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  1. Artikel ; Online: Primary glomerulonephritis

    Jürgen Floege

    Kidney Research and Clinical Practice, Vol 32, Iss 3, Pp 103-

    A review of important recent discoveries

    2013  Band 110

    Abstract: The publication of the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines on the treatment of glomerular diseases in 2012 marked a milestone in this field, as it is the first time that comprehensive guidelines are provided for such disease ... ...

    Abstract The publication of the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines on the treatment of glomerular diseases in 2012 marked a milestone in this field, as it is the first time that comprehensive guidelines are provided for such disease entities. The current review focuses on major findings, both pathogenesis related and clinical, in the primary glomerulonephritis that have been made after the guidelines came into effect.
    Schlagwörter Focal segmental glomerulosclerosis ; IgA nephropathy ; Membranoproliferative glomerulonephritis ; Membranous glomerulonephritis ; Minimal change disease ; Internal medicine ; RC31-1245 ; Specialties of internal medicine ; RC581-951
    Sprache Englisch
    Erscheinungsdatum 2013-09-01T00:00:00Z
    Verlag The Korean Society of Nephrology
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Cardiac Remodeling in Chronic Kidney Disease

    Nadine Kaesler / Anne Babler / Jürgen Floege / Rafael Kramann

    Toxins, Vol 12, Iss 3, p

    2020  Band 161

    Abstract: Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart ... ...

    Abstract Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
    Schlagwörter uremia ; uremic cardiomyopathy ; organ crosstalk ; cardiorenal syndrome ; chronic kidney disease ; left-ventricular hypertrophy ; heart failure ; cardiac fibrosis ; Medicine ; R
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-03-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Impact of sucroferric oxyhydroxide on the oral and intestinal microbiome in hemodialysis patients

    Mohamed M. H. Abdelbary / Christoph Kuppe / Sareh Said-Yekta Michael / Thilo Krüger / Jürgen Floege / Georg Conrads

    Scientific Reports, Vol 12, Iss 1, Pp 1-

    2022  Band 15

    Abstract: Abstract Hyperphosphatemia is a consequence of chronic kidney disease associated with mineral/bone impairment, increased cardiovascular events and mortality. Therapeutically, most dialysis patients have to take phosphate binders. Here, we investigated ... ...

    Abstract Abstract Hyperphosphatemia is a consequence of chronic kidney disease associated with mineral/bone impairment, increased cardiovascular events and mortality. Therapeutically, most dialysis patients have to take phosphate binders. Here, we investigated effects of the Fe(3+)-based phosphate binder sucroferric oxyhydroxide (SFOH) on the oral and gastrointestinal microbiome of 11 hemodialysis patients. Saliva, dental plaque and stool were collected at baseline, one and four weeks of SFOH intake and subjected to 16S rRNA gene (V3-V4 region) directed Illumina MiSeq-based analysis. Total Fe, Fe(2+) and Fe(3+) were determined in stool and saliva. Overall, the microbiome did not change significantly. However, some patient-, sample- and taxon-specific differences were noted, which allowed patients to be divided into those with a shift in their microbiome (6/11) and those without a shift (5/11). Total Fe and Fe(2+) were highest after one week of SFOH, particularly in patients who exhibited a shift in microbiome composition. Eight bacterial taxa showed significant unidirectional changes during treatment. In-depth microbiome analysis revealed that taxa that significantly benefited from iron plethora had no iron-binding siderophores or alternatives, which was in contrast to taxa that significantly declined under iron plethora. Patients with microbiome-shift were significantly younger and had higher serum phosphate concentrations. In conclusion, this study sheds light on the impact of iron on the microbiome of hemodialysis patients.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2022-06-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: New Aspects of Kidney Fibrosis–From Mechanisms of Injury to Modulation of Disease

    Marcus J. Moeller / Rafael Kramann / Twan Lammers / Bernd Hoppe / Eicke Latz / Isis Ludwig-Portugall / Peter Boor / Jürgen Floege / Christian Kurts / Ralf Weiskirchen / Tammo Ostendorf

    Frontiers in Medicine, Vol

    2022  Band 8

    Abstract: Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative ... ...

    Abstract Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative Research Center “Organ Fibrosis: From Mechanisms of Injury to Modulation of Disease” (referred to as SFB/TRR57) was hosted from 2009 to 2021 by the Medical Faculties of RWTH Aachen University and the University of Bonn. This consortium had the ultimate goal of discovering new common but also different fibrosis pathways in the liver and kidneys. It finally successfully identified new mechanisms and established novel therapeutic approaches to interfere with hepatic and renal fibrosis. This review covers the consortium's key kidney-related findings, where three overarching questions were addressed: (i) What are new relevant mechanisms and signaling pathways triggering renal fibrosis? (ii) What are new immunological mechanisms, cells and molecules that contribute to renal fibrosis?, and finally (iii) How can renal fibrosis be modulated?
    Schlagwörter renal fibrosis ; myofibroblast ; parietal epithelial cell ; inflammasome ; crystals ; lupus erythematodes ; Medicine (General) ; R5-920
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2022-01-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: MicroRNAs in Chronic Kidney Disease

    Linsey J. F. Peters / Jürgen Floege / Erik A. L. Biessen / Joachim Jankowski / Emiel P. C. van der Vorst

    International Journal of Molecular Sciences, Vol 21, Iss 6547, p

    Four Candidates for Clinical Application

    2020  Band 6547

    Abstract: There are still major challenges regarding the early diagnosis and treatment of chronic kidney disease (CKD), which is in part due to the fact that its pathophysiology is very complex and not clarified in detail. The diagnosis of CKD commonly is made ... ...

    Abstract There are still major challenges regarding the early diagnosis and treatment of chronic kidney disease (CKD), which is in part due to the fact that its pathophysiology is very complex and not clarified in detail. The diagnosis of CKD commonly is made after kidney damage has occurred. This highlights the need for better mechanistic insight into CKD as well as improved clinical tools for both diagnosis and treatment. In the last decade, many studies have focused on microRNAs (miRs) as novel diagnostic tools or clinical targets. MiRs are small non-coding RNA molecules that are involved in post-transcriptional gene regulation and many have been studied in CKD. A wide array of pre-clinical and clinical studies have highlighted the potential role for miRs in the pathogenesis of hypertensive nephropathy, diabetic nephropathy, glomerulonephritis, kidney tubulointerstitial fibrosis, and some of the associated cardiovascular complications. In this review, we will provide an overview of the miRs studied in CKD, especially highlighting miR-103a-3p, miR-192-5p, the miR-29 family and miR-21-5p as these have the greatest potential to result in novel therapeutic and diagnostic strategies.
    Schlagwörter MicroRNAs ; kidney fibrosis ; chronic kidney disease ; clinical application ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-09-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate.

    Anne Babler / Carlo Schmitz / Andrea Buescher / Marietta Herrmann / Felix Gremse / Theo Gorgels / Juergen Floege / Willi Jahnen-Dechent

    PLoS ONE, Vol 15, Iss 2, p e

    2020  Band 0228938

    Abstract: Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly ...

    Abstract Calcifications can disrupt organ function in the cardiovascular system and the kidney, and are particularly common in patients with chronic kidney disease (CKD). Fetuin-A deficient mice maintained against the genetic background DBA/2 exhibit particularly severe soft tissue calcifications, while fetuin-A deficient C57BL/6 mice remain healthy. We employed molecular genetic analysis to identify risk factors of calcification in fetuin-A deficient mice. We sought to identify pharmaceutical therapeutic targets that could be influenced by dietary of parenteral supplementation. We studied the progeny of an intercross of fetuin-A deficient DBA/2 and C57BL/6 mice to identify candidate risk genes involved in calcification. We determined that a hypomorphic mutation of the Abcc6 gene, a liver ATP transporter supplying systemic pyrophosphate, and failure to regulate the Trpm6 magnesium transporter in kidney were associated with severity of calcification. Calcification prone fetuin-A deficient mice were alternatively treated with parenteral administration of fetuin-A dietary magnesium supplementation, phosphate restriction, or by or parenteral pyrophosphate. All treatments markedly reduced soft tissue calcification, demonstrated by computed tomography, histology and tissue calcium measurement. We show that pathological ectopic calcification in fetuin-A deficient DBA/2 mice is caused by a compound deficiency of three major extracellular and systemic inhibitors of calcification, namely fetuin-A, magnesium, and pyrophosphate. All three of these are individually known to contribute to stabilize protein-mineral complexes and thus inhibit mineral precipitation from extracellular fluid. We show for the first time a compound triple deficiency that can be treated by simple dietary or parenteral supplementation. This is of special importance in patients with advanced CKD, who commonly exhibit reduced serum fetuin-A, magnesium and pyrophosphate levels.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Hypoglycemia following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function.

    Armando Coca / Ana Lucia Valencia / Jesus Bustamante / Alicia Mendiluce / Jürgen Floege

    PLoS ONE, Vol 12, Iss 2, p e

    2017  Band 0172961

    Abstract: BACKGROUND:Hypoglycemia is a serious complication following the administration of insulin for hyperkalemia. We determined the incidence of hypoglycemia and severe hypoglycemia (blood glucose <70 or ≤40 mg/dl, respectively) in a cohort of AKI and non- ... ...

    Abstract BACKGROUND:Hypoglycemia is a serious complication following the administration of insulin for hyperkalemia. We determined the incidence of hypoglycemia and severe hypoglycemia (blood glucose <70 or ≤40 mg/dl, respectively) in a cohort of AKI and non-dialysis dependent CKD patients who received an intravenous infusion of insulin plus glucose to treat hyperkalemia. METHODS:We retrospectively reviewed charts of all AKI and non-dialysis dependent CKD patients who received 10 U of insulin plus 50 g glucose to treat hyperkalemia from December 1, 2013 to May 31, 2015 at our Department. RESULTS:One hundred sixty four episodes of hyperkalemia were treated with insulin plus glucose and were eligible for analysis. Serum potassium levels dropped by 1.18 ± 1.01 mmol/l. Eleven treatments (6.1%) resulted in hypoglycemia and two (1.2%) in severe hypoglycemia. A lower pretreatment blood glucose tended to associate with a higher subsequent risk of hypoglycemia. Age, sex, renal function, an established diagnosis of diabetes or previous treatment were not associated with the development of this complication. We did not register any significant adverse events. CONCLUSION:Our intravenous regimen combining an infusion of insulin plus glucose effectively reduced serum potassium levels compared to previous studies and associated a low risk of symptomatic hypoglycemia and other complications.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2017-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Next-Generation Morphometry for pathomics-data mining in histopathology

    David L. Hölscher / Nassim Bouteldja / Mehdi Joodaki / Maria L. Russo / Yu-Chia Lan / Alireza Vafaei Sadr / Mingbo Cheng / Vladimir Tesar / Saskia V. Stillfried / Barbara M. Klinkhammer / Jonathan Barratt / Jürgen Floege / Ian S. D. Roberts / Rosanna Coppo / Ivan G. Costa / Roman D. Bülow / Peter Boor

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Band 14

    Abstract: Pathology diagnostics still rely on tissue morphology assessment by trained experts. Here, the authors perform deep-learning-based segmentation followed by large-scale feature extraction of histological images, i.e., next-generation morphometry, to ... ...

    Abstract Pathology diagnostics still rely on tissue morphology assessment by trained experts. Here, the authors perform deep-learning-based segmentation followed by large-scale feature extraction of histological images, i.e., next-generation morphometry, to enable outcome-relevant and disease-specific pathomics analysis of non-tumor kidney pathology.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2023-01-01T00:00:00Z
    Verlag Nature Portfolio
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    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury

    Yuki Sato / Akiko Oguchi / Yuji Fukushima / Kyoko Masuda / Naoya Toriu / Keisuke Taniguchi / Takahisa Yoshikawa / Xiaotong Cui / Makiko Kondo / Takeshi Hosoi / Shota Komidori / Yoko Shimizu / Harumi Fujita / Li Jiang / Yingyi Kong / Takashi Yamanashi / Jun Seita / Takuya Yamamoto / Shinya Toyokuni /
    Yoko Hamazaki / Masakazu Hattori / Yasunobu Yoshikai / Peter Boor / Jürgen Floege / Hiroshi Kawamoto / Yasuhiro Murakawa / Nagahiro Minato / Motoko Yanagita

    The Journal of Clinical Investigation, Vol 132, Iss

    2022  Band 2

    Abstract: Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling ... ...

    Abstract Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.
    Schlagwörter Inflammation ; Nephrology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-01-01T00:00:00Z
    Verlag American Society for Clinical Investigation
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    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Urinary exosomes

    Silvia Spanu / Claudia R C van Roeyen / Bernd Denecke / Jürgen Floege / Anja S Mühlfeld

    PLoS ONE, Vol 9, Iss 10, p e

    a novel means to non-invasively assess changes in renal gene and protein expression.

    2014  Band 109631

    Abstract: BACKGROUND: In clinical practice, there is a lack of markers for the non-invasive diagnosis and follow-up of kidney disease. Exosomes are membrane vesicles, which are secreted from their cells of origin into surrounding body fluids and contain proteins ... ...

    Abstract BACKGROUND: In clinical practice, there is a lack of markers for the non-invasive diagnosis and follow-up of kidney disease. Exosomes are membrane vesicles, which are secreted from their cells of origin into surrounding body fluids and contain proteins and mRNA which are protected from digestive enzymes by a cell membrane. METHODS: Toxic podocyte damage was induced by puromycin aminonucleoside in rats (PAN). Urinary exosomes were isolated by ultracentrifugation at different time points during the disease. Exosomal mRNA was isolated, amplified, and the mRNA species were globally assessed by gene array analysis. Tissue-specific gene and protein expression was assessed by RT-qPCR analysis and immunohistochemistry. RESULTS: Gene array analysis of mRNA isolated from urinary exosomes revealed cystatin C mRNA as one of the most highly regulated genes. Its gene expression increased 7.5-fold by day 5 and remained high with a 1.9-fold increase until day 10. This was paralleled by a 2-fold increase in cystatin C mRNA expression in the renal cortex. Protein expression in the kidneys also dramatically increased with de novo expression of cystatin C in glomerular podocytes in parts of the proximal tubule and the renal medulla. Urinary excretion of cystatin C increased approximately 2-fold. CONCLUSION: In this proof-of-concept study, we could demonstrate that changes in urinary exosomal cystatin C mRNA expression are representative of changes in renal mRNA and protein expression. Because cells lining the urinary tract produce urinary exosomal cystatin C mRNA, it might be a more specific marker of renal damage than glomerular-filtered free cystatin C.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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