LIVIVO - Search results -

Search results

Result 1 - 10 of total 31

Search options

Article ; Online: Adaptive immune changes associate with clinical progression of Alzheimer's disease.

van Olst, Lynn / Kamermans, Alwin / Halters, Sem / van der Pol, Susanne M A / Rodriguez, Ernesto / Verberk, Inge M W / Verberk, Sanne G S / Wessels, Danielle W R / Rodriguez-Mogeda, Carla / Verhoeff, Jan / Wouters, Dorine / Van den Bossche, Jan / Garcia-Vallejo, Juan J / Lemstra, Afina W / Witte, Maarten E / van der Flier, Wiesje M / Teunissen, Charlotte E / de Vries, Helga E

Molecular neurodegeneration

2024 Volume 19, Issue 1, Page(s) 38

Abstract: Background: Alzheimer's disease (AD) is the most frequent cause of dementia. Recent evidence suggests the involvement of peripheral immune cells in the disease, but the underlying mechanisms remain unclear.: Methods: We comprehensively mapped ... ...

Abstract	Background: Alzheimer's disease (AD) is the most frequent cause of dementia. Recent evidence suggests the involvement of peripheral immune cells in the disease, but the underlying mechanisms remain unclear. Methods: We comprehensively mapped peripheral immune changes in AD patients with mild cognitive impairment (MCI) or dementia compared to controls, using cytometry by time-of-flight (CyTOF). Results: We found an adaptive immune signature in AD, and specifically highlight the accumulation of PD1 Conclusions: Our findings illustrate significant peripheral immune alterations associated with both early and late clinical stages of AD, emphasizing the necessity for further investigation into how these changes influence underlying brain pathology.
MeSH term(s)	Humans ; Alzheimer Disease/immunology ; Alzheimer Disease/cerebrospinal fluid ; Aged ; Disease Progression ; Male ; Cognitive Dysfunction/immunology ; Female ; Adaptive Immunity/immunology ; Biomarkers/cerebrospinal fluid ; Aged, 80 and over ; Middle Aged
Chemical Substances	Biomarkers
Language	English
Publishing date	2024-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-024-00726-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: Inflammation-induced TRPV4 channels exacerbate blood-brain barrier dysfunction in multiple sclerosis.

Hansen, Cathrin E / Kamermans, Alwin / Mol, Kevin / Berve, Kristina / Rodriguez-Mogeda, Carla / Fung, Wing Ka / van Het Hof, Bert / Fontijn, Ruud D / van der Pol, Susanne M A / Michalick, Laura / Kuebler, Wolfgang M / Kenkhuis, Boyd / van Roon-Mom, Willeke / Liedtke, Wolfgang / Engelhardt, Britta / Kooij, Gijs / Witte, Maarten E / de Vries, Helga E

Journal of neuroinflammation

2024 Volume 21, Issue 1, Page(s) 72

Abstract: Background: Blood-brain barrier (BBB) dysfunction and immune cell migration into the central nervous system (CNS) are pathogenic drivers of multiple sclerosis (MS). Ways to reinstate BBB function and subsequently limit neuroinflammation present ... ...

Abstract	Background: Blood-brain barrier (BBB) dysfunction and immune cell migration into the central nervous system (CNS) are pathogenic drivers of multiple sclerosis (MS). Ways to reinstate BBB function and subsequently limit neuroinflammation present promising strategies to restrict disease progression. However, to date, the molecular players directing BBB impairment in MS remain poorly understood. One suggested candidate to impact BBB function is the transient receptor potential vanilloid-type 4 ion channel (TRPV4), but its specific role in MS pathogenesis remains unclear. Here, we investigated the role of TRPV4 in BBB dysfunction in MS. Main text: In human post-mortem MS brain tissue, we observed a region-specific increase in endothelial TRPV4 expression around mixed active/inactive lesions, which coincided with perivascular microglia enrichment in the same area. Using in vitro models, we identified that microglia-derived tumor necrosis factor-α (TNFα) induced brain endothelial TRPV4 expression. Also, we found that TRPV4 levels influenced brain endothelial barrier formation via expression of the brain endothelial tight junction molecule claudin-5. In contrast, during an inflammatory insult, TRPV4 promoted a pathological endothelial molecular signature, as evidenced by enhanced expression of inflammatory mediators and cell adhesion molecules. Moreover, TRPV4 activity mediated T cell extravasation across the brain endothelium. Conclusion: Collectively, our findings suggest a novel role for endothelial TRPV4 in MS, in which enhanced expression contributes to MS pathogenesis by driving BBB dysfunction and immune cell migration.
MeSH term(s)	Humans ; Blood-Brain Barrier/metabolism ; Central Nervous System/metabolism ; Inflammation/metabolism ; Multiple Sclerosis/pathology ; TRPV Cation Channels/metabolism
Chemical Substances	TRPV Cation Channels ; TRPV4 protein, human
Language	English
Publishing date	2024-03-23
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/s12974-024-03069-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Extended interval dosing of ocrelizumab modifies the repopulation of B cells without altering the clinical efficacy in multiple sclerosis.

Rodriguez-Mogeda, Carla / van Lierop, Zoë Y G J / van der Pol, Susanne M A / Coenen, Loet / Hogenboom, Laura / Kamermans, Alwin / Rodriguez, Ernesto / van Horssen, Jack / van Kempen, Zoé L E / Uitdehaag, Bernard M J / Teunissen, Charlotte E / Witte, Maarten E / Killestein, Joep / de Vries, Helga E

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 215

Abstract: Background: Recent studies suggest that extended interval dosing of ocrelizumab, an anti-B cell therapy, does not affect its clinical effectiveness in most patients with multiple sclerosis (MS). However, it remains to be established whether certain B ... ...

Abstract	Background: Recent studies suggest that extended interval dosing of ocrelizumab, an anti-B cell therapy, does not affect its clinical effectiveness in most patients with multiple sclerosis (MS). However, it remains to be established whether certain B cell subsets are differentially repopulated after different dosing intervals and whether these subsets relate to clinical efficacy. Methods: We performed high-dimensional single-cell characterization of the peripheral immune landscape of patients with MS after standard (SID; n = 43) or extended interval dosing (EID; n = 37) of ocrelizumab and in non-ocrelizumab-treated (control group, CG; n = 28) patients with MS, using mass cytometry by time of flight (CyTOF). Results: The first B cells that repopulate after both ocrelizumab dosing schemes were immature, transitional and regulatory CD1d Conclusions: Taken together, our data highlight that extending the dosing interval of ocrelizumab does not lead to increased repopulation of effector B cells. We show that the increase of CD20 expression on B cell subsets in EID might lead to longer depletion or less repopulation of B cells after the next infusion of ocrelizumab. Lastly, even though extending the ocrelizumab interval dosing alters B cell repopulation, it does not affect the clinical efficacy of ocrelizumab in our cohort of patients with MS.
MeSH term(s)	Humans ; Multiple Sclerosis ; Antibodies, Monoclonal, Humanized/therapeutic use ; B-Lymphocytes ; Treatment Outcome ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Immunologic Factors/therapeutic use
Chemical Substances	ocrelizumab (A10SJL62JY) ; Antibodies, Monoclonal, Humanized ; Immunologic Factors
Language	English
Publishing date	2023-09-26
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/s12974-023-02900-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Single-cell profiling reveals periventricular CD56

Rodríguez-Lorenzo, Sabela / van Olst, Lynn / Rodriguez-Mogeda, Carla / Kamermans, Alwin / van der Pol, Susanne M A / Rodríguez, Ernesto / Kooij, Gijs / de Vries, Helga E

eLife

2022 Volume 11

Abstract: Multiple sclerosis (MS) is a chronic demyelinating disease characterised by immune cell infiltration resulting in lesions that preferentially affect periventricular areas of the brain. Despite research efforts to define the role of various immune cells ... ...

Abstract	Multiple sclerosis (MS) is a chronic demyelinating disease characterised by immune cell infiltration resulting in lesions that preferentially affect periventricular areas of the brain. Despite research efforts to define the role of various immune cells in MS pathogenesis, the focus has been on a few immune cell populations while full-spectrum analysis, encompassing others such as natural killer (NK) cells, has not been performed. Here, we used single-cell mass cytometry (CyTOF) to profile the immune landscape of brain periventricular areas - septum and choroid plexus - and of the circulation from donors with MS, dementia and controls without neurological disease. Using a 37-marker panel, we revealed the infiltration of T cells and antibody-secreting cells in periventricular brain regions and identified a novel NK cell signature specific to MS. CD56
MeSH term(s)	CD56 Antigen/metabolism ; Granzymes ; Humans ; Killer Cells, Natural ; Multiple Sclerosis/metabolism ; Neural Cell Adhesion Molecules/metabolism ; T-Lymphocytes
Chemical Substances	CD56 Antigen ; Neural Cell Adhesion Molecules ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2022-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.73849
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Single-cell profiling reveals periventricular CD56bright NK cell accumulation in multiple sclerosis

Sabela Rodríguez-Lorenzo / Lynn van Olst / Carla Rodriguez-Mogeda / Alwin Kamermans / Susanne MA van der Pol / Ernesto Rodríguez / Gijs Kooij / Helga E de Vries

eLife, Vol

2022 Volume 11

Abstract	Multiple sclerosis (MS) is a chronic demyelinating disease characterised by immune cell infiltration resulting in lesions that preferentially affect periventricular areas of the brain. Despite research efforts to define the role of various immune cells in MS pathogenesis, the focus has been on a few immune cell populations while full-spectrum analysis, encompassing others such as natural killer (NK) cells, has not been performed. Here, we used single-cell mass cytometry (CyTOF) to profile the immune landscape of brain periventricular areas – septum and choroid plexus – and of the circulation from donors with MS, dementia and controls without neurological disease. Using a 37-marker panel, we revealed the infiltration of T cells and antibody-secreting cells in periventricular brain regions and identified a novel NK cell signature specific to MS. CD56bright NK cells were accumulated in the septum of MS donors and displayed an activated and migratory phenotype, similar to that of CD56bright NK cells in the circulation. We validated this signature by multiplex immunohistochemistry and found that the number of NK cells with high expression of granzyme K, typical of the CD56bright subset, was increased in both periventricular lesions and the choroid plexus of donors with MS. Together, our multi-tissue single-cell data shows that CD56bright NK cells accumulate in the periventricular brain regions of MS patients, bringing NK cells back to the spotlight of MS pathology.
Keywords	multiple sclerosis ; natural killer cells ; single-cell mass cytometry ; periventricular ; choroid plexus ; septum ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Correction to: Inflammation of the choroid plexus in progressive multiple sclerosis: accumulation of granulocytes and T cells.

Rodríguez-Lorenzo, Sabela / Konings, Julia / van der Pol, Susanne / Kamermans, Alwin / Amor, Sandra / van Horssen, Jack / Witte, Maarten E / Kooij, Gijs / de Vries, Helga E

Acta neuropathologica communications

2020 Volume 8, Issue 1, Page(s) 24

Abstract: The original publication of this article [1] contained an incorrect author name. The correct and incorrect information is shown in this correction article. The original article has been updated. ...

Abstract	The original publication of this article [1] contained an incorrect author name. The correct and incorrect information is shown in this correction article. The original article has been updated.
Language	English
Publishing date	2020-02-26
Publishing country	England
Document type	Published Erratum
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-020-00899-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Reactive astrocytes in multiple sclerosis impair neuronal outgrowth through TRPM7-mediated chondroitin sulfate proteoglycan production.

Kamermans, Alwin / Planting, Kirsten E / Jalink, Kees / van Horssen, Jack / de Vries, Helga E

Glia

2018 Volume 67, Issue 1, Page(s) 68–77

Abstract: Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS), characterized by inflammation-mediated demyelination, axonal injury and neurodegeneration. The mechanisms underlying impaired neuronal function are not fully ... ...

Abstract	Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS), characterized by inflammation-mediated demyelination, axonal injury and neurodegeneration. The mechanisms underlying impaired neuronal function are not fully understood, but evidence is accumulating that the presence of the gliotic scar produced by reactive astrocytes play a critical role in these detrimental processes. Here, we identified astrocytic Transient Receptor Potential cation channel, subfamily M, member 7 (TRPM7), a Ca
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Animals ; Astrocytes/metabolism ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/biosynthesis ; Chondroitin Sulfate Proteoglycans/genetics ; Female ; Humans ; Male ; Middle Aged ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Neurons/metabolism ; Neurons/pathology ; Protein-Serine-Threonine Kinases/biosynthesis ; Protein-Serine-Threonine Kinases/genetics ; Rats ; TRPM Cation Channels/biosynthesis ; TRPM Cation Channels/genetics
Chemical Substances	Chondroitin Sulfate Proteoglycans ; TRPM Cation Channels ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; TRPM7 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2018-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23526
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 2345: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Neurovascular dysfunction in GRN-associated frontotemporal dementia identified by single-nucleus RNA sequencing of human cerebral cortex.

Gerrits, Emma / Giannini, Lucia A A / Brouwer, Nieske / Melhem, Shamiram / Seilhean, Danielle / Le Ber, Isabelle / Kamermans, Alwin / Kooij, Gijs / de Vries, Helga E / Boddeke, Erik W G M / Seelaar, Harro / van Swieten, John C / Eggen, Bart J L

Nature neuroscience

2022 Volume 25, Issue 8, Page(s) 1034–1048

Abstract: Frontotemporal dementia (FTD) is the second most prevalent form of early-onset dementia, affecting predominantly frontal and temporal cerebral lobes. Heterozygous mutations in the progranulin gene (GRN) cause autosomal-dominant FTD (FTD-GRN), associated ... ...

Abstract	Frontotemporal dementia (FTD) is the second most prevalent form of early-onset dementia, affecting predominantly frontal and temporal cerebral lobes. Heterozygous mutations in the progranulin gene (GRN) cause autosomal-dominant FTD (FTD-GRN), associated with TDP-43 inclusions, neuronal loss, axonal degeneration and gliosis, but FTD-GRN pathogenesis is largely unresolved. Here we report single-nucleus RNA sequencing of microglia, astrocytes and the neurovasculature from frontal, temporal and occipital cortical tissue from control and FTD-GRN brains. We show that fibroblast and mesenchymal cell numbers were enriched in FTD-GRN, and we identified disease-associated subtypes of astrocytes and endothelial cells. Expression of gene modules associated with blood-brain barrier (BBB) dysfunction was significantly enriched in FTD-GRN endothelial cells. The vasculature supportive function and capillary coverage by pericytes was reduced in FTD-GRN tissue, with increased and hypertrophic vascularization and an enrichment of perivascular T cells. Our results indicate a perturbed BBB and suggest that the neurovascular unit is severely affected in FTD-GRN.
MeSH term(s)	Blood-Brain Barrier/physiopathology ; Endothelial Cells/pathology ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/pathology ; Humans ; Intercellular Signaling Peptides and Proteins/genetics ; Mutation ; Progranulins/genetics ; Sequence Analysis, RNA ; Temporal Lobe/pathology
Chemical Substances	GRN protein, human ; Intercellular Signaling Peptides and Proteins ; Progranulins
Language	English
Publishing date	2022-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-022-01124-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Contribution of Gut Microbiota to Immunological Changes in Alzheimer's Disease.

van Olst, Lynn / Roks, Sigrid J M / Kamermans, Alwin / Verhaar, Barbara J H / van der Geest, Anne M / Muller, Majon / van der Flier, Wiesje M / de Vries, Helga E

Frontiers in immunology

2021 Volume 12, Page(s) 683068

Abstract: Emerging evidence suggests that both central and peripheral immunological processes play an important role in the pathogenesis of Alzheimer's disease (AD), but regulatory mechanisms remain unknown. The gut microbiota and its key metabolites are known to ... ...

Abstract	Emerging evidence suggests that both central and peripheral immunological processes play an important role in the pathogenesis of Alzheimer's disease (AD), but regulatory mechanisms remain unknown. The gut microbiota and its key metabolites are known to affect neuroinflammation by modulating the activity of peripheral and brain-resident immune cells, yet an overview on how the gut microbiota contribute to immunological alterations in AD is lacking. In this review, we discuss current literature on microbiota composition in AD patients and relevant animal models. Next, we highlight how microbiota and their metabolites may contribute to peripheral and central immunological changes in AD. Finally, we offer a future perspective on the translation of these findings into clinical practice by targeting gut microbiota to modulate inflammation in AD. Since we find that gut microbiota alterations in AD can induce peripheral and central immunological changes
MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/therapy ; Animals ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Brain/physiopathology ; Disease Models, Animal ; Disease Susceptibility/immunology ; Dysbiosis ; Feedback, Physiological ; Gastrointestinal Microbiome/immunology ; Gastrointestinal Tract/immunology ; Gastrointestinal Tract/metabolism ; Humans ; Immune System/immunology ; Immune System/metabolism ; Immunomodulation
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-05-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.683068
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Reduced Angiopoietin-Like 4 Expression in Multiple Sclerosis Lesions Facilitates Lipid Uptake by Phagocytes via Modulation of Lipoprotein-Lipase Activity.

Kamermans, Alwin / Rijnsburger, Merel / Chakraborty, Ananya / van der Pol, Susanne / de Vries, Helga E / van Horssen, Jack

Frontiers in immunology

2019 Volume 10, Page(s) 950

Abstract: Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) characterized by the presence of focal demyelinated plaques. Sufficient clearance of myelin and cellular debris is one of the requirements for proper tissue ... ...

Abstract	Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) characterized by the presence of focal demyelinated plaques. Sufficient clearance of myelin and cellular debris is one of the requirements for proper tissue repair and remyelination. The mechanisms underlying the clearance of such debris by phagocytes are not fully understood, but recent findings suggest a prominent role for lipoprotein-lipase (LPL) in this process. Here, we demonstrate that angiopoietin-like 4 (ANGPTL4), a potent inhibitor of LPL, is abundantly expressed in astrocytes in control white matter tissue and its expression is markedly reduced in active MS lesions. We provide evidence that ANGPTL4 inhibits the uptake of myelin-derived lipids by LPL-immunoreactive phagocytes. Taken together, our data suggest that the strong reduction in astrocytic ANGPTL4 expression in active demyelinating MS lesions enables phagocytes to adequately clear myelin debris, setting the stage for remyelination.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Angiopoietin-like 4 Protein/metabolism ; Brain/metabolism ; Cell Line, Tumor ; Female ; Humans ; Lipid Metabolism ; Lipoprotein Lipase/metabolism ; Macrophages/metabolism ; Male ; Middle Aged ; Multiple Sclerosis/metabolism ; Myelin Sheath/metabolism ; Phagocytes/metabolism
Chemical Substances	ANGPTL4 protein, human ; Angiopoietin-like 4 Protein ; Lipoprotein Lipase (EC 3.1.1.34)
Language	English
Publishing date	2019-05-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.00950
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

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

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito