32 research outputs found

    Development and Evolution of a Model Interprofessional Education Program in Parkinson’s disease: A Ten-year Experience

    Get PDF
    OBJECTIVE This paper describes development, evolution and learner reactions in a model interprofessional education program for medical, nursing, physician assistant, occupational therapy, physical therapy, music therapy, social work and speech-language pathology practitioners. Sponsored by the National Parkinson Foundation (NPF) (currently Parkinson’s Foundation), Allied Team Training for Parkinson (ATTP) is a U.S.-based multi-day interprofessional education program in best practices for integrated, interprofessional team-based Parkinson’s disease (PD) care. NPF sponsored 26 ATTP trainings from 2003 to 2013. METHODS This mixed methods evaluation uses case study document review and observation to outline ATTP curriculum development, evolution, and implementation challenges. Learner-perceived effectiveness ratings, knowledge change, pre-post ratings on the Team Skills Scale, confidence in working with people with PD and caregivers, and trainee-reported practice changes at 6-month follow-up were collected. RESULTS Qualitative results identified multiple factors in building an effective interprofessional education program, including interprofessional team practice opportunities through case-based learning, engaging care networks and continuous feedback loops for program improvement. Quantitative results showed that trainees across professions, geographic regions and work settings rated the overall program and curriculum effectiveness, amount of new knowledge and knowledge change very highly. ATTP resulted in significant post-training improvement in team skills, confidence in working with PD, and post-training self-reported practice changes. CONCLUSION Findings suggest that ATTP is an effective interprofessional education program that could be replicated or adapted to other settings and neurodegenerative or chronic illnesses. The model of combining interprofessional team training with disease-specific curriculum content appears to be an effective “next practice” in continuing professional development

    Does Progesterone Alter Toll-Like Receptor-Stimulated Monocyte Production of Cytokines?

    No full text
    OBJECTIVE: Current models for infection-mediated preterm birth suggest that bacteria stimulate the production of proinflammatory cytokines and cause the fetus to lose its immunological privileges. Pharmacological levels of progesterone (P4) have been proposed to inhibit preterm birth by suppressing such immune reactions that lead to rejection of the fetal allograft. Bacteria stimulate the production of proinflammatory cytokines through interactions with the Toll-Like Receptors (TLRs). We studied whether P4 alters TLR-2 and TLR-4 agonist-stimulated IL-1b and TNF-a production by human monocytes in vitro. STUDY DESIGN: Human monocytes (THP-1 cells) were plated and preincubated overnight. Progesterone was added at increasing doses of 0 to 10 mg/ ml and incubated for 24 h. Cells were then stimulated with 0 to 8 mg/ml Pam3Cys (a TLR-2 agonist), 0 to 10 mg/ml Lipopolysaccharide (LPS, a TLR-4 agonist) or 0 to10 mg/ml Lipid A (a TLR-4 agonist) for an additional 24 h. Concentrations of IL-1b and TNF-a in the conditioned medium were then quantified by ELISA. Each experiment was replicated three times. RESULTS: For monocytes stimulated with 1 mg/ml Pam3Cys, 1 mg/ml LPS, or 1 mg/ml Lipid A, pre-treatment with 10 mg/ml P4 inhibited the production of TNF-a but enhanced the production of IL-1b. Progesterone at this superphysiological concentration also inhibited the dose-dependent rise in TNF-a production but enhanced the dose-dependent rise in IL-1b production caused by each TLR agonist. CONCLUSION: High levels of P4 inhibit the production of TNF-a but increase the production of IL-1b by monocytes stimulated with TLR-2 or TLR-4 agonists. These results suggest that any potential immunomodulatory effects of P4 are similar for TLR-2 and TLR-4 mediated inflammation
    corecore