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Article ; Online: Appearance of claudin-5

Krajewski, Dylan / Paul, Debayon / Ge, Shujun / Jellison, Evan / Pachter, Joel S

2021 Volume 18, Issue 1, Page(s) 296

Abstract: Background: Tight junctions (TJs) are membrane specializations characteristic of barrier-forming membranes, which function to seal the aqueous pathway between endothelial cells or epithelial cells and, thereby, obstruct intercellular solute and cellular ...

Abstract	Background: Tight junctions (TJs) are membrane specializations characteristic of barrier-forming membranes, which function to seal the aqueous pathway between endothelial cells or epithelial cells and, thereby, obstruct intercellular solute and cellular movement. However, previous work from our laboratory found that claudin-5 (CLN-5), a TJ protein prominent at the blood-brain barrier (BBB), was also detected, ectopically, on leukocytes (CLN-5 Methods: To begin clarifying the significance of CLN-5 Results: Flow cytometric analysis revealed CLN-5 Conclusion: Several leukocyte subtypes variably acquire CLN-5 in blood before they enter the CNS, an event that may represent a novel mechanism to guide leukocytes to sites for paracellular diapedesis across the BBB.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Claudin-5/blood ; Claudin-5/genetics ; Claudin-5/metabolism ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Flow Cytometry ; Leukocytes/pathology ; Mice ; Mice, Inbred C57BL ; Neuroinflammatory Diseases/genetics ; Neuroinflammatory Diseases/metabolism ; Neuroinflammatory Diseases/pathology ; Tight Junction Proteins/metabolism
Chemical Substances	Claudin-5 ; Cldn5 protein, mouse ; Tight Junction Proteins
Language	English
Publishing date	2021-12-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-021-02328-3
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Article ; Online: Human ESC-Derived MSCs Outperform Bone Marrow MSCs in the Treatment of an EAE Model of Multiple Sclerosis.

Wang, Xiaofang / Kimbrel, Erin A / Ijichi, Kumiko / Paul, Debayon / Lazorchak, Adam S / Chu, Jianlin / Kouris, Nicholas A / Yavanian, Gregory J / Lu, Shi-Jiang / Pachter, Joel S / Crocker, Stephen J / Lanza, Robert / Xu, Ren-He

Stem cell reports

2021 Volume 16, Issue 2, Page(s) 370–371

Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2021.01.004
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Article ; Online: Extracellular vesicles: mediators and biomarkers of pathology along CNS barriers.

Ramirez, Servio H / Andrews, Allison M / Paul, Debayon / Pachter, Joel S

Fluids and barriers of the CNS

2018 Volume 15, Issue 1, Page(s) 19

Abstract: Extracellular vesicles (EVs) are heterogeneous, nano-sized vesicles that are shed into the blood and other body fluids, which disperse a variety of bioactive molecules (e.g., protein, mRNA, miRNA, DNA and lipids) to cellular targets over long and short ... ...

Abstract	Extracellular vesicles (EVs) are heterogeneous, nano-sized vesicles that are shed into the blood and other body fluids, which disperse a variety of bioactive molecules (e.g., protein, mRNA, miRNA, DNA and lipids) to cellular targets over long and short distances. EVs are thought to be produced by nearly every cell type, however this review will focus specifically on EVs that originate from cells at the interface of CNS barriers. Highlighted topics include, EV biogenesis, the production of EVs in response to neuroinflammation, role in intercellular communication and their utility as a therapeutic platform. In this review, novel concepts regarding the use of EVs as biomarkers for BBB status and as facilitators for immune neuroinvasion are also discussed. Future directions and prospective are covered along with important unanswered questions in the field of CNS endothelial EV biology.
MeSH term(s)	Central Nervous System/blood supply ; Central Nervous System/metabolism ; Exosomes/metabolism ; Extracellular Vesicles/metabolism ; Humans ; Inflammation/metabolism
Language	English
Publishing date	2018-07-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-018-0104-7
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Article ; Online: Human ES-derived MSCs correct TNF-α-mediated alterations in a blood-brain barrier model.

Ge, Shujun / Jiang, Xi / Paul, Debayon / Song, Li / Wang, Xiaofang / Pachter, Joel S

Fluids and barriers of the CNS

2019 Volume 16, Issue 1, Page(s) 18

Abstract: Background: Immune cell trafficking into the CNS is considered to contribute to pathogenesis in MS and its animal model, EAE. Disruption of the blood-brain barrier (BBB) is a hallmark of these pathologies and a potential target of therapeutics. Human ... ...

Abstract	Background: Immune cell trafficking into the CNS is considered to contribute to pathogenesis in MS and its animal model, EAE. Disruption of the blood-brain barrier (BBB) is a hallmark of these pathologies and a potential target of therapeutics. Human embryonic stem cell-derived mesenchymal stem/stromal cells (hES-MSCs) have shown superior therapeutic efficacy, compared to bone marrow-derived MSCs, in reducing clinical symptoms and neuropathology of EAE. However, it has not yet been reported whether hES-MSCs inhibit and/or repair the BBB damage associated with neuroinflammation that accompanies EAE. Methods: BMECs were cultured on Transwell inserts as a BBB model for all the experiments. Disruption of BBB models was induced by TNF-α, a pro-inflammatory cytokine that is a hallmark of acute and chronic neuroinflammation. Results: Results indicated that hES-MSCs reversed the TNF-α-induced changes in tight junction proteins, permeability, transendothelial electrical resistance, and expression of adhesion molecules, especially when these cells were placed in direct contact with BMEC. Conclusions: hES-MSCs and/or products derived from them could potentially serve as novel therapeutics to repair BBB disturbances in MS.
MeSH term(s)	Animals ; Blood-Brain Barrier/cytology ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Cell Line, Transformed ; Embryonic Stem Cells/drug effects ; Embryonic Stem Cells/metabolism ; Humans ; Mesenchymal Stem Cells/drug effects ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Tumor Necrosis Factor-alpha
Language	English
Publishing date	2019-07-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-019-0138-5
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Article ; Online: Spatiotemporal resolution of spinal meningeal and parenchymal inflammation during experimental autoimmune encephalomyelitis.

Shrestha, Bandana / Jiang, Xi / Ge, Shujun / Paul, Debayon / Chianchiano, Peter / Pachter, Joel S

Neurobiology of disease

2017 Volume 108, Page(s) 159–172

Abstract: Experimental autoimmune encephalomyelitis (EAE) induced by active immunization of C57BL/6 mice with peptide from myelin oligodendrocyte protein ( ... ...

Abstract	Experimental autoimmune encephalomyelitis (EAE) induced by active immunization of C57BL/6 mice with peptide from myelin oligodendrocyte protein (MOG
MeSH term(s)	Animals ; Cervical Vertebrae ; Disease Progression ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Gene Expression ; Inflammation/pathology ; Inflammation/physiopathology ; Leukocytes/immunology ; Leukocytes/pathology ; Lumbar Vertebrae ; Meninges/immunology ; Meninges/pathology ; Mice, Inbred C57BL ; Microvessels/immunology ; Microvessels/pathology ; Myelin-Oligodendrocyte Glycoprotein ; Parenchymal Tissue/immunology ; Parenchymal Tissue/pathology ; Peptide Fragments ; Spinal Cord/immunology ; Spinal Cord/pathology
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; myelin oligodendrocyte glycoprotein (35-55)
Language	English
Publishing date	2017-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2017.08.010
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Article ; Online: Alterations in tight junction protein and IgG permeability accompany leukocyte extravasation across the choroid plexus during neuroinflammation.

Shrestha, Bandana / Paul, Debayon / Pachter, Joel S

Journal of neuropathology and experimental neurology

2014 Volume 73, Issue 11, Page(s) 1047–1061

Abstract: The choroid plexus (CP) is considered to be a point of leukocyte entry into the CNS during normal immune surveillance and in neuroinflammatory diseases. The structural and functional alterations within the CP that support this migration are not ... ...

Abstract	The choroid plexus (CP) is considered to be a point of leukocyte entry into the CNS during normal immune surveillance and in neuroinflammatory diseases. The structural and functional alterations within the CP that support this migration are not understood. We used quantitative, high-resolution, 3-dimensional (3-D) fluorescence imaging to analyze CP alterations associated with inflammatory responses in C57/Bl6 mice after the induction of experimental autoimmune encephalomyelitis by immunization with myelin oligodendrocyte glycoprotein (MOG) and complete Freund adjuvant/pertussis toxin (MOG-CFA/PTX) or adjuvants alone (CFA-PTX). The MOG-CFA/PTX and CFA/PTX produced similar effects, although those caused by the former were consistently more marked. Both treatments resulted in the accumulation of serum immunoglobulin G and leukocytes in the CP stroma, consistent with elevated stromal capillary permeability. They also provoked distortions and diminished immunostaining patterns of the tight junction adaptor protein ZO-1 in the choroidal epithelium but no obvious change in the patterns of the tight junction associated protein claudin-2. Only MOG-CFA/PTX triggered visible extravasation of immunoglobulin G and leukocytes across the choroidal epithelium. Our results suggest that CFA/PTX primes the CP for neuroinflammation by inducing structural changes that are exacerbated when there is an immune response to MOG and reinforce the CP as a gateway for leukocytes to enter the CNS by accessing the CSF and leptomeninges.
MeSH term(s)	Amino Acid Sequence ; Animals ; Capillary Permeability/physiology ; Choroid Plexus/immunology ; Choroid Plexus/metabolism ; Female ; Immunoglobulin G/immunology ; Immunoglobulin G/metabolism ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Leukocytes/immunology ; Leukocytes/metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Tight Junction Proteins/immunology ; Tight Junction Proteins/metabolism ; Tight Junctions/immunology ; Tight Junctions/metabolism
Chemical Substances	Immunoglobulin G ; Inflammation Mediators ; Tight Junction Proteins
Language	English
Publishing date	2014-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1097/NEN.0000000000000127
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Article ; Online: Active induction of experimental autoimmune encephalomyelitis by MOG35-55 peptide immunization is associated with differential responses in separate compartments of the choroid plexus.

Murugesan, Nivetha / Paul, Debayon / Lemire, Yen / Shrestha, Bandana / Ge, Shujun / Pachter, Joel S

Fluids and barriers of the CNS

2012 Volume 9, Issue 1, Page(s) 15

Language	English
Publishing date	2012-08-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/2045-8118-9-15
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Article ; Online: Systemic TLR2 tolerance enhances central nervous system remyelination.

Wasko, Nicholas J / Kulak, Meghan Horne / Paul, Debayon / Nicaise, Alexandra M / Yeung, Stephen T / Nichols, Frank C / Khanna, Kamal M / Crocker, Stephen / Pachter, Joel S / Clark, Robert B

Journal of neuroinflammation

2019 Volume 16, Issue 1, Page(s) 158

Abstract: Background: Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease characterized by both inflammatory demyelination and impaired remyelination. Studies indicate that Toll-like receptor 2 (TLR2) signaling contributes to both the ... ...

Abstract	Background: Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease characterized by both inflammatory demyelination and impaired remyelination. Studies indicate that Toll-like receptor 2 (TLR2) signaling contributes to both the inflammatory component and the defective remyelination in MS. While most MS therapeutics target adaptive immunity, we recently reported that reducing TLR2 signaling in innate immune cells by inducing TLR2 tolerance attenuates adoptively transferred experimental autoimmune encephalomyelitis. Given that previous reports suggest TLR2 signaling also inhibits myelin repair, the objective of this study was to assess how reducing TLR2 signaling through TLR2 tolerance induction affects CNS myelin repair. Methods: Chow containing 0.2% cuprizone was fed to male and female wild-type (WT) C57BL/6 mice or TLR2-deficient (TLR2 Results: Inducing TLR2 tolerance in WT mice during remyelination significantly enhanced myelin recovery, restoring unmyelinated axon frequency and myelin thickness to baseline levels compared to VC-treated mice. Mechanistically, enhanced remyelination in TLR2 tolerized mice was associated with a shift in corpus callosum microglia from a pro-inflammatory iNOS Discussion: Our results suggest that reducing TLR2 signaling in vivo by inducing TLR2 tolerance significantly enhances myelin repair. Furthermore, the enhanced remyelination resulting from TLR2 tolerance induction is associated with a shift in corpus callosum microglia from a pro-inflammatory iNOS
MeSH term(s)	Animals ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Female ; Lipopeptides/therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/metabolism ; Oligodendroglia/metabolism ; Remyelination/physiology ; Toll-Like Receptor 2/metabolism ; Treatment Outcome
Chemical Substances	Lipopeptides ; Pam(3)CSK(4) peptide ; Tlr2 protein, mouse ; Toll-Like Receptor 2
Language	English
Publishing date	2019-07-27
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-019-1540-2
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Article ; Online: Novel 3D analysis of Claudin-5 reveals significant endothelial heterogeneity among CNS microvessels.

Paul, Debayon / Cowan, Ann E / Ge, Shujun / Pachter, Joel S

Microvascular research

2012 Volume 86, Page(s) 1–10

Abstract: Tight junctions (TJs) feature critically in maintaining the integrity of the blood-brain barrier (BBB), and undergo significant disruption during neuroinflammatory diseases. Accordingly, the expression and distribution of CLN-5, a prominent TJ protein in ...

Abstract	Tight junctions (TJs) feature critically in maintaining the integrity of the blood-brain barrier (BBB), and undergo significant disruption during neuroinflammatory diseases. Accordingly, the expression and distribution of CLN-5, a prominent TJ protein in central nervous system (CNS) microvessels and BBB determinant, has been shown to parallel physiological and pathophysiological changes in microvascular function. However, efforts to quantify CLN-5 within the CNS microvasculature in situ, by using conventional two-dimensional immunohistochemical analysis of thin sections, are encumbered by the tortuosity of capillaries and distorted diameters of inflamed venules. Herein, we describe a novel contour-based 3D image visualization and quantification method, employing high-resolution confocal z-stacks from thick immunofluorescently-stained thoraco-lumbar spinal cord cryosections, to analyze CLN-5 along the junctional regions of different-sized CNS microvascular segments. Analysis was performed on spinal cords of both healthy mice, and mice experiencing experimental autoimmune encephalomyelitis (EAE), an animal model of the neuroinflammatory disease multiple sclerosis. Results indicated that, under normal conditions, the density of CLN-5 staining (CLN-5 intensity/ endothelial surface area) was greatest in the capillaries and smaller venules, and least in the larger venules. This heterogeneity in junctional CLN-5 staining was exacerbated during EAE, as spinal venules revealed a significant loss of junctional CLN-5 staining that was associated with focal leukocyte extravasation, while adjacent capillaries exhibited neither CLN-5 loss nor infiltrating leukocytes. However, despite only venules displaying these behaviors, both capillaries and venules evidenced leakage of IgG during disease, further underscoring the heterogeneity of the inflammatory response in CNS microvessels. This method should be readily adaptable to analyzing other junctional proteins of the CNS and peripheral microvasculature, and serve to highlight their role(s) in health and disease.
MeSH term(s)	Animals ; Blood-Brain Barrier ; Capillaries/chemistry ; Capillaries/ultrastructure ; Capillary Permeability ; Claudin-5/analysis ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/blood ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Endothelium, Vascular/chemistry ; Endothelium, Vascular/ultrastructure ; Female ; Imaging, Three-Dimensional/methods ; Immunoglobulin G/metabolism ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal/methods ; Microscopy, Fluorescence ; Microvessels/chemistry ; Multiple Sclerosis ; Spinal Cord/blood supply ; Tight Junctions/chemistry ; Tight Junctions/ultrastructure ; Venules/chemistry ; Venules/ultrastructure
Chemical Substances	Claudin-5 ; Cldn5 protein, mouse ; Immunoglobulin G
Language	English
Publishing date	2012-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80307-8
ISSN	1095-9319 ; 0026-2862
ISSN (online)	1095-9319
ISSN	0026-2862
DOI	10.1016/j.mvr.2012.12.001
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Zs.A 746: Show issues

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Article ; Online: Mesenchymal stem cell: present challenges and prospective cellular cardiomyoplasty approaches for myocardial regeneration.

Paul, Debayon / Samuel, Samson Mathews / Maulik, Nilanjana

Antioxidants & redox signaling

2009 Volume 11, Issue 8, Page(s) 1841–1855

Abstract: Myocardial ischemia and cardiac dysfunction have been known to follow ischemic heart diseases (IHDs). Despite a plethora of conventional treatment options, their efficacies are associated with skepticism. Cell therapies harbor a promising potential for ... ...

Abstract	Myocardial ischemia and cardiac dysfunction have been known to follow ischemic heart diseases (IHDs). Despite a plethora of conventional treatment options, their efficacies are associated with skepticism. Cell therapies harbor a promising potential for vascular and cardiac repair, which is corroborated by adequate preclinical evidence. The underlying objectives behind cardiac regenerative therapies subsume enhancing angiomyogenesis in the ischemic myocardium, ameliorating cellular apoptosis, regenerating the damaged myocardium, repopulating the lost resident myocardial cells (smooth muscle, cardiomyocyte, and endothelial cells), and finally, decreasing fibrosis with a consequent reduction in ventricular remodeling. Although-cell based cardiomyoplasty approaches have an immense potential, their clinical utilization is limited owing to the increased need for better candidates for cellular cardiomyoplasty, better routes of delivery, appropriate dose for efficient engraftment, and better preconditioning or genetic-modification strategies for the progenitor and stem cells. Mesenchymal stem cells (MSCs) have emerged as powerful candidates in mediating myocardial repair owing to their unique properties of multipotency, transdifferentiation, intercellular connection with the resident cardiomyocytes via connexin 43 (Cx43)-positive gap junctions in the myocardium, and most important, immunomodulation. In this review, we present an in-depth discussion on the complexities associated with stem and progenitor cell therapies, the potential of preclinical approaches involving MSCs for myocardial repair, and an account of the past milestones and ongoing MSC-based trials in humans.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Transplantation ; Female ; Heart/physiopathology ; Mesenchymal Stem Cells/cytology ; Mice ; Mice, Inbred C57BL ; Myocardial Ischemia/therapy ; Rats ; Rats, Inbred F344 ; Regeneration
Language	English
Publishing date	2009-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ARS.2009.2455
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