Implementing SAFER Responses to Misconduct and Responding to Biased Patient Requests ASAP.

Background: In response to encounters involving misconduct, discrimination, and harassment toward healthcare workers, the Experience Training, Education, and Coaching (XTEC) team was tasked with empowering staff members to respond to biased requests and misconduct appropriately and consistently. The aim of this article is to discuss communication strategies for how to respond to patient bias and misconduct. Methods: XTEC developed a training program with two focused communication strategies: (1) SAFER, a stepped approach to respond to patient and visitor misconduct and (2) ASAP, an approach for responding to patient bias which we describe as requests related to race, religion, ethnicity, gender, and other personal attributes of staff. Intervention: SAFER ASAP workshops were delivered to 2154 health care professionals through 109 face-to-face training over a 15-month period between January 2019 and March 2020. All trainings were discussion- and scenario-based, ranging in duration from 60 to 90 min. Participants were given pre- and post-training test case scenarios, in which respondents wrote responses to a challenging behavior to assess skill attainment post-training. Results:Seventy-one percent demonstrated higher levels of response ability post-training, and 92% of respondents indicated they would likely recommend this training to others. Conclusions: SAFER ASAP is an effective communication training program for responding to patient and visitor bias and misconduct.

Loss of Id3 increases VCAM-1 expression, macrophage accumulation, and atherogenesis in Ldlr-/- mice.

OBJECTIVE: Inhibitor of differention-3 (Id3) promotes B cells homing to the aorta and atheroprotection in Apoe(-/-) mice. We sought to determine the impact of loss of Id3 in the Ldlr((-/-)) mouse model of diet-induced atherosclerosis and identify novel Id3 targets in the vessel wall. METHODS AND RESULTS: Ex vivo optical imaging confirmed that Id3((-/-)) Ldlr((-/-)) mice have significantly fewer aortic B cells than Id3((+/+)) Ldlr(-/-) mice. After 8 and 16 weeks of Western diet, Id3((-/-)) Ldlr((-/-)) mice developed significantly more atherosclerosis than Id3((+/+)) Ldlr((-/-)) mice, with Id3(+/-) Ldlr(-/-) mice demonstrating an intermediate phenotype. There were no differences in serum lipid levels between genotypes. Immunostaining demonstrated that aortas from Id3((-/-)) Ldlr((-/-)) mice had greater intimal macrophage density and C-C chemokine ligand 20 and vascular cell adhesion molecule 1 (VCAM-1) expression compared with Id3((+/+)) Ldlr(-/-) mice. Real-time polymerase chain reaction demonstrated increased VCAM-1 mRNA levels in the aortas of Id3(-/-) Ldlr(-/-) mice. Primary vascular smooth muscle cells from Id3((-/-)) mice expressed greater amounts of VCAM-1 protein compared with control. Gain and loss of function studies in primary vascular smooth muscle cells identified a role for Id3 in repressing VCAM-1 promoter activation. Chromatin immunoprecipitation demonstrated interaction of E12 with the VCAM-1 promoter, which is inhibited by Id3. CONCLUSIONS: Id3 is an atheroprotective transcription regulator with targets in both B cells and vessel wall cells leading to reduced macrophage accumulation and reduced atherosclerosis formation.