Consequences of COVID-19 Vaccine Hesitancy Among Healthcare Providers During the First 10 Months of Vaccine Availability: Scoping Review.

BACKGROUND: Throughout the COVID-19 pandemic, healthcare providers (HCPs)-including nurses-have played important roles in the vaccination effort. It is expected that COVID-19 vaccine hesitancy among HCPs has numerous consequences; however, the scope of these consequences and their impacts on providers, patients, and the broader healthcare system remained unclear. PURPOSE: To identify existing and emerging evidence to understand the state of knowledge of the consequences of COVID-19 vaccine hesitancy among HCPs. METHODS: A scoping review was completed based upon the JBI scoping review methodology. The databases searched included OVID Medline, EBSCOhost CINAHL, ProQuest Nursing and Allied Health Source, ProQuest APA PsycInfo, and ProQuest Dissertations and Theses. The final literature search was completed on June 2, 2022. Studies were screened and retrieved based on predefined inclusion and exclusion criteria using Covidence reference management software. Data extraction followed criteria recommended in the JBI scoping review framework with additional relevant variables identified by the authors. RESULTS: A total of 33 sources were included in the review. Consequences of HCP COVID-19 vaccine hesitancy were grouped under three themes and seven subthemes. Consequences affecting HCPs included health-related, psychosocial, and employment-related consequences. Consequences affecting patients pertained to COVID-19 vaccination communication and COVID-19 vaccination practices of HCPs. Consequences to the healthcare system involved consequences to coworkers and employment/attendance/staffing-related consequences. CONCLUSIONS: Healthcare provider COVID-19 vaccine hesitancy was found to have numerous consequences. By understanding the scope and extent of these consequences, healthcare leaders, researchers, and HCPs can work together to protect providers, patients, and healthcare systems.

"My problems aren't severe enough to seek help": Stress levels and use of mental health supports by Canadian hospital employees during the COVID-19 pandemic.

Due to the unique set of stressors associated with the COVID-19 pandemic, healthcare workers in acute care settings may be facing elevated rates of mental health symptomatology. The purpose of this study was to assess levels of depression, anxiety, and stress in a sample of healthcare employees working in hospitals and their use of formal and informal mental health supports. Data was gathered over a three-week period in December 2020 as COVID cases began to rise sharply in Ontario, Canada. Results from an online survey of 650 healthcare employees suggested that overall levels of depression, anxiety, and stress were mild. However, a significant minority of participants reported severe or extremely severe levels of depression (14.4%), anxiety (21.8%), and stress (13.5%). Levels of distress were higher among women, younger participants, those who did not work directly with COVID+ patients, and those who were redeployed. Use of formal mental health supports (e.g., Employee Assistance Plans, teletherapy) was very low (<10%), with the most frequently-reported reason for not using supports being "problems not severe enough to require this service". Implications are considered for healthcare policy decisions as hospital systems attempt to address the mental health needs of their employees.

High-Fidelity Simulation and Clinical Judgment of Nursing Students in a Maternal-Newborn Course.

Clinical judgment, one's ability to think like a nurse, is an essential skill for safe nursing practice. With the rise of simulation to replace clinical experiences, there is limited evidence regarding the effectiveness of simulation on the development of clinical judgment. This study explored differences in clinical judgment in maternal-newborn courses between undergraduate nursing students participating exclusively in simulation and those participating in hospital-based clinical experiences. Following completion of the clinical rotation, students participated in an evaluative maternal-newborn high-fidelity simulation experience that was recorded and evaluated using the Lasater's Clinical Judgment Rubric (2007). Lasater's Clinical Judgment Rubric scores between the simulation and clinical practice groups were compared using an independent sample t-test. There was no statistical difference in clinical judgment scores between the simulation and hospital-based clinical groups (t = -1.056, P = .295). Our findings suggest that simulation may be a comparable alternative to clinical experience in nursing education.

Effects of Maternal Vitamin D Supplementation on the Maternal and Infant Epigenome.

INTRODUCTION: Mothers and infants are at high risk for inadequate vitamin D status. Mechanisms by which vitamin D may affect maternal and infant DNA methylation are poorly understood. OBJECTIVE: This study quantified the effects of vitamin D3 supplementation on DNA methylation in pregnant and lactating women and their breastfed infants. MATERIALS AND METHODS: In this randomized controlled pilot study, pregnant women received vitamin D3 400 international units (IU) (n = 6; control) or 3,800 IU (n = 7; intervention) daily from late second trimester through 4-6 weeks postpartum. Epigenome-wide DNA methylation was quantified in leukocytes collected from mothers at birth and mother-infant dyads at 4-6 weeks postpartum. RESULTS: At birth, intervention group mothers showed DNA methylation gain and loss at 76 and 89 cytosine-guanine (CpG) dinucleotides, respectively, compared to controls. Postpartum, methylation gain was noted at 200 and loss at 102 CpGs. Associated gene clusters showed strongest biologic relevance for cell migration/motility and cellular membrane function at birth and cadherin signaling and immune function at postpartum. Breastfed 4-6-week-old infants of intervention mothers showed DNA methylation gain and loss in 217 and 213 CpGs, respectively, compared to controls. Genes showing differential methylation mapped most strongly to collagen metabolic processes and regulation of apoptosis. CONCLUSIONS: Maternal vitamin D supplementation during pregnancy and lactation alters DNA methylation in mothers and breastfed infants. Additional work is needed to fully elucidate the short- and long-term biologic effects of vitamin D supplementation at varying doses, which could hold important implications for establishing clinical recommendations for prenatal and offspring health promotion.

DNA Methylation Patterns in Peripheral Blood of Pregnant Women With Group B Streptococcus Colonization.

The primary risk factor for neonatal Group B streptococcus (GBS) infection, which is the leading cause of infectious neonatal morbidity and mortality, is maternal colonization. However, no definitive maternal risk factors for GBS colonization have been identified and no systematic efforts have been made to prevent maternal colonization. The purpose of this exploratory secondary analysis was to evaluate genome-wide DNA methylation patterns in maternal peripheral blood early in pregnancy for association with GBS colonization status in the third trimester. Genome-wide DNA methylation was analyzed from 18 nulliparous GBS-positive and -negative women (n = 9/group) recruited for a previous study. No statistically significant differences in baseline characteristics or DNA methylation in peripheral blood were identified between GBS-positive and -negative women in early pregnancy. The results suggest that DNA methylation patterns in peripheral blood are not associated with risk for GBS colonization.

First trimester vitamin D status and placental epigenomics in preeclampsia among Northern Plains primiparas.

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.

DNA methylation as a biomarker for preeclampsia.

BACKGROUND: Preeclampsia contributes significantly to pregnancy-associated morbidity and mortality as well as future risk of cardiovascular disease in mother and offspring, and preeclampsia in offspring. The lack of reliable methods for early detection limits the opportunities for prevention, diagnosis, and timely treatment. PURPOSE: The purpose of this study was to explore distinct DNA methylation patterns associated with preeclampsia in both maternal cells and fetal-derived tissue that represent potential biomarkers to predict future preeclampsia and inheritance in children. METHOD: A convenience sample of nulliparous women (N = 55) in the first trimester of pregnancy was recruited for this prospective study. Genome-wide DNA methylation was quantified in first-trimester maternal peripheral white blood cells and placental chorionic tissue from normotensive women and those with preeclampsia (n = 6/group). RESULTS: Late-onset preeclampsia developed in 12.7% of women. Significant differences in DNA methylation were identified in 207 individual linked cytosine and guanine (CpG) sites in maternal white blood cells collected in the first trimester (132 sites with gain and 75 sites with loss of methylation), which were common to approximately 75% of the differentially methylated CpG sites identified in chorionic tissue of fetal origin. CONCLUSION: This study is the first to identify maternal epigenetic targets and common targets in fetal-derived tissue that represent putative biomarkers for early detection and heritable risk of preeclampsia. Findings may pave the way for diagnosis of preeclampsia prior to its clinical presentation and acute damaging effects, and the potential for prevention of the detrimental long-term sequelae.

First trimester dietary intake, biochemical measures, and subsequent gestational hypertension among nulliparous women.

INTRODUCTION: The purpose of this study was to evaluate the relationships between first-trimester dietary factors and biochemical measures and subsequent risk of gestational hypertension. METHODS: This pilot study used a prospective design utilizing a convenience sample of nulliparous women enrolled at their first prenatal visit. A total of 57 women completed the study. Participants were divided into 2 groups for data analysis: normotensive pregnancy and gestational hypertension. RESULTS: Nearly one-quarter of study participants (22.8%) developed gestational hypertension, of whom 84.6% had significant proteinuria meeting the criteria for preeclampsia. There were no significant differences in micronutrient or macronutrient dietary intakes between groups. Serum iron and zinc levels were lower for the gestational hypertension group compared with the normotensive pregnancy group (P ≤ .01). Low serum zinc levels were related to a risk of developing gestational hypertension (adjusted odds ratio, 0.930; 95% confidence interval, 0.872-0.992). DISCUSSION: Ensuring adequate intake of zinc and monitoring serum zinc levels in nulliparous pregnant women may help to prevent or contribute to early detection of gestational hypertension.

DNA methylation in complex disease: applications in nursing research, practice, and policy.

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.

Diet assessment methods: a guide for oncology nurses.

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.

YB-1 is upregulated during prostate cancer tumor progression and increases P-glycoprotein activity.

BACKGROUND: Currently, the main obstacle to curing advanced prostate cancer is development of androgen independence (AI), where malignant cells acquire the ability to survive in the absence of androgens. Our initial experimental approach used cDNA microarrays to characterize changes in gene expression in the LNCaP human prostate tumor model during progression to AI. The transcription factor Y-box binding protein (YB-1) was shown to be one of the genes upregulated. We focused on increased YB-1 expression during progression in clinical specimens, and further examined one of its downstream targets, P-glycoprotein (P-gp). METHODS: Northern blot analysis was performed on LNCaP tumor series, as well as immunohistochemical analyses of human prostate cancer tissue samples. YB-1 was transiently transfected and transport analysis were performed to analyze P-gp efflux activity. RESULTS: YB-1 expression is markedly increased during benign to malignant transformation and further following androgen ablation. In addition, increased YB-1 expression after castration in the LNCaP model is linked to upregulation of P-gp. We demonstrate that YB-1 upregulates P-gp activity resulting in a 40% intracellular decrease in the P-gp substrate vinblastine. We have also found that P-gp increases the efflux of the endogenous androgen, dihydrotestosterone (DHT), from prostate cells and leads to decreased androgen regulated gene expression. CONCLUSIONS: We hypothesize that early in prostate cancer progression, increased expression of YB-1 may increase P-gp activity which may in turn lower androgen levels in the prostate tumor cells. Suppression of androgen levels may activate cell survival pathways and lead to an adaptive survival advantage of androgen independent prostate cancer cells following androgen ablation therapy.

Disruption of androgen regulation in the prostate by the environmental contaminant hexachlorobenzene.

Hexachlorobenzene (HCB) is a persistent environmental contaminant that has the potential to interfere with steroid hormone regulation. The prostate requires precise control by androgens to regulate its growth and function. To determine if HCB impacts androgen action in the prostate, we used a number of methods. Our in vitro cell-culture-based assay used a firefly luciferase reporter gene driven by an androgen-responsive promoter. In the presence of dihydrotestosterone, low concentrations (0.5-5 nM) of HCB increased the androgen-responsive production of firefly luciferase and high concentrations of HCB (> 10 microM) suppressed this transcriptional activity. Results from a binding assay showed no evidence of affinity between HCB and the androgen receptor. We also tested HCB for in vivo effects using transgenic mice in which the transgene was a prostate-specific, androgen-responsive promoter upstream of a chloramphenicol acetyl transferase (CAT) reporter gene. In 4-week-old mice, the proportion of dilated prostate acini, a marker of sexual maturity, increased in the low HCB dose group and decreased in the high HCB dose mice. In the 8-week-old mice, there was a significant decrease in both CAT activity and prostate weight upon exposure to 20 mg/kg/day HCB. Therefore, in vitro and in vivo data suggest that HCB weakly agonizes androgen action, and consequently, low levels of HCB enhanced androgen action but high levels of HCB interfered. Environmental contaminants have been implicated in the rising incidence of prostate cancer, and insight into the mechanisms of endocrine disruption will help to clarify their role.