Predictors of mental health in healthcare workers during the COVID-19 pandemic: The role of experiential avoidance, emotion regulation and resilience.

AIMS: This study explores the mediational role of resilience, experiential avoidance and emotion regulation in the levels of anxiety, depression and posttraumatic stress disorder (PTSD) of healthcare workers during the COVID-19 pandemic. Additionally, we explored the association of such levels with personal and professional variables. DESIGN: Cross-sectional study. METHODS: Healthcare professionals working in Spain (N = 786) were recruited following a snowball approach in November and December 2021. Resilience, emotion regulation, experiential avoidance, depression, anxiety, PTSD and work-related variables were measured. Mean differences and correlations were computed, and a path analysis with latent variables (PALV) model was tested. RESULTS: In total, 18.8% of the sample scored above the cut-off score for depression, 24.6% for anxiety and 36.4% for PTSD. Higher resilience and lower experiential avoidance and expression suppression were correlated with better mental health. The PALV model explained 42%-53% of mental health outcomes. Experiential avoidance showed the greatest explanatory power and mediated the impact that stressors had on mental health. Some work-related variables correlated with greater psychological impact. These factors encompassed being a nurse, feeling that their job remained stressful and had not yet returned to its pre-pandemic state and having interacted with individuals facing economic difficulties due to the pandemic, and those who had lost their lives to COVID-19. CONCLUSION: Healthcare workers showed high levels of psychological impact during the COVID-19 pandemic. Such impact was predicted from some work-stress variables and the reliance on maladaptive strategies such as experiential avoidance and expressive suppression. IMPACT: Training healthcare professionals to use coping strategies incompatible with experiential avoidance may improve their mental health. Additionally, better working conditions are fundamental for reducing the impact of critical situations on healthcare workers' mental health. PATIENT OR PUBLIC CONTRIBUTION: No patient or public contribution.

The Mitochondrial Isoform of FASTK Modulates Nonopsonic Phagocytosis of Bacteria by Macrophages via Regulation of Respiratory Complex I.

Phagocytosis is a pivotal process by which innate immune cells eliminate bacteria. In this study, we explore novel regulatory mechanisms of phagocytosis driven by the mitochondria. Fas-activated serine/threonine kinase (FASTK) is an RNA-binding protein with two isoforms, one localized to the mitochondria (mitoFASTK) and the other isoform to cytosol and nucleus. The mitoFASTK isoform has been reported to be necessary for the biogenesis of the mitochondrial ND6 mRNA, which encodes an essential subunit of mitochondrial respiratory complex I (CI, NADH:ubiquinone oxidoreductase). This study investigates the role and the mechanisms of action of FASTK in phagocytosis. Macrophages from FASTK─/─ mice exhibited a marked increase in nonopsonic phagocytosis of bacteria. As expected, CI activity was specifically reduced by almost 50% in those cells. To explore if decreased CI activity could underlie the phagocytic phenotype, we tested the effect of CI inhibition on phagocytosis. Indeed, treatment with CI inhibitor rotenone or short hairpin RNAs against two CI subunits (NDUFS3 and NDUFS4) resulted in a marked increase in nonopsonic phagocytosis of bacteria. Importantly, re-expression of mitoFASTK in FASTK-depleted macrophages was sufficient to rescue the phagocytic phenotype. In addition, we also report that the decrease in CI activity in FASTK─/─ macrophages is associated with an increase in phosphorylation of the energy sensor AMP-activated protein kinase (AMPK) and that its inhibition using Compound C reverted the phagocytosis phenotype. Taken together, our results clearly demonstrate for the first time, to our knowledge, that mitoFASTK plays a negative regulatory role on nonopsonic phagocytosis of bacteria in macrophages through its action on CI activity.

Changing face of socio-economic vulnerability and COVID-19: An analysis of country wealth during the first two years of the pandemic.

There are numerous academic studies on the relationship between population wealth and the incidence of COVID-19. However, research developed shows contradictory results on their relationship. In accordance with this question, this work pursues two objectives: on the one hand, to check whether wealth and disease incidence have a unidirectional and stable relationship. And on the other hand, to find out if the country's statistical production capacity is masking the real incidence of the COVID-19 pandemic. In order to achieve this objective, an ecological study has been designed at international level with the countries established as study units. The analytical strategy utilized involves the consecutive application of cross-sectional analysis, specifically employing multivariate linear regression daily throughout the first two years of the pandemic (from 03/14/2020 to 03/28/2022). The application of multiple cross-sectional analysis has shown that country wealth has a dynamic relationship with the incidence of COVID-19. Initially, it appears as a risk factor and, in the long term, as a protective element. In turn, statistical capacity appears as an explanatory variable for the number of published COVID-19 cases and deaths. Therefore, the inadequate statistical production capacity of low income countries may be masking the real incidence of the disease.

The Non-Linear Impact of Financial Development on Environmental Quality and Sustainability: Evidence from G7 Countries.

This paper analyses the impact of financial development on the environmental quality and sustainability for the group of G7 countries over the period 1990-2019 based on static panel data-fixed effect models. The objective is to explore if there exists a non-linear relationship between the whole financial system development and a wide array of measures of environmental sustainability and degradation, namely adjusted net savings, greenhouse gas, CO2, methane, nitrous oxide emissions and ecological footprint. We define a new Financial Environmental Kuznets Curve (FEKC) by introducing the square term of financial development on the environment-finance relationship. Empirical results prove the existence of non-linear relationships between the composite index of financial development and environmental degradation for the group of advanced economies. In the case of methane, we validate the presence of an inverted-U shape association in line with the FEKC hypothesis, while for greenhouse gas and CO2 the link follows a U-shaped pattern. The impact of financial development on environmental sustainability is monotonically positive and statistically significant while the ecological footprint is not statistically linked with the level of financial development within G7 countries. Economic growth, human capital, population density and primary energy consumption appear as significant drivers of environmental quality and sustainability.

Multivariate Analysis of Risk Factors of the COVID-19 Pandemic in the Community of Madrid, Spain.

It has been more than one year since Chinese authorities identified a deadly new strain of coronavirus, SARS-CoV-2. Since then, the scientific work regarding the transmission risk factors of COVID-19 has been intense. The relationship between COVID-19 and environmental conditions is becoming an increasingly popular research topic. Based on the findings of the early research, we focused on the community of Madrid, Spain, which is one of the world's most significant pandemic hotspots. We employed different multivariate statistical analyses, including principal component analysis, analysis of variance, clustering, and linear regression models. Principal component analysis was employed in order to reduce the number of risk factors down to three new components that explained 71% of the original variance. Cluster analysis was used to delimit the territory of Madrid according to these new risk components. An ANOVA test revealed different incidence rates between the territories delimited by the previously identified components. Finally, a set of linear models was applied to demonstrate how environmental factors present a greater influence on COVID-19 infections than socioeconomic dimensions. This type of local research provides valuable information that could help societies become more resilient in the face of future pandemics.

Focal adhesion kinase as a mechanotransducer during rapid brain growth of the chick embryo.

Expansion of the hollow fluid-filled embryonic brain occurs by an increase in intraluminal pressure created by accumulation of cerebrospinal fluid (CSF). Experiments have shown a direct correlation between cavity pressure and cell proliferation within the neuroepithelium. These findings lead us to ask how mechanistically this might come about. Are there perhaps molecules on the luminal surface of the embryonic neuroepithelium, such as focal adhesion kinases (FAKs) known to respond to tension in other epithelial cells? Immunodetection using antibodies to total FAK and p-FAK was performed with subsequent confocal analysis of the pattern of their activation under normal intraluminal pressure and induced chronic pressure. Western analysis was also done to look at the amount of FAK expression, as well as its activation under these same conditions. Using immunolocalization, we have shown that FAK is present and activated on both apical and basolateral surfaces and within the cytoplasm of the neuroepithelial cells. This pattern changed profoundly when the neuroepithelium was under pressure. By Western blot, we have shown that FAK was upregulated and activated in the neuroepithelium of the embryos just after the neural tube becomes a closed pressurized system, with phosphorylation detected on the luminal instead of the basal surface, along with an increase in cell proliferation. Chronic hyper-pressure does not induce an increase in phosphorylation of FAK. In conclusion, here we show that neuroepithelial cells respond to intraluminal pressure via FAK phosphorylation on the luminal surface.