Mother and father depression symptoms and child emotional difficulties: a Network model

INTRODUCTION: Enhancing understanding of depression symptom interactions between parents and associations with subsequent child emotional difficulties will inform targeted treatment of depression to prevent transmission within families. OBJECTIVES: To use a network approach to identify ‘bridge’ symptoms that reinforce mother and father depression, and whether bridge symptoms, as well as other symptoms, impact subsequent child emotional difficulties. METHODS: Symptoms were examined using two unregularized partial correlation network models. The study included 4,492 mother-father-child trios from a prospective, population-based cohort in the United Kingdom. Mother and father reports of depression symptoms were assessed when the child was twenty-one months old. Child emotional difficulties were reported by the mother at ages nine, eleven and thirteen years. RESULTS: Bridge symptoms mutually reinforcing mother and father depression symptoms were feelings of guilt and self-harm ideation, whereas anhedonia acted as a bridge from the father to the mother, but not vice-versa (fig.1, network 1). The symptom of feelings of guilt in mothers was the only bridge symptom which directly associated with child emotional difficulties. Other symptoms that directly associated with child emotional difficulties were feeling overwhelmed for fathers and anhedonia, sadness, and panic in mothers (fig.1, network 2). CONCLUSIONS: Specific symptom interactions are central to the co-occurrence of depression symptoms between parents. Of interest, only one of the bridge symptoms associated with later child emotional difficulties. In addition, specific symptom-to-child outcomes were identified, suggesting that different symptoms in mothers and fathers are central for increased vulnerability in children. DISCLOSURE: No significant relationships

Maintaining Well-Being During the COVID-19 Pandemic: A Network Analysis of Well-Being Responses from British Youth

COVID-19 has significant impacts on young peoples’ lives and emotions. Understanding how young people maintain well-being in the face of challenges can inform future mental health intervention development. Here we applied network analysis to well-being data gathered from 2532 young people (12-25 years) residing in the UK during the COVID-19 pandemic to identify the structure across well-being and crucially, its central defining features. Gender and age differences in networks were also investigated. Across all participants, items emerged in two clusters: 1) optimism, positive self-perception, and social connectedness, and 2) processing problems and ideas. The two central features of well-being were: “I’ve been dealing with problems well” and “I’ve been thinking clearly”. There were minimal age and gender differences. Our findings suggest that the perception of being able to process problems and ideas efficiently could be a hallmark of well-being, particularly in the face of challenging circumstances. These findings contrast with pre-pandemic studies that point to positive affect as central aspects of well-being networks. Future interventions that encourage problem-solving and mental flexibility could be useful in helping young people maintain well-being during times of stress and uncertainty

Role of polygenic and environmental factors in the co-occurrence of depression and psychosis symptoms:a network analysis

Depression and psychosis are often comorbid; they also have overlapping genetic and environmental risk factors, including trauma and area-level exposures. The present study aimed to advance understanding of this comorbidity via a network approach, by (1) identifying bridge nodes that connect clusters of lifetime depression and psychosis symptoms and (2) evaluating the influence of polygenic and environmental risk factors in these symptoms. This study included data from European ancestry participants in UK Biobank, a large population-based sample (N = 77,650). In Step 1, a network model identified bridge nodes between lifetime symptoms of depression and psychosis and functional impairment. In Step 2, genetic and environmental risk factors were incorporated to examine the degree to which symptoms associated with polygenic risk scores for depression and schizophrenia, lifetime exposure to trauma and area-level factors (including deprivation, air pollution and greenspace). Feelings of worthlessness, beliefs in unreal conspiracy against oneself, depression impairment and psychosis impairment emerged as bridges between depression and psychosis symptoms. Polygenic risk scores for depression and schizophrenia were predominantly linked with depression and psychosis impairment, respectively, rather than with specific symptoms. Cumulative trauma emerged as a bridge node associating deprivation with feelings of worthlessness and beliefs in unreal conspiracy, indicating that the experience of trauma is prominently linked with the co-occurrence of depression and psychosis symptoms related to negative views of oneself and others. These key symptoms and risk factors provide insights into the lifetime co-occurrence of depression and psychosis

Determination of and Effects of Taxifolin and Epirubicin on Epithelial–Mesenchymal Transition in Mouse Breast Cancer Cells

Background: One of the most significant characteristics of cancer is epithelial–mesenchymal transition and research on the relationship between phenolic compounds and anticancer medications and epithelial–mesenchymal transition is widespread. Methods: In order to investigate the potential effects of Taxifolin on enhancing the effectiveness of Epirubicin in treating breast cancer, specifically in 4T1 cells and an allograft BALB/c model, the effects of Taxifolin and Epirubicin, both individually and in combination, were examined. Cell viability assays and cytotoxicity assays in 4T1 cells were performed. In addition, 4T1 cells were implanted into female BALB/c mice to conduct in vivo studies and evaluate the therapeutic efficacy of Taxifolin and Epirubicin alone or in combination. Tumor volumes and histological analysis were also assessed in mice. To further understand the mechanisms involved, we examined the messenger RNA and protein levels of epithelial–mesenchymal transition-related genes, as well as active Caspase-3/7 levels, using quantitative real-time polymerase chain reaction, western blot, and enzyme-linked immunosorbent assays, respectively. Results: In vitro results demonstrated that the coadministration of Taxifolin and Epirubicin reduced cell viability and cytotoxicity in 4T1 cell lines. In vivo , coadministration of Taxifolin and Epirubicin suppressed tumor growth in BALB/c mice with 4T1 breast cancer cells. Additionally, this combination treatment significantly increased the levels of active caspase-3/7 and downregulated the messenger RNA and protein levels of N-cadherin, β-catenin, vimentin, snail, and slug, but upregulated the E-cadherin gene. It significantly decreased the messenger RNA levels of the Zeb1 and Zeb2 genes. Conclusion: The in vitro and in vivo results of our study indicate that the concurrent use of Epirubicin with Taxifolin has supportive effects on breast cancer treatment