Pascal Geschwill
Heidelberg University
5 Papers
9 Citations
Pascal Geschwill is an academic researcher from Heidelberg University. The author has contributed to research in topics: Cardiomyopathy & Induced pluripotent stem cell. The author has an hindex of 4, co-authored 5 publications.
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Papers
Subtype-specific differentiation of cardiac pacemaker cell clusters from human induced pluripotent stem cells.
Patrick A. Schweizer,Patrick A. Schweizer,Fabrice F Darche,Nina D. Ullrich,Pascal Geschwill,Boris Greber,Rasmus Rivinius,Claudia Seyler,Claudia Seyler,Karin Müller-Decker,Andreas Draguhn,Jochen Utikal,Jochen Utikal,Michael Koenen,Michael Koenen,Hugo A. Katus,Hugo A. Katus,Dierk Thomas,Dierk Thomas +18 more
TL;DR: A novel culture media-based, transgene-free approach for targeted generation of hiPSC-derived pacemaker-type cells that grow in clusters and offer the potential for disease modeling, drug testing, and individualized cell-based replacement therapy of the SAN is provided.
TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control.
Patrick Lugenbiel,Fabian Wenz,Pascal Syren,Pascal Geschwill,Katharina Govorov,Claudia Seyler,Derk Frank,Patrick A. Schweizer,Jennifer Franke,Tanja Weis,Claus Bruehl,Bastian Schmack,Arjang Ruhparwar,Matthias Karck,Norbert Frey,Hugo A. Katus,Dierk Thomas +16 more
TL;DR: Mechanistic and potential therapeutic significance of TREK-1 channels are suggested in a subgroup of AF patients with HF and prolonged atrial effective refractory periods, consistent with prior observations in humans with HF.
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The C-terminal HCN4 variant P883R alters channel properties and acts as genetic modifier of atrial fibrillation and structural heart disease.
Isabel Weigl,Pascal Geschwill,Miriam Reiss,Claus Bruehl,Andreas Draguhn,Michael Koenen,Farbod Sedaghat-Hamedani,Benjamin Meder,Dierk Thomas,Hugo A. Katus,Patrick A. Schweizer +10 more
TL;DR: HCN4-P883R may increase ectopic trigger and maintenance of AF by shifting the activation voltage of If to more positive potentials and producing higher current density, which may provide a substrate for the development of AF and TIC.
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Augmentation of myocardial If dysregulates calcium homeostasis and causes adverse cardiac remodeling.
Pessah Yampolsky,Pessah Yampolsky,Michael Koenen,Michael Koenen,Matias Mosqueira,Pascal Geschwill,Sebastian Nauck,Sebastian Nauck,Monika Witzenberger,Claudia Seyler,Claudia Seyler,Thomas Fink,Mathieu Kruska,Claus Bruehl,Alexander P. Schwoerer,Heimo Ehmke,Rainer H. A. Fink,Andreas Draguhn,Dierk Thomas,Dierk Thomas,Hugo A. Katus,Hugo A. Katus,Patrick A. Schweizer,Patrick A. Schweizer +23 more
TL;DR: It is shown that upregulation of funny current to the levels observed in human heart failure alters calcium homeostasis leading to cardiac remodelling and arrhythmia and inhibition of myocardial If per se may constitute a therapeutic mechanism to prevent cardiomyopathy.
Synchronicity of excitatory inputs drives hippocampal networks to distinct oscillatory patterns.
Pascal Geschwill,Martin Kaiser,Paul Grube,Nadja Lehmann,Christian Thome,Andreas Draguhn,Jan-Oliver Hollnagel,Martin Both +7 more
TL;DR: This work reports that the pattern of the evoked oscillation depends strongly on the initial synchrony of activation of excitatory cells within CA3, and induction of these two fundamental network patterns does not depend on the presence of any neuromodulatory transmitter like acetylcholine, but is merely based on a different synchrony in the initial activation pattern.