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Purpose: This population-representative study examined the association of Medicaid expansion under the Patient Protection and Affordable Care Act (ACA) with postpartum depressive symptoms among low-income women., Methods: We used data from the 2009 - 2018 Pregnancy Risk Assessment Monitoring System (PRAMS) surveys for 13 Medicaid expansion and 7 non-expansion states. We used a generalized difference-in-differences approach and log-binomial regression models to calculate prevalence ratios (PRs) and 95% confidence intervals (CIs) comparing the likelihood of postpartum depressive symptoms among low-income women (≤138% of the federal poverty level) who delivered in expansion and non-expansion states., Results: Adjusting for state and year fixed-effects and individual- and state-level confounders, low-income women who delivered in Medicaid expansion states had a decreased likelihood of postpartum depressive symptoms compared to low-income women who delivered in non-expansion states (PR = 0.93, 95% CI 0.80, 1.07). Results were largely consistent across multiple sensitivity analysis specifications. Results were robust to falsification tests among women with incomes >138% of the federal poverty level., Conclusion: Our results indicate that Medicaid expansion may be associated with a small reduction in the likelihood of postpartum depressive symptoms. Future research should examine the potential for implementation of multiple supportive policies to achieve larger gains in treatment and prevention., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Alzheimer disease (AD) is a complex neurodegenerative disorder predisposed by multiple genetic factors. Mutations in amyloid beta precursor protein (APP) are known to be associated with autosomal dominant, early onset familial AD and possibly also late onset AD (LOAD). A number of genes encoding proteins capable of binding to APP have been identified, but their contribution to AD pathobiology remains unclear. Conceivably, mutations in these genes may play a role in affecting AD susceptibility, which appears to be substantiated by some genetic studies. Here we report results of the first genetic association study with APBB2, an APP binding protein (also known as FE65L), and LOAD, in three independently collected case-control series totaling approximately 2,000 samples. Two SNPs were significantly associated with LOAD in two sample series and in meta-analyses of all three sample sets (for rs13133980: odds ratio [OR](hom)=1.36 [95% CI: 1.05-1.75], OR(het)=1.32 [95% CI: 1.04-1.67], minor allele frequency=43%, P=0.041; and for hCV1558625: OR(hom)=1.37 [95% CI: 1.06-1.77], OR(het)=1.02 [95% CI: 0.82-1.26], minor allele frequency=48%, P=0.026). One of these SNPs, located in a region conserved between the human and mouse genome, showed a significant interaction with age of disease onset. For this marker, the association with LOAD was most pronounced in subjects with disease onset before 75 years of age (OR(hom)=2.43 [95% CI: 1.61-3.67]; OR(het)=2.15 [95% CI: 1.46-3.17]; P=0.00006) in the combined sample set. Our data raise the possibility that genetic variations in APBB2 may affect LOAD susceptibility.

A Tufts University study released in mid-2003 indicates that increasing numbers of clinical trials for U.S.-produced pharmaceutical are being conducted outside the United States, mainly by contract research organizations. This process speeds up clinical trials, but raises ethical issues of the possible coercion or exploitation of more vulnerable and naive patient populations.