LIVIVO - Search results -

Search results

Result 1 - 10 of total 50

Search options

Article: The landscape of regional missense mutational intolerance quantified from 125,748 exomes.

Chao, Katherine R / Wang, Lily / Panchal, Ruchit / Liao, Calwing / Abderrazzaq, Haneen / Ye, Robert / Schultz, Patrick / Compitello, John / Grant, Riley H / Kosmicki, Jack A / Weisburd, Ben / Phu, William / Wilson, Michael W / Laricchia, Kristen M / Goodrich, Julia K / Goldstein, Daniel / Goldstein, Jacqueline I / Vittal, Christopher / Poterba, Timothy /

Baxter, Samantha / Watts, Nicholas A / Solomonson, Matthew / Tiao, Grace / Rehm, Heidi L / Neale, Benjamin M / Talkowski, Michael E / MacArthur, Daniel G / O'Donnell-Luria, Anne / Karczewski, Konrad J / Radivojac, Predrag / Daly, Mark J / Samocha, Kaitlin E

bioRxiv : the preprint server for biology

2024

Abstract: Missense variants can have a range of functional impacts depending on factors such as the specific amino acid substitution and location within the gene. To interpret their deleteriousness, studies have sought to identify regions within genes that are ... ...

Abstract	Missense variants can have a range of functional impacts depending on factors such as the specific amino acid substitution and location within the gene. To interpret their deleteriousness, studies have sought to identify regions within genes that are specifically intolerant of missense variation
Language	English
Publishing date	2024-04-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.11.588920
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: Discovery of rare variants for complex phenotypes.

Kosmicki, Jack A / Churchhouse, Claire L / Rivas, Manuel A / Neale, Benjamin M

Human genetics

2016 Volume 135, Issue 6, Page(s) 625–634

Abstract: With the rise of sequencing technologies, it is now feasible to assess the role rare variants play in the genetic contribution to complex trait variation. While some of the earlier targeted sequencing studies successfully identified rare variants of ... ...

Abstract	With the rise of sequencing technologies, it is now feasible to assess the role rare variants play in the genetic contribution to complex trait variation. While some of the earlier targeted sequencing studies successfully identified rare variants of large effect, unbiased gene discovery using exome sequencing has experienced limited success for complex traits. Nevertheless, rare variant association studies have demonstrated that rare variants do contribute to phenotypic variability, but sample sizes will likely have to be even larger than those of common variant association studies to be powered for the detection of genes and loci. Large-scale sequencing efforts of tens of thousands of individuals, such as the UK10K Project and aggregation efforts such as the Exome Aggregation Consortium, have made great strides in advancing our knowledge of the landscape of rare variation, but there remain many considerations when studying rare variation in the context of complex traits. We discuss these considerations in this review, presenting a broad range of topics at a high level as an introduction to rare variant analysis in complex traits including the issues of power, study design, sample ascertainment, de novo variation, and statistical testing approaches. Ultimately, as sequencing costs continue to decline, larger sequencing studies will yield clearer insights into the biological consequence of rare mutations and may reveal which genes play a role in the etiology of complex traits.
MeSH term(s)	Exome/genetics ; Genetic Predisposition to Disease ; Genetic Variation ; High-Throughput Nucleotide Sequencing ; Humans ; Mutation/genetics ; Phenotype
Language	English
Publishing date	2016-05-24
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	223009-4
ISSN	1432-1203 ; 0340-6717
ISSN (online)	1432-1203
ISSN	0340-6717
DOI	10.1007/s00439-016-1679-1
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 256: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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 ▾

Article ; Online: Author Correction: Transcript expression-aware annotation improves rare variant interpretation.

Cummings, Beryl B / Karczewski, Konrad J / Kosmicki, Jack A / Seaby, Eleanor G / Watts, Nicholas A / Singer-Berk, Moriel / Mudge, Jonathan M / Karjalainen, Juha / Satterstrom, F Kyle / O'Donnell-Luria, Anne H / Poterba, Timothy / Seed, Cotton / Solomonson, Matthew / Alföldi, Jessica / Daly, Mark J / MacArthur, Daniel G

Nature

2021 Volume 590, Issue 7846, Page(s) E54

Language	English
Publishing date	2021-02-03
Publishing country	England
Document type	Published Erratum
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-020-03175-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 9: Show issues
Zs.MO 244: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Applicability of the Mutation-Selection Balance Model to Population Genetics of Heterozygous Protein-Truncating Variants in Humans.

Weghorn, Donate / Balick, Daniel J / Cassa, Christopher / Kosmicki, Jack A / Daly, Mark J / Beier, David R / Sunyaev, Shamil R

Molecular biology and evolution

2019 Volume 36, Issue 8, Page(s) 1701–1710

Abstract: The fate of alleles in the human population is believed to be highly affected by the stochastic force of genetic drift. Estimation of the strength of natural selection in humans generally necessitates a careful modeling of drift including complex effects ...

Abstract	The fate of alleles in the human population is believed to be highly affected by the stochastic force of genetic drift. Estimation of the strength of natural selection in humans generally necessitates a careful modeling of drift including complex effects of the population history and structure. Protein-truncating variants (PTVs) are expected to evolve under strong purifying selection and to have a relatively high per-gene mutation rate. Thus, it is appealing to model the population genetics of PTVs under a simple deterministic mutation-selection balance, as has been proposed earlier (Cassa et al. 2017). Here, we investigated the limits of this approximation using both computer simulations and data-driven approaches. Our simulations rely on a model of demographic history estimated from 33,370 individual exomes of the Non-Finnish European subset of the ExAC data set (Lek et al. 2016). Additionally, we compared the African and European subset of the ExAC study and analyzed de novo PTVs. We show that the mutation-selection balance model is applicable to the majority of human genes, but not to genes under the weakest selection.
MeSH term(s)	Codon, Nonsense ; Genetic Drift ; Humans ; Models, Genetic ; Population Growth ; Selection, Genetic
Chemical Substances	Codon, Nonsense
Language	English
Publishing date	2019-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	998579-7
ISSN	1537-1719 ; 0737-4038
ISSN (online)	1537-1719
ISSN	0737-4038
DOI	10.1093/molbev/msz092
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 2137: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Converging evidence from exome sequencing and common variants implicates target genes for osteoporosis.

Zhou, Sirui / Sosina, Olukayode A / Bovijn, Jonas / Laurent, Laetitia / Sharma, Vasundhara / Akbari, Parsa / Forgetta, Vincenzo / Jiang, Lai / Kosmicki, Jack A / Banerjee, Nilanjana / Morris, John A / Oerton, Erin / Jones, Marcus / LeBlanc, Michelle G / Idone, Vincent / Overton, John D / Reid, Jeffrey G / Cantor, Michael / Abecasis, Goncalo R /

Goltzman, David / Greenwood, Celia M T / Langenberg, Claudia / Baras, Aris / Economides, Aris N / Ferreira, Manuel A R / Hatsell, Sarah / Ohlsson, Claes / Richards, J Brent / Lotta, Luca A

Nature genetics

2023 Volume 55, Issue 8, Page(s) 1277–1287

Abstract: In this study, we leveraged the combined evidence of rare coding variants and common alleles to identify therapeutic targets for osteoporosis. We undertook a large-scale multiancestry exome-wide association study for estimated bone mineral density, which ...

Abstract	In this study, we leveraged the combined evidence of rare coding variants and common alleles to identify therapeutic targets for osteoporosis. We undertook a large-scale multiancestry exome-wide association study for estimated bone mineral density, which showed that the burden of rare coding alleles in 19 genes was associated with estimated bone mineral density (P < 3.6 × 10
MeSH term(s)	Humans ; Genetic Predisposition to Disease ; Exome Sequencing ; Osteoporosis/genetics ; Bone Density/genetics ; Alleles ; Transcription Factors/genetics ; Genome-Wide Association Study
Chemical Substances	Transcription Factors
Language	English
Publishing date	2023-08-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-023-01444-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3613: 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 46: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Computationally efficient whole-genome regression for quantitative and binary traits.

Mbatchou, Joelle / Barnard, Leland / Backman, Joshua / Marcketta, Anthony / Kosmicki, Jack A / Ziyatdinov, Andrey / Benner, Christian / O'Dushlaine, Colm / Barber, Mathew / Boutkov, Boris / Habegger, Lukas / Ferreira, Manuel / Baras, Aris / Reid, Jeffrey / Abecasis, Goncalo / Maxwell, Evan / Marchini, Jonathan

Nature genetics

2021 Volume 53, Issue 7, Page(s) 1097–1103

Abstract: Genome-wide association analysis of cohorts with thousands of phenotypes is computationally expensive, particularly when accounting for sample relatedness or population structure. Here we present a novel machine-learning method called REGENIE for fitting ...

Abstract	Genome-wide association analysis of cohorts with thousands of phenotypes is computationally expensive, particularly when accounting for sample relatedness or population structure. Here we present a novel machine-learning method called REGENIE for fitting a whole-genome regression model for quantitative and binary phenotypes that is substantially faster than alternatives in multi-trait analyses while maintaining statistical efficiency. The method naturally accommodates parallel analysis of multiple phenotypes and requires only local segments of the genotype matrix to be loaded in memory, in contrast to existing alternatives, which must load genome-wide matrices into memory. This results in substantial savings in compute time and memory usage. We introduce a fast, approximate Firth logistic regression test for unbalanced case-control phenotypes. The method is ideally suited to take advantage of distributed computing frameworks. We demonstrate the accuracy and computational benefits of this approach using the UK Biobank dataset with up to 407,746 individuals.
MeSH term(s)	Case-Control Studies ; Computational Biology/methods ; Genome-Wide Association Study/methods ; Genomics/methods ; Genotype ; Humans ; Logistic Models ; Machine Learning ; Phenotype ; Reproducibility of Results
Language	English
Publishing date	2021-05-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-021-00870-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3613: 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 46: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: ERAP1, ERAP2, and Two Copies of HLA-Aw19 Alleles Increase the Risk for Birdshot Chorioretinopathy in HLA-A29 Carriers.

Gelfman, Sahar / Monnet, Dominique / Ligocki, Ann J / Tabary, Thierry / Moscati, Arden / Bai, Xiaodong / Freudenberg, Jan / Cooper, Blerta / Kosmicki, Jack A / Wolf, Sarah / Ferreira, Manuel A R / Overton, John / Weyne, Jonathan / Stahl, Eli A / Baras, Aris / Romano, Carmelo / Cohen, Jacques H M / Coppola, Giovanni / Brézin, Antoine

Investigative ophthalmology & visual science

2021 Volume 62, Issue 14, Page(s) 3

Abstract: Purpose: Birdshot chorioretinopathy (BSCR) is strongly associated with HLA-A29. This study was designed to elucidate the genetic modifiers of BSCR in HLA-A29 carriers.: Methods: We sequenced the largest BSCR cohort to date, including 286 cases and ... ...

Abstract	Purpose: Birdshot chorioretinopathy (BSCR) is strongly associated with HLA-A29. This study was designed to elucidate the genetic modifiers of BSCR in HLA-A29 carriers. Methods: We sequenced the largest BSCR cohort to date, including 286 cases and 108 HLA-A29-positive controls to determine genome-wide common and rare variant associations. We further typed the HLA alleles of cases and 45,386 HLA-A29 controls of European ancestry to identify HLA alleles that associate with BSCR risk. Results: Carrying a second allele that belongs to the HLA-Aw19 broad antigen family (including HLA-A29, -A30, -A31, and -A33) increases the risk for BSCR (odds ratio [OR] = 4.44; P = 2.2e-03). This result was validated by comparing allele frequencies to large HLA-A29-controlled cohorts (n = 45,386; OR > 2.5; P < 1.3e-06). We also confirm that ERAP1 and ERAP2 haplotypes modulate disease risk. A meta-analysis with an independent dataset confirmed that ERAP1 and ERAP2 haplotypes modulate the risk for disease at a genome-wide significant level: ERAP1-rs27432 (OR = 2.46; 95% confidence interval [CI], 1.85-3.26; P = 4.07e-10), an expression quantitative trait locus (eQTL) decreasing ERAP1 expression; and ERAP2-rs10044354 (OR = 1.95; 95% CI, 1.55-2.44; P = 6.2e-09), an eQTL increasing ERAP2 expression. Furthermore, ERAP2-rs2248374 that disrupts ERAP2 expression is protective (OR = 0.56; 95% CI, 0.45-0.70; P = 2.39e-07). BSCR risk is additively increased when combining ERAP1/ERAP2 risk genotypes with two copies of HLA-Aw19 alleles (OR = 13.53; 95% CI, 3.79-54.77; P = 1.17e-05). Conclusions: The genetic factors increasing BSCR risk demonstrate a pattern of increased processing, as well as increased presentation of ERAP2-specific peptides. This suggests a mechanism in which exceeding a peptide presentation threshold activates the immune response in choroids of A29 carriers.
MeSH term(s)	Alleles ; Aminopeptidases/genetics ; Birdshot Chorioretinopathy/diagnosis ; Birdshot Chorioretinopathy/genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotyping Techniques ; HLA-A Antigens/genetics ; Haplotypes ; Heterozygote ; Humans ; Minor Histocompatibility Antigens/genetics ; Multiplex Polymerase Chain Reaction ; Odds Ratio ; Polymorphism, Single Nucleotide ; Risk Factors
Chemical Substances	HLA-A Antigens ; HLA-A19 antigen ; HLA-A29 antigen ; Minor Histocompatibility Antigens ; Aminopeptidases (EC 3.4.11.-) ; ERAP1 protein, human (EC 3.4.11.-) ; ERAP2 protein, human (EC 3.4.11.-)
Language	English
Publishing date	2021-11-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.62.14.3
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 45: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Transcript expression-aware annotation improves rare variant interpretation.

Nature

2020 Volume 581, Issue 7809, Page(s) 452–458

Abstract: The acceleration of DNA sequencing in samples from patients and population studies has resulted in extensive catalogues of human genetic variation, but the interpretation of rare genetic variants remains problematic. A notable example of this challenge ... ...

Abstract	The acceleration of DNA sequencing in samples from patients and population studies has resulted in extensive catalogues of human genetic variation, but the interpretation of rare genetic variants remains problematic. A notable example of this challenge is the existence of disruptive variants in dosage-sensitive disease genes, even in apparently healthy individuals. Here, by manual curation of putative loss-of-function (pLoF) variants in haploinsufficient disease genes in the Genome Aggregation Database (gnomAD)
MeSH term(s)	Autism Spectrum Disorder/genetics ; Datasets as Topic ; Developmental Disabilities/genetics ; Disease/genetics ; Exons/genetics ; Female ; Genotype ; Haploinsufficiency/genetics ; Humans ; Intellectual Disability/genetics ; Loss of Function Mutation/genetics ; Male ; Molecular Sequence Annotation/standards ; Poisson Distribution ; RNA, Messenger/analysis ; RNA, Messenger/genetics ; Rare Diseases/diagnosis ; Rare Diseases/genetics ; Reproducibility of Results ; Transcription, Genetic ; Transcriptome/genetics ; Exome Sequencing
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2020-05-27
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-020-2329-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 9: Show issues
Zs.MO 244: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Author Correction: Predicting the clinical impact of human mutation with deep neural networks.

Sundaram, Laksshman / Gao, Hong / Padigepati, Samskruthi Reddy / McRae, Jeremy F / Li, Yanjun / Kosmicki, Jack A / Fritzilas, Nondas / Hakenberg, Jörg / Dutta, Anindita / Shon, John / Xu, Jinbo / Batzoglou, Serafim / Li, Xiaolin / Farh, Kyle Kai-How

Nature genetics

2018 Volume 51, Issue 2, Page(s) 364

Abstract: In the version of this article originally published, the name of author Serafim Batzoglou was misspelled. The error has been corrected in the HTML and PDF versions of the article. ...

Abstract	In the version of this article originally published, the name of author Serafim Batzoglou was misspelled. The error has been corrected in the HTML and PDF versions of the article.
Language	English
Publishing date	2018-12-17
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-018-0329-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3613: 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 46: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Loss of heterozygosity of essential genes represents a widespread class of potential cancer vulnerabilities.

Nichols, Caitlin A / Gibson, William J / Brown, Meredith S / Kosmicki, Jack A / Busanovich, John P / Wei, Hope / Urbanski, Laura M / Curimjee, Naomi / Berger, Ashton C / Gao, Galen F / Cherniack, Andrew D / Dhe-Paganon, Sirano / Paolella, Brenton R / Beroukhim, Rameen

Nature communications

2020 Volume 11, Issue 1, Page(s) 2517

Abstract: Alterations in non-driver genes represent an emerging class of potential therapeutic targets in cancer. Hundreds to thousands of non-driver genes undergo loss of heterozygosity (LOH) events per tumor, generating discrete differences between tumor and ... ...

Abstract	Alterations in non-driver genes represent an emerging class of potential therapeutic targets in cancer. Hundreds to thousands of non-driver genes undergo loss of heterozygosity (LOH) events per tumor, generating discrete differences between tumor and normal cells. Here we interrogate LOH of polymorphisms in essential genes as a novel class of therapeutic targets. We hypothesized that monoallelic inactivation of the allele retained in tumors can selectively kill cancer cells but not somatic cells, which retain both alleles. We identified 5664 variants in 1278 essential genes that undergo LOH in cancer and evaluated the potential for each to be targeted using allele-specific gene-editing, RNAi, or small-molecule approaches. We further show that allele-specific inactivation of either of two essential genes (PRIM1 and EXOSC8) reduces growth of cells harboring that allele, while cells harboring the non-targeted allele remain intact. We conclude that LOH of essential genes represents a rich class of non-driver cancer vulnerabilities.
MeSH term(s)	Alleles ; Cell Proliferation ; DNA Primase/genetics ; Exosome Multienzyme Ribonuclease Complex/genetics ; Genes, Essential ; Humans ; Loss of Heterozygosity ; Models, Genetic ; Neoplasms/genetics ; Neoplasms/physiopathology ; RNA-Binding Proteins/genetics
Chemical Substances	RNA-Binding Proteins ; DNA Primase (EC 2.7.7.-) ; PRIM1 protein, human (EC 2.7.7.-) ; EXOSC8 protein, human (EC 3.1.-) ; Exosome Multienzyme Ribonuclease Complex (EC 3.1.-)
Language	English
Publishing date	2020-05-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-16399-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Inter-library loan at ZB MED

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

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

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

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito