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Article ; Online: Resident Macrophages in the Heart: Cardioprotective Under Pressure.

Ismahil, Mohamed Ameen / Prabhu, Sumanth D

2021 Volume 129, Issue 12, Page(s) 1102–1104

MeSH term(s)	Heart ; Macrophages
Language	English
Publishing date	2021-12-02
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; 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.121.320328
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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: Neutrophils are indispensable for adverse cardiac remodeling in heart failure.

Antipenko, Sergey / Mayfield, Nicolas / Jinno, Miki / Gunzer, Matthias / Ismahil, Mohamed Ameen / Hamid, Tariq / Prabhu, Sumanth D / Rokosh, Gregg

Journal of molecular and cellular cardiology

2024 Volume 189, Page(s) 1–11

Abstract: Persistent immune activation contributes significantly to left ventricular (LV) dysfunction and adverse remodeling in heart failure (HF). In contrast to their well-known essential role in acute myocardial infarction (MI) as first responders that clear ... ...

Abstract	Persistent immune activation contributes significantly to left ventricular (LV) dysfunction and adverse remodeling in heart failure (HF). In contrast to their well-known essential role in acute myocardial infarction (MI) as first responders that clear dead cells and facilitate subsequent reparative macrophage polarization, the role of neutrophils in the pathobiology of chronic ischemic HF is poorly defined. To determine the importance of neutrophils in the progression of ischemic cardiomyopathy, we measured their production, levels, and activation in a mouse model of chronic HF 8 weeks after permanent coronary artery ligation and large MI. In HF mice, neutrophils were more abundant both locally in failing myocardium (more in the border zone) and systemically in the blood, spleen, and bone marrow, together with increased BM granulopoiesis. There were heightened stimuli for neutrophil recruitment and trafficking in HF, with increased myocardial expression of the neutrophil chemoattract chemokines CXCL1 and CXCL5, and increased neutrophil chemotactic factors in the circulation. HF neutrophil NETotic activity was increased in vitro with coordinate increases in circulating neutrophil extracellular traps (NETs) in vivo. Neutrophil depletion with either antibody-based or genetic approaches abrogated the progression of LV remodeling and fibrosis at both intermediate and late stages of HF. Moreover, analogous to murine HF, the plasma milieu in human acute decompensated HF strongly promoted neutrophil trafficking. Collectively, these results support a key tissue-injurious role for neutrophils and their associated cytotoxic products in ischemic cardiomyopathy and suggest that neutrophils are potential targets for therapeutic immunomodulation in this disease.
MeSH term(s)	Humans ; Animals ; Mice ; Neutrophils/metabolism ; Ventricular Remodeling ; Heart Failure ; Myocardium/metabolism ; Myocardial Ischemia/metabolism ; Cardiomyopathies/metabolism ; Mice, Inbred C57BL
Language	English
Publishing date	2024-02-22
Publishing country	England
Document type	Journal Article
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2024.02.005
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Zs.A 426: Show issues

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Article ; Online: Cardiac Mesenchymal Stem Cells Promote Fibrosis and Remodeling in Heart Failure: Role of PDGF Signaling.

Hamid, Tariq / Xu, Yuanyuan / Ismahil, Mohamed Ameen / Rokosh, Gregg / Jinno, Miki / Zhou, Guihua / Wang, Qiongxin / Prabhu, Sumanth D

JACC. Basic to translational science

2022 Volume 7, Issue 5, Page(s) 465–483

Abstract: Heart failure (HF) is characterized by progressive fibrosis. Both fibroblasts and mesenchymal stem cells (MSCs) can differentiate into pro-fibrotic myofibroblasts. MSCs secrete and express platelet-derived growth factor (PDGF) and its receptors. We ... ...

Abstract	Heart failure (HF) is characterized by progressive fibrosis. Both fibroblasts and mesenchymal stem cells (MSCs) can differentiate into pro-fibrotic myofibroblasts. MSCs secrete and express platelet-derived growth factor (PDGF) and its receptors. We hypothesized that PDGF signaling in cardiac MSCs (cMSCs) promotes their myofibroblast differentiation and aggravates post-myocardial infarction left ventricular remodeling and fibrosis. We show that cMSCs from failing hearts post-myocardial infarction exhibit an altered phenotype. Inhibition of PDGF signaling in vitro inhibited cMSC-myofibroblast differentiation, whereas in vivo inhibition during established ischemic HF alleviated left ventricular remodeling and function, and decreased myocardial fibrosis, hypertrophy, and inflammation. Modulating cMSC PDGF receptor expression may thus represent a novel approach to limit pathologic cardiac fibrosis in HF.
Language	English
Publishing date	2022-04-20
Publishing country	United States
Document type	Journal Article
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2022.01.004
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cardiac immune cell remodeling after myocardial infarction.

Ismahil, Mohamed Ameen / Prabhu, Sumanth D

Journal of molecular and cellular cardiology

2013 Volume 62, Page(s) 142–143

MeSH term(s)	Animals ; Macrophages/cytology ; Myocardial Infarction/immunology
Language	English
Publishing date	2013-09
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2013.05.017
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Article ; Online: The Apolipoprotein A-I Mimetic L-4F Attenuates Monocyte Activation and Adverse Cardiac Remodeling after Myocardial Infarction.

Hamid, Tariq / Ismahil, Mohamed Ameen / Bansal, Shyam S / Patel, Bindiya / Goel, Mehak / White, C Roger / Anantharamaiah, G M / Prabhu, Sumanth D

International journal of molecular sciences

2020 Volume 21, Issue 10

Abstract: Excessive inflammation after myocardial infarction (MI) can promote infarct expansion and adverse left ventricular (LV) remodeling. L-4F, a mimetic peptide of apolipoprotein A-I (apoA-I), exhibits anti-inflammatory and anti-atherogenic properties; ... ...

Abstract	Excessive inflammation after myocardial infarction (MI) can promote infarct expansion and adverse left ventricular (LV) remodeling. L-4F, a mimetic peptide of apolipoprotein A-I (apoA-I), exhibits anti-inflammatory and anti-atherogenic properties; however, whether L-4F imparts beneficial effects after myocardial infarction (MI) is unknown. Here we demonstrate that L-4F suppresses the expansion of blood, splenic, and myocardial pro-inflammatory monocytes and macrophages in a mouse model of reperfused MI. Changes in immune cell profiles were accompanied by alleviation of post-MI LV remodeling and dysfunction. In vitro, L-4F also inhibited pro-inflammatory and glycolytic gene expression in macrophages. In summary, L-4F treatment prevents prolonged and excessive inflammation after MI, in part through modulation of pro-inflammatory monocytes and macrophages, and improves post-MI LV remodeling. These data suggest that L-4F could be a used as a therapeutic adjunct in humans with MI to limit inflammation and alleviate the progression to heart failure.
MeSH term(s)	Animals ; Apolipoprotein A-I/metabolism ; Cell Plasticity/drug effects ; Inflammation/pathology ; Macrophage Activation/drug effects ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/drug effects ; Monocytes/pathology ; Myocardial Infarction/physiopathology ; Peptides/pharmacology ; RAW 264.7 Cells ; Systole/drug effects ; Ventricular Dysfunction, Left/physiopathology ; Ventricular Remodeling/drug effects
Chemical Substances	Apolipoprotein A-I ; L-4F peptide ; Peptides
Language	English
Publishing date	2020-05-15
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/ijms21103519
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: CCR2

Patel, Bindiya / Bansal, Shyam S / Ismahil, Mohamed Ameen / Hamid, Tariq / Rokosh, Gregg / Mack, Matthias / Prabhu, Sumanth D

JACC. Basic to translational science

2018 Volume 3, Issue 2, Page(s) 230–244

Abstract: Although chronic inflammation is a central feature of heart failure (HF), the immune cell profiles differ with different underlying causes. This suggests that for immunomodulatory therapy in HF to be successful, it needs to be tailored to the specific ... ...

Abstract	Although chronic inflammation is a central feature of heart failure (HF), the immune cell profiles differ with different underlying causes. This suggests that for immunomodulatory therapy in HF to be successful, it needs to be tailored to the specific etiology. Here, the authors demonstrate that monocyte-derived C-C chemokine receptor 2 (CCR2)
Language	English
Publishing date	2018-03-14
Publishing country	United States
Document type	Journal Article
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2017.12.006
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Article ; Online: Optimized protocols for isolation, fixation, and flow cytometric characterization of leukocytes in ischemic hearts.

Covarrubias, Roman / Ismahil, Mohamed Ameen / Rokosh, Gregg / Hamid, Tariq / Accornero, Federica / Singh, Harpreet / Gumina, Richard J / Prabhu, Sumanth D / Bansal, Shyam S

American journal of physiology. Heart and circulatory physiology

2019 Volume 317, Issue 3, Page(s) H658–H666

Abstract: Immune activation post-myocardial infarction is an orchestrated sequence of cellular responses to effect tissue repair and healing. However, excessive and dysregulated inflammation can result in left ventricular remodeling and pathological alterations in ...

Abstract	Immune activation post-myocardial infarction is an orchestrated sequence of cellular responses to effect tissue repair and healing. However, excessive and dysregulated inflammation can result in left ventricular remodeling and pathological alterations in the structural and mechanical attributes of the heart. Identification of key pathways and critical cellular mediators of inflammation is thus essential to design immunomodulatory therapies for myocardial infarction and ischemic heart failure. Despite this, the experimental approaches to isolate mononuclear cells from the heart are diverse, and detailed protocols to enable maximum yield of live cells in the shortest time possible are not readily available. Here, we describe optimized protocols for the isolation, fixation, and flow cytometric characterization of cardiac CD45
MeSH term(s)	Animals ; Biomarkers/analysis ; Cell Separation/methods ; Centrifugation, Density Gradient ; Disease Models, Animal ; Fixatives/chemistry ; Flow Cytometry/methods ; Immunophenotyping ; Leukocyte Common Antigens/analysis ; Leukocytes/immunology ; Leukocytes/pathology ; Male ; Mice, Inbred C57BL ; Myocardial Infarction/immunology ; Myocardial Infarction/pathology ; Myocardium/immunology ; Myocardium/pathology ; Tissue Fixation/methods
Chemical Substances	Biomarkers ; Fixatives ; Leukocyte Common Antigens (EC 3.1.3.48) ; Ptprc protein, mouse (EC 3.1.3.48)
Language	English
Publishing date	2019-08-02
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00137.2019
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Article ; Online: Mononuclear Phagocytes Are Dispensable for Cardiac Remodeling in Established Pressure-Overload Heart Failure.

Patel, Bindiya / Ismahil, Mohamed Ameen / Hamid, Tariq / Bansal, Shyam S / Prabhu, Sumanth D

PloS one

2017 Volume 12, Issue 1, Page(s) e0170781

Abstract: Background: Although cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. ...

Abstract	Background: Although cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. We tested the hypothesis that these immune cells are required for the progression of remodeling in pressure-overload heart failure (HF), and that MP depletion would ameliorate remodeling. Methods and results: C57BL/6 mice were subjected to transverse aortic constriction (TAC) or sham operation, and assessed for alterations in MPs. As compared with sham, TAC mice exhibited expansion of circulating LyC6hi monocytes and pro-inflammatory CD206- cardiac macrophages early (1 w) after pressure-overload, prior to significant hypertrophy and systolic dysfunction, with subsequent resolution during chronic HF. In contrast, classical DCs were expanded in the heart in a biphasic manner, with peaks both early, analogous to macrophages, and late (8 w), during established HF. There was no significant expansion of circulating DCs, or Ly6C+ monocytes and DCs in the spleen. Periodic systemic MP depletion from 2 to 16 w after TAC in macrophage Fas-induced apoptosis (MaFIA) transgenic mice did not alter cardiac remodeling progression, nor did splenectomy in mice with established HF after TAC. Lastly, adoptive transfer of splenocytes from TAC HF mice into naïve recipients did not induce immediate or long-term cardiac dysfunction in recipient mice. Conclusions: Mononuclear phagocytes populations expand in a phasic manner in the heart during pressure-overload. However, they are dispensable for the progression of remodeling and failure once significant hypertrophy is evident and blood monocytosis has normalized.
MeSH term(s)	Adoptive Transfer ; Animals ; Aorta/immunology ; Aorta/pathology ; Cell Count ; Constriction, Pathologic/immunology ; Constriction, Pathologic/pathology ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Dendritic Cells/transplantation ; Disease Models, Animal ; Disease Progression ; Heart Failure/immunology ; Heart Failure/pathology ; Lymphocyte Transfusion ; Lymphocytes/immunology ; Lymphocytes/pathology ; Macrophages/immunology ; Macrophages/pathology ; Macrophages/transplantation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Monocytes/immunology ; Monocytes/pathology ; Monocytes/transplantation ; Pressure ; Spleen/immunology ; Spleen/pathology ; Ventricular Remodeling
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0170781
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dysfunctional and Proinflammatory Regulatory T-Lymphocytes Are Essential for Adverse Cardiac Remodeling in Ischemic Cardiomyopathy.

Bansal, Shyam S / Ismahil, Mohamed Ameen / Goel, Mehak / Zhou, Guihua / Rokosh, Gregg / Hamid, Tariq / Prabhu, Sumanth D

Circulation

2018 Volume 139, Issue 2, Page(s) 206–221

Abstract: Background: Heart failure (HF) is a state of inappropriately sustained inflammation, suggesting the loss of normal immunosuppressive mechanisms. Regulatory T-lymphocytes (Tregs) are considered key suppressors of immune responses; however, their role in ... ...

Abstract	Background: Heart failure (HF) is a state of inappropriately sustained inflammation, suggesting the loss of normal immunosuppressive mechanisms. Regulatory T-lymphocytes (Tregs) are considered key suppressors of immune responses; however, their role in HF is unknown. We hypothesized that Tregs are dysfunctional in ischemic cardiomyopathy and HF, and they promote immune activation and left ventricular (LV) remodeling. Methods: Adult male wild-type C57BL/6 mice, Foxp3-diphtheria toxin receptor transgenic mice, and tumor necrosis factor (TNF) α receptor-1 (TNFR1) Results: Compared with wild-type sham mice, CD4 Conclusions: Proinflammatory and antiangiogenic Tregs play an essential pathogenetic role in chronic ischemic HF to promote immune activation and pathological LV remodeling. The restoration of normal Treg function may be a viable approach to therapeutic immunomodulation in this disease.
MeSH term(s)	Angiogenic Proteins/metabolism ; Animals ; Cardiomyopathies/immunology ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cardiomyopathies/physiopathology ; Cells, Cultured ; Coculture Techniques ; Disease Models, Animal ; Endothelial Cells/immunology ; Endothelial Cells/metabolism ; Fibrosis ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Infarction/immunology ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardium/immunology ; Myocardium/metabolism ; Myocardium/pathology ; Neovascularization, Physiologic ; Phenotype ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Ventricular Function, Left ; Ventricular Remodeling
Chemical Substances	Angiogenic Proteins ; Inflammation Mediators ; Receptors, Tumor Necrosis Factor, Type I ; Tnfrsf1a protein, mouse
Language	English
Publishing date	2018-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
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.118.036065
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Ui IV Zs.60: Show issues

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Article ; Online: Mononuclear Phagocytes Are Dispensable for Cardiac Remodeling in Established Pressure-Overload Heart Failure.

Bindiya Patel / Mohamed Ameen Ismahil / Tariq Hamid / Shyam S Bansal / Sumanth D Prabhu

PLoS ONE, Vol 12, Iss 1, p e

2017 Volume 0170781

Abstract: Although cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. We tested ... ...

Abstract	Although cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. We tested the hypothesis that these immune cells are required for the progression of remodeling in pressure-overload heart failure (HF), and that MP depletion would ameliorate remodeling.C57BL/6 mice were subjected to transverse aortic constriction (TAC) or sham operation, and assessed for alterations in MPs. As compared with sham, TAC mice exhibited expansion of circulating LyC6hi monocytes and pro-inflammatory CD206- cardiac macrophages early (1 w) after pressure-overload, prior to significant hypertrophy and systolic dysfunction, with subsequent resolution during chronic HF. In contrast, classical DCs were expanded in the heart in a biphasic manner, with peaks both early, analogous to macrophages, and late (8 w), during established HF. There was no significant expansion of circulating DCs, or Ly6C+ monocytes and DCs in the spleen. Periodic systemic MP depletion from 2 to 16 w after TAC in macrophage Fas-induced apoptosis (MaFIA) transgenic mice did not alter cardiac remodeling progression, nor did splenectomy in mice with established HF after TAC. Lastly, adoptive transfer of splenocytes from TAC HF mice into naïve recipients did not induce immediate or long-term cardiac dysfunction in recipient mice.Mononuclear phagocytes populations expand in a phasic manner in the heart during pressure-overload. However, they are dispensable for the progression of remodeling and failure once significant hypertrophy is evident and blood monocytosis has normalized.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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