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Article ; Online: Mechanistic dissection unmasks colibactin as a prevalent mutagenic driver of cancer.

Berger, Hilmar / Meyer, Thomas F

2021 Volume 39, Issue 11, Page(s) 1439–1441

Abstract: Gut colonization by colibactin-producing bacteria is associated with colorectal cancer. A mutational signature of this genotoxin in human cancer indicates causality but only partially accounts for cell transformation. Instead, the failure of adequately ... ...

Abstract	Gut colonization by colibactin-producing bacteria is associated with colorectal cancer. A mutational signature of this genotoxin in human cancer indicates causality but only partially accounts for cell transformation. Instead, the failure of adequately resolving DNA damage causes genomic aberrations and chromosomal instability, constituting the main starting point for colibactin-driven cancer.
MeSH term(s)	Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/genetics ; Chromosome Aberrations ; Colorectal Neoplasms/chemically induced ; Colorectal Neoplasms/genetics ; DNA Damage ; Humans ; Mutation ; Peptides/toxicity ; Polyketides/toxicity
Chemical Substances	Peptides ; Polyketides ; colibactin
Language	English
Publishing date	2021-11-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2021.10.010
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Zs.A 5650: 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)
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Article ; Online: Advancing one health in our communities.

Meyer, Thomas F

Journal of the American Veterinary Medical Association

2017 Volume 250, Issue 3, Page(s) 240

MeSH term(s)	Animals ; Animals, Domestic ; Animals, Wild ; Food Supply ; Global Health ; Health Promotion ; Humans ; Societies, Scientific/organization & administration ; United States ; Veterinary Medicine/organization & administration
Language	English
Publishing date	2017-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	390811-2
ISSN	1943-569X ; 0003-1488
ISSN (online)	1943-569X
ISSN	0003-1488
DOI	10.2460/javma.250.3.240
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Article: The Sweeping Role of Cholesterol Depletion in the Persistence of Helicobacter pylori Infections.

Morey, Pau / Meyer, Thomas F

Current topics in microbiology and immunology

2019 Volume 421, Page(s) 209–227

Abstract: The ability of Helicobacter pylori to persist lifelong in the human gastric mucosa is a striking phenomenon. It is even more surprising since infection is typically associated with a vivid inflammatory response. Recent studies revealed the mechanism by ... ...

Abstract	The ability of Helicobacter pylori to persist lifelong in the human gastric mucosa is a striking phenomenon. It is even more surprising since infection is typically associated with a vivid inflammatory response. Recent studies revealed the mechanism by which this pathogen inhibits the epithelial responses to IFN-γ and other central inflammatory cytokines in order to abolish an effective antimicrobial defense. The mechanism is based on the modification and depletion of cholesterol by the pathogen's cholesterol-α-glucosyltransferase. It abrogates the assembly of numerous cytokine receptors due to the reduction of lipid rafts. Particularly, the receptors for IFN-γ, IL-22, and IL-6 then fail to assemble properly and to activate JAK/STAT signaling. Consequently, cholesterol depletion prevents the release of antimicrobial peptides, including the highly effective β-defensin-3. Intriguingly, the inhibition is spatially restricted to heavily infected cells, while the surrounding epithelium continues to respond normally to cytokine stimulation, thus providing a platform of the intense inflammation typically observed in H. pylori infections. It appears that pathogen and host establish a homeostatic balance between tightly colonized and rather inflamed sites. This homeostasis is influenced by the levels of available cholesterol, which potentially exacerbate H. pylori-induced inflammation. The observed blockage of epithelial effector mechanisms by H. pylori constitutes a convincing explanation for the previous failures of T-cell-based vaccination against H. pylori, since infected epithelial cells remain inert upon stimulation by effector cytokines. Moreover, the mechanism provides a rationale for the carcinogenic action of this pathogen in that persistent infection and chronic inflammation represent a pro-carcinogenic environment. Thus, cholesterol-α-glucosyltransferase has been revealed as a central pathogenesis determinant of H. pylori.
MeSH term(s)	Cholesterol/deficiency ; Cholesterol/metabolism ; Epithelial Cells/microbiology ; Gastric Mucosa/microbiology ; Glucosyltransferases/metabolism ; Helicobacter Infections/blood ; Helicobacter Infections/metabolism ; Helicobacter Infections/microbiology ; Helicobacter pylori/enzymology ; Helicobacter pylori/pathogenicity ; Humans
Chemical Substances	Cholesterol (97C5T2UQ7J) ; Glucosyltransferases (EC 2.4.1.-) ; Hp0421 protein, Helicobacter pylori (EC 2.4.1.-)
Language	English
Publishing date	2019-05-23
Publishing country	Germany
Document type	Journal Article
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-030-15138-6_9
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Book ; Online ; Thesis: Mechanistic regulation of gastroesophageal junction and role of retinoic acid in the development of Barrett's esophagus

Nirchal, Naveen Kumar [Verfasser] / Chumduri, Cindrilla [Gutachter] / Engstler, Markus [Gutachter] / Meyer, Thomas F. [Gutachter] / Seyfried, Florian [Gutachter]

2024

Author's details	Naveen Kumar Nirchal ; Gutachter: Cindrilla Chumduri, Markus Engstler, Thomas F. Meyer, Florian Seyfried
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Publisher	Universität Würzburg
Publishing place	Würzburg
Document type	Book ; Online ; Thesis
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Article ; Online: Patient-derived and mouse endo-ectocervical organoid generation, genetic manipulation and applications to model infection.

Gurumurthy, Rajendra Kumar / Koster, Stefanie / Kumar, Naveen / Meyer, Thomas F / Chumduri, Cindrilla

Nature protocols

2022 Volume 17, Issue 7, Page(s) 1658–1690

Abstract: The cervix is the gateway to the upper female reproductive tract, connecting the uterus and vagina. It plays crucial roles in fertility and pregnancy maintenance from onset until delivery of the fetus, and prevents pathogen ascension. Compromised ... ...

Abstract	The cervix is the gateway to the upper female reproductive tract, connecting the uterus and vagina. It plays crucial roles in fertility and pregnancy maintenance from onset until delivery of the fetus, and prevents pathogen ascension. Compromised functionality of the cervix can lead to disorders, including infertility, chronic infections and cancers. The cervix comprises two regions: columnar epithelium-lined endocervix and stratified squamous epithelium-lined ectocervix, meeting at the squamocolumnar transition zone. So far, two-dimensional cultures of genetically unstable immortalized or cancer cell lines have been primarily used to study cervix biology in vitro. The lack of an in vitro system that reflects the cellular, physiological and functional properties of the two epithelial types has hampered the study of normal physiology, disease development and infection processes. Here we describe a protocol for cell isolation, establishment, long-term culture and expansion of adult epithelial stem cell-derived endocervical and ectocervical organoids from human biopsies and mouse tissue. These two organoid types require unique combinations of growth factors reminiscent of their in vivo tissue niches and different culturing procedures. They recapitulate native three-dimensional tissue architecture and patterning. The protocol to generate these organoids takes 4-6 weeks. We also describe procedures to introduce human papillomavirus oncogenes into the cervical stem cells by genetic manipulation to model cervical cancer and infection of the organoids with the highly prevalent sexually transmitted bacterial pathogen Chlamydia trachomatis. These organoid systems open new possibilities to study cervix biology, infections and cancer evolution, and have potential applications in personalized medicine, drug screening, genome editing and disease modeling.
MeSH term(s)	Animals ; Cervix Uteri/pathology ; Female ; Mice ; Organoids ; Pregnancy ; Stem Cells
Language	English
Publishing date	2022-05-11
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2244966-8
ISSN	1750-2799 ; 1754-2189
ISSN (online)	1750-2799
ISSN	1754-2189
DOI	10.1038/s41596-022-00695-6
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Article ; Online: Single object profiles regression analysis (SOPRA): a novel method for analyzing high-content cell-based screens.

Gurumurthy, Rajendra Kumar / Pleissner, Klaus-Peter / Chumduri, Cindrilla / Meyer, Thomas F / Mäurer, André P

BMC bioinformatics

2022 Volume 23, Issue 1, Page(s) 440

Abstract: Background: High-content screening (HCS) experiments generate complex data from multiple object features for each cell within a treated population. Usually, these data are analyzed by using population-averaged values of the features of interest, ... ...

Abstract	Background: High-content screening (HCS) experiments generate complex data from multiple object features for each cell within a treated population. Usually, these data are analyzed by using population-averaged values of the features of interest, increasing the amount of false positives and the need for intensive follow-up validation. Therefore, there is a strong need for novel approaches with reproducible hit prediction by identifying significantly altered cell populations. Results: Here we describe SOPRA, a workflow for analyzing image-based HCS data based on regression analysis of non-averaged object features from cell populations, which can be run on hundreds of samples using different cell features. Following plate-wise normalization, the values are counted within predetermined binning intervals, generating unique frequency distribution profiles (histograms) for each population, which are then normalized to control populations (control-based normalization). These control-normalized frequency distribution profiles are analyzed using the Bioconductor R-package maSigPro, originally developed to analyze time profiles. However, statistically significant altered frequency distributions are also identified by maSigPro when integrating it into the SOPRA workflow. Finally, significantly changed profiles can be used to generate a heatmap from which altered cell populations with similar phenotypes can be identified, enabling the detection of siRNAs and compounds with the same 'on-target' profile and reducing the number of false positive hits. Conclusions: SOPRA is a novel analysis workflow for the detection of statistically significant normalized frequency distribution profiles of cellular features generated in high-throughput RNAi screens. For the validation of the SOPRA software workflow, a screen for cell cycle progression was used. We were able to identify such profiles for siRNA-mediated gene perturbations and chemical inhibitors of different cell cycle stages. The SOPRA software is freely available from Github.
MeSH term(s)	RNA, Small Interfering/metabolism ; RNA Interference ; Regression Analysis ; Software ; Phenotype
Chemical Substances	RNA, Small Interfering
Language	English
Publishing date	2022-10-21
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/s12859-022-04981-8
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Article ; Online: Copper regulates the host innate immune response against bacterial infection via activation of ALPK1 kinase.

Lu, Jing / Liu, Xue / Li, Xinghua / Li, Hongyan / Shi, Liwa / Xia, Xin / He, Bai-Liang / Meyer, Thomas F / Li, Xiaofeng / Sun, Hongzhe / Yang, Xinming

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

2024 Volume 121, Issue 4, Page(s) e2311630121

Abstract: Copper is an essential trace element for the human body, and its requirement for optimistic immune functions has been recognized for decades. How copper is involved in the innate immune pathway, however, remains to be clarified. Here, we report that ... ...

Abstract	Copper is an essential trace element for the human body, and its requirement for optimistic immune functions has been recognized for decades. How copper is involved in the innate immune pathway, however, remains to be clarified. Here, we report that copper serves as a signal molecule to regulate the kinase activity of alpha-kinase 1 (ALPK1), a cytosolic pattern-recognition receptor (PRR), and therefore promotes host cell defense against bacterial infection. We show that in response to infection, host cells actively accumulate copper in the cytosol, and the accumulated cytosolic copper enhances host cell defense against evading pathogens, including intracellular and, unexpectedly, extracellular bacteria. Subsequently, we demonstrate that copper activates the innate immune pathway of host cells in an ALPK1-dependent manner. Further mechanistic studies reveal that copper binds to ALPK1 directly and is essential for the kinase activity of this cytosolic PRR. Moreover, the binding of copper to ALPK1 enhances the sensitivity of ALPK1 to the bacterial metabolite ADP-heptose and eventually prompts host cells to elicit an enhanced immune response during bacterial infection. Finally, using a zebrafish in vivo model, we show that a copper-treated host shows an increased production of proinflammatory cytokines, enhanced recruitment of phagosome cells, and promoted bacterial clearance. Our findings uncover a previously unrecognized role of copper in the modulation of host innate immune response against bacterial pathogens and advance our knowledge on the cross talk between cytosolic copper homeostasis and immune system.
MeSH term(s)	Animals ; Humans ; Copper ; Zebrafish ; Immunity, Innate ; Cytokines ; Bacterial Infections ; Receptors, Pattern Recognition
Chemical Substances	Copper (789U1901C5) ; Cytokines ; Receptors, Pattern Recognition
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2311630121
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Article ; Online: Enhanced LRP8 expression induced by Helicobacter pylori drives gastric cancer progression by facilitating β-Catenin nuclear translocation.

Liu, Bin / Bukhari, Ihtisham / Li, Fazhan / Ren, Feifei / Xia, Xue / Hu, Baitong / Liu, Haipeng / Meyer, Thomas F / Marshall, Barry J / Tay, Alfred / Fu, Yuming / Wu, Wanqing / Tang, Youcai / Mi, Yang / Zheng, Peng-Yuan

Journal of advanced research

2024

Abstract: Introduction: Helicobacter pylori (H. pylori) infection has been associated with gastric carcinogenesis. However, the precise involvement of LRP8, the low-density lipoprotein receptor-related protein 8, in H. pylori pathogenesis and gastric cancer (GC) ... ...

Abstract	Introduction: Helicobacter pylori (H. pylori) infection has been associated with gastric carcinogenesis. However, the precise involvement of LRP8, the low-density lipoprotein receptor-related protein 8, in H. pylori pathogenesis and gastric cancer (GC) remains poorly understood. Objectives: To investigate the potential role of LRP8 in H. pylori infection and gastric carcinogenesis. Methods: Three-dimensional human-derived gastric organoids (hGO) and gastric cancer organoids (hGCO) were synthesized from the tissues obtained from human donors. In this work, multi-omics combined with in vivo and in vitro studies were conducted to investigate the potential involvement of LRP8 in H. pylori-induced GC. Results: We found that H. pylori infection significantly upregulated the expression of LRP8 in human GC tissues, cells, organoids, and mouse gastric mucous. In particular, LRP8 exhibited a distinct enrichment in cancer stem cells (CSC). Functionally, silencing of LRP8 affected the formation and proliferation of tumor spheroids, while increased expression of LRP8 was associated with increased proliferation and stemness of GC cells and organoids. Mechanistically, LRP8 promotes the binding of E-cadherin to β-catenin, thereby promoting nuclear translocation and transcriptional activity of β-catenin. Furthermore, LRP8 interacts with the cytotoxin-associated gene A (CagA) to form the CagA/LRP8/β-catenin complex. This complex further amplifies H. pylori-induced β-catenin nuclear translocation, leading to increased transcription of inflammatory factors and CSC markers. Clinical analysis demonstrated that abnormal overexpression of LRP8 is correlated with a poor prognosis and resistance to 5-Fluorouracil in patients with GC. Conclusion: Our findings provide valuable information on the molecular intricacies of H. pylori-induced gastric carcinogenesis, offering potential therapeutic targets and prognostic markers for GC.
Language	English
Publishing date	2024-04-10
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2541849-X
ISSN	2090-1224 ; 2090-1224
ISSN (online)	2090-1224
ISSN	2090-1224
DOI	10.1016/j.jare.2024.04.002
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Article ; Online: Revealing the pathogenesis of gastric intestinal metaplasia based on the mucosoid air-liquid interface.

Liu, Simeng / Wen, Huijuan / Li, Fazhan / Xue, Xia / Sun, Xiangdong / Li, Fuhao / Hu, Ruoyu / Xi, Huayuan / Boccellato, Francesco / Meyer, Thomas F / Mi, Yang / Zheng, Pengyuan

Journal of translational medicine

2024 Volume 22, Issue 1, Page(s) 468

Abstract: Background: Gastric intestinal metaplasia (GIM) is an essential precancerous lesion. Although the reversal of GIM is challenging, it potentially brings a state-to-art strategy for gastric cancer therapeutics (GC). The lack of the appropriate in vitro ... ...

Abstract	Background: Gastric intestinal metaplasia (GIM) is an essential precancerous lesion. Although the reversal of GIM is challenging, it potentially brings a state-to-art strategy for gastric cancer therapeutics (GC). The lack of the appropriate in vitro model limits studies of GIM pathogenesis, which is the issue this work aims to address for further studies. Method: The air-liquid interface (ALI) model was adopted for the long-term culture of GIM cells in the present work. This study conducted Immunofluorescence (IF), quantitative real-time polymerase chain reaction (qRT-PCR), transcriptomic sequencing, and mucoproteomic sequencing (MS) techniques to identify the pathways for differential expressed genes (DEGs) enrichment among different groups, furthermore, to verify novel biomarkers of GIM cells. Result: Our study suggests that GIM-ALI model is analog to the innate GIM cells, which thus can be used for mucus collection and drug screening. We found genes MUC17, CDA, TRIM15, TBX3, FLVCR2, ONECUT2, ACY3, NMUR2, and MAL2 were highly expressed in GIM cells, while GLDN, SLC5A5, MAL, and MALAT1 showed down-regulated, which can be used as potential biomarkers for GIM cells. In parallel, these genes that highly expressed in GIM samples were mainly involved in cancer-related pathways, such as the MAPK signal pathway and oxidative phosphorylation signal pathway. Conclusion: The ALI model is validated for the first time for the in vitro study of GIM. GIM-ALI model is a novel in vitro model that can mimic the tissue micro-environment in GIM patients and further provide an avenue for studying the characteristics of GIM mucus. Our study identified new markers of GIM as well as pathways associated with GIM, which provides outstanding insight for exploring GIM pathogenesis and potentially other related conditions.
MeSH term(s)	Metaplasia ; Humans ; Air ; Models, Biological ; Gastric Mucosa/pathology ; Gastric Mucosa/metabolism ; Stomach/pathology ; Organoids/pathology ; Stomach Neoplasms/pathology ; Stomach Neoplasms/genetics ; Gene Expression Regulation, Neoplastic ; Transcriptome/genetics ; Intestines/pathology
Language	English
Publishing date	2024-05-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2118570-0
ISSN	1479-5876 ; 1479-5876
ISSN (online)	1479-5876
ISSN	1479-5876
DOI	10.1186/s12967-024-05276-7
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Article ; Online: hGBP1 Coordinates Chlamydia Restriction and Inflammasome Activation through Sequential GTP Hydrolysis.

Xavier, Audrey / Al-Zeer, Munir A / Meyer, Thomas F / Daumke, Oliver

Cell reports

2020 Volume 31, Issue 7, Page(s) 107667

Abstract: Human guanylate binding protein 1 (hGBP1) belongs to the dynamin superfamily of GTPases and conveys host defense against intracellular bacteria and parasites. During infection, hGBP1 is recruited to pathogen-containing vacuoles, such as Chlamydia ... ...

Abstract	Human guanylate binding protein 1 (hGBP1) belongs to the dynamin superfamily of GTPases and conveys host defense against intracellular bacteria and parasites. During infection, hGBP1 is recruited to pathogen-containing vacuoles, such as Chlamydia trachomatis inclusions, restricts pathogenic growth, and induces the activation of the inflammasome pathway. hGBP1 has a unique catalytic activity to hydrolyze guanosine triphosphate (GTP) to guanosine monophosphate (GMP) in two consecutive cleavage steps. However, the functional significance of this activity in host defense remains elusive. Here, we generate a structure-guided mutant that specifically abrogates GMP production, while maintaining fast cooperative GTP hydrolysis. Complementation experiments in human monocytes/macrophages show that hGBP1-mediated GMP production is dispensable for restricting Chlamydia trachomatis growth but is necessary for inflammasome activation. Mechanistically, GMP is catabolized to uric acid, which in turn activates the NLRP3 inflammasome. Our study demonstrates that the unique enzymology of hGBP1 coordinates bacterial growth restriction and inflammasome signaling.
MeSH term(s)	Chlamydia Infections/immunology ; Chlamydia Infections/metabolism ; Chlamydia Infections/microbiology ; Chlamydia trachomatis/growth & development ; Cyclic GMP ; GTP-Binding Proteins/chemistry ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/immunology ; GTP-Binding Proteins/metabolism ; Guanine Nucleotides/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Hydrolysis ; Inflammasomes/immunology ; Inflammasomes/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; Signal Transduction ; THP-1 Cells ; Uric Acid/metabolism
Chemical Substances	GBP1 protein, human ; Guanine Nucleotides ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Uric Acid (268B43MJ25) ; Guanosine Triphosphate (86-01-1) ; GTP-Binding Proteins (EC 3.6.1.-) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2020-05-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.107667
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