Community Partnership to Co-Develop an Intervention to Promote Equitable Uptake of the COVID-19 Vaccine Among Pediatric Populations.

Objective: To describe the process of engaging community, caregiver, and youth partners in codeveloping an intervention to promote equitable uptake of the COVID-19 vaccine in non-Hispanic Black (Black) and Hispanic youth who experience higher rates of COVID-19 transmission, morbidity, and mortality but were less likely to receive the COVID-19 vaccine. Methods: A team of 11 Black and Hispanic community partners was assembled to codevelop intervention strategies with our interdisciplinary research team. We used a mixed-methods crowdsourcing approach with Black and Hispanic youth (n=15) and caregivers of Black and Hispanic youth (n=20) who had not yet been vaccinated against COVID-19, recruited from primary care clinics, to elicit perspectives on the acceptability of these intervention strategies. Results: We codeveloped five strategies: (1) community-tailored handouts and posters, (2) videos featuring local youth, (3) family-centered language to offer vaccines in the primary care clinic, (4) communication-skills training for primary care providers, and (5) use of community health workers to counsel families about the vaccine. The majority (56-96.9%) of youth and caregivers rated each of these strategies as acceptable, especially because they addressed common concerns and facilitated shared decision-making. Conclusions: Engaging community and family partners led to the co-development of culturally- and locally-tailored strategies to promote dialogue and shared decision-making about the COVID-19 vaccine. This process can be used to codevelop interventions to address other forms of public health disparities. Policy Implications: Intervention strategies that promote dialogues with trusted healthcare providers and support shared decision-making are acceptable strategies to promote COVID-19 vaccine uptake among youth from historically underserved communities. Stakeholder-engaged methods may also help in the development of interventions to address other forms of health disparities.

Black-White Risk Differentials in Pediatric COVID-19 Hospitalization and Intensive Care Unit Admissions in the USA.

PURPOSE: The COVID-19 morbidity with SARS-CoV-2 as a causative pathogenic microbe remains a pandemic with children experiencing less mortality but with severe manifestations. The current study aimed to assess SARS-CoV-2 cumulative incidence, COVID-19 hospitalization, and ICU admission with respect to racial differentials. MATERIALS AND METHODS: A cross-sectional nonexperimental epidemiologic design was used to examine pediatric COVID-19 data from CDC during 2020. The variables assessed were ICU admissions, hospitalization, sex, race, and region. The Chi-Square (X2) statistic was used to examine the independence of the variables by race, while the binomial regression model was used to predict racial risk differentials in hospitalization and ICU admissions. RESULTS: The pediatric COVID-19 data observed the cumulative incidence of hospitalization to be 96,376, while ICU admission was 12,448. Racial differences were observed in hospitalization, ICU admissions, sex, and region. With respect to COVID-19 hospitalization, Black/African American (AA) children were two times as likely to be hospitalized compared to their White counterparts, prevalence risk ratio (pRR) = 2.20, 99% confidence interval (CI = 2.12-2.28). Similarly, Asians were 45% more likely to be hospitalized relative to their White counterparts, pRR = 1.45, 99% CI = 1.32-1.60. Regarding ICU admission, there was a disproportionate racial burden, implying excess ICU admission among Black/AA children relative to their White counterparts, pRR = 5.18, 99% CI = 4.44-6.04. Likewise, Asian children were 3 times as likely to be admitted to the ICU compared to their White counterparts, pRR = 3.36, 99% CI = 2.37-4.77. Additionally, American Indians/Alaska Natives were 2 times as likely to be admitted to ICU, pRR = 2.54, 99% CI = 0.82-7.85. CONCLUSION: Racial disparities were observed in COVID-19 hospitalization and ICU admission among the US children, with Black/AA children being disproportionately affected, implying health equity transformation.

Black-White Risk Differentials in COVID-19 (SARS-COV2) Transmission, Mortality and Case Fatality in the United States: Translational Epidemiologic Perspective and Challenges.

BACKGROUND: Social and health inequities predispose vulnerable populations to adverse morbidity and mortality outcomes of epidemics and pandemics. While racial disparities in cumulative incidence (CmI) and mortality from the influenza pandemics of 1918 and 2009 implicated Blacks with survival disadvantage relative to Whites in the United States, COVID-19 currently indicates comparable disparities. We aimed to: (a) assess COVID-19 CmI by race, (b) determine the Black-White case fatality (CF) and risk differentials, and (c) apply explanatory model for mortality risk differentials. METHODS: COVID-19 data on confirmed cases and deaths by selective states health departments were assessed using a cross-sectional ecologic design. Chi-square was used for CF independence, while binomial regression model for the Black-White risk differentials. RESULTS: The COVID-19 mortality CmI indicated Blacks/AA with 34% of the total mortality in the United States, albeit their 13% population size. The COVID-19 CF was higher among Blacks/AA relative to Whites; Maryland, (2.7% vs. 2.5%), Wisconsin (7.4% vs. 4.8%), Illinois (4.8% vs. 4.2%), Chicago (5.9% vs. 3.2%), Detroit (Michigan), 7.2% and St. John the Baptist Parish (Louisiana), 7.9%. Blacks/AA compared to Whites in Michigan were 15% more likely to die, CmI risk ratio (CmIRR) = 1.15, 95% CI, 1.01-1.32. Blacks/AA relative to Whites in Illinois were 13% more likely to die, CmIRR = 1.13, 95% CI, 0.93-1.39, while Blacks/AA compared to Whites in Wisconsin were 51% more likely to die, CmIRR = 1.51, 95% CI, 1.10-2.10. In Chicago, Blacks/AA were more than twice as likely to die, CmIRR = 2.24, 95% CI, 1.36-3.88. CONCLUSION: Substantial racial/ethnic disparities are observed in COVID-19 CF and mortality with Blacks/AA disproportionately affected across the United States.

Implication of Vaginal and Cesarean Section Delivery Method in Black-White Differentials in Infant Mortality in the United States: Linked Birth/Infant Death Records, 2007-2016.

Racial/ethnic disparities in infant mortality (IM) continue to persist in the United States, with Black/African Americans (AA) being disproportionally affected with a three-fold increase in mortality compared to Whites. Epidemiological data have identified maternal characteristics in IM risk such as preeclampsia, eclampsia, maternal education, smoking, maternal weight, maternal socioeconomic status (SES), and family structure. Understanding the social gradient in health including implicit bias, as inherent in the method of labor and delivery and the racial heterogeneity, may facilitate intervention mapping in narrowing the Black-White IM risk differences. We aimed to assess the temporal/racial trends and the methods of delivery, mainly vaginal vs. cesarean section (C-section) as an exposure function of IM. The United States linked birth/infant death records (2007-2016) were used with a cross-sectional ecological design. The analysis involved chi squared statistic, incidence rate estimation by binomial regression model, and period percent change. Of the 40,445,070 births between 2007 and 2016, cumulative mortality incidence was 249,135 (1.16 per 1000). The IM rate was highest among Black/AA (11.41 per 1000), intermediate among Whites (5.19 per 1000), and lowest among Asian /Pacific Islanders (4.24 per 1000). The cumulative incidence rate difference, comparing vaginal to cesarean procedure was 1.73 per 1000 infants, implying excess IM with C-section. Compared to C-section, there was a 31% decreased risk of IM among mothers with vaginal delivery, rate ratio (RR) = 0.69, 95% confidence interval (CI): 0.64-0.74. Racial disparities were observed in the method of delivery associated with IM. Black/AA mothers with vaginal delivery had a 6% decreased risk of IM compared to C-section, RR = 0.94, 95% CI: 0.92-0.95, while Whites with vaginal delivery had a 38% decrease risk of IM relative to C-section, RR= 0.68, 95% CI: 0.67-0.69, p < 0.001. Infant mortality varied by race, with Black/AA disproportionally affected, which is explained in part by labor and delivery procedures, suggestive of reliable and equitable intrapartum assessment of Black/AA mothers during labor, as well as implicit bias marginalization in the healthcare system.

Implication of Spiritual Network Support System in Epigenomic Modulation and Health Trajectory.

With challenges in understanding the multifactorial etiologies of disease and individual treatment effect heterogeneities over the past four decades, much has been acquired on how physical, chemical and social environments affect human health, predisposing certain subpopulations to adverse health outcomes, especially the socio-environmentally disadvantaged (SED). Current translational data on gene and adverse environment interaction have revealed how adverse gene-environment interaction, termed aberrant epigenomic modulation, translates into impaired gene expression via messenger ribonucleic acid (mRNA) dysregulation, reflecting abnormal protein synthesis and hence dysfunctional cellular differentiation and maturation. The environmental influence on gene expression observed in most literature includes physical, chemical, physicochemical and recently social environment. However, data are limited on spiritual or religious environment network support systems, which reflect human psychosocial conditions and gene interaction. With this limited information, we aimed to examine the available data on spiritual activities characterized by prayers and meditation for a possible explanation of the nexus between the spiritual network support system (SNSS) as a component of psychosocial conditions, implicated in social signal transduction, and the gene expression correlate. With the intent to incorporate SNSS in human psychosocial conditions, we assessed the available data on bereavement, loss of spouse, loneliness, social isolation, low socio-economic status (SES), chronic stress, low social status, social adversity (SA) and early life stress (ELS), as surrogates for spiritual support network connectome. Adverse human psychosocial conditions have the tendency for impaired gene expression through an up-regulated conserved transcriptional response to adversity (CTRA) gene expression via social signal transduction, involving the sympathetic nervous system (SNS), beta-adrenergic receptors, the hypothalamus-pituitary-adrenal (HPA) axis and the glucocorticoid response. This review specifically explored CTRA gene expression and the nuclear receptor subfamily 3 group C member 1 (NR3C1) gene, a glucocorticoid receptor gene, in response to stress and the impaired negative feedback, given allostatic overload as a result of prolonged and sustained stress and social isolation as well as the implied social interaction associated with religiosity. While more remains to be investigated on psychosocial and immune cell response and gene expression, current data on human models do implicate appropriate gene expression via the CTRA and NR3C1 gene in the SNSS as observed in meditation, yoga and thai-chi, implicated in malignant neoplasm remission. However, prospective epigenomic studies in this context are required in the disease causal pathway, prognosis and survival, as well as cautious optimism in the application of these findings in clinical and public health settings, due to unmeasured and potential confoundings implicated in these correlations.

Aberrant Epigenomic Modulation of Glucocorticoid Receptor Gene (NR3C1) in Early Life Stress and Major Depressive Disorder Correlation: Systematic Review and Quantitative Evidence Synthesis.

Early life stress (ELS) induced by psychological trauma, child maltreatment, maternal separation, and domestic violence predisposes to psycho-behavioral pathologies during adulthood, namely major depressive disorder (MDD), anxiety, and bipolar affective disorder. While environmental data are available in illustrating this association, data remain to be established on the epigenomic underpinning of the nexus between ELS and MDD predisposition. Specifically, despite the observed aberrant epigenomic modulation of the NR3C1, a glucocorticoid receptor gene, in early social adversity and social threats in animal and human models, reliable scientific data for intervention mapping in reducing social adversity and improving human health is required. We sought to synthesize the findings of studies evaluating (a) epigenomic modulations, mainly DNA methylation resulting in MDD following ELS, (b) epigenomic modifications associated with ELS, and (c) epigenomic alterations associated with MDD. A systematic review and quantitative evidence synthesis (QES) were utilized with the random effect meta-analytic procedure. The search strategy involved both the PubMed and hand search of relevant references. Of the 1534 studies identified through electronic search, 592 studies were screened, 11 met the eligibility criteria for inclusion in the QES, and 5 examined ELS and MDD; 4 studies assessed epigenomic modulation and ELS, while 2 studies examined epigenomic modulations and MDD. The dense DNA methylation of the 1F exon of the NR3C1, implying the hypermethylated region of the glucocorticoid receptor gene, was observed in the nexus between ELS and MDD, common effect size (CES) = 14.96, 95%CI, 10.06-19.85. With respect to epigenomic modulation associated with child ELS, hypermethylation was observed, CES = 23.2%, 95%CI, 8.00-38.48. In addition, marginal epigenomic alteration was indicated in MDD, where hypermethylation was associated with increased risk of MDD, CES = 2.12%, 95%CI, -0.63-4.86. Substantial evidence supports the implication of NR3C1 and environmental interaction, mainly DNA methylation, in the predisposition to MDD following ELS. This QES further supports aberrant epigenomic modulation identified in ELS as well as major depressive episodes involving dysfunctional glucocorticoid-mediated negative feedback as a result of allostatic overload. These findings recommend prospective investigation of social adversity and its predisposition to the MDD epidemic via aberrant epigenomic modulation. Such data will facilitate early intervention mapping in reducing MDD in the United States population.