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    • Paul J D Winyard
    • Paul J D Winyard: Influence Statistics

      Paul J D Winyard

      Paul J D Winyard

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      UCL Great Ormond Street Institute of Child Health, London, UK | University College London Great Ormond Street, Institute of Child Health, London, UK. | Nephro-Urology Research ...

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      Paul J D Winyard:Expert Impact

      Concepts for whichPaul J D Winyardhas direct influence:Kidney injury,Young people,Urinary tract,Thymosin β4,Human kidney,Children adpkd,Hyperechogenic kidneys,Polycystic kidney.

      Paul J D Winyard:KOL impact

      Concepts related to the work of other authors for whichfor which Paul J D Winyard has influence:Urinary tract,Kidney disease,Congenital anomalies,Kallmann syndrome,Renal dysplasia,Primary cilia,Growth factor.

      KOL Resume for Paul J D Winyard

      Year
      2022

      UCL Great Ormond Street Institute of Child Health, London, UK

      2021

      Nephro-Urology Research Group, Developmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK

      2019

      UCL Great Ormond Street Institute of Child Health, 30 Guilford St, Holborn, WC1N 1EH, London, UK

      From the Department of General Pediatrics, Adolescent Medicine and Neonatology, Center for Pediatrics, Medical Center-University of Freiburg, Mathildenstr 1, 79106 Freiburg, Germany (C.G.); Department of Pediatric Radiology, Jeanne de Flandre Mother and Child Hospital, University of Lille, Lille, France (E.F.A.); Department of Pediatric Radiology, University Hospital of Leuven, Leuven, Belgium (L.B.); Department of Pediatrics, University Hospital of Cologne, Cologne, Germany (K.B.); Department of Bioengineering, IRCCS Mario Negri Institute for Pharmacological Research, Bergamo, Italy (A.C.); Department of Pediatrics II, University Hospital Essen, Essen, Germany (M.C.); Department of Pediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School, Hannover, Germany (D.H., D.F., L.P.); Division of Nephrology, Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, Pa (E.A.H.); Department of General Pediatrics, University Children's Hospital, Münster, Germany (J.K., A.T.); Department of Pediatrics and Center for Molecular Medicine, University Hospital of Cologne, Cologne, Germany (M.C.L.); Department of Pediatric Nephrology, University Hospital of Leuven, Leuven, Belgium (D.M.); PKD Research Group, Laboratory of Pediatrics, Department of Development and Regeneration, GPURE, KU Leuven, Leuven, Belgium (D.M.); PKD Research Group, Department of Development and Regeneration, Catholic University Leuven (KU Leuven), Leuven, Belgium (D.M.); Academic Nephrology Unit, Department of Infection Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, England (A.C.M.O.); Department of Nephrology, Fundació Puigvert, Autonomous University of Barcelona, IIB Sant Pau, REDINREN, Barcelona, Spain (R.T.); University College London Great Ormond Street, Institute of Child Health, London, England (P.J.D.W.); and Division of Pediatric Nephrology, Center for Pediatrics and Adolescent Medicine, Heidelberg University Hospital, Heidelberg, Germany (F.S.).

      2018

      Fetal Medicine Unit, Elizabeth Garrett Anderson Hospital, University College Hospitals London, Huntley Street, London WC1N 6AU, UK; Nephro-Urology Group, Developmental Biology and Cancer programme, University College London Great Ormond Street Institute of Child Health, 30 Guildford Street, London WC1N 1EH, UK. Electronic address:

      Developmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK

      UCL Great Ormond Street Institute of Child Health, University College London, London, England

      2017

      Developmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, University College London, London WC1N 1EH, UK

      2016

      Nephrology Section , Developmental Biology and Cancer Programme (DBCP), UCL Institute of Child Health (ICH), London, UK

      Developmental Biology and Cancer Programme, UCL Institute of Child Health, London, United Kingdom

      2015

      Developmental Biology and Cancer, Institute of Child Health, University College London, London, United Kingdom

      2013

      Nephro-Urology Unit, UCL Institute of Child Health, 30 Guilford Street, London, UK

      2011

      Nephro-Urology Unit, UCL Institute of Child Health, 30 Guilford St, London, WC1N 1EH, UK

      2010

      Nephrourology, UCL Institute of Child Health, London, England

      2009

      *Nephrology, Urology, and Clinical Genetics Units, Great Ormond Street Hospital NHS Trust, and §Centre for Nephrology, Royal Free Hospital, University College London, London, and †Peninsula Medical School, Institute of Biomedical and Clinical Science, Exeter, United Kingdom; and ‡Institut für Zellbiologie, Universitätsklinikum Essen, Universität Duisburg-Essen, Essen, Germany

      2008

      *Nephro-Urology Unit, †Centre for Paediatric Epidemiology and Biostatistics, and ‡Centre for Evidence-Based Child Health, University College London Institute of Child Health, London, United Kingdom

      Nephro‐urology Unit, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK

      2007

      Nephro‐Urology, and

      UCL Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK

      2006

      Nephro-Urology Unit, University College London, London, United Kingdom

      Institute of Child Health, Royal Free and University College London, London, UK.

      2005

      *Nephro-Urology; †Clinical & Molecular Genetics Units, Institute of Child Health, University College London, London, United Kingdom; ‡Ronald O. Perelman Department of Dermatology and Departments of Pharmacology and Urology, New York University School of Medicine, New York, New York; and §Departments of Paediatric Urology and Nephrology, St. James’ University Hospital, Leeds, United Kingdom

      2004

      Nephro-Urology and Paediatric Epidemiology and Biostatistics Units, Institute of Child Health, University College London, London, UK

      2003

      Nephro-Urology Unit, Institute of Child Health, University College London, London, United Kingdom

      2002

      Centre for Nephrology, Institute of Urology and Nephrology, Middlesex Hospital, Nephro-Urology Unit, Institute of Child Health and, Autonomic Neuroscience Unit, Royal Free and University College Medical School, University College London, London, UK

      From the Nephro-Urology Unit, Institute of Child Health, Division of Applied Physiology, Institute of Urology and Nephrology and Department of Obstetrics and Gynaecology, University College London, London, United Kingdom

      2001

      Nephro-Urology Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK

      Division of Protein Structure, National Institute for Medical Research, London, United Kingdom.

      2000

      Nephro-Urology Units, Institute of Child Health, University College, London, United Kingdom

      1997

      Nephrourology, Units, Institute of Child Health, WC1N 1EH, London, United Kingdom

      Department of Nephrourology and Developmental Biology On behalf of the Institute of Child Health and Great Ormond Street clinical research fellows and lecturers forum

      1996

      Development Biology and Nephro-Urology Units, Institute of Child Health, London, UK.

      Queen Elizabeth Hospital for Children, London, United Kingdon

      Department of Paediatric Nephrology, Sophia Childrens Hospital, Rottterdam, The Netherlands

      1995

      Developmental Biology Unit, Institute of Child Health, London WC1N 1EH, UK

      Unit of Medicine, Institute of Child Health, London.

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      Sample of concepts for which Paul J D Winyard is among the top experts in the world.
      Concept World rank
      deregulates pax2 #1
      dysplastic kidneys #1
      large hyperechogenic #1
      orpk cystic mice #1
      uk career path #1
      native nephrogenic niche #1
      order clinical implications #1
      equally variable implications #1
      induces calcium influx #1
      4 anhydramnios #1
      accounts pathogenesis #1
      academic paediatric medicine #1
      cakut contributing factors #1
      fetus future pregnancies #1
      tide strategies #1
      recapitulate nephrogenesis #1
      applied embryology pathogenesis #1
      functiondevelopmental anatomy nephrogenesistranscription #1
      renal cells kidney #1
      structurally abnormal cilia #1
      hyperechogenic kidneys #1
      introductionstructure functiondevelopmental anatomy #1
      dysplastic polycystic #1
      failure ckd5 #1
      renal malformationsagenda #1
      detectable monogenic mutations #1
      severe bilateral dysplasia #1
      renal malformationsagenda futureconclusionreferences #1
      future leaders medical #1
      nonsyndromic sporadic cases #1
      impairment deregulates #1
      apical surface cilia #1
      pathogenesis congenital anomalies #1
      academic paediatric trainee #1
      cystic epithelia #1
      cystic renal conditions #1
      cakut teratogens #1
      multiple cakut genes #1
      classical 92 cilia #1
      nephrogenesistranscription #1
      mechanisms renal pathology #1
      prominent vascular spaces #1
      human kidney repair #1
      nephrons regenerative #1
      correct human markers #1
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      Prominent publications by Paul J D Winyard

      KOL-Index: 11727

      Defects of either anosmin-1 or fibroblast growth factor receptor 1 (FGFR1) are known to underlie hereditary Kallmann's syndrome (KS), a human disorder of olfactory and gonadotropin-releasing hormone (GnRH) neuronal ontogeny. Here, we report a functional interaction between anosmin-1 and the FGFR1-FGF2-heparan sulfate complex, leading to amplified responses in the FGFR1 signaling pathway. In human embryonic GnRH olfactory neuroblasts, wild-type anosmin-1, but not proteins with ...

      Known for Fibroblast Growth | Receptor 1 | Releasing Hormone | Heparan Sulfate | Mitogen Activated
      KOL-Index: 11657

      BACKGROUND: Recently, we identified a microduplication in chromosomal band 1q21.1 encompassing the CHD1L/ALC1 gene encoding a chromatin-remodelling enzyme in congenital anomalies of the kidneys and urinary tract (CAKUT) patient.

      METHODS: To explore the role of CHD1L in CAKUT, we screened 85 CAKUT patients for mutations in the CHD1L gene and performed functional analyses of the three heterozygous missense variants detected. In addition, we quantitatively determined CHD1L expression in ...

      Known for Urinary Tract | Congenital Anomalies | Role Chd1l | Gene Cakut | Kidney Development
      KOL-Index: 11088

      Mutations in hepatocyte nuclear factor 1B (HNF1B), which is a transcription factor expressed in tissues including renal epithelia, associate with abnormal renal development. While studying renal phenotypes of children with HNF1B mutations, we identified a teenager who presented with tetany and hypomagnesemia. We retrospectively reviewed radiographic and laboratory data for all patients from a single center who had been screened for an HNF1B mutation. We found heterozygous mutations in 21 ...

      Known for Hnf1b Mutations | Renal Magnesium | Nuclear Factor | Chronic Kidney Disease | 1 Beta
      KOL-Index: 10395

      The last 10 years has witnessed an explosion in research into roles of cilia in cystic renal disease. Cilia are membrane-enclosed finger-like projections from the cell, usually on the apical surface or facing into a lumen, duct or airway. Ten years ago, the major recognised functions related to classical "9+2" cilia in the respiratory and reproductive tracts, where co-ordinated beating clears secretions and assists fertilisation respectively. Primary cilia, which have a "9+0" arrangement ...

      Known for Polycystic Kidney Disease | Primary Cilia | Apical Surface | Cell Differentiation | Basal Body
      KOL-Index: 9473

      Renal hypodysplasia (RHD) is characterized by reduced kidney size and/or maldevelopment of the renal tissue following abnormal organogenesis. Mutations in renal developmental genes have been identified in a subset of affected individuals. Here, we report the first mutations in BMP4 and SIX2 identified in patients with RHD. We detected 3 BMP4 mutations in 5 RHD patients, and 3 SIX2 mutations in 5 different RHD patients. Overexpression assays in zebrafish demonstrated that these mutations ...

      Known for Bmp4 Mutations | Kidney Development | Zebrafish Proteins | Renal Tissue | Six2 Patients
      KOL-Index: 9005

      Galectin-3 is a β-galactoside binding lectin with roles in diverse processes including proliferation, apoptosis, inflammation and fibrosis which are dependent on different domains of the molecule and subcellular distribution. Although galectin-3 is known to be upregulated in acute kidney injury, the relative importance of its different domains and functions are poorly understood in the underlying pathogenesis. Therefore we experimentally modulated galectin-3 in folic acid (FA)-induced ...

      Known for Kidney Injury | Modified Citrus Pectin | Folic Acid | Mcp Galectin3 | Renal Fibrosis
      KOL-Index: 8985

      Autosomal Dominant Polycystic Kidney Disease (ADPKD) is thought to affect about 1 in 1000 people in the UK. ADPKD causes a progressive decline in kidney function, with kidney failure tending to occur in middle age. Children and young people with ADPKD may not have any symptoms. However they may have high blood pressure, which may accelerate progression to later stages of chronic kidney disease.There is uncertainty and variation in how health professionals manage children and young people ...

      Known for Adpkd Children | Polycystic Kidney | Autosomal Dominant | Blood Pressure | Genetic Testing
      KOL-Index: 8721

      Renal malformations are the commonest cause of chronic renal failure in children and they are often associated with urinary tract abnormalities that impair fetal urine flow. Up-regulation of transforming growth factor-beta1 (TGF-beta1) occurs after experimental postnatal urinary tract obstruction and we recently reported increased levels of TGF-beta1 in human renal malformations (Yang SP et al, Am J Pathol 2000, 157:1633-1647). These findings led us to propose that obstruction-induced ...

      Known for Growth Factor | Fetal Sheep | Messenger Receptors | Tgf Beta1 | Renal Malformations
      KOL-Index: 8203

      Hepatocyte growth factor/scatter factor (HGF/SF) is secreted by mesenchymal cells and elicits proliferation, motility, differentiation, and morphogenesis of epithelia and other cells. These effects are mediated by binding to MET, a receptor tyrosine kinase. Genetically engineered mice lacking HGF/SF die in utero due to a failure of placental and hepatocyte differentiation, but little information exists regarding the expression of this signaling system in human development. Using reverse ...

      Known for Growth Factor | Hgf Protein | Human Embryonic | Mesenchymal Cells | Chain Reaction
      KOL-Index: 8045

      Human dysplastic kidneys are developmental aberrations which are responsible for many of the very young children with chronic renal failure. They contain poorly differentiated metanephric cells in addition to metaplastic elements. We recently demonstrated that apoptosis was prominent in undifferentiated cells around dysplastic tubules (Winyard, P.J.D., J. Nauta, D.S. Lirenman, P. Hardman, V.R. Sams, R.A. Risdon, and A.S. Woolf. 1996. Kidney Int. 49:135-146), perhaps explaining the ...

      Known for Dysplastic Epithelia | Human Kidney | Pax2 Transcription | Cell Proliferation | Proto Oncogene
      KOL-Index: 7856

      PURPOSE: Congenital bladder outflow obstruction caused by posterior urethral valves is a common cause of end stage renal failure in boys. We hypothesized that fetal bladder outflow obstruction perturbs detrusor contractility and innervation and bladder storage volume-pressure relationships.

      MATERIALS AND METHODS: Severe bladder outflow obstruction was induced in male fetal sheep by placing a urethral ring and urachal ligation midway through gestation at 75 days. Fetuses were examined 30 ...

      Known for Outflow Obstruction | Fetal Sheep | Urinary Bladder | Detrusor Contractility | Urachal Ligation
      KOL-Index: 7735

      CONTEXT: Autosomal dominant polycystic kidney disease (ADPKD) is a common disorder that can cause hypertension during childhood, but the true prevalence of hypertension during childhood is not known.

      OBJECTIVE: We undertook a systematic review and meta-analysis to determine the prevalence of hypertension in children with ADPKD.

      DATA SOURCES: Systematic review of articles published between 1980 and 2015 in MEDLINE and EMBASE.

      STUDY SELECTION: Studies selected by two authors independently ...

      Known for Children Adpkd | Polycystic Kidney | Autosomal Dominant | Hypertension Proteinuria | Renal Function
      KOL-Index: 7522

      FSGS is a CKD with heavy proteinuria that eventually progresses to ESRD. Hereditary forms of FSGS have been linked to mutations in the transient receptor potential cation channel, subfamily C, member 6 (TRPC6) gene encoding a nonselective cation channel. Most of these TRPC6 mutations cause a gain-of-function phenotype, leading to calcium-triggered podocyte cell death, but the underlying molecular mechanisms are unclear. We studied the molecular effect of disease-related mutations using ...

      Known for Trpc6 Mutations | Cation Channel | Function Mutation | Dominant Negative | Focal Segmental
      KOL-Index: 7386

      Kallmann's syndrome (KS) is characterised by the association of anosmia and isolated hypogonadotrophic hypogonadism (IHH). Mutations of the KAL gene which is located at Xp22.3 cause X-linked KS (XKS). In this study we used the reverse transcriptase polymerase chain reaction and in situ hybridisation to examine the developmental expression of KAL in the first trimester of pregnancy, the earliest stage of human gestation examined thus far. At 45 days after fertilisation KAL mRNA was ...

      Known for Human Development | Kal Gene | Olfactory Bulb | Spinal Cord | Expression Pattern
      KOL-Index: 7359

      Congenital anomalies of the kidney and urinary tract (CAKUT) are the commonest cause of chronic kidney disease in children. Structural anomalies within the CAKUT spectrum include renal agenesis, kidney hypo-/dysplasia, multicystic kidney dysplasia, duplex collecting system, posterior urethral valves and ureter abnormalities. While most CAKUT cases are sporadic, familial clustering of CAKUT is common, emphasizing a strong genetic contribution to CAKUT origin. Animal experiments ...

      Known for Congenital Anomalies | Urinary Tract | Human Cakut | Renal Agenesis | Kidney Development

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      UCL Great Ormond Street Institute of Child Health, London, UK | University College London Great Ormond Street, Institute of Child Health, London, UK. | Nephro-Urology Research Group, Developmental Biology and Cancer Programme, UCL Great Ormond Street

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