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Article ; Online: Glomeruloid Hemangioma in a Patient with TAFRO Syndrome.

Osano, Keiichi / Hanai, Shunichiro / Takahashi, Kazuya / Furuya, Fumihiko

2022 Volume 61, Issue 16, Page(s) 2545–2546

MeSH term(s)	Castleman Disease ; Hemangioma/diagnosis ; Hemangioma/diagnostic imaging ; Humans ; POEMS Syndrome
Language	English
Publishing date	2022-02-01
Publishing country	Japan
Document type	Journal Article
ZDB-ID	32371-8
ISSN	1349-7235 ; 0021-5120 ; 0918-2918
ISSN (online)	1349-7235
ISSN	0021-5120 ; 0918-2918
DOI	10.2169/internalmedicine.8888-21
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Article ; Online: Membrane protease prostasin promotes insulin secretion by regulating the epidermal growth factor receptor pathway.

Ishii, Toshihisa / Miyasato, Yoshikazu / Ichijo, Masashi / Uchimura, Kohei / Furuya, Fumihiko

Scientific reports

2023 Volume 13, Issue 1, Page(s) 9086

Abstract: Prostasin (PRSS8) is a serine protease that metabolizes and moderates the effect of specific substrates. Epidermal growth factor receptor (EGFR), which modulates insulin secretion and pancreatic β-cell proliferation, is regulated via proteolytic shedding ...

Abstract	Prostasin (PRSS8) is a serine protease that metabolizes and moderates the effect of specific substrates. Epidermal growth factor receptor (EGFR), which modulates insulin secretion and pancreatic β-cell proliferation, is regulated via proteolytic shedding by PRSS8. We first detected PRSS8 expression in β-cells of pancreatic islets of mice. To better understand the molecular processes involved in PRSS8-associated insulin secretion, pancreatic β-cell-specific PRSS8 knockout (βKO) and PRSS8-overexpressing (βTG) male mice were generated. We found that glucose intolerance and reduction in glucose-stimulated insulin secretion developed in βKO mice compared with the control subjects. A higher response to glucose was noted in islets retrieved from βTG mice. Erlotinib, a specific blocker of EGFR, blocks EGF- and glucose-stimulated secretion of insulin among MIN6 cells, and glucose improves EGF release from β-cells. After silencing PRSS8 in MIN6 cells, glucose-stimulated insulin secretion decreased, and EGFR signaling was impaired. Conversely, overexpression of PRSS8 in MIN6 cells induced higher concentrations of both basal and glucose-stimulated insulin secretion and increased phospho-EGFR concentrations. Furthermore, short-term exposure to glucose improved the concentration of endogenous PRSS8 in MIN6 cells through inhibition of intracellular degradation. These findings suggest that PRSS8 is involved in glucose-dependent physiological regulation of insulin secretion via the EGF-EGFR signaling pathway in pancreatic β-cells.
MeSH term(s)	Male ; Animals ; Mice ; Insulin Secretion ; Peptide Hydrolases/metabolism ; Epidermal Growth Factor/metabolism ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Glucose/metabolism ; ErbB Receptors/metabolism
Chemical Substances	prostasin (EC 3.4.21.-) ; Peptide Hydrolases (EC 3.4.-) ; Epidermal Growth Factor (62229-50-9) ; Insulin ; Glucose (IY9XDZ35W2) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2023-06-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-36326-7
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Article ; Online: Membrane protease prostasin promotes insulin secretion by regulating the epidermal growth factor receptor pathway

Toshihisa Ishii / Yoshikazu Miyasato / Masashi Ichijo / Kohei Uchimura / Fumihiko Furuya

Scientific Reports, Vol 13, Iss 1, Pp 1-

2023 Volume 13

Abstract: Abstract Prostasin (PRSS8) is a serine protease that metabolizes and moderates the effect of specific substrates. Epidermal growth factor receptor (EGFR), which modulates insulin secretion and pancreatic β-cell proliferation, is regulated via proteolytic ...

Abstract	Abstract Prostasin (PRSS8) is a serine protease that metabolizes and moderates the effect of specific substrates. Epidermal growth factor receptor (EGFR), which modulates insulin secretion and pancreatic β-cell proliferation, is regulated via proteolytic shedding by PRSS8. We first detected PRSS8 expression in β-cells of pancreatic islets of mice. To better understand the molecular processes involved in PRSS8-associated insulin secretion, pancreatic β-cell-specific PRSS8 knockout (βKO) and PRSS8-overexpressing (βTG) male mice were generated. We found that glucose intolerance and reduction in glucose-stimulated insulin secretion developed in βKO mice compared with the control subjects. A higher response to glucose was noted in islets retrieved from βTG mice. Erlotinib, a specific blocker of EGFR, blocks EGF- and glucose-stimulated secretion of insulin among MIN6 cells, and glucose improves EGF release from β-cells. After silencing PRSS8 in MIN6 cells, glucose-stimulated insulin secretion decreased, and EGFR signaling was impaired. Conversely, overexpression of PRSS8 in MIN6 cells induced higher concentrations of both basal and glucose-stimulated insulin secretion and increased phospho-EGFR concentrations. Furthermore, short-term exposure to glucose improved the concentration of endogenous PRSS8 in MIN6 cells through inhibition of intracellular degradation. These findings suggest that PRSS8 is involved in glucose-dependent physiological regulation of insulin secretion via the EGF–EGFR signaling pathway in pancreatic β-cells.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: NKX2-1 re-expression induces cell death through apoptosis and necrosis in dedifferentiated thyroid carcinoma cells.

Ito, Yuko / Furuya, Fumihiko / Taki, Katsumi / Suzuki, Hideaki / Shimura, Hiroki

PloS one

2021 Volume 16, Issue 11, Page(s) e0259558

Abstract: NK2 homeobox 1 (NKX2-1) is a thyroid transcription factor essential for proper thyroid formation and maintaining its physiological function. In thyroid cancer, NKX2-1 expression decreases in parallel with declined differentiation. However, the molecular ... ...

Abstract	NK2 homeobox 1 (NKX2-1) is a thyroid transcription factor essential for proper thyroid formation and maintaining its physiological function. In thyroid cancer, NKX2-1 expression decreases in parallel with declined differentiation. However, the molecular pathways and mechanisms connecting NKX2-1 to thyroid cancer phenotypes are largely unknown. This study aimed to examine the effects of NKX2-1 re-expression on dedifferentiated thyroid cancer cell death and explore the underlying mechanisms. A human papillary thyroid carcinoma cell line lacking NKX2-1 expression was infected with an adenoviral vector containing Nkx2-1. Cell viability decreased after Nkx2-1 transduction and apoptosis and necrosis were detected. Arginase 2 (ARG2), regulator of G protein signaling 4 (RGS4), and RGS5 mRNA expression was greatly increased in Nkx2-1-transducted cells. After suppressing these genes by siRNA, cell death, apoptosis, and necrosis decreased in RGS4 knockdown cells. These findings demonstrated that cell death was induced via apoptosis and necrosis by NKX2-1 re-expression and involves RGS4.
MeSH term(s)	Apoptosis ; Genes, Homeobox ; Humans ; Necrosis ; Thyroid Nuclear Factor 1
Chemical Substances	NKX2-1 protein, human ; Thyroid Nuclear Factor 1
Language	English
Publishing date	2021-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0259558
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Article ; Online: NKX2-1 re-expression induces cell death through apoptosis and necrosis in dedifferentiated thyroid carcinoma cells

Yuko Ito / Fumihiko Furuya / Katsumi Taki / Hideaki Suzuki / Hiroki Shimura

PLoS ONE, Vol 16, Iss

2021 Volume 11

Abstract	NK2 homeobox 1 (NKX2-1) is a thyroid transcription factor essential for proper thyroid formation and maintaining its physiological function. In thyroid cancer, NKX2-1 expression decreases in parallel with declined differentiation. However, the molecular pathways and mechanisms connecting NKX2-1 to thyroid cancer phenotypes are largely unknown. This study aimed to examine the effects of NKX2-1 re-expression on dedifferentiated thyroid cancer cell death and explore the underlying mechanisms. A human papillary thyroid carcinoma cell line lacking NKX2-1 expression was infected with an adenoviral vector containing Nkx2-1. Cell viability decreased after Nkx2-1 transduction and apoptosis and necrosis were detected. Arginase 2 (ARG2), regulator of G protein signaling 4 (RGS4), and RGS5 mRNA expression was greatly increased in Nkx2-1-transducted cells. After suppressing these genes by siRNA, cell death, apoptosis, and necrosis decreased in RGS4 knockdown cells. These findings demonstrated that cell death was induced via apoptosis and necrosis by NKX2-1 re-expression and involves RGS4.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: NKX2-1 re-expression induces cell death through apoptosis and necrosis in dedifferentiated thyroid carcinoma cells.

Yuko Ito / Fumihiko Furuya / Katsumi Taki / Hideaki Suzuki / Hiroki Shimura

PLoS ONE, Vol 16, Iss 11, p e

2021 Volume 0259558

Abstract	NK2 homeobox 1 (NKX2-1) is a thyroid transcription factor essential for proper thyroid formation and maintaining its physiological function. In thyroid cancer, NKX2-1 expression decreases in parallel with declined differentiation. However, the molecular pathways and mechanisms connecting NKX2-1 to thyroid cancer phenotypes are largely unknown. This study aimed to examine the effects of NKX2-1 re-expression on dedifferentiated thyroid cancer cell death and explore the underlying mechanisms. A human papillary thyroid carcinoma cell line lacking NKX2-1 expression was infected with an adenoviral vector containing Nkx2-1. Cell viability decreased after Nkx2-1 transduction and apoptosis and necrosis were detected. Arginase 2 (ARG2), regulator of G protein signaling 4 (RGS4), and RGS5 mRNA expression was greatly increased in Nkx2-1-transducted cells. After suppressing these genes by siRNA, cell death, apoptosis, and necrosis decreased in RGS4 knockdown cells. These findings demonstrated that cell death was induced via apoptosis and necrosis by NKX2-1 re-expression and involves RGS4.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Chronic Inflammation and Progression of Diabetic Kidney Disease.

Furuya, Fumihiko / Ishii, Toshihisa / Kitamura, Kenichiro

Contributions to nephrology

2019 Volume 198, Page(s) 33–39

Abstract: Background: From a global perspective, diabetic kidney disease (DKD) is the leading cause of not only chronic kidney disease and end-stage renal disease but also cardiovascular disease (CVD).: Summary: In the early stages of diabetes, patients have a ...

Abstract	Background: From a global perspective, diabetic kidney disease (DKD) is the leading cause of not only chronic kidney disease and end-stage renal disease but also cardiovascular disease (CVD). Summary: In the early stages of diabetes, patients have a high risk of developing microvascular complications, loss of kidney function, CVD, infection, and death. Hyperglycemia, free fatty acids, and insulin resistance induce metabolic imbalance and DKD initiation. Inflammation is recognized to play a role in DKD pathogenesis. Our recent study indicated that angiopoietin-like protein 2, which is a circulating proinflammatory protein, might be a strong mediator for the development of DKD and a good predictive biomarker of its progression. The need for effective and safe treatment options for complications such as DKD or CVD becomes ever more urgent. Key Messages: Inflammatory mediators have emerged as potential biomarkers and therapeutic targets for DKD.
MeSH term(s)	Angiopoietin-like Proteins/blood ; Biomarkers/blood ; Cardiovascular Diseases/etiology ; Diabetic Nephropathies/complications ; Diabetic Nephropathies/pathology ; Disease Progression ; Humans ; Inflammation ; Inflammation Mediators/blood ; Kidney Failure, Chronic/etiology ; Prognosis
Chemical Substances	Angiopoietin-like Proteins ; Biomarkers ; Inflammation Mediators
Language	English
Publishing date	2019-04-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1662-2782 ; 0302-5144
ISSN (online)	1662-2782
ISSN	0302-5144
DOI	10.1159/000496526
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Article ; Online: Intelectin1 ameliorates macrophage activation via inhibiting the nuclear factor kappa B pathway.

Kobayashi, Hidetoshi / Uchimura, Kohei / Ishii, Toshihisa / Takahashi, Kazuya / Mori, Kentaro / Tsuchiya, Kyoichiro / Furuya, Fumihiko

Endocrine journal

2021 Volume 69, Issue 5, Page(s) 539–546

Abstract: Inteletin1 (Itln1) is an adipokine that is abundantly expressed in intestine, ovary, and lung. The expression levels of ITLN1 are decreased in the presence of diabetes or obesity, but the mechanisms of its production and function are still controversial. ...

Abstract	Inteletin1 (Itln1) is an adipokine that is abundantly expressed in intestine, ovary, and lung. The expression levels of ITLN1 are decreased in the presence of diabetes or obesity, but the mechanisms of its production and function are still controversial. The aim of this study is to elucidate the mechanisms of ITLN1 synthesis and ITLN1-associated macrophage activation. To analyze the effects of high fat and high-carbohydrate diet (HFHCD) on the expression of ITLN1 in the intestine, the mice were fed a HFHCD for 8 weeks. HFHCD feeding enhanced the endoplasmic reticulum (ER)-stress in the intestine and inhibited the expression of Itln1 in the intestinal endocrine cells and lowered circulating ITLN1 levels. In contrast, treatment with a chemical chaperone and reduction of ER-stress restored the expression of Itln1 in the intestine of HFHCD-fed mice. Furthermore, in vitro studies indicated that ITLN1 physically interacts with adiponectin receptor 1 and suppresses lipopolysaccharide-induced mRNA expressions of pro-inflammatory cytokines and phagocytosis activities via inhibition of the nuclear factor kappa B-signaling pathway in macrophages. These results suggest that diet-induced ER-stress decreases circulating ITLN1 via inhibition of its synthesis in the intestine, and a reduction of circulating ITLN1 might enhanced the expression of proinflammatory cytokines and macrophage activation, following exacerbate the chronic inflammation of metabolic syndrome.
MeSH term(s)	Animals ; Cytokines/metabolism ; Endoplasmic Reticulum Stress ; Female ; GPI-Linked Proteins/metabolism ; Inflammation ; Lectins/metabolism ; Macrophage Activation ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Signal Transduction
Chemical Substances	Cytokines ; GPI-Linked Proteins ; Itln1 protein, mouse ; Lectins ; NF-kappa B
Language	English
Publishing date	2021-12-03
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1151918-6
ISSN	1348-4540 ; 0918-8959
ISSN (online)	1348-4540
ISSN	0918-8959
DOI	10.1507/endocrj.EJ21-0438
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Article ; Online: Hyperthyroidism exacerbates ischemic reperfusion injury in the kidney.

Yamaguchi, Yasuno / Uchimura, Kohei / Takahashi, Kazuya / Ishii, Toshihisa / Hanai, Shunichiro / Furuya, Fumihiko

Endocrine journal

2021 Volume 69, Issue 3, Page(s) 263–272

Abstract: Thyroid hormones are critical regulators of vertebrate development and metabolism. Under hyperthyroid conditions, excess thyroid hormones induce expression of several enzymes and activities via activation of ligand-bound thyroid hormone receptors (TRs). ... ...

Abstract	Thyroid hormones are critical regulators of vertebrate development and metabolism. Under hyperthyroid conditions, excess thyroid hormones induce expression of several enzymes and activities via activation of ligand-bound thyroid hormone receptors (TRs). Arginase (ARG) is downstream of a ligand-bound TR and overexpression of ARG2 induces the production of reactive oxygen species and subsequent exacerbation of kidney ischemia/reperfusion (I/R) injury. To clarify the association between I/R-induced kidney injury and hyperthyroidism, mice were pretreated with L-thyroxine (LT4) or vehicle alone, then subjected to I/R. Proximal tubular cell-specific conditional knockout of thyroid hormone receptor β (TRβcKO) mice was generated and the effects of I/R were analyzed. Hyperthyroidism enhanced tubular damage and fibrosis in the kidneys of mice after I/R. Hyperthyroidism induced tubular cell necroptosis following inflammatory cell accumulation in the kidney after I/R. ARG2 expressions and reactive oxygen species accumulated in the kidneys of hyperthyroid mice after I/R, but these changes were ameliorated in the kidneys of TRβcKO mice. Hyperthyroidism-enhanced kidney injury was ameliorated in the kidney of TRβcKO mice after I/R. These results suggest that excess thyroid hormones are disadvantageous for the kidney under ischemic stress. Overt hypothyroidism represents a severe thyroid hormone deficiency disease that requires LT4 treatment, while overreplacement or iatrogenic thyrotoxicosis might cause kidney injury.
MeSH term(s)	Animals ; Hyperthyroidism/complications ; Hyperthyroidism/genetics ; Hypothyroidism/metabolism ; Kidney/metabolism ; Mice ; Reperfusion Injury/complications ; Reperfusion Injury/metabolism ; Thyroid Hormones/metabolism
Chemical Substances	Thyroid Hormones
Language	English
Publishing date	2021-10-09
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1151918-6
ISSN	1348-4540 ; 0918-8959
ISSN (online)	1348-4540
ISSN	0918-8959
DOI	10.1507/endocrj.EJ21-0395
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Article ; Online: Hypoxia-induced thyroid hormone receptor expression regulates cell-cycle progression in renal tubule epithelial cells.

Hanai, Shunichiro / Uchimura, Kohei / Takahashi, Kazuya / Ishii, Toshihisa / Mitsui, Takahiko / Furuya, Fumihiko

Endocrine journal

2021 Volume 68, Issue 11, Page(s) 1309–1320

Abstract: Hypoxia occurs in the kidneys of chronic kidney disease (CKD) patients, inducing interstitial fibrosis and tubule cell death. Renal tubule cell death is an important determinant of mortality in CKD. We focused on the regulation of cell-cycle-mediated ... ...

Abstract	Hypoxia occurs in the kidneys of chronic kidney disease (CKD) patients, inducing interstitial fibrosis and tubule cell death. Renal tubule cell death is an important determinant of mortality in CKD. We focused on the regulation of cell-cycle-mediated protein expression to prevent cell death under chronic hypoxia in the kidneys of CKD patients. Paraffin-embedded kidney sections from patients with CKD (diabetes nephropathy, nephrosclerosis, or IgA nephropathy) were analyzed for the expression of hypoxia-inducible factor (HIF), thyroid hormone receptor (TR) β, or p21 and levels of interstitial fibrosis. Human renal proximal tubule cells were exposed to hypoxia and analyzed for the expression of HIF, TRβ, or p21 and the cell-cycle stage. TRβ expression was enhanced early on when fibrosis was not fully developed in the tubule cells of CKD patients. HIF1α bound to the TRβ promoter and directly induced its transcription. Further, HIF1α expression induced the expression of TRβ and inhibited cell-cycle progression. In the early stage of kidney injury, TRβ might act as a guardian to prepare and organize cell-cycle proliferation and prevent cell death. While the molecular mechanism that regulates the expression of cell-cycle regulators in renal tubule cells remains controversial, TRβ has strong potential as a new therapeutic target.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Cell Cycle/physiology ; Cell Line ; Cell Proliferation ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Female ; Humans ; Hypoxia/genetics ; Hypoxia/metabolism ; Hypoxia/pathology ; Kidney Tubules, Proximal/metabolism ; Kidney Tubules, Proximal/pathology ; Male ; Middle Aged ; Receptors, Thyroid Hormone/genetics ; Receptors, Thyroid Hormone/metabolism ; Young Adult
Chemical Substances	Receptors, Thyroid Hormone
Language	English
Publishing date	2021-06-08
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1151918-6
ISSN	1348-4540 ; 0918-8959
ISSN (online)	1348-4540
ISSN	0918-8959
DOI	10.1507/endocrj.EJ21-0245
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