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Background: In March 2023, there was no comprehensive overview of job demands, resources, and mental health consequences for nurses in Germany during the COVID-19 pandemic. Because of country-specific differences with regard to the course/management of the pandemic and the organization of the healthcare system, data from Germany were analyzed specifically., Methods: A systematic search in databases (PubMed/Medline, PsycINFO) yielded 50 relevant studies that were included in the scoping review., Results: The studies were based on cross-sectional designs, mostly from the hospital setting and the first year of the pandemic. Frequently investigated job demands were work intensification, lack of protective equipment, rapidly changing regulations, contact with COVID-19 patients, and pandemic-related worries/anxieties. Pandemic phase and setting-specific demand cascades became clear. Frequently examined mental health problems (including stress experience, anxiety, depression, burnout, and intention to change career/job) were higher in groups with higher levels of reported job demands. Nurses generally reported less favorable values than medical professionals. Social support, reward/appreciation, humor, resilience, and sense of coherence proved to be resources., Conclusion: In preparation for further pandemics and crises, pre-pandemic job demands should be reduced through targeted measures and relevant resources should be strengthened. Pandemic-specific job demands should be systematically reflected and cross-organizational solutions developed. Longitudinal studies using validated instruments and intervention studies should be the focus of future research funding., Competing Interests: Einhaltung ethischer Richtlinien. Interessenkonflikt: D. Arndt und T. Hering geben an, dass kein Interessenkonflikt besteht. Für diesen Beitrag wurden von den Autor/-innen keine Studien an Menschen oder Tieren durchgeführt. Für die aufgeführten Studien gelten die jeweils dort angegebenen ethischen Richtlinien., (© 2024. The Author(s).)

Huntington's disease (HD) predominantly affects the brain, causing a mixed movement disorder, cognitive decline and behavioural abnormalities. It also causes a peripheral phenotype involving skeletal muscle. Mitochondrial dysfunction has been reported in tissues of HD models, including skeletal muscle, and lymphoblast and fibroblast cultures from patients with HD. Mutant huntingtin protein (mutHTT) expression can impair mitochondrial quality control and accelerate mitochondrial ageing. Here, we obtained fresh human skeletal muscle, a post-mitotic tissue expressing the mutated HTT allele at physiological levels since birth, and primary cell lines from HTT CAG repeat expansion mutation carriers and matched healthy volunteers to examine whether such a mitochondrial phenotype exists in human HD. Using ultra-deep mitochondrial DNA (mtDNA) sequencing, we showed an accumulation of mtDNA mutations affecting oxidative phosphorylation. Tissue proteomics indicated impairments in mtDNA maintenance with increased mitochondrial biogenesis of less efficient oxidative phosphorylation (lower complex I and IV activity). In full-length mutHTT expressing primary human cell lines, fission-inducing mitochondrial stress resulted in normal mitophagy. In contrast, expression of high levels of N-terminal mutHTT fragments promoted mitochondrial fission and resulted in slower, less dynamic mitophagy. Expression of high levels of mutHTT fragments due to somatic nuclear HTT CAG instability can thus affect mitochondrial network dynamics and mitophagy, leading to pathogenic mtDNA mutations. We show that life-long expression of mutant HTT causes a mitochondrial phenotype indicative of mtDNA instability in fresh post-mitotic human skeletal muscle. Thus, genomic instability may not be limited to nuclear DNA, where it results in somatic expansion of the HTT CAG repeat length in particularly vulnerable cells such as striatal neurons. In addition to efforts targeting the causative mutation, promoting mitochondrial health may be a complementary strategy in treating diseases with DNA instability such as HD., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Introduction: Tobacco smoking is related with a substantial morbidity and mortality as well as with tremendous socioeconomic burden. Therefore, an early successful smoking cessation bears an enormous medical and socioeconomic importance. The gold standard of smoking cessation, a combination of behavioral und pharmacologic therapy reaches only few smokers every year and so, guideline-based, low-threshold and broadly available digital cessation support could considerably increase the annual cessation rate. With the digital cessation program "Nichtraucherhelden" such a guideline-based program is available in Germany since December 2016., Methods: The program consists of 2 preparation days and 10 program days und contains the major features of common smoking cessation courses. The present study examined the participants from December 2016 to November 2019 (n = 2491) regarding acceptance, adherence and effectivity. 69 % were female and the average age was 46 years., Results: On average cessation was attained after 19 days. One year after the program a cessation rate of 15 % was achieved. Surprisingly, the cessation rate was higher in more addictive compared to less addictive participants., Conclusion: The study shows that a digital guideline-based cessation program is feasible and effectual. For confirmation a control and randomized study is required., Competing Interests: Alena M. Bubeck war während der Auswertung der Daten und der Publikation nebenberuflich für die NichtraucherHelden GmbH tätig.Alexander Rupp, Thomas Hering und Michael Kreuter beraten als wissenschaftlicher Beirat die NichtraucherHelden GmbH., (The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).)

The Questionnaire "Monitoring of Exacerbation Probability" (MEP) provides a novel simple tool to assist detection and semiquantitative numerical documentation of exacerbation (ECOPD) in daily routine. In a prospective multi-center trial involving 3751 visits of 810 patients in 21 centers, MEP was evaluated and compared to the application of the EXACT-Pro questionnaire under real world conditions. The population of COPD patients included in this study is a typical COPD population demographically and clinically. Defining a MEP score of one or more as a positive test result, we found a sensitivity of 91% and a specificity of 66%. Additionally, MEP results correlated clearly with EXACT-Pro results. This qualifies the MEP questionnaire as a valid tool for the detection of ECOPD and longitudinal characterization of COPD patients., Competing Interests: Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht., (The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).)

Background: A major challenge in neurodegenerative diseases concerns identifying biological disease signatures that track with disease progression or respond to an intervention. Several clinical trials in Huntington disease (HD), an inherited, progressive neurodegenerative disease, are currently ongoing. Therefore, we examine whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in HD patients., Results: We generate large, high-quality human datasets from skeletal muscle, skin and adipose tissue to probe molecular changes in human premanifest and early manifest HD patients-those most likely involved in clinical trials. The analysis of the transcriptomics and proteomics data shows robust, stage-dependent dysregulation. Gene ontology analysis confirms the involvement of inflammation and energy metabolism in peripheral HD pathogenesis. Furthermore, we observe changes in the homeostasis of extracellular vesicles, where we find consistent changes of genes and proteins involved in this process. In-depth single nucleotide polymorphism data across the HTT gene are derived from the generated primary cell lines., Conclusions: Our 'omics data document the involvement of inflammation, energy metabolism, and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials. The generated data, complemented by the primary cell lines established from peripheral tissues, and a large panel of iPSC lines that can serve as human models of HD are a valuable and unique resource to advance the current understanding of molecular mechanisms driving HD pathogenesis., (© 2022. The Author(s).)