful of stroke loci have been identified by large-scale genetic association studies to date. Hypothesizing that genetic effects might be stronger for early- versus late-onset stroke, we conducted a 2-stage meta-analysis of genome-wide association studies, focusing on stroke cases with an age of onset <60 years.
Methods: The discovery stage of our genome-wide association studies included 4505 cases and 21 968 controls of European, South-Asian, and African ancestry, drawn from 6 studies.
Acetaminophen use and risk of myocardial infarction and stroke in a hypertensive cohort.
Hypertension
May 2015
From the Institute of Cardiovascular and Medical Sciences (R.L.F., M.R.W., R.M.T., A.F.D., S.P., G.T.M., J.D.), School of Medicine (R.M., P.A.M.), and West of Scotland Cancer Surveillance Unit (D.S.M.), College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Recent data suggest that self-reported acetaminophen use is associated with increased risk of cardiovascular events and that acetaminophen causes a modest blood pressure rise. There are no randomized trials or studies using verified prescription data of this relationship. We aimed to assess the relationship between verified acetaminophen prescription data and risk of myocardial infarction or stroke in patients with hypertension.
View Article and Find Full Text PDFIron homeostasis and pulmonary hypertension: iron deficiency leads to pulmonary vascular remodeling in the rat.
Circ Res
May 2015
From the Centre for Pharmacology and Therapeutics, Department of Medicine (E.C., A.A., L.W., J.W., O.D., S.B., M.R.W., L.Z.) and Division of Brain Sciences, Department of Medicine (K.N.A.), Imperial College London, Hammersmith Hospital, London, United Kingdom; and Clinical Biochemistry, Imperial College Healthcare NHS Trust, London, United Kingdom (M.B.).
Rationale: Iron deficiency without anemia is prevalent in patients with idiopathic pulmonary arterial hypertension and associated with reduced exercise capacity and survival.
Objectives: We hypothesized that iron deficiency is involved in the pathogenesis of pulmonary hypertension and iron replacement is a possible therapeutic strategy.
Methods And Results: Rats were fed an iron-deficient diet (IDD, 7 mg/kg) and investigated for 4 weeks.
Pathophysiology and treatment of high-altitude pulmonary vascular disease.
Circulation
February 2015
From Experimental Medicine, Imperial College London, Hammersmith Hospital, United Kingdom (M.R.W., H.-A.G., L.Z.); Excellence Cluster Cardio-Pulmonary System, Universities of Giessen, Germany (M.R.W., H.-A.G., N.W., L.Z.); University of Giessen Marburg Lung Center, Justus-Liebig-University, Germany (M.R.W., H.-A.G., N.W., L.Z.); Kerckhoff Clinic, Bad Nauheim, Germany (H.-A.G.); Institute of Molecular Biology and Medicine, Bishkek, Kyrgyzstan (A.A.).
α1-A680T variant in GUCY1A3 as a candidate conferring protection from pulmonary hypertension among Kyrgyz highlanders.
Circ Cardiovasc Genet
December 2014
From the Department of Medicine, Imperial College London, London, United Kingdom (M.R.W., J.W., C.J.R., S.R.); National Academy of Sciences of Kyrgyz Republic, Bishkek, Kyrgyz Republic (A.A.A.); Physiological Genomics and Medicine Group, MRC Clinical Sciences Centre, Hammersmith Hospital, London, United Kingdom (J.V., T.J.A.); NIHR BRC Clinical Genome Informatics Facility, Imperial College London, London, United Kingdom (D.K., S.G.B., M.M.); Cardiology Research, Bayer Pharma AG, Wuppertal, Germany (S.G., J.-P.S.); Department of Pharmacology, The School of Pharmacy, Martin-Luther-University, Halle, Germany (J.-P.S.); Department of Pulmonary Pharmacotherapy, University of Giessen and Marburg Lung Center, Giessen, Germany (B.K.); Department of Medicine, University of Cambridge, Cambridge, United Kingdom (N.W.M.); Department of Pharmacology, Toxicology, and Clinical Pharmacy, University of Braunschweig-Center of Pharmaceutical Engineering, Braunschweig, Germany (I.N., S.B.); and Department of Chemistry, The Scripps Research Institute, La Jolla, CA (N.B.S., M.A.M.).
Background: Human variation in susceptibility to hypoxia-induced pulmonary hypertension is well recognized. High-altitude residents who do not develop pulmonary hypertension may host protective gene mutations.
Methods And Results: Exome sequencing was conducted on 24 unrelated Kyrgyz highlanders living 2400 to 3800 m above sea level, 12 (10 men; mean age, 54 years) with an elevated mean pulmonary artery pressure (mean±SD, 38.
Aberrant chloride intracellular channel 4 expression contributes to endothelial dysfunction in pulmonary arterial hypertension.
Circulation
April 2014
Centre for Pharmacology and Therapeutics, Department of Medicine, Imperial College London, London, UK (B.W.-S., V.B.A.-S., K.H.L., H.T., R.J.E., C.J.R., J.W., L.Z., M.R.W.); Cardiovascular Pulmonary Research Group, University of Colorado Denver Health Sciences Center, Aurora (D.C.I., C.L., Z.L., K.R.S.); Division of Nephrology, Department of Internal Medicine, St. Louis University, St. Louis MO (J.C.E.); Laboratory of Cancer Biology & Genetics, Centre for Cancer Research, Bethesda, MD (S.H.Y.); and National Pulmonary Hypertension Service and National Heart & Lung Institute, Imperial College Healthcare NHS Trust, London, UK (L.S.H., J.S.R.G.).
Background: Chloride intracellular channel 4 (CLIC4) is highly expressed in the endothelium of remodeled pulmonary vessels and plexiform lesions of patients with pulmonary arterial hypertension. CLIC4 regulates vasculogenesis through endothelial tube formation. Aberrant CLIC4 expression may contribute to the vascular pathology of pulmonary arterial hypertension.
View Article and Find Full Text PDFImproving the efficiency of stroke trials: feasibility and efficacy of group adjudication of functional end points.
Stroke
December 2013
From the Institute of Cardiovascular and Medical Sciences (K.S.M., T.J.Q., P.H., P.L., M.R.W., J.D., K.R.L.) and Robertson Centre for Biostatistics (P.C.D.J.), University of Glasgow, United Kingdom; and MRC Hub for Trials Methodology Research, Centre for Population Health Sciences, University of Edinburgh Medical School, United Kingdom (C.J.W.).
Background And Purpose: Use of the modified Rankin scale (mRS) in multicenter trials may be limited by interobserver variability. We assessed the effect of this on trial power and developed a novel group adjudication approach.
Methods: We generated power and sample size estimates from simulated trials modeled with varying mRS reliability.
Heterogeneity in lung (18)FDG uptake in pulmonary arterial hypertension: potential of dynamic (18)FDG positron emission tomography with kinetic analysis as a bridging biomarker for pulmonary vascular remodeling targeted treatments.
Circulation
September 2013
Centre for Pharmacology and Therapeutics, Experimental Medicine, Imperial College London, Hammersmith Hospital, London, UK (L.Z., A.A., L.W., O.D., J.C., E.C., H.J., G.B., M.R.W.); Department of Nuclear Medicine, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (W.F.); Max-Planck Institute for Heart and Lung Research and University of Giessen and Marburg Lung Center, German Center for Lung Research, Bad Nauheim, Germany (S.D., S.S.P.); Comprehensive Cancer Imaging Centre, Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital, London, UK (G.T., Q.N., E.O.A.); Department of Histopathology, Imperial College London, UK (M.A.E.-B.); National Heart and Lung Institute, Imperial College London, and National Pulmonary Hypertension Service, Department of Cardiology, Hammersmith Hospital, London, UK (L.S.H., J.S.R.G.); Biological Imaging Centre, Medical Research Council Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, UK (W.G.); and Center for Diagnosis and Management of Pulmonary Vascular Diseases, Department of Cardiology, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (J.H.).
Background: Pulmonary arterial hypertension (PAH) is a disease of progressive vascular remodeling, characterized by dysregulated growth of pulmonary vascular cells and inflammation. A prevailing view is that abnormal cellular metabolism, notably aerobic glycolysis that increases glucose demand, underlies the pathogenesis of PAH. Increased lung glucose uptake has been reported in animal models.
View Article and Find Full Text PDFUnexplored reservoirs of pathogenic bacteria: protozoa and biofilms.
Trends Microbiol
January 1999
Pharmaceutical Sciences Institute, School of Life and Health Sciences, Aston University, Birmingham, UK.
In the natural, industrial, hospital and domestic environments, there are numerous phenotypes of pathogenic microorganisms, which vary considerably in chemical, physical and biological properties. A link exists between survival, resistance and virulence. In particular, surface-adherent biofilms and bacteria living within protozoa pose potential health problems that are unrecognized by conventional laboratory culture methods.
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