Background: Ensuring the strength of the physician workforce is essential to optimizing patient care. Challenges that undermine the profession include inequities in advancement, high levels of burnout, reduced career duration, and elevated risk for mental health problems, including suicide. This narrative review explores whether physicians within four subpopulations represented in the workforce at levels lower than predicted from their numbers in the general population-women, racial and ethnic minorities in medicine, sexual and gender minorities, and people with disabilities-are at elevated risk for these problems, and if present, how these problems might be addressed to support patient care. In essence, the underlying question this narrative review explores is as follows: Do physician workforce disparities affect patient care? While numerous articles and high-profile reports have examined the relationship between workforce diversity and patient care, to our knowledge, this is the first review to examine the important relationship between diversity-related workforce disparities and patient care. Methods: Five databases (PubMed, the Cochrane Library of Systematic Reviews, EMBASE, Web of Knowledge, and EBSCO Discovery Service) were searched by a librarian. Additional resources were included by authors, as deemed relevant to the investigation. Results: The initial database searches identified 440 potentially relevant articles. Articles were categorized according to subtopics, including (1) underrepresented physicians and support for vulnerable patient populations; (2) factors that could exacerbate the projected physician deficit; (3) methods of addressing disparities among underrepresented physicians to support patient care; or (4) excluded (n = 155). The authors identified another 220 potentially relevant articles. Of 505 potentially relevant articles, 199 (39.4%) were included in this review. Conclusions: This report demonstrates an important gap in the literature regarding the impact of physician workforce disparities and their effect on patient care. This is a critical public health issue and should be urgently addressed in future research and considered in clinical practice and policy decision-making.
BackgroundNocturnin was originally identified by differential display as a circadian clock regulated gene with high expression at night in photoreceptors of the African clawed frog, Xenopus laevis. Although encoding a novel protein, the nocturnin cDNA had strong sequence similarity with a C-terminal domain of the yeast transcription factor CCR4, and with mouse and human ESTs. Since its original identification others have cloned mouse and human homologues of nocturnin/CCR4, and we have cloned a full-length cDNA from mouse retina, along with partial cDNAs from human, cow and chicken. The goal of this study was to determine the temporal pattern of nocturnin mRNA expression in multiple tissues of the mouse.ResultscDNA sequence analysis revealed a high degree of conservation among vertebrate nocturnin/CCR4 homologues along with a possible homologue in Drosophila. Northern analysis of mRNA in C3H/He and C57/Bl6 mice revealed that the mNoc gene is expressed in a broad range of tissues, with greatest abundance in liver, kidney and testis. mNoc is also expressed in multiple brain regions including suprachiasmatic nucleus and pineal gland. Furthermore, mNoc exhibits circadian rhythmicity of mRNA abundance with peak levels at the time of light offset in the retina, spleen, heart, kidney and liver.ConclusionThe widespread expression and rhythmicity of mNoc mRNA parallels the widespread expression of other circadian clock genes in mammalian tissues, and suggests that nocturnin plays an important role in clock function or as a circadian clock effector.
AimTo determine the association between dementia and age-related macular degeneration (AMD) using meta-analysis.MethodsWe searched in the MEDLINE, EMBASE, Web of Knowledge, PsycInfo and Cochrane database of systematic reviews for studies published from March 1959 to March 2018. We included cross-sectional, case–control and cohort studies that evaluated the association of dementia/Alzheimer's disease (AD) with AMD (as outcome) and the association of AMD with dementia/AD (as outcome). Studies that compared cognitive functions between AMD and controls were also included. The summary outcomes, namely odds ratio (OR), relative risk, mean differences and corresponding 95% CIs, were estimated using random effects models. We performed sensitivity analysis based on study quality and individual study effect to control for potential biases.ResultsAmong 2159 citation records, we identified 21 studies consisting of 7 876 499 study subjects for meta-analysis. Patients with dementia (padjusted≤0.017, OR≥1.24, I2≤9%) or AD (p=0.001, ORunadjusted=2.22, I2=50%) were at risk for AMD, particularly for late AMD (padjusted<0.001, OR=1.37, I2=0). AMD was also significantly associated with increased risk of AD/cognitive impairment (padjusted=0.037, OR=2.42, I2=38%). Moreover, patients with AMD had poorer cognitive functions when compared with controls, including Mini-Mental State Examination (p<0.001, I2≤79%) and Trail Making Test A (p<0.001, I2=0). Sensitivity analysis and Egger’s test indicated our results were less likely biased.ConclusionsA significant association between dementia/AD and AMD calls for greater clinical awareness. The cost-effectiveness of routine screening for the other condition in patients with primary diagnosis of dementia/AD or AMD requires further study.
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