Do social support and community engagement act as mechanisms in the association between neighbourhood income inequality and the mental health of mothers in Calgary,Canada? A mediation analysis

PurposeAccording to the social determinants of health framework, income inequality is a potential risk factor for adverse mental health. However, few studies have explored the mechanisms suspected to mediate this relationship. The current study addresses this gap through a mediation analysis to determine if social support and community engagement act as mediators linking neighbourhood income inequality to maternal anxiety and depressive symptoms within a cohort of new mothers living in the City of Calgary, Canada.MethodsData collected at three years postpartum from mothers belonging to the All Our Families (AOF) cohort were used in the current study. Maternal data were collected between 2012 and 2015 and linked to neighbourhood socioeconomic data from the 2006 Canadian Census. Income inequality was measured using Gini coefficients derived from 2006 after-tax census data. Generalized structural equation models were used to quantify the associations between income inequality and mental health symptoms, and to assess the potential direct and indirect mediating effects of maternal social support and community engagement.ResultsIncome inequality was not significantly associated with higher depressive symptoms (β = 0.32, 95%CI = −0.067, 0.70), anxiety symptoms (β = 0.11, 95%CI = −0.39, 0.60), or lower social support. Income inequality was not associated with community engagement. For the depression models, higher social support was significantly associated with lower depressive symptoms (β = −0.13, 95%CI = −0.15, −0.097), while community engagement was not significantly associated with depressive symptoms (β = 0.059, 95%CI = −0.15, 0.27). Similarly, for the anxiety models, lower anxiety symptoms were significantly associated with higher levels of social support (β = −0.17, 95%CI = −0.20, −0.13) but not with higher levels of community engagement (β = 0.14, 95%CI = −0.14, 0.41).ConclusionThe current study did not find clear evidence for social support or community engagement mediating the relationship between neighbourhood income inequality and maternal mental health. Future investigations should employ a broader longitudinal approach to capture changes in income inequality, potential mediators, and mental health symptomatology over time.     

Mortality in patients with intracerebral hemorrhage associated with antiplatelet agents,oral anticoagulants or no antithrombotic therapy

The association between preceding treatment with antiplatelet agents (APs), vitamin K antagonists (VKAs) or direct oral anticoagulants (DOACs) and mortality after intracerebral hemorrhage (ICH) remains unclear.The aim of this multicenter, prospective cohort study was to assess the risk for death after ICH in consecutive patients who were on treatment with APs, VKAs, DOACs, or no antithrombotic agent. The primary outcome was in-hospital death by day 30. ICH volume at admission and volume expansion were centrally assessed.Out of 598 study patients, in-hospital death occurred in 21% of patients who were on treatment with APs, 25% with VKAs, 30% with DOACs, and 13% with no antithrombotics. Crude death rate was higher in patients on antithrombotics as compared to patients receiving no antithrombotic agent. At multivariate analysis, age (HR 1.07; 95% CI 1.04–1.10), previous stroke (HR 1.83; 95% CI 1.14–2.93), GCS ≤8 at admission (HR 6.06; 95% CI 3.16–9.74) and GCS 9–12 (HR 3.38; 95% CI 1.81–6.33) were independent predictors of death. Treatment with APs (HR 1.29; 95% CI 0.61–2.76), VKAs (HR 1.42; 95% CI 0.70–2.88) or DOACs (HR 1.28; 95% CI 0.61–2.73) were not predictors of death in the overall study population, in non-trauma associated ICH as well as when GCS was not included in the model. ICH volume and volume expansion were independent predictors of death.In conclusion, preceding treatment with antithrombotic is associated with the severity of ICH. Age, previous stroke and clinical severity at presentation were independent predictors of in-hospital death in patients with ICH.     

Inequalities in the Distribution of Childhood Adversity From Birth to 11 Years

ObjectiveExposure to early adversity carries long term harmful consequences for children's health and development. This study aims to 1) estimate the prevalence of childhood adversity for Australian children from infancy to 10–11 years, and 2) document inequalities in the distribution of adversity according to socioeconomic position (SEP), Indigenous status, and ethnicity.MethodsAdversity was assessed every 2 years from 0–1 to 10–11 years in the nationally representative birth cohort of the Longitudinal Study of Australian Children (N = 5107). Adversity included legal problems; family violence; household mental illness; household substance abuse; harsh parenting; parental separation/divorce; unsafe neighborhood; family member death; and bullying (from 4 to 5 years). Adversities were examined individually and summed for a measure of multiple adversity (2+ adverse experiences).ResultsBy 10–11 years, 52.8% (95% confidence interval [CI] 51.0–54.7) of children had been exposed to 2 or more adversities. When combined with low SEP, children from ethnic minority and from Indigenous backgrounds had 4 to 8 times the odds of exposure to 2 or more adversities than children from higher SEP Anglo-Euro backgrounds, respectively (odds ratio [OR] 4.3, 95% CI 2.8–6.6 and OR 8.1, 95% CI 4.4–14.8). Ethnic minority and Indigenous children from higher SEP backgrounds had increased odds of exposure to multiple adversity than similarly advantaged Anglo-Euro children (OR 1.8, 95% CI 1.4–2.3 and OR 2.3, 95% CI 1.3–4.3, respectively).ConclusionsAddressing early adversity is a significant opportunity to promote health over the life course, and reduce health inequalities experienced by marginalized groups of children.     

Proteases and their inhibitors as prognostic factors for high-grade serous ovarian cancer

Ovarian carcinoma is one of the most lethal malignancies, but only very few prognostic biomarkers are known. The degradome, comprising proteases, protease non-proteolytic homologues and inhibitors, have been involved in the prognosis of many cancer types, including ovarian carcinoma. The prognostic significance of the whole degradome family has not been specifically studied in high-grade serous ovarian cancer. A targeted DNA microarray known as the CLIP-CHIP microarray was used to identify potential prognostic factors in ten high-grade serous ovarian cancer women who had early recurrence (<1.6 years) or late/no recurrence after first line surgery and chemotherapy. In women with early recurrence, we identified seven upregulated genes (TMPRSS4, MASP1/3, SPC18, PSMB1, IGFBP2, CFI – encoding Complement Factor I – and MMP9) and one down-regulated gene (ADAM-10). Using immunohistochemistry, we evaluated the prognostic effect of these 8 candidate genes in an independent cohort of 112 high-grade serous ovarian cancer women. Outcomes were progression, defined according to CA-125 criteria, and death. Multivariate Cox proportional hazard regression models were done to estimate the associations between each protein and each outcome. High ADAM-10 expression (intensity of 2–3) was associated with a lower risk of progression (adjusted hazard ratio (HR): 0.51; 95% confidence interval (CI): 0.29-0.87). High complement factor I expression (intensity 2–3) was associated with a higher risk of progression (adjusted HR: 2.30, 95% CI: 1.17–4.53) and death (adjusted HR: 3.42; 95% CI: 1.72–6.79). Overall, we identified the prognostic value of two proteases, ADAM-10 and complement factor I, for high-grade serous ovarian cancer which could have clinical significance.