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Objective: The objective of this formative study was to gather women's perspectives in the design and communication modalities of a health kiosk set within a Planned Parenthood setting to promote patient education about the Human papillomavirus (HPV) and to motivate uptake of the HPV vaccine., Methods: Twenty-four women aged 18-35 participated in in-depth one-on-one interviews at a Planned Parenthood health center, which were analyzed in code-associated categories using NVivo11 Pro., Results: Most women showed receptivity to using an on-site health kiosk, as well as QR codes linked to text messages, to receive HPV-related health information outside of the clinic setting and reminders. Participants provided suggestions for kiosk design and communication modalities., Conclusions: Among low-income women we interviewed at Planned Parenthood, increasing HPV vaccination rates necessitates engaging digital health tools which incorporate both the preferences and needs of vulnerable populations., Innovation: Designing a point-of-service health kiosk that 1) draws on user preferences early in the design phase, 2) integrates multiple communication technologies, and 3) disseminates culturally grounded HPV vaccination decisions narratives that are tailored to vaccination awareness level is a promising approach in reducing barriers to HPV vaccine education and vaccine uptake among low-income women at safety-net clinics., (© 2022 The Authors.)

Human papilloma virus (HPV) is the most common sexually transmitted infection in the United States. Disease-associated strains of HPV can cause genital warts and six cancer types. HPV-associated cervical cancer disproportionately impacts medically underserved women including Black and Latina women with respect to incidence, prevalence, and mortality rates. Although safe and effective vaccines are available, HPV vaccination rates remain low among low-income individuals and women of color. The current study examined individual and structural motivators and barriers to HPV vaccination among medically underserved women utilizing a Planned Parenthood health center in Southeast Pennsylvania. Guided by narrative engagement theory (NET), qualitative interviews (N = 24) were used to elicit HPV vaccine decision stories from both vaccinated and unvaccinated women. Using a phronetic iterative data analysis approach, we identified three motivators to vaccinate against HPV: (1) receiving an explicit vaccine recommendation from a healthcare provider (a structural determinant), (2) feeling empowered to take control of one's health (an individual determinant), and (3) knowing someone infected with HPV (an individual determinant). Among unvaccinated participants, barriers to HPV vaccination included: (1) not receiving an explicit vaccine recommendation from a healthcare provider (a structural determinant), (2) low perceived risk for acquiring HPV or that HPV is not severe (an individual determinant), and (3) lack of maternal support to vaccinate (a structural determinant). Healthcare providers are optimally positioned to fill the gap in prior missed vaccine opportunities and empower women by recommending HPV vaccination.

Adolescent COVID-19 vaccination has stalled at 53% in the United States. Vaccinating adolescents remains critical to preventing the continued transmission of COVID-19, the emergence of variants, and rare but serious disease in children, and it is the best preventive measure available to return to in-person schooling. We investigated parent-adolescent COVID-19 vaccine decision-making. Between 24 February and 15 March 2021, we conducted surveys and 12 focus groups with 46 parent-adolescent dyads in Southern California. Parents and adolescents completed a survey prior to participation in a focus group discussion, which focused on exploring COVID-19 vaccine acceptance or uncertainty and was guided by the 5C vaccine hesitancy model. Parents uncertain about vaccinating adolescents expressed low vaccine confidence and high COVID-19 disease risk complacency. Parents who accepted COVID-19 vaccination for adolescents expressed high confidence in health authority vaccine recommendations, high perceived COVID-19 risk, and collective responsibility to vaccinate children. Additionally, unique pandemic-related factors of vaccine acceptance included vaccinating for emotional health, resuming social activities, and vaccine mandates. Among parents, 46% were willing to vaccinate their adolescent, 11% were not, and 43% were unsure. Among adolescents, 63% were willing to vaccinate. Despite vaccine availability, 47% of adolescents remain unvaccinated against COVID-19. Factors associated with vaccine uncertainty and acceptability inform health care practitioner, school, community, and public health messaging to reach parents and adolescents.

Introduction: Twitter represents a mainstream news source for the American public, offering a valuable vehicle for learning how citizens make sense of pandemic health threats like Covid-19. Masking as a risk mitigation measure became controversial in the US. The social amplification risk framework offers insight into how a risk event interacts with psychological, social, institutional, and cultural communication processes to shape Covid-19 risk perception., Methods: Qualitative content analysis was conducted on 7,024 mask tweets reflecting 6,286 users between January 24 and July 7, 2020, to identify how citizens expressed Covid-19 risk perception over time. Descriptive statistics were computed for (a) proportion of tweets using hyperlinks, (b) mentions, (c) hashtags, (d) questions, and (e) location., Results: Six themes emerged regarding how mask tweets amplified and attenuated Covid-19 risk: (a) severity perceptions (18.0%) steadily increased across 5 months; (b) mask effectiveness debates (10.7%) persisted; (c) who is at risk (26.4%) peaked in April and May 2020; (d) mask guidelines (15.6%) peaked April 3, 2020, with federal guidelines; (e) political legitimizing of Covid-19 risk (18.3%) steadily increased; and (f) mask behavior of others (31.6%) composed the largest discussion category and increased over time. Of tweets, 45% contained a hyperlink, 40% contained mentions, 33% contained hashtags, and 16.5% were expressed as a question., Conclusions: Users ascribed many meanings to mask wearing in the social media information environment revealing that COVID-19 risk was expressed in a more expanded range than objective risk. The simultaneous amplification and attenuation of COVID-19 risk perception on social media complicates public health messaging about mask wearing., Competing Interests: No authors have competing interests.

Human dilated cardiomyopathy (DCM) is characterized by congestive heart failure and altered myocardial gene expression. Epigenetic changes, including DNA methylation, are implicated in the development of DCM but have not been studied extensively. Clinical human DCM and nonfailing control left ventricle samples were individually analyzed for DNA methylation and expressional changes. Expression microarrays were used to identify 393 overexpressed and 349 underexpressed genes in DCM (GEO accession number: GSE43435). Gene promoter microarrays were utilized for DNA methylation analysis, and the resulting data were analyzed by two different computational methods. In the first method, we utilized subtractive analysis of DNA methylation peak data to identify 158 gene promoters exhibiting DNA methylation changes that correlated with expression changes. In the second method, a two-stage approach combined a particle swarm optimization feature selection algorithm and a discriminant analysis via mixed integer programming classifier to identify differentially methylated gene promoters. This analysis identified 51 hypermethylated promoters and six hypomethylated promoters in DCM with 100% cross-validation accuracy in the group assignment. Generation of a composite list of genes identified by subtractive analysis and two-stage computation analysis revealed four genes that exhibited differential DNA methylation by both methods in addition to altered gene expression. Computationally identified genes (AURKB, BTNL9, CLDN5, and TK1) define a central set of differentially methylated gene promoters that are important in classifying DCM. These genes have no previously reported role in DCM. This study documents that rigorous computational analysis applied to microarray analysis of healthy and diseased human heart samples helps to define clinically relevant DNA methylation and expressional changes in DCM.

This study addresses how depletion of human cardiac left ventricle (LV) mitochondrial DNA (mtDNA) and epigenetic nuclear DNA methylation promote cardiac dysfunction in human dilated cardiomyopathy (DCM) through regulation of pyrimidine nucleotide kinases. Samples of DCM LV and right ventricle (n = 18) were obtained fresh at heart transplant surgery. Parallel samples from nonfailing (NF) controls (n = 12) were from donor hearts found unsuitable for clinical use. We analyzed abundance of mtDNA and nuclear DNA (nDNA) using qPCR. LV mtDNA was depleted in DCM (50%, P < 0.05 each) compared with NF. No detectable change in RV mtDNA abundance occurred. DNA methylation and gene expression were determined using microarray analysis (GEO accession number: GSE43435). Fifty-seven gene promoters exhibited DNA hypermethylation or hypomethylation in DCM LVs. Among those, cytosolic thymidine kinase 1 (TK1) was hypermethylated. Expression arrays revealed decreased abundance of the TK1 mRNA transcript with no change in transcripts for other relevant thymidine metabolism enzymes. Quantitative immunoblots confirmed decreased TK1 polypeptide steady state abundance. TK1 activity remained unchanged in DCM samples while mitochondrial thymidine kinase (TK2) activity was significantly reduced. Compensatory TK activity was found in cardiac myocytes in the DCM LV. Diminished TK2 activity is mechanistically important to reduced mtDNA abundance and identified in DCM LV samples here. Epigenetic and genetic changes result in changes in mtDNA and in nucleotide substrates for mtDNA replication and underpin energy starvation in DCM.

A mitochondrial matrix-specific p53 construct (termed p53-290) in HepG2 cells was utilized to determine the impact of p53 in the mitochondrial matrix following oxidative stress. H₂O₂ exposure reduced cellular proliferation similarly in both p53-290 and vector cells, and p53-290 cells demonstrating decreased cell viability at 1mM H₂O₂ (~85% viable). Mitochondrial DNA (mtDNA) abundance was decreased in a dose-dependent manner in p53-290 cells while no change was observed in vector cells. Oximetric analysis revealed reduced maximal respiration and reserve capacity in p53-290 cells. Our results demonstrate that mitochondrial matrix p53 sensitizes cells to oxidative stress by reducing mtDNA abundance and mitochondrial function., (Copyright © 2013. Published by Elsevier B.V.)

Purpose: To establish the phenotype of reproductive aging in our mouse model. To test the hypotheses that reproductive aging is associated with a decrease in mitochondrial abundance that could ultimately reflect dysfunction in oocytes., Methods: Breeding studies were performed in young and aged female virgin wild type C57BL6J mice to establish their reproductive phenotype by measuring time to conception, litter size, and live birth per dam. Individual oocytes were analyzed for mtDNA content. Transmission electron microscopy was used to study ultrastructure of mitochondria in oocytes., Results: Old females were found to have significantly prolonged time to conception and fewer surviving pups in their litters. Oocytes from old mice had 2.7-fold less mtDNA compared to younger controls (p < 0.001; 95 % CI 2.1-3.5). Decrease in mitochondrial organelle abundance in old animal's oocytes was confirmed with transmission electron microscopy. Distinct morphological changes were noted in mitochondria, suggesting altered mitochondrial biogenesis in the old animals' oocytes., Conclusions: Reproductive aging in mice is associated with reduced reproductive competence. Aging is associated with a significant decrease in number of mitochondria in oocytes. Our data support mitochondrial organelle loss and dysfunction in oocytes as a potential etiology for reproductive senescence.