Improving resident education through unstable chicken hips: a novel way to teach an infant hip examination.

Current clinical screening for infantile hip dysplasia relies on combined Ortolani and Barlow maneuvers, which have a quoted sensitivity and specificity of 74-98 and 84-99%, respectively. Teaching this delicate physical examination maneuver is difficult as it requires a distinct tactile feel. The purpose of this study is to validate a benchtop learning grocery-bought chicken simulator model of newborn hip instability through a pre- and post-test surveys. This model of hip dysplasia uses whole chickens. A posterior capsulotomy of the chicken's hip joint was performed to create instability. Provocative maneuvers to dislocate and relocate the hip were taught by a pediatric orthopedic surgeon. All participants completed an anonymous pre- and post-training surveys. A total of 58 participants were included in the study: 10 medical students, 13 pediatric residents, 15 orthopedic residents, and 20 orthopedic or pediatric attending physicians. The pediatric residents had performed the Barlow/Ortolani tests more than the orthopedic residents (96.15 ± 83.19 vs. 37.53 ± 60.89; P = 0.01); however, fewer pediatric residents reported feeling a positive examination (31 vs. 67%). The majority of the group agreed that the simulation felt and moved like an infant's hip (3.95 and 4.13; Likert five-point scale). The participants unanimously agreed that the model could be used to teach someone new to pediatrics the basic steps of the examination (4.91; Likert five-point scale) and should be implemented in the teaching curriculum (100%). The current study validates the benchtop model in teaching the clinical steps in detecting hip dysplasia. The model improved confidence and comfort level for all participants and proved to be a valuable tool for resident education in multiple specialties. By improving education with this model, we hope to improve early identification of hip dysplasia with increased accuracy across subspecialties.

Sensing Microbial Viability through Bacterial RNA Augments T Follicular Helper Cell and Antibody Responses.

Live vaccines historically afford superior protection, yet the cellular and molecular mechanisms mediating protective immunity remain unclear. Here we found that vaccination of mice with live, but not dead, Gram-negative bacteria heightened follicular T helper cell (Tfh) differentiation, germinal center formation, and protective antibody production through the signaling adaptor TRIF. Complementing the dead vaccine with an innate signature of bacterial viability, bacterial RNA, recapitulated these responses. The interferon (IFN) and inflammasome pathways downstream of TRIF orchestrated Tfh responses extrinsically to B cells and classical dendritic cells. Instead, CX3CR1+CCR2- monocytes instructed Tfh differentiation through interleukin-1ß (IL-1ß), a tightly regulated cytokine secreted upon TRIF-dependent IFN licensing of the inflammasome. Hierarchical production of IFN-ß and IL-1ß dictated Tfh differentiation and elicited the augmented humoral responses characteristic of live vaccines. These findings identify bacterial RNA, an innate signature of microbial viability, as a trigger for Tfh differentiation and suggest new approaches toward vaccine formulations for coordinating augmented Tfh and B cell responses.