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Article ; Online: Systemic Lupus Erythematosus Pathogenesis: Interferon and Beyond.

Caielli, Simone / Wan, Zurong / Pascual, Virginia

2023 Volume 41, Page(s) 533–560

Abstract: Autoreactive B cells and interferons are central players in systemic lupus erythematosus (SLE) pathogenesis. The partial success of drugs targeting these pathways, however, supports heterogeneity in upstream mechanisms contributing to disease ... ...

Abstract	Autoreactive B cells and interferons are central players in systemic lupus erythematosus (SLE) pathogenesis. The partial success of drugs targeting these pathways, however, supports heterogeneity in upstream mechanisms contributing to disease pathogenesis. In this review, we focus on recent insights from genetic and immune monitoring studies of patients that are refining our understanding of these basic mechanisms. Among them, novel mutations in genes affecting intrinsic B cell activation or clearance of interferogenic nucleic acids have been described. Mitochondria have emerged as relevant inducers and/or amplifiers of SLE pathogenesis through a variety of mechanisms that include disruption of organelle integrity or compartmentalization, defective metabolism, and failure of quality control measures. These result in extra- or intracellular release of interferogenic nucleic acids as well as in innate and/or adaptive immune cell activation. A variety of classic and novel SLE autoantibody specificities have been found to recapitulate genetic alterations associated with monogenic lupus or to trigger interferogenic amplification loops. Finally, atypical B cells and novel extrafollicular T helper cell subsets have been proposed to contribute to the generation of SLE autoantibodies. Overall, these novel insights provide opportunities to deepen the immunophenotypic surveillance of patients and open the door to patient stratification and personalized, rational approaches to therapy.
MeSH term(s)	Humans ; Animals ; Interferons/therapeutic use ; Lupus Erythematosus, Systemic ; B-Lymphocytes ; T-Lymphocytes, Helper-Inducer ; Autoantibodies
Chemical Substances	Interferons (9008-11-1) ; Autoantibodies
Language	English
Publishing date	2023-02-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-101921-042422
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Article ; Online: Morpholinium‐Modified, Polyketone‐Based Anion Exchange Membranes for Water Electrolysis

Dr. Simone Bonizzoni / Diego Stucchi / Tommaso Caielli / Dr. Eva Sediva / Prof. Dr. Michele Mauri / Prof. Dr. Piercarlo Mustarelli

ChemElectroChem, Vol 10, Iss 6, Pp n/a-n/a (2023)

2023

Abstract: Abstract Water electrolysis is by far the most appealing method to produce green hydrogen. Among the possible technologies, Anion Exchange Membrane (AEM) water electrolyzers are promising in the medium term, as they make it possible to avoid critical and ...

Abstract	Abstract Water electrolysis is by far the most appealing method to produce green hydrogen. Among the possible technologies, Anion Exchange Membrane (AEM) water electrolyzers are promising in the medium term, as they make it possible to avoid critical and noble materials as catalyst components. However, AEMs are still lacking in performance and stability, which has become the current research focus. Here, we report the facile and inexpensive chemical modification of polyketone (PK) with a functional unit encompassing morpholinium as the positively charged group, and the fabrication of self‐standing membranes. The synthesis products are investigated with an ensemble of physico‐chemical and spectroscopic techniques, including solid‐state and time‐domain NMR, FT‐IR, and thermal analysis. The membranes show good Ion Exchange Capacity values in the range 1.48–2.24 mmol g−1. A preliminary electrolysis test shows that the PK‐based membrane has performance comparable to that of a commercial one.
Keywords	Anion Exchange Membrane ; fuel cell ; electrolysis ; hydrogen ; polyketone ; Industrial electrochemistry ; TP250-261 ; Chemistry ; QD1-999
Subject code	660
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Wiley-VCH
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: An unconventional mechanism of IL-1β secretion that requires Type I IFN in lupus monocytes.

Caielli, Simone / Balasubramanian, Preetha / Rodriguez-Alcazar, Juan / Balaji, Uthra / Wan, Zurong / Baisch, Jeanine / Smitherman, Cynthia / Walters, Lynnette / Sparagana, Paola / Nehar-Belaid, Djamel / Marches, Radu / Nassi, Lorien / Stewart, Katie / Fuller, Julie / Banchereau, Jacques F / Gu, Jinghua / Wright, Tracey / Pascual, Virginia

bioRxiv : the preprint server for biology

2023

Abstract: Systemic Lupus Erythematosus (SLE) is characterized by autoreactive B cell activation, upregulation of Type I Interferon (IFN) and widespread inflammation. Mitochondrial nucleic acids (NAs) are increasingly recognized as triggers of ... ...

Abstract	Systemic Lupus Erythematosus (SLE) is characterized by autoreactive B cell activation, upregulation of Type I Interferon (IFN) and widespread inflammation. Mitochondrial nucleic acids (NAs) are increasingly recognized as triggers of IFN
Language	English
Publishing date	2023-08-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.08.03.551696
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Article ; Online: Extracellular vesicle- and particle-mediated communication shapes innate and adaptive immune responses.

Pelissier Vatter, Fanny A / Cioffi, Michele / Hanna, Samer J / Castarede, Ines / Caielli, Simone / Pascual, Virginia / Matei, Irina / Lyden, David

The Journal of experimental medicine

2021 Volume 218, Issue 8

Abstract: Intercellular communication among immune cells is vital for the coordination of proper immune responses. Extracellular vesicles and particles (EVPs) act as messengers in intercellular communication, with important consequences for target cell and organ ... ...

Abstract	Intercellular communication among immune cells is vital for the coordination of proper immune responses. Extracellular vesicles and particles (EVPs) act as messengers in intercellular communication, with important consequences for target cell and organ physiology in both health and disease. Under normal physiological conditions, immune cell-derived EVPs participate in immune responses by regulating innate and adaptive immune responses. EVPs play a major role in antigen presentation and immune activation. On the other hand, immune cell-derived EVPs exert immunosuppressive and regulatory effects. Consequently, EVPs may contribute to pathological conditions, such as autoimmune and inflammatory diseases, graft rejection, and cancer progression and metastasis. Here, we provide an overview of the role of EVPs in immune homeostasis and pathophysiology, with a particular focus on their contribution to innate and adaptive immunity and their potential use for immunotherapies.
MeSH term(s)	Adaptive Immunity ; Animals ; Cell Communication/immunology ; Cell-Derived Microparticles/immunology ; Extracellular Vesicles/immunology ; Humans ; Immunity, Innate ; Immunotherapy
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20202579
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Article ; Online: Association of Juvenile Dermatomyositis Disease Activity With the Expansion of Blood Memory B and T Cell Subsets Lacking Follicular Markers.

Gofshteyn, Jacqueline S / Mansfield, Leanne / Spitznagle, Jacob / Balasubramanian, Preetha / Cardenas, Jacob / Miller, Thomas / Gu, Jinghua / Wang, Xuan / Punaro, Marilynn / Fuller, Julie / Nassi, Lorien / Stewart, Katie / Ohouo, Marina / Stagnar, Cristy / Baisch, Jeanine / Walters, Lynnette / Wang, Yuanyuan / Yan, Helena / Rinchai, Darawan /

Chaussabel, Damien / Caielli, Simone / Hong, Seunghee / Onel, Karen / Wright, Tracey / Pascual, Virginia

Arthritis & rheumatology (Hoboken, N.J.)

2023 Volume 75, Issue 7, Page(s) 1246–1261

Abstract: Objective: This study was undertaken to identify blood markers of juvenile dermatomyositis (DM) disease activity (DA), which are needed to improve disease management.: Methods: The study comprised a total of 123 juvenile DM patients and 53 healthy ... ...

Abstract	Objective: This study was undertaken to identify blood markers of juvenile dermatomyositis (DM) disease activity (DA), which are needed to improve disease management. Methods: The study comprised a total of 123 juvenile DM patients and 53 healthy controls. Results of laboratory tests (aldolase, creatinine kinase, lactate dehydrogenase [LDH], aspartate aminotransferase) and clinical measures of DA in patients with juvenile DM, including the Manual Muscle Testing in 8 muscles (MMT-8), Childhood Myositis Assessment Scale (CMAS), and disease activity scores (DAS) (total DAS for juvenile DM, the muscle DAS, and the skin DAS), were recorded when available. Surface phenotype of peripheral blood mononuclear cells was assessed using flow cytometry. Whole blood transcriptional profiles were studied using either RNA-sequencing or microarrays. Differential gene expression was determined using DESeq and compared by pathway and gene ontology analyses. Results: Conventional memory (CD27+IgD-) B cells expressing low CXCR5 levels (CXCR5 Conclusion: These findings suggest that both CM B cells lacking the CXCR5 follicular marker and CXCR5- Th2 cells represent potential biomarkers of DA in juvenile DM and may contribute to its pathogenesis.
MeSH term(s)	Humans ; Dermatomyositis/metabolism ; Leukocytes, Mononuclear ; T-Lymphocytes, Helper-Inducer/metabolism ; CD4-Positive T-Lymphocytes/metabolism ; Aldehyde-Lyases/metabolism
Chemical Substances	Aldehyde-Lyases (EC 4.1.2.-)
Language	English
Publishing date	2023-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.42446
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Article ; Online: Neutrophils come of age in chronic inflammation.

Caielli, Simone / Banchereau, Jacques / Pascual, Virginia

Current opinion in immunology

2012 Volume 24, Issue 6, Page(s) 671–677

Abstract: Neutrophils have long been known to participate in acute inflammation, but a role in chronic inflammatory and autoimmune diseases is now emerging. These cells are key players in the recognition and elimination of pathogens, but they also sense self ... ...

Abstract	Neutrophils have long been known to participate in acute inflammation, but a role in chronic inflammatory and autoimmune diseases is now emerging. These cells are key players in the recognition and elimination of pathogens, but they also sense self components, including nucleic acids and products of sterile tissue damage. While this normally contributes to tissue repair, it can also lead to the release of highly immunogenic products that can trigger and/or amplify autoimmune pathogenic loops. Understanding the mechanisms that underlie neutrophil activation, migration, survival and their various forms of death in health and disease might provide us with new approaches to treat chronic inflammatory conditions.
MeSH term(s)	Autoimmune Diseases/immunology ; Chronic Disease ; Humans ; Immune System Diseases ; Inflammation/immunology ; Leukocyte Disorders ; Neutrophil Activation/physiology ; Neutrophils/physiology
Language	English
Publishing date	2012-11-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2012.09.008
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Article: Neutrophils come of age in chronic inflammation

Caielli, Simone / Banchereau, Jacques / Pascual, Virginia

Current Opinion in Immunology. 2012 Dec., v. 24, no. 6

2012

Abstract	Neutrophils have long been known to participate in acute inflammation, but a role in chronic inflammatory and autoimmune diseases is now emerging. These cells are key players in the recognition and elimination of pathogens, but they also sense self components, including nucleic acids and products of sterile tissue damage. While this normally contributes to tissue repair, it can also lead to the release of highly immunogenic products that can trigger and/or amplify autoimmune pathogenic loops. Understanding the mechanisms that underlie neutrophil activation, migration, survival and their various forms of death in health and disease might provide us with new approaches to treat chronic inflammatory conditions.
Keywords	autoimmune diseases ; inflammation ; neutrophils ; nucleic acids ; pathogens ; tissue repair
Language	English
Dates of publication	2012-12
Size	p. 671-677.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2012.09.008
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Article ; Online: Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLE.

Caielli, Simone / Cardenas, Jacob / de Jesus, Adriana Almeida / Baisch, Jeanine / Walters, Lynnette / Blanck, Jean Philippe / Balasubramanian, Preetha / Stagnar, Cristy / Ohouo, Marina / Hong, Seunghee / Nassi, Lorien / Stewart, Katie / Fuller, Julie / Gu, Jinghua / Banchereau, Jacques F / Wright, Tracey / Goldbach-Mansky, Raphaela / Pascual, Virginia

Cell

2021 Volume 184, Issue 17, Page(s) 4464–4479.e19

Abstract: Emerging evidence supports that mitochondrial dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis. Here we show that programmed mitochondrial removal, a hallmark of mammalian erythropoiesis, is defective in SLE. Specifically, we ... ...

Abstract	Emerging evidence supports that mitochondrial dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis. Here we show that programmed mitochondrial removal, a hallmark of mammalian erythropoiesis, is defective in SLE. Specifically, we demonstrate that during human erythroid cell maturation, a hypoxia-inducible factor (HIF)-mediated metabolic switch is responsible for the activation of the ubiquitin-proteasome system (UPS), which precedes and is necessary for the autophagic removal of mitochondria. A defect in this pathway leads to accumulation of red blood cells (RBCs) carrying mitochondria (Mito
MeSH term(s)	Adolescent ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Child ; Child, Preschool ; Erythroblasts/metabolism ; Erythroblasts/ultrastructure ; Erythrocytes/metabolism ; Erythropoiesis ; Humans ; Interferon Type I/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Mitochondria/metabolism ; Mitophagy ; Myeloid Cells/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Ubiquitin/metabolism
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Interferon Type I ; Ubiquitin ; endothelial PAS domain-containing protein 1 (1B37H0967P) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2021-08-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2021.07.021
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Article ; Online: The dangerous liaison between iNKT cells and dendritic cells: does it prevent or promote autoimmune diseases?

Caielli, Simone / Sorini, Chiara / Falcone, Marika

Autoimmunity

2011 Volume 44, Issue 1, Page(s) 11–22

Abstract: Invariant natural killer T (iNKT) cells represent an important regulatory T-cell subset that perceives signals of danger and/or cellular distress and modulate the adaptive immune response accordingly. In the presence of pathogens, iNKT cells acquire an ... ...

Abstract	Invariant natural killer T (iNKT) cells represent an important regulatory T-cell subset that perceives signals of danger and/or cellular distress and modulate the adaptive immune response accordingly. In the presence of pathogens, iNKT cells acquire an adjuvant function that is fundamental to boost anti-microbial and anti-tumor immunity. At the same time, iNKT cells can play a negative regulatory function to maintain peripheral T-cell tolerance toward self-antigens and to prevent autoimmune disease. Both these effects of iNKT cells involve the modulation of the activity of dendritic cells (DCs) through cell-cell interaction. Indeed, iNKT cells can either boost Th1 immunity by enhancing maturation of pro-inflammatory DCs or promote immune tolerance through the maturation of tolerogenic DCs. This dual action of iNKT cells opens questions on the modalities by which a single-cell subset can exert opposite effects on DCs and may even put in question the overall immunosuppressive properties of iNKT cells. This review presents the large body of evidence that shows the ability of iNKT cells to negatively regulate autoimmunity and to prevent autoimmune diseases including multiple sclerosis, type 1 diabetes, rheumatoid arthritis, and systemic lupus erythematosus. In addition, an update is provided on the mechanisms of iNKT-DCs interactions and how this can result in inflammatory or tolerogenic responses.
MeSH term(s)	Adaptive Immunity ; Autoimmune Diseases/immunology ; Autoimmune Diseases/prevention & control ; Dendritic Cells/immunology ; Humans ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Self Tolerance ; Th1 Cells/immunology ; Transplantation Tolerance
Language	English
Publishing date	2011-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1025450-x
ISSN	1607-842X ; 0891-6934
ISSN (online)	1607-842X
ISSN	0891-6934
DOI	10.3109/08916931003782130
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Article: Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLE

Caielli, Simone / Cardenas, Jacob / de Jesus, Adriana Almeida / Baisch, Jeanine / Walters, Lynnette / Blanck, Jean Philippe / Balasubramanian, Preetha / Stagnar, Cristy / Ohouo, Marina / Hong, Seunghee / Nassi, Lorien / Stewart, Katie / Fuller, Julie / Gu, Jinghua / Banchereau, Jacques F. / Wright, Tracey / Goldbach-Mansky, Raphaela / Pascual, Virginia

Cell. 2021 Aug. 19, v. 184, no. 17

2021

Abstract	Emerging evidence supports that mitochondrial dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis. Here we show that programmed mitochondrial removal, a hallmark of mammalian erythropoiesis, is defective in SLE. Specifically, we demonstrate that during human erythroid cell maturation, a hypoxia-inducible factor (HIF)-mediated metabolic switch is responsible for the activation of the ubiquitin-proteasome system (UPS), which precedes and is necessary for the autophagic removal of mitochondria. A defect in this pathway leads to accumulation of red blood cells (RBCs) carrying mitochondria (Mito⁺ RBCs) in SLE patients and in correlation with disease activity. Antibody-mediated internalization of Mito⁺ RBCs induces type I interferon (IFN) production through activation of cGAS in macrophages. Accordingly, SLE patients carrying both Mito⁺ RBCs and opsonizing antibodies display the highest levels of blood IFN-stimulated gene (ISG) signatures, a distinctive feature of SLE.
Keywords	erythropoiesis ; genes ; humans ; interferons ; lupus erythematosus ; macrophages ; mitochondria ; pathogenesis
Language	English
Dates of publication	2021-0819
Size	p. 4464-4479.e19.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2021.07.021
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