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Article ; Online: Chronic Traumatic Encephalopathy and Neuropathological Comorbidities.

Stein, Thor D / Crary, John F

2020 Volume 40, Issue 4, Page(s) 384–393

Abstract: With age, the presence of multiple neuropathologies in a single individual becomes increasingly common. Given that traumatic brain injury and the repetitive head impacts (RHIs) that occur in contact sports have been associated with the development of ... ...

Abstract	With age, the presence of multiple neuropathologies in a single individual becomes increasingly common. Given that traumatic brain injury and the repetitive head impacts (RHIs) that occur in contact sports have been associated with the development of many neurodegenerative diseases, including chronic traumatic encephalopathy (CTE), Alzheimer's disease, Lewy body disease, and amyotrophic lateral sclerosis, it is becoming critical to understand the relationship and interactions between these pathologies. In fact, comorbid pathology is common in CTE and likely influenced by both age and the severity and type of exposure to RHI as well as underlying genetic predisposition. Here, we review the major comorbid pathologies seen with CTE and in former contact sports athletes and discuss what is known about the associations between RHI, age, and the development of neuropathologies. In addition, we examine the distinction between CTE and age-related pathology including primary age-related tauopathy and age-related tau astrogliopathy.
MeSH term(s)	Alzheimer Disease/epidemiology ; Alzheimer Disease/pathology ; Amyotrophic Lateral Sclerosis/epidemiology ; Amyotrophic Lateral Sclerosis/pathology ; Chronic Traumatic Encephalopathy/epidemiology ; Chronic Traumatic Encephalopathy/pathology ; Comorbidity ; Humans ; Lewy Body Disease/epidemiology ; Lewy Body Disease/pathology ; Tauopathies/epidemiology ; Tauopathies/pathology
Language	English
Publishing date	2020-06-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603165-1
ISSN	1098-9021 ; 0271-8235
ISSN (online)	1098-9021
ISSN	0271-8235
DOI	10.1055/s-0040-1713628
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Article ; Online: APOE genotype-specific methylation patterns are linked to Alzheimer disease pathology and estrogen response.

Panitch, Rebecca / Sahelijo, Nathan / Hu, Junming / Nho, Kwangsik / Bennett, David A / Lunetta, Kathryn L / Au, Rhoda / Stein, Thor D / Farrer, Lindsay A / Jun, Gyungah R

Translational psychiatry

2024 Volume 14, Issue 1, Page(s) 129

Abstract: The joint effects of APOE genotype and DNA methylation on Alzheimer disease (AD) risk is relatively unknown. We conducted genome-wide methylation analyses using 2,021 samples in blood (91 AD cases, 329 mild cognitive impairment, 1,391 controls) and 697 ... ...

Abstract	The joint effects of APOE genotype and DNA methylation on Alzheimer disease (AD) risk is relatively unknown. We conducted genome-wide methylation analyses using 2,021 samples in blood (91 AD cases, 329 mild cognitive impairment, 1,391 controls) and 697 samples in brain (417 AD cases, 280 controls). We identified differentially methylated levels in AD compared to controls in an APOE genotype-specific manner at 25 cytosine-phosphate-guanine (CpG) sites in brain and 36 CpG sites in blood. Additionally, we identified seven CpG sites in the APOE region containing TOMM40, APOE, and APOC1 genes with P < 5 × 10
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; DNA Methylation ; Estrogens ; Genotype
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E ; Estrogens ; ApoE protein, human
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-024-02834-x
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Article ; Online: Bulk brain tissue cell-type deconvolution with bias correction for single-nuclei RNA sequencing data using DeTREM.

O'Neill, Nicholas K / Stein, Thor D / Hu, Junming / Rehman, Habbiburr / Campbell, Joshua D / Yajima, Masanao / Zhang, Xiaoling / Farrer, Lindsay A

BMC bioinformatics

2023 Volume 24, Issue 1, Page(s) 349

Abstract: Background: Quantifying cell-type abundance in bulk tissue RNA-sequencing enables researchers to better understand complex systems. Newer deconvolution methodologies, such as MuSiC, use cell-type signatures derived from single-cell RNA-sequencing (scRNA- ...

Abstract	Background: Quantifying cell-type abundance in bulk tissue RNA-sequencing enables researchers to better understand complex systems. Newer deconvolution methodologies, such as MuSiC, use cell-type signatures derived from single-cell RNA-sequencing (scRNA-seq) data to make these calculations. Single-nuclei RNA-sequencing (snRNA-seq) reference data can be used instead of scRNA-seq data for tissues such as human brain where single-cell data are difficult to obtain, but accuracy suffers due to sequencing differences between the technologies. Results: We propose a modification to MuSiC entitled 'DeTREM' which compensates for sequencing differences between the cell-type signature and bulk RNA-seq datasets in order to better predict cell-type fractions. We show DeTREM to be more accurate than MuSiC in simulated and real human brain bulk RNA-sequencing datasets with various cell-type abundance estimates. We also compare DeTREM to SCDC and CIBERSORTx, two recent deconvolution methods that use scRNA-seq cell-type signatures. We find that they perform well in simulated data but produce less accurate results than DeTREM when used to deconvolute human brain data. Conclusion: DeTREM improves the deconvolution accuracy of MuSiC and outperforms other deconvolution methods when applied to snRNA-seq data. DeTREM enables accurate cell-type deconvolution in situations where scRNA-seq data are not available. This modification improves characterization cell-type specific effects in brain tissue and identification of cell-type abundance differences under various conditions.
MeSH term(s)	Humans ; RNA/genetics ; Brain ; RNA, Small Nuclear ; RNA-Seq ; Base Sequence
Chemical Substances	RNA (63231-63-0) ; RNA, Small Nuclear
Language	English
Publishing date	2023-09-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2041484-5
ISSN	1471-2105 ; 1471-2105
ISSN (online)	1471-2105
ISSN	1471-2105
DOI	10.1186/s12859-023-05476-w
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Article ; Online: Authors' Response.

Bieniek, Kevin F / Crary, John F / Dickson, Dennis W / Stein, Thor D / Mez, Jesse / Alosco, Michael E / McKee, Ann C

Journal of neuropathology and experimental neurology

2021 Volume 80, Issue 10, Page(s) 1008–1010

Language	English
Publishing date	2021-10-27
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nlab066.001
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Article ; Online: Identification of circRNAs linked to Alzheimer's disease and related dementias.

Puri, Sambhavi / Hu, Junming / Sun, Zhuorui / Lin, Mintao / Stein, Thor D / Farrer, Lindsay A / Wolozin, Benjamin / Zhang, Xiaoling

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19, Issue 8, Page(s) 3389–3405

Abstract: Introduction: Circular RNAs (circRNAs) exhibit selective expression in the brain and differential regulation in Alzheimer's disease (AD). To explore the role of circRNAs in AD, we investigated how circRNA expression varies between brain regions and with ...

Abstract	Introduction: Circular RNAs (circRNAs) exhibit selective expression in the brain and differential regulation in Alzheimer's disease (AD). To explore the role of circRNAs in AD, we investigated how circRNA expression varies between brain regions and with AD-related stress in human neuronal precursor cells (NPCs). Methods: Ribosomal RNA-depleted hippocampus RNA-sequencing data were generated. Differentially regulated circRNAs in AD and related dementias were detected using CIRCexplorer3 and limma. circRNA results were validated using quantitative real-time PCR of cDNA from the brain and NPCs. Results: We identified 48 circRNAs that were significantly associated with AD. We observed that circRNA expression differed by dementia subtype. Using NPCs, we demonstrated that exposure to oligomeric tau elicits downregulation of circRNA similar to that observed in the AD brain. Discussion: Our study shows that differential expression of circRNA can vary by dementia subtype and brain region. We also demonstrated that circRNAs can be regulated by AD-linked neuronal stress independently from their cognate linear messenger RNAs (mRNAs).
MeSH term(s)	Humans ; RNA, Circular/genetics ; RNA, Circular/metabolism ; Alzheimer Disease/genetics ; MicroRNAs/genetics ; RNA, Messenger/metabolism ; Down-Regulation
Chemical Substances	RNA, Circular ; MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2023-02-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.12960
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Zs.MO 540: Show issues

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Article: Repetitive head impacts induce neuronal loss and neuroinflammation in young athletes.

Butler, Morgane L M D / Pervaiz, Nida / Ypsilantis, Petra / Wang, Yichen / Cammasola Breda, Julia / Mazzilli, Sarah / Nicks, Raymond / Spurlock, Elizabeth / Hefti, Marco M / Huber, Bertrand R / Alvarez, Victor E / Stein, Thor D / Campbell, Joshua D / McKee, Ann C / Cherry, Jonathan D

bioRxiv : the preprint server for biology

2024

Abstract: Repetitive head impacts (RHI) sustained from contact sports are the largest risk factor for chronic traumatic encephalopathy (CTE). Currently, CTE can only be diagnosed after death and the multicellular cascade of events that trigger initial ... ...

Abstract	Repetitive head impacts (RHI) sustained from contact sports are the largest risk factor for chronic traumatic encephalopathy (CTE). Currently, CTE can only be diagnosed after death and the multicellular cascade of events that trigger initial hyperphosphorylated tau (p-tau) deposition remain unclear. Further, the symptoms endorsed by young individuals with early disease are not fully explained by the extent of p-tau deposition, severely hampering development of therapeutic interventions. Here, we show that RHI exposure associates with a multicellular response in young individuals (<51 years old) prior to the onset of CTE p-tau pathology that correlates with number of years of RHI exposure. Leveraging single nucleus RNA sequencing of tissue from 8 control, 9 RHI-exposed, and 11 low stage CTE individuals, we identify SPP1+ inflammatory microglia, angiogenic and inflamed endothelial cell profiles, reactive astrocytes, and altered synaptic gene expression in excitatory and inhibitory neurons in all individuals with exposure to RHI. Surprisingly, we also observe a significant loss of cortical sulcus layer 2/3 neurons in contact sport athletes compared to controls independent of p-tau pathology. These results provide robust evidence that multiple years of RHI exposure is sufficient to induce lasting cellular alterations that may underlie p-tau deposition and help explain the early clinical symptoms observed in young former contact sport athletes. Furthermore, these data identify specific cellular responses to repetitive head impacts that may direct future identification of diagnostic and therapeutic strategies for CTE.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.26.586815
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Article ; Online: Inflammation and neuronal gene expression changes differ in early versus late chronic traumatic encephalopathy brain.

Labadorf, Adam / Agus, Filisia / Aytan, Nurgul / Cherry, Jonathan / Mez, Jesse / McKee, Ann / Stein, Thor D

BMC medical genomics

2023 Volume 16, Issue 1, Page(s) 49

Abstract: Background: Our understanding of the molecular underpinnings of chronic traumatic encephalopathy (CTE) and its associated pathology in post-mortem brain is incomplete. Factors including years of play and genetic risk variants influence the extent of tau ...

Abstract	Background: Our understanding of the molecular underpinnings of chronic traumatic encephalopathy (CTE) and its associated pathology in post-mortem brain is incomplete. Factors including years of play and genetic risk variants influence the extent of tau pathology associated with disease expression, but how these factors affect gene expression, and whether those effects are consistent across the development of disease, is unknown. Methods: To address these questions, we conducted an analysis of the largest post-mortem brain CTE mRNASeq whole-transcriptome dataset available to date. We examined the genes and biological processes associated with disease by comparing individuals with CTE with control individuals with a history of repetitive head impacts that lack CTE pathology. We then identified genes and biological processes associated with total years of play as a measure of exposure, amount of tau pathology present at time of death, and the presence of APOE and TMEM106B risk variants. Samples were stratified into low and high pathology groups based on McKee CTE staging criteria to model early versus late changes in response to exposure, and the relative effects associated with these factors were compared between these groups. Results: Substantial gene expression changes were associated with severe disease for most of these factors, primarily implicating diverse, strongly involved neuroinflammatory and neuroimmune processes. In contrast, low pathology groups had many fewer genes and processes implicated and show striking differences for some factors when compared with severe disease. Specifically, gene expression associated with amount of tau pathology showed a nearly perfect inverse relationship when compared between these two groups. Conclusions: Together, these results suggest the early CTE disease process may be mechanistically different than what occurs in late stages, that total years of play and tau pathology influence disease expression differently, and that related pathology-modifying risk variants may do so via distinct biological pathways.
MeSH term(s)	Humans ; Chronic Traumatic Encephalopathy/genetics ; Chronic Traumatic Encephalopathy/metabolism ; Chronic Traumatic Encephalopathy/pathology ; tau Proteins/genetics ; tau Proteins/metabolism ; Brain/metabolism ; Inflammation/metabolism ; Transcriptome ; Membrane Proteins/genetics ; Nerve Tissue Proteins/genetics
Chemical Substances	tau Proteins ; TMEM106B protein, human ; Membrane Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2023-03-09
Publishing country	England
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	2411865-5
ISSN	1755-8794 ; 1755-8794
ISSN (online)	1755-8794
ISSN	1755-8794
DOI	10.1186/s12920-023-01471-5
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Article ; Online: Progressive mechanical and structural changes in anterior cerebral arteries with Alzheimer's disease.

Liu, Xiaozhu / Halvorsen, Samuel / Blanke, Nathan / Downs, Margaret / Stein, Thor D / Bigio, Irving J / Zaia, Joseph / Zhang, Yanhang

Alzheimer's research & therapy

2023 Volume 15, Issue 1, Page(s) 185

Abstract: Alzheimer's disease (AD) is a neurodegenerative disease and the main cause for dementia. The irreversible neurodegeneration leads to a gradual loss of brain function characterized predominantly by memory loss. Cerebrovascular changes are common ... ...

Abstract	Alzheimer's disease (AD) is a neurodegenerative disease and the main cause for dementia. The irreversible neurodegeneration leads to a gradual loss of brain function characterized predominantly by memory loss. Cerebrovascular changes are common neuropathologic findings in aged subjects with dementia. Cerebrovascular integrity is critical for proper metabolism and perfusion of the brain, as cerebrovascular remodeling may render the brain more susceptible to pulse pressure and may be associated with poorer cognitive performance and greater risk of cerebrovascular events. The objective of this study is to provide understanding of cerebrovascular remodeling with AD progression. Anterior cerebral arteries (ACAs) from a total of 19 brain donor participants from controls and pathologically diagnosed AD groups (early-Braak stages I-II; intermediate-Braak stages III-IV; and advanced-Braak stages V-VI) were included in this study. Mechanical testing, histology, advanced optical imaging, and mass spectrometry were performed to study the progressive structural and functional changes of ACAs with AD progression. Biaxial extension-inflation tests showed that ACAs became progressively less compliant, and the longitudinal stress in the intermediate and advanced AD groups was significantly higher than that from the control group. With pathological AD development, the inner and outer diameters of the ACAs remained almost unchanged; however, histology study revealed progressive smooth muscle cell atrophy and loss of elastic fibers which led to compromised structural integrity of the arterial wall. Multiphoton imaging demonstrated elastin degradation at the media-adventitia interface, which led to the formation of an empty band of 21.0 ± 15.4 μm and 32.8 ± 9.24 μm in width for the intermediate and advanced AD groups, respectively. Furthermore, quantitative birefringence microscopy showed disorganized adventitial collagen with AD development. Mass spectrometry analysis provided further evidence of altered collagen content and other extracellular matrix (ECM) molecule and smooth muscle cell changes that were consistent with the mechanical and structural alterations. Collectively, our study provides understanding of the mechanical and structural cerebrovascular deterioration in cerebral arteries with AD, which may be related to neurodegenration and pathology in the brain.
MeSH term(s)	Humans ; Aged ; Alzheimer Disease/pathology ; Anterior Cerebral Artery/metabolism ; Anterior Cerebral Artery/pathology ; Neurodegenerative Diseases/metabolism ; Brain/metabolism ; Collagen/metabolism
Chemical Substances	Collagen (9007-34-5)
Language	English
Publishing date	2023-10-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-023-01331-5
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Article: Progressive Mechanical and Structural Changes in Anterior Cerebral Arteries with Alzheimer's Disease.

Liu, Xiaozhu / Halvorsen, Samuel / Blanke, Nathan / Downs, Margaret / Stein, Thor D / Bigio, Irving J / Zaia, Joseph / Zhang, Yanhang

Research square

2023

Abstract: Alzheimer disease (AD) is a neurodegenerative disease and the main cause for dementia. The irreversible neurodegeneration leads to a gradual loss of brain function characterized predominantly by memory loss. Cerebrovascular changes are common ... ...

Abstract	Alzheimer disease (AD) is a neurodegenerative disease and the main cause for dementia. The irreversible neurodegeneration leads to a gradual loss of brain function characterized predominantly by memory loss. Cerebrovascular changes are common neuropathologic findings in aged subjects with dementia. Cerebrovascular integrity is critical for proper metabolism and perfusion of the brain, as cerebrovascular remodeling may render the brain more susceptible to pulse pressure and may be associated with poorer cognitive performance and greater risk of cerebrovascular events. The objective of this study is to provide understanding of cerebrovascular remodeling with AD progression. A total of 28 brain donor participants with human anterior cerebral artery (ACA) from controls and pathologically diagnosed AD groups (early - Braak stages I-II; intermediate - Braak stages III-IV; and advanced - Braak stages V-VI) were included in this study. Mechanical testing, histology, advanced optical imaging, and mass spectrometry were performed to study the progressive structural and functional changes of ACAs with AD progression. Biaxial extension-inflation tests showed that ACAs became progressively less compliant, and the longitudinal stress in the intermediate& advanced AD groups was significantly higher than that from the control group. With pathological AD development, the inner and outer diameter of ACA remained almost unchanged; however, histology study revealed progressive smooth muscle cell atrophy and loss of elastic fibers which led to compromised structural integrity of the arterial wall. Multiphoton imaging demonstrated elastin degradation at the media-adventitia interface, which led to the formation of an empty band of 21.0 ± 15.4 μm and 32.8 ± 9.24 μm in width for the intermediate& advanced AD groups, respectively. Furthermore, quantitative birefringence microscopy showed disorganized adventitial collagen with AD development. Mass spectrometry analysis provided further evidence of altered collagen content and other extracellular matrix (ECM) molecule and smooth muscle cell changes that were consistent with the mechanical and structural alterations. Collectively, our study provides understanding of the mechanical and structural cerebrovascular deterioration in cerebral arteries with AD, which may be related to neurodegenration and pathology in the brain.
Language	English
Publishing date	2023-08-29
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3283587/v1
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Article: Chronic Traumatic Encephalopathy and Neuropathological Comorbidities

Stein, Thor D. / Crary, John F.

Seminars in Neurology

(Chronic Traumatic Encephalopathy)

2020 Volume 40, Issue 04, Page(s) 384–393

Series title	Chronic Traumatic Encephalopathy
Abstract	With age, the presence of multiple neuropathologies in a single individual becomes increasingly common. Given that traumatic brain injury and the repetitive head impacts (RHIs) that occur in contact sports have been associated with the development of many neurodegenerative diseases, including chronic traumatic encephalopathy (CTE), Alzheimer's disease, Lewy body disease, and amyotrophic lateral sclerosis, it is becoming critical to understand the relationship and interactions between these pathologies. In fact, comorbid pathology is common in CTE and likely influenced by both age and the severity and type of exposure to RHI as well as underlying genetic predisposition. Here, we review the major comorbid pathologies seen with CTE and in former contact sports athletes and discuss what is known about the associations between RHI, age, and the development of neuropathologies. In addition, we examine the distinction between CTE and age-related pathology including primary age-related tauopathy and age-related tau astrogliopathy.
Keywords	chronic traumatic encephalopathy ; traumatic brain injury ; neurodegenerative disease ; Alzheimer's disease ; comorbidity
Language	English
Publishing date	2020-06-30
Publisher	Thieme Medical Publishers
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	603165-1
ISSN	1098-9021 ; 0271-8235
ISSN (online)	1098-9021
ISSN	0271-8235
DOI	10.1055/s-0040-1713628
Database	Thieme publisher's database

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Zs.A 1737: Show issues

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ab Jg. 2022: Lesesaal (EG)

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