Adolescent Participation in HPV Vaccine Clinical Trials: Are Parents Willing?

Approximately one-quarter of human papillomavirus (HPV) infections are acquired by adolescents, with a higher burden among racial/ethnic minorities. However, racial/ethnic minorities have been underrepresented in previous HPV vaccine trials. Ongoing and future HPV vaccine optimization trials would benefit from racially- and ethnically-diverse sample of adolescent trial participants. This study examined factors influencing parental willingness to consent to their adolescents' participation in HPV vaccine clinical trials and tested for possible racial differences. A convenience sample of parents of adolescents (N = 256) completed a cross-sectional survey. Chi square analyses were used to assess racial differences in parental HPV vaccine awareness and intentions and willingness to consent to their child participating in an HPV vaccine clinical trial. Ordinal logistic regression was used to identify factors associated with willingness. Approximately 47% of parents were willing to allow their adolescent to participate in HPV vaccine clinical trials (30.7% African American and 48.3% Caucasian, p = .081). African Americans had lower HPV vaccine awareness (p = .006) but not lower intentions to vaccinate (p = .086). Parental willingness was positively associated with the following variables: Child's age (p < .039), Perceived Advantages of HPV Vaccination for Adolescents (p = .002), Parental Trust in Medical Researchers (p < .001), and Level of Ease in Understanding Clinical Trial Information (p = .010). Educating parents about the advantages of HPV vaccines for younger adolescents using low-literacy educational materials and building trust between parents and researchers may increase parental willingness to consent to adolescent participation in HPV vaccine clinical trials.

Self-Administration of a Boar Priming Pheromone Stimulates Puberty in Gilts without Boar Exposure.

Labor is in short supply in animal agriculture. One time-consuming task is estrus detection in gilts. Stimulation with a live boar causes the onset of puberty in young gilts. Typically, a live boar is used to stimulate and identify estrus in the gilts by exposing the gilts to him. Recently, a boar pheromone (BB) was developed to replace the use of a live boar for sows. Additionally, a novel automatic sprayer used as environmental enrichment (EE) by gilts for the self-administration of BB has been developed by this laboratory. A commercial study was conducted to determine whether the use of a live boar could be replaced with a simple EE sprayer, allowing gilts to self-administer BB. Our objective was to determine whether the number and percentage of gilts in estrus obtained using live boars was comparable to self-administration using an EE sprayer containing BB. A total of 242 gilts were randomly assigned to either a live boar (BOAR) or BB self-administration using the environmental enrichment (EE) sprayer. Gilts began simultaneous exposure to either the BOAR or the BB when they were about 4-5 months of age and this continued until they were found in estrus or were injured, died, or never cycled about 2 months later. A total of 83.3% of gilts with exposure to BOAR were identified in estrus and bred, while exposure to BB resulted in 92.9% of gilts reaching puberty and being bred (p < 0.05). The days to reach estrus were 11 days longer for gilts exposed to BB than BOAR. Eight percent more gilts were injured by the BOAR than by using BB (and no boar). The use of BB as a priming pheromone could prevent gilt injuries, save labor, and reduce costs for pig farmers while not inhibiting reproductive output.

MAP3K4 Controls the Chromatin Modifier HDAC6 during Trophoblast Stem Cell Epithelial-to-Mesenchymal Transition.

The first epithelial-to-mesenchymal transition (EMT) occurs in trophoblast stem (TS) cells during implantation. Inactivation of the serine/threonine kinase MAP3K4 in TS cells (TSKI4 cells) induces an intermediate state of EMT, where cells retain stemness, lose epithelial markers, and gain mesenchymal characteristics. Investigation of relationships among MAP3K4 activity, stemness, and EMT in TS cells may reveal key regulators of EMT. Here, we show that MAP3K4 activity controls EMT through the ubiquitination and degradation of HDAC6. Loss of MAP3K4 activity in TSKI4 cells results in elevated HDAC6 expression and the deacetylation of cytoplasmic and nuclear targets. In the nucleus, HDAC6 deacetylates the promoters of tight junction genes, promoting the dissolution of tight junctions. Importantly, HDAC6 knockdown in TSKI4 cells restores epithelial features, including cell-cell adhesion and barrier formation. These data define a role for HDAC6 in regulating gene expression during transitions between epithelial and mesenchymal phenotypes.