The Effect of Large-scale Health Coverage Expansions in Wealthy Nations on Society-Wide Healthcare Utilization.
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ABSTRACT:
SUBMITTER: Gaffney A
PROVIDER: S-EPMC7403378 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundUnited Nations (UN) personnel address a diverse range of political, social, and cultural crises throughout the world. Compared with other occupations routinely exposed to traumatic stress, there remains a paucity of research on mental health disorders and access to mental healthcare in this population. To fill this gap, personnel from UN agencies were surveyed for mental health disorders and mental healthcare utilization.MethodsUN personnel (N = 17 363) from 11 UN entities completed online measures of generalized anxiety disorder (GAD), major depressive disorder (MDD), posttraumatic stress disorder (PTSD), trauma exposure, mental healthcare usage, and socio-demographic information.ResultsExposure to one or more traumatic events was reported by 36.2% of survey responders. Additionally, 17.9% screened positive for GAD, 22.8% for MDD, and 19.9% for PTSD. Employing multivariable logistic regressions, low job satisfaction, younger age (<35 years of age), greater length of employment, and trauma exposure on or off-duty was significantly associated with all the three disorders. Among individuals screening positive for a mental health disorder, 2.05% sought mental health treatment within and 10.01% outside the UN in the past year.ConclusionsUN personnel appear to be at high risk for trauma exposure and screening positive for a mental health disorder, yet a small percentage screening positive for mental health disorders sought treatment. Despite the mental health gaps observed in this study, additional research is needed, as these data reflect a large sample of convenience and it cannot be determined if the findings are representative of the UN.
| S-EPMC7056861 | biostudies-literature
Project description:Large-scale expansions of DNA repeats are implicated in numerous hereditary disorders in humans. We describe a yeast experimental system to analyze large-scale expansions of triplet GAA repeats responsible for the human disease Friedreich's ataxia. When GAA repeats were placed into an intron of the chimeric URA3 gene, their expansions caused gene inactivation, which was detected on the selective media. We found that the rates of expansions of GAA repeats increased exponentially with their lengths. These rates were only mildly dependent on the repeat's orientation within the replicon, whereas the repeat-mediated replication fork stalling was exquisitely orientation dependent. Expansion rates were significantly elevated upon inactivation of the replication fork stabilizers, Tof1 and Csm3, but decreased in the knockouts of postreplication DNA repair proteins, Rad6 and Rad5, and the DNA helicase Sgs1. We propose a model for large-scale repeat expansions based on template switching during replication fork progression through repetitive DNA.
| S-EPMC2722067 | biostudies-literature
Project description:ObjectivesWe aim to clarify the pathogenic role of intermediate size repeat expansions of SCA2, SCA3, SCA6, and SCA17 as risk factors for idiopathic Parkinson disease (PD).MethodsWe invited researchers from the Genetic Epidemiology of Parkinson's Disease Consortium to participate in the study. There were 12,346 cases and 8,164 controls genotyped, for a total of 4 repeats within the SCA2, SCA3, SCA6, and SCA17 genes. Fixed- and random-effects models were used to estimate the summary risk estimates for the genes. We investigated between-study heterogeneity and heterogeneity between different ethnic populations.ResultsWe did not observe any definite pathogenic repeat expansions for SCA2, SCA3, SCA6, and SCA17 genes in patients with idiopathic PD from Caucasian and Asian populations. Furthermore, overall analysis did not reveal any significant association between intermediate repeats and PD. The effect estimates (odds ratio) ranged from 0.93 to 1.01 in the overall cohort for the SCA2, SCA3, SCA6, and SCA17 loci.ConclusionsOur study did not support a major role for definite pathogenic repeat expansions in SCA2, SCA3, SCA6, and SCA17 genes for idiopathic PD. Thus, results of this large study do not support diagnostic screening of SCA2, SCA3, SCA6, and SCA17 gene repeats in the common idiopathic form of PD. Likewise, this largest multicentered study performed to date excludes the role of intermediate repeats of these genes as a risk factor for PD.
| S-EPMC4617164 | biostudies-literature
Project description:Expansions of simple DNA repeats cause numerous hereditary disorders in humans. Replication, repair, and transcription are implicated in the expansion process, but their relative contributions are yet to be distinguished. To separate the roles of replication and transcription in the expansion of Friedreich's ataxia (GAA)n repeats, we designed two yeast genetic systems that utilize a galactose-inducible GAL1 promoter but contain these repeats in either the transcribed or nontranscribed region of a selectable cassette. We found that large-scale repeat expansions can occur in the lack of transcription. Induction of transcription strongly elevated the rate of expansions in both systems, indicating that active transcriptional state rather than transcription through the repeat per se affects this process. Furthermore, replication defects increased the rate of repeat expansions irrespective of transcriptional state. We present a model in which transcriptional state, linked to the nucleosomal density of a region, acts as a modulator of large-scale repeat expansions.
| S-EPMC4268310 | biostudies-literature
Project description:ObjectiveTo evaluate impacts of state Medicaid expansions for low-income parents on the health insurance coverage, pregnancy intention, and use of prenatal care among mothers who became pregnant.Data sources/study settingPerson-level data for women with a live birth from the 1997-2012 Pregnancy Risk Assessment Monitoring System.Data collection/extraction methodsThe sample was restricted to women who were already parents using information on previous live births and combined with information on state Medicaid policies for low-income parents.Study designI used a measure of expanded generosity of state Medicaid eligibility for low-income parents to estimate changes in health insurance, pregnancy intention, and prenatal care for pregnant mothers associated with Medicaid expansion.Principal findingsI found an increase in prepregnancy health insurance coverage and coverage during pregnancy among pregnant mothers, as well as earlier initiation of prenatal care, associated with the expansions. Among pregnant mothers with less education, I found an increase in the adequacy of prenatal care utilization.ConclusionsExpanded Medicaid coverage for low-income adults has the potential to increase a woman's health insurance coverage prior to pregnancy, as well as her insurance coverage and medical care receipt during pregnancy.
| S-EPMC6153180 | biostudies-literature
Project description:BackgroundIn 2014, only 26 states and the District of Columbia chose to implement the Patient Protection and Affordable Care Act (ACA) Medicaid expansions for low-income adults.ObjectiveTo evaluate whether the state Medicaid expansions were associated with changes in insurance coverage, access to and utilization of health care, and self-reported health.DesignComparison of outcomes before and after the expansions in states that did and did not expand Medicaid.SettingUnited States.ParticipantsCitizens aged 19 to 64 years with family incomes below 138% of the federal poverty level in the 2010 to 2014 National Health Interview Surveys.MeasurementsHealth insurance coverage (private, Medicaid, or none); improvements in coverage over the previous year; visits to physicians in general practice and specialists; hospitalizations and emergency department visits; skipped or delayed medical care; usual source of care; diagnoses of diabetes, high cholesterol, and hypertension; self-reported health; and depression.ResultsIn the second half of 2014, adults in expansion states experienced increased health insurance (7.4 percentage points [95% CI, 3.4 to 11.3 percentage points]) and Medicaid (10.5 percentage points [CI, 6.5 to 14.5 percentage points]) coverage and better coverage than 1 year before (7.1 percentage points [CI, 2.7 to 11.5 percentage points]) compared with adults in nonexpansion states. Medicaid expansions were associated with increased visits to physicians in general practice (6.6 percentage points [CI, 1.3 to 12.0 percentage points]), overnight hospital stays (2.4 percentage points [CI, 0.7 to 4.2 percentage points]), and rates of diagnosis of diabetes (5.2 percentage points [CI, 2.4 to 8.1 percentage points]) and high cholesterol (5.7 percentage points [CI, 2.0 to 9.4 percentage points]). Changes in other outcomes were not statistically significant.LimitationObservational study may be susceptible to unmeasured confounders; reliance on self-reported data; limited post-ACA time frame provided information on short-term changes only.ConclusionThe ACA Medicaid expansions were associated with higher rates of insurance coverage, improved quality of coverage, increased utilization of some types of health care, and higher rates of diagnosis of chronic health conditions for low-income adults.Primary funding sourceNone.
| S-EPMC5021068 | biostudies-literature
Project description:Many genetic variants influence complex traits by modulating gene expression, thus altering the abundance of one or multiple proteins. Here we introduce a powerful strategy that integrates gene expression measurements with summary association statistics from large-scale genome-wide association studies (GWAS) to identify genes whose cis-regulated expression is associated with complex traits. We leverage expression imputation from genetic data to perform a transcriptome-wide association study (TWAS) to identify significant expression-trait associations. We applied our approaches to expression data from blood and adipose tissue measured in ∼ 3,000 individuals overall. We imputed gene expression into GWAS data from over 900,000 phenotype measurements to identify 69 new genes significantly associated with obesity-related traits (BMI, lipids and height). Many of these genes are associated with relevant phenotypes in the Hybrid Mouse Diversity Panel. Our results showcase the power of integrating genotype, gene expression and phenotype to gain insights into the genetic basis of complex traits.
| S-EPMC4767558 | biostudies-other
Project description:Healthcare providers are routinely being assessed for metrics designed to assess the quality of the care they deliver. There is growing consensus that these measurements, which typically assess the percentage of patients meeting a specific standard of care, should be adjusted for the clinical complexity of the providers. This study will assess whether adjusting for the social complexity of the patient panel adds significantly to adjustment for clinical complexity in explaining apparent differences in quality of care provided by Primary care providers and clinics.
| 2257794 | ecrin-mdr-crc
Project description:Expansions of (CAG)n/(CTG)n trinucleotide repeats are responsible for over a dozen neuromuscular and neurodegenerative disorders. Large-scale expansions are commonly observed in human pedigrees and may be explained by iterative small-scale events such as strand slippage during replication or repair DNA synthesis. Alternatively, a distinct mechanism may lead to a large-scale repeat expansion as a single step. To distinguish between these possibilities, we developed a novel experimental system specifically tuned to analyze large-scale expansions of (CAG)n/(CTG)n repeats in Saccharomyces cerevisiae. The median size of repeat expansions was ?60 triplets, although we also observed additions of more than 150 triplets. Genetic analysis revealed that Rad51, Rad52, Mre11, Pol32, Pif1, and Mus81 and/or Yen1 proteins are required for large-scale expansions, whereas proteins previously implicated in small-scale expansions are not involved. From these results, we propose a new model for large-scale expansions, which is based on the recovery of replication forks broken at (CAG)n/(CTG)n repeats via break-induced replication.
| S-EPMC5215974 | biostudies-literature
Project description:Study designRetrospective observational cohort study.ObjectivesEstimate spinal cord injury (SCI) prevalence in First Nations and non-First Nations populations and compare healthcare utilization as an indirect marker of health inequities.SettingAlberta, Canada.MethodsWe created a prevalent adult SCI cohort by identifying cases between April 1, 2002 and December 31, 2017 who were followed for common SCI complications and location of healthcare access from January 1, 2018 to December 31, 2019 using administrative data sources housed within Alberta Health Services (AHS). First Nations and non-First Nations SCI cohorts were divided into SCI etiology: traumatic SCI (TSCI) and non-traumatic SCI (NTSCI). Statistical analyses compared prevalence, demographics, healthcare utilization, and SCI complication rates. A secondary analysis was performed using case matching for demographics, injury type, injury level, and comorbidities.ResultsTSCI prevalence: 248 and 117 per 100,000 in First Nations and non-First Nations cohorts, respectively. NTSCI prevalence: 74 and 50 per 100,000 in First Nations and non-First Nations cohorts, respectively. Visit rates were higher in the TSCI First Nations cohort for visits to General Practitioner (GP), Emergency Department (ED), inpatient visits, and inpatient days with higher complication rates due to pulmonary, genitourinary, skin, and 'other' causes after case matching. Visits rates were higher in the NTSCI First Nations cohort for GP and specialists without differences in complication types after case matching.ConclusionsSignificant differences exist between First Nations and non-First Nations cohorts living with SCI in Alberta, suggesting healthcare inequities against First Nations Peoples in this province.
| S-EPMC10484972 | biostudies-literature