LIVIVO - Search results -

Search results

Result 1 - 10 of total 62

Search options

Article: Structural insights into regulation of CCN protein activities and functions.

Monsen, Vivi Talstad / Attramadal, Håvard

Journal of cell communication and signaling

2023 Volume 17, Issue 2, Page(s) 371–390

Abstract: CCN proteins play important functions during development, in repair mechanisms following tissue injury, as well as in pathophysiologic mechanisms of metastasis of cancer. CCNs are secreted proteins that have a multimodular structure and are categorized ... ...

Abstract	CCN proteins play important functions during development, in repair mechanisms following tissue injury, as well as in pathophysiologic mechanisms of metastasis of cancer. CCNs are secreted proteins that have a multimodular structure and are categorized as matricellular proteins. Although the prevailing view is that CCN proteins regulate biologic processes by interacting with a wide array of other proteins in the microenvironment of the extracellular matrix, the molecular mechanisms of action of CCN proteins are still poorly understood. Not dissuading the current view, however, the recent appreciation that these proteins are signaling proteins in their own right and may even be considered preproproteins controlled by endopeptidases to release a C-terminal bioactive peptide has opened new avenues of research. Also, the recent resolution of the crystal structure of two of the domains of CCN3 have provided new knowledge with implications for the entire CCN family. These resolved structures in combination with structural predictions based upon the AlphaFold artificial intelligence tool provide means to shed new light on CCN functions in context of the notable literature in the field. CCN proteins have emerged as important therapeutic targets in several disease conditions, and clinical trials are currently ongoing. Thus, a review that critically discusses structure - function relationship of CCN proteins, in particular as it relates to interactions with other proteins in the extracellular milieu and on the cell surface, as well as to cell signaling activities of these proteins, is very timely. Suggested mechanism for activation and inhibition of signaling by the CCN protein family (graphics generated with BioRender.com ).
Language	English
Publishing date	2023-05-28
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2299380-0
ISSN	1873-961X ; 1873-9601
ISSN (online)	1873-961X
ISSN	1873-9601
DOI	10.1007/s12079-023-00768-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

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 ▾
- Full text online
- Order with fees

Article ; Online: Inflammatory augmentation of the delayed type hypersensitivity arthritis mouse model.

Tønnessen, Theis Christian / Ueland, Thor / Ahmed, Muhammad Shakil / Attramadal, Håvard / Sjaastad, Ivar / Vinge, Leif Erik

Basic & clinical pharmacology & toxicology

2023 Volume 132, Issue 6, Page(s) 551–555

MeSH term(s)	Animals ; Mice ; Arthritis ; Disease Models, Animal ; Arthritis, Experimental ; Hypersensitivity, Delayed
Language	English
Publishing date	2023-03-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2134679-3
ISSN	1742-7843 ; 1742-7835
ISSN (online)	1742-7843
ISSN	1742-7835
DOI	10.1111/bcpt.13864
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

Uf I Zs.144: 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: The carboxyl-terminal TSP1-homology domain is the biologically active effector peptide of matricellular protein CCN5 that counteracts profibrotic CCN2.

Zolfaghari, Sima / Kaasbøll, Ole Jørgen / Monsen, Vivi T / Sredic, Bojana / Hagelin, Else Marie V / Attramadal, Håvard

The Journal of biological chemistry

2022 Volume 299, Issue 1, Page(s) 102803

Abstract: Cellular Communication Network (CCN) proteins have multimodular structures important for their roles in cellular responses associated with organ development and tissue homeostasis. CCN2 has previously been reported to be secreted as a preproprotein that ... ...

Abstract	Cellular Communication Network (CCN) proteins have multimodular structures important for their roles in cellular responses associated with organ development and tissue homeostasis. CCN2 has previously been reported to be secreted as a preproprotein that requires proteolytic activation to release its bioactive carboxyl-terminal fragment. Here, our goal was to resolve whether CCN5, a divergent member of the CCN family with converse functions relative to CCN2, releases the TSP1 homology domain as its bioactive signaling entity. The recombinant CCN5 or CCN3 TSP1 homology domains were produced in ExpiCHO-S or DG44 CHO cells as secretory fusion proteins appended to the carboxyl-terminal end of His-Halo-Sumo or amino-terminal end of human albumin and purified from the cell culture medium. We tested these fusion proteins in various phosphokinase signaling pathways or cell physiologic assays. Fusion proteins with the CCN5 TSP1 domain inhibited key signaling pathways previously reported to be stimulated by CCN2, irrespective of fusion partner. The fusion proteins also efficiently inhibited CCN1/2-stimulated cell migration and gap closure following scratch wound of fibroblasts. Fusion protein with the CCN3 TSP1 domain inhibited these functions with similar efficacy and potency as that of the CCN5 TSP1 domain. The CCN5 TSP1 domain also recapitulated a positive regulatory function previously assigned to full-length CCN5, that is, induction of estrogen receptor-α mRNA expression in triple negative MDA-MB-231 mammary adenocarcinoma cells and inhibited epithelial-to-mesenchymal transition and CCN2-induced mammosphere formation of MCF-7 adenocarcinoma cells. In conclusion, the CCN5 TSP1 domain is the bioactive entity that confers the biologic functions of unprocessed CCN5.
MeSH term(s)	Animals ; Cricetinae ; Humans ; Connective Tissue Growth Factor/metabolism ; Cricetulus ; CCN Intercellular Signaling Proteins/genetics ; CCN Intercellular Signaling Proteins/metabolism ; Peptides ; Recombinant Proteins ; Adenocarcinoma
Chemical Substances	Connective Tissue Growth Factor (139568-91-5) ; CCN Intercellular Signaling Proteins ; Peptides ; Recombinant Proteins
Language	English
Publishing date	2022-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.102803
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.108: 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 ▾
- See ZB MED holdings
- Order with fees

Article: Report on the 11th international workshop on the CCN family of genes, Nice, October 20-24, 2022.

Attramadal, Havard / Banerjee, Sushanta K / Chaqour, Brahim / Fisher, Gary / Lau, Lester / Perbal, Bernard / Smith, Ulf / Yeger, Herman

Journal of cell communication and signaling

2023 Volume 17, Issue 1, Page(s) 7–11

Abstract: In celebration of the twentieth anniversary of the inception of the CCN society, and of the first post-Covid-19 live meeting, the executive board of the ICCNS had chosen Nice as the venue for the 11th International workshop on the CCN family of genes. On ...

Abstract	In celebration of the twentieth anniversary of the inception of the CCN society, and of the first post-Covid-19 live meeting, the executive board of the ICCNS had chosen Nice as the venue for the 11th International workshop on the CCN family of genes. On this occasion participation in the meeting was extended to colleagues from other cell signaling fields who were invited to present both an overview of their work and the future directions of their laboratory. Also, for the first time, the members of the JCCS Editorial Board were invited to participate in a JCCS special session during which all aspects of the journal « life » were addressed and opened to free critical discussion. The scientific presentations and the discussions that followed showed once more that an expansion of the session topics was beneficial to the quality of the meeting and confirmed that the ARBIOCOM project discussed last April in Nice was now on track to be launched in 2023. The participants unanimously welcomed Professor Attramadal's proposition to organize the 2024, 12th International CCN workshop in Oslo, Norway.
Language	English
Publishing date	2023-02-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2299380-0
ISSN	1873-961X ; 1873-9601
ISSN (online)	1873-961X
ISSN	1873-9601
DOI	10.1007/s12079-023-00731-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Hypertension: Are we beta-ARKing up the right tree?

Attramadal, Håvard

Hypertension (Dallas, Tex. : 1979)

2009 Volume 54, Issue 1, Page(s) 27–28

MeSH term(s)	African Americans/statistics & numerical data ; Blood Pressure/physiology ; Cyclic AMP/metabolism ; G-Protein-Coupled Receptor Kinase 2/genetics ; G-Protein-Coupled Receptor Kinase 2/metabolism ; G-Protein-Coupled Receptor Kinase 5/genetics ; G-Protein-Coupled Receptor Kinase 5/metabolism ; Humans ; Hypertension/enzymology ; Hypertension/ethnology ; Hypertension/physiopathology ; Models, Biological ; Norepinephrine/blood
Chemical Substances	Cyclic AMP (E0399OZS9N) ; GRK2 protein, human (EC 2.7.11.15) ; G-Protein-Coupled Receptor Kinase 2 (EC 2.7.11.16) ; G-Protein-Coupled Receptor Kinase 5 (EC 2.7.11.16) ; GRK5 protein, human (EC 2.7.11.16) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2009-06-01
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.109.131904
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1488: 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

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: SLAMF1-derived peptide exhibits cardio protection after permanent left anterior descending artery ligation in mice.

Olsen, Maria Belland / Kong, Xiang Yi / Louwe, Mieke C / Lauritzen, Knut H / Schanke, Ylva / Kaasbøll, Ole Jørgen / Attramadal, Håvard / Øgaard, Jonas / Holm, Sverre / Aukrust, Pål / Ryan, Liv / Espevik, Terje / Yurchenko, Maria / Halvorsen, Bente

Frontiers in immunology

2024 Volume 15, Page(s) 1383505

Abstract: Acute myocardial infarction (MI) results in tissue damage to affected areas of the myocardium. The initial inflammatory response is the most damaging for residual cardiac function, while at later stages inflammation is a prerequisite for proper healing ... ...

Abstract	Acute myocardial infarction (MI) results in tissue damage to affected areas of the myocardium. The initial inflammatory response is the most damaging for residual cardiac function, while at later stages inflammation is a prerequisite for proper healing and scar formation. Balancing the extent and duration of inflammation during various stages after MI is thus pivotal for preserving cardiac function. Recently, a signaling lymphocytic activation molecule 1 (SLAMF1)-derived peptide (P7) was shown to reduce the secretion of inflammatory cytokines and protected against acute lipopolysaccharide-induced death in mice. In the present study, we experimentally induced MI by permanent ligation of the left anterior descending artery (LAD) in mice and explored the beneficial effect of immediately administering P7, with the aim of dampening the initial inflammatory phase without compromising the healing and remodeling phase. Blood samples taken 9 h post-LAD surgery and P7 administration dampened the secretion of inflammatory cytokines, but this dampening effect of P7 was diminished after 3 days. Echocardiography revealed less deterioration of cardiac contraction in mice receiving P7. In line with this, less myocardial damage was observed histologically in P7-treated mice. In conclusion, the administration of a SLAMF1-derived peptide (P7) immediately after induction of MI reduces the initial myocardial inflammation, reduces infarct expansion, and leads to less deterioration of cardiac contraction.
MeSH term(s)	Animals ; Mice ; Myocardial Infarction ; Male ; Disease Models, Animal ; Cytokines/metabolism ; Mice, Inbred C57BL ; Antigens, CD/metabolism ; Ligation ; Myocardium/pathology ; Myocardium/metabolism ; Peptides/pharmacology ; Receptors, Cell Surface/metabolism ; Coronary Vessels/drug effects ; Coronary Vessels/pathology
Chemical Substances	Cytokines ; Antigens, CD ; Ly78 protein, mouse ; Peptides ; Receptors, Cell Surface
Language	English
Publishing date	2024-04-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1383505
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Prokineticins and the heart: diverging actions elicited by signalling through prokineticin receptor-1 or -2.

Attramadal, Håvard

Cardiovascular research

2009 Volume 81, Issue 1, Page(s) 3–4

MeSH term(s)	Animals ; Capillary Leak Syndrome/metabolism ; Capillary Leak Syndrome/pathology ; Cardiomyopathy, Dilated/metabolism ; Cardiomyopathy, Dilated/pathology ; Disease Models, Animal ; Gastrointestinal Hormones/metabolism ; Mice ; Mice, Transgenic ; Myocardium/metabolism ; Myocardium/pathology ; Neuropeptides/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/physiology ; Vascular Endothelial Growth Factor, Endocrine-Gland-Derived/metabolism ; Ventricular Remodeling
Chemical Substances	Gastrointestinal Hormones ; Neuropeptides ; PKR1 protein, mouse ; PKR2 protein, mouse ; Prok2 protein, mouse ; Receptors, G-Protein-Coupled ; Vascular Endothelial Growth Factor, Endocrine-Gland-Derived
Language	English
Publishing date	2009-01-01
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvn306
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

Details ▾
- See ZB MED holdings
- Order with fees

Article: Tissue distribution and transcriptional regulation of CCN5 in the heart after myocardial infarction.

Zolfaghari, Sima / Kaasbøll, Ole Jørgen / Ahmed, M Shakil / Line, Fabian A / Hagelin, Else Marie V / Monsen, Vivi T / Attramadal, Håvard

Journal of cell communication and signaling

2021 Volume 16, Issue 3, Page(s) 377–395

Abstract: CCN5 is a divergent member of the cellular communication network factor (CCN) family in that it lacks the carboxyl terminal cystine knot domain common to the other CCN family members. CCN5 has been reported to antagonize the profibrotic actions of CCN2 ... ...

Abstract	CCN5 is a divergent member of the cellular communication network factor (CCN) family in that it lacks the carboxyl terminal cystine knot domain common to the other CCN family members. CCN5 has been reported to antagonize the profibrotic actions of CCN2 and to inhibit myocardial collagen deposition and fibrosis in chronic pressure overload of the heart. However, what mechanisms that regulate CCN5 activity in the heart remain unknown. Recombinant, replication defective adenovirus encoding firefly luciferase under control of the human CCN5 promoter was prepared and used to investigate what mechanisms regulate CCN5 transcription in relevant cells. Tissue distribution of CCN5 in hearts from healthy mice and from mice subjected to myocardial infarction was investigated. Contrary to the profibrotic immediate early gene CCN2, we find that CCN5 is induced in the late proliferation and maturation phases of scar healing. CCN5 was identified principally in endothelial cells, fibroblasts, smooth muscle cells, and macrophages. Our data show that CCN5 gene transcription and protein levels are induced by catecholamines via β
Language	English
Publishing date	2021-12-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2299380-0
ISSN	1873-961X ; 1873-9601
ISSN (online)	1873-961X
ISSN	1873-9601
DOI	10.1007/s12079-021-00659-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Cardiomyocyte-specific overexpression of syndecan-4 in mice results in activation of calcineurin-NFAT signalling and exacerbated cardiac hypertrophy

Lunde, Ida G. / Aronsen, J. Magnus / Melleby, A. Olav / Strand, Mari E. / Skogestad, Jonas / Bendiksen, Bård A. / Ahmed, M. Shakil / Sjaastad, Ivar / Attramadal, Håvard / Carlson, Cathrine R. / Christensen, Geir

Mol Biol Rep. 2022 Dec., v. 49, no. 12 p.11795-11809

2022

Abstract: BACKGROUND: Cardiomyocyte hypertrophy is a hallmark of cardiac dysfunction in patients with aortic stenosis (AS), and can be triggered by left ventricular (LV) pressure overload in mice by aortic banding (AB). Syndecan-4 is a transmembrane heparan ... ...

Abstract	BACKGROUND: Cardiomyocyte hypertrophy is a hallmark of cardiac dysfunction in patients with aortic stenosis (AS), and can be triggered by left ventricular (LV) pressure overload in mice by aortic banding (AB). Syndecan-4 is a transmembrane heparan sulphate proteoglycan which is found increased in the myocardium of AS patients and AB mice. The role of syndecan-4 in cardiomyocyte hypertrophy is not well understood. PURPOSE OF THE STUDY: We developed mice with cardiomyocyte-specific overexpression of syndecan-4 (Sdc4-Tg) and subjected these to AB to examine the role of syndecan-4 in hypertrophy and activation of the pro-hypertrophic calcineurin-NFAT signalling pathway. METHODS AND RESULTS: Sdc4-Tg mice showed exacerbated cardiac remodelling upon AB compared to wild type (WT). At 2–6 weeks post-AB, Sdc4-Tg and WT mice showed similar hypertrophic growth, while at 20 weeks post-AB, exacerbated hypertrophy and dysfunction were evident in Sdc4-Tg mice. After cross-breeding of Sdc4-Tg mice with NFAT-luciferase reporter mice, we found increased NFAT activation in Sdc4-Tg hearts after AB. Immunoprecipitation showed that calcineurin bound to syndecan-4 in Sdc4-Tg hearts. Isolated cardiomyocytes from Sdc4-Tg mice showed alterations in Ca²⁺ fluxes, suggesting that syndecan-4 regulated Ca²⁺ levels, and thereby, activating the syndecan-4-calcineurin complex resulting in NFAT activation and hypertrophic growth. Similarly, primary cardiomyocyte cultures from neonatal rats showed increased calcineurin-NFAT-dependent hypertrophic growth upon viral Sdc4 overexpression. CONCLUSION: Our study of mice with cardiomyocyte-specific overexpression of Sdc4 have revealed that syndecan-4 is important for activation of the Ca²⁺-dependent calcineurin-NFAT signalling pathway, hypertrophic remodelling and dysfunction in cardiomyocytes in response to pressure overload.
Keywords	calcium ; cardiomyocytes ; crossing ; heparan sulfate ; hypertrophy ; precipitin tests ; proteoglycans ; syndecans
Language	English
Dates of publication	2022-12
Size	p. 11795-11809.
Publishing place	Springer Netherlands
Document type	Article ; Online
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-022-07985-y
Database	NAL-Catalogue (AGRICOLA)

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Bonn / Germany

Z 78/728: Show issues

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 ▾

Article ; Online: Impact of delayed type hypersensitivity arthritis on development of heart failure by aortic constriction in mice.

Tønnessen, Theis Christian / Melleby, Arne Olav / Hauge-Iversen, Ida Marie / Espe, Emil Knut Stenersen / Ahmed, Mohammed Shakil / Ueland, Thor / Haavardsholm, Espen Andre / Atkinson, Sara Marie / Melum, Espen / Attramadal, Håvard / Sjaastad, Ivar / Vinge, Leif Erik

PloS one

2022 Volume 17, Issue 1, Page(s) e0262821

Abstract: Aims: Patients with rheumatoid arthritis (RA) have increased risk of heart failure (HF). The mechanisms and cardiac prerequisites explaining this association remain unresolved. In this study, we sought to determine the potential cardiac impact of an ... ...

Abstract	Aims: Patients with rheumatoid arthritis (RA) have increased risk of heart failure (HF). The mechanisms and cardiac prerequisites explaining this association remain unresolved. In this study, we sought to determine the potential cardiac impact of an experimental model of RA in mice subjected to HF by constriction of the ascending aorta. Methods: Aorta was constricted via thoracotomy and placement of o-rings with inner diameter 0.55 mm or 0.66 mm, or sham operated. RA-like phenotype was instigated by delayed-type hypersensitivity arthritis (DTHA) two weeks after surgery and re-iterated after additional 18 days. Cardiac magnetic resonance imaging (MRI) was performed before surgery and at successive time points throughout the study. Six weeks after surgery the mice were euthanized, blood and tissue were collected, organ weights were documented, and expression levels of cardiac foetal genes were analysed. In a supplemental study, DTHA-mice were euthanized throughout 14 days after induction of arthritis, and blood was analysed for important markers and mediators of RA (SAP, TNF-α and IL-6). In order to put the latter findings into clinical context, the same molecules were analysed in serum from untreated RA patients and compared to healthy controls. Results: Significant elevations of inflammatory markers were found in both patient- and murine blood. Furthermore, the DTHA model appeared clinically relevant when compared to the inflammatory responses observed in three prespecified RA severity disease states. Two distinct trajectories of cardiac dysfunction and HF development were found using the two o-ring sizes. These differences were consistent by both MRI, organ weights and cardiac foetal gene expression levels. Still, no difference within the HF groups, nor within the sham groups, could be found when DTHA was induced. Conclusion: DTHA mediated systemic inflammation did not cause, nor modify HF caused by aortic constriction. This indicates other prerequisites for RA-induced cardiac dysfunction.
MeSH term(s)	Animals ; Aortic Valve Stenosis/etiology ; Aortic Valve Stenosis/physiopathology ; Arthritis, Experimental/complications ; Arthritis, Experimental/physiopathology ; Disease Models, Animal ; Heart Failure/etiology ; Heart Failure/physiopathology ; Humans ; Mice
Language	English
Publishing date	2022-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0262821
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Bonn / Germany

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito