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To help maximize the real-world applicability of available interventions in clinical and community healthcare practice, there has been greater emphasis over the past two decades on engaging local communities in health-related research. While there have been numerous successful community-academic partnered collaborations, there continues to be a need to articulate the common barriers experienced during the evolution of these partnerships, and to provide a roadmap for best practices that engage healthcare providers, patients, families, caregivers, community leaders, healthcare systems, public agencies and academic medical centers. To this end, this paper presents a summary of a forum discussion from the 2014 Southern California Dissemination, Implementation and Improvement (DII) Science Symposium, sponsored by the University of California Los Angeles (UCLA) Clinical Translational Science Institute (CTSI), University of Southern California (USC) CTSI, and Kaiser Permanente. During this forum, a diverse group of individuals representing multiple constituencies identified four key barriers to success in community-partnered participatory research (CPPR) and discussed consensus recommendations to enhance the development, implementation, and dissemination of community health-related research. In addition, this group identified several ways in which the over 60 NIH funded Clinical and Translational Science Institutes across the country could engage communities and researchers to advance DII science.

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PURPOSE: This study explored the relationships between systemic- and individual-level contextual factors and health-related quality of life (HRQOL) in a cohort of African American and Latina breast cancer survivors (BCS). METHODS: Baseline questionnaire data of 320 BCS who participated in a HRQOL psycho-educational intervention were abstracted from the parent study. Hierarchical regression analysis tested the independent effects of contextual factors on HRQOL. RESULTS: HRQOL was higher in BCS who: were diagnosed at < stage 2 (b = -1.38, p < 0.05), expressed satisfaction with their health care (b = 0.20, p < 0.001), had fewer comorbidities (b = - 0.60, p < 0.001) and depressive symptoms (b = -0.30, p < 0.001), and practiced healthy diet and exercise habits (b = 0.02, p < 0.05). Demographic and cancer-related factors accounted for 14 % of the variance in HRQOL (F[6, 274] = 7.25, p < 0.001). The socio-cultural context (i.e., ethnicity, life stress, perceived social support) explained 20 % of the variance in HRQOL (FΔ[3, 271] = 27.32, p < 0.001). The health care system context contributed an additional 8 % to explaining HRQOL (FΔ[1, 270] = 34.88, p < 0.001). Health status and behavioral factors accounted for 18 % of the variance (FΔ[4, 266] = 29.55, p < 0.001). The full model explained 59 % of the variance in HRQOL (F[14, 266] = 27.76, p < 0.001). CONCLUSIONS: HRQOL in ethnic minority BCS is multifaceted and is significantly influenced by cancer-related, socio-cultural, health care system, health status, and behavioral contextual factors. Therefore, survivorship research and practice must address broad multi-level domains to achieve equitable and optimal breast cancer outcomes. IMPLICATIONS FOR CANCER SURVIVORS: To enhance HRQOL, survivors must be provided the know-how and support to maintain healthy lifestyle and self-management practices. Advocates must engage the care team to consider systemic factors, including life stress and community resources, to be more patient-centered.

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This paper will present the multiple roles and the impact of cancer advocates. The emerging literature provides evidence for the consideration and integration of African American BC survivors as advocates in practice, policy and research relevant to cancer prevention and control. We present a practical outline for organizational assessment for the inclusion of advocates in these arenas. This assessment can be conducted by all levels of partners, including community advocacy and scientific organizations.

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In the cephalopod retina, light/dark adaptation is accompanied by a decrease/increase in rhabdom size and redistribution of rhodopsin and retinochrome. Rearrangements in the actin cytoskeleton probably govern changes in rhabdom size by regulating the degradation/formation of rhabdomere microvilli. Photopigment movements may be directed by microtubules present in the outer segment core cytoplasm. We believe that rhodopsin activation by light stimulates Rho and Rac signaling pathways, affecting these cytoskeletal systems and their possible functions in controlling rhabdom morphology and protein movements. In this study, we localized cytoskeletal and signaling proteins in octopus photoreceptors to determine their concurrence between the lighting conditions. We used toxin B from Clostridium difficile to inhibit the activity of Rho/Rac and observed its effect on the location of signaling proteins and actin and tubulin. In both lighting conditions, we found Rho in specific sets of juxtaposed rhabdomeres in embryonic and adult retinas. In the light, Rho and actin were localized along the length of the rhabdomere, but, in the dark, both proteins were absent from a space beneath the inner limiting membrane. Rac colocalized with tubulin in the outer segment core cytoplasm and, like Rho, the two proteins were also absent beneath the inner limiting membrane in the dark. The distribution of actin and Rho was affected by toxin B and, in dark-adapted retinas, actin and Rho distribution was similar to that observed in the light. Our results suggest that the Rho/Rac GTPases are candidates for the regulation of rhabdomere size and protein movements in light-dark-adapted octopus photoreceptors.

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Previous studies of Delta 4-androstene-3,17-dione (4-androstenedione) administration in men have not demonstrated sustained increments in testosterone levels, fat-free mass (FFM), and muscle strength, and failure to demonstrate androstenedione's androgenic/anabolic effects has stifled efforts to regulate its sales. To determine whether 4-androstenedione has androgenic/anabolic properties, we evaluated its association with androgen receptor (AR) and its effects on myogenesis in vitro. Additionally, we studied the effects of a high dose of 4-androstenedione on testosterone levels, FFM, and muscle strength in hypogonadal men. We determined the dissociation constant (K(d)) for 4-androstenedione using fluorescence anisotropy measurement of competitive displacement of fluorescent androgen from AR ligand-binding domain. AR nuclear translocation and myogenic activity of androstenedione were evaluated in mesenchymal, pluripotent C3H10T1/2 cells, in which androgens stimulate myogenesis through an AR pathway. We determined effects of a high dose of androstenedione (500 mg thrice daily) given for 12 wk on FFM, muscle strength, and hormone levels in nine healthy, hypogonadal men. 4-Androstenedione competitively displaced fluorescent androgen from AR ligand-binding domain with a lower affinity than dihydrotestosterone (K(d), 648 +/- 21 and 10 +/- 0.4 nm, respectively). In C3H10T1/2 cells, 4-androstenedione caused nuclear translocation of AR and stimulated myogenesis, as indicated by a dose-dependent increase in myosin heavy chain II+ myotube area and up-regulation of MyoD protein. Stimulatory effects of 4-androstenedione on myosin heavy chain II+ myotubes and myogenic determination factor expression were attenuated by bicalutamide, an AR antagonist. Administration of 1500 mg 4-androstenedione daily to hypogonadal men significantly increased serum androstenedione, total and free testosterone, estradiol, and estrone levels and suppressed SHBG and high-density lipoprotein cholesterol levels. 4-androstenedione administration was associated with significant gains in FFM (+1.7 +/- 0.5 kg; P = 0.012) and muscle strength in bench press (+4.3 +/- 3.1 kg; P = 0.006) and leg press exercises (+18.8 +/- 17.3 kg; P = 0.045). 4-androstenedione is an androgen that binds AR, induces AR nuclear translocation, and promotes myogenesis in vitro, with substantially lower potency than dihydrotestosterone. 4-androstenedione administration in high doses to hypogonadal men increases testosterone levels, FFM, and muscle strength, although at the dose tested, the anabolic effects in hypogonadal men are likely because of its conversion to testosterone.

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