No abstract

This study suggests that longer working hours are associated with poorer mental health status and increasing levels of anxiety and depression symptoms. There was a positive correlation between these symptoms and sleep disturbances.

Background Mental health-related positive and negative aspects of telework are understudied. This study aimed to evaluate anxiety, depression and sleep quality in full-time teleworkers during lockdown imposed by the coronavirus disease 2019 (COVID-19) pandemic and explore potential relationships between these variables, sociodemographic characteristics, quality of life and perceived productivity. Methods A cross-sectional study was conducted on 143 full-time teleworkers. Participants were assessed for anxiety, depression and sleep quality using validated clinical instruments. Results This study found a high prevalence of poor sleep quality (74%, N = 106). Participants reported anxiety/depressive symptoms with the predominance of anxiety and very high levels of sleep impairment. Better sleep quality was associated with longer sleep duration and better job satisfaction, whereas the use of hypnotic medication and higher depression/anxiety scores seem to point a correlation with sleep impairment. Anxiety/depression positively correlated with worse sleep quality and negatively associated with quality of life. Male sex was negatively associated with perceived productivity. Conclusions A higher prevalence of poor sleep quality was found in comparison with other studies performed during the COVID-19 pandemic as well as high levels of anxiety and depression. These results highlight the relevance of considering the potential negative impact of telework on mental health.

Missense mutations result in full-length proteins containing an amino acid substitution that can be neutral or deleterious, interfering with the normal conformation, localization, and function of a protein. A striking example is the presence of CDH1 (E-cadherin gene) germline missense variants in hereditary diffuse gastric cancer (HDGC), which represent a clinical burden for genetic counseling and surveillance of mutation carriers and their families. CDH1 missense variants can compromise not only the function of E-cadherin but also its expression pattern. Here, we propose a novel method to characterize E-cadherin signature in order to identify cases with E-cadherin deregulation and functional impairment. The strategy includes a bioimaging pipeline to quantify the expression level and characterize the distribution of the protein from in situ immunofluorescence images. The algorithm computes 1D (dimension intensity) radial and internuclear fluorescence profiles to generate expression outlines and 2D virtual cells representing a typical cell within the populations analyzed. Using this new approach, we verify that cells expressing mutant forms of E-cadherin display fluorescence profiles distinct from those of the wild-type cells. Mutant proteins showed a significantly decrease of fluorescence intensity at the membrane and often abnormal expression peaks in the cytoplasm, reflecting the underlying molecular mechanism of trafficking deregulation. Our results suggest employing this methodology as a complementary approach to evaluate the pathogenicity of E-cadherin missense variants. Moreover, it can be applied to a wide range of proteins and, more importantly, to diseases characterized by aberrant protein expression or trafficking deregulation.