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Article ; Online: Mouse models for pendrin-associated loss of cochlear and vestibular function.

Wangemann, Philine

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2013 Volume 32, Issue 7, Page(s) 157–165

Abstract: The human gene SLC26A4 and the mouse ortholog Slc26a4 code for the protein pendrin, which is an anion exchanger expressed in apical membranes of selected epithelia. In the inner ear, pendrin is expressed in the cochlea, the vestibular labyrinth and the ... ...

Abstract	The human gene SLC26A4 and the mouse ortholog Slc26a4 code for the protein pendrin, which is an anion exchanger expressed in apical membranes of selected epithelia. In the inner ear, pendrin is expressed in the cochlea, the vestibular labyrinth and the endolymphatic sac. Loss-of-function and hypo-functional mutations cause an enlargement of the vestibular aqueduct (EVA) and sensorineural hearing loss. The relatively high prevalence of SLC26A4 mutations provides a strong imperative to develop rational interventions that delay, ameliorate or prevent pendrin-associated loss of cochlear and vestibular function. This review summarizes recent studies in mouse models that have been developed to delineate the role of pendrin in the physiology of hearing and balance and that have brought forward the concept that a temporally and spatially limited therapy may be sufficient to secure a life-time of normal hearing in children bearing mutations of SLC26A4.
MeSH term(s)	Animals ; Anion Transport Proteins/genetics ; Anion Transport Proteins/metabolism ; Cochlea/metabolism ; Cochlea/pathology ; Cochlear Diseases/genetics ; Cochlear Diseases/metabolism ; Cochlear Diseases/pathology ; Disease Models, Animal ; Humans ; Mice ; Sulfate Transporters ; Vestibular Diseases/genetics ; Vestibular Diseases/metabolism ; Vestibular Diseases/pathology ; Vestibular Function Tests
Chemical Substances	Anion Transport Proteins ; Slc26a4 protein, mouse ; Sulfate Transporters
Language	English
Publishing date	2013-12-18
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000356635
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Article ; Online: The role of pendrin in the development of the murine inner ear.

Wangemann, Philine

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2011 Volume 28, Issue 3, Page(s) 527–534

Abstract: Enlargement of the vestibular aqueduct (EVA) is a common inner ear malformation found in children with sensorineural hearing loss that is frequently associated with loss-of-function or hypo-function mutations of SLC26A4. SLC26A4 codes for pendrin, which ... ...

Abstract	Enlargement of the vestibular aqueduct (EVA) is a common inner ear malformation found in children with sensorineural hearing loss that is frequently associated with loss-of-function or hypo-function mutations of SLC26A4. SLC26A4 codes for pendrin, which is a protein that is expressed in apical membranes of selected epithelia and functions as an anion exchanger. The comparatively high prevalence of EVA provides a strong imperative to develop rational interventions that delay, ameliorate or prevent hearing loss associated with this phenotype. The development of rational interventions requires a fundamental understanding of the role that pendrin plays in the normal development of hearing, as well as a detailed understanding of the pathobiologic mechanisms that, in the absence of fully functional pendrin, lead to an unstable hearing phenotype, with fluctuating or progressive loss of hearing. This review summarizes studies in mouse models that have focused on delineating the role of pendrin in the physiology of the inner ear and the pathobiology that leads to hearing loss.
MeSH term(s)	Animals ; Anion Transport Proteins/analysis ; Anion Transport Proteins/metabolism ; Anions/metabolism ; Cell Communication ; Ear, Inner/embryology ; Ear, Inner/metabolism ; Hearing Loss, Sensorineural/genetics ; Hearing Loss, Sensorineural/metabolism ; Hearing Loss, Sensorineural/pathology ; Humans ; Potassium Channels, Inwardly Rectifying/metabolism ; Sulfate Transporters
Chemical Substances	Anion Transport Proteins ; Anions ; Kcnj10 (channel) ; Potassium Channels, Inwardly Rectifying ; Slc26a4 protein, mouse ; Sulfate Transporters
Language	English
Publishing date	2011-11-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000335113
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Article ; Online: Mouse Models for Pendrin-Associated Loss of Cochlear and Vestibular Function

Wangemann, Philine

Cellular Physiology and Biochemistry - International Journal of Experimental Cellular Physiology, Biochemistry and Pharmacology

2013 Volume 32, Issue S1, Page(s) 157–165

Abstract	The human gene SLC26A4 and the mouse ortholog Slc26a4 code for the protein pendrin, which is an anion exchanger expressed in apical membranes of selected epithelia. In the inner ear, pendrin is expressed in the cochlea, the vestibular labyrinth and the endolymphatic sac. Loss-of-function and hypo-functional mutations cause an enlargement of the vestibular aqueduct (EVA) and sensorineural hearing loss. The relatively high prevalence of SLC26A4 mutations provides a strong imperative to develop rational interventions that delay, ameliorate or prevent pendrin-associated loss of cochlear and vestibular function. This review summarizes recent studies in mouse models that have been developed to delineate the role of pendrin in the physiology of hearing and balance and that have brought forward the concept that a temporally and spatially limited therapy may be sufficient to secure a life-time of normal hearing in children bearing mutations of SLC26A4.© 2014 S. Karger AG, Basel
Keywords	Slc26a4 ; Enlarged vestibular aqueduct ; Hearing ; Cochlea ; Endolymphatic sac ; Genetic disease model
Language	English
Publisher	S. Karger AG
Publishing place	Basel
Publishing country	Switzerland
Document type	Article ; Online
ISSN	1421-9778 ; 1015-8987 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000356635
Database	Karger publisher's database

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Article: Mouse Models for Pendrin-Associated Loss of Cochlear and Vestibular Function

Wangemann, Philine

Cellular Physiology and Biochemistry

2013 Volume 32, Issue 1, Page(s) 157–165

Institution	Anatomy & Physiology Department, Kansas State University, Manhattan, Kansas, USA
Abstract	The human gene SLC26A4 and the mouse ortholog Slc26a4 code for the protein pendrin, which is an anion exchanger expressed in apical membranes of selected epithelia. In the inner ear, pendrin is expressed in the cochlea, the vestibular labyrinth and the endolymphatic sac. Loss-of-function and hypo-functional mutations cause an enlargement of the vestibular aqueduct (EVA) and sensorineural hearing loss. The relatively high prevalence of SLC26A4 mutations provides a strong imperative to develop rational interventions that delay, ameliorate or prevent pendrin-associated loss of cochlear and vestibular function. This review summarizes recent studies in mouse models that have been developed to delineate the role of pendrin in the physiology of hearing and balance and that have brought forward the concept that a temporally and spatially limited therapy may be sufficient to secure a life-time of normal hearing in children bearing mutations of SLC26A4
Keywords	Enlarged vestibular aqueduct ; Hearing ; Cochlea ; Endolymphatic sac ; Genetic disease model
Language	English
Publishing date	2013-12-18
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
ZDB-ID	1067572-3
ISBN	978-3-318-05402-6 ; 3-318-05402-X
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000356635
Database	Karger publisher's database

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Article ; Online: Claudin expression during early postnatal development of the murine cochlea.

Kudo, Takayuki / Wangemann, Philine / Marcus, Daniel C

BMC physiology

2018 Volume 18, Issue 1, Page(s) 1

Abstract: Background: Claudins are major components of tight junctions, which form the paracellular barrier between the cochlear luminal and abluminal fluid compartments that supports the large transepithelial voltage difference and the large concentration ... ...

Abstract	Background: Claudins are major components of tight junctions, which form the paracellular barrier between the cochlear luminal and abluminal fluid compartments that supports the large transepithelial voltage difference and the large concentration differences of K Results: We examined by quantitative RT-PCR the expression of the mRNA of 24 claudin isoforms in mouse cochlea during postnatal development and localized the expression in separated fractions of the cochlea. Transcripts of 21 claudin isoforms were detected at all ages, while 3 isoforms (Cldn-16, - 17 and - 18) were not detected. Claudins that increased expression during development include Cldn-9, - 13, - 14, - 15, and -19v2, while Cldn-6 decreased. Those that do not change expression level during postnatal development include Cldn-1, - 2, - 3, - 4, - 5, - 7, - 8, -10v1, -10v2, - 11, - 12, -19v1, - 20, - 22, and - 23. Our investigation revealed unique localization of some claudins. In particular, Cldn-13 expression rapidly increases during early development and is mainly expressed in bone but only minimally in the lateral wall (including stria vascularis) and in the medial region (including the organ of Corti). No statistically significant changes in expression of Cldn-11, - 13, or - 14 were found in the cochlea of Slc26a4 Conclusions: We demonstrated developmental patterns of claudin isoform transcript expression in the murine cochlea. Most of the claudins were associated with stria vascularis and organ of Corti, tissue fractions rich in tight junctions. However, this study suggests a novel function of Cldn-13 in the cochlea, which may be linked to cochlear bone marrow maturation.
MeSH term(s)	Animals ; Anion Transport Proteins/genetics ; Claudins/metabolism ; Cochlea/growth & development ; Cochlea/metabolism ; Female ; Male ; Mice, Knockout ; Protein Isoforms/metabolism ; RNA, Messenger/metabolism ; Sulfate Transporters
Chemical Substances	Anion Transport Proteins ; Claudins ; Protein Isoforms ; RNA, Messenger ; Slc26a4 protein, mouse ; Sulfate Transporters
Language	English
Publishing date	2018-01-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2041340-3
ISSN	1472-6793 ; 1472-6793
ISSN (online)	1472-6793
ISSN	1472-6793
DOI	10.1186/s12899-018-0035-1
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Article: The Role of Pendrin in the Development of the Murine Inner Ear

Wangemann, Philine

Cellular Physiology and Biochemistry

2011 Volume 28, Issue 3, Page(s) 527–534

Institution	Anatomy & Physiology Department, Kansas State University, Manhattan, Kansas
Abstract	Enlargement of the vestibular aqueduct (EVA) is a common inner ear malformation found in children with sensorineural hearing loss that is frequently associated with loss-of-function or hypo-function mutations of SLC26A4. SLC26A4 codes for pendrin, which is a protein that is expressed in apical membranes of selected epithelia and functions as an anion exchanger. The comparatively high prevalence of EVA provides a strong imperative to develop rational interventions that delay, ameliorate or prevent hearing loss associated with this phenotype. The development of rational interventions requires a fundamental understanding of the role that pendrin plays in the normal development of hearing, as well as a detailed understanding of the pathobiologic mechanisms that, in the absence of fully functional pendrin, lead to an unstable hearing phenotype, with fluctuating or progressive loss of hearing. This review summarizes studies in mouse models that have focused on delineating the role of pendrin in the physiology of the inner ear and the pathobiology that leads to hearing loss.
Keywords	Enlarged vestibular aqueduct ; Development ; Hearing ; Cochlea ; Endolymphatic sac ; Genetic disease model
Language	English
Publishing date	2011-11-18
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Review
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000335113
Database	Karger publisher's database

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Article: Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential.

Wangemann, Philine

The Journal of physiology

2006 Volume 576, Issue Pt 1, Page(s) 11–21

Abstract: The exquisite sensitivity of the cochlea, which mediates the transduction of sound waves into nerve impulses, depends on the endocochlear potential and requires a highly specialized environment that enables and sustains sensory function. Disturbance of ... ...

Abstract	The exquisite sensitivity of the cochlea, which mediates the transduction of sound waves into nerve impulses, depends on the endocochlear potential and requires a highly specialized environment that enables and sustains sensory function. Disturbance of cochlear homeostasis is the cause of many forms of hearing loss including the most frequently occurring syndromic and non-syndromic forms of hereditary hearing loss, Pendred syndrome and Cx26-related deafness. The occurrence of these and other monogenetic disorders illustrates that cochlear fluid homeostasis and the generation of the endocochlear potential are poorly secured by functional redundancy. This review summarizes the most prominent aspects of cochlear fluid homeostasis. It covers cochlear fluid composition, the generation of the endocochlear potential, K(+) secretion and cycling and its regulation, the role of gap junctions, mechanisms of acid-base homeostasis, and Ca(2+) transport.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Animals ; Cochlea/cytology ; Cochlea/innervation ; Cochlea/physiology ; Connexin 26 ; Connexins ; Evoked Potentials, Auditory/physiology ; Extracellular Fluid/physiology ; Gap Junctions/physiology ; Hearing Loss/physiopathology ; Homeostasis/physiology ; Humans ; Neurons, Afferent/physiology ; Potassium/metabolism ; Potassium Channels/physiology ; Signal Transduction/physiology ; Sodium-Potassium-Exchanging ATPase/physiology
Chemical Substances	Connexins ; GJB2 protein, human ; Potassium Channels ; Connexin 26 (127120-53-0) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2006-07-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2006.112888
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Article ; Online: Ryanodine-induced vasoconstriction of the gerbil spiral modiolar artery depends on the Ca

Krishnamoorthy, Gayathri / Reimann, Katrin / Wangemann, Philine

BMC physiology

2016 Volume 16, Issue 1, Page(s) 6

Abstract: Background: In many vascular smooth muscle cells (SMCs), ryanodine receptor-mediated Ca: Methods: SMAs were isolated from adult female gerbils, loaded with the Ca: Results: Ca: Conclusions: The results suggest that ... ...

Abstract	Background: In many vascular smooth muscle cells (SMCs), ryanodine receptor-mediated Ca Methods: SMAs were isolated from adult female gerbils, loaded with the Ca Results: Ca Conclusions: The results suggest that Ca
MeSH term(s)	Animals ; Calcium Signaling/drug effects ; Cochlea/blood supply ; Cochlea/drug effects ; Cochlea/physiology ; Endothelin-1/administration & dosage ; Female ; Gerbillinae ; Large-Conductance Calcium-Activated Potassium Channels/physiology ; Muscle, Smooth, Vascular/blood supply ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/physiology ; Ryanodine/administration & dosage ; Vasoconstriction/drug effects
Chemical Substances	Endothelin-1 ; Large-Conductance Calcium-Activated Potassium Channels ; Ryanodine (15662-33-6)
Language	English
Publishing date	2016-11-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2041340-3
ISSN	1472-6793 ; 1472-6793
ISSN (online)	1472-6793
ISSN	1472-6793
DOI	10.1186/s12899-016-0026-z
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Article ; Online: The gastric H,K-ATPase in stria vascularis contributes to pH regulation of cochlear endolymph but not to K secretion.

Miyazaki, Hiromitsu / Wangemann, Philine / Marcus, Daniel C

BMC physiology

2016 Volume 17, Issue 1, Page(s) 1

Abstract: Background: Disturbance of acid-base balance in the inner ear is known to be associated with hearing loss in a number of conditions including genetic mutations and pharmacologic interventions. Several previous physiologic and immunohistochemical ... ...

Abstract	Background: Disturbance of acid-base balance in the inner ear is known to be associated with hearing loss in a number of conditions including genetic mutations and pharmacologic interventions. Several previous physiologic and immunohistochemical observations lead to proposals of the involvement of acid-base transporters in stria vascularis. Results: We directly measured acid flux in vitro from the apical side of isolated stria vascularis from adult C57Bl/6 mice with a novel constant-perfusion pH-selective self-referencing probe. Acid efflux that depended on metabolism and ion transport was observed from the apical side of stria vascularis. The acid flux was decreased to about 40 % of control by removal of the metabolic substrate (glucose-free) and by inhibition of the sodium pump (ouabain). The flux was also decreased a) by inhibition of Na,H-exchangers by amiloride, dimethylamiloride (DMA), S3226 and Hoe694, b) by inhibition of Na,2Cl,K-cotransporter (NKCC1) by bumetanide, and c) by the likely inhibition of HCO3/anion exchange by DIDS. By contrast, the acid flux was increased by inhibition of gastric H,K-ATPase (SCH28080) but was not affected by an inhibitor of vH-ATPase (bafilomycin). K flux from stria vascularis was reduced less than 5 % by SCH28080. Conclusions: These observations suggest that stria vascularis may be an important site of control of cochlear acid-base balance and demonstrate a functional role of several acid-base transporters in stria vascularis, including basolateral H,K-ATPase and apical Na,H-exchange. Previous suggestions that H secretion is mediated by an apical vH-ATPase and that basolateral H,K-ATPase contributes importantly to K secretion in stria vascularis are not supported. These results advance our understanding of inner ear acid-base balance and provide a stronger basis to interpret the etiology of genetic and pharmacologic cochlear dysfunctions that are influenced by endolymphatic pH.
MeSH term(s)	Acid-Base Equilibrium ; Animals ; Endolymph/metabolism ; Female ; H(+)-K(+)-Exchanging ATPase/metabolism ; Hydrogen-Ion Concentration ; Male ; Mice ; Mice, Inbred C57BL ; Potassium/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Stria Vascularis/enzymology ; Stria Vascularis/metabolism
Chemical Substances	H(+)-K(+)-Exchanging ATPase (EC 3.6.3.10) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2016-08-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2041340-3
ISSN	1472-6793 ; 1472-6793
ISSN (online)	1472-6793
ISSN	1472-6793
DOI	10.1186/s12899-016-0024-1
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Article: Cochlear blood flow regulation.

Wangemann, Philine

Advances in oto-rhino-laryngology

2003 Volume 59, Page(s) 51–57

Abstract: The regulation of cochlear blood flow is crucial for auditory function due to the sensitivity of this sensory organ to hypoxia. Part of the regulation of cochlear blood flow occurs in the spiral modiolar artery, which provides the main blood supply to ... ...

Abstract	The regulation of cochlear blood flow is crucial for auditory function due to the sensitivity of this sensory organ to hypoxia. Part of the regulation of cochlear blood flow occurs in the spiral modiolar artery, which provides the main blood supply to the cochlea. Blood flow in general is most effectively regulated through the control of the vascular diameter. The vascular diameter is determined by the degree of constriction of the smooth muscle cells in the vascular wall. A constriction of the smooth muscle cells reduces the diameter of the vascular lumen and thereby decreases blood flow, whereas a relaxation of the smooth muscle cells increases blood flow. The degree of constriction of the smooth muscle cells in the spiral modiolar artery is carefully controlled and must be adjusted properly to the demands of the cochlear tissues. To achieve proper control, smooth muscle cells integrate information from various sources. Vasoconstrictors and dilators may originate from the innervation surrounding the vessel, from endothelial cells lining the vascular lumen or from the smooth muscle cells themselves. Recent advances revealed that smooth muscle cells from different arterioles differ widely in their endowment with mechanisms that regulate the degree of smooth muscle cell tone. Signal transduction mechanisms, which mediate these neurogenic, local and paracrine regulations of smooth muscle contractility are now beginning to be understood. This report reviews recently obtained evidence for adrenergic regulation of cochlear blood flow and then focuses on a novel vasodilation mechanism that involves ryanodine receptors, Ca2+ sparks and the activation of Ca2+-activated K+ channels.
MeSH term(s)	Calcium Channels/metabolism ; Cochlea/blood supply ; Cochlea/metabolism ; Humans ; Muscle Contraction/physiology ; Muscle, Smooth/blood supply ; Muscle, Smooth/metabolism ; Potassium Channels/metabolism ; Receptors, Adrenergic/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Signal Transduction/physiology ; Stellate Ganglion/metabolism
Chemical Substances	Calcium Channels ; Potassium Channels ; Receptors, Adrenergic ; Ryanodine Receptor Calcium Release Channel
Language	English
Publishing date	2003-02-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ISSN	0065-3071
ISSN	0065-3071
DOI	10.1159/000059241
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