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Resilience, thriving in the face of adversity, is a critical component of well-being in African American women. However, traditional definitions and approaches to operationalize resilience may not capture race- and gender-related resilience experiences of African American women. A more complete conceptualization of resilience may help facilitate future investigation of the mechanisms through which resilience influences health in this group. Our team conducted a scoping review of the literature published during twenty years, between 2000 and 2019, on resilience and health in African American women. We included a multidisciplinary set of databases (PubMed, CINAHL, PsycINFO, Scopus, Social Work Abstracts, Sociological Abstracts, Academic Search Premier). Using Covidence software a multi-step review process was conducted; 904 abstracts were initially screened for eligibility, 219 full-text studies were screened in stage two, and 22 remaining studies were reviewed for extraction. The studies reviewed revealed limitations of unidimensional approaches to conceptualizing/operationalizing resilience in African American women. The review highlighted culturally-relevant components of resilience including spirituality/religion, strength, survival, active coping, and social support. Findings highlight the importance of operationalizing resilience as a multidimensional construct so it can be optimally included in research designed to investigate the quality of life, cardiovascular risk, and other health outcomes in African American women. • Resilience, thriving in the face of adversity, is a critical component of well-being in African American women. • Existing definitions of resilience may not capture race- and gender-related experiences of African American women. • African American women's resilience includes spirituality/religion, strength, survival, active coping, and social support. • It is important to define resilience multidimensionally for research designed to improve health in African American women. [ABSTRACT FROM AUTHOR]

There is a dearth of literature describing factors supporting a successful transition from a career-development fellowship to resumption of the full complement of faculty roles. Because little is known about the transition back to the full faculty role, a subset of Robert Wood Johnson Foundation (RWJF) Nurse Faculty Scholars (NFS) was interviewed to evaluate the self-identified challenges and opportunities that the scholars faced and factors contributing to their success when they reassumed the full faculty role. A subset of scholars from cohorts beginning the RWJF NFS program between 2008 and 2012 (n = 10) was interviewed by members of the NFS National Advisory Committee. NFSs identified challenges and opportunities faced as they transitioned to their faculty roles following completion of the career development fellowship as well as the character of support received from individuals in their organizational influencing the experience of the faculty transition. Evaluation outcomes include recommendations for transition planning for home institutions, colleagues and fellows. NFSs identified transition challenges including managing multiple responsibilities and increased teaching demands coupled with loss of protected time and funding for scholarly work. Opportunities for career advancement were influenced by effective mentorship, institutional supports including advocacy and allocation of time and responsibilities consistent with continued research productivity. Issues contributing to a more difficult transition included non-supportive relationships among administrators and colleagues and newly assigned responsibilities that detracted from success in meeting expectations for tenure and promotion. Effective transition from fellow to faculty included plans for continued mentorship and stakeholder engagement of administration, mentors and faculty colleagues. Effective transition from fellow to the full complement of the faculty role benefits both the home institution and scholar. Positive outcomes may be contingent on scholar support and organizational investment during the transition period. • Fellowship transition to faculty requires a balance of responsibilities to support career development, tenure and promotion • Effective transition to the full faculty role includes intentional planning in anticipation of and after transition • Investment in successful transition of fellows to faculty reaps long term benefits for the home institution and individual. [ABSTRACT FROM AUTHOR]

The challenge to increase the diversity, inclusivity, and equity of nurse scientists is a critical issue to enhance nursing knowledge development, health care, health equity, and health outcomes in the United States. The purpose of this paper is to highlight the current nurse scholars in the Robert Wood Johnson Foundation (RWJF) Harold Amos Medical Faculty Development Program (AMFDP). Profiles and the programs of research and scholarship of the current AMFDP nurse scholars are described and discussed. Scholars share lessons learned, and how the AMFDP program has influenced their thinking and commitments to future action in service of nursing science, diversity efforts, legacy leadership, issues of health equity. RWJF has a history of supporting the development of nursing scholars. AMFDP is an example of legacy leadership program that contributes to a culture of health and the development of next-generation nursing science scholars. • The is a need to address issues of nursing faculty development with specific attention to diversity, inclusion. • The Robert Wood Johnson Foundation (RWJF) has a history of supporting faculty development of nurse-scholar-scientists. • This paper describes the Harold Amos Medical Faculty Development Program. [ABSTRACT FROM AUTHOR]

• The genome and the exposome affect epigenetic age and health over time. • Epigenetic age surpasses chronologic age in health and disease prediction. • Precision prevention may benefit from targeting biological indicators of aging. A rapidly expanding literature suggests that individuals of the same chronological age show significant variation in biological age. The purpose of this article is to review the literature surrounding epigenetic age as estimated by DNA methylation, involving the addition or removal of methyl groups to DNA that can alter gene expression without changing the DNA sequence. This state of the science literature review summarizes current approaches in epigenetic age determination and applications of aging algorithms. A number of algorithms estimate epigenetic age using DNA methylation markers, primarily among adults. Algorithm application has focused on determining predictive value for risk of disease and death and identifying antecedents to age acceleration. Several studies have incorporated epigenetic age to evaluate intervention effectiveness. As the research community continues to refine aging algorithms, there may be opportunity to promote health from a precision health perspective. [ABSTRACT FROM AUTHOR]

Abstract Rationale Psychological stress-induced cortisol elevations appear to contribute to preterm birth. Yet, some studies suggest that the biological ramifications of racial discrimination-associated stress are unique and may involve development of decreased glucocorticoid sensitivity despite normalized cortisol levels. Objective In this study, we examined the effects of racial discrimination on maternal cortisol output, leukocyte glucocorticoid sensitivity, and the degree of correspondence between cortisol levels and birth timing in an African American cohort. Method A generally healthy prospective cohort was enrolled at 28–32 weeks gestation (n = 91). The Experiences of Discrimination scale was administered, whole blood collected, and plasma cortisol levels, cytokine levels, and leukocyte counts quantified for examination of patterns of endogenous feedback. Results Racial discrimination in the mid-tertile was associated with greater maternal cortisol levels than the bottom tertile among women reporting internalizing responses (b* = 0.68, p = 0.001). Decreased leukocyte glucocorticoid sensitivity was witnessed at greater frequencies of experiences of racial discrimination, as evidenced by decreased correspondence between maternal cortisol levels and plasma IL-8 levels, monocyte counts, and lymphocyte counts (p values ≤ 0.043). The association between maternal cortisol levels and birth timing differed by discrimination tertile (p values ≤ 0.005), with greater cortisol levels predictive of earlier birth among women without (b* = −0.59, p < 0.001) but not with racial discrimination (p s ≥ 0.497). Conclusion We provide novel evidence of decreased glucocorticoid sensitivity at increasing frequency of exposure to racial discrimination. Our findings suggest that the biology of preterm birth may depend upon racial discriminatory exposures, favoring pathways dependent upon glucocorticoid-induced increases in leukocyte tissue surveillance versus glucocorticoid resistance-associated inflammatory aberrations at increasing levels of exposure. Precision approaches to prenatal care are sorely needed to combat preterm birth, particularly among African American women, with efforts dependent upon further research examining the pathways contributing to the syndrome dependent upon the totality of an individual's exposures. Highlights • Racial discrimination predicts lower maternal leukocyte glucocorticoid sensitivity. • Elevated cortisol levels predict earlier birth in women without past discrimination. • Findings suggest biology of preterm birth may be unique based on prior exposures. [ABSTRACT FROM AUTHOR]

Background Pending revisions to the Common Rule include topics consistent with respect for persons, justice, and beneficence for research subjects in studies using omics technologies and are relevant to omics research. Purpose Synthesize trends in bioethics, precision health, and omics nursing science for novice and experienced nursing scholars from which to consider bioethics questions. Methods Review topics addressed in the National Institute of Nursing Research (NINR) strategic plan, Common Rule pending revisions, and publications regarding human subjects protection policies. Discussion Omics research involves decisions regarding understandable informed consent, broad consent, data sharing, trust, equal benefit, equal access, societal variables, privacy, data security, and return of findings to participants. Conclusion Principles of respect for persons, justice, and beneficence as articulated in the Belmont report and reflected in the American Nurses Association (ANA) Code of Ethics provide guidance for human subjects protection procedures to advance omics and nursing science. [ABSTRACT FROM AUTHOR]

Prevention of disease is a cornerstone of nursing care. Through our endeavors in research, teaching, and clinical care, nurses consistently seek to change the trajectory of disease development. The theoretical framework known as the Developmental Origins of Health and Disease (DOHaD) offers a new lens that shifts the current disease prevention paradigm upstream, encouraging intensified care of pregnant girls/women, neonates, and infants. This new focus parallels other emerging ecobiodevelopmental, life-course theories, which identify the long-term impact of early environments and stressors on the later risk of chronic adult diseases. Nurses have the potential to influence the health of multiple generations by incorporating DOHaD perspectives and interventions into their research and patient care. [ABSTRACT FROM AUTHOR]

Preparing the next generation of nursing scientists to conduct high-impact, competitive, sustainable, innovative, and interdisciplinary programs of research requires that the curricula for PhD programs keep pace with emerging areas of knowledge and health care/biomedical science. A field of inquiry that holds great potential to influence our understanding of the underlying biology and mechanisms of health and disease is omics. For the purpose of this article, omics refers to genomics, transcriptomics, proteomics, epigenomics, exposomics, microbiomics, and metabolomics. Traditionally, most PhD programs in schools of nursing do not incorporate this content into their core curricula. As part of the Council for the Advancement of Nursing Science's Idea Festival for Nursing Science Education, a work group charged with addressing omics preparation for the next generation of nursing scientists was convened. The purpose of this article is to describe key findings and recommendations from the work group that unanimously and enthusiastically support the incorporation of omics content into the curricula of PhD programs in nursing. The work group also calls to action faculty in schools of nursing to develop strategies to enable students needing immersion in omics science and methods to execute their research goals. [ABSTRACT FROM AUTHOR]

Aims As maternal vitamin D status has been associated with preeclampsia, the purpose of this study was to determine variations in DNA methylation patterns and associated protein expression in placental genes regulating vitamin D metabolism. Main methods A convenience sample of 48 pregnant nulliparous women, including 11 later diagnosed with preeclampsia, were recruited in this prospective study. Using a case–control design in two groups of women, we administered a food frequency questionnaire to determine vitamin D dietary intake. Laboratory measures included serum vitamin D levels (25[OH]D), DNA methylation patterns and protein expression in placental genes regulating vitamin D metabolism (1α-hydroxylase, CYP27B1; vitamin D receptor, VDR; retinoid X receptor, RXR) from placental tissue collected at delivery among those diagnosed with preeclampsia and those who remained normotensive throughout pregnancy. Key findings There were no significant differences in vitamin D dietary intake or mean serum 25[OH]D levels, although the proportion of women with deficient 25[OH]D levels was higher in the preeclampsia group (46%) than the normotensive group (20%). Placenta samples from women with preeclampsia also had increased DNA methylation of CYP27B1, VDR and RXR genes with lower protein expression levels limited to RXR. Significance Hypermethylation of key placental genes involved in vitamin D metabolism suggests uncoupling of processes that may interfere with placentation and availability of vitamin D at the maternal–fetal interface. [ABSTRACT FROM AUTHOR]

DNA methylation is an epigenomic modification that is essential to normal human development and biological processes. DNA methylation patterns are heritable and dynamic throughout the life span. Environmental exposures can alter DNA methylation patterns, contributing to the development of complex disease. Identification and modulation of environmental factors influencing disease susceptibility through alterations in DNA methylation are amenable to nursing intervention and form the basis for individualized patient care. Here we describe the evidence supporting the translation of DNA methylation analyses as a tool for screening, diagnosis, and treatment of complex disease in nursing research and practice. The ethical, legal, social, and economic considerations of advances in genomics are considered as a model for epigenomic policy. We conclude that contemporary and informed nurse scientists and clinicians are uniquely poised to apply innovations in epigenomic research to clinical populations and develop appropriate policies that guide equitable and ethical use of new strategies to improve patient care. [ABSTRACT FROM AUTHOR]

It has been reported previously that the offspring of rat dams consuming low dietary copper (Cu) during pregnancy and lactation experience a deficiency in cardiac cytochrome c oxidase (CCO) characterized by reduced catalytic activity and mitochondrial and nuclear subunit content after postnatal d 10. The present study was undertaken to determine whether the cardiac CCO deficiency was caused directly by low postnatal Cu intake or whether it was a prenatal effect of low Cu intake by the dams that became manifest postnatally. Dams were fed either a Cu-adequate diet (6 mg Cu/kg) or Cu- deficient diet (1 mg Cu/kg) beginning 3 wk before conception and throughout gestation and lactation. One day following parturitiori, several litters from Cu-adequate dams were cross fostered to Cu-deficient dams and several litters from Cu- deficient dams were cross fostered to Cu-adequate dams. Litters that remained with their birth dams served as controls. CCO activity, the content of the mitochondrial-encoded CCO subunit 1 )COX1), and the content of the nuclear-encoded subunit COX4 in cardiac mitochondria were reduced in the 21-d-old offspring of Cu-deficient dams. COX1 content was normal in the 21-d-old cross-fostered offspring of Cu-deficient dams, but CCO activity and COX4 were reduced. Cross fostering the offspring of Cu-adequate dams to Cu-deficient dams did not significantly affect CCO activity, COX1 content, or COX4 content in cardiac mitochondria of 21-d-old offspring. These data indicate that low prenatal Cu intake by dams was the determinant of CCO activity in cardiac mitochondria of the 21-d-old offspring and may have led to the assembly of a less-than-fully active holoenzyme. [ABSTRACT FROM AUTHOR]

It has been reported previously that the offspring of rat dams consuming low dietary copper (Cu) during pregnancy and lactation experience a deficiency in cardiac cytochrome c oxidase (CCO) characterized by reduced catalytic activity and mitochondrial and nuclear subunit content after postnatal d 10. The present study was undertaken to determine whether the cardiac CCO deficiency was caused directly by low postnatal Cu intake or whether it was a prenatal effect of low Cu intake by the dams that became manifest postnatally. Dams were fed either a Cu-adequate diet (6 mg Cu/kg) or Cu-deficient diet (1 mg Cu/kg) beginning 3 wk before conception and throughout gestation and lactation. One day following parturition, several litters from Cu-adequate dams were cross fostered to Cu-deficient dams and several litters from Cu-deficient dams were cross fostered to Cu-adequate dams. Litters that remained with their birth dams served as controls. CCO activity, the content of the mitochondrial-encoded CCO subunit 1 (COX1), and the content of the nuclear-encoded subunit COX4 in cardiac mitochondria were reduced in the 21-d-old offspring of Cu-deficient dams. COX1 content was normal in the 21-d-old cross-fostered offspring of Cu-deficient dams, but CCO activity and COX4 were reduced. Cross fostering the offspring of Cu-adequate dams to Cu-deficient dams did not significantly affect CCO activity, COX1 content, or COX4 content in cardiac mitochondria of 21-d-old offspring. These data indicate that low prenatal Cu intake by dams was the determinant of CCO activity in cardiac mitochondria of the 21-d-old offspring and may have led to the assembly of a less-than-fully active holoenzyme. [ABSTRACT FROM AUTHOR]

• African Americans are at heightened risk for coronary heart disease. • Biologic pathways are poorly understood. • In this study, depressive symptoms were associated with allostatic load in females. • Depressive symptoms and allostatic load predicted incident coronary heart disease. • Metabolic allostatic load was a partial mediator in the pathway among females. African Americans are at heightened risk for coronary heart disease (CHD), with biologic pathways poorly understood. We examined the role of allostatic load (AL) in the association of depressive symptoms with incident CHD among 2,670 African American men and women in the prospective Jackson Heart Study. Depressive symptoms were quantified using the Center for Epidemiologic Studies Depression Scale (CES-D). Incident CHD was ascertained by self-report, death certificate survey, and adjudicated medical record surveillance. Baseline AL was quantified using biologic parameters of metabolic, cardiovascular, immune, and neuroendocrine subsystems and as a combined meta-factor. Sequential models adjusted for demographic, socioeconomic, and behavioral covariates, stratified to examine differences by sex. Greater depressive symptomatology was associated with greater metabolic, cardiovascular, and immune AL (p -values≤0.036) and AL meta-factor z-scores (p = 0.007), with findings driven by observations among females. Each 1-point increase in baseline depressive symptomatology, and 1-SD increase in metabolic AL, neuroendocrine AL, and AL meta-factor z-scores was associated with 3.3%, 88%, 39%, and 130% increases in CHD risk, respectively (p- values <0.001). Neuroendocrine AL and AL meta-factor scores predicted incident CHD among males but not females in stratified analyses. Metabolic AL partially mediated the association of depressive symptoms with incident CHD (5.79% mediation, p = 0.044), a finding present among females (p = 0.016) but not males (p = 0.840). Among African American adults, we present novel findings of an association between depressive symptomatology and incident CHD, partially mediated by metabolic AL. These findings appear to be unique to females, an important consideration in the design of targeted interventions for CHD prevention. [ABSTRACT FROM AUTHOR]