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Background: In the United States, Black women experience preterm birth (PTB; <37 weeks gestation) at more than 1.5 times the rate of non-Hispanic White women. Social determinants of health including the neighborhood environment have been recognized as contributing to the risk of PTB. Due to historical segregation, Black women are more likely to live in neighborhoods with higher levels of neighborhood disorder compared with White women. Perceived neighborhood disorder appears to be a risk factor for maternal psychological distress in Black women and psychological distress has mediated the association between neighborhood disorder and the risk for PTB. However, the biological pathways underpinning these associations are not clear. Objective: We examined the associations among neighborhood disorder; psychological distress; DNA methylation of six stress-related, glucocorticoid candidate genes (AVP, CRH, CRHBP, FKBP5, HSD11B2, NR3C1); and gestational age at birth among 44 Black pregnant women. Methods: Women who were 18–45 years old and 8–18 weeks gestation had blood drawn and completed questionnaires measuring perceived neighborhood disorder, neighborhood crime, and psychological distress. Results: Three CpG sites were associated with neighborhood disorder (cg03405789 [ CRH ], cg14939152 and cg15910486 [ NR3C1 ]). One CpG site, cg03098337 (FKBP5) was associated with psychological distress. Three of the identified CpG sites were located within gene CpG islands or shores—areas at which DNA methylation is known to affect gene transcription. Conclusion: These findings warrant further research to clarify intermediate biological pathways and potential biomarkers to identify women at risk for PTB. Identification of PTB risk early in pregnancy would allow for interventions to prevent PTB. [ABSTRACT FROM AUTHOR]

Preterm birth (PTB; <37 weeks gestation) rates have increased for 5 of the last 6 consecutive years in the United States. These rates are particularly alarming for U.S. non-Hispanic Black women who give birth prematurely at 1.5 times the rate of non-Hispanic White women. Previous research suggests that psychological stress is associated with PTB in Black women. However, the biological pathways by which stress alters birth timing are not clear. We examined DNA methylation (DNAm) in peripheral blood leukocytes in 6 glucocorticoid, stress-related genes in 44 (22 PTB; 22 term birth) pregnant Black women. Four cytosine-phosphate-guanine (CpG) sites were identified as differentially methylated (p < 0.05) between women with PTB and women with term births. The ability to identify stress-related biological markers that are associated with PTB among Black women would provide a critical step toward decreasing the PTB disparity among these women. Future studies should include larger sample sizes and gene expression analyses of the stress-related biological pathways to PTB. [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]

Junior faculty follow a research path replete with challenges as they strive to create knowledge in their area of interest while balancing new responsibilities. Unlike graduate school, where students focus inward on personal development, junior faculty must add responsibilities in ways that hold them accountable as members of a university. This special article deals with three themes of interest to new junior faulty launching research programs: personal development, collaboration and team development within university settings, and funding advice. Strategies in these areas provide guidance on navigating early careers and finding success in the academic setting. [ABSTRACT FROM AUTHOR]

Preeclampsia, one of four hypertensive disorders of pregnancy, has traditionally been characterized as new-onset hypertension and proteinuria developing after 20 weeks' gestation. It is, however, now understood to be a complex, progressive, multisystem disorder with a highly variable presentation and a number of potentially life-threatening complications. The American College of Obstetricians and Gynecologists Task Force on Hypertension in Pregnancy has refined preeclampsia diagnostic criteria accordingly, and as the disorder's pathogenesis has been more clearly defined, new targets for screening, diagnosis, prevention, and treatment have emerged. This clinical update provides a review of current practice related to preeclampsia risk assessment, prediction, and management. It discusses preeclampsia pathophysiology and points readers to valuable health care resources on the topic. [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]

Regulatory process may be altered in response to the intrauterine environment, leading to the development of altered growth trajectory and disease later in life. Previously, our lab reported reduced leptin levels in pregnant hypertensive Sprague-Dawley rat dams with placental insufficiency. The purposes of this study were to investigate the relationship between leptin levels, growth and hypertension in two generations of offspring exposed to placental insufficiency. Leptin levels were significantly different only at 12 weeks in female first generation offspring (p < 0.05). Variations in postnatal body and organ weights were evident in first generation females at 3 and 12 weeks of age. There were no significant correlations with plasma leptin levels and systolic blood pressure in offspring groups at any age point. Our findings indicate that fetal exposure to maternal hypertension and hypoleptinemia is associated with altered leptin and growth patterns in mature female offspring and not perpetuated to a second generation. [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]

Background: Leadership development, career advancement, and collaboration among scholars are essential to nurturing nursing research excellence and sustainability. The Midwest Nursing Research Society (MNRS) has incorporated several strategies to advance nursing science and to increase the pool of future nurse leaders. In this article, we describe the process, activities, and outcomes of the Leadership Academy (LA), an innovative initiative from MNRS developed to identify, engage, and nurture future generations of leaders. Methods: For the LA 2022 to 2023 period, the MNRS leaders selected a cohort of 5 nurse scholars and engaged them in activities to develop, enhance, and advance their leadership skills. By following the LA purposes, the cohort participated in monthly meetings with MNRS leaders, received individual mentoring sessions, assessed strengths and areas for further development, attended seminars, participated in a book club, and implemented a cohort project that focused on the promotion and support of early career scholars. Results: Outcomes showed increased knowledge about organizational governance, direction, and resource development; leadership confidence culminating with leadership positions inside and outside MNRS; career development plans; engagement with board members, and enhanced networking. Moreover, the cohort members planned and executed a well-attended conference special session that engaged a large group of scholars to discuss challenges and opportunities for career development at the MNRS Annual Conference. Conclusion: The MNRS LA is a thriving organizational initiative that promotes engagement and leadership skills development thereby increasing the pool of candidates confidently prepared to lead the nursing profession. [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]

Topic: Early‐life experiences, the transmission of health and disease within families, and the influence of cumulative risks as well as protective factors throughout life shape the trajectory of health, including mental health. Long‐term health trajectories established early in life are influenced by biologic, social, and environmental factors. Negative trajectories may be more salient if exposures to adversity occur during critical developmental periods. Purpose: The purpose of this brief is to (a) review pediatric health disparities related to depression and the intergenerational transmission of pediatric depression using a Life Course Health Development (LCHD) model and (b) provide recommendations for pediatric mental health research. Sources: Peer‐reviewed papers available for PubMed, CINAL, and Medline. Other sources include published books, papers, and gray materials. Conclusions: The LCHD model is a perspective to guide and foster new scientific inquiry about the development of mental health outcomes over the life course. The model enables synthesis of mental health, nursing, and public health, linking mental health prevention, risk reduction, and treatment in children. [ABSTRACT FROM AUTHOR]

An abstract of the article "Validation of DNA Methylation Patterns: Potential Biomarker for Heritable Risk of Preeclampsia" by Michelle L. Wright et al. is presented.

Background:The prevalence of variant alleles among single nucleotide polymorphisms (SNPs) is not well known for many minority populations. These population allele frequencies (PAFs) are necessary to guide genetic epidemiology studies and to understand the population specific contribution of these variants to disease risk. Large differences in PAF among certain functional groups of genes could also indicate possible selection pressure or founder effects of interest. The 50K SNP, custom genotyping microarray (CARe) was developed, focusing on about 2,000 candidate genes and pathways with demonstrated pathophysiologic influence on cardiovascular disease (CVD). Methods:The CARe microarray was used to genotype 216 unaffected controls in a study of pre-eclampsia among a Northern Plains, American Indian tribe. The allelic prevalences of 34,240 SNPs suitable for analysis, were determined and compared with corresponding HapMap prevalences for the Caucasian population. Further analysis was conducted to compare the frequency of statistically different prevalences among functionally related SNPs, as determined by the DAVID Bioinformatics Resource. Results:Of the SNPs with PAFs in both datasets, 9.8%,37.2% and 47.1% showed allele frequencies among the American Indian population greater than, less than and either greater or less than (respectively) the HapMap Caucasian population. The 2,547 genes were divided into 53 functional groups using the highest stringency criteria. While none of these groups reached the Bonferroni corrected p value of 0.00094, there were 7 of these 53 groups with significantly more or less differing PAFs, each with a probability of less than 0.05 and an overall probability of 0.0046. Conclusion:In comparison to the HapMap Caucasian population, there are substantial differences in the prevalence among an American Indian community of SNPs related to CVD. Certain functional groups of genes and related SNPs show possible evidence of selection pressure or founder effects. [ABSTRACT FROM AUTHOR]

Preceding studies have shown that cardiac cytochrome c oxidase (CCO) deficiency occurs in the offspring of Cu-deficient rats on postnatal days (PND) 15 and 21. In order to determine if the CCO deficiency resulted from low prenatal Cu intake rather than from low postnatal Cu intake, pups from dams fed AIN93G diet containing 1 mg Cu/kg (CuD dams) were cross fostered to dams fed diet containing 6 mg Cu/kg (CuA dams) and vice versa on PND 1. Pups that remained with their birth dams served as controls. All dams began dietary treatment with either CuD or CuA diets 3 weeks before conception and remained on their respective diets until PND 21. On PND 21, CCO activities (U/mg protein, mean±SEM) in isolated cardiac mitochondria were 3.25±0.06 in pups of CuA dams (N=26), 3.30±0.11 in pups of CuA dams cross fostered to CuD dams (N=8), 2.52±0.10 in pups of CuD dams cross fostered to CuA dams (N=10), and 1.81±0.07 in pups of CuD dams (N=18). CCO activity was lower (P<0.05, Tukey's test) in pups of CuDdams cross fostered to CuA dams compared to pups of CuA dams or pups of CuA dams cross fostered to CuD dams, but higher (P<0.05) compared to pups of CuD dams. Differences in heart Cu concentrations corresponded to the differences in CCO activity. These findings indicate that Cu intake during pregnancy has a greater influence than postnatal Cu intake on cardiac CCO in the first generation. [ABSTRACT FROM AUTHOR]

• We examined lifetime stressors and inflammation in Black pregnant women. • Greater lifetime stressor severity was related to higher prenatal IL-1β levels. • Stressor severity mediated the association between stressors and IL-1β levels. • Prenatal IL-6 levels were higher preceding preterm versus full-term birth. • Therefore, assessing and reducing maternal stress is potentially important. Although Black American mothers and infants are at higher risk for morbidity and mortality than their White counterparts, the biological mechanisms underlying these phenomena remain largely unknown. To investigate the role that lifetime stressor exposure, perceived stressor severity, and systemic inflammatory markers might play, we studied how these factors were interrelated in 92 pregnant Black American women. We also compared inflammatory marker levels for women who did versus did not go on to give birth preterm. During the early third trimester, women completed the Stress and Adversity Inventory for Adults to assess the stressors they experienced over their lifetime. Women also provided blood samples for plasma interleukin (IL)-6, IL-8, IL-1β, and tumor necrosis factor (TNF)-α quantification. Preterm births were identified by medical record review. Controlling for relevant covariates, there were significant positive associations between average levels of both overall and acute perceived stressor severity and plasma IL-1β levels. Controlling for perceived stress at assessment and exposure to racial discrimination did not affect these results. Mediation models revealed that exposure to more chronic stressors was related to higher plasma IL-1β levels, as mediated by higher average levels of overall perceived stressor severity. Exposure to fewer acute stressors was related to higher plasma IL-1β levels, as mediated by higher average levels of acute perceived stressor severity. Finally, women who went on to give birth preterm had higher levels of plasma IL-6. These data thus highlight the potential importance of assessing and addressing lifetime stressor exposure among mothers before and during maternal-infant care. [ABSTRACT FROM AUTHOR]

Background: The etiology of pre-eclampsia (PE) is unknown; but it is accepted that normal pregnancy represents a distinctive challenge to the maternal immune system. C-reactive protein is a prominent component of the innate immune system; and we previously reported an association between PE and the CRP polymorphism, rs1205. Our aim was to explore the effects of additional CRP variants. The IBC (Cardiochip) genotyping microarray focuses on candidate genes and pathways related to the pathophysiology of cardiovascular disease. Methods: This study recruited 140 cases of PE and 270 matched controls, of which 95 cases met criteria as severe PE, from an American Indian community. IBC array genotypes from 10 suitable CRP SNPs were analyzed. A replication sample of 178 cases and 427 controls of European ancestry was also genotyped. Results: A nominally significant difference (p value <0.05) was seen in the distribution of discordant matched pairs for rs3093068; and Bonferroni corrected differences (P<0.005) were seen for rs876538, rs2794521, and rs3091244. Univariate conditional logistic regression odds ratios (OR) were nominally significant for rs3093068 and rs876538 models only. Multivariate logistic models with adjustment for mother's age, nulliparity and BMI attenuated the effect (OR 1.58, P = 0.066, 95% CI 0.97–2.58) for rs876538 and (OR 2.59, P = 0.050, 95% CI 1.00–6.68) for rs3093068. An additive risk score of the above two risk genotypes shows a multivariate adjusted OR of 2.04 (P = 0.013, 95% CI 1.16–3.56). The replication sample also demonstrated significant association between PE and the rs876538 allele (OR = 1.55, P = 0.01, 95% CI 2.16–1.10). We also show putative functionality for the rs876538 and rs3093068 CRP variants. Conclusion: The CRP variants, rs876538 and rs3093068, previously associated with other cardiovascular disease phenotypes, show suggestive association with PE in this American Indian population, further supporting a possible role for CRP in PE. [ABSTRACT FROM AUTHOR]

We explored the associations among perceived stress, depressive symptoms, loneliness, and social support during the COVID-19 pandemic; and differences in perceived stress, depressive symptoms, and social support prior to the pandemic and during the pandemic among pregnant Black women. A sample of 33 pregnant Black women who participated in the Biosocial Impact on Black Births (BIBB) and were still pregnant in May–June 2020 were invited to complete an online survey about their experiences during the pandemic. Fifteen women responded very much or somewhat to experiencing stress and anxiety because of the COVID-19 pandemic. Eight women had CES-D scores ≥23, which have been correlated with depression diagnosis. Women who reported higher levels of loneliness during the COVID-19 pandemic also reported higher levels of perceived stress and depressive symptoms and lower levels of social support during the pandemic. Women who reported lower levels of social support during the pandemic also reported higher levels of perceived stress and depressive symptoms during the pandemic. There were no changes in perceived stress, depressive symptoms, or social support prior to the pandemic and during the pandemic. Clinicians should assess for signs of loneliness and depressive symptoms for pregnant women and offer recommendations for therapy and support groups. [ABSTRACT FROM AUTHOR]

Epigenetic modifications are chemical changes that can modify gene expression without changing the sequence of the gene. These modifications are potentially identifiable and reversible, making the epigenome an important area of research for discovering biomarkers to identify those who may be at risk and providing therapeutic interventions to prevent adverse health outcomes. African Americans bear a disproportionate risk of adverse health outcomes (e.g., hypertension, cancer). Indeed, African American women experience preterm birth (PTB; <37 completed weeks gestation) at more than twice the rate of non-Hispanic White women. Research suggests that environmental influences may play a significant role in PTB outcomes for this population. However, the biological pathways by which these influences contribute to PTB are poorly understood. This paper describes research methods and ethical considerations for the collection and analysis of biological samples based on our study examining the epigenetic regulation of stress pathways in PTB in pregnant African American women. [ABSTRACT FROM AUTHOR]

Supplemental digital content is available in the text. Background: Despite strong prevention efforts and advances in neonatal care in recent decades, low birth weight remains a serious public health problem in the United States, and survivors remain at increased risk for lifelong problems including cognitive deficits. Current regional and local strategies for referral often rely on variable thresholds for birth weight and gestational age that may be poor analogues to cognitive risk. Improving early referral criteria offers many benefits, including improved cognitive outcomes for children and improved cost-effectiveness and resource utilization in resource-limited communities. Objectives: We hypothesized that social determinants measurable at birth or at birth hospital discharge, when combined with birth weight and gestational age, would offer an improvement over birth weight and gestational age alone in predicting cognitive test scores in school-aged children with low birth weight. Methods: We conducted a secondary analysis using a birth cohort of children from the Fragile Families and Child Wellbeing Study. We created a panel of maternal, familial, and community-level social determinant indicators from the data and examined associations with cognitive measures assessed at age of 9 years. Results: The final social determinant model was statistically significant and explained 35% of the total variance in composite test scores. The "standard care" model (birth weight and gestational age) only explained 9% of the variance. Discussion: Assessment of social determinants may offer improvement over traditional referral criteria to identify children most at risk of cognitive deficits after low birth weight. [ABSTRACT FROM AUTHOR]

Objective: We compared blood-based DNA methylation levels of endoglin (ENG) and transforming growth factor beta receptor 2 (TGFβR2) gene promoter regions between women with clinically-overt preeclampsia and women with uncomplicated, normotensive pregnancies. Methods: We used EpiTect Methyl II PCR Assays to evaluate DNA methylation of CpG islands located in promoter regions of ENG (CpG Island 114642) and TGFβR2 (CpG Island 110111). Preeclampsia was diagnosed based on blood pressure, protein, and uric acid criteria. N = 21 nulliparous preeclampsia case participants were 1:1 frequency matched to N = 21 nulliparous normotensive control participants on gestational age at sample collection (±2 weeks), smoking status, and labor status at sample collection. Methylation values were compared between case and control participant groups [(ENG subset: n = 20 (9 cases, 11 controls); TGFβR2 subset: n = 28 (15 cases, 13 controls)]. Results: The majority of the preeclampsia cases delivered at ⩾34 weeks' gestation (83%). Average methylation levels for ENG ([M ± (SD)]; Case Participant Group = 6.54% ± 4.57 versus Control Participant group = 4.81% ± 5.08; P =.102) and TGFβR2 (Case Participant Group = 1.50% ± 1.37 vs Control Participant Group = 1.70% ± 1.40; P =.695) promoter CpG islands did not differ significantly between the participant groups. Removal of 2 extreme outliers in the ENG analytic subset revealed a trend between levels of ENG methylation and pregnancy outcome (Case Participant Group = 5.17% ± 2.16 vs Control Participant Group = 3.36% ± 1.73; P =.062). Conclusion: Additional epigenetic studies that include larger sample sizes, investigate preeclampsia subtypes, and capture methylation status of CpG island shores and shelves are needed to further inform us of the potential role that ENG and TGFβR2 DNA methylation plays in preeclampsia pathophysiology. [ABSTRACT FROM AUTHOR]

Objective: This study examined whether cigarette smoking mediated the association of racial discrimination with depressive symptoms among pregnant Black women. Design: Cross‐sectional. Sample: Two hundred Black women at 8–29 weeks gestation. Measurements: Women completed questionnaires including the Experiences of Discrimination and the Center for Epidemiologic Studies‐Depression (CES‐D) scales, as well as questions about sociodemographic characteristics and cigarette smoking. Results: The mean age of the sample was 26.9 ± 5.7 years and the mean gestational age at data collection was 15.6 ± 5.7 weeks. Approximately 17% of women reported prenatal cigarette smoking; 27% had prenatal CES‐D scores ≥23, which have been correlated with depression diagnoses; and 59% reported ever (lifetime) experiencing discrimination in at least one situation (e.g., at work). Path analysis results indicated that the standardized indirect effect of experiences of racial discrimination on CES‐D scores through prenatal smoking was statistically significant (standardized indirect effect = 0.03; 95% CI: 0.001, 0.094; p =.042). Conclusion: Cigarette smoking during pregnancy partially mediated the association between lifetime experiences of racial discrimination and prenatal depressive symptoms among pregnant Black women. Smoking cessation programs should focus on identifying and treating depressive symptoms among pregnant Black women. [ABSTRACT FROM AUTHOR]

Objective: We compared blood-based DNA methylation levels of endoglin (ENG) and transforming growth factor beta receptor 2 (TGFβR2) gene promoter regions between women with clinically-overt preeclampsia and women with uncomplicated, normotensive pregnancies. Methods: We used EpiTect Methyl II PCR Assays to evaluate DNA methylation of CpG islands located in promoter regions of ENG (CpG Island 114642) and TGFβR2 (CpG Island 110111). Preeclampsia was diagnosed based on blood pressure, protein, and uric acid criteria. N = 21 nulliparous preeclampsia case participants were 1:1 frequency matched to N = 21 nulliparous normotensive control participants on gestational age at sample collection (±2 weeks), smoking status, and labor status at sample collection. Methylation values were compared between case and control participant groups [(ENG subset: n = 20 (9 cases, 11 controls); TGFβR2 subset: n = 28 (15 cases, 13 controls)]. Results: The majority of the preeclampsia cases delivered at ⩾34 weeks' gestation (83%). Average methylation levels for ENG ([M ± (SD)]; Case Participant Group = 6.54% ± 4.57 versus Control Participant group = 4.81% ± 5.08; P =.102) and TGFβR2 (Case Participant Group = 1.50% ± 1.37 vs Control Participant Group = 1.70% ± 1.40; P =.695) promoter CpG islands did not differ significantly between the participant groups. Removal of 2 extreme outliers in the ENG analytic subset revealed a trend between levels of ENG methylation and pregnancy outcome (Case Participant Group = 5.17% ± 2.16 vs Control Participant Group = 3.36% ± 1.73; P =.062). Conclusion: Additional epigenetic studies that include larger sample sizes, investigate preeclampsia subtypes, and capture methylation status of CpG island shores and shelves are needed to further inform us of the potential role that ENG and TGFβR2 DNA methylation plays in preeclampsia pathophysiology. [ABSTRACT FROM AUTHOR]

Low birth weight is an ongoing public health problem with severe consequences for those affected, including early morbidity and mortality and elevated risk for lifelong deficits in cognitive function. These deficits can be ameliorated by early intervention in many cases. To contribute to criteria for earlier identification of at-risk children prior to the onset of delays or deficits, we examined relationships between three gene candidates— SLC6A4, BDNF, COMT— and cognitive outcomes at school age in a secondary analysis of existing data from a nationally representative cohort. Single nucleotide polymorphism rs4074134, a variant of BDNF, and a rare insertion/deletion in the intron region of SLC6A4 were significant predictors of cognitive performance. Our final model predicted 17% of the variance in composite cognitive test scores among children with low birth weight at school age (F = 96.36, p <.001, R 2 =.17). Specifically, children homozygous for cytosine at rs4074134 scored.62 standard deviations higher on a measure of global cognition than children with one or more thymine. Similarly, children with an extra-long copy number variant of SLC6A4 scored.88 standard deviations higher than children who had one or more short forms of the gene. These findings support the potential for an approach to identifying children with low birth weights who are most at need of early intervention services. Future research should focus on validation of these findings in an independent sample and confirmation of the biological mechanisms through which these genes influence cognitive development. [ABSTRACT FROM AUTHOR]

Formidable health problems are often best addressed by teams of scientists with varied expertise. This diversity among team members and complexities in managing teams can lead to challenges in designing, funding, conducting, and reporting research. Team science difficulties can be addressed by sophisticated planning, frequent reassessment and realignment of team strategies with goals, and consistent transparent communication. This article addresses specific strategies to build and sustain research teams, manage team meetings, strategically develop publications and grants, thrive in the midst of disciplinary and individual team member differences, embrace new ideas and change to maintain creativity, and build future team scientists and projects. The potential value in team science justifies the effort required to build and maintain efficient and effective research teams. [ABSTRACT FROM AUTHOR]

Exposure to chronic stress such as living in disadvantaged neighborhoods has been related to cardiovascular disease (CVD). Chronic stress may increase the risk for CVD by increasing levels of systemic inflammation (e.g., higher levels of pro-inflammatory cytokines). Differential DNA methylation of inflammation-related candidate genes is also related to higher risk for CVD. Thus, the purpose of this review was to examine the association of neighborhood disadvantage with DNA methylation. A search of literature was conducted using Scopus, CINAHL, PubMed, Medline, and Embase databases. The keywords neighborhood, neighborhood disorder, neighborhood crime, neighborhood violence, neighborhood safety, built environment, and housing vacancy were combined with the keywords DNA methylation and epigenetics. Five studies were included in this review (n = 3 adult blood samples and n = 2 fetal blood samples). Four of the five studies reported an association of neighborhood socioeconomic status, social environment, and crime with either global or gene-specific DNA methylation. Only two studies examined the association of neighborhood disadvantage with inflammation-related candidate genes. One of these studies found a significant association of neighborhood socioeconomic disadvantage and social environment with DNA methylation in inflammation-related candidate genes. Thus, data are limited on the association between neighborhood disadvantage and DNA methylation of inflammation-related candidate genes, as well as genes in other potential mechanistic pathways including psychosocial stress, toxin response, and adiposity. Future studies should examine these associations and the potential epigenetic mechanisms by which neighborhood disadvantage increases the risk for CVD. [ABSTRACT FROM AUTHOR]

Publication in refereed journals is an important responsibility of PhD-prepared nurses. Specialized writing skills are crucial for effective professional publication. The capacity to develop and publish articles is best learned during doctoral education. This Western Journal of Nursing Research Editorial Board Special Article addresses multi-dimensional strategies to develop authorship competence among doctoral students. The article outlines structured PhD program experiences to provide the context for students to develop authorship capacity. The authors identify multi-faceted faculty endeavors and student activities that are essential to foster authorship competence. Students who embrace opportunities to acquire authorship qualifications will be well prepared for their post-graduation role as stewards of the nursing discipline. [ABSTRACT FROM AUTHOR]

Getting turned down for grant funding or having a manuscript rejected is an uncomfortable but not unusual occurrence during the course of a nurse researcher’s professional life. Rejection can evoke an emotional response akin to the grieving process that can slow or even undermine productivity. Only by “normalizing” rejection, that is, by accepting it as an integral part of the scientific process, can researchers more quickly overcome negative emotions and instead use rejection to refine and advance their scientific programs. This article provides practical advice for coming to emotional terms with rejection and delineates methods for working constructively to address reviewer comments. [ABSTRACT FROM AUTHOR]

Objective. To determine the prevalence in an American Indian population of genetic variants with putative effects on endothelial function and determine whether they are associated with preeclampsia. Methods. Five genetic polymorphisms potentially related to endothelial function in the NOS3, GNB3, and DDAH1 genes were genotyped from a total of 101 cases, 198 controls, and an additional 110 population-based controls among an American Indian population. Results. The minor allele frequencies for NOS3 (rs1799983, rs3918227), GNB3 (rs5442), and DDAH1 (rs10158674, rs233115) among those with and without PE in this population were 25, 10, 5, 11, and 30%%, respectively. Although not statistically significant, the maximum risk associated with any of these SNPs was 2.22 (0.734-6.73, 95%% CI, p == 0.156) in a multivariate analysis of the A allele of the rs233115 SNP incorporated in a recessive model. Conclusion. Although endothelial dysfunction likely plays a role in the pathophysiology of PE, this study was unable to find evidence for an association between these five SNPs on three genes influencing endothelial function and PE. This may be due to insufficient power to detect an association, investigation of SNPs without linkage to risk of PE in this population or other factors. Investigation of additional SNPs in these or related genes and other populations seems warranted. [ABSTRACT FROM AUTHOR]

Citation Best LG, Nadeau M, Davis K, Lamb F, Bercier S, Anderson CM. Genetic variants, immune function, and risk of pre-eclampsia among American Indians. Am J Reprod Immunol 2012; 67: 152-159 Problem To determine the prevalence in an American Indian population of genetic variants with putative effects on immune function and determine if they are associated with pre-eclampsia (PE). Method of study In a study of 66 cases and 130 matched controls, six single nucleotide polymorphisms (SNP) with either previously demonstrated or postulated modulating effects on the immune system were genotyped. Allele frequencies and various genetic models were evaluated by conditional logistic regression in both univariate and multiply adjusted models. Results Although most genetic variants lacked evidence of association with PE, the minor allele of the CRP related, rs1205 SNP in a dominant model with adjustment for age at delivery, nulliparity, and body mass index, exhibited an odds ratio of 0.259 (95% CI of 0.08-0.81, P = 0.020) in relation to severe PE (48 cases). The allelic prevalence of this variant was 46.1% in this population. Conclusion Of the six SNPs related to immune function in this study, a functional variant in the 3′UTR of the CRP gene was shown to be associated with severe PE in an American Indian population. [ABSTRACT FROM AUTHOR]

Diet may play a significant role in cancer prevention, disease progression, and treatment tolerance. An in-depth search of the literature revealed limited information geared toward nurses about diet assessment methods used in research. The purpose of this review is to synthesize the evidence regarding diet assessment methods important in oncology studies. The method used varied based on the study size, duration, and research question. For example, studies focusing on mean nutrient intake of a group used a 24-hour dietary recall, estimated food diary or dietary record, or food frequency questionnaire. Studies investigating usual nutrient intake predominately used multiple 24-hour dietary recalls, dietary records, biomarkers, or food frequency questionnaires. Measuring dietary intake accurately in a cost-effective manner is a difficult task. Selection of the appropriate assessment tool is critical for the generation of quality data. Oncology nurses are increasing their involvement in nutrition research, and the findings from this review may promote a better understanding of the published and ongoing research in this important field of study. [ABSTRACT FROM AUTHOR]

Objective: To determine the prevalence of thrombophilic genetic variants in an American Indian population and determine if they are associated with preeclampsia.Methods: A total of 87 cases, 165 controls and an additional 75 population-based controls were genotyped for two thrombophilic polymorphisms.Results: The allelic prevalence of the factor V Leiden and 20210 G/A prothrombin variants in this population was 2.1% and 0.5% respectively. No statistically significant associations between these genetic variants and preeclampsia were found.Conclusion: The prevalence of thrombophilic variants is of possible public health significance for other morbidity; but perhaps not in relation to preeclampsia. [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]