An innovative medical school curriculum to address human papillomavirus vaccine hesitancy.

BACKGROUND: Vaccination rates against Human Papillomavirus (HPV) in the US remain alarmingly low. Physicians can significantly influence a parent's decision to vaccinate their children. However, medical education often lacks training on specific strategies for communicating with vaccine hesitant parents. METHODS: We created an innovative curriculum designed to teach medical students how to address HPV vaccine hesitancy. The curriculum consisted of (1) a presentation on the epidemiology, biology, and disease morbidity associated with HPV, (2) a video that teaches specific communication strategies and (3) role-playing simulations. This curriculum was delivered to medical students at two separate sites. Medical students were surveyed before and after completing the educational curriculum. The surveys assessed student comfort talking to HPV vaccine hesitant parents and their likelihood to recommend the HPV vaccine. RESULTS: Pre- and post-intervention surveys were completed by 101 of the 132 participants (77% response rate). After the intervention, student awareness of the benefits of the HPV vaccine increased by a mean of 0.82 points (Likert scale 1-5, p < 0.01) and student comfort talking to vaccine hesitant parents increased by a mean of 1.37 points (p < 0.01). Prior to the intervention, students more strongly recommended the HPV vaccine to females compared to males, but this gender disparity was eliminated after the intervention (p < 0.01). Personal vaccination status was independately associated with a higher likelihood of recommending the HPV vaccine both before and after the intervention. CONCLUSION: Our innovative curriculum improved medical student comfort level discussing HPV vaccination with hesitant parents and increased the perceived likelihood of recommending HPV vaccination. The intervention is easy to implement, scalable, and requires minimal resources. Educating future providers on this important topic has the potential to improve vaccination rates nationwide and thus should be considered for all medical students.

CD11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus.

Genetic variations in the ITGAM gene (encoding CD11b) strongly associate with risk for systemic lupus erythematosus (SLE). Here we have shown that 3 nonsynonymous ITGAM variants that produce defective CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link between reduced CD11b activity and the chronically increased inflammatory status in patients. Treatment with the small-molecule CD11b agonist LA1 led to partial integrin activation, reduced IFN-I responses in WT but not CD11b-deficient mice, and protected lupus-prone MRL/Lpr mice from end-organ injury. CD11b activation reduced TLR-dependent proinflammatory signaling in leukocytes and suppressed IFN-I signaling via an AKT/FOXO3/IFN regulatory factor 3/7 pathway. TLR-stimulated macrophages from CD11B SNP carriers showed increased basal expression of IFN regulatory factor 7 (IRF7) and IFN-ß, as well as increased nuclear exclusion of FOXO3, which was suppressed by LA1-dependent activation of CD11b. This suggests that pharmacologic activation of CD11b could be a potential mechanism for developing SLE therapeutics.

Nickel-catalyzed decarboxylative cross-coupling of perfluorobenzoates with aryl halides and sulfonates.

A Ni-catalyzed method for the coupling of perfluorobenzoates with aryl halides and pseudohalides is described. Aryl iodides, bromides, chlorides, triflates, and tosylates participate in these transformations to afford the products in good yields. Penta-, tetra-, and trifluorinated biaryl compounds are obtained using these newly developed Ni-catalyzed decarboxylative cross-coupling reactions.