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Article ; Online: Identification of signalling pathways involved in gill regeneration in zebrafish.

Cadiz, Laura / Reed, Maddison / Monis, Simon / Akimenko, Marie-Andrée / Jonz, Michael G

2024 Volume 227, Issue 2

Abstract: The occurrence of regeneration of the organs involved in respiratory gas exchange amongst vertebrates is heterogeneous. In some species of amphibians and fishes, the gills regenerate completely following resection or amputation, whereas in mammals, only ... ...

Abstract	The occurrence of regeneration of the organs involved in respiratory gas exchange amongst vertebrates is heterogeneous. In some species of amphibians and fishes, the gills regenerate completely following resection or amputation, whereas in mammals, only partial, facultative regeneration of lung tissue occurs following injury. Given the homology between gills and lungs, the capacity of gill regeneration in aquatic species is of major interest in determining the underlying molecular or signalling pathways involved in respiratory organ regeneration. In the present study, we used adult zebrafish (Danio rerio) to characterize signalling pathways involved in the early stages of gill regeneration. Regeneration of the gills was induced by resection of gill filaments and observed over a period of up to 10 days. We screened for the effects on regeneration of the drugs SU5402, dorsomorphin and LY411575, which inhibit FGF, BMP or Notch signalling pathways, respectively. Exposure to each drug for 5 days significantly reduced regrowth of filament tips in regenerating tissue, compared with unresected controls. In separate experiments under normal conditions of regeneration, we used reverse transcription quantitative PCR and observed an increased expression of genes encoding for the bone morphogenetic factor, Bmp2b, fibroblast growth factor, Fgf8a, a transcriptional regulator (Her6) involved in Notch signalling, and Sonic Hedgehog (Shha), in regenerating gills at 10 day post-resection, compared with unresected controls. In situ hybridization confirmed that all four genes were expressed in regenerating gill tissue. This study implicates BMP, FGF, Notch and Shh signalling in gill regeneration in zebrafish.
MeSH term(s)	Animals ; Zebrafish/genetics ; Zebrafish/metabolism ; Gills/metabolism ; Hedgehog Proteins ; Signal Transduction/genetics ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Zebrafish Proteins/genetics ; Mammals/metabolism
Chemical Substances	Hedgehog Proteins ; Fibroblast Growth Factors (62031-54-3) ; Zebrafish Proteins
Language	English
Publishing date	2024-01-26
Publishing country	England
Document type	Journal Article
ZDB-ID	218085-6
ISSN	1477-9145 ; 0022-0949
ISSN (online)	1477-9145
ISSN	0022-0949
DOI	10.1242/jeb.246290
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Article ; Online: Contributions of 5'HoxA/D regulation to actinodin evolution and the fin-to-limb transition.

Lalonde, Robert L / Akimenko, Marie-Andrée

The International journal of developmental biology

2019 Volume 62, Issue 11-12, Page(s) 705–716

Abstract: The evolution of tetrapod limbs from paired fish fins comprised major changes to the appendicular dermal and endochondral skeleton. Fish fin rays were lost, and the endochondral bone was modified and elaborated to form three distinct segments common to ... ...

Abstract	The evolution of tetrapod limbs from paired fish fins comprised major changes to the appendicular dermal and endochondral skeleton. Fish fin rays were lost, and the endochondral bone was modified and elaborated to form three distinct segments common to all tetrapod limbs: the stylopod, the zeugopod and the autopod. Identifying the molecular mechanisms that contributed to these morphological changes presents a unique insight into our own evolutionary history. This review first summarizes previously identified cis-acting regulatory elements for the 5'HoxA/D genes and actinodin1 that were tested using transgenic swap experiments between fish and tetrapods. Conserved regulatory networks provide evidence for a deep homology between distal fin structures and the autopod, while diverging regulatory strategies highlight potential molecular mechanisms that contributed to the fin-to-limb transition. Next, we summarize studies that performed functional analysis to recapitulate fish-tetrapod diverging regulatory strategies and then discuss their potential morphological consequences during limb evolution. Finally, we also discuss here some of the advantages and disadvantages of using zebrafish to study molecular and morphological changes during the fin-to-limb transition.
MeSH term(s)	Animal Fins/physiology ; Animals ; Animals, Genetically Modified ; Biological Evolution ; Evolution, Molecular ; Extremities/physiology ; Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Genes, Homeobox ; Regulatory Elements, Transcriptional ; Zebrafish/genetics ; Zebrafish Proteins/genetics
Chemical Substances	Zebrafish Proteins ; actinodin 1, zebrafish
Language	English
Publishing date	2019-01-02
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036070-0
ISSN	1696-3547 ; 0214-6282
ISSN (online)	1696-3547
ISSN	0214-6282
DOI	10.1387/ijdb.180248rl
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Article ; Online: Effects of fin fold mesenchyme ablation on fin development in zebrafish.

Lalonde, Robert L / Akimenko, Marie-Andrée

PloS one

2018 Volume 13, Issue 2, Page(s) e0192500

Abstract: The evolution of the tetrapod limb involved an expansion and elaboration of the endoskeletal elements, while the fish fin rays were lost. Loss of fin-specific genes, and regulatory changes in key appendicular patterning genes have been identified as ... ...

Abstract	The evolution of the tetrapod limb involved an expansion and elaboration of the endoskeletal elements, while the fish fin rays were lost. Loss of fin-specific genes, and regulatory changes in key appendicular patterning genes have been identified as mechanisms of limb evolution, however their contributions to cellular organization and tissue differences between fins and limbs remains poorly understood. During early larval fin development, hoxa13a/hoxd13a-expressing fin fold mesenchyme migrate through the median and pectoral fin along actinotrichia fibrils, non-calcified skeletal elements crucial for supporting the fin fold. Fin fold mesenchyme migration defects have previously been proposed as a mechanism of fin dermal bone loss during tetrapod evolution as it has been shown they contribute directly to the fin ray osteoblast population. Using the nitroreductase/metronidazole system, we genetically ablated a subset of hoxa13a/hoxd13a-expressing fin fold mesenchyme to assess its contributions to fin development. Following the ablation of fin fold mesenchyme in larvae, the actinotrichia are unable to remain rigid and the median and pectoral fin folds collapse, resulting in a reduced fin fold size. The remaining cells following ablation are unable to migrate and show decreased actinodin1 mesenchymal reporter activity. Actinodin proteins are crucial structural component of the actinotrichia. Additionally, we show a decrease in hoxa13a, hoxd13a, fgf10a and altered shha, and ptch2 expression during larval fin development. A continuous treatment of metronidazole leads to fin ray defects at 30dpf. Fewer rays are present compared to stage-matched control larvae, and these rays are shorter and less defined. These results suggest the targeted hoxa13a/hoxd13a-expressing mesenchyme contribute to their own successful migration through their contributions to actinotrichia. Furthermore, due to their fate as fin ray osteoblasts, we propose their initial ablation, and subsequent disorganization produces truncated fin dermal bone elements during late larval stages.
MeSH term(s)	Animal Fins/growth & development ; Animals ; Gene Expression Regulation, Developmental ; Larva/drug effects ; Mesoderm/growth & development ; Metronidazole/pharmacology ; Zebrafish/genetics ; Zebrafish/growth & development
Chemical Substances	Metronidazole (140QMO216E)
Language	English
Publishing date	2018-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0192500
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Article ; Online: Cellular and Animal Models of Striated Muscle Laminopathies

Hannah A. Nicolas / Marie-Andrée Akimenko / Frédérique Tesson

Cells, Vol 8, Iss 4, p

2019 Volume 291

Abstract: The lamin A/C ( LMNA ) gene codes for nuclear intermediate filaments constitutive of the nuclear lamina. LMNA has 12 exons and alternative splicing of exon 10 results in two major isoforms—lamins A and C. Mutations found throughout the LMNA gene cause a ... ...

Abstract	The lamin A/C ( LMNA ) gene codes for nuclear intermediate filaments constitutive of the nuclear lamina. LMNA has 12 exons and alternative splicing of exon 10 results in two major isoforms—lamins A and C. Mutations found throughout the LMNA gene cause a group of diseases collectively known as laminopathies, of which the type, diversity, penetrance and severity of phenotypes can vary from one individual to the other, even between individuals carrying the same mutation. The majority of the laminopathies affect cardiac and/or skeletal muscles. The underlying molecular mechanisms contributing to such tissue-specific phenotypes caused by mutations in a ubiquitously expressed gene are not yet well elucidated. This review will explore the different phenotypes observed in established models of striated muscle laminopathies and their respective contributions to advancing our understanding of cardiac and skeletal muscle-related laminopathies. Potential future directions for developing effective treatments for patients with lamin A/C mutation-associated cardiac and/or skeletal muscle conditions will be discussed.
Keywords	lamin A/C ; striated muscle laminopathies ; DCM ; EDMD ; L-CMD ; LGMD ; cellular models ; animal models ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Cellular and Animal Models of Striated Muscle Laminopathies.

Nicolas, Hannah A / Akimenko, Marie-Andrée / Tesson, Frédérique

Cells

2019 Volume 8, Issue 4

Abstract: The lamin A/C ( ...

Abstract	The lamin A/C (
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Lamins/genetics ; Models, Biological ; Muscle, Striated/pathology ; Muscular Diseases/pathology ; Phenotype
Chemical Substances	Lamins
Language	English
Publishing date	2019-03-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8040291
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Article ; Online: Inhibition of mmp13a during zebrafish fin regeneration disrupts fin growth, osteoblasts differentiation, and Laminin organization.

Li, Li / Zhang, Jing / Akimenko, Marie-Andrée

Developmental dynamics : an official publication of the American Association of Anatomists

2019 Volume 249, Issue 2, Page(s) 187–198

Abstract: Background: Matrix metalloproteinases 13 (MMP13) is a potent endopeptidase that regulate cell growth, migration, and extracellular matrix remodeling. However, its role in fin regeneration remains unclear.: Results: mmp13a expression is strongly ... ...

Abstract	Background: Matrix metalloproteinases 13 (MMP13) is a potent endopeptidase that regulate cell growth, migration, and extracellular matrix remodeling. However, its role in fin regeneration remains unclear. Results: mmp13a expression is strongly upregulated during blastema formation and persists in the distal blastema. mmp13a knockdown via morpholino electroporation impairs regenerative outgrowth by decreasing cell proliferation, which correlates with a downregulation of fgf10a and sall4 expression in the blastema. Laminin distribution in the basement membrane is also affected in mmp13a MO-injected rays. Another impact of mmp13a knockdown is observed in the skeletal elements of the fin rays. Expression of two main components of actinotrichia, Collagen II and Actinodin 1 is highly reduced in mmp13a MO-injected rays leading to highly disorganized actinotrichia pattern. Inhibition of mmp13a strongly affects bone formation as shown by a reduction of Zns5 and sp7 expression and of bone matrix mineralization in rays. These defects are accompanied by a significant increase in apoptosis in mmp13a MO-injected fin regenerates. Conclusion: Defects of expression of this multifunctional proteinase drastically affects osteoblast differentiation, bone and actinotrichia formation as well as Laminin distribution in the basement membrane of the fin regenerate, suggesting the important role of Mmp13 during the regenerative process.
MeSH term(s)	Animal Fins/cytology ; Animal Fins/metabolism ; Animals ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Gene Expression Regulation, Developmental/genetics ; Gene Expression Regulation, Developmental/physiology ; Laminin/metabolism ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	Laminin ; Zebrafish Proteins
Language	English
Publishing date	2019-09-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/dvdy.112
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Article ; Online: A CRISPR/Cas9 zebrafish lamin A/C mutant model of muscular laminopathy.

Nicolas, Hannah A / Hua, Khang / Quigley, Hailey / Ivare, Joshua / Tesson, Frédérique / Akimenko, Marie-Andrée

Developmental dynamics : an official publication of the American Association of Anatomists

2021 Volume 251, Issue 4, Page(s) 645–661

Abstract: Background: Lamin A/C gene (LMNA) mutations frequently cause cardiac and/or skeletal muscle diseases called striated muscle laminopathies. We created a zebrafish muscular laminopathy model using CRISPR/Cas9 technology to target the zebrafish lmna gene.!# ...

Abstract	Background: Lamin A/C gene (LMNA) mutations frequently cause cardiac and/or skeletal muscle diseases called striated muscle laminopathies. We created a zebrafish muscular laminopathy model using CRISPR/Cas9 technology to target the zebrafish lmna gene. Results: Heterozygous and homozygous lmna mutants present skeletal muscle damage at 1 day post-fertilization (dpf), and mobility impairment at 4 to 7 dpf. Cardiac structure and function analyses between 1 and 7 dpf show mild and transient defects in the lmna mutants compared to wild type (WT). Quantitative RT-PCR analysis of genes implicated in striated muscle laminopathies show a decrease in jun and nfκb2 expression in 7 dpf homozygous lmna mutants compared to WT. Homozygous lmna mutants have a 1.26-fold protein increase in activated Erk 1/2, kinases associated with striated muscle laminopathies, compared to WT at 7 dpf. Activated Protein Kinase C alpha (Pkc α), a kinase that interacts with lamin A/C and Erk 1/2, is also upregulated in 7 dpf homozygous lmna mutants compared to WT. Conclusions: This study presents an animal model of skeletal muscle laminopathy where heterozygous and homozygous lmna mutants exhibit prominent skeletal muscle abnormalities during the first week of development. Furthermore, this is the first animal model that potentially implicates Pkc α in muscular laminopathies.
MeSH term(s)	Animals ; CRISPR-Cas Systems ; Disease Models, Animal ; Lamin Type A/genetics ; Lamin Type A/metabolism ; Laminopathies ; Muscle, Skeletal ; Mutation ; Zebrafish/genetics ; Zebrafish/metabolism
Chemical Substances	Lamin Type A
Language	English
Publishing date	2021-10-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/dvdy.427
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Article ; Online: Effects of fin fold mesenchyme ablation on fin development in zebrafish.

Robert L Lalonde / Marie-Andrée Akimenko

PLoS ONE, Vol 13, Iss 2, p e

2018 Volume 0192500

Abstract	The evolution of the tetrapod limb involved an expansion and elaboration of the endoskeletal elements, while the fish fin rays were lost. Loss of fin-specific genes, and regulatory changes in key appendicular patterning genes have been identified as mechanisms of limb evolution, however their contributions to cellular organization and tissue differences between fins and limbs remains poorly understood. During early larval fin development, hoxa13a/hoxd13a-expressing fin fold mesenchyme migrate through the median and pectoral fin along actinotrichia fibrils, non-calcified skeletal elements crucial for supporting the fin fold. Fin fold mesenchyme migration defects have previously been proposed as a mechanism of fin dermal bone loss during tetrapod evolution as it has been shown they contribute directly to the fin ray osteoblast population. Using the nitroreductase/metronidazole system, we genetically ablated a subset of hoxa13a/hoxd13a-expressing fin fold mesenchyme to assess its contributions to fin development. Following the ablation of fin fold mesenchyme in larvae, the actinotrichia are unable to remain rigid and the median and pectoral fin folds collapse, resulting in a reduced fin fold size. The remaining cells following ablation are unable to migrate and show decreased actinodin1 mesenchymal reporter activity. Actinodin proteins are crucial structural component of the actinotrichia. Additionally, we show a decrease in hoxa13a, hoxd13a, fgf10a and altered shha, and ptch2 expression during larval fin development. A continuous treatment of metronidazole leads to fin ray defects at 30dpf. Fewer rays are present compared to stage-matched control larvae, and these rays are shorter and less defined. These results suggest the targeted hoxa13a/hoxd13a-expressing mesenchyme contribute to their own successful migration through their contributions to actinotrichia. Furthermore, due to their fate as fin ray osteoblasts, we propose their initial ablation, and subsequent disorganization produces truncated fin dermal bone ...
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2018-01-01T00:00:00Z
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: Scales Radi(i)cally Remodel Sensory Axons and Vasculature.

McMillan, Stephanie C / Akimenko, Marie-Andrée

Developmental cell

2018 Volume 46, Issue 3, Page(s) 253–254

Abstract: Peripheral axons of sensory neurons innervate skin cells to form a functional sensory organ. In this issue of Developmental Cell, Rasmussen et al. (2018) demonstrate that scale formation is essential for the development and regeneration of zebrafish ... ...

Abstract	Peripheral axons of sensory neurons innervate skin cells to form a functional sensory organ. In this issue of Developmental Cell, Rasmussen et al. (2018) demonstrate that scale formation is essential for the development and regeneration of zebrafish sensory axons and vasculature.
MeSH term(s)	Animals ; Axons ; Nerve Regeneration ; Sensory Receptor Cells ; Skin ; Zebrafish ; Zebrafish Proteins
Chemical Substances	Zebrafish Proteins
Language	English
Publishing date	2018-08-04
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2018.07.016
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Article ; Online: Differential actinodin1 regulation in embryonic development and adult fin regeneration in Danio rerio.

Hue-Eileen Phan / Marissa Northorp / Robert L Lalonde / Dung Ngo / Marie-Andrée Akimenko

PLoS ONE, Vol 14, Iss 5, p e

2019 Volume 0216370

Abstract: Actinotrichia are the first exoskeletal elements formed during zebrafish fin development. These rigid fibrils serve as skeletal support for the fin fold and as substrates for mesenchymal cell migration. In the adult intact fins, actinotrichia are ... ...

Abstract	Actinotrichia are the first exoskeletal elements formed during zebrafish fin development. These rigid fibrils serve as skeletal support for the fin fold and as substrates for mesenchymal cell migration. In the adult intact fins, actinotrichia are restricted to the distal domain of the fin. Following fin amputation, actinotrichia also reform during regeneration. The actinodin gene family codes for structural proteins of actinotrichia. We have previously identified cis-acting regulatory elements in a 2kb genomic region upstream of the first exon of actinodin1, termed 2P, required for tissue-specific expression in the fin fold ectoderm and mesenchyme during embryonic development. Indeed, 2P contains an ectodermal enhancer in a 150bp region named epi. Deletion of epi from 2P results in loss of ectodermal-specific activity. In the present study, we sought to further characterize the activity of these regulatory sequences throughout fin development and during adult fin regeneration. Using a reporter transgenic approach, we show that a site within the epi region, termed epi3, contains an early mesenchymal-specific repressor. We also show that the larval fin fold ectodermal enhancer within epi3 remains functional in the basal epithelial layer during fin regeneration. We show that the first non-coding exon and first intron of actinodin1 contains a transcriptional enhancer and an alternative promoter that are necessary for the persistence of reporter expression reminiscent of actinodin1 expression during adulthood. Altogether, we have identified cis-acting regulatory elements that are required for tissue-specific expression as well as full recapitulation of actinodin1 expression during adulthood. Furthermore, the characterization of these elements provides us with useful molecular tools for the enhancement of transgene expression in adulthood.
Keywords	Medicine ; R ; Science ; Q
Subject code	572
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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