Primary care collaborative practice in quality improvement: Description of an interprofessional curriculum.

PURPOSE: An innovative quality improvement (QI)-focused interprofessional training curriculum for pharmacy residents and other healthcare trainees is described. SUMMARY: Effective interprofessional collaboration and the ability to carry out QI initiatives are important skills for all healthcare trainees to develop when they are in training. To cultivate those skills, in 2011 a Veterans Affairs medical center in Idaho implemented a unique yearlong interprofessional curriculum for healthcare trainees, including postgraduate year 1 (PGY1) and postgraduate year 2 (PGY2) pharmacy residents, physician trainees in internal medicine, nurses, and psychologists. The curriculum has both didactic and experiential components. After attending a series of 1-hour workshops early in the academic year, trainees are assigned to interprofessional teams and work for the remainder of the year to complete QI projects. Over 100 trainees have participated in the interprofessional QI curriculum, with the majority of trainee projects based in the primary care setting. Pharmacy residents were involved in 62% of the projects completed in the 6 academic years ending with the 2016-17 year. CONCLUSION: Establishing an interprofessional QI curriculum allowed pharmacy residents in PGY1 and PGY2 programs to collaborate with other members of the healthcare team. Benefits include QI skills development, a greater understanding of QI initiatives at the institution, stronger relationships with other healthcare trainees and mentors, and improvements to patient care and safety and facility performance.

Cadmium-induced decrease in RUNX2 mRNA expression and recovery by the antioxidant N-acetylcysteine (NAC) in the human osteoblast-like cell line, Saos-2.

Exposure to cadmium poses a threat to human health, including increased susceptibility to developing the bone disease osteoporosis. Despite its recognized importance as an environmental toxin, little is known about how cadmium directly impacts bone-forming osteoblasts. We previously reported that cadmium induces apoptosis in human osteoblast-like Saos-2 cells. In this work, we hypothesize that cadmium exposure induces oxidative stress which leads to decreased RUNX2 mRNA expression and increased apoptotic death, and predict that the antioxidant NAC mitigates the damaging effects of cadmium. Oxidative stress is implicated in osteoporosis; furthermore the osteoblast transcriptional factor RUNX2 is reported to play a protective role against osteoporosis in postmenopausal women. Cells treated with 10 microM CdCl2 exhibited signs of oxidative damage including depletion in glutathione, increased reactive oxygen species formation, and enhanced lipid peroxidation. RUNX2 mRNA expression, by RT-PCR, was significantly reduced after exposure to 10 microM CdCl2. Pretreatment with the antioxidant NAC (1mM) prevented cadmium-induced decrease in RUNX2 mRNA and protected cells from apoptotic death. This study provides insight into the mechanisms underlying cadmium-induced osteotoxicity. In addition, this study distinguishes itself by identifying RUNX2 as a target for heavy metal-induced osteotoxicity.