A patient-centredness improvement study for efficacy of behaviour change for healthy lifestyle and weight loss in a student-run free clinic.

BACKGROUND: Primary care is the ideal place to implement behaviour change interventions for weight management. However, most primary care physicians are not managing patient weight as a standard of care due to lack of knowledge, skills and reimbursement. Generating more physicians who are familiar and comfortable with providing weight management is essential in leveraging a global change. In our university free clinic, medical students provide healthy lifestyle counselling using shared decision making to each patient at every clinic visit. OBJECTIVE: Improve the efficacy of behaviour change interventions via increased patient responsiveness and adherence. METHODS: The needs assessment demonstrated a subpar patient response rate to check-ins regarding behavioural change goals. In the first and second interventions, check-in message structure and contact schedule were varied to maximize patient responsiveness and goal achievement. RESULTS: In the needs assessment, 58% of patients responded to follow-ups and 58% of patients accomplished their goal. The first intervention cycle resulted in an improvement of responsiveness to 70% and accomplishment of goals to 59%. The second intervention cycle resulted in an improvement of responsiveness to 78% and accomplishment of goals to 74%. CONCLUSIONS: Messages that were frequent, unique, succinct and delivered within 4 weeks after the clinic visit resulted in the highest response rate and goal attainment. Other primary care clinics can use these interventions to increase patient completion of implemented behaviour changes for a healthier lifestyle.

MicroRNAs as Guardians of the Prostate: Those Who Stand before Cancer. What Do We Really Know about the Role of microRNAs in Prostate Biology?

Prostate cancer is the second leading cause of cancer-related deaths of men in the Western world. Despite recent advancement in genomics, transcriptomics and proteomics to understand prostate cancer biology and disease progression, castration resistant metastatic prostate cancer remains a major clinical challenge and often becomes incurable. MicroRNAs (miRNAs), about 22-nucleotide-long non-coding RNAs, are a group of regulatory molecules that mainly work through post-transcriptional gene silencing via translational repression. Expression analysis studies have revealed that miRNAs are aberrantly expressed in cancers and have been recognized as regulators of prostate cancer progression. In this critical review, we provide an analysis of reported miRNA functions and conflicting studies as they relate to expression levels of specific miRNAs and prostate cancer progression; oncogenic and/or tumor suppressor roles; androgen receptor signaling; epithelial plasticity; and the current status of diagnostic and therapeutic applications. This review focuses on select miRNAs, highly expressed in normal and cancer tissue, to emphasize the current obstacles faced in utilizing miRNA data for significant impacts on prostate cancer therapeutics.

Expression of FGD4 positively correlates with the aggressive phenotype of prostate cancer.

BACKGROUND: FGD4 (Frabin) is an F-actin binding protein with GTP/GDP exchange activity specific for CDC42. It is involved in reorganization of the actin cytoskeleton, which requires both actin binding and CDC42 activating function of FGD4. Expression of FGD4 is altered in patients with heterogeneous hereditary motor and sensory neuropathies as a result of demyelination of peripheral nerves. METHODS: In this study, we examined the expression of FGD4 in prostate cancer specimens using immunohistochemistry and studied the function of FGD4 in maintaining cell phenotype, behavior and drug sensitivity using overexpression and siRNA-based silencing approaches. We used Mann-Whitney test for comparative analysis of FGD4 expression. RESULTS: Our results show that the expression of FGD4 is upregulated in cancerous prostates compared to the luminal cells in benign prostatic hyperplasia, although the basal cells showed high staining intensities. We noted a gradual increase in the staining intensity of FGD4 with increasing aggressiveness of the disease. Inhibition of expression of FGD4 using siRNAs showed reduced proliferation and cell cycle arrest in G2/M phase of androgen dependent LNCaP-104S and androgen refractory PC-3 cells. Inhibition of FGD4 also resulted in reduced cell migration and CDC42 activities in PC-3 cells whereas, ectopic expression of FGD4 induced cell migration, altered expression of mesenchymal and epithelial markers and activation of CDC42/PAK signaling pathway. Reduced expression of FGD4 improved sensitivity of LNCaP-104S cells to the anti-androgen drug Casodex and PC-3 cells to the microtubule stabilizing drug docetaxel. CONCLUSIONS: Our data demonstrate a tumor promoting and a cell migratory function of FGD4 in prostate cancer cells and that inhibition of FGD4 expression enhances the response for both androgen-dependent and independent prostate cancer cells towards currently used prostate cancer drugs.