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Article ; Online: NDRG1: A New Regulator of Vascular Inflammation and Atherothrombosis.

Bursill, Christina A

2023 Volume 132, Issue 3, Page(s) 320–322

MeSH term(s)	Humans ; Cell Cycle Proteins ; Inflammation
Chemical Substances	Cell Cycle Proteins
Language	English
Publishing date	2023-02-02
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.122.322377
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Ui IV Zs.70: 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)
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)

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Article ; Online: The Mechanisms of Restenosis and Relevance to Next Generation Stent Design.

Clare, Jessie / Ganly, Justin / Bursill, Christina A / Sumer, Huseyin / Kingshott, Peter / de Haan, Judy B

Biomolecules

2022 Volume 12, Issue 3

Abstract: Stents are lifesaving mechanical devices that re-establish essential blood flow to the coronary circulation after significant vessel occlusion due to coronary vessel disease or thrombolytic blockade. Improvements in stent surface engineering over the ... ...

Abstract	Stents are lifesaving mechanical devices that re-establish essential blood flow to the coronary circulation after significant vessel occlusion due to coronary vessel disease or thrombolytic blockade. Improvements in stent surface engineering over the last 20 years have seen significant reductions in complications arising due to restenosis and thrombosis. However, under certain conditions such as diabetes mellitus (DM), the incidence of stent-mediated complications remains 2-4-fold higher than seen in non-diabetic patients. The stents with the largest market share are designed to target the mechanisms behind neointimal hyperplasia (NIH) through anti-proliferative drugs that prevent the formation of a neointima by halting the cell cycle of vascular smooth muscle cells (VSMCs). Thrombosis is treated through dual anti-platelet therapy (DAPT), which is the continual use of aspirin and a P2Y
MeSH term(s)	Coronary Restenosis/etiology ; Drug-Eluting Stents/adverse effects ; Humans ; Inflammation/complications ; Neointima/complications ; Percutaneous Coronary Intervention/adverse effects ; Stents/adverse effects ; Thrombosis/etiology
Language	English
Publishing date	2022-03-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12030430
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TRIM2 Selectively Regulates Inflammation-Driven Pathological Angiogenesis without Affecting Physiological Hypoxia-Mediated Angiogenesis.

Wong, Nathan K P / Solly, Emma L / Le, Richard / Nankivell, Victoria A / Mulangala, Jocelyne / Psaltis, Peter J / Nicholls, Stephen J / Ng, Martin K C / Bursill, Christina A / Tan, Joanne T M

International journal of molecular sciences

2024 Volume 25, Issue 6

Abstract: Angiogenesis is a critical physiological response to ischemia but becomes pathological when dysregulated and driven excessively by inflammation. We recently identified a novel angiogenic role for tripartite-motif-containing protein 2 (TRIM2) whereby ... ...

Abstract	Angiogenesis is a critical physiological response to ischemia but becomes pathological when dysregulated and driven excessively by inflammation. We recently identified a novel angiogenic role for tripartite-motif-containing protein 2 (TRIM2) whereby lentiviral shRNA-mediated TRIM2 knockdown impaired endothelial angiogenic functions in vitro. This study sought to determine whether these effects could be translated in vivo and to determine the molecular mechanisms involved. CRISPR/Cas9-generated
MeSH term(s)	Animals ; Mice ; Angiogenesis ; Endothelial Cells/metabolism ; Hindlimb/blood supply ; Hypoxia/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Inflammation/metabolism ; Ischemia/metabolism ; Neovascularization, Pathologic/metabolism ; Neovascularization, Physiologic/genetics
Chemical Substances	Hypoxia-Inducible Factor 1, alpha Subunit ; Trim2 protein, mouse (EC 2.3.2.27)
Language	English
Publishing date	2024-03-15
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/ijms25063343
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Article ; Online: Targeting macrophages with multifunctional nanoparticles to detect and prevent atherosclerotic cardiovascular disease.

Nankivell, Victoria / Vidanapathirana, Achini K / Hoogendoorn, Ayla / Tan, Joanne T M / Verjans, Johan / Psaltis, Peter J / Hutchinson, Mark R / Gibson, Brant C / Lu, Yiqing / Goldys, Eva / Zheng, Gang / Bursill, Christina A

Cardiovascular research

2024

Abstract: Despite the emergence of novel diagnostic, pharmacological, interventional and prevention strategies, atherosclerotic cardiovascular disease remains a significant cause of morbidity and mortality. Nanoparticle-based platforms encompass diverse imaging, ... ...

Abstract	Despite the emergence of novel diagnostic, pharmacological, interventional and prevention strategies, atherosclerotic cardiovascular disease remains a significant cause of morbidity and mortality. Nanoparticle-based platforms encompass diverse imaging, delivery and pharmacological properties that provide novel opportunities for refining diagnostic and therapeutic interventions for atherosclerosis at the cellular and molecular level. Macrophages play a critical role in atherosclerosis and therefore represent an important disease-related diagnostic and therapeutic target, especially given their inherent ability for passive and active nanoparticle uptake. In this review, we discuss an array of inorganic, carbon-based and lipid-based nanoparticles that provide magnetic, radiographic and fluorescent imaging capabilities for a range of highly promising research and clinical applications in atherosclerosis. We discuss the design of nanoparticles that target a range of macrophage-related functions such as lipoprotein oxidation, cholesterol efflux, vascular inflammation and defective efferocytosis. We also provide examples of nanoparticle systems that were developed for other pathologies such as cancer and highlight their potential for repurposing in cardiovascular disease. Finally, we discuss the current state of play and the future of theranostic nanoparticles. Whilst this is not without its challenges, the array of multifunctional capabilities that are possible in nanoparticle design ensures they will be part of the next frontier of exciting new therapies that simultaneously improve the accuracy of plaque diagnosis and more effectively reduce atherosclerosis with limited side effects.
Language	English
Publishing date	2024-05-02
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/cvae099
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Article: The Role of miR-181c in Mechanisms of Diabetes-Impaired Angiogenesis: An Emerging Therapeutic Target for Diabetic Vascular Complications.

Solly, Emma L / Psaltis, Peter J / Bursill, Christina A / Tan, Joanne T M

Frontiers in pharmacology

2021 Volume 12, Page(s) 718679

Abstract: Diabetes mellitus is estimated to affect up to 700 million people by the year 2045, contributing to an immense health and economic burden. People living with diabetes have a higher risk of developing numerous debilitating vascular complications, leading ... ...

Abstract	Diabetes mellitus is estimated to affect up to 700 million people by the year 2045, contributing to an immense health and economic burden. People living with diabetes have a higher risk of developing numerous debilitating vascular complications, leading to an increased need for medical care, a reduced quality of life and increased risk of early death. Current treatments are not satisfactory for many patients who suffer from impaired angiogenesis in response to ischaemia, increasing their risk of ischaemic cardiovascular conditions. These vascular pathologies are characterised by endothelial dysfunction and abnormal angiogenesis, amongst a host of impaired signaling pathways. Therapeutic stimulation of angiogenesis holds promise for the treatment of diabetic vascular complications that stem from impaired ischaemic responses. However, despite significant effort and research, there are no established therapies that directly stimulate angiogenesis to improve ischaemic complications such as ischaemic heart disease and peripheral artery disease, highlighting the immense unmet need. However, despite significant effort and research, there are no established therapies that directly stimulate angiogenesis in a clinical setting, highlighting the immense unmet need. MicroRNAs (miRNAs) are emerging as powerful targets for multifaceted diseases including diabetes and cardiovascular disease. This review highlights the potential role of microRNAs as therapeutic targets for rescuing diabetes-impaired angiogenesis, with a specific focus on miR-181c, which we have previously identified as an important angiogenic regulator. Here we summarise the pathways currently known to be regulated by miR-181c, which include the classical angiogenesis pathways that are dysregulated in diabetes, mitochondrial function and axonal guidance, and describe how these relate both directly and indirectly to angiogenesis. The pleiotropic actions of miR-181c across multiple key angiogenic signaling pathways and critical cellular processes highlight its therapeutic potential as a novel target for treating diabetic vascular complications.
Language	English
Publishing date	2021-08-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.718679
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Article ; Online: The Role of Chemokines in Wound Healing.

Ridiandries, Anisyah / Tan, Joanne T M / Bursill, Christina A

International journal of molecular sciences

2018 Volume 19, Issue 10

Abstract: Wound healing is a multistep process with four overlapping but distinct stages: hemostasis, inflammation, proliferation, and remodeling. An alteration at any stage may lead to the development of chronic non-healing wounds or excessive scar formation. ... ...

Abstract	Wound healing is a multistep process with four overlapping but distinct stages: hemostasis, inflammation, proliferation, and remodeling. An alteration at any stage may lead to the development of chronic non-healing wounds or excessive scar formation. Impaired wound healing presents a significant health and economic burden to millions of individuals worldwide, with diabetes mellitus and aging being major risk factors. Ongoing understanding of the mechanisms that underly wound healing is required for the development of new and improved therapies that increase repair. Chemokines are key regulators of the wound healing process. They are involved in the promotion and inhibition of angiogenesis and the recruitment of inflammatory cells, which release growth factors and cytokines to facilitate the wound healing process. Preclinical research studies in mice show that the administration of CCL2, CCL21, CXCL12, and a CXCR4 antagonist as well as broad-spectrum inhibition of the CC-chemokine class improve the wound healing process. The focus of this review is to highlight the contributions of chemokines during each stage of wound healing and to discuss the related molecular pathologies in complex and chronic non-healing wounds. We explore the therapeutic potential of targeting chemokines as a novel approach to overcome the debilitating effects of impaired wound healing.
MeSH term(s)	Animals ; Biomarkers ; Cell Proliferation ; Chemokines/genetics ; Chemokines/metabolism ; Homeostasis ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Molecular Targeted Therapy ; Neovascularization, Pathologic ; Neovascularization, Physiologic ; Wound Healing/physiology
Chemical Substances	Biomarkers ; Chemokines
Language	English
Publishing date	2018-10-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19103217
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Article ; Online: Broad-spectrum chemokine inhibition blocks inflammation-induced angiogenesis, but preserves ischemia-driven angiogenesis.

Ravindran, Dhanya / Cartland, Siân P / Bursill, Christina A / Kavurma, Mary M

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 33, Issue 12, Page(s) 13423–13434

Abstract: M3 is a broad-spectrum chemokine-binding protein that inactivates inflammatory chemokines, including CCL2, CCL5, and ... ...

Abstract	M3 is a broad-spectrum chemokine-binding protein that inactivates inflammatory chemokines, including CCL2, CCL5, and CX
MeSH term(s)	Adenoviridae/genetics ; Animals ; Cell Movement ; Cell Proliferation ; Chemokines/metabolism ; Hindlimb/physiology ; Hypoxia/complications ; Inflammation/complications ; Ischemia/complications ; Kruppel-Like Factor 4 ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout, ApoE ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Neovascularization, Pathologic/etiology ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/prevention & control ; Regional Blood Flow ; Signal Transduction ; Viral Proteins/antagonists & inhibitors ; Viral Proteins/genetics
Chemical Substances	Chemokines ; KLF4 protein, human ; Klf4 protein, mouse ; Kruppel-Like Factor 4 ; M3 protein, Murine gammaherpesvirus ; Viral Proteins
Language	English
Publishing date	2019-10-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201900232RR
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Zs.A 2266: 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 296: Show issues

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Article ; Online: The multiple roles of chemokines in the mechanisms of stent biocompatibility.

Ravindran, Dhanya / Karimi Galougahi, Keyvan / Tan, Joanne T M / Kavurma, Mary M / Bursill, Christina A

Cardiovascular research

2020 Volume 117, Issue 11, Page(s) 2299–2308

Abstract: While the advent of drug-eluting stents has been clinically effective in substantially reducing the rates of major stent-related adverse events compared with bare metal stents, vascular biological problems such as neointimal hyperplasia, delayed re- ... ...

Abstract	While the advent of drug-eluting stents has been clinically effective in substantially reducing the rates of major stent-related adverse events compared with bare metal stents, vascular biological problems such as neointimal hyperplasia, delayed re-endothelialization, late stent thrombosis are not eliminated and, increasingly, neoatherosclerosis is the underlying mechanism for very late stent failure. Further understanding regarding the mechanisms underlying the biological responses to stent deployment is therefore required so that new and improved therapies can be developed. This review will discuss the accumulating evidence that the chemokines, small inflammatory proteins, play a role in each key biological process of stent biocompatibility. It will address the chemokine system in its specialized roles in regulating the multiple facets of vascular biocompatibility including neointimal hyperplasia, endothelial progenitor cell (EPC) mobilization and re-endothelialization after vascular injury, platelet activation and thrombosis, as well as neoatherosclerosis. The evidence in this review suggests that chemokine-targeting strategies may be effective in controlling the pathobiological processes that lead to stent failure. Preclinical studies provide evidence that inhibition of specific chemokines and/or broad-spectrum inhibition of the CC-chemokine class prevents neointimal hyperplasia, reduces thrombosis and suppresses the development of neoatherosclerosis. In contrast, however, to these apparent deleterious effects of chemokines on stent biocompatibility, the CXC chemokine, CXCL12, is essential for the mobilization and recruitment of EPCs that make important contributions to re-endothelialization post-stent deployment. This suggests that future chemokine inhibition strategies would need to be correctly targeted so that all key stent biocompatibility areas could be addressed, without compromising important adaptive biological responses.
MeSH term(s)	Animals ; Biocompatible Materials ; Chemokines/immunology ; Chemokines/metabolism ; Coronary Artery Disease/immunology ; Coronary Artery Disease/metabolism ; Coronary Artery Disease/pathology ; Coronary Artery Disease/therapy ; Coronary Restenosis/immunology ; Coronary Restenosis/metabolism ; Coronary Restenosis/pathology ; Coronary Thrombosis/immunology ; Coronary Thrombosis/metabolism ; Coronary Thrombosis/pathology ; Coronary Vessels/immunology ; Coronary Vessels/metabolism ; Coronary Vessels/pathology ; Drug-Eluting Stents ; Humans ; Hyperplasia ; Neointima ; Percutaneous Coronary Intervention/adverse effects ; Percutaneous Coronary Intervention/instrumentation ; Prosthesis Design ; Signal Transduction ; Stents ; Treatment Outcome
Chemical Substances	Biocompatible Materials ; Chemokines
Language	English
Publishing date	2020-02-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvaa072
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Article ; Online: The Role of High-Density Lipoproteins in Endothelial Cell Metabolism and Diabetes-Impaired Angiogenesis.

Primer, Khalia R / Psaltis, Peter J / Tan, Joanne T M / Bursill, Christina A

International journal of molecular sciences

2020 Volume 21, Issue 10

Abstract: Diabetes mellitus affects millions of people worldwide and is associated with devastating vascular complications. A number of these complications, such as impaired wound healing and poor coronary collateral circulation, are characterised by impaired ... ...

Abstract	Diabetes mellitus affects millions of people worldwide and is associated with devastating vascular complications. A number of these complications, such as impaired wound healing and poor coronary collateral circulation, are characterised by impaired ischaemia-driven angiogenesis. There is increasing evidence that high-density lipoproteins (HDL) can rescue diabetes-impaired angiogenesis through a number of mechanisms, including the modulation of endothelial cell metabolic reprogramming. Endothelial cell metabolic reprogramming in response to tissue ischaemia is a driver of angiogenesis and is dysregulated by diabetes. Specifically, diabetes impairs pathways that allow endothelial cells to upregulate glycolysis in response to hypoxia adequately and impairs suppression of mitochondrial respiration. HDL rescues the impairment of the central hypoxia signalling pathway, which regulates these metabolic changes, and this may underpin several of its known pro-angiogenic effects. This review discusses the current understanding of endothelial cell metabolism and how diabetes leads to its dysregulation whilst examining the various positive effects of HDL on endothelial cell function.
MeSH term(s)	Animals ; Diabetic Angiopathies/metabolism ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Humans ; Lipoproteins, HDL/metabolism
Chemical Substances	Lipoproteins, HDL
Language	English
Publishing date	2020-05-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21103633
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Article ; Online: Cardiovascular bioimaging of nitric oxide: Achievements, challenges, and the future.

Vidanapathirana, Achini K / Psaltis, Peter J / Bursill, Christina A / Abell, Andrew D / Nicholls, Stephen J

Medicinal research reviews

2020 Volume 41, Issue 1, Page(s) 435–463

Abstract: Nitric oxide (NO) is a ubiquitous, volatile, cellular signaling molecule that operates across a wide physiological concentration range (pM-µM) in different tissues. It is a highly diffusible messenger and intermediate in various metabolic pathways. NO ... ...

Abstract	Nitric oxide (NO) is a ubiquitous, volatile, cellular signaling molecule that operates across a wide physiological concentration range (pM-µM) in different tissues. It is a highly diffusible messenger and intermediate in various metabolic pathways. NO plays a pivotal role in maintaining optimum cardiovascular function, particularly by regulating vascular tone and blood flow. This review highlights the need for accurate, real-time bioimaging of NO in clinical diagnostic, therapeutic, monitoring, and theranostic applications within the cardiovascular system. We summarize electrochemical, optical, and nanoscale sensors that allow measurement and imaging of NO, both directly and indirectly via surrogate measurements. The physical properties of NO render it difficult to accurately measure in tissues using direct methods. There are also significant limitations associated with the NO metabolites used as surrogates to indirectly estimate NO levels. All these factors added to significant variability in the measurement of NO using available methodology have led to a lack of sensors and imaging techniques of clinical applicability in relevant vascular pathologies such as atherosclerosis and ischemic heart disease. Challenges in applying current methods to biomedical and clinical translational research, including the wide physiological range of NO and limitations due to the characteristics and toxicity of the sensors are discussed, as are potential targets and modifications for future studies. The development of biocompatible nanoscale sensors for use in combination with existing clinical imaging modalities provides a feasible opportunity for bioimaging NO within the cardiovascular system.
MeSH term(s)	Atherosclerosis ; Cardiovascular System ; Humans ; Nitric Oxide ; Signal Transduction
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603210-2
ISSN	1098-1128 ; 0198-6325
ISSN (online)	1098-1128
ISSN	0198-6325
DOI	10.1002/med.21736
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