Evaluation of an assessment model to reduce waitlist times for occupational therapy in a rural community health setting.

OBJECTIVE: Community occupational therapy services have seen an increase in demand over the last three years, resulting in longer waitlist times for service provision, particularly in rural areas where it is difficult to recruit experienced occupational therapists. Utilising a demand management model, the Basic Assessment Model Pre-Screening Tool was developed by a team of Occupational Therapists and allied health assistants to decrease client waitlist times at one rural community health service. DESIGN: An evaluation of the implementation of an assessment model with comparison of quantitative data pre and post intervention. SETTING: Rural Community Health Service in Victoria, Australia PARTICIPANTS: 456 clients that were registered as community-based clients requiring occupational therapy services. MAIN OUTCOME MEASURE: Following the implementation of the newly developed Basic Assessment Model the number of occupational therapy assessments increased and there was a decrease in the median wait time that clients were on the waitlist in comparison to pre implementation. RESULTS: There was a statistically significant decrease (p<0.001) in the median number of days spent on the waitlist for the post intervention group (80 days) compared to the pre intervention group (105 days). CONCLUSION: The results of this study suggest that waiting lists for community occupational therapy services can be reduced by implementing this basic assessment model ultimately improving the health outcomes of clients.

Normalizing glycosphingolipids restores function in CD4+ T cells from lupus patients.

Patients with the autoimmune rheumatic disease systemic lupus erythematosus (SLE) have multiple defects in lymphocyte signaling and function that contribute to disease pathogenesis. Such defects could be attributed to alterations in metabolic processes, including abnormal control of lipid biosynthesis pathways. Here, we reveal that CD4+ T cells from SLE patients displayed an altered profile of lipid raft-associated glycosphingolipids (GSLs) compared with that of healthy controls. In particular, lactosylceramide, globotriaosylceramide (Gb3), and monosialotetrahexosylganglioside (GM1) levels were markedly increased. Elevated GSLs in SLE patients were associated with increased expression of liver X receptor ß (LXRß), a nuclear receptor that controls cellular lipid metabolism and trafficking and influences acquired immune responses. Stimulation of CD4+ T cells isolated from healthy donors with synthetic and endogenous LXR agonists promoted GSL expression, which was blocked by an LXR antagonist. Increased GSL expression in CD4+ T cells was associated with intracellular accumulation and accelerated trafficking of GSL, reminiscent of cells from patients with glycolipid storage diseases. Inhibition of GSL biosynthesis in vitro with a clinically approved inhibitor (N-butyldeoxynojirimycin) normalized GSL metabolism, corrected CD4+ T cell signaling and functional defects, and decreased anti-dsDNA antibody production by autologous B cells in SLE patients. Our data demonstrate that lipid metabolism defects contribute to SLE pathogenesis and suggest that targeting GSL biosynthesis restores T cell function in SLE.