The SARS-CoV-2 health emergency has led to a restructuring of health care systems and the reassignment of medical specialists from their usual duties to attend COVID-19 patients. The aim of this paper is to describe the levels of insomnia, anxiety, depression, and the impact on quality of life of doctors who were on the frontline of COVID-19 during the first two waves of the pandemic. Self-report surveys were conducted on said physicians during both waves, with 83 and 61 responses in the first and second waves, respectively. The reported presence of insomnia was frequent (71.8%), although it decreased in the second survey. Anxiety was moderate, decreasing from 57.1% to 43.1% between measurements. Overall, depression rates decreased between the two surveys. Substance use was found to have an indirect correlation with personal and professional satisfaction. In the light of the unforeseeable evolution of the pandemic and the medium- to long-term repercussions on professionals, we believe the adaptation of health resources is crucial to meet the new unpredictable mental health needs of this group.

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Since the beginning of the COVID-19 pandemic, the need to implement protocols that respond to the mental health demands of the population has been demonstrated. The PASMICOR programme started in March 2020, involving a total of 210 requests for treatment. Out of those subjects, the intervention was performed in 53 patients with COVID-19 without history of past psychiatric illness, 57 relatives and 60 health professionals, all of them within the area of Salamanca (Spain). Interventions were carried out by professionals of the public mental health service mostly by telephone. Depending on clinical severity, patients received basic (level I) or complex psychotherapeutic care combined with psychiatric care (level II). The majority of attended subjects were women (76.5%). Anxious-depressive symptoms were predominant, although sadness was more frequent in patients, insomnia in relatives and anxiety and fear in health professionals. 80% of the sample, particularly most of the health professionals, required a high-intensity intervention (level II). Nearly 50% of the people treated were discharged after an average of 5 interventions. Providing early care to COVID-19 patients, relatives and professionals by using community mental health resources can help to reduce the negative impact of crises, such as the pandemic, on the most affected population groups.

Background: Iron nanoparticles, mainly in magnetite phase (Fe3O4 NPs), are released to the environment in areas with high traffic density and braking frequency. Fe3O4 NPs were found in postmortem human brains and are assumed to get directly into the brain through the olfactory nerve. However, these pollution-derived NPs may also translocate from the lungs to the bloodstream and then, through the blood-brain barrier (BBB), into the brain inducing oxidative and inflammatory responses that contribute to neurodegeneration. Objective: To describe the interaction and toxicity of pollution-derived Fe3O4 NPs on primary rat brain microvascular endothelial cells (rBMECs), main constituents of in vitro BBB models. Methods: Synthetic bare Fe3O4 NPs that mimic the environmental ones (miFe3O4) were synthesized by co-precipitation and characterized using complementary techniques. The rBMECs were cultured in Transwell® plates. The NPs-cell interaction was evaluated through transmission electron microscopy and standard colorimetric in vitro assays. Results: The miFe3O4 NPs, with a mean diameter of 8.45 ± 0.14 nm, presented both magnetite and maghemite phases, and showed super-paramagnetic properties. Results suggest that miFe3O4 NPs are internalized by rBMECs through endocytosis and that they are able to cross the cells monolayer. The lowest miFe3O4 NPs concentration tested induced mid cytotoxicity in terms of 1) membrane integrity (LDH release) and 2) metabolic activity (MTS transformation). Conclusion: Pollution-derived Fe3O4 NPs may interact and cross the microvascular endothelial cells forming the BBB and cause biological damage.