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Peer support is effective in improving self-management behaviors and health outcomes among individuals with Type 2 diabetes. Volunteer peer support programs offer a cost-effective resource for diabetes self-management support; however, factors affecting the retention of volunteer peer leaders remain understudied. Herein, we examined factors associated with volunteer retention and satisfaction among 34 predominantly Mexican-origin peer leaders who assisted patients from a Federally Qualified Health Center located on the US/Mexico border with their diabetes management. Peer leaders completed surveys with open- and close-ended questions at baseline, 6 months and 12 months. Quantitative and qualitative data analyses were guided by the Volunteer Process Model. Using nonparametric Mann-Whitney U tests, self-efficacy as a peer leader at 6 months was most associated with interest to continue volunteering (P = 0.01), and satisfaction with support from the program at 12 months was most associated with interest to continue volunteering (P = 0.01). The qualitative data indicated that the relationship between the peer leaders and their patients was the primary factor for a satisfying volunteer experience. Future research should focus on increasing peer leaders' self-efficacy and satisfaction with program support and examine how organizations can support the development of the patient--peer relationship. Practitioners should consider appealing to volunteer peers' motivations to promote their retention.

Summary: Background: Obesity disproportionately affects Latino youth. Community clinics are an important resource, yet there is little evidence for the efficacy of clinic‐based approaches in this population. Objective: The purpose of this study was to test the efficacy of a clinic‐based intervention to lower body mass index (BMI) and improve body composition among overweight Latino children. Methods: A randomized trial (2 group × 3 repeated measures) was conducted among 297 randomly sampled, overweight paediatric patients (5–10 years old) and their parents. The 12‐month family‐based culturally tailored behavioural intervention (Luces de Cambio) was based on the 'traffic light' concepts to address behaviour change and was delivered by clinic health educators and mid‐level providers. The primary study outcome was child BMI (kg m−2) assessed at baseline, 6‐month (n = 191) and 12‐month (n = 201) post‐baseline. A subsample of the children was examined for overall and site‐specific adiposity using dual‐energy X‐ray absorptiometry (n = 79). Results: There were no significant intervention effects on child BMI (p > 0.05); however, intervention children showed significantly (p < 0.05) lower total and trunk per cent fat compared with the usual care condition. Conclusions: The Luces intervention did not reduce child BMI, yet small but significant reductions were observed for child per cent body fat. Further research is needed to identify and reduce barriers to recruitment and participation among Latino families. [ABSTRACT FROM AUTHOR]

Even though farnesyltransferase inhibitors (FTIs), a novel class of therapeutic agents presently in clinical trials, have preclinically outstanding anticancer activity and impressive lack of toxicity, their mechanism of action is not well understood. To enhance our understanding of how FTIs inhibit the growth of tumors, we have investigated their effects on cell cycle progression of two human lung cancer cell lines, A-549 and Calu-1. In this report, we show in synchronized A-549 and Calu-1 cells that FTI-2153 treatment resulted in a large accumulation of cells in the mitosis phase of the cell division cycle, with some cells in the G(0)/G(1) phase. Furthermore, microtubule immunostaining and 4,6-diamidino-2-phenylindole DNA staining demonstrated that the FTI-2153-induced accumulation in mitosis is due to the inability of these cells to progress from prophase to metaphase. FTI-2153 inhibited the ability of A-549 and Calu-1 cells to form bipolar spindles and caused formation of monoasteral spindles. Furthermore, FTI-2153 induced a ring-shaped chromosome morphology and inhibited chromosome alignment. Time-lapse videomicroscopy confirmed this result by showing that FTI-2153-treated cells are unable to align their chromosomes at the metaphase plate. FTI-2153 did not affect the localization to the kinetochores of two farnesylated centromeric proteins, CENP-E and CENP-F. Thus, a mechanism by which FTIs inhibit progression through mitosis and tumor growth is by blocking bipolar spindle formation and chromosome alignment.

Farnesyltransferase inhibitors (FTIs) represent a novel class of anticancer drugs that exhibit a remarkable ability to inhibit malignant transformation without toxicity to normal cells. However, the mechanism by which FTIs inhibit tumor growth is not well understood. Here, we demonstrate that FTI-277 inhibits phosphatidylinositol 3-OH kinase (PI 3-kinase)/AKT2-mediated growth factor- and adhesion-dependent survival pathways and induces apoptosis in human cancer cells that overexpress AKT2. Furthermore, overexpression of AKT2, but not oncogenic H-Ras, sensitizes NIH 3T3 cells to FTI-277, and a high serum level prevents FTI-277-induced apoptosis in H-Ras- but not AKT2-transformed NIH 3T3 cells. A constitutively active form of AKT2 rescues human cancer cells from FTI-277-induced apoptosis. FTI-277 inhibits insulin-like growth factor 1-induced PI 3-kinase and AKT2 activation and subsequent phosphorylation of the proapoptotic protein BAD. Integrin-dependent activation of AKT2 is also blocked by FTI-277. Thus, a mechanism for FTI inhibition of human tumor growth is by inducing apoptosis through inhibition of PI 3-kinase/AKT2-mediated cell survival and adhesion pathway.