Publications by authors named "G Nagel"
Optogenetics is a valuable tool for studying the mechanisms of neurological diseases and is now being developed for therapeutic applications. In rodents and macaques, improved channelrhodopsins have been applied to achieve transcranial optogenetic stimulation. While transcranial photoexcitation of neurons has been achieved, noninvasive optogenetic inhibition for treating hyperexcitability-induced neurological disorders has remained elusive.
View Article and Find Full Text PDFEarly plant responses to different stress situations often encompass cytosolic Ca increases, plasma membrane depolarization and the generation of reactive oxygen species. However, the mechanisms by which these signalling elements are translated into defined physiological outcomes are poorly understood. Here, to study the basis for encoding of specificity in plant signal processing, we used light-gated ion channels (channelrhodopsins).
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- * In a study involving 790 ALS patients and 570 control participants, levels of NfL and pNfH were measured, revealing that NfL is more effective than pNfH for diagnostics and prognosis, especially when considering a new population-based ALS Z-score.
- * The research highlights the importance of factors like age, ALS symptoms, body mass index (BMI), and kidney function in interpreting neurofilament levels, showing that with
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- The study examined the link between long-term air pollution exposure and end-stage kidney disease (ESKD) in two large European cohorts, highlighting the burden ESKD poses on patients and healthcare systems.
- In the Austrian cohort (VHM&PP), increased black carbon and nitrogen dioxide showed potential associations with ESKD, but findings were not statistically significant.
- Conversely, in the Italian cohort (RoLS), fine particulate matter was significantly associated with ESKD, indicating that the impact of air pollution on kidney health may differ based on the specific pollutants present in different regions.
Cellular senescence, a major driver of aging, can be stimulated by DNA damage, and is counteracted by the DNA repair machinery. Here we show that in p16INK4a-deficient cells, senescence induction by the environmental genotoxin B[a]P or ionizing radiation (IR) completely depends on p21CIP1. Immunoprecipitation-based mass spectrometry interactomics data revealed that during senescence induction and maintenance, p21CIP1 specifically inhibits CDK4 and thereby activates the DREAM complex.
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