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Article ; Online: Die Rolle des Komplementsystems bei Nierenerkrankungen – Neue Aspekte.

Zipfel, Peter F / Zipfel, Svante / Wiech, Thorsten

Deutsche medizinische Wochenschrift (1946)

2023 Volume 148, Issue 12, Page(s) 774–779

Abstract: Complement is a central part of the immune system. In the human body, complement is responsible for recognition of infectious microbes, for coordinating the adaptive immune response, controlling homeotic reactions and for the non-inflammatory removal of ... ...

Title translation	Role of Complement in Kidney Diseases - New Aspects.
Abstract	Complement is a central part of the immune system. In the human body, complement is responsible for recognition of infectious microbes, for coordinating the adaptive immune response, controlling homeotic reactions and for the non-inflammatory removal of modified self-cells and infectious microbes. Complement is also closely linked to another proteolytic cascade, the coagulation system. Defective activation and altered complement regulation drives pathology of several severe human kidney diseases.This manuscript summarizes the latest developments on the role of complement in kidney diseases, on new complement inhibitors and on recent complement targeting therapies. In particular focusing on diseases (1) atypical Hemolytic Uremic Syndrome, (2) C3 Glomerulopathy, (3) Anti Neutrophil Cytoplasmic Antibody Mediated Vasculitis, (4) IgA Nephropathy, (5) Membranous Glomerulopathy, (6) Systemic Lupus Erythematosus, (7) Transplant rejection and (8) COVID 19 Infection-Triggered Kidney Diseases. More excitement is generated in this field, as more and more complement mediated diseases can be treated. Several complement targeting compounds are approved by the EMA and FDA and an increasing number of new candidates are in late phase clinical trials. In addition, clinical guidelines are developed for Diagnosis and Therapy of complement mediated diseases, new biomarkers are evaluated in clinical studies, and diagnostic guidelines are in development. The recent Covid infections showed a clear link of complement in thrombo inflammation, which ultimately results in kidney damage. These aspects have increased further the focus of complement inhibitors in COVID infections.
MeSH term(s)	Humans ; Complement Activation ; COVID-19 ; Complement System Proteins/therapeutic use ; Kidney Diseases/drug therapy ; Complement Inactivating Agents/therapeutic use ; Glomerulonephritis, IGA/drug therapy ; Glomerulonephritis, IGA/pathology ; Kidney/pathology
Chemical Substances	Complement System Proteins (9007-36-7) ; Complement Inactivating Agents
Language	German
Publishing date	2023-05-31
Publishing country	Germany
Document type	English Abstract ; Journal Article
ZDB-ID	200446-x
ISSN	1439-4413 ; 0012-0472
ISSN (online)	1439-4413
ISSN	0012-0472
DOI	10.1055/a-1936-6697
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Article: Die Rolle des Komplementsystems bei Nierenerkrankungen – Neue Aspekte

Zipfel, Peter F. / Zipfel, Svante / Wiech, Thorsten

DMW - Deutsche Medizinische Wochenschrift

2023 Volume 148, Issue 12, Page(s) 774–779

Abstract: Genaue Darstellung von Komplement bei Nierenerkrankungen nachgewiesen : Eine fehlerhafte Komplementaktivierung bzw. eine defekte, unpräzise Regulation von einzelnen Reaktionen dieses Immunsystems sind in der Zwischenzeit bei mehreren unterschiedlichen ... ...

Abstract	Genaue Darstellung von Komplement bei Nierenerkrankungen nachgewiesen : Eine fehlerhafte Komplementaktivierung bzw. eine defekte, unpräzise Regulation von einzelnen Reaktionen dieses Immunsystems sind in der Zwischenzeit bei mehreren unterschiedlichen Nierenerkrankungen klar aufgezeigt worden. Komplementdefekte sind therapierbar : Die komplementvermittelten Pathophysiologien bei den einzelnen Erkrankungen zeigen häufig eine stetige Überaktivierung einzelner Reaktionsschritte. Das genaue Verständnis dieser Mechanismen, die oft einhergehen mit Entzündungsreaktionen, Zellrekrutierung und Zellschädigung, erlauben eine gezielte Target-Identifizierung und den Einsatz von neuen Wirkstoffen. Aktuell gibt es eine Reihe von therapeutischen Wirkstoffen, die in die Komplementkaskade eingreifen. Mehrere Wirkstoffe sind schon für den therapeutischen Einsatz zugelassen, andere befinden sich in fortgeschrittener klinischer Erprobung und sind auf dem Weg zu einer Zulassung. Bei den Wirkstoffklassen für Nierenerkrankungen handelt es sich um monoklonale Antikörper, Nanobodies, die von der variablen Domäne von einzelsträngigen Lama- oder Kameliden-Antikörpern abgeleitet sind, kleine chemische Verbindungen, RNA-basierte Moleküle, sowie rekombinante Proteine. Diagnostik von Komplement-Erkrankungen : Aktuell werden Leitlinien zu unterschiedlichen Aspekten der Rolle des Komplementsystems bei Nierenerkrankungen erstellt. Viele der für die Komplement-Diagnostik relevanten Untersuchungen werden häufig nur von Speziallaboren angeboten. Präzisierung von Biomarkern in klinischen Studien und Diagnostik-Leitfaden : Die Identifikation von selektiven krankheitsspezifischen Biomarkern ist hochrelevant. Sie sind für die präzise Diagnose und für das Monitoring nach einer (komplement-)gerichteten Therapie von größter Bedeutung. Komplement-Infektionen – Covid und Nierenerkrankung : Bei COVID-19-Infektionen hat sich gezeigt, dass das stark aktivierte Komplementsystem zur Thromboinflammation und Schädigung der Niere beiträgt und einen erheblichen Faktor bei dieser Infektion darstellt.
Keywords	Komplement-System ; Komplement-Therapie ; Nierenerkrankungen ; Komplement-Diagnostik ; Infektions-getriggerte Komplement-Aktivierung ; complement ; treatment of complement mediated diseases ; kidney diseases ; diagnosis of complement mediated diseases ; infection-induced complement acitvation
Language	German
Publishing date	2023-05-31
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	200446-x
ISSN	1439-4413 ; 0012-0472
ISSN (online)	1439-4413
ISSN	0012-0472
DOI	10.1055/a-1936-6697
Database	Thieme publisher's database

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Article: Association of HbA1c and utilization of internal mammary arteries with wound infections in CABG.

Knochenhauer, Tim / Schaefer, Andreas / Brickwedel, Jens / Reiter, Beate / Naito, Shiho / Zipfel, Svante / Schneeberger, Yvonne / Reichenspurner, Hermann / Sill, Bjoern

Frontiers in cardiovascular medicine

2024 Volume 11, Page(s) 1345726

Abstract: Background: Deep sternal wound infection (DSWI) remains a serious complication after coronary artery bypass grafting (CABG). We herein aimed to stratify diabetic patients who underwent CABG using bilateral internal mammary artery (BIMA) for levels of ... ...

Abstract	Background: Deep sternal wound infection (DSWI) remains a serious complication after coronary artery bypass grafting (CABG). We herein aimed to stratify diabetic patients who underwent CABG using bilateral internal mammary artery (BIMA) for levels of glycated hemoglobin A1C (HbA1c) and compare postoperative outcomes. Methods: Between January 2010 and August 2020, 4,186 consecutive patients underwent isolated CABG at our center. In 3,229 patients, preoperative HbA1c levels were available. Primary endpoints were wound healing disorder (WHD), DSWI, and 30-day mortality. Patients were stratified according to preoperative HbA1c levels. Patients were further divided into subgroups according to utilization of BIMA. Results: After adjustment, no differences in mortality and stroke rates were seen between group 1 (HbA1c < 6.5%) vs. group 2 (HbA1c ≥ 6.5%). WHD was more frequent in group 2 [2.8 vs. 5.6%; adjusted Conclusions: Intraoperative utilization of BIMA is not connected with an increase of DSWI but higher rates of WHD in patients with poor diabetic status and HbA1c ≥ 6.5%. Therefore, application of BIMA should be taken into consideration even in patients with poor diabetic status, while identification of special subsets of patients who are at particular high risk for DSWI is of paramount importance to prevent this serious complication.
Language	English
Publishing date	2024-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2024.1345726
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Article: Antegrade axillary arterial perfusion in 3D endoscopic minimally-invasive mitral valve surgery.

Petersen, Johannes / Naito, Shiho / Kloth, Benjamin / Pecha, Simon / Zipfel, Svante / Alassar, Yousuf / Detter, Christian / Conradi, Lenard / Reichenspurner, Hermann / Girdauskas, Evaldas

Frontiers in cardiovascular medicine

2022 Volume 9, Page(s) 980074

Abstract: Background: Minimally-invasive (MIS) mitral valve (MV) surgery has become standard therapy in many cardiac surgery centers. While femoral arterial perfusion is the preferred cannulation strategy in MIS mitral valve surgery, retrograde arterial perfusion ...

Abstract	Background: Minimally-invasive (MIS) mitral valve (MV) surgery has become standard therapy in many cardiac surgery centers. While femoral arterial perfusion is the preferred cannulation strategy in MIS mitral valve surgery, retrograde arterial perfusion is known to be associated with an increased risk for cerebral atheroembolism, particularly in atherosclerosis patients. Therefore, antegrade perfusion may be beneficial in such cases. This analysis aimed to compare outcomes of antegrade axillary vs. retrograde femoral perfusion in the MIS mitral valve surgery. Methods: This analysis includes 50 consecutive patients who underwent MIS between 2016 and 2020 using arterial cannulation of right axillary artery (Group A) due to severe aortic arteriosclerosis. Perioperative outcomes of the study group were compared with a historical control group of retrograde femoral perfusion (Group F) which was adjusted for age and gender ( Results: Patients in group A had a significantly higher perioperative risk as compared to Group F (EuroSCORE II: 3.9 ± 2.5 vs. 1.6 ± 1.5; Conclusion: Selective use of antegrade axillary artery perfusion in patients with systemic atherosclerosis shows similar in-hospital outcomes as compared to lower risk patients undergoing retrograde femoral perfusion. Patients with higher perioperative risk and severe atherosclerosis can be safely treated
Language	English
Publishing date	2022-09-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.980074
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Article ; Online: Factor H-related protein 1: a complement regulatory protein and guardian of necrotic-type surfaces.

Skerka, Christine / Pradel, Gabriele / Halder, Luke D / Zipfel, Peter F / Zipfel, Svante L H / Strauß, Olaf

British journal of pharmacology

2020 Volume 178, Issue 14, Page(s) 2823–2831

Abstract: Factor H-related protein 1 (FHR-1) is a member of the factor H protein family, which is involved in regulating innate immune complement reactions. Genetic modification of the encoding gene, CFHR1 on human chromosome 1, is involved in diseases such as age- ...

Abstract	Factor H-related protein 1 (FHR-1) is a member of the factor H protein family, which is involved in regulating innate immune complement reactions. Genetic modification of the encoding gene, CFHR1 on human chromosome 1, is involved in diseases such as age-related macular degeneration, C3 glomerulopathy and atypical haemolytic uraemic syndrome, indicating an important role for FHR-1 in human health. Recent research data demonstrate that FHR-1 levels increase in IgA nephropathy and anti-neutrophilic cytoplasmic autoantibodies (ANCA) vasculitis and that FHR-1 induces strong inflammation in monocytes on necrotic-type surfaces, suggesting a complement-independent role. These new results increase our knowledge about the role of this complement protein in pathology and provide a new therapeutic target, particularly in the context of inflammatory diseases induced by necrosis. This review summarizes current knowledge about FHR-1 and discusses its role in complement reactions and inflammation. LINKED ARTICLES: This article is part of a themed issue on Canonical and non-canonical functions of the complement system in health and disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.14/issuetoc.
MeSH term(s)	Blood Proteins ; Complement Factor H ; Complement System Proteins ; Humans ; Inflammation ; Necrosis
Chemical Substances	Blood Proteins ; factor H-related protein 1 ; Complement Factor H (80295-65-4) ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2020-12-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15290
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Article ; Online: Mapping genetic changes in the cAMP-signaling cascade in human atria.

Garnier, Anne / Bork, Nadja I / Jacquet, Eric / Zipfel, Svante / Muñoz-Guijosa, Christian / Baczkó, Istvan / Reichenspurner, Hermann / Donzeau-Gouge, Patrick / Maier, Lars S / Dobrev, Dobromir / Girdauskas, Evaldas / Nikolaev, Viacheslav O / Fischmeister, Rodolphe / Molina, Cristina E

Journal of molecular and cellular cardiology

2021 Volume 155, Page(s) 10–20

Abstract: Aim: To obtain a quantitative expression profile of the main genes involved in the cAMP-signaling cascade in human control atria and in different cardiac pathologies.: Methods and results: Expression of 48 target genes playing a relevant role in the ... ...

Abstract	Aim: To obtain a quantitative expression profile of the main genes involved in the cAMP-signaling cascade in human control atria and in different cardiac pathologies. Methods and results: Expression of 48 target genes playing a relevant role in the cAMP-signaling cascade was assessed by RT-qPCR. 113 samples were obtained from right atrial appendages (RAA) of patients in sinus rhythm (SR) with or without atrium dilation, paroxysmal atrial fibrillation (AF), persistent AF or heart failure (HF); and left atrial appendages (LAA) from patients in SR or with AF. Our results show that right and left atrial appendages in donor hearts or from SR patients have similar expression values except for AC7 and PDE2A. Despite the enormous chamber-dependent variability in the gene-expression changes between pathologies, several distinguishable patterns could be identified. PDE8A, PI3Kγ and EPAC2 were upregulated in AF. Different phosphodiesterase (PDE) families showed specific pathology-dependent changes. Conclusion: By comparing mRNA-expression patterns of the cAMP-signaling cascade related genes in right and left atrial appendages of human hearts and across different pathologies, we show that 1) gene expression is not significantly affected by cardioplegic solution content, 2) it is appropriate to use SR atrial samples as controls, and 3) many genes in the cAMP-signaling cascade are affected in AF and HF but only few of them appear to be chamber (right or left) specific. Topic: Genetic changes in human diseased atria. Translational perspective: The cyclic AMP signaling pathway is important for atrial function. However, expression patterns of the genes involved in the atria of healthy and diseased hearts are still unclear. We give here a general overview of how different pathologies affect the expression of key genes in the cAMP signaling pathway in human right and left atria appendages. Our study may help identifying new genes of interest as potential therapeutic targets or clinical biomarkers for these pathologies and could serve as a guide in future gene therapy studies.
MeSH term(s)	Aged ; Alleles ; Atrial Appendage/metabolism ; Atrial Fibrillation/complications ; Atrial Fibrillation/diagnosis ; Atrial Fibrillation/genetics ; Atrial Fibrillation/physiopathology ; Biomarkers ; Cyclic AMP/metabolism ; Disease Susceptibility ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Genetic Variation ; Heart Atria/metabolism ; Heart Failure/diagnosis ; Heart Failure/drug therapy ; Heart Failure/etiology ; Humans ; Male ; Middle Aged ; Proteome ; Proteomics/methods ; Second Messenger Systems/genetics
Chemical Substances	Biomarkers ; Proteome ; Cyclic AMP (E0399OZS9N)
Language	English
Publishing date	2021-02-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2021.02.006
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Article ; Online: Postcardiotomy Venoarterial Extracorporeal Membrane Oxygenation With and Without Intra-Aortic Balloon Pump.

Björnsdóttir, Björk / Biancari, Fausto / Dalén, Magnus / Dell'Aquila, Angelo M / Jónsson, Kristján / Fiore, Antonio / Mariscalco, Giovanni / El-Dean, Zein / Gatti, Giuseppe / Zipfel, Svante / Perrotti, Andrea / Bounader, Karl / Alkhamees, Khalid / Loforte, Antonio / Lechiancole, Andrea / Pol, Marek / Spadaccio, Cristiano / Pettinari, Matteo / De Keyzer, Dieter /

Welp, Henryk / Speziale, Giuseppe / Lichtenberg, Artur / Ruggieri, Vito G / Yusuf, Hakeem / Ragnarsson, Sigurdur

Journal of cardiothoracic and vascular anesthesia

2022 Volume 36, Issue 8 Pt B, Page(s) 2876–2883

Abstract: Objectives: To compare the outcomes of patients with postcardiotomy shock treated with venoarterial extracorporeal membrane oxygenation (VA-ECMO) only compared with VA-ECMO and intra-aortic balloon pump (IABP).: Design: A retrospective multicenter ... ...

Abstract	Objectives: To compare the outcomes of patients with postcardiotomy shock treated with venoarterial extracorporeal membrane oxygenation (VA-ECMO) only compared with VA-ECMO and intra-aortic balloon pump (IABP). Design: A retrospective multicenter registry study. Setting: At 19 cardiac surgery units. Participants: A total of 615 adult patients who required VA-ECMO from 2010 to 2018. The patients were divided into 2 groups depending on whether they received VA-ECMO only (ECMO only group) or VA-ECMO plus IABP (ECMO-IABP group). Measurements and main results: The overall series mean age was 63 ± 13 years, and 33% were female. The ECMO-only group included 499 patients, and 116 patients were in the ECMO-IABP group. Urgent and/or emergent procedures were more common in the ECMO-only group. Central cannulation was performed in 47% (n = 54) in the ECMO-IABP group compared to 27% (n = 132) in the ECMO-only group. In the ECMO-IABP group, 58% (n = 67) were successfully weaned from ECMO, compared to 46% (n = 231) in the ECMO-only group (p = 0.026). However, in-hospital mortality was 63% in the ECMO-IABP group compared to 65% in the ECMO-only group (p = 0.66). Among 114 propensity score-matched pairs, ECMO-IABP group had comparable weaning rates (57% v 53%, p = 0.51) and in-hospital mortality (64% v 58%, p = 0.78). Conclusions: This multicenter study showed that adjunctive IABP did not translate into better outcomes in patients treated with VA-ECMO for postcardiotomy shock.
MeSH term(s)	Adult ; Aged ; Cardiac Surgical Procedures/adverse effects ; Extracorporeal Membrane Oxygenation/methods ; Female ; Heart-Assist Devices ; Humans ; Intra-Aortic Balloon Pumping/methods ; Male ; Middle Aged ; Retrospective Studies ; Shock/etiology ; Shock, Cardiogenic/etiology ; Shock, Cardiogenic/therapy
Language	English
Publishing date	2022-02-11
Publishing country	United States
Document type	Journal Article ; Multicenter Study
ZDB-ID	1067317-9
ISSN	1532-8422 ; 1053-0770
ISSN (online)	1532-8422
ISSN	1053-0770
DOI	10.1053/j.jvca.2022.02.006
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Article ; Online: Serum FHR1 binding to necrotic-type cells activates monocytic inflammasome and marks necrotic sites in vasculopathies.

Irmscher, Sarah / Brix, Silke R / Zipfel, Svante L H / Halder, Luke D / Mutlutürk, Sibel / Wulf, Sonia / Girdauskas, Evaldas / Reichenspurner, Hermann / Stahl, Rolf A K / Jungnickel, Berit / Wiech, Thorsten / Zipfel, Peter F / Skerka, Christine

Nature communications

2019 Volume 10, Issue 1, Page(s) 2961

Abstract: Persistent inflammation is a hallmark of many human diseases, including anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) and atherosclerosis. Here, we describe a dominant trigger of inflammation: human serum factor H-related protein FHR1. ...

Abstract	Persistent inflammation is a hallmark of many human diseases, including anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) and atherosclerosis. Here, we describe a dominant trigger of inflammation: human serum factor H-related protein FHR1. In vitro, this protein selectively binds to necrotic cells via its N-terminus; in addition, it binds near necrotic glomerular sites of AAV patients and necrotic areas in atherosclerotic plaques. FHR1, but not factor H, FHR2 or FHR3 strongly induces inflammasome NLRP3 in blood-derived human monocytes, which subsequently secrete IL-1β, TNFα, IL-18 and IL-6. FHR1 triggers the phospholipase C-pathway via the G-protein coupled receptor EMR2 independent of complement. Moreover, FHR1 concentrations of AAV patients negatively correlate with glomerular filtration rates and associate with the levels of inflammation and progressive disease. These data highlight an unexpected role for FHR1 during sterile inflammation, may explain why FHR1-deficiency protects against certain diseases, and identifies potential targets for treatment of auto-inflammatory diseases.
MeSH term(s)	C-Reactive Protein/metabolism ; Complement C3b Inactivator Proteins/metabolism ; Complement System Proteins/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Immobilized Proteins/metabolism ; Inflammasomes/metabolism ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Interleukin-1beta/metabolism ; Lipoproteins, LDL/metabolism ; Malondialdehyde/metabolism ; Models, Biological ; Monocytes/metabolism ; Monocytes/pathology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Necrosis ; Protein Binding ; Receptors, G-Protein-Coupled/metabolism ; Serum/metabolism ; Type C Phospholipases/metabolism ; Vascular Diseases/metabolism ; Vascular Diseases/pathology
Chemical Substances	ADGRE2 protein, human ; CFHR1 protein, human ; Complement C3b Inactivator Proteins ; Immobilized Proteins ; Inflammasomes ; Inflammation Mediators ; Interleukin-1beta ; Lipoproteins, LDL ; NLR Family, Pyrin Domain-Containing 3 Protein ; Receptors, G-Protein-Coupled ; Malondialdehyde (4Y8F71G49Q) ; Complement System Proteins (9007-36-7) ; C-Reactive Protein (9007-41-4) ; Type C Phospholipases (EC 3.1.4.-)
Language	English
Publishing date	2019-07-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-10766-0
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Article ; Online: Switching to Impella 5.0 decreases need for transfusion in patients undergoing temporary mechanical circulatory support.

Castro, Liesa / Zipfel, Svante / Braunsteiner, Josephine / Schaefer, Andreas / Sill, Björn / Söffker, Gerold / Kluge, Stefan / Lubos, Edith / Rybczinski, Meike / Grahn, Hanno / Schrage, Benedikt / Becher, Peter M / Barten, Markus J / Westermann, Dirk / Blankenberg, Stefan / Reichenspurner, Hermann / Bernhardt, Alexander M

Journal of critical care

2020 Volume 57, Page(s) 253–258

Abstract: Purpose: Various options of temporary mechanical circulatory support (tMCS) exist for the treatment of cardiogenic shock, however, all forms of tMCS carry a risk of complications. The aim of this study was to compare bleeding complications and ... ...

Abstract	Purpose: Various options of temporary mechanical circulatory support (tMCS) exist for the treatment of cardiogenic shock, however, all forms of tMCS carry a risk of complications. The aim of this study was to compare bleeding complications and thromboembolic events under extracorporeal life support + Impella 2.5/CP (ECMELLA) and isolated Impella 5.0 therapy in the same patient cohort. Material: We retrospectively analyzed data of patients who underwent ECMELLA implantation and subsequent Impella 5.0 therapy. Implantation strategy and anticoagulation protocol were comparable in both groups. Results: We included 15 patients (mean age 57.2 years; 80% of male patients) who were weaned from ECMELLA undergoing subsequent Impella 5.0 implantation. Mean duration of ECMELLA and Impella 5.0 therapy (10.5 vs. 11.2 days) did not differ significantly (p = .731). The average number of transfused packed red blood cells (PRBC) and thrombocyte concentrates (TC) was significantly decreased during Impella 5.0 treatment (PRBC: 30.3 vs 12.3, p = .001; TC: 5.9 vs 2.2, p = .045). Additionally, the transfusion rates per day were significantly reduced under Impella 5.0 support. Conclusions: The need for transfusions is significantly lower in the phase of Impella 5.0 therapy compared to the initial phase on ECMELLA. Therefore, we recommend replacing ECMELLA by an Impella 5.0 device early, if possible.
MeSH term(s)	Aged ; Anticoagulants/therapeutic use ; Blood Platelets/cytology ; Blood Transfusion/methods ; Erythrocytes/cytology ; Extracorporeal Membrane Oxygenation/adverse effects ; Extracorporeal Membrane Oxygenation/instrumentation ; Female ; Heart-Assist Devices/adverse effects ; Hemoglobins/analysis ; Hemorrhage/complications ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Risk ; Shock, Cardiogenic/therapy ; Treatment Outcome
Chemical Substances	Anticoagulants ; Hemoglobins
Language	English
Publishing date	2020-05-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	632818-0
ISSN	1557-8615 ; 0883-9441
ISSN (online)	1557-8615
ISSN	0883-9441
DOI	10.1016/j.jcrc.2019.11.007
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Article ; Online: Factor H-related protein 1 (FHR-1) is associated with atherosclerotic cardiovascular disease.

Irmscher, Sarah / Zipfel, Svante L H / Halder, Luke D / Ivanov, Lia / Gonzalez-Delgado, Andres / Waldeyer, Christoph / Seiffert, Moritz / Brunner, Fabian J / von der Heide, Monika / Löschmann, Ina / Wulf, Sonia / Czamara, Darina / Papac-Milicevic, Nikolina / Strauß, Olaf / Lorkowski, Stefan / Reichenspurner, Hermann / Holers, Michael V / Banda, Nirmal K / Zeller, Tania /

Binder, Elisabeth B / Binder, Christoph J / Wiech, Thorsten / Zipfel, Peter F / Skerka, Christine

Scientific reports

2021 Volume 11, Issue 1, Page(s) 22511

Abstract: Atherosclerotic cardiovascular disease (ACVD) is a lipid-driven inflammatory disease and one of the leading causes of death worldwide. Lipid deposits in the arterial wall lead to the formation of plaques that involve lipid oxidation, cellular necrosis, ... ...

Abstract	Atherosclerotic cardiovascular disease (ACVD) is a lipid-driven inflammatory disease and one of the leading causes of death worldwide. Lipid deposits in the arterial wall lead to the formation of plaques that involve lipid oxidation, cellular necrosis, and complement activation, resulting in inflammation and thrombosis. The present study found that homozygous deletion of the CFHR1 gene, which encodes the plasma complement protein factor H-related protein 1 (FHR-1), was protective in two cohorts of patients with ACVD, suggesting that FHR-1 accelerates inflammation and exacerbates the disease. To test this hypothesis, FHR-1 was isolated from human plasma and was found to circulate on extracellular vesicles and to be deposited in atherosclerotic plaques. Surface-bound FHR-1 induced the expression of pro-inflammatory cytokines and tissue factor in both monocytes and neutrophils. Notably, plasma concentrations of FHR-1, but not of factor H, were significantly (p < 0.001) elevated in patients with ACVD, and correlated with the expression of the inflammation markers C-reactive protein, apolipoprotein serum amyloid protein A, and neopterin. FHR-1 expression also significantly correlated with plasma concentrations of low-density lipoprotein (LDL) (p < 0.0001) but not high-density lipoprotein (HDL). Taken together, these findings suggest that FHR-1 is associated with ACVD.
MeSH term(s)	Aged ; Atherosclerosis/metabolism ; Cardiology ; Cardiovascular Diseases/metabolism ; Chromosome Deletion ; Complement Activation ; Complement C3b Inactivator Proteins/biosynthesis ; Complement C3b Inactivator Proteins/genetics ; Complement C3b Inactivator Proteins/physiology ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Homozygote ; Humans ; Inflammation ; Lipids/chemistry ; Male ; Middle Aged ; Necrosis ; Oxygen/chemistry ; Sequence Deletion
Chemical Substances	CFHR1 protein, human ; Complement C3b Inactivator Proteins ; Lipids ; Oxygen (S88TT14065)
Language	English
Publishing date	2021-11-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-02011-w
Database	MEDical Literature Analysis and Retrieval System OnLINE

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