Regulation of mutant huntingtin mitochondrial toxicity by phosphomimetic mutations within its N-terminal region.

Huntington's disease (HD), a neurodegenerative disease, affects approximately 30,000 people in the United States, with 200,000 more at risk. Mitochondrial dysfunction caused by mutant huntingtin (mHTT) drives early HD pathophysiology. mHTT binds the translocase of mitochondrial inner membrane (TIM23) complex, inhibiting mitochondrial protein import and altering the mitochondrial proteome.

Designing, implementing and evaluating multidisciplinary healthcare training programmes in the wartime humanitarian context of Ukraine.

Introduction: Civilian healthcare workers (HCW) and medical facilities are directly and indirectly impacted by armed conflict. In the Russia-Ukraine war, acute trauma care needs grew, the workforce was destabilised by HCW migrating or shifting roles to meet conflict needs, and facilities faced surge events. Chemical, biological, radiological, nuclear and explosive (CBRNE) exposure risks created unique preparedness needs.

Two hit mitochondrial-driven model of synapse loss in neurodegeneration.

In healthy neurons, a mitochondrial membrane potential gradient exists whereby membrane potential is highest in the soma and decreases with distance from the nucleus. Correspondingly, distal mitochondria have more oxidative damage and slower protein import than somal mitochondria. Due to these differences, distal mitochondria have an intrinsic first stressor that somal mitochondria do not have, resulting in synaptic mitochondrial vulnerability.