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Book ; Online ; Thesis: Evidence-based pharmacotherapy and drug development in autism spectrum disorder: a systematic review, network meta-analysis and meta-regression of placebo-effects

Siafis, Spyridon [Verfasser] / Leucht, Stefan M. [Akademischer Betreuer] / Andreas, Dinkel [Gutachter] / Leucht, Stefan M. [Gutachter] / Welling, Andrea [Gutachter]

2023

Author's details	Spyridon Siafis ; Gutachter: Dinkel Andreas, Stefan M. Leucht, Andrea Welling ; Betreuer: Stefan M. Leucht
Keywords	Psychologie ; Psychology
Subject code	sg150
Language	English
Publisher	Universitätsbibliothek der TU München
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Book ; Online ; Thesis: Epidemiologische Zusammenhänge und Hintergründe von Intoxikationen mit suizidaler oder parasuizidaler Intention im Zeitraum von 2012 bis 2016

Lumpe, Maja Christiane Verfasser] / [Eyer, Florian [Akademischer Betreuer] / Welling, Andrea Gutachter] / [Eyer, Florian [Gutachter]

2022

Author's details	Maja Christiane Lumpe ; Gutachter: Andrea Welling, Florian Eyer ; Betreuer: Florian Eyer
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	German
Publisher	Universitätsbibliothek der TU München
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Book: Kardiomyozyten aus patientenspezifischen induzierbaren pluripotenten Stammzellen als Modellsystem zur Analyse des LQT2-Syndroms

Welling, Andrea

Title variant	Molecular Dissection of Cardiovascular functions ; Cardiac myocytes from patient-specific inducible pluripotent stem cells as a model system for the analysis of the LQT2 syndrome
Institution	Technische Universitaet Muenchen, Institut fuer Pharmakologie und Toxikologie, Biedersteiner Str. 29, 80802, Muenchen, DE
Keywords	Medizin ; Toxikologie ; Chemische Analyse ; Biotechnologie
Document type	Book
Remark	project start: 08/01/2010 project end: 07/31/2013 grant ID: WE 1693/3-1
Database	Environmental research database (UFORDAT) of the German Federal Environment Agency (UBA)

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Article ; Online: The inhibitor of connexin Cx36 channels, mefloquine, inhibits voltage-dependent Ca

Seemann, Nele / Welling, Andrea / Rustenbeck, Ingo

Molecular and cellular endocrinology

2017 Volume 472, Page(s) 97–106

Abstract: The antimalarial agent, mefloquine, inhibits the function of connexin Cx36 gap junctions and hemichannels and has thus become a tool to investigate their physiological relevance in pancreatic islets. In view of earlier reports on a ... ...

Abstract	The antimalarial agent, mefloquine, inhibits the function of connexin Cx36 gap junctions and hemichannels and has thus become a tool to investigate their physiological relevance in pancreatic islets. In view of earlier reports on a K
MeSH term(s)	3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester/pharmacology ; Action Potentials/drug effects ; Animals ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels/metabolism ; Connexins/antagonists & inhibitors ; Connexins/metabolism ; Dihydropyridines/pharmacology ; Glucose/pharmacology ; Insulin Secretion/drug effects ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Ion Channel Gating/drug effects ; Mefloquine/pharmacology ; Mice ; Nisoldipine/pharmacology ; Potassium Chloride/pharmacology ; Tolbutamide/pharmacology ; Gap Junction delta-2 Protein
Chemical Substances	Calcium Channel Blockers ; Calcium Channels ; Connexins ; Dihydropyridines ; Nisoldipine (4I8HAB65SZ) ; Potassium Chloride (660YQ98I10) ; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester (71145-03-4) ; 1,4-dihydropyridine (7M8K3P6I89) ; Tolbutamide (982XCM1FOI) ; Glucose (IY9XDZ35W2) ; Calcium (SY7Q814VUP) ; Mefloquine (TML814419R)
Language	English
Publishing date	2017-12-05
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2017.11.024
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Book ; Online ; Thesis: Die Häufigkeit thromboembolischer Ereignisse unter Behandlung mit Antipsychotika der zweiten Generation und Placebo im Rahmen randomisiert-kontrollierter Studien

Dörries, Carola [Verfasser] / Leucht, Stefan M. [Akademischer Betreuer] / Leucht, Stefan M. [Gutachter] / Welling, Andrea [Gutachter]

2021

Author's details	Carola Dörries ; Gutachter: Stefan M. Leucht, Andrea Welling ; Betreuer: Stefan M. Leucht
Keywords	Psychologie ; Psychology
Subject code	sg150
Language	German
Publisher	Universitätsbibliothek der TU München
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Reduced excitability of gp130-deficient nociceptors is associated with increased voltage-gated potassium currents and Kcna4 channel upregulation.

Langeslag, Michiel / Malsch, Philipp / Welling, Andrea / Kress, Michaela

Pflugers Archiv : European journal of physiology

2014 Volume 466, Issue 11, Page(s) 2153–2165

Abstract: Neuropathic pain and pain arising from local inflammation are characterized by increased release of inflammatory mediators like interleukin-6 (IL-6) by immune cells. The levels of IL-6 is increased in various painfull conditions and correlates with the ... ...

Abstract	Neuropathic pain and pain arising from local inflammation are characterized by increased release of inflammatory mediators like interleukin-6 (IL-6) by immune cells. The levels of IL-6 is increased in various painfull conditions and correlates with the severity of thermal and mechanical hypersensitivity. Deletion of the IL-6 signal transducer glycoprotein 130 (gp130) reduces inflammation associated with hypersensitivity to thermal and mechanical stimuli. In this study, we show that nociceptor-specific deletion of gp130 alters excitability parameters that are linked to changes in the potassium conductance. In SNS-gp130(-/-) sensory neurons, the resting membrane potential was reduced. Moreover the repolarization speed of the action potential and afterhypolarization was augmented, however, voltage-gated Na(+) and Ca(2+) current were not obviously altered. The main difference between gp130-deficient and control neurons was a significant increase in the conductance of both delayed rectifier as well as A-type potassium currents. Taqman RT-PCR analysis revealed significantly higher levels of Kcna4 mRNA, encoding A-type Kv1.4 potassium channel, in neuron cultures from SNS-gp130(-/-) versus control mice, which may account for the electrophysiological data. No difference in other voltage-gated ion channel mRNAs was observed. The present data show for the first time increased A-type K(+) currents and expression of voltage-gated potassium channel Kcna4 (Kv1.4) in SNS-gp130(-/-) nociceptors. This suggests that gp130 acts as a break for the expression of potassium channels and important regulator hub for nociceptor excitability.
MeSH term(s)	Animals ; Calcium/metabolism ; Glycoproteins/deficiency ; Glycoproteins/genetics ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Kv1.4 Potassium Channel/genetics ; Kv1.4 Potassium Channel/metabolism ; Membrane Potentials/genetics ; Membrane Potentials/physiology ; Mice ; Nociceptors/metabolism ; Potassium/metabolism ; Potassium Channels, Voltage-Gated/genetics ; Potassium Channels, Voltage-Gated/metabolism ; RNA, Messenger/genetics ; Sensory Receptor Cells/metabolism ; Sensory Receptor Cells/physiology ; Sodium/metabolism ; Up-Regulation
Chemical Substances	Glycoproteins ; Interleukin-6 ; Kcna4 protein, mouse ; Kv1.4 Potassium Channel ; Potassium Channels, Voltage-Gated ; RNA, Messenger ; Sodium (9NEZ333N27) ; Potassium (RWP5GA015D) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-01-25
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-014-1443-0
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Article ; Online: Cyclic GMP kinase I modulates glucagon release from pancreatic α-cells.

Leiss, Veronika / Friebe, Andreas / Welling, Andrea / Hofmann, Franz / Lukowski, Robert

Diabetes

2010 Volume 60, Issue 1, Page(s) 148–156

Abstract: Objective: The physiologic significance of the nitric oxide (NO)/cGMP signaling pathway in islets is unclear. We hypothesized that cGMP-dependent protein kinase type I (cGKI) is directly involved in the secretion of islet hormones and glucose ... ...

Abstract	Objective: The physiologic significance of the nitric oxide (NO)/cGMP signaling pathway in islets is unclear. We hypothesized that cGMP-dependent protein kinase type I (cGKI) is directly involved in the secretion of islet hormones and glucose homeostasis. Research design and methods: Gene-targeted mice that lack cGKI in islets (conventional cGKI mutants and cGKIα and Iβ rescue mice [α/βRM] that express cGKI only in smooth muscle) were studied in comparison to control (CTR) mice. cGKI expression was mapped in the endocrine pancreas by Western blot, immuno-histochemistry, and islet-specific recombination analysis. Insulin, glucagon secretion, and cytosolic Ca²(+) ([Ca²(+)](i)) were assayed by radioimmunoassay and FURA-2 measurements, respectively. Serum levels of islet hormones were analyzed at fasting and upon glucose challenge (2 g/kg) in vivo. Results: Immunohistochemistry showed that cGKI is present in α- but not in β-cells in islets of Langerhans. Mice that lack α-cell cGKI had significantly elevated fasting glucose and glucagon levels, whereas serum insulin levels were unchanged. High glucose concentrations strongly suppressed the glucagon release in CTR mice, but had only a moderate effect on islets that lacked cGKI. 8-Br-cGMP reduced stimulated [Ca²(+)](i) levels and glucagon release rates of CTR islets at 0.5 mmol/l glucose, but was without effect on [Ca²(+)](i) or hormone release in cGKI-deficient islets. Conclusions: We propose that cGKI modulates glucagon release by suppression of [Ca²(+)](i) in α-cells.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Calcium/physiology ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/deficiency ; Cyclic GMP-Dependent Protein Kinases/genetics ; DNA Primers ; Gene Amplification ; Genes, Reporter ; Glucagon/blood ; Glucagon/metabolism ; Glucagon-Secreting Cells/enzymology ; Glucagon-Secreting Cells/metabolism ; Glucose Tolerance Test ; Guanylate Kinases/metabolism ; Homeostasis ; Hypoxanthine Phosphoribosyltransferase/genetics ; Insulin/blood ; Insulin/metabolism ; Insulin Secretion ; Islets of Langerhans/cytology ; Luminescent Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal/physiology ; Muscle, Smooth/enzymology ; RNA/genetics ; RNA/isolation & purification ; Recombination, Genetic ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Blood Glucose ; DNA Primers ; Insulin ; Luminescent Proteins ; RNA (63231-63-0) ; Glucagon (9007-92-5) ; Hypoxanthine Phosphoribosyltransferase (EC 2.4.2.8) ; Cyclic GMP-Dependent Protein Kinase Type I (EC 2.7.11.12) ; Cyclic GMP-Dependent Protein Kinases (EC 2.7.11.12) ; Prkg1 protein, mouse (EC 2.7.11.12) ; Guanylate Kinases (EC 2.7.4.8) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2010-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db10-0595
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Article ; Online: Antihypertensive effects of the putative T-type calcium channel antagonist mibefradil are mediated by the L-type calcium channel Cav1.2.

Moosmang, Sven / Haider, Nicole / Brüderl, Birgit / Welling, Andrea / Hofmann, Franz

Circulation research

2006 Volume 98, Issue 1, Page(s) 105–110

Abstract: The role of T-type Ca2+ channels for cardiovascular physiology, in particular blood pressure regulation, is controversial. Selective blockade of T-type Ca2+ channels in resistance arteries has been proposed to explain the effect of the antihypertensive ... ...

Abstract	The role of T-type Ca2+ channels for cardiovascular physiology, in particular blood pressure regulation, is controversial. Selective blockade of T-type Ca2+ channels in resistance arteries has been proposed to explain the effect of the antihypertensive drug mibefradil. In the present study, we used a third generation, time- and tissue-specific conditional knockout model of the L-type Ca2+ channel Cav1.2 (Cav1.2SMAKO mice) to genetically dissect the effects of mibefradil on T- and L-type Ca2+ channels. Myogenic tone and phenylephrine-induced contraction in hindlimb perfusion experiments were sensitive to mibefradil in control mice, whereas the drug showed no effect in Cav1.2-deficient animals. Mean arterial blood pressure in awake, freely moving control mice was reduced by 38+/-2.5 mm Hg at a dose of 1.25 mg/kg bodyweight mibefradil, but not changed in Cav1.2SMAKO mice. These results demonstrate that the effect of the putative T-type Ca2+ channel-selective blocker mibefradil on blood pressure and small vessel myogenic tone is mediated by the Cav1.2 L-type Ca2+ channel.
MeSH term(s)	Animals ; Antihypertensive Agents/pharmacology ; Blood Pressure/drug effects ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/physiology ; Calcium Channels, T-Type/physiology ; Male ; Membrane Potentials ; Mibefradil/pharmacology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/physiology
Chemical Substances	Antihypertensive Agents ; Calcium Channel Blockers ; Calcium Channels, L-Type ; Calcium Channels, T-Type ; L-type calcium channel alpha(1C) ; Mibefradil (27B90X776A)
Language	English
Publishing date	2006-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/01.RES.0000197851.11031.9c
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Article: Characterization of voltage-dependent sodium and calcium channels in mouse pancreatic A- and B-cells.

Vignali, Sheila / Leiss, Veronika / Karl, Rosi / Hofmann, Franz / Welling, Andrea

The Journal of physiology

2006 Volume 572, Issue Pt 3, Page(s) 691–706

Abstract: Insulin and glucagon are the major hormones of the islets of Langerhans that are stored and released from the B- and A-cells, respectively. Both hormones are secreted when the intracellular cytosolic Ca2+ concentration ([Ca2+]i) increases. The [Ca2+]i is ...

Abstract	Insulin and glucagon are the major hormones of the islets of Langerhans that are stored and released from the B- and A-cells, respectively. Both hormones are secreted when the intracellular cytosolic Ca2+ concentration ([Ca2+]i) increases. The [Ca2+]i is modulated by mutual inhibition and activation of different voltage-gated ion channels. The precise interplay of these ion channels in either glucagon or insulin release is unknown, owing in part to the difficulties in distinguishing A- from B-cells in electrophysiological experiments. We have established a single-cell RT-PCR method to identify A- and B-cells from the mouse. A combination of PCR, RT-PCR, electrophysiology and pharmacology enabled us to characterize the different sodium and calcium channels in mouse islet cells. In both A- and B-cells, 60% of the inward calcium current (I(Ca)) is carried by L-type calcium channels. In B-cells, the predominant calcium channel is Ca(v)1.2, whereas Ca(v)1.2 and Ca(v)1.3 were identified in A-cells. These results were confirmed by using mice carrying A- or B-cell-specific inactivation of the Ca(v)1.2 gene. In B-cells, the remaining I(Ca) flows in equal amounts through Ca(v)2.1, Ca(v)2.2 and Ca(v)2.3. In A-cells, 30 and 15% of I(Ca) is due to Ca(v)2.3 and Ca(v)2.1 activity, respectively, whereas Ca(v)2.2 current was not found in these cells. Low-voltage-activated T-type calcium channels could not be identified in A- and B-cells. Instead, two TTX-sensitive sodium currents were found: an early inactivating and a residual current. The residual current was only recovered in a subpopulation of B-cells. A putative genetic background for these currents is Na(v)1.7.
MeSH term(s)	Animals ; Calcium Channels/metabolism ; Cells, Cultured ; Glucagon-Secreting Cells/metabolism ; Insulin-Secreting Cells/metabolism ; Ion Channel Gating/physiology ; Membrane Potentials/physiology ; Mice ; Sodium Channels/metabolism ; Tissue Distribution
Chemical Substances	Calcium Channels ; Sodium Channels
Language	English
Publishing date	2006-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2005.102368
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Article: Facilitation of murine cardiac L-type Cav1.2 channel is modulated by Calmodulin kinase II-dependent phosphorylation of S1512 and S1570

Blaich, Anne / Welling, Andrea / Fischer, Stefanie / Wegener, JÃ¶rg Werner / KÃ¶stner, Katharina / Hofmann, Franz / Moosmang, Sven

Proceedings of the National Academy of Sciences of the United States of America. 2010 June 1, v. 107, no. 22

2010

Abstract: Activity-dependent means of altering calcium (CaÂ²âº) influx are assumed to be of great physiological consequence, although definitive tests of this assumption have only begun to emerge. Facilitation and inactivation offer two opposing, activity- ... ...

Abstract	Activity-dependent means of altering calcium (CaÂ²âº) influx are assumed to be of great physiological consequence, although definitive tests of this assumption have only begun to emerge. Facilitation and inactivation offer two opposing, activity-dependent means of altering CaÂ²âº influx via cardiac Cav1.2 calcium channels. Voltage- and frequency-dependent facilitation of Cav1.2 has been reported to depend on Calmodulin (CaM) and/or the activity of Calmodulin kinase II (CaMKII). Several sites within the cardiac L-type calcium channel complex have been proposed as the targets of CaMKII. Here, we generated mice with knockin mutations of Î±â1.2 S1512 and S1570 phosphorylation sites [sine facilitation (SF) mice]. Homocygote SF mice were viable and reproduced in a Mendelian ratio. Voltage-dependent facilitation in ventricular cardiomyocytes carrying the SF mutation was decreased from 1.58- to 1.18-fold. The CaMKII inhibitor KN-93 reduced facilitation to 1.28 in control cardiomyocytes. SF mutation negatively shifted the voltage-dependent inactivation and slowed recovery from inactivation, thereby making fewer channels available for activation. Telemetric ECG recordings at different heart rates showed that QT time decreased significantly more in SF than in control mice at higher rates. Our results strongly support the notion that CaMKII-dependent phosphorylation of Cav1.2 at S1512 and S1570 mediates CaÂ²âº current facilitation in the murine heart.
Keywords	calcium ; calcium channels ; calcium-calmodulin-dependent protein kinase ; calmodulin ; cardiomyocytes ; heart rate ; mice ; mutation ; phosphorylation
Language	English
Dates of publication	2010-0601
Size	p. 10285-10289.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0914287107
Database	NAL-Catalogue (AGRICOLA)

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