Afrontamiento del estrés post Covid-19 mediante un programa psicológico virtual / Coping with post-Covid-19 stress through a virtual psychological program

La pandemia Covid-19 ha impactado en el bienestar psicológico a nivel mundial y los estudiantes universitarios no están exentos, manifestando respuestas emocionales-patológicas como estrés, ansiedad y depresión provocadas por factores individuales, socio-familiares y académicos. El objetivo es conocer los tipos de estrategias de afrontamiento en 100 estudiantes de una universidad privada de Huancayo frente a la Covid-19, determinando la eficacia de un programa virtual. La investigación fue cuantitativa-descriptiva de corte trasversal y aplicada, mediante un programa virtual denominado "Cuidando mi salud psicológica" con 16 sesiones de 50 minutos/3 semanas, entre septiembre-noviembre 2021, el procesamiento de datos se realizó mediante el uso de estadística descriptiva y medidas de tendencia central. Los resultados determinaron 14 principales factores generadores de estrés y ansiedad en los estudiantes, categorizados en 3 núcleos; factor individual, socio-familiar y académico. El grupo T0 (no diagnosticado) y T1 (diagnosticado) expresaron como factor individual el temor a enfermar de Covid-19 con 0,72 y 0,88, en el factor socio-familiar se evidenció en T0 con conflictos con los integrantes de la familia (0,52) y T1 temor de contagiar personas del entorno cercano (0,62). En el factor académico fue la adaptación a otras modalidades de estudio con 0,56 (T0) y 0,42 (T1). La influencia del PSV sobre las estrategias de afrontamiento fue moderada, positiva y altamente positiva a excepción del grupo T0 en la evitación de problemas que paso de medio 7,57 (bajo) a 8,68 (medio) con influencia del PSV negativa. Demostrando así, la eficacia del programa virtual "Cuidando mi salud psicológica"(AU)

The Covid-19 pandemic has impacted psychological well-being worldwide and university students are not exempt, manifesting emotional-pathological responses such as stress, anxiety and depression caused by individual, socio-family and academic factors. The objective is to know the types of coping strategies in 100 students from a private university in Huancayo against Covid-19, determining the effectiveness of a virtual program. The research was quantitative-descriptive, cross-sectional and applied, through a virtual program called "Caring for my psychological health" with 16 sessions of 50 minutes/3 weeks, between September-November 2021, the data processing was carried out through the use of statistics descriptive and measures of central tendency. The results determined 14 main factors that generate stress and anxiety in students, categorized into 3 cores; individual, socio-family and academic factor. The group T0 (undiagnosed) and T1 (diagnosed) expressed as an individual factor the fear of getting sick from Covid-19 with 0.72 and 0.88, in the socio-family factor it was evidenced in T0 with conflicts with the members of the family (0.52) and T1 fear of infecting people in the immediate environment (0.62). In the academic factor it was the adaptation to other study modalities with 0.56 (T0) and 0.42 (T1). The influence of PSV on coping strategies was moderate, positive and highly positive, except for the T0 group in problem avoidance, which went from a mean of 7.57 (low) to 8.68 (medium) with a negative influence of PSV. Thus demonstrating the effectiveness of the virtual program "Caring for my psychological health"

Prion pathogenesis is faithfully reproduced in cerebellar organotypic slice cultures.

Prions cause neurodegeneration in vivo, yet prion-infected cultured cells do not show cytotoxicity. This has hampered mechanistic studies of prion-induced neurodegeneration. Here we report that prion-infected cultured organotypic cerebellar slices (COCS) experienced progressive spongiform neurodegeneration closely reproducing prion disease, with three different prion strains giving rise to three distinct patterns of prion protein deposition. Neurodegeneration did not occur when PrP was genetically removed from neurons, and a comprehensive pharmacological screen indicated that neurodegeneration was abrogated by compounds known to antagonize prion replication. Prion infection of COCS and mice led to enhanced fodrin cleavage, suggesting the involvement of calpains or caspases in pathogenesis. Accordingly, neurotoxicity and fodrin cleavage were prevented by calpain inhibitors but not by caspase inhibitors, whereas prion replication proceeded unimpeded. Hence calpain inhibition can uncouple prion replication from its neurotoxic sequelae. These data validate COCS as a powerful model system that faithfully reproduces most morphological hallmarks of prion infections. The exquisite accessibility of COCS to pharmacological manipulations was instrumental in recognizing the role of calpains in neurotoxicity, and significantly extends the collection of tools necessary for rigorously dissecting prion pathogenesis.