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Article ; Online: Drug repurposing in autosomal dominant polycystic kidney disease.

Zhou, Julie Xia / Torres, Vicente E

2023 Volume 103, Issue 5, Page(s) 859–871

Abstract: Autosomal dominant polycystic kidney disease is characterized by progressive kidney cyst formation that leads to kidney failure. Tolvaptan, a vasopressin 2 receptor antagonist, is the only drug approved to treat patients with autosomal dominant ... ...

Abstract	Autosomal dominant polycystic kidney disease is characterized by progressive kidney cyst formation that leads to kidney failure. Tolvaptan, a vasopressin 2 receptor antagonist, is the only drug approved to treat patients with autosomal dominant polycystic kidney disease who have rapid disease progression. The use of tolvaptan is limited by reduced tolerability from aquaretic effects and potential hepatotoxicity. Thus, the search for more effective drugs to slow down the progression of autosomal dominant polycystic kidney disease is urgent and challenging. Drug repurposing is a strategy for identifying new clinical indications for approved or investigational medications. Drug repurposing is increasingly becoming an attractive proposition because of its cost-efficiency and time-efficiency and known pharmacokinetic and safety profiles. In this review, we focus on the repurposing approaches to identify suitable drug candidates to treat autosomal dominant polycystic kidney disease and prioritization and implementation of candidates with high probability of success. Identification of drug candidates through understanding of disease pathogenesis and signaling pathways is highlighted.
MeSH term(s)	Humans ; Tolvaptan/therapeutic use ; Polycystic Kidney, Autosomal Dominant/pathology ; Drug Repositioning ; Antidiuretic Hormone Receptor Antagonists/adverse effects ; Kidney/pathology
Chemical Substances	Tolvaptan (21G72T1950) ; Antidiuretic Hormone Receptor Antagonists
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.02.010
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Article ; Online: Autosomal Dominant Polycystic Kidney Disease Therapies on the Horizon.

Zhou, Julie Xia / Torres, Vicente E

Advances in kidney disease and health

2023 Volume 30, Issue 3, Page(s) 245–260

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of numerous kidney cysts which leads to kidney failure. ADPKD is responsible for approximately 10% of patients with kidney failure. Overwhelming evidence supports that ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of numerous kidney cysts which leads to kidney failure. ADPKD is responsible for approximately 10% of patients with kidney failure. Overwhelming evidence supports that vasopressin and its downstream cyclic adenosine monophosphate signaling promote cystogenesis, and targeting vasopressin 2 receptor with tolvaptan and other antagonists ameliorates cyst growth in preclinical studies. Tolvaptan is the only drug approved by Food and Drug Administration to treat ADPKD patients at the risk of rapid disease progression. A major limitation of the widespread use of tolvaptan is aquaretic events. This review discusses the potential strategies to improve the tolerability of tolvaptan, the progress on the use of an alternative vasopressin 2 receptor antagonist lixivaptan, and somatostatin analogs. Recent advances in understanding the pathophysiology of PKD have led to new approaches of treatment via targeting different signaling pathways. We review the new pharmacotherapies and dietary interventions of ADPKD that are promising in the preclinical studies and investigated in clinical trials.
MeSH term(s)	United States ; Humans ; Polycystic Kidney, Autosomal Dominant/drug therapy ; Tolvaptan/therapeutic use ; Antidiuretic Hormone Receptor Antagonists/therapeutic use ; Vasopressins/therapeutic use ; Receptors, Vasopressin/metabolism ; Renal Insufficiency/drug therapy
Chemical Substances	Tolvaptan (21G72T1950) ; Antidiuretic Hormone Receptor Antagonists ; Vasopressins (11000-17-2) ; Receptors, Vasopressin
Language	English
Publishing date	2023-04-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	3156601-7
ISSN	2949-8139
ISSN (online)	2949-8139
DOI	10.1053/j.akdh.2023.01.003
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Zs.A 4627: Show issues

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Article ; Online: Salt, water, and vasopressin in polycystic kidney disease.

Torres, Vicente E

Kidney international

2020 Volume 98, Issue 4, Page(s) 831–834

Abstract: Excessive salt intake and vasopressin may promote cyst growth in autosomal dominant polycystic kidney disease and glomerular filtration rate (GFR) decline in chronic kidney disease. Kramers et al. confirmed the effects of salt in a large autosomal ... ...

Abstract	Excessive salt intake and vasopressin may promote cyst growth in autosomal dominant polycystic kidney disease and glomerular filtration rate (GFR) decline in chronic kidney disease. Kramers et al. confirmed the effects of salt in a large autosomal dominant polycystic kidney disease cohort. Copeptin mediated 72% and 25% of the salt effects on GFR decline and kidney growth. Kidney growth did not significantly contribute to the copeptin-mediated salt effect on GFR. Differences in kidney growth and GFR decline trajectories and factors other than cyst growth contributing to GFR decline may explain the divergent effects.
MeSH term(s)	Biomarkers ; Disease Progression ; Glomerular Filtration Rate ; Glycopeptides ; Humans ; Kidney ; Polycystic Kidney, Autosomal Dominant ; Sodium Chloride, Dietary ; Vasopressins ; Water
Chemical Substances	Biomarkers ; Glycopeptides ; Sodium Chloride, Dietary ; Water (059QF0KO0R) ; Vasopressins (11000-17-2)
Language	English
Publishing date	2020-09-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2020.06.001
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Article: Emerging therapies for autosomal dominant polycystic kidney disease with a focus on cAMP signaling.

Zhou, Xia / Torres, Vicente E

Frontiers in molecular biosciences

2022 Volume 9, Page(s) 981963

Abstract: Autosomal dominant polycystic kidney disease (ADPKD), with an estimated genetic prevalence between 1:400 and 1:1,000 individuals, is the third most common cause of end stage kidney disease after diabetes mellitus and hypertension. Over the last 3 decades ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD), with an estimated genetic prevalence between 1:400 and 1:1,000 individuals, is the third most common cause of end stage kidney disease after diabetes mellitus and hypertension. Over the last 3 decades there has been great progress in understanding its pathogenesis. This allows the stratification of therapeutic targets into four levels, gene mutation and polycystin disruption, proximal mechanisms directly caused by disruption of polycystin function, downstream regulatory and signaling pathways, and non-specific pathophysiologic processes shared by many other diseases. Dysfunction of the polycystins, encoded by the PKD genes, is closely associated with disruption of calcium and upregulation of cyclic AMP and protein kinase A (PKA) signaling, affecting most downstream regulatory, signaling, and pathophysiologic pathways altered in this disease. Interventions acting on G protein coupled receptors to inhibit of 3',5'-cyclic adenosine monophosphate (cAMP) production have been effective in preclinical trials and have led to the first approved treatment for ADPKD. However, completely blocking cAMP mediated PKA activation is not feasible and PKA activation independently from cAMP can also occur in ADPKD. Therefore, targeting the cAMP/PKA/CREB pathway beyond cAMP production makes sense. Redundancy of mechanisms, numerous positive and negative feedback loops, and possibly counteracting effects may limit the effectiveness of targeting downstream pathways. Nevertheless, interventions targeting important regulatory, signaling and pathophysiologic pathways downstream from cAMP/PKA activation may provide additive or synergistic value and build on a strategy that has already had success. The purpose of this manuscript is to review the role of cAMP and PKA signaling and their multiple downstream pathways as potential targets for emergent therapies for ADPKD.
Language	English
Publishing date	2022-09-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2022.981963
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Article ; Online: Emerging therapies for autosomal dominant polycystic kidney disease with a focus on cAMP signaling

Xia Zhou / Vicente E. Torres

Frontiers in Molecular Biosciences, Vol

2022 Volume 9

Abstract	Autosomal dominant polycystic kidney disease (ADPKD), with an estimated genetic prevalence between 1:400 and 1:1,000 individuals, is the third most common cause of end stage kidney disease after diabetes mellitus and hypertension. Over the last 3 decades there has been great progress in understanding its pathogenesis. This allows the stratification of therapeutic targets into four levels, gene mutation and polycystin disruption, proximal mechanisms directly caused by disruption of polycystin function, downstream regulatory and signaling pathways, and non-specific pathophysiologic processes shared by many other diseases. Dysfunction of the polycystins, encoded by the PKD genes, is closely associated with disruption of calcium and upregulation of cyclic AMP and protein kinase A (PKA) signaling, affecting most downstream regulatory, signaling, and pathophysiologic pathways altered in this disease. Interventions acting on G protein coupled receptors to inhibit of 3′,5′-cyclic adenosine monophosphate (cAMP) production have been effective in preclinical trials and have led to the first approved treatment for ADPKD. However, completely blocking cAMP mediated PKA activation is not feasible and PKA activation independently from cAMP can also occur in ADPKD. Therefore, targeting the cAMP/PKA/CREB pathway beyond cAMP production makes sense. Redundancy of mechanisms, numerous positive and negative feedback loops, and possibly counteracting effects may limit the effectiveness of targeting downstream pathways. Nevertheless, interventions targeting important regulatory, signaling and pathophysiologic pathways downstream from cAMP/PKA activation may provide additive or synergistic value and build on a strategy that has already had success. The purpose of this manuscript is to review the role of cAMP and PKA signaling and their multiple downstream pathways as potential targets for emergent therapies for ADPKD.
Keywords	cAMP signaling ; protein kinase A (PKA) ; ADPKD (autosomal dominant polycystic kidney disease) ; PKD ; vassopressin ; tolvaptan ; Biology (General) ; QH301-705.5
Subject code	572 ; 570
Language	English
Publishing date	2022-09-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Pro: Tolvaptan delays the progression of autosomal dominant polycystic kidney disease.

Torres, Vicente E

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2018 Volume 34, Issue 1, Page(s) 30–34

Abstract: No treatment until now has directly targeted the mechanisms responsible for the development and growth of cysts in autosomal dominant polycystic kidney disease (ADPKD). Strong rationale and preclinical studies using in vitro and in vivo models justified ... ...

Abstract	No treatment until now has directly targeted the mechanisms responsible for the development and growth of cysts in autosomal dominant polycystic kidney disease (ADPKD). Strong rationale and preclinical studies using in vitro and in vivo models justified the launching of two large phase 3 clinical trials of tolvaptan in early and later stages of ADPKD. Their design was based on preliminary studies informing on the pharmacokinetics, pharmacodynamics, short-term safety and self-reported tolerability in patients with ADPKD. Tolvaptan slowed kidney growth in the early stage and estimated glomerular filtration rate decline in early and later stages of the disease. All participants had the opportunity to enroll in open-label extension trials to ascertain long-term safety and efficacy. In a single-center analysis of long-term outcomes, the effect of tolvaptan was sustained and cumulative over time supporting a disease-modifying effect of tolvaptan in ADPKD. In the countries where tolvaptan has been approved by regulatory agencies, patients with rapidly progressive ADPKD should be informed about the option of treatment including possible benefits and risks. If a decision to initiate treatment is made, prescribing physicians should educate the patients on the prevention of aquaresis-related adverse events and should be vigilant in the surveillance and management of the potential tolvaptan hepatotoxicity. Other vasopressin V2 receptor antagonists, possibly without potential hepatotoxicity, alternative strategies targeting vasopressin and combination with other drugs able to enhance the efficacy or reduce the aquaresis associated with tolvaptan, deserve further study.
MeSH term(s)	Antidiuretic Hormone Receptor Antagonists/therapeutic use ; Humans ; Polycystic Kidney, Autosomal Dominant/drug therapy ; Prognosis ; Tolvaptan/therapeutic use
Chemical Substances	Antidiuretic Hormone Receptor Antagonists ; Tolvaptan (21G72T1950)
Language	English
Publishing date	2018-10-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfy297
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 329: Show issues

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Article ; Online: Assessing Risk of Rapid Progression in Autosomal Dominant Polycystic Kidney Disease and Special Considerations for Disease-Modifying Therapy.

Chebib, Fouad T / Torres, Vicente E

American journal of kidney diseases : the official journal of the National Kidney Foundation

2021 Volume 78, Issue 2, Page(s) 282–292

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of kidney failure, accounting for 5%-10% of cases. Predicting which patients with ADPKD will progress rapidly to kidney failure is critical to assess the risk-benefit ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of kidney failure, accounting for 5%-10% of cases. Predicting which patients with ADPKD will progress rapidly to kidney failure is critical to assess the risk-benefit ratio of any intervention and to consider early initiation of long-term kidney protective measures that will maximize the cumulative benefit of slowing disease progression. Surrogate prognostic biomarkers are required to predict future decline in kidney function. Clinical, genetic, environmental, epigenetic, and radiologic factors have been studied as predictors of progression to kidney failure in ADPKD. A complex interaction of these prognostic factors determines the number of kidney cysts and their growth rates, which affect total kidney volume (TKV). Age-adjusted TKV, represented by the Mayo imaging classification, estimates each patient's unique rate of kidney growth and provides the most individualized approach available clinically so far. Tolvaptan has been approved to slow disease progression in patients at risk of rapidly progressive disease. Several other disease-modifying treatments are being studied in clinical trials. Selection criteria for patients at risk of rapid progression vary widely among countries and are based on a combination of age, baseline glomerular filtration rate (GFR), GFR slope, baseline TKV, and TKV rate of growth. This review details the approach in assessing the risk of disease progression in ADPKD and identifying patients who would benefit from long-term therapy with disease-modifying agents.
MeSH term(s)	Age Factors ; Antidiuretic Hormone Receptor Antagonists/therapeutic use ; Disease Progression ; Glomerular Filtration Rate ; Humans ; Kidney/diagnostic imaging ; Kidney/pathology ; Magnetic Resonance Imaging ; Organ Size ; Polycystic Kidney, Autosomal Dominant/diagnostic imaging ; Polycystic Kidney, Autosomal Dominant/drug therapy ; Polycystic Kidney, Autosomal Dominant/metabolism ; Polycystic Kidney, Autosomal Dominant/physiopathology ; Risk Assessment ; Tolvaptan/therapeutic use ; Tomography, X-Ray Computed ; Ultrasonography
Chemical Substances	Antidiuretic Hormone Receptor Antagonists ; Tolvaptan (21G72T1950)
Language	English
Publishing date	2021-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604539-x
ISSN	1523-6838 ; 0272-6386
ISSN (online)	1523-6838
ISSN	0272-6386
DOI	10.1053/j.ajkd.2020.12.020
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Zs.A 1669: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: CD74 Promotes Cyst Growth and Renal Fibrosis in Autosomal Dominant Polycystic Kidney Disease.

Zhou, Julie Xia / Cheng, Alice Shasha / Chen, Li / Li, Linda Xiaoyan / Agborbesong, Ewud / Torres, Vicente E / Harris, Peter C / Li, Xiaogang

Cells

2024 Volume 13, Issue 6

Abstract: The progression of autosomal dominant polycystic kidney disease (ADPKD), an inherited kidney disease, is associated with renal interstitial inflammation and fibrosis. CD74 has been known not only as a receptor of macrophage migration inhibitory factor ( ... ...

Abstract	The progression of autosomal dominant polycystic kidney disease (ADPKD), an inherited kidney disease, is associated with renal interstitial inflammation and fibrosis. CD74 has been known not only as a receptor of macrophage migration inhibitory factor (MIF) it can also have MIF independent functions. In this study, we report unknown roles and function of CD74 in ADPKD. We show that knockout of CD74 delays cyst growth in
MeSH term(s)	Humans ; Polycystic Kidney, Autosomal Dominant ; Tumor Necrosis Factor-alpha ; Fibrosis ; Cysts ; Polycystic Kidney Diseases
Chemical Substances	Tumor Necrosis Factor-alpha
Language	English
Publishing date	2024-03-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13060489
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Article ; Online: Reactive Oxygen Species and Redox Signaling in Chronic Kidney Disease.

Irazabal, Maria V / Torres, Vicente E

Cells

2020 Volume 9, Issue 6

Abstract: Chronic kidney disease (CKD) remains a worldwide public health problem associated with serious complications and increased mortality rates. Accumulating evidence indicates that elevated intracellular levels of reactive oxygen species (ROS) play a major ... ...

Abstract	Chronic kidney disease (CKD) remains a worldwide public health problem associated with serious complications and increased mortality rates. Accumulating evidence indicates that elevated intracellular levels of reactive oxygen species (ROS) play a major role in the pathogenesis of CKD. Increased intracellular levels of ROS can lead to oxidation of lipids, DNA, and proteins, contributing to cellular damage. On the other hand, ROS are also important secondary messengers in cellular signaling. Consequently, normal kidney cell function relies on the "right" amount of ROS. Mitochondria and NADPH oxidases represent major sources of ROS in the kidney, but renal antioxidant systems, such as superoxide dismutase, catalase, or glutathione peroxidase counterbalance ROS-mediated injury. This review discusses the main sources of ROS and antioxidant systems in the kidney, and redox signaling pathways leading to inflammation and fibrosis, which result in abnormal kidney function and CKD progression. We further discuss the important role of the nuclear factor erythroid 2-related factor 2 (Nrf2) in regulating antioxidant responses, and other mechanisms of redox signaling.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Humans ; Kidney/metabolism ; Kidney/pathology ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction
Chemical Substances	Antioxidants ; Reactive Oxygen Species
Language	English
Publishing date	2020-05-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9061342
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Article ; Online: Progress in the understanding of polycystic kidney disease.

Torres, Vicente E / Harris, Peter C

Nature reviews. Nephrology

2019 Volume 15, Issue 2, Page(s) 70–72

MeSH term(s)	Biomarkers/metabolism ; GTP-Binding Proteins/metabolism ; Genetic Markers ; Humans ; Mutation ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/immunology ; Polycystic Kidney, Autosomal Dominant/metabolism ; Signal Transduction ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism
Chemical Substances	Biomarkers ; Genetic Markers ; TRPP Cation Channels ; polycystic kidney disease 1 protein ; polycystic kidney disease 2 protein ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2019-01-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-018-0108-1
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Zs.MG 107: Show issues

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