Financial Hardship and Sleep Quality Among Black American Women With and Without Systemic Lupus Erythematosus.

OBJECTIVE: To compare dimensions of financial hardship and self-reported sleep quality among Black women with versus without systemic lupus erythematosus (SLE). METHODS: Participants were 402 Black women (50% with validated diagnosis of SLE) living in Georgia between 2017 and 2020. Black women with SLE were recruited from a population-based cohort established in Atlanta, and Black women without SLE were recruited to be of comparable age and from the same geographic areas as SLE women. Financial hardship was measured using three different scales: financial adjustments, financial setbacks, and financial strain. Sleep was assessed continuously using the Pittsburgh Sleep Quality Index (PSQI) scale. Each dimension of financial hardship was analyzed separately in SLE-stratified multivariable linear regression models and adjusted by sociodemographic and health status factors. RESULTS: Dimensions of financial hardship were similarly distributed across the two groups. Sleep quality was worse in Black women with, versus without, SLE (p < .001). Among Black women with SLE, financial adjustment was positively associated with a 0.40-unit increase in poor sleep quality (95% CI = 0.12-0.67, p = .005). When accounting for cognitive depressive symptoms, financial setbacks and strain were somewhat attenuated for Black women with SLE. Overall, no associations between financial hardships and sleep quality were observed for the women without SLE. CONCLUSIONS: Black women with SLE who experience financial hardships may be more at risk for poor sleep quality than Black women without SLE. Economic interventions targeting this population may help improve their overall health and quality of life.

The association between Superwoman schema and subjective sleep quality among Black women.

OBJECTIVES: Similar to women overall, Black women are socialized to be communal and "self-sacrificing," but unlike women from other racial/ethnic backgrounds, Black women are also socialized to be "strong" and "invulnerable." This phenomenon is labeled Superwoman schema. This study examined associations between Superwoman schema endorsement and subjective sleep quality. METHODS: Participants included 405 Black women (ages 30-46). Superwoman schema was measured using a 35-item scale capturing five dimensions: obligation to present strength, suppress emotions, resistance to vulnerability, motivation to succeed, and obligation to help others. Superwoman schema overall and the five dimensions/subscales were analyzed. The Pittsburgh Sleep Quality Index (PSQI) was used to investigate overall subjective sleep quality (range: 0-19), poor sleep quality (PSQI >5), and specific sleep domains (eg, sleep duration, sleep disturbances). We fit linear and binary logistic regression models, adjusting for health-related and sociodemographic factors. RESULTS: Superwoman schema dimension obligation to help others was associated with lower overall subjective sleep quality (ß: .81, 95%CI=0.29, 1.32) and poor sleep quality (OR: 1.55, 95%CI=1.10, 2.19), as well as bad subjective sleep quality (OR: 1.76, 95%CI=1.18, 2.66), sleep disturbances (ß: .73, 95%CI =0.07, 1.41), and daytime sleepiness (OR: 2.01, 95%CI=1.25, 3.26). Suppress emotions (OR: 1.41, 95%CI=1.01, 1.99) was associated with poor subjective sleep quality. Superwoman schema overall was associated with daytime sleepiness (OR: 2.01, 95%CI=1.06, 3.82). CONCLUSION: Superwoman schema endorsement, especially obligation to help others and suppress emotions, may be important psychosocial risk factors for Black women's sleep health.

Immunotolerant p50/NFκB Signaling and Attenuated Hepatic IFNß Expression Increases Neonatal Sensitivity to Endotoxemia.

Sepsis is a major cause of neonatal morbidity and mortality. The current paradigm suggests that neonatal susceptibility to infection is explained by an innate immune response that is functionally immature. Recent studies in adults have questioned a therapeutic role for IFNß in sepsis; however, the role of IFNß in mediating neonatal sensitivity to sepsis is unknown. We evaluated the transcriptional regulation and expression of IFNß in early neonatal (P0) and adult murine models of endotoxemia (IP LPS, 5 mg/kg). We found that hepatic, pulmonary, and serum IFNß expression was significantly attenuated in endotoxemic neonates when compared to similarly exposed adults. Furthermore, endotoxemia induced hepatic p65/NFκB and IRF3 activation exclusively in adults. In contrast, endotoxemia induced immunotolerant p50/NFκB signaling in neonatal mice without evidence of IRF3 activation. Consistent with impaired IFNß expression and attenuated circulating serum levels, neonatal pulmonary STAT1 signaling and target gene expression was significantly lower than adult levels. Using multiple in vivo approaches, the source of hepatic IFNß expression in endotoxemic adult mice was determined to be the hepatic macrophage, and experiments in RAW 264.7 cells confirmed that LPS-induced IFNß expression was NFκB dependent. Finally, treating neonatal mice with IFNß 2 h after endotoxemia stimulated pulmonary STAT1 signaling and STAT1 dependent gene expression. Furthermore, IFNß treatment of endotoxemic neonatal animals resulted in significantly improved survival following exposure to lethal endotoxemia. In conclusion, endotoxemia induced IFNß expression is attenuated in the early neonatal period, secondary to impaired NFκB-p65/IRF3 signaling. Pre-treatment with IFNß decreases neonatal sensitivity to endotoxemia. These results support further study of the role of impaired IFNß expression and neonatal sensitivity to sepsis.