Occupational health and psychological wellbeing in first line nurses during health crisis periods: reliability study of the SOIC tool.

Background: In 2020, the emergence of the new Coronavirus has put health professionals under enormous pressure, as they had to work in difficult and often disadvantaged situations. Prevention of symptoms such as stress, anxiety and burnout therefore become important health management goals. Aim: The aim of this pilot cross-sectional study was to assess the reliability and feasibility of a tool on Occupational Health Nurses after a Pandemic Period such as the COVID-19 pandemic (Salute Oc-cupazionale negli Infermieri in Periodo Pandemico Covid19 - SOIC) that aims to assess the occupational health and psychological wellbeing of nurses during periods of health crisis. Methods: This study was conducted from September to November 2022. The SOIC tool is composed by two preliminary sections and a third part including five validated questionnaires (measuring burnout, work engagement, psychological symptoms, resilience, and mindful awareness). An opportunistic sample of 202 nurses working in a Teaching Hospital of Rome and members of NurSind union were invited to participate: of these, 24 nurses completed the SOIC in two subsequent occasions (T1 and T2). Results: The test-retest assessment showed no differences between the two waves (T1 and T2) in terms of median scores for all questionnaires included in the SOIC tool. The Cronbach alphas, considering all items of each questionnaire included in the SOIC tool, showed good or excellent internal consistencies. Conclusion: The test-retest assessments and the reliability analyses encouraged the usability of the SOIC tool. Furthermore, consistent associations between the five questionnaires were obtained.

Notch signaling in response to excitotoxicity induces neurodegeneration via erroneous cell cycle reentry.

Neurological disorders such as Alzheimer's disease, stroke and epilepsy are currently marred by the lack of effective treatments to prevent neuronal death. Erroneous cell cycle reentry (CCR) is hypothesized to have a causative role in neurodegeneration. We show that forcing S-phase reentry in cultured hippocampal neurons is sufficient to induce neurodegeneration. We found that kainic-acid treatment in vivo induces erroneous CCR and neuronal death through a Notch-dependent mechanism. Ablating Notch signaling in neurons provides neuroprotection against kainic acid-induced neuronal death. We further show that kainic-acid treatment activates Notch signaling, which increases the bioavailability of CyclinD1 through Akt/GSK3ß pathway, leading to aberrant CCR via activation of CyclinD1-Rb-E2F1 axis. In addition, pharmacological blockade of this pathway at critical steps is sufficient to confer resistance to kainic acid-induced neurotoxicity in mice. Taken together, our results demonstrate that excitotoxicity leads to neuronal death in a Notch-dependent manner through erroneous CCR.