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Article ; Online: Daniel Porte Jr., 13 August 1931-13 May 2023.

Kahn, Steven E / Woods, Stephen C / Halter, Jeffrey B / Taborsky, Gerald J / Schwartz, Michael W

2023 Volume 73, Issue 1, Page(s) 5–10

Language	English
Publishing date	2023-12-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db23-0787
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Article ; Online: Islets have a lot of nerve! Or do they?

Taborsky, Gerald J

Cell metabolism

2011 Volume 14, Issue 1, Page(s) 5–6

Abstract: The autonomic nervous system influences insulin and glucagon secretion. In this issue, Rodriguez-Diaz et al. (2011) show that mouse and human islets differ in their innervation patterns, yet the effect of neural activation on islet hormone secretion is ... ...

Abstract	The autonomic nervous system influences insulin and glucagon secretion. In this issue, Rodriguez-Diaz et al. (2011) show that mouse and human islets differ in their innervation patterns, yet the effect of neural activation on islet hormone secretion is similar. Key questions raised by this species difference have potential relevance to diabetic therapeutics.
Language	English
Publishing date	2011-06-24
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2011.06.004
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Article ; Online: Early sympathetic islet neuropathy in autoimmune diabetes: lessons learned and opportunities for investigation.

Mundinger, Thomas O / Taborsky, Gerald J

Diabetologia

2016 Volume 59, Issue 10, Page(s) 2058–2067

Abstract: This review outlines the current state of knowledge regarding a unique neural defect of the pancreatic islet in autoimmune diabetes, one that we have termed early sympathetic islet neuropathy (eSIN). We begin with the findings that a majority of islet ... ...

Abstract	This review outlines the current state of knowledge regarding a unique neural defect of the pancreatic islet in autoimmune diabetes, one that we have termed early sympathetic islet neuropathy (eSIN). We begin with the findings that a majority of islet sympathetic nerves are lost near the onset of type 1, but not type 2, diabetes and that this nerve loss is restricted to the islet. We discuss later work demonstrating that while the loss of islet sympathetic nerves and the loss of islet beta cells in type 1 diabetes both require infiltration of the islet by lymphocytes, their respective mechanisms of tissue destruction differ. Uniquely, eSIN requires the activation of a specific neurotrophin receptor and we propose two possible pathways for activation of this receptor during the immune attack on the islet. We also outline what is known about the functional consequences of eSIN, focusing on impairment of sympathetically mediated glucagon secretion and its application to the clinical problem of insulin-induced hypoglycaemia. Finally, we offer our view on the important remaining questions regarding this unique neural defect.
MeSH term(s)	Autoimmunity/physiology ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/pathology ; Diabetic Neuropathies/immunology ; Diabetic Neuropathies/metabolism ; Diabetic Neuropathies/pathology ; Glucagon/metabolism ; Humans ; Nerve Growth Factors/metabolism ; Sympathetic Nervous System/immunology ; Sympathetic Nervous System/metabolism ; Sympathetic Nervous System/pathology
Chemical Substances	Nerve Growth Factors ; Glucagon (9007-92-5)
Language	English
Publishing date	2016-06-24
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-016-4026-0
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Article ; Online: The physiology of glucagon.

Taborsky, Gerald J

Journal of diabetes science and technology

2010 Volume 4, Issue 6, Page(s) 1338–1344

Abstract: This short review outlines the physiology of glucagon in vivo, with an emphasis on its neural control, the author's area of interest. Glucagon is secreted from alpha cells, which are a minority of the pancreatic islet. Anatomically, they are down stream ... ...

Abstract	This short review outlines the physiology of glucagon in vivo, with an emphasis on its neural control, the author's area of interest. Glucagon is secreted from alpha cells, which are a minority of the pancreatic islet. Anatomically, they are down stream from the majority islet beta cells. Beta-cell secretory products restrain glucagon secretion. Activation of the autonomic nerves, which innervate the islet, increases glucagon secretion. Glucagon is secreted into the portal vein and thus has its major physiologic action at the liver to break down glycogen. Glucagon thereby maintains hepatic glucose production during fasting and increases hepatic glucose production during stress, including the clinically important stress of hypoglycemia. Three different mechanisms proposed to stimulate glucagon secreted during hypoglycemia are discussed: (1) a stimulatory effect of low glucose directly on the alpha cell, (2) withdrawal of an inhibitory effect of adjacent beta cells, and (3) a stimulatory effect of autonomic activation. In type 1 diabetes (T1DM), increased glucagon secretion contributes to the elevated ketones and acidosis present in diabetic ketoacidosis (DKA). It also contributes to the hyperglycemia seen with or without DKA. The glucagon response to insulin-induced hypoglycemia is impaired soon after the development of T1DM. The mediators of this impairment include loss of beta cells and loss of sympathetic nerves from the autoimmune diabetic islet.
MeSH term(s)	Animals ; Autonomic Nervous System/physiopathology ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/physiopathology ; Glucagon/metabolism ; Glucagon-Secreting Cells/metabolism ; Glycogen/metabolism ; Homeostasis ; Humans ; Hypoglycemia/metabolism ; Hypoglycemia/physiopathology ; Insulin/metabolism ; Islets of Langerhans/innervation ; Islets of Langerhans/metabolism ; Liver/metabolism
Chemical Substances	Blood Glucose ; Insulin ; Glycogen (9005-79-2) ; Glucagon (9007-92-5)
Language	English
Publishing date	2010-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ISSN	1932-2968
ISSN (online)	1932-2968
DOI	10.1177/193229681000400607
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Article ; Online: Daniel Porte Jr.: A Leader in Our Understanding of the Role of Defective Insulin Secretion and Action in Obesity and Type 2 Diabetes.

Palmer, Jerry P / Kahn, Steven E / Schwartz, Michael W / Taborsky, Gerald J / Woods, Stephen C

Diabetes care

2020 Volume 43, Issue 4, Page(s) 704–709

MeSH term(s)	Biomedical Research/history ; Blood Glucose/metabolism ; Cardiology/history ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/metabolism ; Endocrinology/history ; History, 20th Century ; History, 21st Century ; Humans ; Insulin/metabolism ; Insulin Resistance/physiology ; Insulin Secretion/physiology ; Leadership ; New York City ; Obesity/etiology ; Obesity/metabolism ; Physicians
Chemical Substances	Blood Glucose ; Insulin
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Biography ; Historical Article ; Journal Article ; Portrait
ZDB-ID	441231-x
ISSN	1935-5548 ; 0149-5992
ISSN (online)	1935-5548
ISSN	0149-5992
DOI	10.2337/dci19-0068
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Zs.A 1434: 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: CNS control of the endocrine pancreas.

Faber, Chelsea L / Deem, Jennifer D / Campos, Carlos A / Taborsky, Gerald J / Morton, Gregory J

Diabetologia

2020 Volume 63, Issue 10, Page(s) 2086–2094

Abstract: Increasing evidence suggests that, although pancreatic islets can function autonomously to detect and respond to changes in the circulating glucose level, the brain cooperates with the islet to maintain glycaemic control. Here, we review the role of the ... ...

Abstract	Increasing evidence suggests that, although pancreatic islets can function autonomously to detect and respond to changes in the circulating glucose level, the brain cooperates with the islet to maintain glycaemic control. Here, we review the role of the central and autonomic nervous systems in the control of the endocrine pancreas, including mechanisms whereby the brain senses circulating blood glucose levels. We also examine whether dysfunction in these systems might contribute to complications of type 1 diabetes and the pathogenesis of type 2 diabetes. Graphical abstract.
MeSH term(s)	Animals ; Autonomic Nervous System/metabolism ; Autonomic Nervous System/physiopathology ; Blood Glucose/metabolism ; Central Nervous System/metabolism ; Central Nervous System/physiopathology ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Glucagon/metabolism ; Humans ; Insulin/metabolism ; Insulin Secretion ; Islets of Langerhans/innervation ; Islets of Langerhans/metabolism ; Sensory Receptor Cells
Chemical Substances	Blood Glucose ; Insulin ; Glucagon (9007-92-5)
Language	English
Publishing date	2020-09-07
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-020-05204-6
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Article ; Online: Minireview: The role of the autonomic nervous system in mediating the glucagon response to hypoglycemia.

Taborsky, Gerald J / Mundinger, Thomas O

Endocrinology

2012 Volume 153, Issue 3, Page(s) 1055–1062

Abstract: In type 1 diabetes, the impairment of the glucagon response to hypoglycemia increases both its severity and duration. In nondiabetic individuals, hypoglycemia activates the autonomic nervous system, which in turn mediates the majority of the glucagon ... ...

Abstract	In type 1 diabetes, the impairment of the glucagon response to hypoglycemia increases both its severity and duration. In nondiabetic individuals, hypoglycemia activates the autonomic nervous system, which in turn mediates the majority of the glucagon response to moderate and marked hypoglycemia. The first goal of this minireview is therefore to illustrate and document these autonomic mechanisms. Specifically we describe the hypoglycemic thresholds for activating the three autonomic inputs to the islet (parasympathetic nerves, sympathetic nerves, and adrenal medullary epinephrine) and their magnitudes of activation as glucose falls from euglycemia to near fatal levels. The implication is that their relative contributions to this glucagon response depend on the severity of hypoglycemia. The second goal of this minireview is to discuss known and suspected down-regulation or damage to these mechanisms in diabetes. We address defects in the central nervous system, the peripheral nervous system, and in the islet itself. They are categorized as either functional defects caused by glucose dysregulation or structural defects caused by the autoimmune attack of the islet. In the last section of the minireview, we outline approaches for reversing these defects. Such reversal has both scientific and clinical benefit. Scientifically, one could determine the contribution of these defects to the impairment of glucagon response seen early in type 1 diabetes. Clinically, restoring this glucagon response would allow more aggressive treatment of the chronic hyperglycemia that is linked to the debilitating long-term complications of this disease.
MeSH term(s)	Animals ; Autoimmunity ; Autonomic Nervous System/physiology ; Central Nervous System/metabolism ; Diabetes Mellitus/physiopathology ; Diabetes Mellitus, Type 1/metabolism ; Gene Expression Regulation ; Glucagon/chemistry ; Glucagon/metabolism ; Glucose/metabolism ; Humans ; Hypoglycemia/metabolism ; Insulin Resistance ; Islets of Langerhans/cytology ; Models, Biological ; Peripheral Nervous System/metabolism
Chemical Substances	Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2012-02-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2011-2040
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Article ; Online: Co-impairment of autonomic and glucagon responses to insulin-induced hypoglycemia in dogs with naturally occurring insulin-dependent diabetes mellitus.

Gilor, Chen / Duesberg, Cynthia / Elliott, Denise A / Feldman, Edward C / Mundinger, Thomas O / Taborsky, Gerald J / Nelson, Richard W / Havel, Peter J

American journal of physiology. Endocrinology and metabolism

2020 Volume 319, Issue 6, Page(s) E1074–E1083

Abstract: This study aimed to investigate the contributions of two factors potentially impairing glucagon response to insulin-induced hypoglycemia (IIH) in insulin-deficient diabetes: ...

Abstract	This study aimed to investigate the contributions of two factors potentially impairing glucagon response to insulin-induced hypoglycemia (IIH) in insulin-deficient diabetes:
MeSH term(s)	Animals ; Autonomic Nervous System/drug effects ; Blood Glucose/metabolism ; C-Peptide/metabolism ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/veterinary ; Dog Diseases/metabolism ; Dogs ; Epinephrine/blood ; Glucagon/pharmacology ; Glucagon-Secreting Cells/drug effects ; Glucose Clamp Technique ; Hypoglycemia/chemically induced ; Hypoglycemia/metabolism ; Hypoglycemic Agents ; Insulin ; Insulin-Secreting Cells/drug effects ; Norepinephrine/blood ; Pancreatic Polypeptide/metabolism
Chemical Substances	Blood Glucose ; C-Peptide ; Hypoglycemic Agents ; Insulin ; Pancreatic Polypeptide (59763-91-6) ; Glucagon (9007-92-5) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2020-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00379.2020
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Article: Islets Have a Lot of Nerve! Or Do They?

Taborsky, Gerald J., Jr

Cell metabolism. 2011 July 6, v. 14, no. 1

2011

Abstract	The autonomic nervous system influences insulin and glucagon secretion. In this issue, Rodriguez-Diaz et al. (2011) show that mouse and human islets differ in their innervation patterns, yet the effect of neural activation on islet hormone secretion is similar. Key questions raised by this species difference have potential relevance to diabetic therapeutics.
Keywords	autonomic nervous system ; glucagon ; hormone secretion ; humans ; innervation ; insulin ; mice ; nerve tissue ; therapeutics
Language	English
Dates of publication	2011-0706
Size	p. 5-6.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2011.06.004
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Short-term diabetic hyperglycemia suppresses celiac ganglia neurotransmission, thereby impairing sympathetically mediated glucagon responses.

Mundinger, Thomas O / Cooper, Ellis / Coleman, Michael P / Taborsky, Gerald J

American journal of physiology. Endocrinology and metabolism

2015 Volume 309, Issue 3, Page(s) E246–55

Abstract: Short-term hyperglycemia suppresses superior cervical ganglia neurotransmission. If this ganglionic dysfunction also occurs in the islet sympathetic pathway, sympathetically mediated glucagon responses could be impaired. Our objectives were 1) to test ... ...

Abstract	Short-term hyperglycemia suppresses superior cervical ganglia neurotransmission. If this ganglionic dysfunction also occurs in the islet sympathetic pathway, sympathetically mediated glucagon responses could be impaired. Our objectives were 1) to test for a suppressive effect of 7 days of streptozotocin (STZ) diabetes on celiac ganglia (CG) activation and on neurotransmitter and glucagon responses to preganglionic nerve stimulation, 2) to isolate the defect in the islet sympathetic pathway to the CG itself, and 3) to test for a protective effect of the WLD(S) mutation. We injected saline or nicotine in nondiabetic and STZ-diabetic rats and measured fos mRNA levels in whole CG. We electrically stimulated the preganglionic or postganglionic nerve trunk of the CG in nondiabetic and STZ-diabetic rats and measured portal venous norepinephrine and glucagon responses. We repeated the nicotine and preganglionic nerve stimulation studies in nondiabetic and STZ-diabetic WLD(S) rats. In STZ-diabetic rats, the CG fos response to nicotine was suppressed, and the norepinephrine and glucagon responses to preganglionic nerve stimulation were impaired. In contrast, the norepinephrine and glucagon responses to postganglionic nerve stimulation were normal. The CG fos response to nicotine, and the norepinephrine and glucagon responses to preganglionic nerve stimulation, were normal in STZ-diabetic WLD(S) rats. In conclusion, short-term hyperglycemia's suppressive effect on nicotinic acetylcholine receptors of the CG impairs sympathetically mediated glucagon responses. WLD(S) rats are protected from this dysfunction. The implication is that this CG dysfunction may contribute to the impaired glucagon response to insulin-induced hypoglycemia seen early in type 1 diabetes.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 1/blood ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/physiopathology ; Down-Regulation/drug effects ; Electric Stimulation ; Ganglia, Sympathetic/drug effects ; Ganglia, Sympathetic/metabolism ; Ganglia, Sympathetic/physiopathology ; Ganglionic Stimulants/pharmacology ; Glucagon/blood ; Glucagon/metabolism ; Hyperglycemia/etiology ; Islets of Langerhans/drug effects ; Islets of Langerhans/innervation ; Islets of Langerhans/metabolism ; Male ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Nicotinic Agonists/pharmacology ; Norepinephrine/blood ; Norepinephrine/metabolism ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-fos/metabolism ; Rats, Sprague-Dawley ; Rats, Transgenic ; Rats, Wistar ; Receptors, Nicotinic/chemistry ; Receptors, Nicotinic/metabolism ; Synaptic Transmission/drug effects ; Wallerian Degeneration/complications
Chemical Substances	Ganglionic Stimulants ; Mutant Proteins ; Nerve Tissue Proteins ; Nicotinic Agonists ; Proto-Oncogene Proteins c-fos ; Receptors, Nicotinic ; Wld protein, rat ; Glucagon (9007-92-5) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2015-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00140.2015
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