Improving Access to Eye Care: A Systematic Review of the Literature.

PURPOSE: The goals were to develop a working and inclusive definition of access to eye care, identify gaps in the current system that preclude access, and highlight recommendations that have been identified in prior studies. This manuscript serves as a narrative summary of the literature. CLINICAL RELEVANCE: Health care disparities continue to plague the nation's well-being, and eye care is no exception. Inequities in eye care negatively affect disease processes (i.e., glaucoma, cataracts, diabetic retinopathy), interventions (surgical treatment, prescription of glasses, referrals), and populations (gender, race and ethnicity, geography, age). METHODS: A systematic review of the existing literature included all study designs, editorials, and opinion pieces and initially yielded nearly 2500 reports. To be included in full-text review, an article had to be US-based, be written in English, and address 1 or more of the key terms "barriers and facilitators to health care," "access," and "disparities in general and sub-specialty eye care." Both patient and health care professional perspectives were included. One hundred ninety-six reports met the inclusion criteria. RESULTS: Four key themes regarding access to eye care from both patient and eye care professional perspectives emerged in the literature: (1) barriers and facilitators to access, (2) utilization, (3) compliance and adherence, and (4) recommendations to improve access. Common barriers and facilitators included many factors identified as social determinants of health (i.e., transportation, insurance, language, education). Utilization of eye care was largely attributable to having coverage for eye care, recommendations from primary care professionals, and improved health status. Geographic proximity, age, and lack of transportation surfaced as factors for compliance and adherence. There were a variety of recommendations to improve access to eye care, including improving presence in community health clinics, reimbursement for physicians, and funding of community-based programs such as DRIVE and REACH. CONCLUSIONS: The eye care profession has abundant evidence of the disparities that continue to affect marginalized communities. Improving community-based programs and clinics, addressing social determinants of health, and acknowledging the effects of discrimination and bias on eye care serve as ways to improve equity in this field.

Mature mice lacking Rbl2/p130 gene have supernumerary inner ear hair cells and supporting cells.

Adult mammalian auditory hair cells (HCs) and their associated supporting cells (SCs) do not proliferate, and HC death leads to irreversible neurosensory hearing loss and balance impairment. In nonmammalian vertebrates, loss of HCs induces mitotic proliferation of adjacent nonsensory SCs and/or direct SC transdifferentiation to generate replacement cells. This results in the structural and functional recovery of the nonmammalian sensory systems. Potential replacement of mammalian auditory HCs, either by transplanting cells or by transforming existing cells through molecular therapy, has long been proposed. However, HC replacement strategies with clear therapeutic potential remain elusive. The retinoblastoma (pRB) family of cell cycle regulators, Rb1, Rbl1 (p107), and Rbl2 (p130), regulate the G(1)- to S-phase transition in proliferating cells. In the inner ear, the biochemical and molecular pathways involving pRBs, particularly p107 and p130, are relatively unexplored and their therapeutic suitability is yet to be determined. In this study, we analyzed the cochleae of adult p130 knock-out (p130(-/-)) mice and showed that lack of the p130 gene results in extra rows of HCs and SCs in the more apical regions of the cochlea. No evidence of transdifferentiation of these supernumerary SCs into HCs was observed in the p130(-/-) mouse. Nevertheless, unscheduled proliferation of SCs in the adult p130(-/-) cochlea coupled to downregulation of bona fide cell cycle inhibitors provides a mechanistic basis for the role of p130 as a regulator of SC and HC mitotic quiescence in the more apical regions of the cochlea. Interestingly, p130(-/-) mice exhibited nearly normal peripheral auditory sensitivity.