Physician Density by Specialty Type in Urban and Rural Counties in the US, 2010 to 2017.
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ABSTRACT:
SUBMITTER: Machado SR
PROVIDER: S-EPMC7823223 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
Publications
Physician Density by Specialty Type in Urban and Rural Counties in the US, 2010 to 2017.
Machado Sara R SR Jayawardana Sahan S Mossialos Elias E Vaduganathan Muthiah M
JAMA network open 20210104 1
Similar Datasets
Project description:ImportanceAs the US population continues to increase and age, there is an unmet need for dermatologic care; therefore, it is important to identify and understand the characteristics and patterns of the dermatologist workforce.ObjectiveTo analyze the longitudinal dermatologist density and urban-rural disparities using a standardized classification scheme.Design, setting, and participantsThis study analyzed county-level data for 1995 to 2013 from the Area Health Resources File to evaluate the longitudinal trends and demographic and environmental factors associated with the geographic distribution of dermatologists.Main outcomes and measuresActive US dermatologist and physician density.ResultsIn this study of nationwide data on dermatologists, dermatologist density increased by 21% from 3.02 per 100 000 people to 3.65 per 100 000 people from 1995 to 2013; the gap between the density of dermatologists in urban and other areas increased from 2.63 to 3.06 in nonmetropolitan areas and from 3.41 to 4.03 in rural areas. The ratio of dermatologists older than 55 years to younger than 55 years increased 75% in nonmetropolitan and rural areas (from 0.32 to 0.56) and 170% in metropolitan areas (from 0.34 to 0.93). Dermatologists tended to be located in well-resourced, urban communities.Conclusions and relevanceOur findings suggest that substantial disparities in the geographic distribution of dermatologists exist and have been increasing with time. Correcting the workforce disparity is important for patient care.
| S-EPMC6248119 | biostudies-literature
Project description:ObjectiveTo understand the role of county characteristics in the growing divide between rural and urban mortality from 1980 to 2010.Data sourceAge-adjusted mortality rates for all U.S. counties from 1980 to 2010 were obtained from the CDC Compressed Mortality File and combined with county characteristics from the U.S. Census Bureau, the Area Health Resources File, and the Inter-University Consortium for Political and Social research.Study designWe used Oaxaca-Blinder decomposition to assess the extent to which rural-urban mortality disparities are explained by observed county characteristics at each decade.Principal findingsDecomposition shows that, at each decade, differences in rural/urban characteristics are sufficient to explain differences in mortality. Furthermore, starting in 1990, rural counties have significantly lower predicted mortality than urban counties when given identical county characteristics. We find changes in the effect of characteristics on mortality, not the characteristics themselves, drive the growing mortality divide.ConclusionsDifferences in economic and demographic characteristics between rural and urban counties largely explain the differences in age-adjusted mortality in any given year. Over time, the role these characteristics play in improving mortality has increased differentially for urban counties. As characteristics continue changing in importance as determinants of health, this divide may continue to widen.
| S-EPMC6232410 | biostudies-literature
Project description:PurposeTo determine the associations of blindness within rural and urban counties using a registry of blind persons and geospatial analytics.MethodsWe used the Oregon Commission for the Blind registry to determine the number of persons who are legally blind, as well as licensure data to determine the density of eye care providers (optometrists and ophthalmologists) within each county of the State of Oregon. We used geospatial statistics, analysis of variance, and logistic regression to determine the explanatory variables associated with blindness within counties.ResultsWe included 8350 individuals who are legally blind within the state of Oregon in the calendar year 2015. The mean observed prevalence of registered blindness was 0.21% and ranged almost 9-fold from 0.04% to 0.58% among counties (p < .001). In univariate models, higher blindness was associated with increasing median age (p = .027), minority race (p < .001), decreased median household income (p < .001), increased poverty within a county (p < .001), and higher density of ophthalmologists (p = .003). Density of optometrists was not associated with prevalence of blindness (p = .89). The final multivariable model showed higher blindness to be associated with lower median household income, higher proportion of black race, and lower proportion of Hispanic race (p < .001 for all).ConclusionGeospatial analytics identified counties with higher and lower than expected proportions of blindness even when adjusted for sociodemographic factors. Clinicians and researchers may use the methods and results of this study to better understand the distribution of individuals with blindness and the associated factors to help design public health interventions.
| S-EPMC9550029 | biostudies-literature
Project description:Atmospheric particulate matter (PM) is a recognized risk factor for the global burden of disease in human populations. We are presenting here the application of toxicogenomics in the evaluation of the toxic effects of organic content of atmospheric particle matter (PM), from urban and rural environments (city of Barcelona and village of La Pobla, NE Spain), using the developing zebrafish embryo. The main goal is to identify the metabolic pathways involved in the adverse effects observed in zebrafish embryos exposed to PM organic content from urban and rural environments, also allowing the selection of genes of interest that are differentially expressed. The relevance of particle size to the PM toxicity is also addressed. Indeed, the zebrafish embryos were exposed to PM of aerodynamic diameter larger than 7.2 μm and smaller than 0.5 μm (PM10 and PM0.5, respectively). PM0.5 concentrated biological and toxic activities linked to organic substances. Transcriptomic analyses showed strong induction of the AhR signalling pathway (a.k.a. dioxin-like activity) for embryos exposed to both rural and urban extracts, correlating with the concentrations of PAHs. Urban extracts, with strong contribution of traffic emissions, specifically de-regulated oxidative stress-related genes, as well as pancreatic and eye-lens specific genes, two organs known to be affected by air pollution in humans. Exposure to rural extracts, with high contribution of wood burning emissions, affected genes implicated in basic cellular functions, in agreement with their strong embryotoxicity. Extracts from rural and urban samples elicited both common and specific transcriptome responses, suggesting different potentially adverse outcomes depending on PM source and composition. The authors thank the financial support of the Spanish Ministry (project TEA-PARTICLE, grant number CGL2011-29621) and the Portuguese Foundation for Science and Technology for the doctoral grant of Sofia R. Mesquita (SFRH/BD/80710/2011) funded by the Program POPH-QREN through the Portuguese Ministry of Education and Science and the European Social Fund, and support through project PEst-C/MAR/LA0015/2013.
2015-10-26 | GSE53522 | GEO
Project description:Atmospheric particulate matter (PM) is a recognized risk factor for the global burden of disease in human populations. We are presenting here the application of toxicogenomics in the evaluation of the toxic effects of organic content of atmospheric particle matter (PM), from urban and rural environments (city of Barcelona and village of La Pobla, NE Spain), using the developing zebrafish embryo. The main goal is to identify the metabolic pathways involved in the adverse effects observed in zebrafish embryos exposed to PM organic content from urban and rural environments, also allowing the selection of genes of interest that are differentially expressed. The relevance of particle size to the PM toxicity is also addressed. Indeed, the zebrafish embryos were exposed to PM of aerodynamic diameter larger than 7.2 μm and smaller than 0.5 μm (PM10 and PM0.5, respectively). PM0.5 concentrated biological and toxic activities linked to organic substances. Transcriptomic analyses showed strong induction of the AhR signalling pathway (a.k.a. dioxin-like activity) for embryos exposed to both rural and urban extracts, correlating with the concentrations of PAHs. Urban extracts, with strong contribution of traffic emissions, specifically de-regulated oxidative stress-related genes, as well as pancreatic and eye-lens specific genes, two organs known to be affected by air pollution in humans. Exposure to rural extracts, with high contribution of wood burning emissions, affected genes implicated in basic cellular functions, in agreement with their strong embryotoxicity. Extracts from rural and urban samples elicited both common and specific transcriptome responses, suggesting different potentially adverse outcomes depending on PM source and composition. The authors thank the financial support of the Spanish Ministry (project TEA-PARTICLE, grant number CGL2011-29621) and the Portuguese Foundation for Science and Technology for the doctoral grant of Sofia R. Mesquita (SFRH/BD/80710/2011) funded by the Program POPH-QREN through the Portuguese Ministry of Education and Science and the European Social Fund, and support through project PEst-C/MAR/LA0015/2013. The PM filter samples used in the present study were PM10 and PM0.5 from the urban site - total of 4 samples from 2 sampling months; and PM0.5 from the rural site - total of 2 samples from 2 sampling months (PM10 samples from the rural site were not tested due to their very low concentration in organic compounds, and insignificant biological activity, previously measured). Sampling occurred during the cold periods of the year 2012/2013. The organic fraction of PM samples was extracted by sonication using a mixture of dichloromethane:methanol. Then, the extracts were filtered, evaporated and re-dissolved in Dimethyl sulfoxide (DMSO). Zebrafish fertilized eggs were exposed to PM organic extracts (0.2% DMSO) from the urban and rural sites from 24 to 120h post-fertilization. Total RNA was isolated from whole embryos (pools of 20 individuals), using Trizol reagent protocol (Invitrogen Life Technologies, Carlsberg, CA). The microarray study was performed using the Agilent Two-colour D. rerio Oligo Microarray v3 platform, following the Agilent Microarray â?? Based Gene Expression Analysis protocol. Three biological replicates were performed for each PM sample and controls. Biological replicates, a technical replicate and a self-to-self, were simultaneously amplified and labelled using Cyanine 3 (Cy3) and Cyanine 5 (Cy5) dye. After cRNA purification (RNeasy Kit, Quiagen GmbH, Hilden, Germany), the cRNA concentration and labelling were quantified in the NanoDrop spectrophotometer, obtaining incorporation rates in the range of 15-20pmol of cyanide dye/µl cRNA and yield values > 0.825ug, as recommended. cRNA was fragmented and hybridized in 4x44K arrays, for 17h at 65oC. After the hybridization the array slides were washed, and immediately scanned using Microarray Scanner Agilent G2505C system. Data was extracted using Agilent Feature Extraction Software v10.5.1.1, and the quality of microarray data was evaluated using the Quality Control report provided by Agilent Software. Based on the microarray data analysis, 22 primers were selected and designed using Primer Express 2.0 software (Applied Biosystems, Foster City, CA). Genes were quantified by real-time PCR to validate the microarray data, and a subset of 13 genes were further selected by their robust behaviour in the validation assays, allowing to differentiate the toxic potential of PM from urban and rural sources.
2015-10-26 | E-GEOD-53522 | biostudies-arrayexpress
Project description: Not available
| S-EPMC10500373 | biostudies-literature
Project description:The molecular basis of evolutionary change is assumed to be genetic variation. However, growing evidence suggests that epigenetic mechanisms, such as DNA methylation, may also be involved in evolutionary change. An important first step in evaluating this hypothesis is to test for the presence of epigenetic variation between natural populations living under different environmental conditions. In the current study we explored variation between populations of Darwin’s finches living in adjacent “urban” and “rural” environments on Santa Cruz Island in the Galápagos. We tested for morphological, genetic, and epigenetic differences between the urban and rural populations of each of two species of ground finches, Geospiza fortis and G. fuliginosa. Using data collected from more than 1000 birds, we found significant morphological differences between populations of G. fortis, but not G. fuliginosa. We did not find genetic differences between populations of either species, based on comparisons of copy number variation (CNV). In contrast, we did find epigenetic differences between the urban and rural populations of both species, based on DNA methylation analysis. We explored genomic features and gene associations of the differentially methylated regions (DMR), as well as their possible functional significance. In summary, our study documents local population epigenetic variation within species of Darwin’s finches.
2017-01-07 | GSE87825 | GEO
Project description:ImportanceLittle is known about recent trends in rural-urban disparities in youth suicide, particularly sex- and method-specific changes. Documenting the extent of these disparities is critical for the development of policies and programs aimed at eliminating geographic disparities.ObjectiveTo examine trends in US suicide mortality for adolescents and young adults across the rural-urban continuum.Design, setting, and participantsLongitudinal trends in suicide rates by rural and urban areas between January 1, 1996, and December 31, 2010, were analyzed using county-level national mortality data linked to a rural-urban continuum measure that classified all 3141 counties in the United States into distinct groups based on population size and adjacency to metropolitan areas. The population included all suicide decedents aged 10 to 24 years.Main outcomes and measuresRates of suicide per 100,000 persons.ResultsAcross the study period, 66,595 youths died by suicide, and rural suicide rates were nearly double those of urban areas for both males (19.93 and 10.31 per 100,000, respectively) and females (4.40 and 2.39 per 100,000, respectively). Even after controlling for a wide array of county-level variables, rural-urban suicide differentials increased over time for males, suggesting widening rural-urban disparities (1996-1998: adjusted incidence rate ratio [IRR], 0.98; 2008-2010: adjusted IRR, 1.19; difference in IRR, P = .02). Firearm suicide rates declined, and the rates of hanging/suffocation for both males and females increased. However, the rates of suicide by firearm (males: 1996-1998, 2.05; and 2008-2010: 2.69 times higher) and hanging/suffocation (males: 1996-1998, 1.24; and 2008-2010: 1.63 times higher) were disproportionately higher in rural areas, and rural-urban differences increased over time (P = .002 for males; P = .06 for females).Conclusions and relevanceSuicide rates for adolescents and young adults are higher in rural than in urban communities regardless of the method used, and rural-urban disparities appear to be increasing over time. Further research should carefully explore the mechanisms whereby rural residence might increase suicide risk in youth and consider suicide-prevention efforts specific to rural settings.
| S-EPMC4551430 | biostudies-literature
Project description:IntroductionThe prevalence of hepatitis C virus infection among women delivering live births in the U.S. may be higher in rural areas where county-level estimates may be unreliable. The aim of this study is to model county-level maternal hepatitis C virus infection among deliveries in the U.S.MethodsIn 2020, U.S. natality files (2010-2018) with county-level maternal residence information were used from states that had adopted the 2003 revised U.S. birth certificate, which included a field for hepatitis C virus infection present during pregnancy. Hierarchical Bayesian spatial models with spatiotemporal random effects were applied to produce stable annual county-level estimates of maternal hepatitis C virus infection for years when all states had adopted the revised birth certificate (2016-2018). Models included a 6-Level Urban-Rural County Classification Scheme along with the birth year and county-specific covariates to improve posterior predictions.ResultsAmong approximately 32 million live births, the overall prevalence of maternal hepatitis C virus infection was 3.5 per 1,000 births (increased from 2.0 in 2010 to 5.0 in 2018). During 2016-2018, posterior predicted median county-level maternal hepatitis C virus infection rates showed that nonurban counties had 3.5-3.8 times higher rates of hepatitis C virus than large central metropolitan counties. The counties in the top 10th percentile for maternal hepatitis C virus rates in 2018 were generally located in Appalachia, in Northern New England, along the northern border in the Upper Midwest, and in New Mexico.ConclusionsFurther implementation of community-level interventions that are effective in reducing maternal hepatitis C virus infection and its subsequent morbidity may help to reduce geographic and rural disparities.
| S-EPMC8154677 | biostudies-literature
