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  1. AU=Coward Richard
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  3. AU="Rebecca A Butcher"
  4. AU="Kimberlyn Roosa"
  5. AU=Chian Ri-Cheng
  6. AU="Alzalzalah, Sayed"
  7. AU=Kaufman Jonathan J
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  15. AU="Teresinha Leal"
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  18. AU="Chauhan, Gaurav B"
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  20. AU=Powell James
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  23. AU="Kreutzer, Susanne" AU="Kreutzer, Susanne"
  24. AU="St John, Maie"
  25. AU=Gerhardy A
  26. AU="Qi, Huixin"
  27. AU="Dobosiewicz, May"
  28. AU="Srivastava, Rakesh"
  29. AU="Grevtsov K.I."

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  1. Artikel ; Online: How to solve a clinical conundrum: Have you tried a trio exome analysis?

    Beal, Felicity / Coward, Richard / Platt, Caroline

    Archives of disease in childhood. Education and practice edition

    2023  Band 108, Heft 6, Seite(n) 456–462

    Abstract: The following report describes the clinical journey of a 5-month-old male infant who presented with a significant kidney injury following a diarrhoeal illness. His course was complicated by severe hypertension and a number of acute life-threatening ... ...

    Abstract The following report describes the clinical journey of a 5-month-old male infant who presented with a significant kidney injury following a diarrhoeal illness. His course was complicated by severe hypertension and a number of acute life-threatening events necessitating periods of time on the intensive care unit, where he received ventilatory support and underwent renal replacement therapy and treatment with a monoclonal antibody therapy.We take the reader on a stepwise journey from presentation through to final diagnosis, discussing important biochemical, haematological and radiological features where learning points are discussed. Guidance on the use of genomic testing strategies for the non-geneticist is provided in some detail with a particular focus on the trio exome analysis that identified the diagnosis for this young boy.This complex case not only provides a number of excellent learning opportunities but also highlights the importance of early involvement of the clinical genetics team and the relevance of the trio exome analysis for rapid identification of rare monogenic diseases.
    Mesh-Begriff(e) Humans ; Infant ; Male ; Exome/genetics ; Kidney Diseases/diagnosis ; Kidney Diseases/etiology ; Kidney Diseases/therapy ; Diarrhea/complications
    Sprache Englisch
    Erscheinungsdatum 2023-07-04
    Erscheinungsland England
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 2148818-6
    ISSN 1743-0593 ; 1743-0585
    ISSN (online) 1743-0593
    ISSN 1743-0585
    DOI 10.1136/archdischild-2021-322910
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: An In Vitro Method to Analyze Glucose Uptake in Podocytes.

    Lay, Abigail C / Coward, Richard J

    Methods in molecular biology (Clifton, N.J.)

    2019  Band 2067, Seite(n) 139–143

    Abstract: ... and insulin sensitivity (Lay & Coward, Nephrol Dial Transplant 29:1127-1133, 2014); thus, reliable ... Nephrol 13:630-638, 2002; Coward, Diabetes 54:3095-3102, 2005); this assay is useful for detecting changes ...

    Abstract Podocytes are terminally differentiated, insulin-sensitive cells of the glomerular filtration barrier, with a central role in filtration barrier maintenance. Podocyte injury is one of the earliest features observed in diabetic nephropathy (DN) and plays a key role in the development of albuminuria. Several factors are associated with diabetes-mediated podocyte injury, including dysregulated metabolic pathways and insulin sensitivity (Lay & Coward, Nephrol Dial Transplant 29:1127-1133, 2014); thus, reliable assays to study these responses are key in understanding podocyte alterations in DN. Here, we detail an in vitro method to analyze glucose uptake in conditionally immortalized human podocytes (Saleem, J Am Soc Nephrol 13:630-638, 2002; Coward, Diabetes 54:3095-3102, 2005); this assay is useful for detecting changes in podocyte metabolism, nutrient sensing, and insulin sensitivity.
    Mesh-Begriff(e) Cell Culture Techniques/methods ; Cell Line ; Deoxyglucose/chemistry ; Deoxyglucose/metabolism ; Diabetic Nephropathies/pathology ; Feasibility Studies ; Glucose/chemistry ; Glucose/metabolism ; Humans ; Insulin/metabolism ; Insulin Resistance ; Podocytes/metabolism ; Podocytes/pathology ; Tritium
    Chemische Substanzen Insulin ; Tritium (10028-17-8) ; Deoxyglucose (9G2MP84A8W) ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2019-11-07
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-9841-8_10
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Modeling Podocyte Biology Using Drosophila Nephrocytes.

    Hartley, Paul S / Coward, Richard J

    Methods in molecular biology (Clifton, N.J.)

    2019  Band 2067, Seite(n) 11–24

    Abstract: Vertebrate podocytes are kidney glomerular cells critically required for normal renal filtration. To fulfill their role, podocytes form molecular sieves known as slit diaphragms that contribute to the glomerular filtration barrier. The disruption of ... ...

    Abstract Vertebrate podocytes are kidney glomerular cells critically required for normal renal filtration. To fulfill their role, podocytes form molecular sieves known as slit diaphragms that contribute to the glomerular filtration barrier. The disruption of podocyte biology or slit diaphragm formation in humans is a precursor to albuminuria, renal failure, and cardiovascular morbidity. Due to genetic and functional similarities, the nephrocytes of Drosophila are increasingly used to model the genetic and metabolic basis of human podocyte biology. They have the advantage that they are a much quicker system to study compared to other murine transgenic models. In this chapter we present methods to modulate and study Drosophila nephrocyte function and diaphragm formation.
    Mesh-Begriff(e) Animals ; Animals, Genetically Modified ; Cell Culture Techniques/methods ; Cell Membrane/metabolism ; Cell Membrane/pathology ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Drosophila melanogaster ; Gene Expression Regulation ; Genetic Engineering/methods ; Humans ; Kidney Diseases/genetics ; Kidney Diseases/pathology ; Kruppel-Like Transcription Factors/genetics ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Nuclear Proteins/genetics ; Optical Imaging/methods ; Podocytes/cytology ; Podocytes/metabolism ; Podocytes/pathology ; Saccharomyces cerevisiae Proteins/genetics ; Transcription Factors/genetics
    Chemische Substanzen DNA-Binding Proteins ; GAL4 protein, S cerevisiae ; Klf15 protein, Drosophila ; Kruppel-Like Transcription Factors ; Membrane Proteins ; Nuclear Proteins ; Saccharomyces cerevisiae Proteins ; Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2019-11-07
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-9841-8_2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Contrasting consequences of podocyte insulin-like growth factor 1 receptor inhibition.

    Hurcombe, Jennifer A / Barrington, Fern / Marchetti, Micol / Betin, Virginie M S / Bowen, Emily E / Lay, Abigail C / Ni, Lan / Dayalan, Lusyan / Pope, Robert J P / Brinkkoetter, Paul T / Holzenberger, Martin / Welsh, Gavin I / Coward, Richard J M

    iScience

    2024  Band 27, Heft 5, Seite(n) 109749

    Abstract: Insulin signaling to the glomerular podocyte via the insulin receptor (IR) is critical for kidney function. In this study we show that near-complete knockout of the closely related insulin-like growth factor 1 receptor (IGF1R) in podocytes is detrimental, ...

    Abstract Insulin signaling to the glomerular podocyte via the insulin receptor (IR) is critical for kidney function. In this study we show that near-complete knockout of the closely related insulin-like growth factor 1 receptor (IGF1R) in podocytes is detrimental, resulting in albuminuria
    Sprache Englisch
    Erscheinungsdatum 2024-04-16
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2024.109749
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: The protective role of peroxisome proliferator-activated receptor gamma in lipotoxic podocytes.

    Carrasco, Almudena G / Izquierdo-Lahuerta, Adriana / Valverde, Ángela M / Ni, Lan / Flores-Salguero, Elena / Coward, Richard J / Medina-Gómez, Gema

    Biochimica et biophysica acta. Molecular and cell biology of lipids

    2023  Band 1868, Heft 7, Seite(n) 159329

    Abstract: Podocytes are specialized epithelial cells that maintain the glomerular filtration barrier. These cells are susceptible to lipotoxicity in the obese state and irreversibly lost during kidney disease leading to proteinuria and renal injury. PPARγ is a ... ...

    Abstract Podocytes are specialized epithelial cells that maintain the glomerular filtration barrier. These cells are susceptible to lipotoxicity in the obese state and irreversibly lost during kidney disease leading to proteinuria and renal injury. PPARγ is a nuclear receptor whose activation can be renoprotective. This study examined the role of PPARγ in the lipotoxic podocyte using a PPARγ knockout (PPARγKO) cell line and since the activation of PPARγ by Thiazolidinediones (TZD) is limited by their side effects, it explored other alternative therapies to prevent podocyte lipotoxic damage. Wild-type and PPARγKO podocytes were exposed to the fatty acid palmitic acid (PA) and treated with the TZD (Pioglitazone) and/or the Retinoid X receptor (RXR) agonist Bexarotene (BX). It revealed that podocyte PPARγ is essential for podocyte function. PPARγ deletion reduced key podocyte proteins including podocin and nephrin while increasing basal levels of oxidative and ER stress causing apoptosis and cell death. A combination therapy of low-dose TZD and BX activated both the PPARγ and RXR receptors reducing PA-induced podocyte damage. This study confirms the crucial role of PPARγ in podocyte biology and that their activation in combination therapy of TZD and BX may be beneficial in the treatment of obesity-related kidney disease.
    Mesh-Begriff(e) Humans ; PPAR gamma/metabolism ; Podocytes ; Pioglitazone/pharmacology ; Thiazolidinediones/metabolism ; Thiazolidinediones/pharmacology ; Thiazolidinediones/therapeutic use ; Kidney Diseases/drug therapy ; Bexarotene/pharmacology
    Chemische Substanzen PPAR gamma ; Pioglitazone (X4OV71U42S) ; Thiazolidinediones ; Bexarotene (A61RXM4375)
    Sprache Englisch
    Erscheinungsdatum 2023-05-06
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbalip.2023.159329
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Adiponectin Reduces Glomerular Endothelial Glycocalyx Disruption and Restores Glomerular Barrier Function in a Mouse Model of Type 2 Diabetes.

    Fawaz, Sarah / Martin Alonso, Aldara / Qiu, Yan / Ramnath, Raina / Stowell-Connolly, Holly / Gamez, Monica / May, Carl / Down, Colin / Coward, Richard J / Butler, Matthew J / Welsh, Gavin I / Satchell, Simon C / Foster, Rebecca R

    Diabetes

    2024  Band 73, Heft 6, Seite(n) 964–976

    Mesh-Begriff(e) Animals ; Glycocalyx/metabolism ; Glycocalyx/drug effects ; Adiponectin/metabolism ; Adiponectin/genetics ; Mice ; Diabetes Mellitus, Type 2/metabolism ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Glomerulus/drug effects ; Humans ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Endothelial Cells/metabolism ; Endothelial Cells/drug effects ; Male ; Glomerular Filtration Barrier/metabolism ; Glomerular Filtration Barrier/drug effects ; Tumor Necrosis Factor-alpha/metabolism ; Syndecan-4/metabolism ; Syndecan-4/genetics ; Disease Models, Animal ; Mice, Inbred C57BL
    Sprache Englisch
    Erscheinungsdatum 2024-03-26
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db23-0455
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: A multi-species, multi-pathogen avian viral disease outbreak event: Investigating potential for virus transmission at the wild bird - poultry interface.

    Reid, Scott M / Byrne, Alexander M P / Lean, Fabian Z X / Ross, Craig S / Pascu, Andrei / Hepple, Richard / Dominguez, Maria / Frost, Susanne / Coward, Vivien J / Núñez, Alejandro / James, Joe / Stephan, Levon / Aegerter, James N / Brown, Ian H / Banyard, Ashley C

    Emerging microbes & infections

    2024  , Seite(n) 2348521

    Abstract: ... ...

    Abstract Abstract
    Sprache Englisch
    Erscheinungsdatum 2024-04-30
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2681359-2
    ISSN 2222-1751 ; 2222-1751
    ISSN (online) 2222-1751
    ISSN 2222-1751
    DOI 10.1080/22221751.2024.2348521
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Peroxisome proliferator activating receptor-γ and the podocyte.

    Platt, Caroline / Coward, Richard J

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

    2016  Band 32, Heft 3, Seite(n) 423–433

    Abstract: Over the past two decades it has become clear that the glomerular podocyte is a key cell in preventing albuminuria, kidney failure and cardiovascular morbidity. Understanding the key pathways that protect the podocyte in times of glomerular stress, which ...

    Abstract Over the past two decades it has become clear that the glomerular podocyte is a key cell in preventing albuminuria, kidney failure and cardiovascular morbidity. Understanding the key pathways that protect the podocyte in times of glomerular stress, which can also be therapeutically manipulated, are highly attractive. In the following review we assess the evidence that the peroxisome proliferator activating receptor (PPAR) agonists are beneficial for podocyte and kidney function with a focus on PPAR-γ. We explain our current understanding of the mechanisms of action of these agonists and the evidence they are beneficial in diabetic and non-diabetic kidney disease. We also outline why these drugs have not been widely used for kidney disease in the past but they may be in the future.
    Mesh-Begriff(e) Albuminuria ; Animals ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/urine ; Humans ; Kidney Diseases/drug therapy ; Kidney Diseases/urine ; Kidney Glomerulus/metabolism ; PPAR gamma/agonists ; PPAR gamma/metabolism ; Peroxisome Proliferator-Activated Receptors ; Podocytes/metabolism ; Thiazolidinediones/therapeutic use
    Chemische Substanzen PPAR gamma ; Peroxisome Proliferator-Activated Receptors ; Thiazolidinediones
    Sprache Englisch
    Erscheinungsdatum 2016-10-03
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 90594-x
    ISSN 1460-2385 ; 0931-0509
    ISSN (online) 1460-2385
    ISSN 0931-0509
    DOI 10.1093/ndt/gfw320
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: MicroRNAs and their delivery in diabetic fibrosis.

    Wonnacott, Alexa / Denby, Laura / Coward, Richard J M / Fraser, Donald J / Bowen, Timothy

    Advanced drug delivery reviews

    2021  Band 182, Seite(n) 114045

    Abstract: The global prevalence of diabetes mellitus was estimated to be 463 million people in 2019 and is predicted to rise to 700 million by 2045. The associated financial and societal costs of this burgeoning epidemic demand an understanding of the pathology of ...

    Abstract The global prevalence of diabetes mellitus was estimated to be 463 million people in 2019 and is predicted to rise to 700 million by 2045. The associated financial and societal costs of this burgeoning epidemic demand an understanding of the pathology of this disease, and its complications, that will inform treatment to enable improved patient outcomes. Nearly two decades after the sequencing of the human genome, the significance of noncoding RNA expression is still being assessed. The family of functional noncoding RNAs known as microRNAs regulates the expression of most genes encoded by the human genome. Altered microRNA expression profiles have been observed both in diabetes and in diabetic complications. These transcripts therefore have significant potential and novelty as targets for therapy, therapeutic agents and biomarkers.
    Mesh-Begriff(e) Biomarkers ; Diabetes Complications/drug therapy ; Diabetes Complications/physiopathology ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/physiopathology ; Drug Carriers ; Fibrosis/drug therapy ; Fibrosis/physiopathology ; Humans ; Hypoglycemic Agents/pharmacology ; Inflammation/metabolism ; MicroRNAs/administration & dosage ; MicroRNAs/pharmacology ; MicroRNAs/therapeutic use ; Nanoparticle Drug Delivery System
    Chemische Substanzen Biomarkers ; Drug Carriers ; Hypoglycemic Agents ; MicroRNAs ; Nanoparticle Drug Delivery System
    Sprache Englisch
    Erscheinungsdatum 2021-11-09
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639113-8
    ISSN 1872-8294 ; 0169-409X
    ISSN (online) 1872-8294
    ISSN 0169-409X
    DOI 10.1016/j.addr.2021.114045
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: The Evolving Importance of Insulin Signaling in Podocyte Health and Disease.

    Lay, Abigail C / Coward, Richard J M

    Frontiers in endocrinology

    2018  Band 9, Seite(n) 693

    Abstract: Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease worldwide, occuring in approximately one-third of diabetic patients. One of the earliest hallmarks of DKD is albuminuria, often occurring following disruptions to the ... ...

    Abstract Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease worldwide, occuring in approximately one-third of diabetic patients. One of the earliest hallmarks of DKD is albuminuria, often occurring following disruptions to the glomerular filtration barrier. Podocytes are highly specialized cells with a central role in filtration barrier maintenance; hence, podocyte dysfunction is a major cause of albuminuria in many settings, including DKD. Numerous studies over the last decade have highlighted the importance of intact podocyte insulin responses in the maintenance of podocyte function. This review summarizes our current perspectives on podocyte insulin signaling, highlighting evidence to support the notion that dysregulated podocyte insulin responses contribute toward podocyte damage, particularly during the pathogenesis of DKD.
    Sprache Englisch
    Erscheinungsdatum 2018-11-21
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2018.00693
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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