Rural-specific identity and associations with lifestyle behaviors and well-being among rural cancer survivors.

BACKGROUND: Disparities in rural cancer survivors' health outcomes are well-documented, yet the role of sociocultural aspects of rurality, such as rural identity, attitudes toward rurality, and social standing on health beliefs and behaviors remain unclear. This study aimed to address these gaps. METHODS: Rural cancer survivors (N = 188) completed a mailed/online survey. Regression analyses identified relationships among rural identity, negative attitudes toward rurality, and social standing with health outcomes, quality of life, cancer fatalism, and cancer information overload. RESULTS: Higher rural identity was associated with believing everything causes cancer (OR = 1.58, p = 0.048), believing "there's not much you can do to lower your chances of getting cancer" (OR = 2.22, p = 0.002), and higher odds of being overloaded with cancer information (OR = 2.05, p  = 0.008). Negative attitudes toward rurality was linked with higher levels of perceived stress (B = 0.83, p = 0.001), and chronic pain (OR = 1.47, p = 0.039). Higher subjective social status was associated with perceived social support (B = 0.09, p = 0.016), better overall health (B = 0.13, p < 0.001), lower levels of perceived stress (B = -0.38, p = 0.007), and chronic pain (OR = 0.80, p = 0.027). CONCLUSION: Sociocultural factors of rurality were associated with indicators of quality of life, cancer fatalism, and information overload. Further exploration of the underlying mechanisms that drive these associations can help improve intervention targets for rural cancer survivors.

Humanin-induced autophagy plays important roles in skeletal muscle function and lifespan extension.

BACKGROUND: Autophagy, a highly conserved homeostatic mechanism, is essential for cell survival. The decline of autophagy function has been implicated in various diseases as well as aging. Although mitochondria play a key role in the autophagy process, whether mitochondrial-derived peptides are involved in this process has not been explored. METHODS: We developed a high through put screening method to identify potential autophagy inducers among mitochondrial-derived peptides. We used three different cell lines, mice, c.elegans, and a human cohort to validate the observation. RESULTS: Humanin, a mitochondrial-derived peptide, increases autophagy and maintains autophagy flux in several cell types. Humanin administration increases the expression of autophagy-related genes and lowers accumulation of harmful misfolded proteins in mice skeletal muscle, suggesting that humanin-induced autophagy potentially contributes to the improved skeletal function. Moreover, autophagy is a critical role in humanin-induced lifespan extension in C. elegans. CONCLUSIONS: Humanin is an autophagy inducer. GENERAL SIGNIFICANCE: This paper presents a significant, novel discovery regarding the role of the mitochondrial derived peptide humanin in autophagy regulation and as a possible therapeutic target for autophagy in various age-related diseases.