RepoMed (Medizinische Hochschule Hannover)
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Comparison of clinicians' and researchers' ratings of proposed diagnostic criteria for compulsive buying-shopping disorder within a Delphi study
No full textBasierend auf den Ergebnissen einer Delphi-Konsensstudie, an der 138 Expert:innen aus 35 Ländern teilnahmen, wurden diagnostische Kriterien für Kaufsucht vorgeschlagen. Diese Daten wurden einer Sekundäranalyse unterzogen, bei der die Antworten der vorrangig klinisch tätigen mit denen der vorrangig wissenschaftlich tätigen Expert:innen analysiert wurden. Die beiden Gruppen wurden hinsichtlich demografischer Variablen sowie ihrer Einschätzung der Wichtigkeit klinischer Merkmale, möglicher Diagnosekriterien, Differentialdiagnosen und Spezifizierungen der Kaufsucht verglichen. Die Originaldaten wurden 2018-2019 i.R. eines SoSci Online Survey (SoSci Survey GmbH, Munich, Germany) von der Arbeitsgruppe "Substanzungebundene Abhängigkeitserkrankungen" der Klinik für Psychosomatik und Psychotherapie der MHH erhoben. Das Projekt wurde von Prof'in Dr. med. Dr. phil. Astrid Müller und Dr. Nora Laskowski geleitet. Im Sinne einer Open-Access-Policy werden die Daten im SPSS-Format für andere Wissenschaftler:innen zugängig gemacht
Autolysosomal activation combined with lysosomal destabilization efficiently targets myeloid leukemia cells for cell death.
Get PDFIntroduction Current cancer research has led to a renewed interest in exploring lysosomal membrane permeabilization and lysosomal cell death as a targeted therapeutic approach for cancer treatment. Evidence suggests that differences in lysosomal biogenesis between cancer and normal cells might open a therapeutic window. Lysosomal membrane stability may be affected by the so-called 'busy lysosomal behaviour' characterized by higher lysosomal abundance and activity and more intensive fusion or interaction with other vacuole compartments. Methods We used a panel of multiple myeloid leukemia (ML) cell lines as well as leukemic patient samples and updated methodology to study auto-lysosomal compartment, lysosomal membrane permeabilization and lysosomal cell death. Results Our analyses demonstrated several-fold higher constitutive autolysosomal activity in ML cells as compared to human CD34+ hematopoietic cells. Importantly, we identified mefloquine as a selective activator of ML cells' lysosomal biogenesis, which induced a sizeable increase in ML lysosomal mass, acidity as well as cathepsin B and L activity. Concomitant mTOR inhibition synergistically increased lysosomal activity and autolysosomal fusion and simultaneously decreased the levels of key lysosomal stabilizing proteins, such as LAMP-1 and 2. Discussion In conclusion, mefloquine treatment combined with mTOR inhibition synergistically induced targeted ML cell death without additional toxicity. Taken together, these data provide a molecular mechanism and thus a rationale for a therapeutic approach for specific targeting of ML lysosomes
Targeted metabolomic profiling of cerebrospinal fluid from patients with progressive multifocal leukoencephalopathy
Get PDFSignaling through the Dystrophin Glycoprotein Complex affects the stress-dependent transcriptome in Drosophila.
Get PDFDeficiencies in the human Dystrophin Glycoprotein Complex (DGC), which links the extracellular matrix with the intracellular cytoskeleton, cause muscular dystrophies (MDs), a group of incurable disorders associated with heterogeneous muscle, brain, and eye abnormalities. Stresses such as nutrient deprivation and aging cause muscle wasting that can be exacerbated by a reduced content of the DGC in membranes, integrity of which is vital for muscle health and function. Moreover, the DGC operates in multiple signaling pathways, demonstrating an important function in gene expression regulation. To advance disease diagnostics and treatment strategies, we strive to understand the genetic pathways that are perturbed by DGC mutations. Here, we utilize a Drosophila model to investigate the transcriptomic changes in mutants of four DGC components under temperature and metabolic stress. We identify DGC-dependent genes; stress-dependent genes; and genes dependent on the DGC for a proper stress response, confirming a novel function of the DGC in stress-response signaling. This perspective yields new insights into the etiology of MD symptoms, possible treatment directions and a better understanding of DGC signaling and regulation under normal and stress conditions
Impressionen : aus dem 11. Durchgang das Ina-Pichlmayr-Mentorings 2021 -2023: Mentoring für Wissenschaftlerinnen an der Medizinischen Hochschule Hannover
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