Prevalence, increase and predictors of family violence during the COVID-19 pandemic, using modern machine learning approaches.

Background: We are facing an ongoing pandemic of coronavirus disease 2019 (COVID-19), which is causing detrimental effects on mental health, including disturbing consequences on child maltreatment and intimate partner violence. Methods: We sought to identify predictors of child maltreatment and intimate partner violence from 380 participants (mean age 36.67 ± 10.61, 63.2% male; Time 3: June 2020) using modern machine learning analysis (random forest and SHAP values). We predicted that COVID-related factors (such as days in lockdown), parents' psychological distress during the pandemic (anxiety, depression), their personality traits, and their intimate partner relationship will be key contributors to child maltreatment. We also examined if there is an increase in family violence during the pandemic by using an additional cohort at two time points (Time 1: March 2020, N = 434; mean age 35.67 ± 9.85, 41.69% male; and Time 2: April 2020, N = 515; mean age 35.3 ± 9.5, 34.33%). Results: Feature importance analysis revealed that parents' affective empathy, psychological well-being, outdoor activities with children as well as a reduction in physical fights between partners are strong predictors of a reduced risk of child maltreatment. We also found a significant increase in physical punishment (Time 3: 66.26%) toward children, as well as in physical (Time 3: 36.24%) and verbal fights (Time 3: 41.08%) among partners between different times. Conclusion: Using modernized predictive algorithms, we present a spectrum of features that can have influential weight on prediction of child maltreatment. Increasing awareness about family violence consequences and promoting parenting programs centered around mental health are imperative.

Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection.

Hyperinflammatory response caused by infections such as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) increases organ failure, intensive care unit admission, and mortality. Cytokine storm in patients with Coronavirus Disease 2019 (COVID-19) drives this pattern of poor clinical outcomes and is dependent upon the activity of the transcription factor complex nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) and its downstream target gene interleukin 6 (IL6) which interacts with IL6 receptor (IL6R) and the IL6 signal transduction protein (IL6ST or gp130) to regulate intracellular inflammatory pathways. In this study, we compare transcriptomic signatures from a variety of drug-treated or genetically suppressed (i.e. knockdown) cell lines in order to identify a mechanism by which antidepressants such as fluoxetine demonstrate non-serotonergic, anti-inflammatory effects. Our results demonstrate a critical role for IL6ST and NF-kappaB Subunit 1 (NFKB1) in fluoxetine's ability to act as a potential therapy for hyperinflammatory states such as asthma, sepsis, and COVID-19.

Oxytocin's anti-inflammatory and proimmune functions in COVID-19: a transcriptomic signature-based approach.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a worldwide pandemic, infecting over 16 million people worldwide with a significant mortality rate. However, there is no current Food and Drug Administration-approved drug that treats coronavirus disease 2019 (COVID-19). Damage to T lymphocytes along with the cytokine storm are important factors that lead to exacerbation of clinical cases. Here, we are proposing intravenous oxytocin (OXT) as a candidate for adjunctive therapy for COVID-19. OXT has anti-inflammatory and proimmune adaptive functions. Using the Library of Integrated Network-Based Cellular Signatures (LINCS), we used the transcriptomic signature for carbetocin, an OXT agonist, and compared it to gene knockdown signatures of inflammatory (such as interleukin IL-1ß and IL-6) and proimmune markers (including T cell and macrophage cell markers like CD40 and ARG1). We found that carbetocin's transcriptomic signature has a pattern of concordance with inflammation and immune marker knockdown signatures that are consistent with reduction of inflammation and promotion and sustaining of immune response. This suggests that carbetocin may have potent effects in modulating inflammation, attenuating T cell inhibition, and enhancing T cell activation. Our results also suggest that carbetocin is more effective at inducing immune cell responses than either lopinavir or hydroxychloroquine, both of which have been explored for the treatment of COVID-19.