Home-based diabetes self-management coaching delivered by paraprofessionals: A randomized controlled trial.

This study evaluated paraprofessional-led diabetes self-management coaching (DSMC) among 94 clients with type 2 diabetes recruited from a Community Care Access Centre in Ontario, Canada. Subjects were randomized to standard care or standard care plus coaching. Measures included the Diabetes Self-Efficacy Scale (DSES), Insulin Management Diabetes Self-Efficacy Scale (IMDSES), and Hospital Anxiety and Depression Scale (HADS). Both groups showed improvement in DSES (6.6 + 1.5 vs. 7.2 + 1.5, p < .001) and IMDSES (113.5 + 20.6 vs. 125.7 + 22.3, p < .001); there were no between-groups differences. There were no between-groups differences in anxiety (p > .05 for all) or depression scores (p > .05 for all), or anxiety (p > .05 for all) or depression (p > .05 for all) categories at baseline, postintervention, or follow-up. While all subjects demonstrated significant improvements in self-efficacy measures, there is no evidence to support paraprofessional-led DSMC as an intervention which conveys additional benefits over standard care.

The role of BRCA1 and BRCA2 mutations in prostate, pancreatic and stomach cancers.

The association of germline mutations in the breast cancer susceptibility gene 1 (BRCA1) and the breast cancer susceptibility gene 2 (BRCA2) with the development of breast and ovarian cancers have been widely researched and recognised. It is known that these genes function at multiple sites in the body. Research has subsequently evolved into the connection of BRCA1/2 with cancers at other sites within the body. This review examines the association of BRCA1/2 germline gene mutations with prostate, pancreatic and stomach cancers. An extensive literature search revealed conflicting findings regarding the association of BRCA1/2 gene mutations with these cancers. Most studies suggest that there is an association between BRCA1/2 mutations and carcinoma of the prostate, pancreas and stomach, but some reports propose that such a correlation may be due to factors other than possessing a mutated BRCA1/2 gene, and other associations may be revealed as further epidemiological information becomes available. The review concludes that as more knowledge arises about the mechanisms of BRCA1/2 gene mutations, it should pave the way for future screening programmes to be applied effectively.

Immune activation in the peripheral blood of patients with acute ischemic stroke.

Lymphocytes, neutrophils and macrophages are found in the brain in areas of acute ischaemic stroke. There is also evidence of modulation of systemic immune function after stroke, with post-stroke immunosuppression being observed. Because lymphocytes are activated in the peripheral immune compartment, before entry to the target organ, we reasoned that activated lymphocytes would be present in the circulation, prior to entering the brain, in patients after stroke. Because immune responses are controlled by regulatory mechanisms, we also reasoned that the post-stroke immunosuppression would involve T regulatory cells. The aim of the study was to look for evidence of immune activation and alterations in regulatory T cells in the peripheral blood of patients after acute ischaemic stroke, in comparison to age-matched healthy controls and patients with other neurological diseases (OND), and to determine the phenotype of the activated cells. The percentages of total and activated T cells, B cells, monocyte/ macrophages, and NK/NK-T cells were determined by labelling peripheral blood leukocytes with specific cell surface markers and analysis with 4-colour flow cytometry. The percentages of activated T cells and regulatory T cells were significantly increased in patients with ischemic stroke compared to healthy subjects and patients with OND. There was also an increase in the percentage of CCR7+ T cells. There were no significant differences in the activation of other cell types. In conclusion, there is evidence of immune activation and Treg cells in acute ischaemic stroke.