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Article ; Online: Molecular subtypes of m

Guan, Bo / Ren, Feng / Shan, Weimin / Zhang, Shangrong

2022 Volume 11, Issue 3, Page(s) 508–518

Abstract: Background: In this study, we sought to investigate the association between N6-methyladenosine (m: Methods: First, the clinical data and the transcriptomes of 530 patients with ccRCC were downloaded from The Cancer Genome Atlas (TCGA). The expression ...

Abstract	Background: In this study, we sought to investigate the association between N6-methyladenosine (m Methods: First, the clinical data and the transcriptomes of 530 patients with ccRCC were downloaded from The Cancer Genome Atlas (TCGA). The expression patterns of m Results: Among the 13 m Conclusions: Following TCGA data-mining, different molecular subtypes of ccRCC based on m
Language	English
Publishing date	2022-03-09
Publishing country	China
Document type	Journal Article
ZDB-ID	2901601-0
ISSN	2219-6803 ; 2218-676X
ISSN (online)	2219-6803
ISSN	2218-676X
DOI	10.21037/tcr-22-117
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Article ; Online: Adverse Effects of Prenatal Exposure to Oxidized Black Carbon Particles on the Reproductive System of Male Mice.

Jiang, Shuanglin / Chen, Li / Shen, Jianyun / Zhang, Di / Wu, Hai / Wang, Rong / Zhang, Shangrong / Jiang, Nan / Li, Wenyong

Toxics

2023 Volume 11, Issue 7

Abstract: Ambient black carbon (BC), a main constituent of atmospheric particulate matter (PM), is a primary particle that is mainly generated by the incomplete combustion of fossil fuel and biomass burning. BC has been identified as a potential health risk via ... ...

Abstract	Ambient black carbon (BC), a main constituent of atmospheric particulate matter (PM), is a primary particle that is mainly generated by the incomplete combustion of fossil fuel and biomass burning. BC has been identified as a potential health risk via exposure. However, the adverse effects of exposure to BC on the male reproductive system remain unclear. In the present study, we explored the effects of maternal exposure to oxidized black carbon (OBC) during pregnancy on testicular development and steroid synthesis in male offspring. Pregnant mice were exposed to OBC (467 μg/kg BW) or nanopure water (as control) by intratracheal instillation from gestation day (GD) 4 to GD 16.5 (every other day). We examined the testicular histology, daily sperm production, serum testosterone, and mRNA expression of hormone synthesis process-related factors of male offspring at postnatal day (PND) 35 and PND 84. Histological examinations exhibited abnormal seminiferous tubules with degenerative changes and low cellular adhesion in testes of OBC-exposed mice at PND 35 and PND 84. Consistent with the decrease in daily sperm production, the serum testosterone level of male offspring of OBC-exposed mice also decreased significantly. Correspondingly, mRNA expression levels of hormone-synthesis-related genes (i.e.,
Language	English
Publishing date	2023-06-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2733883-6
ISSN	2305-6304 ; 2305-6304
ISSN (online)	2305-6304
ISSN	2305-6304
DOI	10.3390/toxics11070556
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Article ; Online: Knockdown of Toe1 causes developmental arrest during the morula-to-blastocyst transition in mice

Wang, Hongcheng / Ming, Xin / Zhang, Shengnan / Chen, Ji / Liu, Xinli / Wu, Xiaoqing / Zhang, Shangrong / Zhang, Yunhai / Cui, Wei / Li, Wenyong / Liu, Yong

Theriogenology. 2022 Dec., v. 194 p.154-161

2022

Abstract: The target of EGR1 protein 1 (TOE1) is evolutionarily conserved from Caenorhabditis elegans to mammals, which plays a critical role in the maturation of a variety of small nuclear RNAs. Mutation in human TOE1 has been reported to cause pontocerebellar ... ...

Abstract	The target of EGR1 protein 1 (TOE1) is evolutionarily conserved from Caenorhabditis elegans to mammals, which plays a critical role in the maturation of a variety of small nuclear RNAs. Mutation in human TOE1 has been reported to cause pontocerebellar hypoplasia type 7, a severe neurodegenerative syndrome. However, the role of TOE1 in early embryonic development remains unclear. Herein, we found that Toe1 mRNA and protein were expressed in mouse preimplantation embryos. Silencing Toe1 by siRNA led to morula-to-blastocyst transition failure. This developmental arrest can be rescued by Toe1 mRNA microinjection. EdU incorporation assay showed a defect in blastomere proliferation within developmentally arrested embryos. Further studies revealed that Toe1 knockdown caused increased signals for γH2AX and micronuclei, indicative of sustained DNA damage. Moreover, mRNA levels of cell cycle inhibitor p21 were significantly upregulated in Toe1 knockdown embryos before developmental arrest. Together, these results suggest that TOE1 is indispensable for mouse early embryo development potentially through maintaining genomic integrity. Our findings provide further insight into the role of TOE1 in mouse preimplantation embryonic development.
Keywords	Caenorhabditis elegans ; DNA damage ; animal reproduction ; cell cycle ; embryogenesis ; genomics ; humans ; mice ; mutation ; TOE1 ; Target of EGR1 protein 1 ; Morula-to-blastocyst transition ; Developmental arrest ; Genomic integrity
Language	English
Dates of publication	2022-12
Size	p. 154-161.
Publishing place	Elsevier Inc.
Document type	Article ; Online
ZDB-ID	189232-0
ISSN	1879-3231 ; 0093-691X
ISSN (online)	1879-3231
ISSN	0093-691X
DOI	10.1016/j.theriogenology.2022.10.011
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Article: MiR-1281 is involved in depression disorder and the antidepressant effects of Kai-Xin-San by targeting ADCY1 and DVL1.

Chen, Chao / Xu, Yuan-Jie / Zhang, Shang-Rong / Wang, Xiao-Hui / Hu, Yuan / Guo, Dai-Hong / Zhou, Xiao-Jiang / Zhu, Wei-Yu / Wen, Ai-Dong / Tan, Qing-Rong / Dong, Xian-Zhe / Liu, Ping

Heliyon

2023 Volume 9, Issue 3, Page(s) e14265

Abstract: Kai-Xin-San (KXS) is a Chinese medicine formulation that is commonly used to treat depression caused by dual deficiencies in the heart and spleen. Recent studies indicated that miRNAs were involved in the pathophysiology of depression. However, there ... ...

Abstract	Kai-Xin-San (KXS) is a Chinese medicine formulation that is commonly used to treat depression caused by dual deficiencies in the heart and spleen. Recent studies indicated that miRNAs were involved in the pathophysiology of depression. However, there have been few studies on the mechanism underlying the miRNAs directly mediating antidepressant at clinical level, especially in nature drugs and TCM compound. In this study, we identified circulating miRNAs defferentially expressed among the depression patients (DPs), DPs who underwent 8weeks of KXS treatment and health controls (HCs). A total of 45 miRNAs (17 were up-regulated and 28 were down-regulated) were significantly differentially expressed among three groups. Subsequently, qRT-PCR was used to verify 10 differentially expressed candidate miRNAs in more serum samples, and the results showed that 6 miRNAs (miR-1281, miR-365a-3p, miR-2861, miR-16-5p, miR-1202 and miR-451a) were consistent with the results of microarray. Among them, miR-1281, was the novel dynamically altered and appeared to be specifically related to depression and antidepressant effects of KXS. MicroRNA-gene-pathway-net analysis showed that miR-1281-regulated genes are mostly key nodes in the classical signaling pathway related to depression. Additionally, our data suggest that ADCY1 and DVL1 were the targets of miR-1281. Thus, based on the discovery of miRNA expression profiles in vivo, our findings suggest a new role for miR-1281 related to depression and demonstrated in vitro that KXS may activate cAMP/PKA/ERK/CREB and Wnt/β-catenin signal transduction pathways by down-regulating miR-1281 that targets ADCY1 and DVL1 to achieve its role in neuronal cell protection.
Language	English
Publishing date	2023-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e14265
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Article ; Online: MiR-1281 is involved in depression disorder and the antidepressant effects of Kai-Xin-San by targeting ADCY1 and DVL1

Chen, Chao / Xu, Yuan-jie / Zhang, Shang-rong / Wang, Xiao-hui / Hu, Yuan / Guo, Dai-hong / Zhou, Xiao-jiang / Zhu, Wei-yu / Wen, Ai-Dong / Tan, Qing-Rong / Dong, Xian-Zhe / Liu, Ping

Heliyon. 2023 Mar., v. 9, no. 3 p.e14265-

2023

Abstract	Kai-Xin-San (KXS) is a Chinese medicine formulation that is commonly used to treat depression caused by dual deficiencies in the heart and spleen. Recent studies indicated that miRNAs were involved in the pathophysiology of depression. However, there have been few studies on the mechanism underlying the miRNAs directly mediating antidepressant at clinical level, especially in nature drugs and TCM compound. In this study, we identified circulating miRNAs defferentially expressed among the depression patients (DPs), DPs who underwent 8weeks of KXS treatment and health controls (HCs). A total of 45 miRNAs (17 were up-regulated and 28 were down-regulated) were significantly differentially expressed among three groups. Subsequently, qRT-PCR was used to verify 10 differentially expressed candidate miRNAs in more serum samples, and the results showed that 6 miRNAs (miR-1281, miR-365a-3p, miR-2861, miR-16-5p, miR-1202 and miR-451a) were consistent with the results of microarray. Among them, miR-1281, was the novel dynamically altered and appeared to be specifically related to depression and antidepressant effects of KXS. MicroRNA-gene-pathway-net analysis showed that miR-1281-regulated genes are mostly key nodes in the classical signaling pathway related to depression. Additionally, our data suggest that ADCY1 and DVL1 were the targets of miR-1281. Thus, based on the discovery of miRNA expression profiles in vivo, our findings suggest a new role for miR-1281 related to depression and demonstrated in vitro that KXS may activate cAMP/PKA/ERK/CREB and Wnt/β-catenin signal transduction pathways by down-regulating miR-1281 that targets ADCY1 and DVL1 to achieve its role in neuronal cell protection.
Keywords	Oriental traditional medicine ; antidepressants ; blood serum ; gene expression regulation ; heart ; microRNA ; microarray technology ; neurons ; pathophysiology ; signal transduction ; spleen ; Depression ; Kai-Xin-San ; miR-1281 ; ADCY1 ; DVL1
Language	English
Dates of publication	2023-03
Publishing place	Elsevier Ltd
Document type	Article ; Online
Note	Use and reproduction
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e14265
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Article ; Online: Knockdown of Toe1 causes developmental arrest during the morula-to-blastocyst transition in mice.

Wang, Hongcheng / Ming, Xin / Zhang, Shengnan / Chen, Ji / Liu, Xinli / Wu, Xiaoqing / Zhang, Shangrong / Zhang, Yunhai / Cui, Wei / Li, Wenyong / Liu, Yong

Theriogenology

2022 Volume 194, Page(s) 154–161

Abstract	The target of EGR1 protein 1 (TOE1) is evolutionarily conserved from Caenorhabditis elegans to mammals, which plays a critical role in the maturation of a variety of small nuclear RNAs. Mutation in human TOE1 has been reported to cause pontocerebellar hypoplasia type 7, a severe neurodegenerative syndrome. However, the role of TOE1 in early embryonic development remains unclear. Herein, we found that Toe1 mRNA and protein were expressed in mouse preimplantation embryos. Silencing Toe1 by siRNA led to morula-to-blastocyst transition failure. This developmental arrest can be rescued by Toe1 mRNA microinjection. EdU incorporation assay showed a defect in blastomere proliferation within developmentally arrested embryos. Further studies revealed that Toe1 knockdown caused increased signals for γH2AX and micronuclei, indicative of sustained DNA damage. Moreover, mRNA levels of cell cycle inhibitor p21 were significantly upregulated in Toe1 knockdown embryos before developmental arrest. Together, these results suggest that TOE1 is indispensable for mouse early embryo development potentially through maintaining genomic integrity. Our findings provide further insight into the role of TOE1 in mouse preimplantation embryonic development.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Pregnancy ; Blastocyst ; Embryonic Development ; Gene Expression Regulation, Developmental ; Genome ; Morula ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	Nuclear Proteins ; RNA, Messenger ; Toe1 protein, mouse
Language	English
Publishing date	2022-10-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	189232-0
ISSN	1879-3231 ; 0093-691X
ISSN (online)	1879-3231
ISSN	0093-691X
DOI	10.1016/j.theriogenology.2022.10.011
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 3929: Show issues

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Article ; Online: Muscarinic acetylcholine receptors regulate inflammatory responses through arginases 1/2 in zebrafish.

Chen, An-Qi / He, Shi-Min / Lv, Shi-Jie / Qiu, Cheng-Zeng / Zhou, Ren / Zhang, Ling / Zhang, Shang-Rong / Zhang, Zijun / Ren, Da-Long

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2022 Volume 153, Page(s) 113321

Abstract: Muscarinic acetylcholine receptors (mAChRs) are widely expressed in various effector cells and have been proved to play vital roles in smooth muscle contraction and digestive secretion. However, there are relatively few literatures revealing the roles of ...

Abstract	Muscarinic acetylcholine receptors (mAChRs) are widely expressed in various effector cells and have been proved to play vital roles in smooth muscle contraction and digestive secretion. However, there are relatively few literatures revealing the roles of mAChRs in inflammatory processes, and its underlying regulatory mechanisms have not been elucidated. Taking the advantages of live imaging of zebrafish, we found that inhibition of mAChRs resulted in increased neutrophils recruitment and proinflammatory cytokines expression, whereas activation of mAChRs led to opposite outcome. Subsequently, we found that mAChRs regulated the expression of arginases (args), and pharmacological intervention of args level could reverse the effects of mAChRs on neutrophils migration and cytokines expression, suggesting that args are important downstream proteins of mAChRs that mediate the regulation of inflammatory response. In this study, we identified args as novel downstream proteins of mAChRs in inflammatory responses, providing additional evidence for system immune regulation of cholinergic receptors.
MeSH term(s)	Animals ; Arginase ; Cytokines ; Receptors, Muscarinic/genetics ; Receptors, Muscarinic/metabolism ; Zebrafish/metabolism
Chemical Substances	Cytokines ; Receptors, Muscarinic ; Arginase (EC 3.5.3.1)
Language	English
Publishing date	2022-06-24
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2022.113321
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Article ; Online: Lansoprazole induces apoptosis of breast cancer cells through inhibition of intracellular proton extrusion.

Zhang, Shangrong / Wang, Yifan / Li, Shu Jie

Biochemical and biophysical research communications

2014 Volume 448, Issue 4, Page(s) 424–429

Abstract: The increased glycolysis and proton secretion in tumors is proposed to contribute to the proliferation and invasion of cancer cells during the process of tumorigenesis and metastasis. Here, treatment of human breast cancer cells with proton pump ... ...

Abstract	The increased glycolysis and proton secretion in tumors is proposed to contribute to the proliferation and invasion of cancer cells during the process of tumorigenesis and metastasis. Here, treatment of human breast cancer cells with proton pump inhibitor (PPI) lansoprazole (LPZ) induces cell apoptosis in a dose-dependent manner. In the implantation of the MDA-MB-231 xenografts in nude mice, administration of LPZ significantly inhibits tumorigenesis and induces large-scale apopotosis of tumor cells. LPZ markedly inhibits intracellular proton extrusion, induces an increase in intracellular ATP level, lysosomal alkalinization and accumulation of reactive oxygen species (ROS) in breast cancer cells. The ROS scavenger N-acetyl-l-cysteine (NAC) and diphenyleneiodonium (DPI), a specific pharmacological inhibitor of NADPH oxidases (NOX), significantly abolish LPZ-induced ROS accumulation in breast cancer cells. Our results suggested that LPZ may be used as a new therapeutic drug for breast tumor.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Female ; Humans ; Hydrogen-Ion Concentration ; Lansoprazole/pharmacology ; Lysosomes/drug effects ; Lysosomes/metabolism ; Mice ; Mice, Nude ; Proton Pump Inhibitors/pharmacology ; Protons ; Reactive Oxygen Species/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Proton Pump Inhibitors ; Protons ; Reactive Oxygen Species ; Lansoprazole (0K5C5T2QPG) ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2014-06-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2014.04.127
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Article: Lansoprazole induces apoptosis of breast cancer cells through inhibition of intracellular proton extrusion

Zhang, Shangrong / Wang, Yifan / Li, Shu Jie

Biochemical and biophysical research communications. 2014 June 13, v. 448

2014

Abstract	The increased glycolysis and proton secretion in tumors is proposed to contribute to the proliferation and invasion of cancer cells during the process of tumorigenesis and metastasis. Here, treatment of human breast cancer cells with proton pump inhibitor (PPI) lansoprazole (LPZ) induces cell apoptosis in a dose-dependent manner. In the implantation of the MDA-MB-231 xenografts in nude mice, administration of LPZ significantly inhibits tumorigenesis and induces large-scale apopotosis of tumor cells. LPZ markedly inhibits intracellular proton extrusion, induces an increase in intracellular ATP level, lysosomal alkalinization and accumulation of reactive oxygen species (ROS) in breast cancer cells. The ROS scavenger N-acetyl-l-cysteine (NAC) and diphenyleneiodonium (DPI), a specific pharmacological inhibitor of NADPH oxidases (NOX), significantly abolish LPZ-induced ROS accumulation in breast cancer cells. Our results suggested that LPZ may be used as a new therapeutic drug for breast tumor.
Keywords	NADP (coenzyme) ; acetylcysteine ; adenosine triphosphate ; alkalinization ; apoptosis ; breast neoplasms ; carcinogenesis ; dose response ; drugs ; extrusion ; glycolysis ; humans ; lansoprazole ; metastasis ; mice ; neoplasm cells ; proton pump inhibitors ; reactive oxygen species ; secretion
Language	English
Dates of publication	2014-0613
Size	p. 424-429.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2014.04.127
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Article ; Online: Melatonin attenuates hypoxia-induced epithelial-mesenchymal transition and cell aggressive via Smad7/ CCL20 in glioma.

Chen, Xueran / Wang, Zhen / Ma, Huihui / Zhang, Shangrong / Yang, Haoran / Wang, Hongzhi / Fang, Zhiyou

Oncotarget

2017 Volume 8, Issue 55, Page(s) 93580–93592

Abstract: Tumor recurrence in gliomas is partly attributed to increased epithelial-mesenchymal transition (EMT) and enhanced tumor cell dissemination in the adjacent brain parenchyma. Thus, exploring effective strategies for against EMT-like changes in glioma ... ...

Abstract	Tumor recurrence in gliomas is partly attributed to increased epithelial-mesenchymal transition (EMT) and enhanced tumor cell dissemination in the adjacent brain parenchyma. Thus, exploring effective strategies for against EMT-like changes in glioma invasion and recurrence will be important for glioma treatment. In this study, we investigated the roles of melatonin in hypoxia-induced EMT suppression, and found that melatonin could significantly suppress the release of the cytokine, CCL20, from cancer cells and antagonize glioma cell metastasis and invasion under hypoxic stress in glioma cells. Furthermore, our findings show that melatonin deregulates Smad7 expression to suppress TGFβ/Smad-mediated increase in CCL20 transcript levels and CCL20-induced EMT occurrence, suggesting a potential anti-EMT therapeutic role for melatonin in malignant transformation in gliomas.
Language	English
Publishing date	2017-11-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.20525
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