LIVIVO - Search results -

Search results

Result 1 - 10 of total 276

Search options

Article ; Online: The Cardiovascular Research community calls for action to address the growing burden of cardiovascular disease.

Pearson, Jeremy / Sipido, Karin R / Musialek, Piotr / van Gilst, Wiek H

2019 Volume 115, Issue 10, Page(s) e96–e98

MeSH term(s)	Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/therapy ; Cooperative Behavior ; Global Health ; Health Services Accessibility ; Health Services Needs and Demand ; Healthcare Disparities ; Humans ; International Cooperation ; Needs Assessment ; Research Design ; Research Personnel
Language	English
Publishing date	2019-05-16
Publishing country	England
Document type	Journal Article
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvz175
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 565: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Galectin-3 and Blood Group: Binding Properties, Effects on Plasma Levels, and Consequences for Prognostic Performance.

Pozder, Carolin / Screever, Elles M / van der Velde, A Rogier / Silljé, Herman H / Suwijn, Janne / de Rond, Saskia / Kleber, Marcus E / Delgado, Graciela / Schuringa, Jan Jacob / van Gilst, Wiek H / Meijers, Wouter C / März, Winfried / de Boer, Rudolf A

International journal of molecular sciences

2023 Volume 24, Issue 5

Abstract: Previous studies have reported an association between ABO type blood group and cardiovascular (CV) events and outcomes. The precise mechanisms underpinning this striking observation remain unknown, although differences in von Willebrand factor (VWF) ... ...

Abstract	Previous studies have reported an association between ABO type blood group and cardiovascular (CV) events and outcomes. The precise mechanisms underpinning this striking observation remain unknown, although differences in von Willebrand factor (VWF) plasma levels have been proposed as an explanation. Recently, galectin-3 was identified as an endogenous ligand of VWF and red blood cells (RBCs) and, therefore, we aimed to explore the role of galectin-3 in different blood groups. Two in vitro assays were used to assess the binding capacity of galectin-3 to RBCs and VWF in different blood groups. Additionally, plasma levels of galectin-3 were measured in different blood groups in the Ludwigshafen Risk and Cardiovascular Health (LURIC) study (2571 patients hospitalized for coronary angiography) and validated in a community-based cohort of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study (3552 participants). To determine the prognostic value of galectin-3 in different blood groups, logistic regression and cox regression models were used with all-cause mortality as the primary outcome. First, we demonstrated that galectin-3 has a higher binding capacity for RBCs and VWF in non-O blood groups, compared to blood group O. Additionally, LURIC patients with non-O blood groups had substantially lower plasma levels of galectin-3 (15.0, 14.9, and 14.0 μg/L in blood groups A, B, and AB, respectively, compared to 17.1 μg/L in blood group O,
MeSH term(s)	Humans ; von Willebrand Factor/metabolism ; Galectin 3 ; Prognosis ; ABO Blood-Group System ; Kidney/metabolism
Chemical Substances	von Willebrand Factor ; Galectin 3 ; ABO Blood-Group System
Language	English
Publishing date	2023-02-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24054415
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A Kinase Interacting Protein 1 (AKIP1) promotes cardiomyocyte elongation and physiological cardiac remodelling.

Nijholt, Kirsten T / Sánchez-Aguilera, Pablo I / Booij, Harmen G / Oberdorf-Maass, Silke U / Dokter, Martin M / Wolters, Anouk H G / Giepmans, Ben N G / van Gilst, Wiek H / Brown, Joan H / de Boer, Rudolf A / Silljé, Herman H W / Westenbrink, B Daan

Scientific reports

2023 Volume 13, Issue 1, Page(s) 4046

Abstract: A Kinase Interacting Protein 1 (AKIP1) is a signalling adaptor that promotes physiological hypertrophy in vitro. The purpose of this study is to determine if AKIP1 promotes physiological cardiomyocyte hypertrophy in vivo. Therefore, adult male mice with ... ...

Abstract	A Kinase Interacting Protein 1 (AKIP1) is a signalling adaptor that promotes physiological hypertrophy in vitro. The purpose of this study is to determine if AKIP1 promotes physiological cardiomyocyte hypertrophy in vivo. Therefore, adult male mice with cardiomyocyte-specific overexpression of AKIP1 (AKIP1-TG) and wild type (WT) littermates were caged individually for four weeks in the presence or absence of a running wheel. Exercise performance, heart weight to tibia length (HW/TL), MRI, histology, and left ventricular (LV) molecular markers were evaluated. While exercise parameters were comparable between genotypes, exercise-induced cardiac hypertrophy was augmented in AKIP1-TG vs. WT mice as evidenced by an increase in HW/TL by weighing scale and in LV mass on MRI. AKIP1-induced hypertrophy was predominantly determined by an increase in cardiomyocyte length, which was associated with reductions in p90 ribosomal S6 kinase 3 (RSK3), increments of phosphatase 2A catalytic subunit (PP2Ac) and dephosphorylation of serum response factor (SRF). With electron microscopy, we detected clusters of AKIP1 protein in the cardiomyocyte nucleus, which can potentially influence signalosome formation and predispose a switch in transcription upon exercise. Mechanistically, AKIP1 promoted exercise-induced activation of protein kinase B (Akt), downregulation of CCAAT Enhancer Binding Protein Beta (C/EBPβ) and de-repression of Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 4 (CITED4). Concludingly, we identified AKIP1 as a novel regulator of cardiomyocyte elongation and physiological cardiac remodelling with activation of the RSK3-PP2Ac-SRF and Akt-C/EBPβ-CITED4 pathway. These findings suggest that AKIP1 may serve as a nodal point for physiological reprogramming of cardiac remodelling.
MeSH term(s)	Animals ; Male ; Mice ; Adaptor Proteins, Signal Transducing/metabolism ; Cardiomegaly/pathology ; Myocytes, Cardiac/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Ventricular Remodeling
Chemical Substances	Adaptor Proteins, Signal Transducing ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; AKIP1 protein, mouse
Language	English
Publishing date	2023-03-10
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/s41598-023-30514-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Fibroblast Growth Factor 23 and Risk of New Onset Heart Failure With Preserved or Reduced Ejection Fraction: The PREVEND Study.

Binnenmars, S Heleen / Hoogslag, Georgette E / Yeung, Stanley M H / Brouwers, Frank P / Bakker, Stephan J L / van Gilst, Wiek H / Gansevoort, Ron T / Navis, Gerjan / Voors, Adriaan A / de Borst, Martin H

Journal of the American Heart Association

2022 Volume 11, Issue 15, Page(s) e024952

Abstract: Background The role of fibroblast growth factor 23 (FGF23) in the development of new-onset heart failure (HF) with reduced (HFrEF) or preserved ejection fraction (HFpEF) in the general population is unknown. Therefore, we set out to investigate ... ...

Abstract	Background The role of fibroblast growth factor 23 (FGF23) in the development of new-onset heart failure (HF) with reduced (HFrEF) or preserved ejection fraction (HFpEF) in the general population is unknown. Therefore, we set out to investigate associations of C-terminal FGF23 with development of new-onset HF and, more specifically, with HFrEF or HFpEF in a large, prospective, population-based cohort. Methods and Results We studied 6830 participants (aged 53.8±12.1 years; 49.7% men; estimated glomerular filtration rate, 93.1±15.7 mL/min per 1.73 m
MeSH term(s)	Adult ; Aged ; Cross-Sectional Studies ; Female ; Fibroblast Growth Factor-23 ; Heart Failure/diagnosis ; Heart Failure/epidemiology ; Humans ; Male ; Middle Aged ; Prognosis ; Prospective Studies ; Risk Factors ; Stroke Volume
Chemical Substances	FGF23 protein, human ; Fibroblast Growth Factor-23 (7Q7P4S7RRE)
Language	English
Publishing date	2022-07-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.121.024952
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Treating oxidative stress in heart failure: past, present and future.

van der Pol, Atze / van Gilst, Wiek H / Voors, Adriaan A / van der Meer, Peter

European journal of heart failure

2018 Volume 21, Issue 4, Page(s) 425–435

Abstract: Advances in cardiovascular research have identified oxidative stress as an important pathophysiological pathway in the development and progression of heart failure. Oxidative stress is defined as the imbalance between the production of reactive oxygen ... ...

Abstract	Advances in cardiovascular research have identified oxidative stress as an important pathophysiological pathway in the development and progression of heart failure. Oxidative stress is defined as the imbalance between the production of reactive oxygen species (ROS) and the endogenous antioxidant defence system. Under physiological conditions, small quantities of ROS are produced intracellularly, which function in cell signalling, and can be readily reduced by the antioxidant defence system. However, under pathophysiological conditions, the production of ROS exceeds the buffering capacity of the antioxidant defence system, resulting in cell damage and death. Over the last decades several studies have tried to target oxidative stress with the aim to improve outcome in patients with heart failure, with very limited success. The reasons as to why these studies failed to demonstrate any beneficial effects remain unclear. However, one plausible explanation might be that currently employed strategies, which target oxidative stress by exogenous inhibition of ROS production or supplementation of exogenous antioxidants, are not effective enough, while bolstering the endogenous antioxidant capacity might be a far more potent avenue for therapeutic intervention. In this review, we provide an overview of oxidative stress in the pathophysiology of heart failure and the strategies utilized to date to target this pathway. We provide novel insights into modulation of endogenous antioxidants, which may lead to novel therapeutic strategies to improve outcome in patients with heart failure.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Disease Models, Animal ; Heart Failure/drug therapy ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Humans ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism
Chemical Substances	Antioxidants ; Reactive Oxygen Species
Language	English
Publishing date	2018-10-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1483672-5
ISSN	1879-0844 ; 1388-9842
ISSN (online)	1879-0844
ISSN	1388-9842
DOI	10.1002/ejhf.1320
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5299: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Emerging role of liver X receptors in cardiac pathophysiology and heart failure.

Cannon, Megan V / van Gilst, Wiek H / de Boer, Rudolf A

Basic research in cardiology

2016 Volume 111, Issue 1, Page(s) 3

Abstract: Liver X receptors (LXRs) are master regulators of metabolism and have been studied for their pharmacological potential in vascular and metabolic disease. Besides their established role in metabolic homeostasis and disease, there is mounting evidence to ... ...

Abstract	Liver X receptors (LXRs) are master regulators of metabolism and have been studied for their pharmacological potential in vascular and metabolic disease. Besides their established role in metabolic homeostasis and disease, there is mounting evidence to suggest that LXRs may exert direct beneficial effects in the heart. Here, we aim to provide a conceptual framework to explain the broad mode of action of LXRs and how LXR signaling may be an important local and systemic target for the treatment of heart failure. We discuss the potential role of LXRs in systemic conditions associated with heart failure, such as hypertension, diabetes, and renal and vascular disease. Further, we expound on recent data that implicate a direct role for LXR activation in the heart, for its impact on cardiomyocyte damage and loss due to ischemia, and effects on cardiac hypertrophy, fibrosis, and myocardial metabolism. Taken together, the accumulating evidence supports the notion that LXRs may represent a novel therapeutic target for the treatment of heart failure.
MeSH term(s)	Animals ; Heart/physiopathology ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Humans ; Liver X Receptors ; Myocytes, Cardiac/metabolism ; Orphan Nuclear Receptors/metabolism
Chemical Substances	Liver X Receptors ; Orphan Nuclear Receptors
Language	English
Publishing date	2016-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-015-0520-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.30: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Pectins from various sources inhibit galectin-3-related cardiac fibrosis.

Pozder Geb Gehlken, Carolin / Rogier van der Velde, A / Meijers, Wouter C / Silljé, Herman H W / Muntendam, Pieter / Dokter, Martin M / van Gilst, Wiek H / Schols, Henk A / de Boer, Rudolf A

Current research in translational medicine

2021 Volume 70, Issue 1, Page(s) 103321

Abstract: Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with ... ...

Abstract	Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with the strongest galectin-3 inhibitory capacity. We evaluated the in vitro inhibitory capacity, identified potent pectins, and tested if this potency could be validated in a mouse model of myocardial fibrosis. Methods: Various pectin fractions were screened in vitro. Modified rhubarb pectin (EMRP) was identified as the most potent inhibitor of galectin-3 and compared to the well-known modified citrus pectin (MCP). Our findings were validated in a mouse model of myocardial fibrosis, which was induced by angiotensin II (Ang II) infusion. Results: Ang II infusion was associated with a 4-5-fold increase in fibrosis signal in the tissue of the left ventricle, compared to the control group (0•22±0•10 to 1•08±0•53%; P < 0•001). After treatment with rhubarb pectin, fibrosis was reduced by 57% vs. Ang II alone while this reduction was 30% with the well-known MCP (P = NS, P < 0•05). Treatment was associated with a reduced cardiac inflammatory response and preserved cardiac function. Conclusion: The galectin-3 inhibitor natural rhubarb pectin has a superior inhibitory capacity over established pectins, substantially attenuates cardiac fibrosis, and preserves cardiac function in vivo. Bioactive pectins are natural sources of galectin-3 inhibitors and may be helpful in the prevention of heart failure or other diseases characterized by fibrosis. Funding: Dr. Meijers is supported by the Mandema-Stipendium of the Junior Scientific Masterclass 2020-10, University Medical Center Groningen and by the Netherlands Heart Foundation (Dekkerbeurs 2021)Dr. de Boer is supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21; CVON RED-CVD, grant 2017-11; CVON PREDICT2, grant 2018-30; and CVON DOUBLE DOSE, grant 2020B005), by a grant from the leDucq Foundation (Cure PhosphoLambaN induced Cardiomyopathy (Cure-PLaN), and by a grant from the European Research Council (ERC CoG 818715, SECRETE-HF).
MeSH term(s)	Animals ; Disease Models, Animal ; Fibrosis ; Galectin 3 ; Mice ; Pectins
Chemical Substances	Galectin 3 ; Pectins (89NA02M4RX)
Language	English
Publishing date	2021-11-23
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2452-3186
ISSN (online)	2452-3186
DOI	10.1016/j.retram.2021.103321
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Pectins from various sources inhibit galectin-3-related cardiac fibrosis

Pozder geb. Gehlken, Carolin / Rogier van der Velde, A. / Meijers, Wouter C. / Silljé, Herman H.W. / Muntendam, Pieter / Dokter, Martin M. / van Gilst, Wiek H. / Schols, Henk A. / de Boer, Rudolf A.

Current Research in Translational Medicine

2022 Volume 70, Issue 1

Abstract	Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with the strongest galectin-3 inhibitory capacity. We evaluated the in vitro inhibitory capacity, identified potent pectins, and tested if this potency could be validated in a mouse model of myocardial fibrosis. Methods: Various pectin fractions were screened in vitro. Modified rhubarb pectin (EMRP) was identified as the most potent inhibitor of galectin-3 and compared to the well-known modified citrus pectin (MCP). Our findings were validated in a mouse model of myocardial fibrosis, which was induced by angiotensin II (Ang II) infusion. Results: Ang II infusion was associated with a 4–5-fold increase in fibrosis signal in the tissue of the left ventricle, compared to the control group (0•22±0•10 to 1•08±0•53%; P < 0•001). After treatment with rhubarb pectin, fibrosis was reduced by 57% vs. Ang II alone while this reduction was 30% with the well-known MCP (P = NS, P < 0•05). Treatment was associated with a reduced cardiac inflammatory response and preserved cardiac function. Conclusion: The galectin-3 inhibitor natural rhubarb pectin has a superior inhibitory capacity over established pectins, substantially attenuates cardiac fibrosis, and preserves cardiac function in vivo. Bioactive pectins are natural sources of galectin-3 inhibitors and may be helpful in the prevention of heart failure or other diseases characterized by fibrosis. Funding: Dr. Meijers is supported by the Mandema-Stipendium of the Junior Scientific Masterclass 2020-10, University Medical Center Groningen and by the Netherlands Heart Foundation (Dekkerbeurs 2021)Dr. de Boer is supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21; CVON RED-CVD, grant 2017-11; CVON PREDICT2, grant 2018-30; and CVON DOUBLE DOSE, grant 2020B005), by a grant from the leDucq Foundation ...
Keywords	Affinity ; Fibrosis ; Galectin-3 ; Heart failure ; Inhibitor ; Pectin
Subject code	610
Language	English
Publishing country	nl
Document type	Article ; Online
ISSN	2452-3186
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Cardiac complications in patients hospitalised with COVID-19.

Linschoten, Marijke / Peters, Sanne / van Smeden, Maarten / Jewbali, Lucia S / Schaap, Jeroen / Siebelink, Hans-Marc / Smits, Peter C / Tieleman, Robert G / van der Harst, Pim / van Gilst, Wiek H / Asselbergs, Folkert W

European heart journal. Acute cardiovascular care

2020 Volume 9, Issue 8, Page(s) 817–823

Abstract: Aims: To determine the frequency and pattern of cardiac complications in patients hospitalised with coronavirus disease (COVID-19).: Methods and results: CAPACITY-COVID is an international patient registry established to determine the role of ... ...

Abstract	Aims: To determine the frequency and pattern of cardiac complications in patients hospitalised with coronavirus disease (COVID-19). Methods and results: CAPACITY-COVID is an international patient registry established to determine the role of cardiovascular disease in the COVID-19 pandemic. In this registry, data generated during routine clinical practice are collected in a standardised manner for patients with a (highly suspected) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection requiring hospitalisation. For the current analysis, consecutive patients with laboratory confirmed COVID-19 registered between 28 March and 3 July 2020 were included. Patients were followed for the occurrence of cardiac complications and pulmonary embolism from admission to discharge. In total, 3011 patients were included, of which 1890 (62.8%) were men. The median age was 67 years (interquartile range 56-76); 937 (31.0%) patients had a history of cardiac disease, with pre-existent coronary artery disease being most common ( Conclusion: This large study among 3011 hospitalised patients with COVID-19 shows that the incidence of cardiac complications during hospital admission is low, despite a frequent history of cardiovascular disease. Long-term cardiac outcomes and the role of pre-existing cardiovascular disease in COVID-19 outcome warrants further investigation.
MeSH term(s)	Acute Coronary Syndrome/epidemiology ; Aged ; Atrial Fibrillation/epidemiology ; COVID-19/complications ; COVID-19/epidemiology ; COVID-19/virology ; Coronary Artery Disease/epidemiology ; Endocarditis, Bacterial/epidemiology ; Female ; Heart Diseases/epidemiology ; Heart Diseases/mortality ; Heart Failure/epidemiology ; Hospitalization/trends ; Humans ; Incidence ; Male ; Middle Aged ; Myocarditis/epidemiology ; Outcome Assessment, Health Care ; Pericarditis/epidemiology ; Pulmonary Embolism/epidemiology ; Registries ; SARS-CoV-2/genetics
Language	English
Publishing date	2020-11-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2663340-1
ISSN	2048-8734 ; 2048-8726
ISSN (online)	2048-8734
ISSN	2048-8726
DOI	10.1177/2048872620974605
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The changing face of heart failure: are we really making progress?

Brouwers, Frank P / van Gilst, Wiek H / van Veldhuisen, Dirk J

European journal of heart failure

2013 Volume 15, Issue 9, Page(s) 960–962

MeSH term(s)	Female ; Heart Failure/epidemiology ; Humans ; Male
Language	English
Publishing date	2013-09
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	1483672-5
ISSN	1879-0844 ; 1388-9842
ISSN (online)	1879-0844
ISSN	1388-9842
DOI	10.1093/eurjhf/hft126
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5299: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito