No abstract

Objectives

We used data from the National Health Interview Survey to compare health care access among individuals involved in same-sex versus opposite-sex relationships.

Methods

We conducted descriptive and logistic regression analyses from pooled data on 614 individuals in same-sex relationships and 93418 individuals in opposite-sex relationships.

Results

Women in same-sex relationships (adjusted odds ratio [OR]=0.60; 95% confidence interval [CI]=0.39, 0.92) were significantly less likely than women in opposite-sex relationships to have health insurance coverage, to have seen a medical provider in the previous 12 months (OR=0.66; 95% CI=0.46, 0.95), and to have a usual source of health care (OR=0.50; 95% CI=0.35, 0.71); they were more likely to have unmet medical needs as a result of cost issues (OR=1.85; 95% CI=1.16, 2.96). In contrast, health care access among men in same-sex relationships was equivalent to or greater than that among men in opposite-sex relationships.

Conclusions

In this study involving a nationwide probability sample, we found some important differences in access to health care between individuals in same-sex and opposite-sex relationships, particularly women.

A unique cluster of childhood leukemia has recently occurred around the city of Fallon in Churchill County, Nevada. From 1999 to 2001, 11 cases were diagnosed in this county of 23,982 people. Exposures related to a nearby naval air station such as jet fuel or an infectious agent carried by naval aviators have been hypothesized as potential causes. The possibility that the cluster could be attributed to chance was also considered. We used data from the Surveillance, Epidemiology, and End Results Program (SEER) to examine the likelihood that chance could explain this cluster. We also used SEER and California Cancer Registry data to evaluate rates of childhood leukemia in other U.S. counties with military aviation facilities. The age-standardized rate ratio (RR) in Churchill County was 12.0 [95% confidence interval (CI), 6.0-21.4; p = 4.3 times symbol 10(-9)]. A cluster of this magnitude would be expected to occur in the United States by chance about once every 22,000 years. The age-standardized RR for the five cases diagnosed after the cluster was first reported was 11.2 (95% CI, 3.6-26.3). In contrast, the incidence rate was not increased in all other U.S. counties with military aviation bases (RR = 1.04; 95% CI, 0.97-1.12) or in the subset of rural counties with military aviation bases (RR = 0.72; 95% CI, 0.48-1.08). These findings suggest that the Churchill County cluster was unlikely due to chance, but no general increase in childhood leukemia was found in other U.S. counties with military aviation bases.

Abstract Background Transcriptional studies suggest Alzheimer's disease (AD) involves dysfunction of many cellular pathways, including synaptic transmission, cytoskeletal dynamics, energetics, and apoptosis. Despite known progression of AD pathologies, it is unclear how such striking regional vulnerability occurs, or which genes play causative roles in disease progression. Methods To address these issues, we performed a large-scale transcriptional analysis in the CA1 and relatively less vulnerable CA3 brain regions of individuals with advanced AD and nondemented controls. In our study, we assessed differential gene expression across region and disease status, compared our results to previous studies of similar design, and performed an unbiased co-expression analysis using weighted gene co-expression network analysis (WGCNA). Several disease genes were identified and validated using qRT-PCR. Results We find disease signatures consistent with several previous microarray studies, then extend these results to show a relationship between disease status and brain region. Specifically, genes showing decreased expression with AD progression tend to show enrichment in CA3 (and vice versa), suggesting transcription levels may reflect a region's vulnerability to disease. Additionally, we find several candidate vulnerability (ABCA1, MT1H, PDK4, RHOBTB3) and protection (FAM13A1, LINGO2, UNC13C) genes based on expression patterns. Finally, we use a systems-biology approach based on WGCNA to uncover disease-relevant expression patterns for major cell types, including pathways consistent with a key role for early microglial activation in AD. Conclusions These results paint a picture of AD as a multifaceted disease involving slight transcriptional changes in many genes between regions, coupled with a systemic immune response, gliosis, and neurodegeneration. Despite this complexity, we find that a consistent picture of gene expression in AD is emerging.

Background

Accumulating evidence indicates that behaviors in Alzheimer's disease and related dementias could result in incarceration. Yet, the proportion of persons diagnosed with dementia and mild cognitive impairment (MCI) before they were incarcerated is largely unknown. By leveraging a national sample of mid- to late-life adults who were incarcerated, we determined the prevalence of dementia and MCI before their incarceration.

Methods

In this current study, participants were Medicare-eligible U.S. veterans who transitioned from incarceration to the community in mid- to late-life from October 1, 2012, to September 30, 2018, after having been incarcerated for ≤10 consecutive years (N = 17,962). Medical claims data were used to determine clinical diagnoses of dementia and MCI up to three years before incarceration. Demographics, comorbidities, and duration of incarceration among those with dementia and MCI were compared to those with neither diagnosis.

Results

Participants were >97% male, 65% non-Hispanic white, 30% non-Hispanic black, and 3.3% had a diagnosis of either dementia (2.5%) or MCI (0.8%) before their most recent incarceration. Individuals with MCI or dementia diagnoses were older, were more likely to be non-Hispanic white, had more medical and psychiatric comorbidities, and experienced homelessness and traumatic brain injury at higher rates than those with neither diagnosis. Average duration of incarceration was significantly shorter among those with MCI (201.8 [±248.0] days) or dementia (312.8 [±548.3] days), as compared to those with neither diagnosis (497.0 [±692.7] days) (p < 0.001).

Conclusions

These findings raise awareness of the proportion of incarcerated persons in the United States who have a diagnosis of MCI or dementia before they are incarcerated. Improved understanding of pathways linking cognitive impairment to incarceration in mid- to late-life are needed to inform appropriateness of incarceration, optimization of health care, and prevention of interpersonal harm in this medically vulnerable population.

Several lines of emerging data point to an imbalance between neuronal excitation and inhibition in at least a subgroup of individuals with autism spectrum disorder (ASD), including in those with fragile X syndrome (FXS), one of the most common genetic syndromes within ASD. In animal models of FXS and of ASD, GABA-B agonists have improved both brain and behavioral phenotypes, including social behavior. A phase 2 randomized, placebo-controlled, crossover trial found that the GABA-B agonist arbaclofen improved social avoidance symptoms in FXS. A pilot open-label trial of arbaclofen suggested similar benefits in ASD. We therefore evaluated arbaclofen in a randomized, placebo-controlled, phase 2 study of 150 participants, aged 5-21 years, with ASD. No difference from placebo was detected on the primary outcome measure, the parent-rated Aberrant Behavior Checklist Social Withdrawal/Lethargy subscale. However, a specified secondary analysis found improvement on the clinician-rated Clinical Global Impression of Severity. An exploratory post hoc analysis of participants with a consistent rater across the trial revealed greater improvement in the Vineland Adaptive Behavior Scales II socialization domain in participants receiving arbaclofen. Affect lability (11%) and sedation (9%) were the most common adverse events. In this exploratory study, secondary analyses suggest that arbaclofen may have the potential to improve symptoms in some children with ASD, but further study will be needed to replicate and extend these initial findings.