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Article: The 10th Santorini conference: Systems medicine, personalised health and therapy. "The odyssey from hope to practice: Patient first.

Visvikis-Siest, Sophie / Stathopoulou, Maria G / Sunder-Plassmann, Raute / Alizadeh, Behrooz Z / Barouki, Robert / Chatzaki, Ekaterina / Dagher, Georges / Dedoussis, George / Deloukas, Panagiotis / Haliassos, Alexander / Hiegel, Brigitte Boisson / Manolopoulos, Vangelis / Masson, Christine / Paré, Guillaume / Paulmichl, Markus / Petrelis, Alexandros M / Sipeky, Csilla / Süsleyici, Belgin / Weryha, Georges /

Chenchik, Alex / Diehl, Paul / Everts, Robin E / Haushofer, Alexander / Lamont, John / Mercado, Ruth / Meyer, Heiko / Munoz-Galeano, Herna / Murray, Helena / Nhat, Ferrier / Nofziger, Charity / Schnitzel, Wolfgang / Kanoni, Stavroula

Frontiers in genetics

2023 Volume 14, Page(s) 1171131

Language	English
Publishing date	2023-03-09
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2023.1171131
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Article: Effect of Genetic Variability in the

Zhang, J E / Klein, Kathrin / Jorgensen, Andrea L / Francis, Ben / Alfirevic, Ana / Bourgeois, Stephane / Deloukas, Panagiotis / Zanger, Ulrich M / Pirmohamed, Munir

Frontiers in pharmacology

2017 Volume 8, Page(s) 323

Abstract: Genetic polymorphisms in the gene encoding cytochrome P450 (CYP) 4F2, a vitamin K oxidase, affect stable warfarin dose requirements and time to therapeutic INR. ...

Abstract	Genetic polymorphisms in the gene encoding cytochrome P450 (CYP) 4F2, a vitamin K oxidase, affect stable warfarin dose requirements and time to therapeutic INR.
Language	English
Publishing date	2017-05-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2017.00323
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Article ; Online: Epigenome-Wide Association Study (EWAS) of Blood Lipids in Healthy Population from STANISLAS Family Study (SFS).

Xie, Ting / Gorenjak, Vesna / G Stathopoulou, Maria / Dadé, Sébastien / Marouli, Eirini / Masson, Christine / Murray, Helena / Lamont, John / Fitzgerald, Peter / Deloukas, Panagiotis / Visvikis-Siest, Sophie

International journal of molecular sciences

2019 Volume 20, Issue 5

Abstract: Epigenome-Wide Association Studies (EWAS) are furthering our knowledge of epigenetic modifications involved in the regulation of lipids' metabolism. Furthermore, epigenetic patterns associated with lipid levels may play an important role in predicting ... ...

Abstract	Epigenome-Wide Association Studies (EWAS) are furthering our knowledge of epigenetic modifications involved in the regulation of lipids' metabolism. Furthermore, epigenetic patterns associated with lipid levels may play an important role in predicting the occurrence of cardiovascular events. To further investigate the relationship between methylation status and lipids, we performed an EWAS in 211 individuals from the STANISLAS Family study (SFS). Methylation at two CpG sites (
MeSH term(s)	Adipose Tissue/metabolism ; Computational Biology ; CpG Islands/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic ; Family ; Genetic Variation ; Genome-Wide Association Study ; Humans ; Lipids/blood ; Promoter Regions, Genetic/genetics ; Reproducibility of Results
Chemical Substances	Lipids
Language	English
Publishing date	2019-02-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20051014
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Article ; Online: A histone map of human chromosome 20q13.12.

Akan, Pelin / Sahlén, Martin / Deloukas, Panagiotis

PloS one

2009 Volume 4, Issue 2, Page(s) e4479

Abstract: Background: We present a systematic search for regulatory elements in a 3.5 Mb region on human chromosome 20q13.12, a region associated with a number of medical conditions such as type II diabetes and obesity.: Methodology/principal findings: We ... ...

Abstract	Background: We present a systematic search for regulatory elements in a 3.5 Mb region on human chromosome 20q13.12, a region associated with a number of medical conditions such as type II diabetes and obesity. Methodology/principal findings: We profiled six histone modifications alongside RNA polymerase II (PolII) and CTCF in two cell lines, HeLa S3 and NTERA-2 clone D1 (NT2/D1), by chromatin immunoprecipitation using an in-house spotted DNA array, constructed with 1.8 kb overlapping plasmid clones. In both cells, more than 90% of transcription start sites (TSSs) of expressed genes showed enrichments with PolII, di-methylated lysine 4 of histone H3 (H3K4me2), tri-methylated lysine 4 of histone H3 (H3K4me3) or acetylated H3 (H3Ac), whereas mono-methylated lysine 4 of histone H3 (H3K4me1) signals did not correlate with expression. No TSSs were enriched with tri-methylated lysine 27 of histone H3 (H3K27me3) in HeLa S3, while eight TSSs (4 expressed) showed enrichments in NT2/D1. We have also located several CTCF binding sites that are potential insulator elements. Conclusions/significance: In summary, we annotated a number of putative regulatory elements in 20q13.12 and went on to verify experimentally a subset of them using dual luciferase reporter assays. Correlating this data to sequence variation can aid identification of disease causing variants.
MeSH term(s)	CCCTC-Binding Factor ; Cell Line ; Chromatin Immunoprecipitation ; Chromosome Mapping/methods ; Chromosomes, Human, Pair 20 ; DNA-Binding Proteins/analysis ; Enhancer Elements, Genetic ; Histones ; Humans ; Methylation ; RNA Polymerase II/analysis ; Repressor Proteins/analysis
Chemical Substances	CCCTC-Binding Factor ; CTCF protein, human ; DNA-Binding Proteins ; Histones ; Repressor Proteins ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2009-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0004479
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Article ; Online: Concordance for clonal hematopoiesis is limited in elderly twins.

Fabre, Margarete A / McKerrell, Thomas / Zwiebel, Maximillian / Vijayabaskar, M S / Park, Naomi / Wells, Philippa M / Rad, Roland / Deloukas, Panagiotis / Small, Kerrin / Steves, Claire J / Vassiliou, George S

Blood

2019 Volume 135, Issue 4, Page(s) 269–273

Abstract: Although acquisition of leukemia-associated somatic mutations by 1 or more hematopoietic stem cells is inevitable with advancing age, its consequences are highly variable, ranging from clinically silent clonal hematopoiesis (CH) to leukemic progression. ... ...

Abstract	Although acquisition of leukemia-associated somatic mutations by 1 or more hematopoietic stem cells is inevitable with advancing age, its consequences are highly variable, ranging from clinically silent clonal hematopoiesis (CH) to leukemic progression. To investigate the influence of heritable factors on CH, we performed deep targeted sequencing of blood DNA from 52 monozygotic (MZ) and 27 dizygotic (DZ) twin pairs (aged 70-99 years). Using this highly sensitive approach, we identified CH (variant allele frequency ≥0.5%) in 62% of individuals. We did not observe higher concordance for CH within MZ twin pairs as compared with that within DZ twin pairs, or to that expected by chance. However, we did identify 2 MZ pairs in which both twins harbored identical rare somatic mutations, suggesting a shared cell of origin. Finally, in 3 MZ twin pairs harboring mutations in the same driver genes, serial blood samples taken 4 to 5 years apart showed substantial twin-to-twin variability in clonal trajectories. Our findings propose that the inherited genome does not exert a dominant influence on the behavior of adult CH and provide evidence that CH mutations may be acquired in utero.
MeSH term(s)	Aged ; Aged, 80 and over ; Cohort Studies ; Diseases in Twins/genetics ; Female ; Hematopoiesis ; Humans ; Leukemia/genetics ; Male ; Mutation ; Twins/genetics ; Twins, Dizygotic/genetics ; Twins, Monozygotic/genetics
Language	English
Publishing date	2019-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2019001807
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Article ; Online: Genome-wide survey of copy number variants finds MAPT duplications in progressive supranuclear palsy.

Chen, Zhongbo / Chen, Jason A / Shatunov, Aleksey / Jones, Ashley R / Kravitz, Stephanie N / Huang, Alden Y / Lawrence, Lauren / Lowe, Jennifer K / Lewis, Cathryn M / Payan, Christine A M / Lieb, Wolfgang / Franke, Andre / Deloukas, Panagiotis / Amouyel, Philippe / Tzourio, Christophe / Dartigues, Jean-François / Ludolph, Albert / Bensimon, Gilbert / Leigh, P Nigel /

Bronstein, Jeff M / Coppola, Giovanni / Geschwind, Daniel H / Al-Chalabi, Ammar

Movement disorders : official journal of the Movement Disorder Society

2019 Volume 34, Issue 7, Page(s) 1049–1059

Abstract: Background: Progressive supranuclear palsy is a neurodegenerative tauopathy manifesting clinically as a progressive akinetic-rigid syndrome. In this study, we sought to identify genetic variants influencing PSP susceptibility through a genome-wide ... ...

Abstract	Background: Progressive supranuclear palsy is a neurodegenerative tauopathy manifesting clinically as a progressive akinetic-rigid syndrome. In this study, we sought to identify genetic variants influencing PSP susceptibility through a genome-wide association analysis of a cohort of well-characterized patients who had participated in the Neuroprotection and Natural History in Parkinson Plus Syndromes and Blood Brain Barrier in Parkinson Plus Syndromes studies. Methods: We genotyped single-nucleotide polymorphisms in 283 PSP cases from the United Kingdom, Germany, and France and compared these with genotypes from 4472 controls. Copy number variants were identified from genotyping data. Results: We observed associations on chromosome 17 within or close to the MAPT gene and explored the genetic architecture at this locus. We confirmed the previously reported association of rs1768208 in the MOBP gene (P = 3.29 × 10 Conclusions: Clinicians should also be aware of MAPT duplication as a possible genetic cause of PSP, especially in patients presenting with young age at onset. © 2019 International Parkinson and Movement Disorder Society.
MeSH term(s)	Adult ; Age of Onset ; Aged ; Aged, 80 and over ; DNA Copy Number Variations/genetics ; Female ; Genome-Wide Association Study ; Genotype ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Supranuclear Palsy, Progressive/genetics ; tau Proteins/genetics
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2019-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.27702
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Article ; Online: Data analysis issues for allele-specific expression using Illumina's GoldenGate assay

Dermitzakis Emmanouil T / Daelemans Caroline / Dimas Antigone S / Forrest Matthew S / Ritchie Matthew E / Deloukas Panagiotis / Tavaré Simon

BMC Bioinformatics, Vol 11, Iss 1, p

2010 Volume 280

Abstract: Abstract Background High-throughput measurement of allele-specific expression (ASE) is a relatively new and exciting application area for array-based technologies. In this paper, we explore several data sets which make use of Illumina's GoldenGate ... ...

Abstract	Abstract Background High-throughput measurement of allele-specific expression (ASE) is a relatively new and exciting application area for array-based technologies. In this paper, we explore several data sets which make use of Illumina's GoldenGate BeadArray technology to measure ASE. This platform exploits coding SNPs to obtain relative expression measurements for alleles at approximately 1500 positions in the genome. Results We analyze data from a mixture experiment where genomic DNA samples from pairs of individuals of known genotypes are pooled to create allelic imbalances at varying levels for the majority of SNPs on the array. We observe that GoldenGate has less sensitivity at detecting subtle allelic imbalances (around 1.3 fold) compared to extreme imbalances, and note the benefit of applying local background correction to the data. Analysis of data from a dye-swap control experiment allowed us to quantify dye-bias, which can be reduced considerably by careful normalization. The need to filter the data before carrying out further downstream analysis to remove non-responding probes, which show either weak, or non-specific signal for each allele, was also demonstrated. Throughout this paper, we find that a linear model analysis of the data from each SNP is a flexible modelling strategy that allows for testing of allelic imbalances in each sample when replicate hybridizations are available. Conclusions Our analysis shows that local background correction carried out by Illumina's software, together with quantile normalization of the red and green channels within each array, provides optimal performance in terms of false positive rates. In addition, we strongly encourage intensity-based filtering to remove SNPs which only measure non-specific signal. We anticipate that a similar analysis strategy will prove useful when quantifying ASE on Illumina's higher density Infinium BeadChips.
Keywords	Computer applications to medicine. Medical informatics ; R858-859.7 ; Biology (General) ; QH301-705.5
Subject code	310
Language	English
Publishing date	2010-05-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Evaluating the glucose raising effect of established loci via a genetic risk score.

Marouli, Eirini / Kanoni, Stavroula / Mamakou, Vasiliki / Hackinger, Sophie / Southam, Lorraine / Prins, Bram / Rentari, Angela / Dimitriou, Maria / Zengini, Eleni / Gonidakis, Fragiskos / Kolovou, Genovefa / Kontaxakis, Vassilis / Rallidis, Loukianos / Tentolouris, Nikolaos / Thanopoulou, Anastasia / Lamnissou, Klea / Dedoussis, George / Zeggini, Eleftheria / Deloukas, Panagiotis

PloS one

2017 Volume 12, Issue 11, Page(s) e0186669

Abstract: Recent genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with glucose levels. We tested the hypothesis here whether the cumulative effect of glucose raising SNPs, assessed via a score, is associated ...

Abstract	Recent genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with glucose levels. We tested the hypothesis here whether the cumulative effect of glucose raising SNPs, assessed via a score, is associated with glucose levels. A total of 1,434 participants of Greek descent from the THISEAS study and 1,160 participants form the GOMAP study were included in this analysis. We developed a genetic risk score (GRS), based on the known glucose-raising loci, in order to investigate the cumulative effect of known glucose loci on glucose levels. In the THISEAS study, the GRS score was significantly associated with increased glucose levels (mmol/L) (β ± SE: 0.024 ± 0.004, P = 8.27e-07). The effect of the genetic risk score was also significant in the GOMAP study (β ± SE: 0.011 ± 0.005, P = 0.031). In the meta-analysis of the two studies both scores were significantly associated with higher glucose levels GRS: β ± SE: 0.019 ± 0.003, P = 1.41e-09. Also, variants at the SLC30A8, PROX1, MTNR1B, ADRA2A, G6PC2, LPIN3 loci indicated nominal evidence for association with glucose levels (p < 0.05). We replicate associations of the established glucose raising variants in the Greek population and confirm directional consistency of effects (binomial sign test p = 6.96e-05). We also demonstrate that the cumulative effect of the established glucose loci yielded a significant association with increasing glucose levels.
MeSH term(s)	Blood Glucose/metabolism ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Male ; Polymorphism, Single Nucleotide
Chemical Substances	Blood Glucose
Language	English
Publishing date	2017-11-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0186669
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Article: Potential Interplay between Dietary Saturated Fats and Genetic Variants of the NLRP3 Inflammasome to Modulate Insulin Resistance and Diabetes Risk: Insights from a Meta‐Analysis of 19 005 Individuals

Murphy, Aoife M / Smith, Caren E / Murphy, Leanne M / Follis, Jack L / Tanaka, Toshiko / Richardson, Kris / Noordam, Raymond / Lemaitre, Rozenn N / Kähönen, Mika / Dupuis, Josée / Voortman, Trudy / Marouli, Eirini / Mook‐Kanamori, Dennis O / Raitakari, Olli T / Hong, Jaeyoung / Dehghan, Abbas / Dedoussis, George / de Mutsert, Renée / Lehtimäki, Terho /

Liu, Ching‐Ti / Rivadeneira, Fernando / Deloukas, Panagiotis / Mikkilä, Vera / Meigs, James B / Uitterlinden, Andre / Ikram, Mohammad A / Franco, Oscar H / Hughes, Maria / O' Gaora, Peadar / Ordovás, José M / Roche, Helen M

Molecular nutrition & food research. 2019 Nov., v. 63, no. 22

2019

Abstract: SCOPE: Insulin resistance (IR) and inflammation are hallmarks of type 2 diabetes (T2D). The nod‐like receptor pyrin domain containing‐3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL‐1β inflammation and ... ...

Abstract	SCOPE: Insulin resistance (IR) and inflammation are hallmarks of type 2 diabetes (T2D). The nod‐like receptor pyrin domain containing‐3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL‐1β inflammation and IR. Interactions between SFA intake and NLRP3‐related genetic variants may alter T2D risk factors. METHODS: Meta‐analyses of six Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (n = 19 005) tested interactions between SFA and NLRP3‐related single‐nucleotide polymorphisms (SNPs) and modulation of fasting insulin, fasting glucose, and homeostasis model assessment of insulin resistance. RESULTS: SFA interacted with rs12143966, wherein each 1% increase in SFA intake increased insulin by 0.0063 IU mL−1 (SE ± 0.002, p = 0.001) per each major (G) allele copy. rs4925663, interacted with SFA (β ± SE = −0.0058 ± 0.002, p = 0.004) to increase insulin by 0.0058 IU mL−1, per additional copy of the major (C) allele. Both associations are close to the significance threshold (p < 0.0001). rs4925663 causes a missense mutation affecting NLRP3 expression. CONCLUSION: Two NLRP3‐related SNPs showed potential interaction with SFA to modulate fasting insulin. Greater dietary SFA intake accentuates T2D risk, which, subject to functional validation, may be further elaborated depending on NLRP3‐related genetic variants.
Keywords	alleles ; epidemiology ; fasting ; genetic variation ; genomics ; glucose ; heart ; homeostasis ; inflammasomes ; inflammation ; insulin ; insulin resistance ; interleukin-1beta ; meta-analysis ; missense mutation ; noninsulin-dependent diabetes mellitus ; risk factors ; saturated fats ; saturated fatty acids ; single nucleotide polymorphism
Language	English
Dates of publication	2019-11
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	JOURNAL ARTICLE
ZDB-ID	2160372-8
ISSN	1613-4133 ; 1613-4125
ISSN (online)	1613-4133
ISSN	1613-4125
DOI	10.1002/mnfr.201900226
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Article: The 9th Santorini Conference: Systems Medicine, Personalised Health and Therapy. "The Odyssey from Hope to Practice", Santorini, Greece, 30 September⁻3 October 2018.

Journal of personalized medicine

2018 Volume 8, Issue 4

Abstract: The 9th traditional biannual conference on Systems Medicine, Personalised Health & Therapy-"The Odyssey from Hope to Practice", inspired by the Greek mythology, was a call to search for practical solutions in cardio-metabolic diseases and cancer, to ... ...

Abstract	The 9th traditional biannual conference on Systems Medicine, Personalised Health & Therapy-"The Odyssey from Hope to Practice", inspired by the Greek mythology, was a call to search for practical solutions in cardio-metabolic diseases and cancer, to resolve and overcome the obstacles in modern medicine by creating more interactions among disciplines, as well as between academic and industrial research, directed towards an effective 'roadmap' for personalised health and therapy. The 9th Santorini Conference, under the Presidency of Sofia Siest, the director of the INSERM U1122; IGE-PCV (www.u1122.inserm.fr), University of Lorraine, France, offered a rich and innovative scientific program. It gathered 34 worldwide distinguished speakers, who shared their passion for personalised medicine with 160 attendees in nine specific sessions on the following topics: First day: The Odyssey from hope to practice: Personalised medicine-landmarks and challenges Second day: Diseases to therapeutics-genotype to phenotype an "-OMICS" approach: focus on personalised therapy and precision medicine Third day: Gene-environment interactions and pharmacovigilance: a pharmacogenetics approach for deciphering disease "bench to clinic to reality" Fourth day: Pharmacogenomics to drug discovery: a big data approach and focus on clinical data and clinical practice. In this article we present the topics shared among the participants of the conference and we highlight the key messages.
Language	English
Publishing date	2018-12-12
Publishing country	Switzerland
Document type	Congress
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm8040043
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