ABSTRACT
COVID-19 has affected the population's mental health, increasing the risk of parental burnout (Griffith, 2020), defined as a syndrome resulting from long-term exposure to chronic stress of parents in their role as caregivers (Mikolajczak et al. 2019). This phenomenon can have serious implications for the upbringing and normal development of children and adolescents, since it affects multiple areas of parental functioning, as well as damage the bond they maintain with their children (Mikolajczak et al, 2018). This study included 693 participants, collected through a non-random sample that included 133 fathers and 560 mothers over 18 years of age who currently live in Chile, living with at least one child. Linear regressions were performed to understand the relationship between parental burnout-measured using the Parental Burnout Assessment (PBA)-and the perceived negative impact of the pandemic on parenting practices;the role of emotional regulation strategies of suppression and reappraisal-measured through the Emotional Regulation Questionnaire (ERQ)-;and gender. Higher levels of parental burnout were found in mothers, who reported a greater negative impact of the COVID-19 crisis, using more suppression strategies and less reappraisal. Copyright © 2022, Sociedad Chilena de Psicologia Clinica. All rights reserved.
ABSTRACT
The COVID-19 pandemic has affected all societies worldwide. The heightened levels of stress that accompanied the crisis were also expected to affect parenting in many families. Since it is known that high levels of stress in the parenting domain can lead to a condition that has severe consequences for health and well-being, we examined whether the prevalence of parental burnout in 26 countries (9,923 parents;75% mothers;mean age 40) increased during COVID-19 compared to few years before the pandemic. In most (but not all) countries, analyses showed a significant increase in the prevalence of parental burnout during the pandemic. The results further revealed that next to governmental measures (e.g., number of days locked down, homeschooling) and factors at the individual and family level (e.g., gender, number of children), parents in less (vs. more) indulgent countries suffered more from parental burnout. The findings suggest that stricter norms regarding their parenting roles and duties in general and during the pandemic in particular might have increased their levels of parental burnout. © 2022 Hogrefe Publishing.
ABSTRACT
Introduction: SARS-CoV-2, the causative pathogen for COVID-19, engages host ACE2 receptor for cellular entry. The brush border of the small intestines express high levels of ACE2. Gastrointestinal (GI) manifestations are common among COVID-19 patients. However, to date, there is limited information regarding intestinal response to SARS-CoV-2 infection. Methods: Intestinal biopsies were obtained from 17 COVID-19 patients (17.3 ± positive nasal swab) for cellular and transcriptomic analyses using mass cytometry and RNA-sequencing, respectively. Ten uninfected individuals served as compartment (EC) and lamina propria (LP) were analyzed separately. Results: The cellular profiles from LP of COVID-19 patients showed reduced frequencies of CD206+ conventional dendritic cells (CDC2s) and plasmacytoid (CD123+) dendritic cells Effector T cell (PD1+CD38+) frequency was increased in the LP and Intraepithelial lymphocytes (IEL) were increased in the EC of COVID-19 patients, with a concomitant decrease in CD206+ CDC2s. RNA sequencing active downregulation of genes involved in inflammatory pathways including IBD-associated pathways, while an upregulation of intestinal barrier function Gene expression of Neuropilin-1 (NRP-1), a putative SARS-CoV-2 receptor as well as key inflammatory cytokines (IL-1b, IFN-g, CCL24 and CXCL8) were significantly reduced in controls. A low intensity antiviral host response signature was observed predominantly in EC as opposed to LP suggesting viral localization to epithelium. Conclusions: Epithelial, myeloid and lymphoid cell alterations characterize intestinal response to SARS-CoV-2 infection with an unanticipated downregulation of key inflammatory pathways that have been implicated in adverse outcomes associated with These data stand in contrast to the inflammatory response reported in the systemic compartments and identify a potential mitigating role of the GI
ABSTRACT
Background: SARS-CoV-2, the etiopathological agent for COVID-19, engages host ACE2 receptor for cellular entry. The brush border of the small intestines express high levels of ACE2 in physiological conditions. Gastrointestinal (GI) manifestations are common among COVID-19 patients. However, to date, there is limited information regarding intestinal response to SARS-CoV-2 infection. Methods: Intestinal biopsies were obtained from 17 COVID-19 patients (17.3-17.5 days from the last positive nasal swab) for cellular and transcriptomic analyses using mass cytometry and RNA-sequencing. Ten COVID-uninfected individuals served as controls. The epithelial compartment (EC) and lamina propria (LP) were analyzed separately. Results: The cellular profiles of intestinal tissues from COVID-19 patients showed reduced frequencies of CD206+ CDC2s and plasmacytoid dendritic cells in the LP of COVID-19 patients by mass cytometry. Effector T cell (PD1+CD38+) frequency was increased in the LP and blood of COVID-19 patients. Intraepithelial lymphocytes (IEL) were increased in the EC of COVID-19 patients, with a concomitant decrease in CD206+ CDC2s. RNA sequencing revealed an active downregulation of genes involved in inflammatory pathways including Th17 and IBD-associated pathways, while an upregulation of intestinal barrier function (mucin biosynthesis), amino acid metabolism and mineral absorption pathways was noted. Gene expression of Neuropilin-1 (NRP-1), a putative SARSCoV-2 receptor as well as key inflammatory cytokines (IL-1β, IFNγ, CCL24 and CXCL8) were significantly reduced in COVID-19 patients compared to controls. A low intensity antiviral host response signature was observed predominantly in EC reflecting the cellular localization of the virus. Conclusion: Epithelial, myeloid and lymphoid cell alterations characterize intestinal response to SARS-CoV-2 infection with an unanticipated downregulation of key inflammatory pathways that have been implicated in adverse outcomes associated with COVID-19. These data stand in contrast to reports from the pulmonary and systemic compartments and identify a potential mitigating role of the GI tract in COVID-19-associated immunopathology.