The effect of a brief, unplanned treatment delay on neovascular age-related macular degeneration patients: a retrospective cohort study.

Non-compliance to intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapy can result in increased disease activity in neovascular age-related macular degeneration (nAMD). Our study aims to determine effects of unplanned delay in anti-VEGF injection treatment for nAMD. This retrospective observational study included patients with delays in receiving intravitreal injections for nAMD treatment from March to May 2020 by at least 21 days. Baseline demographic and clinical characteristics, visual acuity (VA), central macular thickness (CMT) measured on optical coherence tomography (OCT), and duration of delayed treatment were analyzed for 3 time points, the pre-delay visit (v1) and post-delay visits (v2 and v3). Data were compared to age-matched controls treated for nAMD in 2019 without delay. Demographic characteristics were compared using two-sample t-tests for continuous variables and Pearson's chi-square tests for categorical variables. For the two primary outcomes of interest, VA and CMT, means and standard deviations were reported for each combination of group and time. Each outcome was modeled using a linear mixed model with the group, time and group-time interaction as fixed effects. A total of 69 patients (99 eyes) in the treatment delay group and 44 patients (69 eyes) in the control group were identified. Statistically significant differences between control and delayed groups were detected for VA (difference in mean logMAR = 0.16; 95% CI 0.06, 0.27; p = 0.002) and CMT (difference in mean CMT = 29; 95% CI 12, 47; p = 0.001) at v2. No differences were detected for v1 and v3 time points for both outcomes. An unplanned delay in intravitreal injection treatment for nAMD resulted in an increase in CMT and worsening of VA compared to controls observed at v2. At v3, CMT and VA recovered to near v1 levels. This study demonstrates that a one-time, brief interruption in treatment for nAMD results in reversible, temporary worsening.

Medications for opioid use disorder during pregnancy: Access and continuity in a state women's prison facility, 2016-2019.

BACKGROUND: Although medications to treat opioid use disorder (MOUD) are the standard of care during pregnancy, there are many potential gaps in the cascade of care for pregnant people experiencing incarceration. METHODS: We conducted a retrospective cohort study of pregnant people with opioid use disorder incarcerated in a Southeastern women's prison from 2016 to 2019. The primary outcomes were access to MOUD during incarceration and continuity in the community. We used descriptive statistics to summarize aspects of our sample and logistic regression to identify predictors of MOUD receipt during incarceration. RESULTS: Of the 279 pregnant people with OUD included in the analysis, only 40.1% (n = 112) received MOUD during incarceration, including 67 (59.8%) who received methadone and 45 (40.1%) who received buprenorphine. Less than one-third of the participants were referred to a community MOUD provider (n = 83, 30%) on return to the community. Significant predictors of MOUD receipt included medium/close custody level during incarceration, incarceration during the latter portion of the study period, pre-incarceration heroin use, and receipt of pre-incarceration MOUD. CONCLUSIONS: Although prisons can serve as an important site of retention in MOUD for some pregnant people, there were substantial gaps in initiation of MOUD and retention in MOUD among pregnant people with OUD imprisoned in the Southeast during the study period.

Corpora amylacea are associated with tau burden and cognitive status in Alzheimer's disease.

Corpora amylacea (CA) and their murine analogs, periodic acid Schiff (PAS) granules, are age-related, carbohydrate-rich structures that serve as waste repositories for aggregated proteins, damaged cellular organelles, and other cellular debris. The structure, morphology, and suspected functions of CA in the brain imply disease relevance. Despite this, the link between CA and age-related neurodegenerative diseases, particularly Alzheimer's disease (AD), remains poorly defined. We performed a neuropathological analysis of mouse PAS granules and human CA and correlated these findings with AD progression. Increased PAS granule density was observed in symptomatic tau transgenic mice and APOE knock-in mice. Using a cohort of postmortem AD brain samples, we examined CA in cognitively normal and dementia patients across Braak stages with varying APOE status. We identified a Braak-stage dependent bimodal distribution of CA in the dentate gyrus, with CA accumulating and peaking by Braak stages II-III, then steadily declining with increasing tau burden. Refined analysis revealed an association of CA levels with both cognition and APOE status. Finally, tau was detected in whole CA present in human patient cerebrospinal fluid, highlighting CA-tau as a plausible prodromal AD biomarker. Our study connects hallmarks of the aging brain with the emergence of AD pathology and suggests that CA may act as a compensatory factor that becomes depleted with advancing tau burden.