Greenspace redevelopment, pressure of displacement, and sleep quality among Black adults in Southwest Atlanta.

BACKGROUND: Little is known on how greenspace redevelopment-creating or improving existing parks and trails-targeted for low-income and/or majority Black neighborhoods could amplify existing social environmental stressors, increase residents' susceptibility to displacement, and impact their sleep quality. OBJECTIVE: To examine the relationship between social environmental stressors associated with displacement and sleep quality among Black adults. METHODS: Linear regression models were employed on survey data to investigate the association between social environmental stressors, independently and combined, on sleep quality among Black adults residing in block groups targeted for greenspace redevelopment (i.e., exposed) and matched with block groups that were not (i.e., unexposed). RESULTS: The independent associations between everyday discrimination, heightened vigilance, housing unaffordability, and subjective sleep quality were not modified by greenspace redevelopment, controlling for other factors. The association between financial strain and subjective sleep quality was different for exposed and unexposed participants with exposed participants having a poorer sleep quality. The combined model revealed that the association between financial strain and sleep quality persisted. However, for different financial strain categories exposed participants slept poorer and/or better than unexposed participants. SIGNIFICANCE: Our findings suggest a nuanced relationship between social environmental stressors, pressure of displacement related to greenspace redevelopment, and sleep quality among Black adults.

Knockdown of leptin A expression dramatically alters zebrafish development.

Using morpholino antisense oligonucleotide (MO) technology, we blocked leptin A or leptin receptor expression in embryonic zebrafish, and analyzed consequences of leptin A knock-down on fish development. Embryos injected with leptin A or leptin receptor MOs (leptin A or leptin receptor morphants) had smaller bodies and eyes, undeveloped inner ear, enlarged pericardial cavity, curved body and/or tail and larger yolk compared to control embryos of the same stages. The defects persisted in 6-9 days old larvae. We found that blocking leptin A function had little effect on the development of early brain (1 day old), but differentiation of both the morphant dorsal brain and retinal cells was severely disrupted in older (2 days old) embryos. Despite the enlarged pericardial cavity, differentiation of cardiac cells appeared to be similar to control embryos. Formation of the morphants' inner ear is also severely disrupted, which corroborates existing reports of leptin receptor expression in inner ear of both zebrafish and mammals. Co-injection of leptin A MO and recombinant leptin results in partial rescue of the wild-type phenotype. Our results suggest that leptin A plays distinct roles in zebrafish development.