LIVIVO - Search results -

Search results

Result 1 - 10 of total 34

Search options

Article: When worlds collide: autoimmunity and atherosclerosis.

Grainger, David J

2009 Volume 36, Issue 11, Page(s) 2378–2379

MeSH term(s)	Antibodies, Antinuclear/immunology ; Atherosclerosis/immunology ; Autoantibodies/immunology ; Autoimmunity/immunology ; Humans ; Rheumatoid Factor/immunology
Chemical Substances	Antibodies, Antinuclear ; Autoantibodies ; Rheumatoid Factor (9009-79-4)
Language	English
Publishing date	2009-11
Publishing country	Canada
Document type	Comment ; Editorial
ZDB-ID	194928-7
ISSN	1499-2752 ; 0315-162X
ISSN (online)	1499-2752
ISSN	0315-162X
DOI	10.3899/jrheum.091027
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1168: 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)
Zs.MO 135: Show issues

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: Proteostasis is adaptive: Balancing chaperone holdases against foldases.

de Graff, Adam Mr / Mosedale, David E / Sharp, Tilly / Dill, Ken A / Grainger, David J

PLoS computational biology

2020 Volume 16, Issue 12, Page(s) e1008460

Abstract: Because a cell must adapt to different stresses and growth rates, its proteostasis system must too. How do cells detect and adjust proteome folding to different conditions? Here, we explore a biophysical cost-benefit principle, namely that the cell ... ...

Abstract	Because a cell must adapt to different stresses and growth rates, its proteostasis system must too. How do cells detect and adjust proteome folding to different conditions? Here, we explore a biophysical cost-benefit principle, namely that the cell should keep its proteome as folded as possible at the minimum possible energy cost. This can be achieved by differential expression of chaperones-balancing foldases (which accelerate folding) against holdases (which act as parking spots). The model captures changes in the foldase-holdase ratio observed both within organisms during aging and across organisms of varying metabolic rates. This work describes a simple biophysical mechanism by which cellular proteostasis adapts to meet the needs of a changing growth environment.
MeSH term(s)	Animals ; Humans ; Kinetics ; Mammals ; Models, Theoretical ; Molecular Chaperones/metabolism ; Protein Binding ; Protein Folding ; Proteostasis
Chemical Substances	Molecular Chaperones
Language	English
Publishing date	2020-12-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2193340-6
ISSN	1553-7358 ; 1553-734X
ISSN (online)	1553-7358
ISSN	1553-734X
DOI	10.1371/journal.pcbi.1008460
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: TGF-beta and atherosclerosis in man.

Grainger, David J

Cardiovascular research

2007 Volume 74, Issue 2, Page(s) 213–222

Abstract: The transforming growth factor type-beta (TGF-beta) superfamily of ligands, receptors, binding proteins and ligand traps together plays a key role in the maintenance of normal blood vessel wall structure. Specific defects in genes encoding superfamily ... ...

Abstract	The transforming growth factor type-beta (TGF-beta) superfamily of ligands, receptors, binding proteins and ligand traps together plays a key role in the maintenance of normal blood vessel wall structure. Specific defects in genes encoding superfamily members have now been linked to a range of cardiovascular syndromes involving loss of healthy vessel architecture, including hypertension and aneurysm. However the contribution of TGF-beta to the development of atherosclerosis is simultaneously more subtle and more complex. TGF-beta ligands are produced by a range of different cell types, which also regulate release of the active cytokine that, in turn, signals through multiple receptor complexes on different cell types. Recent evidence suggests that the T cell may be both a key source of TGF-beta1 and a key target for its effects during atherogenesis, as in other chronic inflammatory disorders. Here we review the evidence for the role of TGF-beta in the human vasculature during atherogenesis, and evaluate the available data in the context of our knowledge from animal models of the disease.
MeSH term(s)	Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Autoimmunity ; Humans ; Muscle, Smooth, Vascular/immunology ; Muscle, Smooth, Vascular/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction/physiology ; T-Lymphocytes/metabolism ; Transforming Growth Factor beta/metabolism
Chemical Substances	Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta
Language	English
Publishing date	2007-05-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1016/j.cardiores.2007.02.022
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 ; Online: Transforming growth factor beta and atherosclerosis: so far, so good for the protective cytokine hypothesis.

Grainger, David J

Arteriosclerosis, thrombosis, and vascular biology

2004 Volume 24, Issue 3, Page(s) 399–404

Abstract: The role of the anti-inflammatory cytokine transforming growth factor beta (TGF-beta) in atherosclerosis has been the subject of considerable debate for a decade. In the early 1990s, we postulated that TGF-beta played an important role in maintaining ... ...

Abstract	The role of the anti-inflammatory cytokine transforming growth factor beta (TGF-beta) in atherosclerosis has been the subject of considerable debate for a decade. In the early 1990s, we postulated that TGF-beta played an important role in maintaining normal vessel wall structure and that loss of this protective effect contributed to the development of atherosclerosis. We termed this the protective cytokine hypothesis. This proposal was slow to gain broad acceptance, however, because at that time there were little data available on the role of TGF-beta during the development of atherosclerosis but much information about its role during trauma-induced neointima formation. Because TGF-beta apparently aggravates neointima formation, both by inhibiting endothelial regeneration and by promoting fibrosis, it was difficult to accept that its presence might ameliorate the superficially similar atherogenesis process. But several recent studies revealed beyond doubt the fact that TGF-beta protects against lipid lesion formation, at least in mouse models of atherosclerosis. Therefore, two important questions remain. First, is the role of TGF-beta in vascular biology similar in humans and in mice? Secondly, how important, compared with defects in thrombosis or lipoprotein metabolism, is the protective role of TGF-beta during atherogenesis?
MeSH term(s)	Animals ; Arteriosclerosis/etiology ; Arteriosclerosis/metabolism ; Arteriosclerosis/prevention & control ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Humans ; Inflammation ; Mice ; Mice, Knockout ; Models, Biological ; Muscle, Smooth, Vascular/physiology ; Signal Transduction ; Species Specificity ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Transforming Growth Factor beta/deficiency ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/physiology ; Tunica Intima/physiology
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2004-03
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/01.ATV.0000114567.76772.33
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1705: 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: Development and characterisation of an assay for furin activity.

Bourne, Gemma L / Grainger, David J

Journal of immunological methods

2011 Volume 364, Issue 1-2, Page(s) 101–108

Abstract: Furin is a serine endoprotease that is responsible for the proteolytic processing of proteins within the secretory pathway, including cytokines, hormones, integrins, other proteases, and also pathogen-derived proteins. It is likely that the level of ... ...

Abstract	Furin is a serine endoprotease that is responsible for the proteolytic processing of proteins within the secretory pathway, including cytokines, hormones, integrins, other proteases, and also pathogen-derived proteins. It is likely that the level of furin activity determines the extent of processing of these substrates. Furin is ubiquitously expressed across all tissues, at low levels, but can be induced in response to environmental cues such as hypoxia and cytokine stimulation. However, all studies to date that have investigated furin expression have been limited to analysis of furin mRNA; there has been no assay sensitive enough to quantify endogenous furin. Though activity-based assays have been described for furin-like enzyme activity, we demonstrate that these assays are dominated by the activity of other enzymes and cannot be used to approximate furin activity. A sensitive and specific assay for furin activity was therefore developed and characterised, using an antibody capture step to immobilise furin from whole cell lysates. Furin activity is quantified relative to that of recombinant active furin protein, to allow estimation of active furin protein concentration. The assay has a minimum detection limit of 0.006 nM; sensitive enough to determine the furin activity of many of the cell lines tested. The specificity of the assay was demonstrated by genetic modulation of furin expression. Furthermore, the assay was used to demonstrate that the cytokine transforming growth factor beta (TGF-β) stimulates increased furin activity in HepG2 cells, confirming and extending previous reports that TGF-β increases furin expression, and adding to the mounting body of evidence that cellular furin activity can be modulated.
MeSH term(s)	Antibodies/immunology ; Antibodies/metabolism ; Biochemistry/methods ; Cell Extracts/chemistry ; Furin/genetics ; Furin/immunology ; Furin/metabolism ; Gene Expression Regulation, Enzymologic ; Hep G2 Cells ; Humans ; Hypoxia/diagnosis ; Hypoxia/genetics ; Hypoxia/metabolism ; Immunomodulation ; Immunosorbent Techniques ; RNA, Messenger/analysis ; Reference Standards ; Sensitivity and Specificity ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta/metabolism
Chemical Substances	Antibodies ; Cell Extracts ; RNA, Messenger ; Transforming Growth Factor beta ; Furin (EC 3.4.21.75)
Language	English
Publishing date	2011-02-01
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120142-6
ISSN	1872-7905 ; 0022-1759
ISSN (online)	1872-7905
ISSN	0022-1759
DOI	10.1016/j.jim.2010.11.008
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 795: 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 ▾

Article: Development and characterisation of an assay for furin activity

Bourne, Gemma L / Grainger, David J

Journal of immunological methods. 2011 Feb. 1, v. 364, no. 1-2

2011

Abstract	Furin is a serine endoprotease that is responsible for the proteolytic processing of proteins within the secretory pathway, including cytokines, hormones, integrins, other proteases, and also pathogen-derived proteins. It is likely that the level of furin activity determines the extent of processing of these substrates. Furin is ubiquitously expressed across all tissues, at low levels, but can be induced in response to environmental cues such as hypoxia and cytokine stimulation. However, all studies to date that have investigated furin expression have been limited to analysis of furin mRNA; there has been no assay sensitive enough to quantify endogenous furin. Though activity-based assays have been described for furin-like enzyme activity, we demonstrate that these assays are dominated by the activity of other enzymes and cannot be used to approximate furin activity. A sensitive and specific assay for furin activity was therefore developed and characterised, using an antibody capture step to immobilise furin from whole cell lysates. Furin activity is quantified relative to that of recombinant active furin protein, to allow estimation of active furin protein concentration. The assay has a minimum detection limit of 0.006nM; sensitive enough to determine the furin activity of many of the cell lines tested. The specificity of the assay was demonstrated by genetic modulation of furin expression. Furthermore, the assay was used to demonstrate that the cytokine transforming growth factor beta (TGF-β) stimulates increased furin activity in HepG2 cells, confirming and extending previous reports that TGF-β increases furin expression, and adding to the mounting body of evidence that cellular furin activity can be modulated.
Keywords	antibodies ; cytokines ; detection limit ; enzyme activity ; hormones ; human cell lines ; hypoxia ; integrins ; messenger RNA ; proteinases ; proteolysis ; serine ; tissues ; transforming growth factor beta
Language	English
Dates of publication	2011-0201
Size	p. 101-108.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	120142-6
ISSN	1872-7905 ; 0022-1759
ISSN (online)	1872-7905
ISSN	0022-1759
DOI	10.1016/j.jim.2010.11.008
Database	NAL-Catalogue (AGRICOLA)

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 795: 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 ▾

Article ; Online: Molecular basis of ALK1-mediated signalling by BMP9/BMP10 and their prodomain-bound forms.

Salmon, Richard M / Guo, Jingxu / Wood, Jennifer H / Tong, Zhen / Beech, John S / Lawera, Aleksandra / Yu, Minmin / Grainger, David J / Reckless, Jill / Morrell, Nicholas W / Li, Wei

Nature communications

2020 Volume 11, Issue 1, Page(s) 1621

Abstract: Activin receptor-like kinase 1 (ALK1)-mediated endothelial cell signalling in response to bone morphogenetic protein 9 (BMP9) and BMP10 is of significant importance in cardiovascular disease and cancer. However, detailed molecular mechanisms of ALK1- ... ...

Abstract	Activin receptor-like kinase 1 (ALK1)-mediated endothelial cell signalling in response to bone morphogenetic protein 9 (BMP9) and BMP10 is of significant importance in cardiovascular disease and cancer. However, detailed molecular mechanisms of ALK1-mediated signalling remain unclear. Here, we report crystal structures of the BMP10:ALK1 complex at 2.3 Å and the prodomain-bound BMP9:ALK1 complex at 3.3 Å. Structural analyses reveal a tripartite recognition mechanism that defines BMP9 and BMP10 specificity for ALK1, and predict that crossveinless 2 is not an inhibitor of BMP9, which is confirmed by experimental evidence. Introduction of BMP10-specific residues into BMP9 yields BMP10-like ligands with diminished signalling activity in C2C12 cells, validating the tripartite mechanism. The loss of osteogenic signalling in C2C12 does not translate into non-osteogenic activity in vivo and BMP10 also induces bone-formation. Collectively, these data provide insight into ALK1-mediated BMP9 and BMP10 signalling, facilitating therapeutic targeting of this important pathway.
MeSH term(s)	Activin Receptors, Type II/chemistry ; Activin Receptors, Type II/metabolism ; Animals ; Binding Sites ; Bone Morphogenetic Proteins/chemistry ; Bone Morphogenetic Proteins/metabolism ; Bone and Bones/chemistry ; Bone and Bones/metabolism ; Cell Line ; Crystallography, X-Ray ; Endothelial Cells/metabolism ; Growth Differentiation Factor 2/chemistry ; Growth Differentiation Factor 2/metabolism ; Humans ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Models, Molecular ; Protein Conformation ; Protein Domains ; Signal Transduction/physiology ; Transforming Growth Factor beta/metabolism
Chemical Substances	BMP10 protein, human ; Bone Morphogenetic Proteins ; GDF2 protein, human ; Growth Differentiation Factor 2 ; Ligands ; Transforming Growth Factor beta ; ACVRL1 protein, human (EC 2.7.11.30) ; Activin Receptors, Type II (EC 2.7.11.30)
Language	English
Publishing date	2020-04-01
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/s41467-020-15425-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Proposal of a novel diabetogenic mechanism involving the serpin PAI-1.

Griffiths, Sarah L / Grainger, David J

BioEssays : news and reviews in molecular, cellular and developmental biology

2006 Volume 28, Issue 6, Page(s) 629–641

Abstract: Metabolic Syndrome is a cluster of risk factors (including obesity, hypertension and insulin resistance), which is associated with late-onset diabetes and coronary heart disease. Elevated levels of the protease inhibitor PAI-1 are well-known molecular ... ...

Abstract	Metabolic Syndrome is a cluster of risk factors (including obesity, hypertension and insulin resistance), which is associated with late-onset diabetes and coronary heart disease. Elevated levels of the protease inhibitor PAI-1 are well-known molecular markers of the Metabolic Syndrome. Here, however, we present a hypothesis that PAI-1 acts as a causative factor in the development of Metabolic Syndrome and its clinical sequelae. We propose that PAI-1 inhibits the activity of members of the proprotein convertase (PC) class of serine proteases and that this underlies, at a molecular level, many of the other features of the Metabolic Syndrome cluster.
MeSH term(s)	Animals ; Diabetes Mellitus/metabolism ; Humans ; Plasminogen Activator Inhibitor 1/metabolism ; Serpins/metabolism ; Substrate Specificity ; Syndrome ; Thrombin/metabolism
Chemical Substances	Plasminogen Activator Inhibitor 1 ; Serpins ; Thrombin (EC 3.4.21.5)
Language	English
Publishing date	2006-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.20418
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 2024: 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 ▾

Article ; Online: Tamoxifen for the prevention of myocardial infarction in humans: preclinical and early clinical evidence.

Grainger, David J / Schofield, Peter M

Circulation

2005 Volume 112, Issue 19, Page(s) 3018–3024

MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Antioxidants/therapeutic use ; Coronary Disease/prevention & control ; Disease Models, Animal ; Estrogen Antagonists/therapeutic use ; Humans ; Myocardial Infarction/prevention & control ; Tamoxifen/therapeutic use
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Antioxidants ; Estrogen Antagonists ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2005-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.104.531178
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.60: 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: A microtitre format assay for proline in human serum or plasma.

Grainger, David J / Aitken, Sri

Clinica chimica acta; international journal of clinical chemistry

2004 Volume 343, Issue 1-2, Page(s) 113–118

Abstract: Background: Recent studies have suggested that low serum proline concentration may be associated with low bone mineral density. However, further investigation of this association has been hampered by the lack of a relatively high throughput assay for ... ...

Abstract	Background: Recent studies have suggested that low serum proline concentration may be associated with low bone mineral density. However, further investigation of this association has been hampered by the lack of a relatively high throughput assay for proline in biological fluids. Here we report a sensitive and specific microtitre plate format assay for proline which exploits the chemical interaction between proline and isatin. Methods: Human serum or plasma is deproteinised by incubation with sodium citrate buffer pH 4.1 at 95 degrees C, and the supernatant is reacted with isatin at 95 degrees C for 3 h. The resultant blue coloured product is quantitated sprectrophometrically. Results: This assay yields a linear standard curve in the range 15 micromol/l to 1 mmol/l (r=0.998+/-0.002; n=8 determinations) with a sensitivity of 31+/-11 micromol/l. None of the other proteogenic amino acids are detected (<0.3% detection at 10 mmol/l) and the closely related metabolite hydroxyproline is only very weakly detected (3% detection at 10 mmol/l). Using human serum, the assay has linear dilution characteristics and a mean spike recovery of 107+/-5%. Repeated re-measurement of the same serum sample yields an intra-assay coefficient of variation (CV) of 4.8% and an inter-assay CV of 6.1%. Conclusions: This method provides the first reliable micro-titre format assay for proline in human serum.
MeSH term(s)	Buffers ; Humans ; Hydroxyproline/analysis ; Isatin/blood ; Isatin/chemistry ; Kinetics ; Proline/blood ; Proline/chemistry ; Reference Standards ; Sensitivity and Specificity
Chemical Substances	Buffers ; Isatin (82X95S7M06) ; Proline (9DLQ4CIU6V) ; Hydroxyproline (RMB44WO89X)
Language	English
Publishing date	2004-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cccn.2003.12.022
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

Ud II Zs.173: 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 ▾

To top

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

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

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

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

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