TY - JOUR A1 - Schneider-Schaulies, Sibylle A1 - Schneider-Schaulies, Jürgen A1 - Schuster, A. A1 - Bayer, M. A1 - Pavlovic, J. A1 - ter Meulen, V. T1 - Cell type specific MxA-mediated inhibition of measles virus transcription in human brain cells N2 - No abstract available KW - Virologie Y1 - 1994 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-62255 ER - TY - JOUR A1 - Schneider-Schaulies, Jürgen A1 - Schneider-Schaulies, S. A1 - Schuster, A. A1 - Bayer, M. A1 - Pavlovic, J. A1 - ter Meulen, V. T1 - Cell type specific MxA-mediated inhibition of measles virus transcription in human brain cells N2 - Measles virus (MV)-specific transcription in human brain cells is characterized by particularly low abundances of the distal mRNAs encoding the MV envelope proteins. Similar transcriptional restrictions of the closely related vesicular stomatitis virus have been observed in mouse fibroblasts constitutively expressing the interferon-inducible MxA protein (P. Staeheli and J. Pavlovic, J. Virol. 65:4498-4501, 1991). We found that MV infection of human brain cells is accompanied by rapid induction and high-level expression of endogenous MxA proteins. After stable transfection of MxA, human glioblastoma cells (U-87-MxA) released 50- to 100-fold less infectious virus and expression of viral proteinswas highly restricted. The overall MV-specific transcription Ievels were reduced by up to 90%, accompanied by low relative frequencies of the distal MV-specific mRNAs. These restrictions were linked to an inhibition of viral RNA synthesis and not to a decreased stability of the viral RNAs. Our results indicate that expression of MxA is associated with transcriptional attenuation of MV in brain cells, thus probably contributing to the establishment of persistent MV central nervous system infections. In addition, the mechanism of MxA-dependent resistance against MV infection, in contrast to that of vesicular Stomatitis virus, is cell type specific, because an inhibition of MV glycoprotein synthesis independent of transcriptional alterations was observed in MxA-transfected human monocytes Y1 - 1994 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-34313 ER - TY - JOUR A1 - Klingler, Werner A1 - Heiderich, Sebastian A1 - Girard, Thierry A1 - Gravino, Elvira A1 - Heffron, James J. A. A1 - Johannsen, Stephan A1 - Jurkat-Rott, Karin A1 - Rüffert, Henrik A1 - Schuster, Frank A1 - Snoeck, Marc A1 - Sorrentino, Vincenzo A1 - Tegazzin, Vincenzo A1 - Lehmann-Horn, Frank T1 - Functional and genetic characterization of clinical malignant hyperthermia crises: a multi-centre study JF - Orphanet Journal of Rare Diseases N2 - Background: Malignant hyperthermia (MH) is a rare pharmacogenetic disorder which is characterized by life-threatening metabolic crises during general anesthesia. Classical triggering substances are volatile anesthetics and succinylcholine (SCh). The molecular basis of MH is excessive release of Ca2+ in skeletal muscle principally by a mutated ryanodine receptor type 1 (RyR1). To identify factors explaining the variable phenotypic presentation and complex pathomechanism, we analyzed proven MH events in terms of clinical course, muscle contracture, genetic factors and pharmocological triggers. Methods: In a multi-centre study including seven European MH units, patients with a history of a clinical MH episode confirmed by susceptible (MHS) or equivocal (MHE) in vitro contracture tests (IVCT) were investigated. A test result is considered to be MHE if the muscle specimens develop pathological contractures in response to only one of the two test substances, halothane or caffeine. Crises were evaluated using a clinical grading scale (CGS), results of IVCT and genetic screening. The effects of SCh and volatile anesthetics on Ca2+ release from sarcoplasmic reticulum (SR) were studied in vitro. Results: A total of 200 patients met the inclusion criteria. Two MH crises (1%) were triggered by SCh (1 MHS, 1 MHE), 18% by volatile anesthetics and 81% by a combination of both. Patients were 70% male and 50% were younger than 12 years old. Overall, CGS was in accord with IVCT results. Crises triggered by enflurane had a significantly higher CGS compared to halothane, isoflurane and sevoflurane. Of the 200 patients, 103 carried RyR1 variants, of which 14 were novel. CGS varied depending on the location of the mutation within the RyR1 gene. In contrast to volatile anesthetics, SCh did not evoke Ca2+ release from isolated rat SR vesicles. Conclusions: An MH event could depend on patient-related risk factors such as male gender, young age and causative RyR1 mutations as well as on the use of drugs lowering the threshold of myoplasmic Ca2+ release. SCh might act as an accelerant by promoting unspecific Ca2+ influx via the sarcolemma and indirect RyR1 activation. Most MH crises develop in response to the combined administration of SCh and volatile anesthetics. KW - susceptibility KW - central core disease KW - skeletal muscle KW - North American KW - malignant hyperthermia KW - succinylcholine KW - suxamethonium KW - volatile anesthetics KW - RyR1 mutations KW - New Zealand KW - inhalation anesthetics KW - sarcoplasmic reticulum KW - ryanodine receptor gene KW - vitro contracture test Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-117630 SN - 1750-1172 VL - 9 IS - 8 ER - TY - JOUR A1 - Farmer, Adam D. A1 - Strzelczyk, Adam A1 - Finisguerra, Alessandra A1 - Gourine, Alexander V. A1 - Gharabaghi, Alireza A1 - Hasan, Alkomiet A1 - Burger, Andreas M. A1 - Jaramillo, Andrés M. A1 - Mertens, Ann A1 - Majid, Arshad A1 - Verkuil, Bart A1 - Badran, Bashar W. A1 - Ventura-Bort, Carlos A1 - Gaul, Charly A1 - Beste, Christian A1 - Warren, Christopher M. A1 - Quintana, Daniel S. A1 - Hämmerer, Dorothea A1 - Freri, Elena A1 - Frangos, Eleni A1 - Tobaldini, Eleonora A1 - Kaniusas, Eugenijus A1 - Rosenow, Felix A1 - Capone, Fioravante A1 - Panetsos, Fivos A1 - Ackland, Gareth L. A1 - Kaithwas, Gaurav A1 - O'Leary, Georgia H. A1 - Genheimer, Hannah A1 - Jacobs, Heidi I. L. A1 - Van Diest, Ilse A1 - Schoenen, Jean A1 - Redgrave, Jessica A1 - Fang, Jiliang A1 - Deuchars, Jim A1 - Széles, Jozsef C. A1 - Thayer, Julian F. A1 - More, Kaushik A1 - Vonck, Kristl A1 - Steenbergen, Laura A1 - Vianna, Lauro C. A1 - McTeague, Lisa M. A1 - Ludwig, Mareike A1 - Veldhuizen, Maria G. A1 - De Couck, Marijke A1 - Casazza, Marina A1 - Keute, Marius A1 - Bikson, Marom A1 - Andreatta, Marta A1 - D'Agostini, Martina A1 - Weymar, Mathias A1 - Betts, Matthew A1 - Prigge, Matthias A1 - Kaess, Michael A1 - Roden, Michael A1 - Thai, Michelle A1 - Schuster, Nathaniel M. A1 - Montano, Nicola A1 - Hansen, Niels A1 - Kroemer, Nils B. A1 - Rong, Peijing A1 - Fischer, Rico A1 - Howland, Robert H. A1 - Sclocco, Roberta A1 - Sellaro, Roberta A1 - Garcia, Ronald G. A1 - Bauer, Sebastian A1 - Gancheva, Sofiya A1 - Stavrakis, Stavros A1 - Kampusch, Stefan A1 - Deuchars, Susan A. A1 - Wehner, Sven A1 - Laborde, Sylvain A1 - Usichenko, Taras A1 - Polak, Thomas A1 - Zaehle, Tino A1 - Borges, Uirassu A1 - Teckentrup, Vanessa A1 - Jandackova, Vera K. A1 - Napadow, Vitaly A1 - Koenig, Julian T1 - International Consensus Based Review and Recommendations for Minimum Reporting Standards in Research on Transcutaneous Vagus Nerve Stimulation (Version 2020) JF - Frontiers in Human Neuroscience N2 - Given its non-invasive nature, there is increasing interest in the use of transcutaneous vagus nerve stimulation (tVNS) across basic, translational and clinical research. Contemporaneously, tVNS can be achieved by stimulating either the auricular branch or the cervical bundle of the vagus nerve, referred to as transcutaneous auricular vagus nerve stimulation(VNS) and transcutaneous cervical VNS, respectively. In order to advance the field in a systematic manner, studies using these technologies need to adequately report sufficient methodological detail to enable comparison of results between studies, replication of studies, as well as enhancing study participant safety. We systematically reviewed the existing tVNS literature to evaluate current reporting practices. Based on this review, and consensus among participating authors, we propose a set of minimal reporting items to guide future tVNS studies. The suggested items address specific technical aspects of the device and stimulation parameters. We also cover general recommendations including inclusion and exclusion criteria for participants, outcome parameters and the detailed reporting of side effects. Furthermore, we review strategies used to identify the optimal stimulation parameters for a given research setting and summarize ongoing developments in animal research with potential implications for the application of tVNS in humans. Finally, we discuss the potential of tVNS in future research as well as the associated challenges across several disciplines in research and clinical practice. KW - transcutaneous vagus nerve stimulation KW - minimum reporting standards KW - guidelines & recommendations KW - transcutaneous auricular vagus nerve stimulation KW - transcutaneous cervical vagus nerve stimulation Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-234346 SN - 1662-5161 VL - 14 ER -