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Article ; Online: Helminth-virus interactions: determinants of coinfection outcomes.

Desai, Pritesh / Diamond, Michael S / Thackray, Larissa B

Gut microbes

2021 Volume 13, Issue 1, Page(s) 1961202

Abstract: Viral infections are often studied in model mammalian organisms under specific pathogen-free conditions. However, in nature, coinfections are common, and infection with one organism can alter host susceptibility to infection with another. Helminth ... ...

Abstract	Viral infections are often studied in model mammalian organisms under specific pathogen-free conditions. However, in nature, coinfections are common, and infection with one organism can alter host susceptibility to infection with another. Helminth parasites share a long coevolutionary history with mammalian hosts and have shaped host physiology, metabolism, immunity, and the composition of the microbiome. Published studies suggest that helminth infection can either be beneficial or detrimental during viral infection. Here, we discuss coinfection studies in mouse models and use them to define key determinants that impact outcomes, including the type of antiviral immunity, the tissue tropism of both the helminth and the virus, and the timing of viral infection in relation to the helminth lifecycle. We also explore the current mechanistic understanding of how helminth-virus coinfection impacts host immunity and viral pathogenesis. While much attention has been placed on the impact of the gut bacterial microbiome on immunity to infection, we suggest that enteric helminths, as a part of the eukaryotic macrobiome, also represent an important modulator of disease pathogenesis and severity following virus infection.
MeSH term(s)	Animals ; Bacteria/immunology ; Coinfection/immunology ; Disease Models, Animal ; Disease Susceptibility/microbiology ; Gastrointestinal Microbiome/immunology ; Helminthiasis/immunology ; Helminths/immunology ; Humans ; Mice ; Viral Tropism/physiology ; Virus Diseases/immunology ; Viruses/immunology
Language	English
Publishing date	2021-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1949-0984
ISSN (online)	1949-0984
DOI	10.1080/19490976.2021.1961202
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A long-distance relationship: the commensal gut microbiota and systemic viruses.

Winkler, Emma S / Thackray, Larissa B

Current opinion in virology

2019 Volume 37, Page(s) 44–51

Abstract: Recent advances defining the role of the commensal gut microbiota in the development, education, induction, function, and maintenance of the mammalian immune system inform our understanding of how immune responses govern the outcome of systemic virus ... ...

Abstract	Recent advances defining the role of the commensal gut microbiota in the development, education, induction, function, and maintenance of the mammalian immune system inform our understanding of how immune responses govern the outcome of systemic virus infection. While characterization of the impact of the local oral, respiratory, dermal and genitourinary microbiota on host immune responses and systemic virus infection is in its infancy, the gut microbiota interacts with host immunity systemically and at distal non-gastrointestinal tract sites to modulate the pathogenesis of systemic viruses. Gut microbes, microbe-associated molecular patterns, and microbe-derived metabolites engage receptors expressed on the cell surface, in the endosome, or in the cytoplasm to orchestrate optimal innate and adaptive immune responses important for controlling systemic virus infection.
MeSH term(s)	Adaptive Immunity ; Animals ; B-Lymphocytes/immunology ; Cytokines/metabolism ; Gastrointestinal Microbiome/immunology ; Gastrointestinal Tract/immunology ; Gastrointestinal Tract/microbiology ; Gastrointestinal Tract/virology ; Host Microbial Interactions/immunology ; Immunity, Innate ; Interferons/metabolism ; Mice ; Microbial Interactions/immunology ; Pathogen-Associated Molecular Pattern Molecules/immunology ; Pathogen-Associated Molecular Pattern Molecules/metabolism ; Receptors, Pattern Recognition/immunology ; Receptors, Pattern Recognition/metabolism ; Symbiosis ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/metabolism ; Virus Diseases/immunology ; Virus Diseases/microbiology ; Viruses/pathogenicity
Chemical Substances	Cytokines ; Pathogen-Associated Molecular Pattern Molecules ; Receptors, Pattern Recognition ; Toll-Like Receptor 4 ; Interferons (9008-11-1)
Language	English
Publishing date	2019-06-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2611378-8
ISSN	1879-6265 ; 1879-6257
ISSN (online)	1879-6265
ISSN	1879-6257
DOI	10.1016/j.coviro.2019.05.009
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Article ; Online: An Antiviral Role for TRIM14 in Ebola Virus Infection.

Kuroda, Makoto / Halfmann, Peter J / Thackray, Larissa B / Diamond, Michael S / Feldmann, Heinz / Marzi, Andrea / Kawaoka, Yoshihiro

The Journal of infectious diseases

2024 Volume 228, Issue Suppl 7, Page(s) S514–S521

Abstract: Ebola virus (EBOV) is a highly pathogenic virus that encodes 7 multifunctional structural proteins. Multiple host factors have been reported to interact with the EBOV proteins. Here, we found that tripartite motif-containing 14 (TRIM14), an interferon- ... ...

Abstract	Ebola virus (EBOV) is a highly pathogenic virus that encodes 7 multifunctional structural proteins. Multiple host factors have been reported to interact with the EBOV proteins. Here, we found that tripartite motif-containing 14 (TRIM14), an interferon-stimulated gene that mediates cellular signaling pathways associated with type I interferon and inflammatory cytokine production, interacts with EBOV nucleoprotein to enhance interferon-β (IFN-β) and nuclear factor-κB (NF-κB) promotor activation. Moreover, TRIM14 overexpression reduced viral replication in an infectious but biologically contained EBOVΔVP30 system by approximately 10-fold without affecting viral protein expression. Furthermore, TRM14-deficient mice were more susceptible to mouse-adapted EBOV infection than wild-type mice. Our data suggest that TRIM14 is a host factor with anti-EBOV activity that limits EBOV pathogenesis.
MeSH term(s)	Animals ; Mice ; Ebolavirus/genetics ; Hemorrhagic Fever, Ebola ; Interferon Type I/metabolism ; Viral Proteins/metabolism
Chemical Substances	Interferon Type I ; Viral Proteins ; Trim14 protein, mouse
Language	English
Publishing date	2024-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiad325
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Article ; Online: Ipsilateral or contralateral boosting of mice with mRNA vaccines confers equivalent immunity and protection against a SARS-CoV-2 Omicron strain

Ying, Baoling / Liang, Chieh-Yu / Desai, Pritesh / Scheaffer, Suzanne M. / Elbashir, Sayda M. / Edwards, Darin K. / Thackray, Larissa B. / Diamond, Michael S.

bioRxiv

Abstract: Boosting with mRNA vaccines encoding variant-matched spike proteins has been implemented to mitigate their reduced efficacy against emerging SARS-CoV-2 variants. Nonetheless, in humans, it remains unclear whether boosting in the ipsilateral or ... ...

Abstract	Boosting with mRNA vaccines encoding variant-matched spike proteins has been implemented to mitigate their reduced efficacy against emerging SARS-CoV-2 variants. Nonetheless, in humans, it remains unclear whether boosting in the ipsilateral or contralateral arm with respect to the priming doses impacts immunity and protection. Here, we boosted K18-hACE2 mice with either monovalent mRNA-1273 (Wuhan-1 spike) or bivalent mRNA-1273.214 (Wuhan-1 + BA.1 spike) vaccine in the ipsilateral or contralateral leg relative to a two-dose priming series with mRNA-1273. Boosting in the ipsilateral or contralateral leg elicited equivalent levels of serum IgG and neutralizing antibody responses against Wuhan-1 and BA.1. While contralateral boosting with mRNA vaccines resulted in expansion of spike-specific B and T cells beyond the ipsilateral draining lymph node (DLN) to the contralateral DLN, administration of a third mRNA vaccine dose at either site resulted in similar levels of antigen-specific germinal center B cells, plasmablasts/plasma cells, T follicular helper cells and CD8<sup>+</sup> T cells in the DLNs and the spleen. Furthermore, ipsilateral and contralateral boosting with mRNA-1273 or mRNA-1273.214 vaccines conferred similar homologous or heterologous immune protection against SARS-CoV-2 BA.1 virus challenge with equivalent reductions in viral RNA and infectious virus in the nasal turbinates and lungs. Collectively, our data show limited differences in B and T cell immune responses after ipsilateral and contralateral site boosting by mRNA vaccines that do not substantively impact protection against an Omicron strain.
Keywords	covid19
Language	English
Publishing date	2024-04-07
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.04.05.588051
Database	COVID19

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Article: Mesalamine Reduces Intestinal ACE2 Expression Without Modifying SARS-CoV-2 Infection or Disease Severity in Mice.

Alvarado, David M / Son, Juhee / Thackray, Larissa B / Diamond, Michael S / Ding, Siyuan / Ciorba, Matthew A

bioRxiv : the preprint server for biology

2021

Abstract: Introduction: Coronavirus Disease 2019 (COVID-19) is an ongoing public health crisis that has sickened or precipitated death in millions. The etiologic agent of COVID-19, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), infects the ... ...

Abstract	Introduction: Coronavirus Disease 2019 (COVID-19) is an ongoing public health crisis that has sickened or precipitated death in millions. The etiologic agent of COVID-19, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), infects the intestinal epithelium, and can induce GI symptoms similar to the human inflammatory bowel diseases (IBD). An international surveillance epidemiology study (SECURE-IBD) reported that the standardized mortality ratio trends higher in IBD patients (1.5-1.8) and that mesalamine/sulfasalazine therapy correlates with poor outcome. The goal of our study was to experimentally address the relationship between mesalamine and SARS-CoV-2 entry, replication, and/or pathogenesis. Methods: Viral infection was performed with a chimeric vesicular stomatitis virus expressing SARS-CoV-2 spike protein and EGFP (VSV-SARS-CoV-2) and SARS-CoV-2 virus derived from an infectious cDNA clone of 2019n-CoV/USA_WA1/2020. Primary human ileal spheroids derived from healthy donors were grown as 3D spheroids or on 2D transwells. We assessed the effect of 10 mM mesalamine (Millipore Sigma) on viral RNA levels, as well as the expression of the SARS-CoV-2 receptor angiotensin II-converting enzyme 2 (ACE2), Transmembrane Serine Protease 2 (TMPRSS2), TMPRSS4, Cathepsin B (CTSB) and CTSL by qRT-PCR. 8-12 week old K18-ACE2 were treated orally with PBS or mesalamine at 200 mg/kg daily. Mice were inoculated intranasally with 1Ã-10 Results: We found no change in viral RNA levels in human intestinal epithelial cells in response to mesalamine. Expression of Conclusions: Mesalamine did not alter viral entry, replication, or pathogenesis
Language	English
Publishing date	2021-08-02
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.07.23.453393
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Article: Intestinal helminth infection impairs vaccine-induced T cell responses and protection against SARS-CoV-2.

Desai, Pritesh / Karl, Courtney E / Ying, Baoling / Liang, Chieh-Yu / Garcia-Salum, Tamara / Santana, Ana Carolina / Caten, Felipe Ten / Urban, Joseph F / Elbashir, Sayda M / Edwards, Darin K / Ribeiro, Susan P / Thackray, Larissa B / Sekaly, Rafick P / Diamond, Michael S

bioRxiv : the preprint server for biology

2024

Abstract: Although vaccines have reduced COVID-19 disease burden, their efficacy in helminth infection endemic areas is not well characterized. We evaluated the impact of infection ... ...

Abstract	Although vaccines have reduced COVID-19 disease burden, their efficacy in helminth infection endemic areas is not well characterized. We evaluated the impact of infection by
Language	English
Publishing date	2024-01-15
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.14.575588
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Article ; Online: Kathryn V. Holmes: A Career of Contributions to the Coronavirus Field.

Bonavia, Aurelio / Dominguez, Samuel R / Dveksler, Gabriela / Gagneten, Sara / Howard, Megan / Jeffers, Scott / Qian, Zhaohui / Smith, Mary Kathryn / Thackray, Larissa B / Tresnan, Dina B / Wentworth, David E / Wessner, David R / Williams, Richard K / Miura, Tanya A

Viruses

2022 Volume 14, Issue 7

Abstract: Over the past two years, scientific research has moved at an unprecedented rate in response to the COVID-19 pandemic. The rapid development of effective vaccines and therapeutics would not have been possible without extensive background knowledge on ... ...

Abstract	Over the past two years, scientific research has moved at an unprecedented rate in response to the COVID-19 pandemic. The rapid development of effective vaccines and therapeutics would not have been possible without extensive background knowledge on coronaviruses developed over decades by researchers, including Kathryn (Kay) Holmes. Kay's research team discovered the first coronavirus receptors for mouse hepatitis virus and human coronavirus 229E and contributed a wealth of information on coronaviral spike glycoproteins and receptor interactions that are critical determinants of host and tissue specificity. She collaborated with several research laboratories to contribute knowledge in additional areas, including coronaviral pathogenesis, epidemiology, and evolution. Throughout her career, Kay was an extremely dedicated and thoughtful mentor to numerous graduate students and post-doctoral fellows. This article provides a review of her contributions to the coronavirus field and her exemplary mentoring.
MeSH term(s)	Animals ; COVID-19 ; Coronavirus 229E, Human ; History, 21st Century ; Humans ; Mice ; Pandemics ; Receptors, Coronavirus ; Spike Glycoprotein, Coronavirus/genetics
Chemical Substances	Receptors, Coronavirus ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-07-20
Publishing country	Switzerland
Document type	Biography ; Historical Article ; Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14071573
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Article: Kathryn V. Holmes: A Career of Contributions to the Coronavirus Field

Bonavia, Aurelio / Dominguez, Samuel R. / Dveksler, Gabriela / Gagneten, Sara / Howard, Megan / Jeffers, Scott / Qian, Zhaohui / Smith, Mary Kathryn / Thackray, Larissa B. / Tresnan, Dina B. / Wentworth, David E. / Wessner, David R. / Williams, Richard K. / Miura, Tanya A.

Viruses. 2022 July 20, v. 14, no. 7

2022

Abstract	Over the past two years, scientific research has moved at an unprecedented rate in response to the COVID-19 pandemic. The rapid development of effective vaccines and therapeutics would not have been possible without extensive background knowledge on coronaviruses developed over decades by researchers, including Kathryn (Kay) Holmes. Kay’s research team discovered the first coronavirus receptors for mouse hepatitis virus and human coronavirus 229E and contributed a wealth of information on coronaviral spike glycoproteins and receptor interactions that are critical determinants of host and tissue specificity. She collaborated with several research laboratories to contribute knowledge in additional areas, including coronaviral pathogenesis, epidemiology, and evolution. Throughout her career, Kay was an extremely dedicated and thoughtful mentor to numerous graduate students and post-doctoral fellows. This article provides a review of her contributions to the coronavirus field and her exemplary mentoring.
Keywords	COVID-19 infection ; Human coronavirus 229E ; Murine hepatitis virus ; evolution ; glycoproteins ; mentoring ; pathogenesis ; therapeutics
Language	English
Dates of publication	2022-0720
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v14071573
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Intestinal helminth infection impairs vaccine-induced T cell responses and protection against SARS-CoV-2

Desai, Pritesh / Karl, Courtney E. / Ying, Baoling / Liang, Chieh-Yu / Garcia-Salum, Tamara / Santana, Ana Carolina / Caten, Felipe Ten / Urban, Joseph F. / Elbashir, Sayda M. / Edwards, Darin K. / Ribeiro, Susan P. / Thackray, Larissa B. / Sekaly, Rafick P. / Diamond, Michael S.

bioRxiv

Abstract: Although vaccines have reduced COVID-19 disease burden, their efficacy in helminth infection endemic areas is not well characterized. We evaluated the impact of infection by Heligmosomoides polygyrus bakeri (Hpb), a murine intestinal hookworm, on the ... ...

Abstract	Although vaccines have reduced COVID-19 disease burden, their efficacy in helminth infection endemic areas is not well characterized. We evaluated the impact of infection by Heligmosomoides polygyrus bakeri (Hpb), a murine intestinal hookworm, on the efficacy of an mRNA vaccine targeting the Wuhan-1 spike protein of SARS-CoV-2. Although immunization generated similar B cell responses in Hpb-infected and uninfected mice, polyfunctional CD4+ and CD8+ T cell responses were markedly reduced in Hpb-infected mice. Hpb-infected and mRNA vaccinated mice were protected against the ancestral SARS-CoV-2 strain WA1/2020, but control of lung infection was diminished against an Omicron variant compared to animals immunized without Hpb infection. Helminth mediated suppression of spike-specific CD8+ T cell responses occurred independently of STAT6 signaling, whereas blockade of IL-10 rescued vaccine-induced CD8+ T cell responses. In mice, intestinal helminth infection impairs vaccine induced T cell responses via an IL-10 pathway and compromises protection against antigenically shifted SARS-CoV-2 variants.
Keywords	covid19
Language	English
Publishing date	2024-01-15
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.01.14.575588
Database	COVID19

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Article ; Online: mRNA-1273 and Ad26.COV2.S vaccines protect against the B.1.621 variant of SARS-CoV-2.

Darling, Tamarand L / Ying, Baoling / Whitener, Bradley / VanBlargan, Laura A / Bricker, Traci L / Liang, Chieh-Yu / Joshi, Astha / Bamunuarachchi, Gayan / Seehra, Kuljeet / Schmitz, Aaron J / Halfmann, Peter J / Kawaoka, Yoshihiro / Elbashir, Sayda M / Edwards, Darin K / Thackray, Larissa B / Diamond, Michael S / Boon, Adrianus C M

Med (New York, N.Y.)

2022 Volume 3, Issue 5, Page(s) 309–324.e6

Abstract: Background: Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in 2019, viral variants with greater transmissibility or immune-evasion properties have arisen, which could jeopardize recently deployed vaccine- and ... ...

Abstract	Background: Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in 2019, viral variants with greater transmissibility or immune-evasion properties have arisen, which could jeopardize recently deployed vaccine- and antibody-based countermeasures. Methods: Here, we evaluated in mice and hamsters the efficacy of a pre-clinical version of the Moderna mRNA vaccine (mRNA-1273) and the Johnson & Johnson recombinant adenoviral-vectored vaccine (Ad26.COV2.S) against the B.1.621 (Mu) variant of SARS-CoV-2, which contains spike mutations T95I, Y144S, Y145N, R346K, E484K, N501Y, D614G, P681H, and D950N. Findings: Immunization of 129S2 and K18-human ACE2 transgenic mice with the mRNA-1273 vaccine protected against weight loss, lung infection, and lung pathology after challenge with the B.1.621 or WA1/2020 N501Y/D614G SARS-CoV-2 strain. Similarly, immunization of 129S2 mice and Syrian hamsters with a high dose of Ad26.COV2.S reduced lung infection after B.1.621 virus challenge. Conclusions: Thus, immunity induced by the mRNA-1273 or Ad26.COV2.S vaccine can protect against the B.1.621 variant of SARS-CoV-2 in multiple animal models. Funding: This study was supported by the NIH (R01 AI157155 and U01 AI151810), NIAID Centers of Excellence for Influenza Research and Response [CEIRR] contracts 75N93021C00014 and 75N93021C00016, and the Collaborative Influenza Vaccine Innovation Centers [CIVIC] contract 75N93019C00051. It was also supported, in part, by the National Institutes of Allergy and Infectious Diseases Center for Research on Influenza Pathogenesis (HHSN272201400008C) and the Japan Program for Infectious Diseases Research and Infrastructure (JP21wm0125002) from the Japan Agency for Medical Research and Development (AMED).
MeSH term(s)	2019-nCoV Vaccine mRNA-1273/immunology ; 2019-nCoV Vaccine mRNA-1273/pharmacology ; Ad26COVS1 ; Animals ; Antibodies, Neutralizing ; COVID-19/immunology ; COVID-19/prevention & control ; COVID-19/virology ; COVID-19 Vaccines/immunology ; COVID-19 Vaccines/pharmacology ; Cricetinae ; Humans ; Influenza, Human ; Mice ; SARS-CoV-2/genetics ; SARS-CoV-2/immunology ; Spike Glycoprotein, Coronavirus/immunology ; mRNA Vaccines/immunology ; mRNA Vaccines/pharmacology
Chemical Substances	Ad26COVS1 (JT2NS6183B) ; Antibodies, Neutralizing ; COVID-19 Vaccines ; Spike Glycoprotein, Coronavirus ; mRNA Vaccines ; spike protein, SARS-CoV-2 ; 2019-nCoV Vaccine mRNA-1273 (EPK39PL4R4)
Language	English
Publishing date	2022-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-6340
ISSN (online)	2666-6340
DOI	10.1016/j.medj.2022.03.009
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