Community Health Workers in Schools: A Systematic Review.

BACKGROUND: Community health workers (CHWs) are trusted community members who provide health education and care. However, no consensus exists regarding whether community health worker-based interventions are effective within the school setting. OBJECTIVE: To determine outcomes and best practices of school-based community health worker interventions. DATA SOURCES: PubMed, CINAHL, and SCOPUS databases. STUDY ELIGIBILITY CRITERIA: This systematic literature review examined articles that described an intervention led by community health workers, targeted children and/or parents, and took place primarily within a Kindergarten-12th grade school setting. Articles were excluded if they described an intervention outside the United States. PARTICIPANTS: Community health workers, children, and/or their parents INTERVENTIONS: School-based community health worker programs RESULTS: Of 1875 articles identified, 13 met inclusion criteria and were included in the final analysis. Of these, 5 described a statistically significant primary outcome. Seven articles provided details regarding community health worker recruitment, training, and roles that would enable reproduction of the intervention. LIMITATIONS: This review focused on interventions in the United States. Bias of individual studies had a wide range of scores (9-21). Heterogeneity of studies also precluded a meta-analysis of primary outcomes. CONCLUSIONS AND IMPLICATIONS OF KEY FINDINGS: The utilization of Community health workers in school-based interventions for children and/or parents is promising. This review identified a lack of detail and uniformity in program presentation, specifically with Community health worker recruitment, training, and roles. A standardized reporting mechanism for Community health worker interventions in schools would better allow for reproducibility and scalability of existing studies.

Epigenetic changes associated with inflammation in breast cancer patients treated with chemotherapy.

Inflammation has been associated with fatigue during and after various types of breast cancer treatments. We examined whether prior chemotherapy was associated with DNA methylation patterns that could explain persisting inflammation and/or fatigue in women treated for breast cancer. Prior to breast radiation therapy, DNA was extracted from peripheral blood mononuclear cells (PBMCs) of 61 Stage 0-IIIA breast cancer patients who had received partial mastectomy with or without chemotherapy. DNA methylation was assessed at >485,000 CpG sites across the genome along with fatigue and plasma inflammatory markers previously associated with fatigue. Compared to non-chemotherapy-treated, women who had received chemotherapy exhibited significantly decreased methylation at eight CpG sites (p<1.03×10(-7)) including four in exon 11 of transmembrane protein 49 (TMEM49), which demonstrated the largest decreases in methylation. Lower methylation at each identified CpG site was associated with increased plasma soluble tumor necrosis factor receptor 2 (sTNFR2) and interleukin (IL)-6 and mediated the relationship between chemotherapy and increases in these inflammatory biomarkers adjusting for multiple clinical and treatment characteristics. sTNFR2, but not CpG methylation status, was correlated with fatigue. Six months after breast radiation therapy, DNA methylation, inflammatory biomarkers and fatigue assessments were repeated in a subset of subjects (N=39). Reduced methylation in 4 of the 8 identified CpG sites was still observed in chemotherapy versus non-chemotherapy-treated patients, albeit with some decay indicating the dynamic and potentially reversible nature of the changes. Reduced methylation in these 4 CpG sites also continued to correlate with either increased sTNFR2 or IL-6, but not fatigue. In conclusion, prior chemotherapy treatment was associated with decreased methylation of CpG sites in DNA from PBMCs of breast cancer patients, which correlated with increased inflammatory markers prior to and 6months after radiation therapy. Persisting epigenetic changes secondary to chemotherapy may be one factor that contributes to inflammation and its consequences including cancer-related fatigue in vulnerable breast cancer patients.