The Latino Integrative Medical Group Visit as a Model for Pain Reduction in Underserved Spanish Speakers.

OBJECTIVES: Chronic pain is a common problem in the United States, one for which there is a dearth of effective treatments. Nonpharmacological options are a promising alternative, especially for Spanish-speaking Latinos. This pilot study would like to assess the feasibility of an adapted Integrative Medical Group Visit (IMGV) curriculum for a Spanish-speaking Latino chronic pain population. DESIGN AND INTERVENTION: We translated and adapted the curriculum of the IMGV for a Spanish-speaking Latino chronic pain population. We then tested the feasibility of using this model with two pilot groups (N = 19) using a pre-postdesign. SUBJECTS: This intervention was targeted for underserved Spanish-speaking Latino patients with chronic pain. SETTINGS/LOCATION: This study took place at a safety net academic teaching hospital, the Boston Medical Center, and at a community health center located in a majority Latino neighborhood, the East Boston Neighborhood Health Clinic. OUTCOME MEASURES: We used the validated Spanish translations of the Patient-Reported Outcomes Measurement Information System (PROMIS-29) (short version), Personal Health Questionnaire (PHQ-8), and Perceived Stress Scale (PSS-10). We also gathered qualitative information through focus groups and in-depth interviews. RESULTS: Using PROMIS measures, there was a statistically significant reduction in pain interference (p = 0.01), fatigue (p = 0.01), and depression (p = 0.01). Qualitative data also indicated the participants felt they benefited from the visits and having care in Spanish was unique. CONCLUSIONS: This model offers a promising nonpharmacological option for Spanish-speaking patients with chronic pain and could offer an alternative for addressing disparities for this population.

Base excision repair of chemotherapeutically-induced alkylated DNA damage predominantly causes contractions of expanded GAA repeats associated with Friedreich's ataxia.

Expansion of GAA·TTC repeats within the first intron of the frataxin gene is the cause of Friedreich's ataxia (FRDA), an autosomal recessive neurodegenerative disorder. However, no effective treatment for the disease has been developed as yet. In this study, we explored a possibility of shortening expanded GAA repeats associated with FRDA through chemotherapeutically-induced DNA base lesions and subsequent base excision repair (BER). We provide the first evidence that alkylated DNA damage induced by temozolomide, a chemotherapeutic DNA damaging agent can induce massive GAA repeat contractions/deletions, but only limited expansions in FRDA patient lymphoblasts. We showed that temozolomide-induced GAA repeat instability was mediated by BER. Further characterization of BER of an abasic site in the context of (GAA)20 repeats indicates that the lesion mainly resulted in a large deletion of 8 repeats along with small expansions. This was because temozolomide-induced single-stranded breaks initially led to DNA slippage and the formation of a small GAA repeat loop in the upstream region of the damaged strand and a small TTC loop on the template strand. This allowed limited pol ß DNA synthesis and the formation of a short 5'-GAA repeat flap that was cleaved by FEN1, thereby leading to small repeat expansions. At a later stage of BER, the small template loop expanded into a large template loop that resulted in the formation of a long 5'-GAA repeat flap. Pol ß then performed limited DNA synthesis to bypass the loop, and FEN1 removed the long repeat flap ultimately causing a large repeat deletion. Our study indicates that chemotherapeutically-induced alkylated DNA damage can induce large contractions/deletions of expanded GAA repeats through BER in FRDA patient cells. This further suggests the potential of developing chemotherapeutic alkylating agents to shorten expanded GAA repeats for treatment of FRDA.