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Article ; Online: Two Shared Icosahedral Metallacarboranes through Iron: A Joint Experimental and Theoretical Refinement of Mössbauer Spectrum in [Fe(1,2-C

Marco, José F / Dávalos-Prado, Juan Z / Hnyk, Drahomír / Holub, Josef / Oña, Ofelia B / Alcoba, Diego R / Ferrer, Maxime / Elguero, José / Lain, Luis / Torre, Alicia / Oliva-Enrich, Josep M

ACS omega

2023 Volume 8, Issue 15, Page(s) 13993–14004

Abstract: ... of the metallacarborane sandwich complex [Fe(1,2-C ...

Abstract	Mössbauer and X-ray photoelectron spectroscopies (XPS) are complemented with high-level quantum-chemical computations in the study of the geometric and electronic structure of the paramagnetic salt of the metallacarborane sandwich complex [Fe(1,2-C
Language	English
Publishing date	2023-04-07
Publishing country	United States
Document type	Journal Article
ISSN	2470-1343
ISSN (online)	2470-1343
DOI	10.1021/acsomega.3c00422
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Corrigendum to "Acid ceramidase improves mitochondrial function and oxidative stress in Niemann-Pick type C disease by repressing STARD1 expression and mitochondrial cholesterol accumulation" [Redox Biol. 2021 45 102052].

Torres, S / Solsona-Vilarrasa, E / Nuñez, S / Matías, N / Insausti-Urkia, N / Castro, F / Casasempere, M / Fabriás, G / Casas, J / Enrich, C / Fernández-Checa, J C / Garcia-Ruiz, C

Redox biology

2022 Volume 50, Page(s) 102231

Language	English
Publishing date	2022-01-10
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102231
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Article ; Online: Acid ceramidase improves mitochondrial function and oxidative stress in Niemann-Pick type C disease by repressing STARD1 expression and mitochondrial cholesterol accumulation.

Torres, Sandra / Solsona-Vilarrasa, Estel / Nuñez, Susana / Matías, Nuria / Insausti-Urkia, Naroa / Castro, Fernanda / Casasempere, Mireia / Fabriás, Gemma / Casas, Josefina / Enrich, Carlos / Fernández-Checa, José C / Garcia-Ruiz, Carmen

Redox biology

2021 Volume 45, Page(s) 102052

Abstract: Niemann-Pick type C (NPC) disease, a lysosomal storage disorder caused by defective NPC1/NPC2 ...

Abstract	Niemann-Pick type C (NPC) disease, a lysosomal storage disorder caused by defective NPC1/NPC2 function, results in the accumulation of cholesterol and glycosphingolipids in lysosomes of affected organs, such as liver and brain. Moreover, increase of mitochondrial cholesterol (mchol) content and impaired mitochondrial function and GSH depletion contribute to NPC disease. However, the underlying mechanism of mchol accumulation in NPC disease remains unknown. As STARD1 is crucial in intramitochondrial cholesterol trafficking and acid ceramidase (ACDase) has been shown to regulate STARD1, we explored the functional relationship between ACDase and STARD1 in NPC disease. Liver and brain of Npc1
MeSH term(s)	Acid Ceramidase/metabolism ; Animals ; Cholesterol/metabolism ; Humans ; Lysosomes/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Niemann-Pick Disease, Type C/genetics ; Niemann-Pick Disease, Type C/metabolism ; Oxidative Stress ; Phosphoproteins/metabolism
Chemical Substances	Phosphoproteins ; steroidogenic acute regulatory protein ; Cholesterol (97C5T2UQ7J) ; Acid Ceramidase (EC 3.5.1.23)
Language	English
Publishing date	2021-06-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2021.102052
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Article ; Online: Lack of Annexin A6 Exacerbates Liver Dysfunction and Reduces Lifespan of Niemann-Pick Type C Protein-Deficient Mice.

Meneses-Salas, Elsa / Garcia-Forn, Marta / Castany-Pladevall, Carla / Lu, Albert / Fajardo, Alba / Jose, Jaimy / Wahba, Mohamed / Bosch, Marta / Pol, Albert / Tebar, Francesc / Klein, Andrés D / Zanlungo, Silvana / Pérez-Navarro, Esther / Grewal, Thomas / Enrich, Carlos / Rentero, Carles

The American journal of pathology

2020 Volume 191, Issue 3, Page(s) 475–486

Abstract: Niemann-Pick type C (NPC) disease is a lysosomal storage disorder characterized by cholesterol ...

Abstract	Niemann-Pick type C (NPC) disease is a lysosomal storage disorder characterized by cholesterol accumulation caused by loss-of-function mutations in the Npc1 gene. NPC disease primarily affects the brain, causing neuronal damage and affecting motor coordination. In addition, considerable liver malfunction in NPC disease is common. Recently, we found that the depletion of annexin A6 (ANXA6), which is most abundant in the liver and involved in cholesterol transport, ameliorated cholesterol accumulation in Npc1 mutant cells. To evaluate the potential contribution of ANXA6 in the progression of NPC disease, double-knockout mice (Npc1
MeSH term(s)	Animals ; Annexin A6/physiology ; Behavior, Animal ; Intracellular Signaling Peptides and Proteins/physiology ; Liver Diseases/etiology ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Longevity ; Mice ; Mice, Knockout
Chemical Substances	Annexin A6 ; Anxa6 protein, mouse ; Intracellular Signaling Peptides and Proteins ; Npc1 protein, mouse
Language	English
Publishing date	2020-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2020.12.009
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Article ; Online: Corrigendum to “Acid ceramidase improves mitochondrial function and oxidative stress in Niemann-Pick type C disease by repressing STARD1 expression and mitochondrial cholesterol accumulation” [Redox Biol. 2021 45 102052]

S. Torres / E. Solsona-Vilarrasa / S. Nuñez / N. Matías / N. Insausti-Urkia / F. Castro / M. Casasempere / G. Fabriás / J. Casas / C. Enrich / J.C. Fernández-Checa / C. Garcia-Ruiz

Redox Biology, Vol 50, Iss , Pp 102231- (2022)

2022

Keywords	Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Acid ceramidase improves mitochondrial function and oxidative stress in Niemann-Pick type C disease by repressing STARD1 expression and mitochondrial cholesterol accumulation

Sandra Torres / Estel Solsona-Vilarrasa / Susana Nuñez / Nuria Matías / Naroa Insausti-Urkia / Fernanda Castro / Mireia Casasempere / Gemma Fabriás / Josefina Casas / Carlos Enrich / José C. Fernández-Checa / Carmen Garcia-Ruiz

Redox Biology, Vol 45, Iss , Pp 102052- (2021)

2021

Abstract: Niemann-Pick type C (NPC) disease, a lysosomal storage disorder caused by defective NPC1/NPC2 ...

Abstract	Niemann-Pick type C (NPC) disease, a lysosomal storage disorder caused by defective NPC1/NPC2 function, results in the accumulation of cholesterol and glycosphingolipids in lysosomes of affected organs, such as liver and brain. Moreover, increase of mitochondrial cholesterol (mchol) content and impaired mitochondrial function and GSH depletion contribute to NPC disease. However, the underlying mechanism of mchol accumulation in NPC disease remains unknown. As STARD1 is crucial in intramitochondrial cholesterol trafficking and acid ceramidase (ACDase) has been shown to regulate STARD1, we explored the functional relationship between ACDase and STARD1 in NPC disease. Liver and brain of Npc1−/− mice presented a significant increase in mchol levels and STARD1 expression. U18666A, an amphiphilic sterol that inhibits lysosomal cholesterol efflux, increased mchol levels in hepatocytes from Stard1f/f mice but not Stard1ΔHep mice. We dissociate the induction of STARD1 expression from endoplasmic reticulum stress, and establish an inverse relationship between ACDase and STARD1 expression and LRH-1 levels. Hepatocytes from Npc1+/+ mice treated with U18666A exhibited increased mchol accumulation, STARD1 upregulation and decreased ACDase expression, effects that were reversed by cholesterol extraction with 2-hydroxypropyl-β-cyclodextrin. Moreover, transfection of fibroblasts from NPC patients with ACDase, decreased STARD1 expression and mchol accumulation, resulting in increased mitochondrial GSH levels, improved mitochondrial functional performance, decreased oxidative stress and protected NPC fibroblasts against oxidative stress-mediated cell death. Our results demonstrate a cholesterol-dependent inverse relationship between ACDase and STARD1 and provide a novel approach to target the accumulation of cholesterol in mitochondria in NPC disease.
Keywords	Cholesterol ; Acid ceramiase ; Mitochondrial function ; Oxidative stress ; NPC disease ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Determination of HLA-A, -B, -C, -DRB1 and -DQB1 allele and haplotype frequencies in heart failure patients.

Roura, Santiago / Rudilla, Francesc / Gastelurrutia, Paloma / Enrich, Emma / Campos, Eva / Lupón, Josep / Santiago-Vacas, Evelyn / Querol, Sergi / Bayés-Genís, Antoni

ESC heart failure

2019 Volume 6, Issue 2, Page(s) 388–395

Abstract: ... and C) and class II (DRB1 and DQB1) using next-generation sequencing technology ... estimated using HaploStats. A total of 30 HLA-A, 56 HLA-B, 23 HLA-C, 36 HLA-DRB1, and 15 HLA-DQB1 distinct ... HLA-C*07:01, HLA-DRB1*03:01, and HLA-DQB1*02:01 (6.07% haplotype frequency per patient). Remarkably ...

Abstract	Aims: Cell therapy can be used to repair functionally impaired organs and tissues in humans. Although autologous cells have an immunological advantage, it is difficult to obtain high cell numbers for therapy. Well-characterized banks of cells with human leukocyte antigens (HLA) that are representative of a given population are thus needed. The present study investigates the HLA allele and haplotype frequencies in a cohort of heart failure (HF) patients. Methods and results: We carried out the HLA typing and the allele and haplotype frequency analysis in 247 ambulatory HF patients. We determined HLA class I (A, B, and C) and class II (DRB1 and DQB1) using next-generation sequencing technology. The allele frequencies were obtained using Python for Population Genomics (PyPop) software, and HLA haplotypes were estimated using HaploStats. A total of 30 HLA-A, 56 HLA-B, 23 HLA-C, 36 HLA-DRB1, and 15 HLA-DQB1 distinct alleles were identified within the studied cohort. The genotype frequencies of all five HLA loci were in Hardy-Weinberg equilibrium. We detected differences in HLA allele frequencies among patients when the etiological cause of HF was considered. There were a total of 494 five-loci haplotypes, five of which were present six or more times. Moreover, the most common estimated HLA haplotype was HLA-A01:01, HLA-B08:01, HLA-C07:01, HLA-DRB103:01, and HLA-DQB102:01 (6.07% haplotype frequency per patient). Remarkably, the 11 most frequent haplotypes would cover 31.17% of the patients of the cohort in need of allogeneic cell therapy. Conclusions:* Our findings could be useful for improving allogeneic cell administration outcomes without concomitant immunosuppression.
MeSH term(s)	Aged ; Alleles ; Cell- and Tissue-Based Therapy/methods ; Female ; Gene Frequency ; Genotype ; HLA-A Antigens/genetics ; HLA-A Antigens/metabolism ; HLA-B Antigens/genetics ; HLA-B Antigens/metabolism ; HLA-C Antigens/genetics ; HLA-C Antigens/metabolism ; HLA-DQ beta-Chains/genetics ; HLA-DQ beta-Chains/metabolism ; HLA-DRB1 Chains/genetics ; HLA-DRB1 Chains/metabolism ; Haplotypes ; Heart Failure/genetics ; Heart Failure/metabolism ; Heart Failure/therapy ; Humans ; Male
Chemical Substances	HLA-A Antigens ; HLA-B Antigens ; HLA-C Antigens ; HLA-DQ beta-Chains ; HLA-DRB1 Chains
Language	English
Publishing date	2019-01-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2814355-3
ISSN	2055-5822 ; 2055-5822
ISSN (online)	2055-5822
ISSN	2055-5822
DOI	10.1002/ehf2.12406
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Article ; Online: Mitochondrial GSH replenishment as a potential therapeutic approach for Niemann Pick type C disease.

Torres, Sandra / Matías, Nuria / Baulies, Anna / Nuñez, Susana / Alarcon-Vila, Cristina / Martinez, Laura / Nuño, Natalia / Fernandez, Anna / Caballeria, Joan / Levade, Thierry / Gonzalez-Franquesa, Alba / Garcia-Rovés, Pablo / Balboa, Elisa / Zanlungo, Silvana / Fabrías, Gemma / Casas, Josefina / Enrich, Carlos / Garcia-Ruiz, Carmen / Fernández-Checa, José C

Redox biology

2016 Volume 11, Page(s) 60–72

Abstract: Niemann Pick type C (NPC) disease is a progressive lysosomal storage disorder caused by mutations ...

Abstract	Niemann Pick type C (NPC) disease is a progressive lysosomal storage disorder caused by mutations in genes encoding NPC1/NPC2 proteins, characterized by neurological defects, hepatosplenomegaly and premature death. While the primary biochemical feature of NPC disease is the intracellular accumulation of cholesterol and gangliosides, predominantly in endolysosomes, mitochondrial cholesterol accumulation has also been reported. As accumulation of cholesterol in mitochondria is known to impair the transport of GSH into mitochondria, resulting in mitochondrial GSH (mGSH) depletion, we investigated the impact of mGSH recovery in NPC disease. We show that GSH ethyl ester (GSH-EE), but not N-acetylcysteine (NAC), restored the mGSH pool in liver and brain of Npc1
MeSH term(s)	Acetylcysteine/metabolism ; Animals ; Cerebellum/metabolism ; Cerebellum/pathology ; Cholesterol/metabolism ; Glutathione/metabolism ; Glutathione/pharmacology ; Humans ; Intracellular Signaling Peptides and Proteins ; Lysosomes/genetics ; Lysosomes/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Mitochondria/pathology ; Mutation ; Niemann-Pick C1 Protein ; Niemann-Pick Disease, Type C/genetics ; Niemann-Pick Disease, Type C/metabolism ; Niemann-Pick Disease, Type C/pathology ; Oxidative Phosphorylation ; Proteins/genetics ; Proteins/metabolism ; Purkinje Cells/metabolism ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Niemann-Pick C1 Protein ; Npc1 protein, mouse ; Npc2 protein, mouse ; Proteins ; Vesicular Transport Proteins ; Cholesterol (97C5T2UQ7J) ; Glutathione (GAN16C9B8O) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2016-11-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2016.11.010
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Article ; Online: HLA-A, -B, -C, -DRB1, and -DQB1 allele and haplotype frequencies: An analysis of umbilical cord blood units at the Barcelona Cord Blood Bank.

Enrich, Emma / Campos, Eva / Martorell, Lluís / Herrero, María José / Vidal, Francisco / Querol, Sergi / Rudilla, Francesc

HLA

2019 Volume 94, Issue 4, Page(s) 347–359

Abstract: ... is an important step towards improving the quality of cord blood banks. We analyzed HLA-A, -B, -C ... Bank and identified 275 class I and 121 class II HLA alleles. A*02:01, B*44:03, C*07:01, DRB1*07:01 and ... to determine the presence or absence of some null alleles, including C*04:09N, in a large number of units ...

Abstract	Allele-level HLA compatibility in cord blood transplantation has been associated with better transplant outcomes and is recommended as a selection criterion. It is also a crucial aspect for other therapeutic applications involving cord blood-derived cells. Determination of high-resolution HLA frequencies is an important step towards improving the quality of cord blood banks. We analyzed HLA-A, -B, -C, -DRB1, and -DQB1 allele frequencies in 5458 high-quality cord blood units from the Barcelona Cord Blood Bank and identified 275 class I and 121 class II HLA alleles. A02:01, B44:03, C07:01, DRB107:01 and DQB103:01 were the most frequent alleles at each locus. We detected 26 novel alleles and were able to determine the presence or absence of some null alleles, including C04:09N, in a large number of units. We also analyzed maternal HLA typing information for 1877 units to determine real haplotype frequencies and linkage disequilibrium. A29:02-B44:03-C16:01-DRB107:01-DQB1*02:02 was the most frequent HLA haplotype and the DRB1-DQB1 gene pair contained the two-locus haplotypes with the strongest linkage disequilibrium values. Four of the 11 unique haplotypes identified in the HLA-homozygous cord blood units were the top-ranking haplotypes identified and were present in 18% of the cohort. This is the first study to report on HLA allele and haplotype frequencies for umbilical cord blood units from the Barcelona Cord Blood Bank and the largest study to date involving two fields of HLA resolution typing of Spanish registry data.
MeSH term(s)	3' Untranslated Regions ; Alleles ; Blood Banks ; Female ; Fetal Blood/immunology ; Gene Frequency ; Genotype ; HLA-A Antigens/genetics ; HLA-A2 Antigen/genetics ; HLA-B Antigens/genetics ; HLA-B44 Antigen/genetics ; HLA-C Antigens/genetics ; HLA-DQ beta-Chains/genetics ; HLA-DRB1 Chains/genetics ; Haplotypes ; Homozygote ; Humans ; Linkage Disequilibrium ; Male ; Mothers ; Polymorphism, Single Nucleotide ; Pregnancy
Chemical Substances	3' Untranslated Regions ; HLA-A Antigens ; HLA-A02:01 antigen ; HLA-A2 Antigen ; HLA-A29 antigen ; HLA-B Antigens ; HLA-B44:03 antigen ; HLA-B44 Antigen ; HLA-C Antigens ; HLA-C04:09N antigen ; HLA-C16 antigen ; HLA-DQ beta-Chains ; HLA-DQB1 antigen ; HLA-DRB1 Chains ; HLA-DRB1*07 antigen
Language	English
Publishing date	2019-08-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2845111-9
ISSN	2059-2310 ; 2059-2302
ISSN (online)	2059-2310
ISSN	2059-2302
DOI	10.1111/tan.13644
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Article ; Online: Mitochondrial GSH replenishment as a potential therapeutic approach for Niemann Pick type C disease

Sandra Torres / Nuria Matías / Anna Baulies / Susana Nuñez / Cristina Alarcon-Vila / Laura Martinez / Natalia Nuño / Anna Fernandez / Joan Caballeria / Thierry Levade / Alba Gonzalez-Franquesa / Pablo Garcia-Rovés / Elisa Balboa / Silvana Zanlungo / Gemma Fabrías / Josefina Casas / Carlos Enrich / Carmen Garcia-Ruiz / José C. Fernández-Checa

Redox Biology, Vol 11, Iss , Pp 60-

2017 Volume 72

Abstract: Niemann Pick type C (NPC) disease is a progressive lysosomal storage disorder caused by mutations ...

Abstract	Niemann Pick type C (NPC) disease is a progressive lysosomal storage disorder caused by mutations in genes encoding NPC1/NPC2 proteins, characterized by neurological defects, hepatosplenomegaly and premature death. While the primary biochemical feature of NPC disease is the intracellular accumulation of cholesterol and gangliosides, predominantly in endolysosomes, mitochondrial cholesterol accumulation has also been reported. As accumulation of cholesterol in mitochondria is known to impair the transport of GSH into mitochondria, resulting in mitochondrial GSH (mGSH) depletion, we investigated the impact of mGSH recovery in NPC disease. We show that GSH ethyl ester (GSH-EE), but not N-acetylcysteine (NAC), restored the mGSH pool in liver and brain of Npc1-/- mice and in fibroblasts from NPC patients, while both GSH-EE and NAC increased total GSH levels. GSH-EE but not NAC increased the median survival and maximal life span of Npc1-/- mice. Moreover, intraperitoneal therapy with GSH-EE protected against oxidative stress and oxidant-induced cell death, restored calbindin levels in cerebellar Purkinje cells and reversed locomotor impairment in Npc1-/- mice. High-resolution respirometry analyses revealed that GSH-EE improved oxidative phosphorylation, coupled respiration and maximal electron transfer in cerebellum of Npc1-/- mice. Lipidomic analyses showed that GSH-EE treatment had not effect in the profile of most sphingolipids in liver and brain, except for some particular species in brain of Npc1-/- mice. These findings indicate that the specific replenishment of mGSH may be a potential promising therapy for NPC disease, worth exploring alone or in combination with other options. Keywords: Ceramide, Sphingolipids, Mitochondrial GSH, Cerebellum, Hepatosplenomegaly, Lysosomal disorders
Keywords	Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2017-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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