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Article ; Online: Connexin37 Regulates Cell Cycle in the Vasculature.

Fang, Jennifer S / Burt, Janis M

2022 Volume 60, Issue 2, Page(s) 73–86

Abstract: Control of vascular cell growth responses is critical for development and maintenance of a healthy vasculature. Connexins - the proteins comprising gap junction channels - are key regulators of cell growth in diseases such as cancer, but their ... ...

Abstract	Control of vascular cell growth responses is critical for development and maintenance of a healthy vasculature. Connexins - the proteins comprising gap junction channels - are key regulators of cell growth in diseases such as cancer, but their involvement in controlling cell growth in the vasculature is less well appreciated. Connexin37 (Cx37) is one of four connexin isotypes expressed in the vessel wall. Its primary role in blood vessels relies on its unique ability to transduce flow-sensitive signals into changes in cell cycle status of endothelial (and perhaps, mural) cells. Here, we review available evidence for Cx37's role in the regulation of vascular growth, vessel organization, and vascular tone in healthy and diseased vasculature. We propose a novel mechanism whereby Cx37 accomplishes this with a phosphorylation-dependent transition between closed (growth-suppressive) and multiple open (growth-permissive) channel conformations that result from interactions of the C-terminus with cell-cycle regulators to limit or support cell cycle progression. Lastly, we discuss Cx37 and its downstream signaling as a novel potential target in the treatment of cardiovascular disease, and we address outstanding research questions that still challenge the development of such therapies.
MeSH term(s)	Connexins/metabolism ; Cell Cycle
Chemical Substances	Connexins
Language	English
Publishing date	2022-09-06
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1105259-4
ISSN	1423-0135 ; 1018-1172
ISSN (online)	1423-0135
ISSN	1018-1172
DOI	10.1159/000525619
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Article ; Online: Author Correction: Sema3C signaling is an alternative activator of the canonical WNT pathway in glioblastoma.

Hao, Jing / Han, Xiangzi / Huang, Haidong / Yu, Xingjiang / Fang, Jiankang / Zhao, Jianjun / Prayson, Richard A / Bao, Shideng / Yu, Jennifer S

Nature communications

2023 Volume 14, Issue 1, Page(s) 6018

Language	English
Publishing date	2023-09-27
Publishing country	England
Document type	Published Erratum
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41842-1
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Article ; Online: Mechanisms of cognitive behavioral therapy vs. supportive psychotherapy in body dysmorphic disorder: An exploratory mediation analysis.

Greenberg, Jennifer L / Phillips, Katharine A / Hoeppner, Susanne S / Jacobson, Nicholas C / Fang, Angela / Wilhelm, Sabine

Behaviour research and therapy

2023 Volume 161, Page(s) 104251

Abstract: Body dysmorphic disorder (BDD) is common, severe, and often chronic. Cognitive behavioral therapy (CBT) is the first-line psychosocial treatment for BDD, with well-established efficacy. However, some patients do not improve with CBT, and little is known ... ...

Abstract	Body dysmorphic disorder (BDD) is common, severe, and often chronic. Cognitive behavioral therapy (CBT) is the first-line psychosocial treatment for BDD, with well-established efficacy. However, some patients do not improve with CBT, and little is known about how CBT confers its effects. Neurocognitive processes have been implicated in the etiology and maintenance of BDD and are targeted by CBT-BDD treatment components. Yet, the malleability of these factors in BDD, and their potential role in mediating symptom improvement, are not well understood. Understanding how treatment works could help optimize treatment outcomes. In this secondary data analysis of a randomized clinical trial of CBT vs. supportive psychotherapy (SPT) in BDD (n = 120), we examined whether treatment-related changes in detail processing (Rey-Osterrieth Complex Figure test), maladaptive appearance beliefs (Appearance Schemas Inventory-Revised), and emotion recognition (Emotion Recognition Task) mediated treatment outcome. All constructs improved over time and were associated with symptom improvement. CBT was associated with greater improvements in maladaptive beliefs than SPT. None of the variables examined mediated symptom improvement. Findings suggest that with successful treatment, individuals with BDD demonstrate reduced neurocognitive deficits (detail processing, emotion recognition, maladaptive beliefs) and that CBT is more likely than SPT to improve maladaptive appearance beliefs. More work is needed to understand mechanisms of change and thus maximize treatment outcomes.
MeSH term(s)	Humans ; Body Dysmorphic Disorders/therapy ; Body Dysmorphic Disorders/psychology ; Mediation Analysis ; Psychotherapy ; Cognitive Behavioral Therapy ; Treatment Outcome
Language	English
Publishing date	2023-01-10
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	211997-3
ISSN	1873-622X ; 0005-7967
ISSN (online)	1873-622X
ISSN	0005-7967
DOI	10.1016/j.brat.2022.104251
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Article ; Online: Polygenic Risk and Social Support in Predicting Depression Under Stress.

Cleary, Jennifer L / Fang, Yu / Zahodne, Laura B / Bohnert, Amy S B / Burmeister, Margit / Sen, Srijan

The American journal of psychiatry

2023 Volume 180, Issue 2, Page(s) 139–145

Abstract: Objective: Despite substantial progress in identifying genomic variation associated with major depression, the mechanisms by which genomic and environmental factors jointly influence depression risk remain unclear. Genomically conferred sensitivity to ... ...

Abstract	Objective: Despite substantial progress in identifying genomic variation associated with major depression, the mechanisms by which genomic and environmental factors jointly influence depression risk remain unclear. Genomically conferred sensitivity to the social environment may be one mechanism linking genomic variation and depressive symptoms. The authors assessed whether social support affects the likelihood of depression development differently across the spectrum of genomic risk in two samples that experienced substantial life stress: 1,011 first-year training physicians (interns) in the Intern Health Study (IHS) and 435 recently widowed Health and Retirement Study (HRS) participants. Methods: Participants' depressive symptoms and social support were assessed with questionnaires that were administered before and after the life stressor. Polygenic risk scores (PRSs) for major depressive disorder were calculated for both samples. Results: Depressive symptom scores increased by 126% after the start of internship in the IHS sample and by 34% after widowing in the HRS sample. There was an interaction between depression PRS and change in social support in the prediction of depressive symptoms in both the IHS sample (incidence rate ratio [IRR]=0.96, 95% CI=0.93, 0.98) and the HRS sample (IRR=0.78, 95% CI=0.66, 0.92), with higher depression PRS associated with greater sensitivity to changes in social support. Johnson-Neyman intervals indicated a crossover effect, with losses and gains in social support moderating the effect of PRS on depressive symptoms. (Johnson-Neyman interval in the IHS sample, -0.02, 0.71; in the HRS sample, -0.49, 1.92). Conclusions: The study findings suggest that individuals with high genomic risk for developing increased depressive symptoms under adverse social conditions also benefit more from nurturing social environments.
MeSH term(s)	Humans ; Depressive Disorder, Major/diagnosis ; Depressive Disorder, Major/genetics ; Depression/diagnosis ; Depression/genetics ; Stress, Psychological/genetics ; Social Support ; Social Environment ; Risk Factors
Language	English
Publishing date	2023-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	280045-7
ISSN	1535-7228 ; 0002-953X
ISSN (online)	1535-7228
ISSN	0002-953X
DOI	10.1176/appi.ajp.21111100
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Article: Regulation of Partial and Reversible Endothelial-to-Mesenchymal Transition in Angiogenesis.

Fang, Jennifer S / Hultgren, Nan W / Hughes, Christopher C W

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 702021

Abstract: During development and in several diseases, endothelial cells (EC) can undergo complete endothelial-to-mesenchymal transition (EndoMT or EndMT) to generate endothelial-derived mesenchymal cells. Emerging evidence suggests that ECs can also undergo a ... ...

Abstract	During development and in several diseases, endothelial cells (EC) can undergo complete endothelial-to-mesenchymal transition (EndoMT or EndMT) to generate endothelial-derived mesenchymal cells. Emerging evidence suggests that ECs can also undergo a partial EndoMT to generate cells with intermediate endothelial- and mesenchymal-character. This partial EndoMT event is transient, reversible, and supports both developmental and pathological angiogenesis. Here, we discuss possible regulatory mechanisms that may control the EndoMT program to dictate whether cells undergo complete or partial mesenchymal transition, and we further consider how these pathways might be targeted therapeutically in cancer.
Language	English
Publishing date	2021-10-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.702021
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Article ; Online: Sema3C signaling is an alternative activator of the canonical WNT pathway in glioblastoma.

Hao, Jing / Han, Xiangzi / Huang, Haidong / Yu, Xingjiang / Fang, Jiankang / Zhao, Jianjun / Prayson, Richard A / Bao, Shideng / Yu, Jennifer S

Nature communications

2023 Volume 14, Issue 1, Page(s) 2262

Abstract: The Wnt pathway is frequently dysregulated in many cancers, underscoring it as a therapeutic target. Wnt inhibitors have uniformly failed in clinical trials. Here, we report a mechanism of WNT pathway activation through the Semaphorin 3 C ... ...

Abstract	The Wnt pathway is frequently dysregulated in many cancers, underscoring it as a therapeutic target. Wnt inhibitors have uniformly failed in clinical trials. Here, we report a mechanism of WNT pathway activation through the Semaphorin 3 C neurodevelopmental program in glioma stem-like cells. Sema3C directs β-catenin nuclear accumulation in a Rac1-dependent process, leading to transactivation of Wnt target genes. Sema3C-driven Wnt signaling occurred despite suppression of Wnt ligand secretion, suggesting that Sema3C drives canonical Wnt signaling independent of Wnt ligand binding. In a mouse model of glioblastoma, combined depletion of Sema3C and β-catenin partner TCF1 extended animal survival more than single target inhibition alone. In human glioblastoma, Sema3C expression and Wnt pathway activation were highly concordant. Since Sema3C is frequently overexpressed in glioblastoma, Sema3C signaling may be a significant mechanism of resistance to upstream Wnt pathway inhibitors. Dual targeting of Sema3C and Wnt pathways may achieve clinically significant Wnt pathway inhibition.
MeSH term(s)	Animals ; Humans ; Mice ; beta Catenin/genetics ; beta Catenin/metabolism ; Cell Line, Tumor ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Ligands ; Semaphorins/genetics ; Wnt Signaling Pathway/genetics
Chemical Substances	beta Catenin ; Ligands ; Sema3C protein, human ; Semaphorins ; semaphorin 3C protein, mouse
Language	English
Publishing date	2023-04-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s41467-023-37397-w
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Article: A Microphysiological HHT-on-a-Chip Platform Recapitulates Patient Vascular Lesions.

Fang, Jennifer S / Hatch, Christopher J / Andrejecsk, Jillian / Trigt, William Van / Juat, Damie J / Chen, Yu-Hsi / Matsumoto, Satomi / Lee, Abe P / Hughes, Christopher C W

bioRxiv : the preprint server for biology

2024

Abstract: Hereditary Hemorrhagic Telangiectasia (HHT) is a rare congenital disease in which fragile vascular malformations focally develop in multiple organs. These can be small (telangiectasias) or large (arteriovenous malformations, AVMs) and may rupture leading ...

Abstract	Hereditary Hemorrhagic Telangiectasia (HHT) is a rare congenital disease in which fragile vascular malformations focally develop in multiple organs. These can be small (telangiectasias) or large (arteriovenous malformations, AVMs) and may rupture leading to frequent, uncontrolled bleeding. There are few treatment options and no cure for HHT. Most HHT patients are heterozygous for loss-of-function mutations for Endoglin (ENG) or Alk1 (ACVRL1), however, why loss of these genes manifests as vascular malformations remains poorly understood. To complement ongoing work in animal models, we have developed a microphysiological system model of HHT. Based on our existing vessel-on-a-chip (VMO) platform, our fully human cell-based HHT-VMO recapitulates HHT patient vascular lesions. Using inducible Significance: This manuscript describes development of an organ-on-a-chip model of Hereditary Hemorrhagic Telangiectasia (HHT), a rare genetic disease involving development of vascular malformations. Our VMO-HHT model produces vascular malformations similar to those seen in human HHT patients, including small (telangiectasias) and large (arteriovenous malformations) lesions. We show that VMO-HHT lesions are sensitive to a drug, pazopanib, that appears to be effective in HHT human patients. We further use the VMO-HHT platform to demonstrate that there is a critical window during vessel formation in which the HHT gene, Alk1, is required to prevent vascular malformation. Lastly, we show that lesions in the VMO-HHT model are comprised of both Alk1-deficient and Alk1-intact endothelial cells.
Language	English
Publishing date	2024-03-12
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.11.584490
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Article ; Online: Regulation of Partial and Reversible Endothelial-to-Mesenchymal Transition in Angiogenesis

Jennifer S. Fang / Nan W. Hultgren / Christopher C. W. Hughes

Frontiers in Cell and Developmental Biology, Vol

2021 Volume 9

Abstract	During development and in several diseases, endothelial cells (EC) can undergo complete endothelial-to-mesenchymal transition (EndoMT or EndMT) to generate endothelial-derived mesenchymal cells. Emerging evidence suggests that ECs can also undergo a partial EndoMT to generate cells with intermediate endothelial- and mesenchymal-character. This partial EndoMT event is transient, reversible, and supports both developmental and pathological angiogenesis. Here, we discuss possible regulatory mechanisms that may control the EndoMT program to dictate whether cells undergo complete or partial mesenchymal transition, and we further consider how these pathways might be targeted therapeutically in cancer.
Keywords	EndoMT ; EndMT ; endothelial ; mesenchymal ; cell identity ; cell plasticity ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article: SARS-CoV-2 infection of endothelial cells, dependent on flow-induced ACE2 expression, drives hypercytokinemia in a vascularized microphysiological system.

Hatch, Christopher J / Piombo, Sebastian D / Fang, Jennifer S / Gach, Johannes S / Ewald, Makena L / Van Trigt, William K / Coon, Brian G / Tong, Jay M / Forthal, Donald N / Hughes, Christopher C W

Frontiers in cardiovascular medicine

2024 Volume 11, Page(s) 1360364

Abstract: Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for COVID-19, has caused nearly 7 million deaths worldwide. Severe cases are marked by an aggressive inflammatory response known as hypercytokinemia, contributing to ... ...

Abstract	Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for COVID-19, has caused nearly 7 million deaths worldwide. Severe cases are marked by an aggressive inflammatory response known as hypercytokinemia, contributing to endothelial damage. Although vaccination has reduced hospitalizations, hypercytokinemia persists in breakthrough infections, emphasizing the need for disease models mimicking this response. Using a 3D microphysiological system (MPS), we explored the vascular role in SARS-CoV-2-induced hypercytokinemia. Methods: The vascularized micro-organ (VMO) MPS, consisting of human-derived primary endothelial cells (ECs) and stromal cells within an extracellular matrix, was used to model SARS-CoV-2 infection. A non-replicative pseudotyped virus fused to GFP was employed, allowing visualization of viral entry into human ECs under physiologic flow conditions. Expression of ACE2, TMPRSS2, and AGTR1 was analyzed, and the impact of viral infection on ACE2 expression, vascular inflammation, and vascular morphology was assessed. Results: The VMO platform facilitated the study of COVID-19 vasculature infection, revealing that ACE2 expression increased significantly in direct response to shear stress, thereby enhancing susceptibility to infection by pseudotyped SARS-CoV-2. Infected ECs secreted pro-inflammatory cytokines, including IL-6 along with coagulation factors. Cytokines released by infected cells were able to activate downstream, non-infected EC, providing an amplification mechanism for inflammation and coagulopathy. Discussion: Our findings highlight the crucial role of vasculature in COVID-19 pathogenesis, emphasizing the significance of flow-induced ACE2 expression and subsequent inflammatory responses. The VMO provides a valuable tool for studying SARS-CoV-2 infection dynamics and evaluating potential therapeutics.
Language	English
Publishing date	2024-03-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2024.1360364
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Article ; Online: The key phytochemistry of rosemary (Salvia rosmarinus) contributing to hair protection against UV.

Marsh, Jennifer M / Whitaker, Shane / Li, Lijuan / Fang, Rui / Simmonds, Monique S J / Vagkidis, Nikolaos / Chechik, Victor

International journal of cosmetic science

2023 Volume 45, Issue 6, Page(s) 749–760

Abstract: Extracts from rosemary (Salvia Rosmarinus) are analysed for their phytochemistry using LC-MS and the phytochemistry identified. The same extracts were tested for their efficacy to act as antioxidants by both hydrogen-atom transfer (ORAC) and single ... ...

Abstract	Extracts from rosemary (Salvia Rosmarinus) are analysed for their phytochemistry using LC-MS and the phytochemistry identified. The same extracts were tested for their efficacy to act as antioxidants by both hydrogen-atom transfer (ORAC) and single electron transfer (FRAP). A correlation analysis was performed to identify the key phytochemistry responsible for antioxidant efficacy. The top performing extracts were then tested in a peptide model and in hair with the presence of UV to measure ability to protect against UV-induced peptide and protein damage. Polyphenols (e.g. rosmarinic acid, glycosides of selgin) and abietane diterpenes (e.g. carnosic acid) in rosemary were identified as the principal compounds which enables the extracts to protect hair from UV. Objective: The objective of this work was to correlate the phytochemistry of rosemary (Salvia rosmarinus), a botanical with known antioxidant properties, to a UV protection benefit in hair. These data will give insights into mechanisms of UV damage, the ROS formed and their reactivity. Methods: LC-MS was used to compare the compounds in 10 commercial extracts of rosemary. ORAC (oxygen radical antioxidant capacity) and FRAP (ferric reducing antioxidant power) were used to measure the antioxidant capacity of the rosemary extracts. The ORAC assay measures ability of an antioxidant to react with a peroxyl radical via hydrogen atom extraction and FRAP measures electron transfer through reduction of ferric iron (Fe Results: Ten rosemary extracts were assessed for antioxidant performance and correlated with their compositions. The phytochemistry in each extract varied widely with a total of 33 individual compounds identified. The differences were most likely driven by the solvent and extraction method used by the supplier with extracts varying in the proportion of polar or non-polar compounds. This did influence their reactivity in the ORAC and FRAP assays and their efficacy in preventing protein damage. Two of the key compounds identified were rosmarinic acid and carnosic acid, with rosmarinic acid dominating in extracts with mainly polar compounds and carnosic acid dominating in extracts with mainly nonpolar compounds. Extracts with higher rosmarinic acid correlated with ORAC and FRAP scores, with UV protection on hair and in the peptide model system. The extracts chosen for hair experiments showed hair protection. UV protection was also measured for rosmarinic and carnosic acid. Conclusions: Despite the variation in the profile of phytochemistries in the 10 rosemary extracts, likely driven by the chosen extraction method, all rosemary extracts had antioxidant activity measured. This study suggests that the polyphenols (e.g. rosmarinic acid, glycosides of selgin) and abietane diterpenes (e.g. carnosic acid) are the principal compounds which enables the extracts to protect hair from UV.
MeSH term(s)	Antioxidants/pharmacology ; Abietanes/analysis ; Abietanes/chemistry ; Abietanes/pharmacology ; Rosmarinus/chemistry ; Polyphenols ; Glycosides ; Plant Extracts/pharmacology ; Plant Extracts/chemistry ; Iron ; Peptides ; Hydrogen/analysis ; Salvia ; Rosmarinic Acid
Chemical Substances	Antioxidants ; salvin (LI791SXT24) ; Abietanes ; Polyphenols ; Glycosides ; Plant Extracts ; Iron (E1UOL152H7) ; Peptides ; Hydrogen (7YNJ3PO35Z)
Language	English
Publishing date	2023-08-17
Publishing country	England
Document type	Journal Article
ZDB-ID	198917-0
ISSN	1468-2494 ; 0142-5463
ISSN (online)	1468-2494
ISSN	0142-5463
DOI	10.1111/ics.12883
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