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Article ; Online: Integrated Analysis of DNA Methylation, Hydroxymethylation, and Gene Expression Data Using ME-Class2.

Singh, Manoj K / Edwards, John R

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2198, Page(s) 467–489

Abstract: There is increasing interest in understanding the pathological role of DNA methylation changes in disease by profiling genome-wide methylation changes. This includes both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). The typical profiling ... ...

Abstract	There is increasing interest in understanding the pathological role of DNA methylation changes in disease by profiling genome-wide methylation changes. This includes both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). The typical profiling study is designed to measure 5mC and/or 5hmC levels alongside gene expression in a set of samples and controls to determine a list of candidate genes whose 5mC and/or 5hmC changes are associated with expression changes. We recently showed that ME-Class2 substantially outperforms other bioinformatic approaches at accurately identify genes with highly associated methylation and expression changes. ME-Class2 further illuminated how synergistic changes in 5mC and 5hmC potentially contribute to gene silencing and activation. Here we present a detailed protocol for using ME-Class2 to analyze genome-wide methylation (5mC and/or 5hmC) and expression data. Further, we provide advice about extending ME-Class2 to study the relationships between other epigenetic marks.
MeSH term(s)	5-Methylcytosine/analogs & derivatives ; 5-Methylcytosine/chemistry ; Animals ; Cytosine/metabolism ; DNA/chemistry ; DNA/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic ; Epigenomics/methods ; Gene Expression/genetics ; Gene Silencing ; Genome ; Genomics ; Humans ; Machine Learning ; Sequence Analysis, DNA/methods
Chemical Substances	5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H) ; Cytosine (8J337D1HZY) ; DNA (9007-49-2)
Language	English
Publishing date	2020-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0876-0_34
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Towards constructing the governable worker in nineteenth-century Britain

Edwards, John R

Critical perspectives on accounting : an international journal for social and organizational accountability Vol. 50 , p. 36-55

2018 Volume 50, Page(s) 36–55

Author's details	John Richard Edwards
Keywords	Accounting ; Foucault ; Governable worker ; Piece rates
Language	English
Publisher	Elsevier
Publishing place	Amsterdam
Document type	Article
ZDB-ID	1022791x
ISSN	1045-2354
Database	ECONomics Information System

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Article ; Online: Methylation-directed glycosylation of chromatin factors represses retrotransposon promoters.

Boulard, Mathieu / Rucli, Sofia / Edwards, John R / Bestor, Timothy H

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 25, Page(s) 14292–14298

Abstract: The mechanisms by which methylated mammalian promoters are transcriptionally silenced even in the presence of all of the factors required for their expression have long been a major unresolved issue in the field of epigenetics. Repression requires the ... ...

Abstract	The mechanisms by which methylated mammalian promoters are transcriptionally silenced even in the presence of all of the factors required for their expression have long been a major unresolved issue in the field of epigenetics. Repression requires the assembly of a methylation-dependent silencing complex that contains the TRIM28 protein (also known as KAP1 and TIF1β), a scaffolding protein without intrinsic repressive or DNA-binding properties. The identity of the key effector within this complex that represses transcription is unknown. We developed a methylation-sensitized interaction screen which revealed that TRIM28 was complexed with
MeSH term(s)	Acetylglucosamine/metabolism ; Animals ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase 1/genetics ; DNA (Cytosine-5-)-Methyltransferase 1/metabolism ; DNA Methylation ; Epigenesis, Genetic ; Gene Silencing ; Glycosylation ; Humans ; Methylation ; N-Acetylglucosaminyltransferases ; Nuclear Proteins/metabolism ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Proteomics ; Repressor Proteins/metabolism ; Retroelements/physiology ; Transcription Factors/metabolism ; Tripartite Motif-Containing Protein 28/metabolism
Chemical Substances	Chromatin ; Nuclear Proteins ; Repressor Proteins ; Retroelements ; Transcription Factors ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNMT1 protein, human (EC 2.1.1.37) ; Tripartite Motif-Containing Protein 28 (EC 2.3.2.27) ; N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; UDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferase (EC 2.4.1.-) ; Acetylglucosamine (V956696549)
Language	English
Publishing date	2020-06-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1912074117
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Article: Accounting careers traversing the separate spheres of business and government in Victorian Britain

Black, John / Edwards, John R

Accounting history : journal of the Accounting History Special Interest Group of the Accounting Association of Australia and New Zealand Vol. 21, No. 2/3 , p. 306-328

2016 Volume 21, Issue 2, Page(s) 306–328

Author's details	John Black, John Richard Edwards
Keywords	accounting change ; biography ; military accounting ; professionalization
Language	English
Publisher	SAGE Publ.
Publishing place	Los Angeles [u.a.]
Document type	Article
ZDB-ID	1416503x ; 2211854-8
ISSN	1032-3732
ISSN	1032-3732
Database	ECONomics Information System

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Article ; Online: ME-Class2 reveals context dependent regulatory roles for 5-hydroxymethylcytosine.

Schlosberg, Christopher E / Wu, Dennis Y / Gabel, Harrison W / Edwards, John R

Nucleic acids research

2019 Volume 47, Issue 5, Page(s) e28

Abstract: Since the discovery of 5-hydroxymethylcytosine (5hmC) as a prominent DNA modification found in mammalian genomes, an emergent question has been what role this mark plays in gene regulation. 5hmC is hypothesized to function as an intermediate in the ... ...

Abstract	Since the discovery of 5-hydroxymethylcytosine (5hmC) as a prominent DNA modification found in mammalian genomes, an emergent question has been what role this mark plays in gene regulation. 5hmC is hypothesized to function as an intermediate in the demethylation of 5-methylcytosine (5mC) and in the reactivation of silenced promoters and enhancers. Further, weak positive correlations are observed between gene body 5hmC and gene expression. We previously demonstrated that ME-Class is an effective tool to understand relationships between whole-genome bisulfite sequencing data and expression. In this work, we present ME-Class2, a machine-learning based tool to perform integrative 5mCG, 5hmCG and expression analysis. Using ME-Class2 we analyze whole-genome single-base resolution 5mCG and 5hmCG datasets from 20 primary tissue and cell samples to reveal relationships between 5hmCG and expression. Our analysis indicates that conversion of 5mCG to 5hmCG within 2 kb of the transcription start site associates with distinct functions depending on the summed level of 5mCG + 5hmCG. Unchanged levels of 5mCG + 5hmCG (conversion from 5mCG to stable 5hmCG) associate with repression. Meanwhile, decreases in 5mCG + 5hmCG (5hmCG-mediated demethylation) associate with gene activation. Our results demonstrate that ME-Class2 will prove invaluable to interpret genome-wide 5mC and 5hmC datasets and guide mechanistic studies into the function of 5hmCG.
MeSH term(s)	5-Methylcytosine/analogs & derivatives ; 5-Methylcytosine/metabolism ; Animals ; Brain/metabolism ; Databases, Genetic ; Datasets as Topic ; Genes/genetics ; Genome/genetics ; Humans ; Machine Learning ; Methylation ; Mice ; Organ Specificity/genetics ; Promoter Regions, Genetic/genetics ; Sequence Analysis, RNA/methods ; Sulfites/chemistry ; Sulfites/metabolism
Chemical Substances	Sulfites ; 5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H) ; hydrogen sulfite (OJ9787WBLU)
Language	English
Publishing date	2019-02-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkz001
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Article ; Online: Breast Cancer Mutations HER2V777L and PIK3CAH1047R Activate the p21-CDK4/6-Cyclin D1 Axis to Drive Tumorigenesis and Drug Resistance.

Cheng, Xiaoqing / Sun, Yirui / Highkin, Maureen / Vemalapally, Nagalaxmi / Jin, Xiaohua / Zhou, Brandon / Prior, Julie L / Tipton, Ashley R / Li, Shunqiang / Iliuk, Anton / Achilefu, Samuel / Hagemann, Ian S / Edwards, John R / Bose, Ron

Cancer research

2023 Volume 83, Issue 17, Page(s) 2839–2857

Abstract: In metastatic breast cancer, HER2-activating mutations frequently co-occur with mutations in PIK3CA, TP53, or CDH1. Of these co-occurring mutations, HER2 and PIK3CA are the most commonly comutated gene pair, with approximately 40% of HER2-mutated breast ... ...

Abstract	In metastatic breast cancer, HER2-activating mutations frequently co-occur with mutations in PIK3CA, TP53, or CDH1. Of these co-occurring mutations, HER2 and PIK3CA are the most commonly comutated gene pair, with approximately 40% of HER2-mutated breast cancers also having activating mutations in PIK3CA. To study the effects of co-occurring HER2 and PIK3CA mutations, we generated genetically engineered mice with the HER2V777L; PIK3CAH1047R transgenes (HP mice) and studied the resulting breast cancers both in vivo as well as ex vivo using cancer organoids. HP breast cancers showed accelerated tumor formation in vivo and increased invasion and migration in in vitro assays. HP breast cancer cells were resistant to the pan-HER tyrosine kinase inhibitor, neratinib, but were effectively treated with neratinib plus the HER2-targeted antibody-drug conjugate trastuzumab deruxtecan. Proteomic and RNA-seq analysis of HP breast cancers identified increased gene expression of cyclin D1 and p21WAF1/Cip1 and changes in cell-cycle markers. Combining neratinib with CDK4/6 inhibitors was another effective strategy for treating HP breast cancers, with neratinib plus palbociclib showing a statistically significant reduction in development of mouse HP tumors as compared to either drug alone. The efficacy of both the neratinib plus trastuzumab deruxtecan and neratinib plus palbociclib combinations was validated using a human breast cancer patient-derived xenograft with very similar HER2 and PIK3CA mutations to the HP mice. Further, these two drug combinations effectively treated spontaneous lung metastasis in syngeneic mice transplanted with HP breast cancer organoids. This study provides valuable preclinical data to support the ongoing phase 1 clinical trials of these drug combinations in breast cancer. Significance: In HER2-mutated breast cancer, PIK3CA mutation activates p21-CDK4/6-cyclin D1 signaling to drive resistance to HER2-targeted therapies, which can be overcome using CDK4/6 inhibitors.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Transformation, Neoplastic ; Class I Phosphatidylinositol 3-Kinases/genetics ; Cyclin D1/genetics ; Cyclin-Dependent Kinase 4/genetics ; Drug Resistance, Neoplasm/genetics ; Mutation ; Proteomics ; Receptor, ErbB-2/metabolism
Chemical Substances	CDK4 protein, human (EC 2.7.11.22) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Cyclin D1 (136601-57-5) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Receptor, ErbB-2 (EC 2.7.10.1) ; PIK3CA protein, human (EC 2.7.1.137) ; ERBB2 protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-3558
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A human mitofusin 2 mutation can cause mitophagic cardiomyopathy.

Franco, Antonietta / Li, Jiajia / Kelly, Daniel P / Hershberger, Ray E / Marian, Ali J / Lewis, Renate M / Song, Moshi / Dang, Xiawei / Schmidt, Alina D / Mathyer, Mary E / Edwards, John R / Strong, Cristina de Guzman / Dorn, Gerald W

eLife

2023 Volume 12

Abstract: Cardiac muscle has the highest mitochondrial density of any human tissue, but mitochondrial dysfunction is not a recognized cause of isolated cardiomyopathy. Here, we determined that the rare mitofusin (MFN) 2 R400Q mutation is 15-20× over-represented in ...

Abstract	Cardiac muscle has the highest mitochondrial density of any human tissue, but mitochondrial dysfunction is not a recognized cause of isolated cardiomyopathy. Here, we determined that the rare mitofusin (MFN) 2 R400Q mutation is 15-20× over-represented in clinical cardiomyopathy, whereas this specific mutation is not reported as a cause of MFN2 mutant-induced peripheral neuropathy, Charcot-Marie-Tooth disease type 2A (CMT2A). Accordingly, we interrogated the enzymatic, biophysical, and functional characteristics of MFN2 Q400 versus wild-type and CMT2A-causing MFN2 mutants. All MFN2 mutants had impaired mitochondrial fusion, the canonical MFN2 function. Compared to MFN2 T105M that lacked catalytic GTPase activity and exhibited normal activation-induced changes in conformation, MFN2 R400Q and M376A had normal GTPase activity with impaired conformational shifting. MFN2 R400Q did not suppress mitochondrial motility, provoke mitochondrial depolarization, or dominantly suppress mitochondrial respiration like MFN2 T105M. By contrast to MFN2 T105M and M376A, MFN2 R400Q was uniquely defective in recruiting Parkin to mitochondria. CRISPR editing of the R400Q mutation into the mouse
MeSH term(s)	Pregnancy ; Female ; Humans ; Mice ; Animals ; Membrane Proteins/genetics ; Mitochondrial Proteins/genetics ; Mutation ; GTP Phosphohydrolases/genetics ; Cardiomyopathies/genetics ; Charcot-Marie-Tooth Disease/genetics
Chemical Substances	Membrane Proteins ; Mitochondrial Proteins ; GTP Phosphohydrolases (EC 3.6.1.-)
Language	English
Publishing date	2023-11-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.84235
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Book ; Online: Minority languages and group identity

Edwards, John R

cases and categories

(Impact ; 27)

2010

Abstract: The central concern in this book is the relationship between language and group identity, a relationship that is thrown into greatest relief in 'minority' settings. Since much of the current interest in minority languages revolves around issues of ... ...

Author's details	John Edwards
Series title	Impact ; 27
Abstract	The central concern in this book is the relationship between language and group identity, a relationship that is thrown into greatest relief in 'minority' settings. Since much of the current interest in minority languages revolves around issues of identity politics, language rights and the plight of 'endangered' languages, one aim of the book is to summarise and analyse these and other pivotal themes. Furthermore, since the uniqueness of every language-contact situation does not rest upon unique elements or features - but, rather, upon the particular weightings and combinations of features tha
Keywords	Language attrition ; Linguistic minorities
Language	English
Size	Online-Ressource (ix, 231 p)
Publisher	Benjamins
Publishing place	Amsterdam u.a.
Document type	Book ; Online
Note	Includes bibliographical references and index
ISBN	1282484907 ; 1282484974 ; 9781282484979 ; 9789027218667 ; 9789027288684 ; 9781282484900 ; 9027218668 ; 9027288682
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Determining subpopulation methylation profiles from bisulfite sequencing data of heterogeneous samples using DXM.

Fong, Jerry / Gardner, Jacob R / Andrews, Jared M / Cashen, Amanda F / Payton, Jacqueline E / Weinberger, Kilian Q / Edwards, John R

Nucleic acids research

2021 Volume 49, Issue 16, Page(s) e93

Abstract: Epigenetic changes, such as aberrant DNA methylation, contribute to cancer clonal expansion and disease progression. However, identifying subpopulation-level changes in a heterogeneous sample remains challenging. Thus, we have developed a computational ... ...

Abstract	Epigenetic changes, such as aberrant DNA methylation, contribute to cancer clonal expansion and disease progression. However, identifying subpopulation-level changes in a heterogeneous sample remains challenging. Thus, we have developed a computational approach, DXM, to deconvolve the methylation profiles of major allelic subpopulations from the bisulfite sequencing data of a heterogeneous sample. DXM does not require prior knowledge of the number of subpopulations or types of cells to expect. We benchmark DXM's performance and demonstrate improvement over existing methods. We further experimentally validate DXM predicted allelic subpopulation-methylation profiles in four Diffuse Large B-Cell Lymphomas (DLBCLs). Lastly, as proof-of-concept, we apply DXM to a cohort of 31 DLBCLs and relate allelic subpopulation methylation profiles to relapse. We thus demonstrate that DXM can robustly find allelic subpopulation methylation profiles that may contribute to disease progression using bisulfite sequencing data of any heterogeneous sample.
MeSH term(s)	Algorithms ; Cell Line, Tumor ; DNA Methylation ; Epigenomics/methods ; Epigenomics/standards ; Genetic Heterogeneity ; Humans ; Lymphoma, Large B-Cell, Diffuse/genetics ; Sequence Analysis, DNA/methods ; Sequence Analysis, DNA/standards
Language	English
Publishing date	2021-06-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkab516
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Article: Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10.

Boulard, Mathieu / Edwards, John R / Bestor, Timothy H

Epigenetics & chromatin

2016 Volume 9, Page(s) 22

Abstract: Background: Almost all CpG-rich promoters in the mammalian genome are bound by the multidomain FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1). FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal ... ...

Abstract	Background: Almost all CpG-rich promoters in the mammalian genome are bound by the multidomain FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1). FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal histone demethylase domain with C-terminal F-box, CXXC, PHD, RING, and leucine-rich repeat domains, and FBXL10-2, a shorter form that initiates at an alternative internal exon and which lacks the histone demethylase domain but retains all other annotated domains. Selective deletion of Fbxl10-1 had been reported to produce a low penetrance and variable phenotype; most of the mutant animals were essentially normal. We constructed mutant mouse strains that were either null for Fbxl10-2 but wild type for Fbxl10-1 or null for both Fbxl10-1 and Fbxl10-2. Results: Deletion of Fbxl10-2 (in a manner that does not perturb expression of Fbxl10-1) produced a phenotype very different from the Fbxl10-1 mutant, with craniofacial abnormalities, neural tube defects, and increased lethality, especially in females. Mutants that lacked both FBXL10-1 and FBXL10-2 showed embryonic lethality and even more extreme sexual dimorphism, with more severe gene dysregulation in mutant female embryos. X-linked genes were most severely dysregulated, and there was marked overexpression of Xist in mutant females although genes that encode factors that bind to Xist RNA were globally downregulated in mutant female as compared to male embryos. Conclusions: FBXL10 is the first factor shown to be required both for the normal expression and function of the Xist gene and for normal expression of proteins that associate with Xist RNA; it is proposed that FBXL10 coordinates the expression of Xist RNA with proteins that associate with this RNA. The function of FBXL10 is largely independent of the histone demethylase activity of the long form of the protein.
Language	English
Publishing date	2016
Publishing country	England
Document type	Journal Article
ZDB-ID	2462129-8
ISSN	1756-8935
ISSN	1756-8935
DOI	10.1186/s13072-016-0069-1
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