The impact of physician-directed and patient-directed education on screening, diagnosis, treatment, and referral patterns for urinary incontinence.

INTRODUCTION AND HYPOTHESIS: The objective of this study was to evaluate the impact of patient- and physician-directed education in the primary care setting on screening, diagnosis, treatment, and referral patterns to Urogynecology for urinary incontinence (UI). METHODS: This was a prospective, multi-phase, before-and-after study conducted over a 3-year period. New female patients, 40 years and older, seen in the Internal Medicine (IM) clinic of our institution, were included. Phase 1 intervention consisted of UI lectures for IM residents. Phase 2 intervention involved placement of patient-directed posters throughout the IM clinic. Prior to phase 1, charts of new patients were reviewed as the control group to establish a baseline rate of screening, diagnosis, treatment initiation, and referrals. The same data were collected for 4 months after both phase 1 and phase 2. A washout period of 1 year occurred between phase 1 and phase 2. RESULTS: A total of 410 charts were reviewed and included 200 control, 92 phase 1, and 118 phase 2 patients. In the control group, 13% of patients were screened for UI. There was no significant increase in screening after phase 1 (15% vs 13%, p = 0.6); however, there was a significant increase after phase 2 (32.2% vs 13%, p < 0.001). There was no difference in treatment initiation for patients with a positive screen after either phase. CONCLUSION: In our study, providing an informative lecture to an IM referral base did not improve UI screening. Alternatively, directly targeting patients through posters significantly improved screening rates in the primary care setting, demonstrating that simple interventions can improve screening for conditions that are difficult to discuss such as UI.

Oncogene homologue Sch9 promotes age-dependent mutations by a superoxide and Rev1/Polzeta-dependent mechanism.

Oncogenes contribute to tumorigenesis by promoting growth and inhibiting apoptosis. Here we examine the function of Sch9, the Saccharomyces cerevisiae homologue of the mammalian Akt and S6 kinase, in DNA damage and genomic instability during aging in nondividing cells. Attenuation of age-dependent increases in base substitutions, small DNA insertions/deletions, and gross chromosomal rearrangements (GCRs) in sch9Delta mutants is associated with increased mitochondrial superoxide dismutase (MnSOD) expression, decreased DNA oxidation, reduced REV1 expression and translesion synthesis, and elevated resistance to oxidative stress-induced mutagenesis. Deletion of REV1, the lack of components of the error-prone Polzeta, or the overexpression of SOD1 or SOD2 is sufficient to reduce age-dependent point mutations in SCH9 overexpressors, but REV1 deficiency causes a major increase in GCRs. These results suggest that the proto-oncogene homologue Sch9 promotes the accumulation of superoxide-dependent DNA damage in nondividing cells, which induces error-prone DNA repair that generates point mutations to avoid GCRs and cell death during the first round of replication.