22 results match your criteria: "Charité Medical Faculty and Max Delbrück Center (MDC) for Molecular Medicine[Affiliation]"

Background: Oxylipins, the oxidative metabolites of polyunsaturated fatty acids (PUFAs), serve as key mediators of oxidative stress, inflammatory responses, and vasoactive reactions in vivo. Our previous work has established that hemodialysis affects both long chain fatty acids (LCFAs) and oxylipins in plasma and erythrocytes to varying degrees, which may be responsible for excess cardiovascular complications in end-stage renal disease. In this study, we aimed to determine changes in blood oxylipins during cardiopulmonary bypass (CPB) in patients undergoing cardiac surgery to identify novel biomarkers and potential metabolites of CPB-related complications.

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Article Synopsis
  • * There is still limited understanding of the pathogenesis of VHD, but metabolomics can help in understanding its development, diagnosis, and prognosis.
  • * The study reviews key metabolic biomarkers for different types of VHD, discusses their potential for patient outcome predictions, and addresses challenges in conducting metabolomics research in a clinical setting.
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Corrigendum to "Hemodialysis and Biotransformation of Erythrocyte Epoxy Fatty Acids in Peripheral Tissue".

Prostaglandins Leukot Essent Fatty Acids

December 2023

Experimental and Clinical Research Center (ECRC), a joint institution of the Charité Medical Faculty and Max Delbrück Center (MDC) for Molecular Medicine, 13125 Berlin; Department of Nephrology and Medical Intensive Care, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin; HELIOS Klinikum Berlin-Buch, Schwanebecker Chaussee 50, 13125 Berlin. Electronic address:

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Hemodialysis and biotransformation of erythrocyte epoxy fatty acids in peripheral tissue.

Prostaglandins Leukot Essent Fatty Acids

June 2022

Experimental and Clinical Research Center (ECRC), a joint institution of the Charité Medical Faculty and Max Delbrück Center (MDC) for Molecular Medicine, Berlin 13125, Germany; Department of Nephrology and Medical Intensive Care, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, Berlin 13353; HELIOS Klinikum Berlin-Buch, Schwanebecker Chaussee 50, Berlin 13125, Germany. Electronic address:

Cardiovascular disease is the leading cause of mortality in patients with renal failure. Red blood cells (RBCs) are potential reservoirs for epoxy fatty acids (oxylipins) that regulate cardiovascular function. Hemoglobin exhibits pseudo-lipoxygenase activity in vitro.

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Long-chain fatty acids (LCFAs) serve as energy sources, components of cell membranes, and precursors for signaling molecules. Uremia alters LCFA metabolism so that the risk of cardiovascular events in chronic kidney disease (CKD) is increased. End-stage renal disease (ESRD) patients undergoing dialysis are particularly affected and their hemodialysis (HD) treatment could influence blood LCFA bioaccumulation and transformation.

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Background: There are no systematic reviews of cerebrospinal fluid and blood biomarkers for sporadic Creutzfeldt-Jakob disease (sCJD) in specialized care settings that compare diagnostic accuracies in a network meta-analysis (NMA).

Methods: We searched Medline, Embase, and Cochrane Library for diagnostic studies of sCJD biomarkers. Studies had to use established diagnostic criteria for sCJD and for diseases in the non-CJD groups, which had to represent a consecutive population of patients suspected as a CJD case, as reference standard.

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Factors causing the increased cardiovascular morbidity and mortality in hemodialysis (HD) patients are largely unknown. Oxylipins are a superclass of lipid mediators with potent bioactivities produced from oxygenation of polyunsaturated fatty acids. We previously assessed the impact of HD on oxylipins in arterial blood plasma and found that HD increases several oxylipins.

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Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling.

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Article Synopsis
  • - Previous studies have shown that common genetic variants are linked to eczema, but this research focuses on understanding the impact of rare genetic variants on eczema risk by analyzing 21 different study groups.
  • - The study finds that rare genetic variants in specific genes (DUSP1, NOTCH4, and SLC9A4) are associated with eczema, with some variants likely affecting important protein functions.
  • - Additionally, the researchers identify five new common variants related to other genes, revealing that over 20% of the genetic heritability for eczema is due to these rare and low-frequency variants, opening up potential avenues for new treatments.
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Does the proteasome inhibitor bortezomib sensitize to DNA-damaging therapy in gastroenteropancreatic neuroendocrine neoplasms? - A preclinical assessment in vitro and in vivo.

Neoplasia

January 2021

Department of Hematology, Oncology and Tumor Immunology, Charité-Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany; Department of Gastroenterology and Endocrinology, Zentralklinik Bad Berka GmbH, Bad Berka, Germany; Department of Medical Immunology, Charité Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Berlin, Germany.

Background: Well-differentiated gastroenteropancreatic neuroendocrine neoplasms are rare tumors with a slow proliferation. They are virtually resistant to many DNA-damaging therapeutic approaches, such as chemo- and external beam therapy, which might be overcome by DNA damage inhibition induced by proteasome inhibitors such as bortezomib.

Methods And Results: In this study, we assessed several combined treatment modalities in vitro and in vivo.

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Omega-3 (n-3) fatty acids have beneficial cardiovascular effects, perhaps also in chronic kidney disease (CKD) patients. A low omega-3 index is an independent cardiovascular risk factor in end-stage renal disease (ESRD) dialysis patients. However, the plasma measurements invariably ignore circulating blood cells, including the preponderant erythrocytes (RBCs).

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deletion causes extensive vacuolation that consumes the insulin content of pancreatic β cells.

Proc Natl Acad Sci U S A

October 2019

Molecular Diabetology, Paul Langerhans Institute Dresden (PLID) of the Helmholtz German Center for Diabetes Research (DZD e.V.) Munich, University Hospital Carl Gustav Carus and Faculty of Medicine, TU Dresden, 01307 Dresden, Germany.

Article Synopsis
  • Pancreatic β cells store insulin in granules, which release insulin when blood glucose rises, while damaged granules are degraded through processes like crinophagy and autophagy.* -
  • A study showed that deleting a specific component essential for lysosomal function in mouse β cells led to the buildup of large vacuoles, reduced insulin levels, and poor regulation of glucose.* -
  • The findings highlight that the regulation of insulin granule turnover is crucial for β cell health, suggesting that maintaining this balance is important for preventing diabetes.*
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Omega-3 fatty acids have long been ascribed a positive cardiovascular function. However, the plasma measurements invariably ignore 40% of the blood specimen, cells that engage in continuous exchange with their environment. In our study, we included all components of the circulating blood.

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H S is a gaseous signaling molecule that modifies cysteine residues in proteins to form persulfides (P-SSH). One family of proteins modified by H S are zinc finger (ZF) proteins, which contain multiple zinc-coordinating cysteine residues. Herein, we report the reactivity of H S with a ZF protein called tristetraprolin (TTP).

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In the version of this article initially published, in Fig. 3, the y-axis numbering did not match the log scale indicated in the axis label. The error has been corrected in the HTML and PDF version of the article.

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Genome-wide association and HLA fine-mapping studies identify risk loci and genetic pathways underlying allergic rhinitis.

Nat Genet

August 2018

COPSAC, Copenhagen Prospective Studies on Asthma in Childhood, Herlev and Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark.

Article Synopsis
  • Allergic rhinitis, affecting 400 million people globally, is on the rise in western countries, prompting a detailed genetic analysis involving 59,762 cases and 152,358 controls to identify risk factors.
  • The study found 41 genetic loci linked to allergic rhinitis, including 20 previously unidentified, and validated these findings in an additional group of 60,720 cases and 618,527 controls.
  • The research suggests that common genetic mechanisms underlie different types of rhinitis, paving the way for potential new treatment and prevention strategies targeting the identified genetic factors.
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Members of the transient receptor potential (TRP) cation channel receptor family have unique sites of regulatory function in the kidney which enables them to promote regional vasodilatation and controlled Ca influx into podocytes and tubular cells. Activated TRP vanilloid 1 receptor channels (TRPV1) have been found to elicit renoprotection in rodent models of acute kidney injury following ischaemia/reperfusion. Transient receptor potential cation channel, subfamily C, member 6 (TRPC6) in podocytes is involved in chronic proteinuric kidney disease, particularly in focal segmental glomerulosclerosis (FSGS).

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Hydrogen sulfide (H2S) is known to act protectively during renal ischemia/reperfusion injury (IRI). However, the role of the endogenous H2S in acute kidney injury (AKI) is largely unclear. Here, we analyzed the role of cystathionine gamma-lyase (CTH) in acute renal IRI using CTH-deficient (Cth(-/-)) mice whose renal H2S levels were approximately 50% of control (wild-type) mice.

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Genetic association studies have identified 21 loci associated with atopic dermatitis risk predominantly in populations of European ancestry. To identify further susceptibility loci for this common, complex skin disease, we performed a meta-analysis of >15 million genetic variants in 21,399 cases and 95,464 controls from populations of European, African, Japanese and Latino ancestry, followed by replication in 32,059 cases and 228,628 controls from 18 studies. We identified ten new risk loci, bringing the total number of known atopic dermatitis risk loci to 31 (with new secondary signals at four of these loci).

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Novel childhood asthma genes interact with in utero and early-life tobacco smoke exposure.

J Allergy Clin Immunol

March 2014

Department of Epidemiology, University of Groningen, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands; Groningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. Electronic address:

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Pressure natriuresis in AT(2) receptor-deficient mice with L-NAME hypertension.

J Am Soc Nephrol

February 2003

Max-Delbrück-Center (MDC) for Molecular Medicine, HELIOS-Klinikum-Berlin, Franz Volhard Clinic, Medical Faculty of the Charité, Humboldt University, Berlin, Germany.

AT(2) receptor-disrupted (AT(2) -/-) mice provide a unique opportunity to investigate the cardiovascular and BP-related effects of NO depletion. This study compared the pressure-diuresis-natriuresis relationship in (AT(2) -/-) and wild-type (AT(2) +/+) mice after treating the animals with L-NAME (130 mg/kg body wt per day) for 1 wk. L-NAME increased mean arterial pressure (MAP) more in AT(2) -/- than in AT(2) +/+ mice (118 +/- 2 versus 108 +/- 4 mmHg).

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