LIVIVO - Search results -

Search results

Result 1 - 10 of total 27

Search options

Article: Microglia produce the amyloidogenic ABri peptide in familial British dementia.

Arber, Charles / Casey, Jackie M / Crawford, Samuel / Rambarack, Naiomi / Yaman, Umran / Wiethoff, Sarah / Augustin, Emma / Piers, Thomas M / Rostagno, Agueda / Ghiso, Jorge / Lewis, Patrick A / Revesz, Tamas / Hardy, John / Pocock, Jennifer M / Houlden, Henry / Schott, Jonathan M / Salih, Dervis A / Lashley, Tammaryn / Wray, Selina

bioRxiv : the preprint server for biology

2023

Abstract: Mutations ... ...

Abstract	Mutations in
Language	English
Publishing date	2023-06-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.27.546552
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Details ▾

Article ; Online: Improving Mouse Models for Dementia. Are All the Effects in Tau Mouse Models Due to Overexpression?

Joel, Zelah / Izquierdo, Pablo / Salih, Dervis A / Richardson, Jill C / Cummings, Damian M / Edwards, Frances A

Cold Spring Harbor symposia on quantitative biology

2019 Volume 83, Page(s) 151–161

Abstract: Mouse models of Alzheimer's disease have commonly used transgenic overexpression of genes involved in production of amyloid β ( ...

Abstract	Mouse models of Alzheimer's disease have commonly used transgenic overexpression of genes involved in production of amyloid β (
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article
ISSN	1943-4456 ; 0091-7451
ISSN (online)	1943-4456
ISSN	0091-7451
DOI	10.1101/sqb.2018.83.037531
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

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.

Details ▾
- Full text online
- Order with fees

Article ; Online: Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia.

Molecular neurodegeneration

2021 Volume 16, Issue 1, Page(s) 47

Abstract: Background: Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. We add novel findings concerning these relationships and investigate which of ... ...

Abstract	Background: Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. We add novel findings concerning these relationships and investigate which of our previously reported results from transgenic mice can be validated in knock-in mice, in which overexpression and other artefacts of transgenic technology are avoided. Methods: App Results: Both App knock-in lines showed increased glutamate release probability prior to detection of plaques. Consistent with results in transgenic mice, this persisted throughout life in App Conclusions: Increased glutamate release probability is similar across knock-in and transgenic mouse models of Alzheimer's disease, likely reflecting acute physiological effects of soluble amyloid beta. Microglia respond later to increased amyloid beta levels by proliferating and upregulating Cd68 and Trem2. Partial depletion of microglia suggests that, in wild type mice, alteration of surviving phagocytic microglia, rather than microglial loss, drives age-dependent effects on glutamate release that become exacerbated in Alzheimer's disease.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/genetics ; Animals ; Disease Models, Animal ; Gene Knock-In Techniques/methods ; Humans ; Mice ; Microglia/metabolism ; Plaque, Amyloid/pathology ; Synaptic Transmission/physiology
Chemical Substances	Amyloid beta-Protein Precursor
Language	English
Publishing date	2021-07-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-021-00457-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: FoxO transcription factors in the maintenance of cellular homeostasis during aging.

Salih, Dervis A M / Brunet, Anne

Current opinion in cell biology

2008 Volume 20, Issue 2, Page(s) 126–136

Abstract: The FoxO family of Forkhead transcription factors functions at the interface of tumor suppression, energy metabolism, and organismal longevity. FoxO factors are key downstream targets of insulin, growth factor, nutrient, and oxidative stress stimuli that ...

Abstract	The FoxO family of Forkhead transcription factors functions at the interface of tumor suppression, energy metabolism, and organismal longevity. FoxO factors are key downstream targets of insulin, growth factor, nutrient, and oxidative stress stimuli that coordinate a wide range of cellular outputs. FoxO-dependent cellular responses include gluconeogenesis, neuropeptide secretion, atrophy, autophagy, apoptosis, cell cycle arrest, and stress resistance. This review will discuss the roles of the mammalian FoxO family in a variety of cell types, from stem cells to mature cells, in the context of the whole organism. Given the overwhelming evidence that the FoxO factors promote longevity in invertebrates, this review will also discuss the potential role of the FoxO factors in the aging of mammalian organisms.
MeSH term(s)	Aging/metabolism ; Animals ; Forkhead Transcription Factors/metabolism ; Homeostasis ; Humans ; Invertebrates/metabolism ; Models, Biological ; Neovascularization, Pathologic
Chemical Substances	Forkhead Transcription Factors
Language	English
Publishing date	2008-04-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2008.02.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2963: 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 ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions.

Liu, Wenfei / Taso, Orjona / Wang, Rui / Bayram, Sevinc / Graham, Andrew C / Garcia-Reitboeck, Pablo / Mallach, Anna / Andrews, William D / Piers, Thomas M / Botia, Juan A / Pocock, Jennifer M / Cummings, Damian M / Hardy, John / Edwards, Frances A / Salih, Dervis A

Human molecular genetics

2020 Volume 29, Issue 19, Page(s) 3224–3248

Abstract: Genome-wide association studies have reported that, amongst other microglial genes, variants in TREM2 can profoundly increase the incidence of developing Alzheimer's disease (AD). We have investigated the role of TREM2 in primary microglial cultures from ...

Abstract	Genome-wide association studies have reported that, amongst other microglial genes, variants in TREM2 can profoundly increase the incidence of developing Alzheimer's disease (AD). We have investigated the role of TREM2 in primary microglial cultures from wild type mice by using siRNA to decrease Trem2 expression, and in parallel from knock-in mice heterozygous or homozygous for the Trem2 R47H AD risk variant. The prevailing phenotype of Trem2 R47H knock-in mice was decreased expression levels of Trem2 in microglia, which resulted in decreased density of microglia in the hippocampus. Overall, primary microglia with reduced Trem2 expression, either by siRNA or from the R47H knock-in mice, displayed a similar phenotype. Comparison of the effects of decreased Trem2 expression under conditions of lipopolysaccharide (LPS) pro-inflammatory or IL-4 anti-inflammatory stimulation revealed the importance of Trem2 in driving a number of the genes up-regulated in the anti-inflammatory phenotype. RNA-seq analysis showed that IL-4 induced the expression of a program of genes including Arg1 and Ap1b1 in microglia, which showed an attenuated response to IL-4 when Trem2 expression was decreased. Genes showing a similar expression profile to Arg1 were enriched for STAT6 transcription factor recognition elements in their promoter, and Trem2 knockdown decreased levels of STAT6. LPS-induced pro-inflammatory stimulation suppressed Trem2 expression, thus preventing TREM2's anti-inflammatory drive. Given that anti-inflammatory signaling is associated with tissue repair, understanding the signaling mechanisms downstream of Trem2 in coordinating the pro- and anti-inflammatory balance of microglia, particularly mediating effects of the IL-4-regulated anti-inflammatory pathway, has important implications for fighting neurodegenerative disease.
MeSH term(s)	Animals ; Animals, Newborn ; Gene Expression Regulation ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Membrane Glycoproteins/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia/immunology ; Microglia/metabolism ; Microglia/pathology ; Mutation ; RNA-Seq ; Receptors, Immunologic/physiology ; STAT6 Transcription Factor/genetics ; STAT6 Transcription Factor/metabolism ; Transcriptome
Chemical Substances	Inflammation Mediators ; Membrane Glycoproteins ; Receptors, Immunologic ; STAT6 Transcription Factor ; Trem2 protein, mouse
Language	English
Publishing date	2020-09-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddaa209
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3469: 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 ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A genetic link between risk for Alzheimer's disease and severe COVID-19 outcomes via the OAS1 gene.

Brain : a journal of neurology

2021 Volume 144, Issue 12, Page(s) 3727–3741

Abstract: Recently, we reported oligoadenylate synthetase 1 (OAS1) contributed to the risk of Alzheimer's disease, by its enrichment in transcriptional networks expressed by microglia. However, the function of OAS1 within microglia was not known. Using genotyping ... ...

Abstract	Recently, we reported oligoadenylate synthetase 1 (OAS1) contributed to the risk of Alzheimer's disease, by its enrichment in transcriptional networks expressed by microglia. However, the function of OAS1 within microglia was not known. Using genotyping from 1313 individuals with sporadic Alzheimer's disease and 1234 control individuals, we confirm the OAS1 variant, rs1131454, is associated with increased risk for Alzheimer's disease. The same OAS1 locus has been recently associated with severe coronavirus disease 2019 (COVID-19) outcomes, linking risk for both diseases. The single nucleotide polymorphisms rs1131454(A) and rs4766676(T) are associated with Alzheimer's disease, and rs10735079(A) and rs6489867(T) are associated with severe COVID-19, where the risk alleles are linked with decreased OAS1 expression. Analysing single-cell RNA-sequencing data of myeloid cells from Alzheimer's disease and COVID-19 patients, we identify co-expression networks containing interferon (IFN)-responsive genes, including OAS1, which are significantly upregulated with age and both diseases. In human induced pluripotent stem cell-derived microglia with lowered OAS1 expression, we show exaggerated production of TNF-α with IFN-γ stimulation, indicating OAS1 is required to limit the pro-inflammatory response of myeloid cells. Collectively, our data support a link between genetic risk for Alzheimer's disease and susceptibility to critical illness with COVID-19 centred on OAS1, a finding with potential implications for future treatments of Alzheimer's disease and COVID-19, and development of biomarkers to track disease progression.
MeSH term(s)	2',5'-Oligoadenylate Synthetase/genetics ; Adolescent ; Aged ; Aged, 80 and over ; Alzheimer Disease/diagnosis ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; COVID-19/diagnosis ; COVID-19/epidemiology ; COVID-19/genetics ; Cells, Cultured ; Female ; Gene Regulatory Networks/genetics ; Genetic Linkage/genetics ; Genetic Predisposition to Disease/epidemiology ; Genetic Predisposition to Disease/genetics ; Humans ; Induced Pluripotent Stem Cells/physiology ; Male ; Middle Aged ; Patient Acuity ; Polymorphism, Single Nucleotide/genetics ; Young Adult
Chemical Substances	OAS1 protein, human (EC 2.7.7.-) ; 2',5'-Oligoadenylate Synthetase (EC 2.7.7.84)
Language	English
Publishing date	2021-10-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awab337
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui II Zs.26: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Genetic variability in response to amyloid beta deposition influences Alzheimer's disease risk.

Salih, Dervis A / Bayram, Sevinc / Guelfi, Sebastian / Reynolds, Regina H / Shoai, Maryam / Ryten, Mina / Brenton, Jonathan W / Zhang, David / Matarin, Mar / Botia, Juan A / Shah, Runil / Brookes, Keeley J / Guetta-Baranes, Tamar / Morgan, Kevin / Bellou, Eftychia / Cummings, Damian M / Escott-Price, Valentina / Hardy, John

Brain communications

2019 Volume 1, Issue 1, Page(s) fcz022

Abstract: Genome-wide association studies of late-onset Alzheimer's disease risk have previously identified genes primarily expressed in microglia that form a transcriptional network. Using transgenic mouse models of amyloid deposition, we previously showed that ... ...

Abstract	Genome-wide association studies of late-onset Alzheimer's disease risk have previously identified genes primarily expressed in microglia that form a transcriptional network. Using transgenic mouse models of amyloid deposition, we previously showed that many of the mouse orthologues of these risk genes are co-expressed and associated with amyloid pathology. In this new study, we generate an improved RNA-seq-derived network that is expressed in amyloid-responsive mouse microglia and we statistically compare this with gene-level variation in previous human Alzheimer's disease genome-wide association studies to predict at least four new risk genes for the disease (
Language	English
Publishing date	2019-10-10
Publishing country	England
Document type	Journal Article
ISSN	2632-1297
ISSN (online)	2632-1297
DOI	10.1093/braincomms/fcz022
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

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: Prodromal neuroinflammatory, cholinergic and metabolite dysfunction detected by PET and MRS in the TgF344-AD transgenic rat model of AD: a collaborative multi-modal study.

Chaney, Aisling M / Lopez-Picon, Francisco R / Serrière, Sophie / Wang, Rui / Bochicchio, Daniela / Webb, Samuel D / Vandesquille, Matthias / Harte, Michael K / Georgiadou, Christina / Lawrence, Catherine / Busson, Julie / Vercouillie, Johnny / Tauber, Clovis / Buron, Frédéric / Routier, Sylvain / Reekie, Tristan / Snellman, Anniina / Kassiou, Michael / Rokka, Johanna /

Davies, Karen E / Rinne, Juha O / Salih, Dervis A / Edwards, Frances A / Orton, Llwyd D / Williams, Stephen R / Chalon, Sylvie / Boutin, Hervé

Theranostics

2021 Volume 11, Issue 14, Page(s) 6644–6667

Abstract: Mouse models of Alzheimer's disease (AD) are valuable but do not fully recapitulate human AD pathology, such as spontaneous Tau fibril accumulation and neuronal loss, necessitating the development of new AD models. The transgenic (TG) TgF344-AD rat has ... ...

Abstract	Mouse models of Alzheimer's disease (AD) are valuable but do not fully recapitulate human AD pathology, such as spontaneous Tau fibril accumulation and neuronal loss, necessitating the development of new AD models. The transgenic (TG) TgF344-AD rat has been reported to develop age-dependent AD features including neuronal loss and neurofibrillary tangles, despite only expressing
MeSH term(s)	Aging/metabolism ; Aging/physiology ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Behavior Rating Scale ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/physiopathology ; Disease Models, Animal ; Female ; Fluorine Radioisotopes ; Frontal Lobe/metabolism ; Frontal Lobe/pathology ; Gliosis/metabolism ; Hippocampus/metabolism ; Hippocampus/pathology ; Immunohistochemistry ; Inflammation/metabolism ; Locomotion/genetics ; Locomotion/physiology ; Magnetic Resonance Spectroscopy ; Male ; Neurons/metabolism ; Neurons/pathology ; Plaque, Amyloid/metabolism ; Positron-Emission Tomography ; Rats ; Rats, Transgenic ; Receptors, Cholinergic/metabolism ; Thalamus/metabolism ; Thalamus/pathology ; tau Proteins/metabolism
Chemical Substances	Fluorine Radioisotopes ; Mapt protein, rat ; Receptors, Cholinergic ; tau Proteins
Language	English
Publishing date	2021-05-03
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.56059
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Neuronal and Peripheral Pentraxins Modify Glutamate Release and may Interact in Blood-Brain Barrier Failure.

Cummings, Damian M / Benway, Tiffanie A / Ho, Hinze / Tedoldi, Angelo / Fernandes Freitas, Monica M / Shahab, Lion / Murray, Christina E / Richard-Loendt, Angela / Brandner, Sebastian / Lashley, Tammaryn / Salih, Dervis A / Edwards, Frances A

Cerebral cortex (New York, N.Y. : 1991)

2017 Volume 27, Issue 6, Page(s) 3437–3448

Abstract: Neuronal pentraxin 1 (NPTX1) has been implicated in Alzheimer's disease, being present in and around dystrophic neurons in plaques, affecting glutamatergic transmission postsynaptically and mediating effects of amyloidβ. Here, we confirm the presence of ... ...

Abstract	Neuronal pentraxin 1 (NPTX1) has been implicated in Alzheimer's disease, being present in and around dystrophic neurons in plaques, affecting glutamatergic transmission postsynaptically and mediating effects of amyloidβ. Here, we confirm the presence of NPTX1 around plaques in postmortem Alzheimer's disease brain and report that acutely applied human NPTX1 increases paired-pulse ratio at mouse CA3-CA1 hippocampal synapses, indicating a decrease in glutamate release. In contrast, chronic exposure to NPTX1, NPTX2, or NPTX receptor decreases paired-pulse ratio, mimicking some of the earliest changes in mice expressing familial Alzheimer's disease genes. The peripheral pentraxin, serum amyloid P component (SAP), causes similar synaptic effects to NPTX1. The presence of SAP on amyloid plaques in Alzheimer's disease confirms that it can enter the brain. We show that SAP and neuronal pentraxins can interact and that SAP can enter the brain if the blood-brain barrier is compromised, suggesting that peripheral pentraxins could affect central synaptic transmission via this interaction, especially in the event of blood-brain barrier breakdown.
Language	English
Publishing date	2017-06-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhx046
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3235: 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 ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Effects of rising amyloidβ levels on hippocampal synaptic transmission, microglial response and cognition in APP

Medawar, Evelyn / Benway, Tiffanie A / Liu, Wenfei / Hanan, Taylor A / Haslehurst, Peter / James, Owain T / Yap, Kenrick / Muessig, Laurenz / Moroni, Fabia / Nahaboo Solim, Muzammil A / Baidildinova, Gaukhar / Wang, Rui / Richardson, Jill C / Cacucci, Francesca / Salih, Dervis A / Cummings, Damian M / Edwards, Frances A

EBioMedicine

2018 Volume 39, Page(s) 422–435

Abstract: Background: Progression of Alzheimer's disease is thought initially to depend on rising amyloidβ and its synaptic interactions. Transgenic mice (TASTPM; APP: Methods: CA1 synaptic transmission and plasticity were investigated using in vitro ... ...

Abstract	Background: Progression of Alzheimer's disease is thought initially to depend on rising amyloidβ and its synaptic interactions. Transgenic mice (TASTPM; APP Methods: CA1 synaptic transmission and plasticity were investigated using in vitro electrophysiology. Microglial relationship to plaques was examined with immunohistochemistry. Behaviour was assessed with a forced-alternation T-maze, open field, light/dark box and elevated plus maze. Findings: The most striking finding is the increase in microglial numbers in TASTPM, which, like synaptic changes, begins before plaques are detected. Further increases and a reactive phenotype occur later, concurrent with development of larger plaques. Long-term potentiation is initially enhanced at pre-plaque stages but decrements with the initial appearance of plaques. Finally, despite altered plasticity, TASTPM have little cognitive deficit, even with a heavy plaque load, although they show altered non-cognitive behaviours. Interpretation: The pre-plaque synaptic changes and microglial proliferation are presumably related to low, non-toxic amyloidβ levels in the general neuropil and not directly associated with plaques. However, as plaques grow, microglia proliferate further, clustering around plaques and becoming phagocytic. Like in humans, even when plaque load is heavy, without development of neurofibrillary tangles and neurodegeneration, these alterations do not result in cognitive deficits. Behaviours are seen that could be consistent with pre-diagnosis changes in the human condition. Funding: GlaxoSmithKline; BBSRC; UCL; ARUK; MRC.
MeSH term(s)	Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Animals ; Behavior, Animal ; Cognition/physiology ; Disease Models, Animal ; Hemizygote ; Hippocampus/metabolism ; Hippocampus/physiology ; Humans ; Male ; Maze Learning ; Mice ; Mice, Transgenic ; Microglia/metabolism ; Microglia/physiology ; Presenilin-1/genetics ; Synaptic Transmission
Chemical Substances	APP protein, human ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; PSEN1 protein, human ; Presenilin-1
Language	English
Publishing date	2018-12-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2018.12.006
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 7090: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

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

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

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