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Article: RNAi Therapeutics in Autoimmune Disease.

Pauley, Kaleb M / Cha, Seunghee

2013 Volume 6, Issue 3, Page(s) 287–294

Abstract: Since the discovery of RNA interference (RNAi), excitement has grown over its potential therapeutic uses. Targeting RNAi pathways provides a powerful tool to change biological processes post-transcriptionally in various health conditions such as cancer ... ...

Abstract	Since the discovery of RNA interference (RNAi), excitement has grown over its potential therapeutic uses. Targeting RNAi pathways provides a powerful tool to change biological processes post-transcriptionally in various health conditions such as cancer or autoimmune diseases. Optimum design of shRNA, siRNA, and miRNA enhances stability and specificity of RNAi-based approaches whereas it has to reduce or prevent undesirable immune responses or off-target effects. Recent advances in understanding pathogenesis of autoimmune diseases have allowed application of these tools in vitro as well as in vivo with some degree of success. Further research on the design and delivery of effectors of RNAi pathway and underlying molecular basis of RNAi would warrant practical use of RNAi-based therapeutics in human applications. This review will focus on the approaches used for current therapeutics and their applications in autoimmune diseases, including rheumatoid arthritis and Sjögren's syndrome.
Language	English
Publishing date	2013-03-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph6030287
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Article ; Online: RNAi Therapeutics in Autoimmune Disease

Seunghee Cha / Kaleb M. Pauley

Pharmaceuticals, Vol 6, Iss 3, Pp 287-

2013 Volume 294

Abstract	Since the discovery of RNA interference (RNAi), excitement has grown over its potential therapeutic uses. Targeting RNAi pathways provides a powerful tool to change biological processes post-transcriptionally in various health conditions such as cancer or autoimmune diseases. Optimum design of shRNA, siRNA, and miRNA enhances stability and specificity of RNAi-based approaches whereas it has to reduce or prevent undesirable immune responses or off-target effects. Recent advances in understanding pathogenesis of autoimmune diseases have allowed application of these tools in vitro as well as in vivo with some degree of success. Further research on the design and delivery of effectors of RNAi pathway and underlying molecular basis of RNAi would warrant practical use of RNAi-based therapeutics in human applications. This review will focus on the approaches used for current therapeutics and their applications in autoimmune diseases, including rheumatoid arthritis and Sjögren’s syndrome.
Keywords	RNA interference ; therapeutics ; microRNA ; small interfering RNA ; autoimmune disease ; Medicine ; R ; Pharmacy and materia medica ; RS1-441
Subject code	610
Language	English
Publishing date	2013-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: miRNA-146a in rheumatoid arthritis: a new therapeutic strategy.

Pauley, Kaleb M / Cha, Seunghee

Immunotherapy

2011 Volume 3, Issue 7, Page(s) 829–831

Abstract: Evaluation of: Nakasa T, Shibuya H, Nagata Y, Niimoto T, Ochi M: The inhibitory effect of microRNA ...

Abstract	Evaluation of: Nakasa T, Shibuya H, Nagata Y, Niimoto T, Ochi M: The inhibitory effect of microRNA-146a expression on bone destruction in collagen-induced arthritis. Arthritis Rheum. 63(6), 1582-1590 (2011). miRNA-146a (miR-146a) has been shown to play an important role in the negative regulation of inflammatory innate immune responses, and is differentially expressed in a number of human diseases including rheumatoid arthritis. However, evidence for the potential therapeutic use of miR-146a in human disease has been lacking. The current paper demonstrates the potential therapeutic application of miR-146a for rheumatoid arthritis by demonstrating the inhibitory effect of miR-146a on osteoclastogenesis in vitro. Moreover, using a collagen-induced arthritis mouse model, they were able to demonstrate that intravenous administration of double-stranded miR-146a resulted in the suppression of cartilage and bone destruction, despite relatively unaffected immune cell infiltration of the synovium and inflammatory cytokine expression.
Language	English
Publishing date	2011-07-13
Publishing country	England
Document type	Comment ; Journal Article
ISSN	1750-7448
ISSN (online)	1750-7448
DOI	10.2217/imt.11.70
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Article: Contrast in aberrant microRNA expression in systemic lupus erythematosus and rheumatoid arthritis: is microRNA-146 all we need?

Chan, Edward K L / Satoh, Minoru / Pauley, Kaleb M

Arthritis and rheumatism

2009 Volume 60, Issue 4, Page(s) 912–915

MeSH term(s)	Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Humans ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; MicroRNAs/genetics ; MicroRNAs/immunology
Chemical Substances	MicroRNAs
Language	English
Publishing date	2009-03-31
Publishing country	United States
Document type	Editorial
ZDB-ID	127294-9
ISSN	1529-0131 ; 0004-3591 ; 2326-5191
ISSN (online)	1529-0131
ISSN	0004-3591 ; 2326-5191
DOI	10.1002/art.24421
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Article ; Online: MicroRNA in autoimmunity and autoimmune diseases.

Pauley, Kaleb M / Cha, Seunghee / Chan, Edward K L

Journal of autoimmunity

2009 Volume 32, Issue 3-4, Page(s) 189–194

Abstract: MicroRNAs (miRNAs) are small conserved non-coding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region (UTR) of specific messenger RNAs (mRNAs) for degradation or translational repression. miRNA- ... ...

Abstract	MicroRNAs (miRNAs) are small conserved non-coding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region (UTR) of specific messenger RNAs (mRNAs) for degradation or translational repression. miRNA-mediated gene regulation is critical for normal cellular functions such as the cell cycle, differentiation, and apoptosis, and as much as one-third of human mRNAs may be miRNA targets. Emerging evidence has demonstrated that miRNAs play a vital role in the regulation of immunological functions and the prevention of autoimmunity. Here we review the many newly discovered roles of miRNA regulation in immune functions and in the development of autoimmunity and autoimmune disease. Specifically, we discuss the involvement of miRNA regulation in innate and adaptive immune responses, immune cell development, T regulatory cell stability and function, and differential miRNA expression in rheumatoid arthritis and systemic lupus erythematosus.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/metabolism ; Autoimmunity ; Gene Silencing/immunology ; Humans ; Immunity, Active ; Immunity, Innate ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/metabolism ; MicroRNAs/genetics ; MicroRNAs/immunology ; MicroRNAs/metabolism ; Toll-Like Receptors/immunology ; Toll-Like Receptors/metabolism
Chemical Substances	MicroRNAs ; Toll-Like Receptors
Language	English
Publishing date	2009-03-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2009.02.012
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Article ; Online: MicroRNAs and their emerging roles in immunology.

Pauley, Kaleb M / Chan, Edward K L

Annals of the New York Academy of Sciences

2008 Volume 1143, Page(s) 226–239

Abstract: MicroRNAs (miRNAs) are evolutionarily conserved small noncoding RNAs that post-transcriptionally regulate gene expression by targeting specific messenger RNAs (mRNAs) for degradation or translational repression. Recent evidence indicates that miRNA- ... ...

Abstract	MicroRNAs (miRNAs) are evolutionarily conserved small noncoding RNAs that post-transcriptionally regulate gene expression by targeting specific messenger RNAs (mRNAs) for degradation or translational repression. Recent evidence indicates that miRNA-mediated gene regulation is critical for normal cellular functions, and as much as one-third of human mRNAs may be miRNA targets. Emerging evidence suggests that miRNAs play a key role in the regulation of immunological functions including innate and adaptive immune responses, development and differentiation of immune cells, and the prevention of autoimmunity. Here, we review the mechanisms of miRNA maturation and function, the roles of several miRNAs in immunological functions, and the involvement of miRNAs in disease pathogenesis.
MeSH term(s)	Animals ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Cell Differentiation ; Humans ; Immunity/genetics ; MicroRNAs/metabolism ; MicroRNAs/physiology ; Models, Biological ; Neoplasms/genetics ; Neoplasms/immunology ; RNA, Messenger/metabolism
Chemical Substances	MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2008-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1196/annals.1443.009
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Article ; Online: miR-146a is critical for endotoxin-induced tolerance: IMPLICATION IN INNATE IMMUNITY.

Nahid, Md A / Pauley, Kaleb M / Satoh, Minoru / Chan, Edward K L

The Journal of biological chemistry

2009 Volume 284, Issue 50, Page(s) 34590–34599

Abstract: The human toll-like receptor 4 (TLR4) pathway is activated in response to lipopolysaccharide (LPS), and subsequent signal transductions lead to the production of cytokines such as tumor necrosis factor-alpha (TNF-alpha) by innate immune cells. Defects in ...

Abstract	The human toll-like receptor 4 (TLR4) pathway is activated in response to lipopolysaccharide (LPS), and subsequent signal transductions lead to the production of cytokines such as tumor necrosis factor-alpha (TNF-alpha) by innate immune cells. Defects in innate immune response may contribute to the overproduction of TNF-alpha leading to systemic inflammation and diseases. Thus, the innate immune response needs to be tightly regulated by elaborate mechanisms to control its onset and termination. LPS tolerance is a state of hyporesponsiveness to subsequent LPS challenge and is achieved by monocytic cells after prolonged exposure to LPS. In this report, kinetics of endotoxin-responsive microRNAs expression analysis revealed a unique pattern of gradual increase for miR-146a starting 4 h after LPS stimulation in THP-1 cells and continued up to 35-fold over 24 h. Conversely, TNF-alpha increased up to 4 h and then decreased gradually implicating a negative correlation with miR-146a progression. The characteristic up-regulation of miR-146a toward subsequent LPS challenge in THP-1 cells was studied. Strikingly, microRNA expression analysis during the tolerized state of THP-1 cells showed only miR-146a overexpression suggesting its important role in LPS tolerance. In addition, LPS tolerance was dependent on a LPS-priming dose and associated miR-146a up-regulation. LPS-tolerized cells were observed to regain responsiveness in TNF-alpha production 22 h after LPS removal correlating with a decrease in miR-146a level. Transfection of miR-146a into THP-1 cells mimicked LPS priming, whereas transfection of miR-146a inhibitor largely abolished LPS tolerance. Thus our studies demonstrated that miR-146a is critical for the in vitro monocytic cell-based endotoxin tolerance.
MeSH term(s)	Animals ; Cell Line ; Endotoxins/immunology ; Endotoxins/pharmacology ; Gene Knockdown Techniques ; Humans ; Immune Tolerance/drug effects ; Immune Tolerance/immunology ; Immunity, Innate ; Interleukin-1 Receptor-Associated Kinases/genetics ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Lipopolysaccharides/immunology ; Lipopolysaccharides/pharmacology ; MicroRNAs/genetics ; MicroRNAs/immunology ; Monocytes/cytology ; Monocytes/drug effects ; Monocytes/immunology ; Signal Transduction/immunology ; TNF Receptor-Associated Factor 6/genetics ; TNF Receptor-Associated Factor 6/metabolism ; Toll-Like Receptor 4/immunology ; Tumor Necrosis Factor-alpha/immunology
Chemical Substances	Endotoxins ; Lipopolysaccharides ; MIRN146 microRNA, human ; MicroRNAs ; TLR4 protein, human ; TNF Receptor-Associated Factor 6 ; Toll-Like Receptor 4 ; Tumor Necrosis Factor-alpha ; IRAK1 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2009-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M109.056317
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Article: Presence of Porphyromonas gingivalis in gingival squamous cell carcinoma.

Katz, Joseph / Onate, Mairelys D / Pauley, Kaleb M / Bhattacharyya, Indraneel / Cha, Seunghee

International journal of oral science

2011 Volume 3, Issue 4, Page(s) 209–215

Abstract: Periodontal disease has been recently linked to a variety of systemic conditions such as diabetes, cardiovascular disease, preterm delivery, and oral cancer. The most common bacteria associated with periodontal disease, Porphyromonas gingivalis (P. ... ...

Abstract	Periodontal disease has been recently linked to a variety of systemic conditions such as diabetes, cardiovascular disease, preterm delivery, and oral cancer. The most common bacteria associated with periodontal disease, Porphyromonas gingivalis (P. gingivalis) has not yet been studied in the malignant gingival tissues. The objective of this study was to investigate the presence of P. gingivalis in specimens from squamous cell carcinoma patients. We have performed immunohistochemical staining to investigate the presence of P. gingivalis and Streptococcus gordonii (S. gordonii), a non invasive oral bacteria, in paraffin embedded samples of gingival squamous cell carcinoma (n = 10) and normal gingiva (n = 5). Staining for P. gingivalis revealed the presence of the bacteria in normal gingival tissues and gingival carcinoma, with higher levels (more than 33%, P < 0.05) detected in the carcinoma samples. The staining intensity was also significantly enhanced in the malignant tissue by 2 folds (P < 0.023) compared to specimens stained for the non-invasive S. gordonii. P. gingivalis is abundantly present in malignant oral epithelium suggesting a potential association of the bacteria with gingival squamous cell carcinoma.
MeSH term(s)	Carcinoma, Squamous Cell/microbiology ; Gingiva/microbiology ; Gingival Neoplasms/microbiology ; Humans ; Porphyromonas gingivalis/isolation & purification ; Retrospective Studies ; Statistics, Nonparametric ; Streptococcus gordonii/isolation & purification
Language	English
Publishing date	2011-10-18
Publishing country	India
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2569849-7
ISSN	2049-3169 ; 1674-2818
ISSN (online)	2049-3169
ISSN	1674-2818
DOI	10.4248/IJOS11075
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Article ; Online: Animal models in autoimmune diseases: lessons learned from mouse models for Sjögren's syndrome.

Lee, Byung Ha / Gauna, Adrienne E / Pauley, Kaleb M / Park, Yun-Jong / Cha, Seunghee

Clinical reviews in allergy & immunology

2011 Volume 42, Issue 1, Page(s) 35–44

Abstract: The mouse model is the one of the most frequently used and well-established animal models, and is currently used in many research areas. To date, various mouse models have been utilized to elucidate underlying causes of multifactorial autoimmune ... ...

Abstract	The mouse model is the one of the most frequently used and well-established animal models, and is currently used in many research areas. To date, various mouse models have been utilized to elucidate underlying causes of multifactorial autoimmune conditions, including pathological immune components and specific signaling pathways. This review summarizes the more recent mouse models for Sjögren's syndrome, a systemic autoimmune disease characterized by lymphocytic infiltration in the exocrine glands, such as the salivary and lacrimal glands, and loss of secretory function, resulting in dry mouth and dry eyes in patients. Although every Sjögren's syndrome mouse model resembles the major symptoms or phenotypes of Sjögren's syndrome conditions in humans, the characteristics of each model are variable. Moreover, to date, there is no single mouse model that can completely replicate the human conditions. However, unique features of each mouse model provide insights into the roles of potential etiological and immunological factors in the development and progression of Sjögren's syndrome. Here, we will overview the Sjögren's syndrome mouse models. Lessons from these mouse models will aid us to understand underlying immune dysregulation in autoimmune diseases in general, and will guide us to direct future research towards appropriate diagnostic and therapeutic strategies.
MeSH term(s)	Animals ; Autoimmune Diseases/etiology ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Disease Models, Animal ; Humans ; Sjogren's Syndrome/etiology ; Sjogren's Syndrome/immunology ; Sjogren's Syndrome/pathology
Language	English
Publishing date	2011-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1239045-8
ISSN	1559-0267 ; 1080-0549
ISSN (online)	1559-0267
ISSN	1080-0549
DOI	10.1007/s12016-011-8288-5
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Article ; Online: A secretagogue-small interfering RNA conjugate confers resistance to cytotoxicity in a cell model of Sjögren's syndrome.

Pauley, Kaleb M / Gauna, Adrienne E / Grichtchenko, Irina I / Chan, Edward K L / Cha, Seunghee

Arthritis and rheumatism

2011 Volume 63, Issue 10, Page(s) 3116–3125

Abstract: Objective: Sjögren's syndrome (SS) is characterized by xerophthalmia and xerostomia resulting from loss of secretory function due to immune cell infiltration in lacrimal and salivary glands. Current therapeutic strategies for SS use secretagogues to ... ...

Abstract	Objective: Sjögren's syndrome (SS) is characterized by xerophthalmia and xerostomia resulting from loss of secretory function due to immune cell infiltration in lacrimal and salivary glands. Current therapeutic strategies for SS use secretagogues to induce secretion via muscarinic receptor stimulation. The purpose of this study was to create a secretagogue-small interfering RNA (siRNA) conjugate to deliver siRNA into cells via receptor-mediated endocytosis, thereby altering epithelial cell responses to external cues, such as proinflammatory or death signals, while simultaneously stimulating secretion. Methods: Based on our expertise with type 3 muscarinic receptor (M3), we used carbachol, a ligand specific for muscarinic receptor, as the secretagogue. Carbachol was synthesized with an active choline group and was conjugated with an siRNA that targets caspase 3. A human salivary gland (HSG) cell line was used to test the efficacy of this secretagogue-siRNA conjugate. Results: Lipofectamine transfection of the conjugate into HSG cells resulted in a 78% reduction in the expression of the caspase 3 gene, while external conjugate treatment of HSG cells resulted in intracellular calcium release and induction of endocytosis at levels similar to those of carbachol stimulation, indicating that the siRNA and carbachol portions of the conjugate retained their function after conjugation. HSG cells treated with conjugate (without Lipofectamine transfection) exhibited a 50% reduction in caspase 3 gene and protein expression, indicating that our conjugate was effective in delivering functional siRNA into cells via receptor-mediated endocytosis. Furthermore, tumor necrosis factor α-induced apoptosis was significantly reduced in conjugate-treated cells. Conclusion: Our secretagogue-siRNA conjugate prevented cytokine-induced apoptosis in salivary gland epithelial cells, which is critical to maintaining fluid secretion and potentially reversing the clinical hallmark of SS.
MeSH term(s)	Carbachol/administration & dosage ; Caspase Inhibitors ; Cell Line ; Cholinergic Agonists/administration & dosage ; Humans ; RNA Interference ; RNA, Small Interfering/administration & dosage ; Salivary Glands/cytology ; Salivary Glands/drug effects ; Sjogren's Syndrome/therapy
Chemical Substances	Caspase Inhibitors ; Cholinergic Agonists ; RNA, Small Interfering ; Carbachol (8Y164V895Y)
Language	English
Publishing date	2011-05-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	127294-9
ISSN	1529-0131 ; 0004-3591 ; 2326-5191
ISSN (online)	1529-0131
ISSN	0004-3591 ; 2326-5191
DOI	10.1002/art.30450
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