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Article ; Online: Editorial: Substance abuse and the microbiome.

Nagarkatti, Prakash / Nagarkatti, Mitzi / Buch, Shilpa

Advances in drug and alcohol research

2024 Volume 4, Page(s) 12734

Language	English
Publishing date	2024-03-06
Publishing country	Switzerland
Document type	Editorial
ISSN	2674-0001
ISSN (online)	2674-0001
DOI	10.3389/adar.2024.12734
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Article ; Online: 6-Formylindolo[3,2-b]carbazole, a potent ligand for the aryl hydrocarbon receptor, attenuates concanavalin-induced hepatitis by limiting T-cell activation and infiltration of proinflammatory CD11b+ Kupffer cells.

Cannon, Alkeiver S / Holloman, Bryan L / Wilson, Kiesha / Miranda, Kathryn / Nagarkatti, Prakash S / Nagarkatti, Mitzi

Journal of leukocyte biology

2024

Abstract: FICZ (6-formylindolo[3,2-b]carbazole) is a potent aryl hydrocarbon receptor agonist that has a poorly understood function in the regulation of inflammation. In this study, we investigated the effect of aryl hydrocarbon receptor activation by FICZ in a ... ...

Abstract	FICZ (6-formylindolo[3,2-b]carbazole) is a potent aryl hydrocarbon receptor agonist that has a poorly understood function in the regulation of inflammation. In this study, we investigated the effect of aryl hydrocarbon receptor activation by FICZ in a murine model of autoimmune hepatitis induced by concanavalin A. High-throughput sequencing techniques such as single-cell RNA sequencing and assay for transposase accessible chromatin sequencing were used to explore the mechanisms through which FICZ induces its effects. FICZ treatment attenuated concanavalin A-induced hepatitis, evidenced by decreased T-cell infiltration, decreased circulating alanine transaminase levels, and suppression of proinflammatory cytokines. Concanavalin A revealed an increase in natural killer T cells, T cells, and mature B cells upon concanavalin A injection while FICZ treatment reversed the presence of these subsets. Surprisingly, concanavalin A depleted a subset of CD55+ B cells, while FICZ partially protected this subset. The immune cells showed significant dysregulation in the gene expression profiles, including diverse expression of migratory markers such as CCL4, CCL5, and CXCL2 and critical regulatory markers such as Junb. Assay for transposase accessible chromatin sequencing showed more accessible chromatin in the CD3e promoter in the concanavalin A-only group as compared to the naive and concanavalin A-exposed, FICZ-treated group. While there was overall more accessible chromatin of the Adgre1 (F4/80) promoter in the FICZ-treated group, we observed less open chromatin in the Itgam (CD11b) promoter in Kupffer cells, supporting the ability of FICZ to reduce the infiltration of proinflammatory cytokine producing CD11b+ Kupffer cells. Taken together, these data demonstrate that aryl hydrocarbon receptor activation by FICZ suppresses liver injury through the limitation of CD3+ T-cell activation and CD11b+ Kupffer cell infiltration.
Language	English
Publishing date	2024-02-16
Publishing country	England
Document type	Journal Article
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1093/jleuko/qiae018
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Article ; Online: Characterization of Chemotaxis-Associated Gene Dysregulation in Myeloid Cell Populations in the Lungs during Lipopolysaccharide-Mediated Acute Lung Injury.

Holloman, Bryan Latrell / Cannon, Alkeiver / Wilson, Kiesha / Singh, Narendra / Nagarkatti, Mitzi / Nagarkatti, Prakash

Journal of immunology (Baltimore, Md. : 1950)

2024 Volume 210, Issue 12, Page(s) 2016–2028

Abstract: During endotoxin-induced acute lung injury (ALI), immune cell recruitment resulting from chemotaxis is mediated by CXC and CC chemokines and their receptors. In this study, we investigated the role of chemokines and their receptors in the regulation of ... ...

Abstract	During endotoxin-induced acute lung injury (ALI), immune cell recruitment resulting from chemotaxis is mediated by CXC and CC chemokines and their receptors. In this study, we investigated the role of chemokines and their receptors in the regulation of myeloid cell populations in the circulation and the lungs of C57BL/6J mice exhibiting LPS-mediated ALI using single-cell RNA sequencing. During ALI, there was an increase in the myeloid cells, M1 macrophages, monocytes, neutrophils, and other granulocytes, whereas there was a decrease in the residential alveolar macrophages and M2 macrophages. Interestingly, LPS triggered the upregulation of CCL3, CCL4, CXCL2/3, and CXCL10 genes associated with cellular migration of various subsets of macrophages, neutrophils, and granulocytes. Furthermore, there was an increase in the frequency of myeloid cells expressing CCR1, CCR3, CCR5, and CXCR2 receptors during ALI. MicroRNA sequencing studies of vehicle versus LPS groups identified several dysregulated microRNAs targeting the upregulated chemokine genes. This study suggests that chemokine ligand-receptors interactions are responsible for myeloid cell heterogenicity and cellular recruitment to the lungs during ALI. The single-cell transcriptomics allowed for an in-depth assessment and characterization of myeloid cells involved in immune cell trafficking during ALI.
MeSH term(s)	Animals ; Mice ; Chemotaxis ; Lipopolysaccharides ; Mice, Inbred C57BL ; Lung ; Chemokines ; Acute Lung Injury/chemically induced ; Acute Lung Injury/genetics ; Myeloid Cells ; Receptors, Chemokine/genetics
Chemical Substances	Lipopolysaccharides ; Chemokines ; Receptors, Chemokine
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2200822
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Article: Studying the cellular basis of small bowel enteropathy using high-parameter flow cytometry in mouse models of primary antibody deficiency.

Mohammed, Ahmed D / Ball, Ryan A W / Jolly, Amy / Nagarkatti, Prakash / Nagarkatti, Mitzi / Kubinak, Jason L

bioRxiv : the preprint server for biology

2024

Abstract: Background: Primary immunodeficiencies are heritable defects in immune system function. Antibody deficiency is the most common form of primary immunodeficiency in humans, can be caused by abnormalities in both the development and activation of B cells, ... ...

Abstract	Background: Primary immunodeficiencies are heritable defects in immune system function. Antibody deficiency is the most common form of primary immunodeficiency in humans, can be caused by abnormalities in both the development and activation of B cells, and may result from B-cell-intrinsic defects or defective responses by other cells relevant to humoral immunity. Inflammatory gastrointestinal complications are commonly observed in antibody-deficient patients, but the underlying immune mechanisms driving this are largely undefined. Methods: In this study, several mouse strains reflecting a spectrum of primary antibody deficiency (IgA Results: Results from our experiments indicate that the severity of primary antibody deficiency positively correlates with the degree of immune dysregulation that can be expected to develop in an individual. In the SI of mice, immune dysregulation is primarily explained by defective homeostatic responses in T cell and invariant natural killer-like T (iNKT) cell subsets. These defects are strongly correlated with abnormalities in the balance between protein (MHCII-mediated) versus lipid (CD1d-mediated) antigen presentation by intestinal epithelial cells (IECs) and intestinal stem cells (ISCs), respectively. Conclusions: Multivariate statistical approaches can be used to obtain quantifiable estimates of immune dysregulation based on high-parameter flow cytometry readouts of immune function. Using one such estimate, we reveal a previously unrecognized tradeoff between iNKT cell activation and type 1 immunity that underlies disease in the small bowel. The balance between protein/lipid antigen presentation by ISCs may play a crucial role in regulating this balance and thereby suppressing inflammatory disease in the small bowel.
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.25.577009
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Article ; Online: Identification of miRNAs that target Fcγ receptor-mediated phagocytosis during macrophage activation syndrome.

Varsha, Kontham Kulangara / Yang, Xiaoming / Cannon, Alkeiver S / Zhong, Yin / Nagarkatti, Mitzi / Nagarkatti, Prakash

Frontiers in immunology

2024 Volume 15, Page(s) 1355315

Abstract: Macrophage activation syndrome (MAS) is a life-threatening complication of systemic juvenile arthritis, accompanied by cytokine storm and hemophagocytosis. In addition, COVID-19-related hyperinflammation shares clinical features of MAS. Mechanisms that ... ...

Abstract	Macrophage activation syndrome (MAS) is a life-threatening complication of systemic juvenile arthritis, accompanied by cytokine storm and hemophagocytosis. In addition, COVID-19-related hyperinflammation shares clinical features of MAS. Mechanisms that activate macrophages in MAS remain unclear. Here, we identify the role of miRNA in increased phagocytosis and interleukin-12 (IL-12) production by macrophages in a murine model of MAS. MAS significantly increased F4/80+ macrophages and phagocytosis in the mouse liver. Gene expression profile revealed the induction of Fcγ receptor-mediated phagocytosis (FGRP) and IL-12 production in the liver. Phagocytosis pathways such as High-affinity IgE receptor is known as Fc epsilon RI -signaling and pattern recognition receptors involved in the recognition of bacteria and viruses and phagosome formation were also significantly upregulated. In MAS, miR-136-5p and miR-501-3p targeted and caused increased expression of Fcgr3, Fcgr4, and Fcgr1 genes in FGRP pathway and consequent increase in phagocytosis by macrophages, whereas miR-129-1-3p and miR-150-3p targeted and induced Il-12. Transcriptome analysis of patients with MAS revealed the upregulation of FGRP and FCGR gene expression. A target analysis of gene expression data from a patient with MAS discovered that miR-136-5p targets
MeSH term(s)	Humans ; Animals ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Receptors, IgG/genetics ; Macrophage Activation Syndrome/genetics ; Phagocytosis/genetics ; Interleukin-12
Chemical Substances	MicroRNAs ; Receptors, IgG ; Interleukin-12 (187348-17-0) ; Mirn129 microRNA, human ; MIRN136 microRNA, human
Language	English
Publishing date	2024-03-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1355315
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Article ; Online: Indole-3-carbinol attenuates lipopolysaccharide-induced acute respiratory distress syndrome through activation of AhR: role of CCR2+ monocyte activation and recruitment in the regulation of CXCR2+ neutrophils in the lungs.

Holloman, Bryan Latrell / Wilson, Kiesha / Cannon, Alkeiver / Nagarkatti, Mitzi / Nagarkatti, Prakash S

Frontiers in immunology

2024 Volume 15, Page(s) 1330373

Abstract: Introduction: Indole-3-carbinol (I3C) is found in cruciferous vegetables and used as a dietary supplement. It is known to act as a ligand for aryl hydrocarbon receptor (AhR). In the current study, we investigated the role of AhR and the ability of I3C ... ...

Abstract	Introduction: Indole-3-carbinol (I3C) is found in cruciferous vegetables and used as a dietary supplement. It is known to act as a ligand for aryl hydrocarbon receptor (AhR). In the current study, we investigated the role of AhR and the ability of I3C to attenuate LPS-induced Acute Respiratory Distress Syndrome (ARDS). Methods: To that end, we induced ARDS in wild-type C57BL/6 mice, Ccr2gfp/gfp KI/KO mice (mice deficient in the CCR2 receptor), and LyZcreAhRfl/fl mice (mice deficient in the AhR on myeloid linage cells). Additionally, mice were treated with I3C (65 mg/kg) or vehicle to investigate its efficacy to treat ARDS. Results: I3C decreased the neutrophils expressing CXCR2, a receptor associated with neutrophil recruitment in the lungs. In addition, LPS-exposed mice treated with I3C revealed downregulation of CCR2+ monocytes in the lungs and lowered CCL2 (MCP-1) protein levels in serum and bronchoalveolar lavage fluid. Loss of CCR2 on monocytes blocked the recruitment of CXCR2+ neutrophils and decreased the total number of immune cells in the lungs during ARDS. In addition, loss of the AhR on myeloid linage cells ablated I3C-mediated attenuation of CXCR2+ neutrophils and CCR2+ monocytes in the lungs from ARDS animals. Interestingly, scRNASeq showed that in macrophage/monocyte cell clusters of LPS-exposed mice, I3C reduced the expression of CXCL2 and CXCL3, which bind to CXCR2 and are involved in neutrophil recruitment to the disease site. Discussion: These findings suggest that CCR2+ monocytes are involved in the migration and recruitment of CXCR2+ neutrophils during ARDS, and the AhR ligand, I3C, can suppress ARDS through the regulation of immune cell trafficking.
MeSH term(s)	Mice ; Animals ; Monocytes/metabolism ; Lipopolysaccharides/pharmacology ; Neutrophils/metabolism ; Receptors, Aryl Hydrocarbon/metabolism ; Ligands ; Mice, Inbred C57BL ; Lung/metabolism ; Respiratory Distress Syndrome/chemically induced ; Respiratory Distress Syndrome/drug therapy ; Respiratory Distress Syndrome/metabolism ; Indoles
Chemical Substances	Lipopolysaccharides ; indole-3-carbinol (C11E72455F) ; Receptors, Aryl Hydrocarbon ; Ligands ; Indoles
Language	English
Publishing date	2024-03-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1330373
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Article ; Online: Role of Gut Microbiota in Cannabinoid-Mediated Suppression of Inflammation.

Varsha, Kontham Kulangara / Nagarkatti, Mitzi / Nagarkatti, Prakash

Advances in drug and alcohol research

2022 Volume 2

Abstract: Cannabinoids and the endocannabinoid system have been well established to play a crucial role in the regulation of the immune response. Also, emerging data from numerous investigations unravel the imperative role of gut microbiota and their metabolites ... ...

Abstract	Cannabinoids and the endocannabinoid system have been well established to play a crucial role in the regulation of the immune response. Also, emerging data from numerous investigations unravel the imperative role of gut microbiota and their metabolites in the maintenance of immune homeostasis and gut barrier integrity. In this review, we concisely report the immunosuppressive mechanisms triggered by cannabinoids, and how they are closely associated with the alterations in the gut microbiome and metabolome following exposure to endogenous or exogenous cannabinoids. We discuss how cannabinoid-mediated induction of microbial secondary bile acids, short chain fatty acids, and indole metabolites, produced in the gut, can suppress inflammation even in distal organs. While clearly, more clinical studies are necessary to establish the cross talk between exo- or endocannabinoid system with the gut microbiome and the immune system, the current evidence opens a new avenue of cannabinoid-gut-microbiota-based therapeutics to regulate immunological disorders.
Language	English
Publishing date	2022-07-14
Publishing country	Switzerland
Document type	Journal Article
ISSN	2674-0001
ISSN (online)	2674-0001
DOI	10.3389/adar.2022.10550
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Article ; Online: Effect of TCDD exposure in adult female and male mice on the expression of miRNA in the ovaries and testes and associated reproductive functions.

Hall, Alina / Mattison, Donald / Singh, Narendra / Chatzistamou, Ioulia / Zhang, Jiajia / Nagarkatti, Mitzi / Nagarkatti, Prakash

Frontiers in toxicology

2023 Volume 5, Page(s) 1268293

Abstract: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant found widely across the world. While animal and human studies have shown that exposure to TCDD may cause significant alterations in the reproductive tract, the effect of TCDD on ... ...

Abstract	2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant found widely across the world. While animal and human studies have shown that exposure to TCDD may cause significant alterations in the reproductive tract, the effect of TCDD on the expression of miRNA in the reproductive organs has not been previously tested. In the current study, we exposed adult female or male mice to TCDD or vehicle and bred them to study the impact on reproduction. The data showed that while TCDD treatment of females caused no significant change in litter size, it did alter the survival of the pups. Also, TCDD exposure of either the male or female mice led to an increase in the gestational period. While TCDD did not alter the gross morphology of the ovaries and testes, it induced significant alterations in the miRNA expression. The ovaries showed the differential expression of 426 miRNAs, of which 315 miRNAs were upregulated and 111 miRNA that were downregulated after TCDD exposure when compared to the vehicle controls. In the testes, TCDD caused the differential expression of 433 miRNAs, with 247 miRNAs upregulated and 186 miRNAs downregulated. Pathway analysis showed that several of these dysregulated miRNAs targeted reproductive functions. The current study suggests that the reproductive toxicity of TCDD may result from alterations in the miRNA expression in the reproductive organs. Because miRNAs also represent one of the epigenetic pathways of gene expression, our studies suggest that the transgenerational toxicity of TCDD may also result from dysregulation in the miRNAs.
Language	English
Publishing date	2023-10-03
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-3080
ISSN (online)	2673-3080
DOI	10.3389/ftox.2023.1268293
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Article ; Online: Aryl Hydrocarbon Receptor Activation Ameliorates Acute Respiratory Distress Syndrome through Regulation of Th17 and Th22 Cells in the Lungs.

Holloman, Bryan Latrell / Cannon, Alkeiver / Wilson, Kiesha / Nagarkatti, Prakash / Nagarkatti, Mitzi

mBio

2023 Volume 14, Issue 2, Page(s) e0313722

Abstract: Acute respiratory distress syndrome (ARDS) is triggered by a variety of insults, including bacterial and viral infections, and this leads to high mortality. While the role of the aryl hydrocarbon receptor (AhR) in mucosal immunity is being increasingly ... ...

Abstract	Acute respiratory distress syndrome (ARDS) is triggered by a variety of insults, including bacterial and viral infections, and this leads to high mortality. While the role of the aryl hydrocarbon receptor (AhR) in mucosal immunity is being increasingly recognized, its function during ARDS is unclear. In the current study, we investigated the role of AhR in LPS-induced ARDS. AhR ligand, indole-3-carbinol (I3C), attenuated ARDS which was associated with a decrease in CD4
MeSH term(s)	Humans ; Interleukin-17 ; Lipopolysaccharides ; Lung/metabolism ; MicroRNAs ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Respiratory Distress Syndrome/pathology ; RNA, Viral ; SARS-CoV-2/metabolism ; Th17 Cells
Chemical Substances	Interleukin-17 ; Lipopolysaccharides ; MicroRNAs ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Aryl Hydrocarbon ; RNA, Viral
Language	English
Publishing date	2023-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.03137-22
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Article ; Online: Targeting AhR as a Novel Therapeutic Modality against Inflammatory Diseases.

Cannon, Alkeiver S / Nagarkatti, Prakash S / Nagarkatti, Mitzi

International journal of molecular sciences

2021 Volume 23, Issue 1

Abstract: For decades, activation of Aryl Hydrocarbon Receptor (AhR) was excluded from consideration as a therapeutic approach due to the potential toxic effects of AhR ligands and the induction of the cytochrome P450 enzyme, Cyp1a1, following AhR activation. ... ...

Abstract	For decades, activation of Aryl Hydrocarbon Receptor (AhR) was excluded from consideration as a therapeutic approach due to the potential toxic effects of AhR ligands and the induction of the cytochrome P450 enzyme, Cyp1a1, following AhR activation. However, it is now understood that AhR activation not only serves as an environmental sensor that regulates the effects of environmental toxins, but also as a key immunomodulator where ligands induce a variety of cellular and epigenetic mechanisms to attenuate inflammation. Thus, the emergence of further in-depth research into diverse groups of compounds capable of activating this receptor has prompted reconsideration of its use therapeutically. The aim of this review is to summarize the body of research surrounding AhR and its role in regulating inflammation. Specifically, evidence supporting the potential of targeting this receptor to modulate the immune response in inflammatory and autoimmune diseases will be highlighted. Additionally, the opportunities and challenges of developing AhR-based therapies to suppress inflammation will be discussed.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Humans ; Inflammation/drug therapy ; Inflammation/genetics ; Inflammation/immunology ; Molecular Targeted Therapy ; Mutation/genetics ; Receptors, Aryl Hydrocarbon/chemistry ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Receptors, Aryl Hydrocarbon
Language	English
Publishing date	2021-12-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23010288
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