Sebastian Maier

Bio: Sebastian Maier is an academic researcher from University of Würzburg. The author has contributed to research in topics: Quantum dot & Photon. The author has an hindex of 35, co-authored 84 publications receiving 5268 citations. Previous affiliations of Sebastian Maier include University of Washington.

On-Demand Single Photons with High Extraction Efficiency and Near-Unity Indistinguishability from a Resonantly Driven Quantum Dot in a Micropillar.

Abstract: This work was supported by the National Natural Science Foundation of China, the Chinese Academy of Sciences, and the National Fundamental Research Program. We acknowledge financial support by the State of Bavaria and the German Ministry of Education and Research (BMBF) within the projects Q.com-H and the Chist-era project SSQN. N. G. acknowledges support from the Danish Research Council for Technology and Production.

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

Abstract: In heart failure (HF), Ca2+/calmodulin kinase II (CaMKII) expression is increased. Altered Na+ channel gating is linked to and may promote ventricular tachyarrhythmias (VTs) in HF. Calmodulin regulates Na+ channel gating, in part perhaps via CaMKII. We investigated effects of adenovirus-mediated (acute) and Tg (chronic) overexpression of cytosolic CaMKIIδC on Na+ current (INa) in rabbit and mouse ventricular myocytes, respectively (in whole-cell patch clamp). Both acute and chronic CaMKIIδC overexpression shifted voltage dependence of Na+ channel availability by –6 mV (P < 0.05), and the shift was Ca2+ dependent. CaMKII also enhanced intermediate inactivation and slowed recovery from inactivation (prevented by CaMKII inhibitors autocamtide 2–related inhibitory peptide [AIP] or KN93). CaMKIIδC markedly increased persistent (late) inward INa and intracellular Na+ concentration (as measured by the Na+ indicator sodium-binding benzofuran isophthalate [SBFI]), which was prevented by CaMKII inhibition in the case of acute CaMKIIδC overexpression. CaMKII coimmunoprecipitates with and phosphorylates Na+ channels. In vivo, transgenic CaMKIIδC overexpression prolonged QRS duration and repolarization (QT intervals), decreased effective refractory periods, and increased the propensity to develop VT. We conclude that CaMKII associates with and phosphorylates cardiac Na+ channels. This alters INa gating to reduce availability at high heart rate, while enhancing late INa (which could prolong action potential duration). In mice, enhanced CaMKIIδC activity predisposed to VT. Thus, CaMKII-dependent regulation of Na+ channel function may contribute to arrhythmogenesis in HF.

Quantum-dot spin-photon entanglement via frequency downconversion to telecom wavelength

Abstract: Future quantum networks will combine ideally stationary quantum bits (qubits), such as single electron spins, with 'flying' qubits, which are photons that transfer quantum states between distant qubits. It has therefore been a long-standing challenge in the field of quantum computation and communication to couple a single electron spin to a single photon in a solid-state platform. Two groups working independently have now achieved that goal, by demonstrating entanglement between a photon and a single electron spin trapped in a semiconductor 'quantum dot' structure. The quantum dot acts as the stationary node. This achievement is a small step towards eventual implementation of quantum networks that can support long-distance quantum communication.

An unexpected role for brain-type sodium channels in coupling of cell surface depolarization to contraction in the heart

Abstract: Voltage-gated sodium channels composed of pore-forming α and auxiliary β subunits are responsible for the rising phase of the action potential in cardiac muscle, but the functional roles of distinct sodium channel subtypes have not been clearly defined. Immunocytochemical studies show that the principal cardiac pore-forming α subunit isoform Nav1.5 is preferentially localized in intercalated disks, whereas the brain α subunit isoforms Nav1.1, Nav1.3, and Nav1.6 are localized in the transverse tubules. Sodium currents due to the highly tetrodotoxin (TTX)-sensitive brain isoforms in the transverse tubules are small and are detectable only after activation with β scorpion toxin. Nevertheless, they play an important role in coupling depolarization of the cell surface membrane to contraction, because low TTX concentrations reduce left ventricular function. Our results suggest that the principal cardiac isoform in the intercalated disks is primarily responsible for action potential conduction between cells and reveal an unexpected role for brain sodium channel isoforms in the transverse tubules in coupling electrical excitation to contraction in cardiac muscle.

Distinct Subcellular Localization of Different Sodium Channel α and β Subunits in Single Ventricular Myocytes From Mouse Heart

Abstract: Background— Voltage-gated sodium channels composed of pore-forming α and auxiliary β subunits are responsible for the rising phase of the action potential in cardiac muscle, but their localizations have not yet been clearly defined Methods and Results— Immunocytochemical studies show that the principal cardiac α subunit isoform Nav15 and the β2 subunit are preferentially localized in intercalated disks, identified by immunostaining of connexin 43, the major protein of cardiac gap junctions The brain α subunit isoforms Nav11, Nav13, and Nav16 are preferentially localized with β1 and β3 subunits in the transverse tubules, identified by immunostaining of α-actinin, a cardiac z-line protein The β1 subunit is also present in a small fraction of intercalated disks The recently cloned β4 subunit, which closely resembles β2 in amino acid sequence, is also expressed in ventricular myocytes and is localized in intercalated disks as are β2 and Nav15 Conclusions— Our results suggest that the primary sodium

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society

Abstract: Jeffrey L. Anderson, MD, FACC, FAHA, Chair Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect Nancy M. Albert, PhD, RN, FAHA Biykem Bozkurt, MD, PhD, FACC, FAHA Ralph G. Brindis, MD, MPH, MACC Mark A. Creager, MD, FACC, FAHA[#][1] Lesley H. Curtis, PhD, FAHA David DeMets, PhD[#][1] Robert A

International Union of Pharmacology. XLVIII. Nomenclature and Structure-Function Relationships of Voltage-Gated Calcium Channels

Abstract: The family of voltage-gated sodium channels initiates action potentials in all types of excitable cells. Nine members of the voltage-gated sodium channel family have been characterized in mammals, and a 10th member has been recognized as a related protein. These distinct sodium channels have similar structural and functional properties, but they initiate action potentials in different cell types and have distinct regulatory and pharmacological properties. This article presents the molecular relationships and physiological roles of these sodium channel proteins and provides comprehensive information on their molecular, genetic, physiological, and pharmacological properties.

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary

Abstract: Preamble 2072 1. Introduction 2074 2. Clinical Characteristics and Evaluation of AF 2076 3. Thromboembolic Risk and Treatment 2077 4. Rate Control: Recommendations 2079 5. Rhythm Control: Recommendations 2080 6. Specific Patient Groups and AF: Recommendations 2086 7. Evidence Gaps and Future Research Directions 2089 References 2090 Appendix 1. Author Relationships With Industry and Other Entities (Relevant) 2095 Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) 2097 Appendix 3. Initial Clinical Evaluation in Patients With AF 2104 The medical profession should play a central role in evaluating the evidence related to drugs, devices, and procedures for the detection, management, and prevention of disease. When properly applied, expert analysis of available data on the benefits and risks of these therapies and procedures can improve the quality of care, optimize patient outcomes, and favorably affect costs by focusing resources on the most effective strategies. An organized …