Current data on the prevalence of prior illicit drug use among the prison population in Europe is scarce. The aim of this study is to identify the prevalence of illicit drug use prior to incarceration, as reported by studies conducted in 30 European countries. A comprehensive literature review was conducted from the 5–31 of March 2018 using the databases Cochrane Library, Embase, MEDLINE, PsychINFO and PubMed. After the deletion of duplications, 2607 articles meeting the eligibility criteria for review were identified. In total, 26 studies from 12 different countries have been included in this review. The review found that the lifetime prevalence of illicit drug use before imprisonment ranged from 30 to 93%; last year prevalence from 51 to 69%; last 6 months prevalence from 13 to 75% and last month prevalence from 58 to 62%. The prevalence of illicit drug use was especially high among women. The rates varied across the 26 studies although high prevalence values are reported in most studies and variations are partly related to methodological differences in the reviewed studies. The high levels of prior involvement with drugs, necessitates prisons to develop clear strategies to deal with illicit drug use.

Hospitals operate in increasingly complex and dynamically uncertain environments. To understand how hospital organizations can cope with such profound uncertainty, this article presents a multiple case study of five hospitals during the COVID-19 crisis in a heavily hit region of the Netherlands. We find that hospitals make adaptations in five key categories, namely: reorganization, decision-making, human resources, material resources, and planning. These adaptations offer insights into the core capabilities needed by hospitals to cope with dynamic uncertainty. Our findings highlight the need for hospitals to become more flexible without sacrificing efficiency. Organizations can accomplish this by building in more sensing and seizing capabilities to be better prepared for and respond to environmental change. Furthermore, transforming capabilities allow organizations to be more resilient and responsive in the face of ongoing uncertainty. We make recommendations on how hospitals can build these capabilities and address the core challenges they face in this pursuit.

The contribution of modifiable risk factors to social inequalities in dementia, observed in longitudinal studies, remains unclear. We aimed to quantify the role of cardiovascular health factors, assessed using Life's Essential 8 (LE8) score, in mediating social inequalities in incidence of dementia and, for comparison, in incidence of stroke, coronary heart disease, and mortality. In this prospective, population-based cohort study, we collected data from the UK Whitehall II Study and UK Biobank databases. Participants were included if data were available on SEP, outcomes and LE8 (smoking, physical activity, diet, body mass index, blood pressure, fasting blood glucose, lipid levels, sleep duration). The primary outcome was incident dementia and secondary outcomes were stroke, coronary heart disease, and mortality. Outcomes were derived from electronic healthcare records. Socioeconomic position (SEP) was measured by occupation in Whitehall II and education in UK Biobank. Counterfactual mediation analysis was used to quantify the extent to which LE8 score explained the associations of SEP with all outcomes. Analyses involved Cox regression, accelerated failure time models, and linear regression; and were adjusted for age, sex, and ethnicity. Between 10.09.1985 and 29.03.1988, a total of 9688 participants (mean age ± SD 44.9 ± 6.0; 67% men) from the Whitehall II study, and between 19.12.2006 and 01.10.2010, 278,215 participants (mean age ± SD 56.0 ± 8.1; 47% men) from the UK Biobank were included. There were 606 and 4649 incident dementia cases over a median (interquartile range) follow-up of 31.7 (31.1–32.7) and 13.5 (12.7–14.1) years respectively in Whitehall II and UK Biobank. In Whitehall II, the hazard ratio was 1.85 [95% CI 1.42, 2.32] for the total effect of SEP on dementia and 1.20 [1.12, 1.28] for the indirect effect via the LE8, the proportion mediated being 36%. In UK Biobank, the total effect of SEP on dementia was 1.65 [1.54, 1.78]; the indirect effect was 1.11 [1.09, 1.12], and the proportion mediated was 24%. The proportions mediated for stroke, coronary heart disease, and mortality were higher, ranging between 34% and 63% in Whitehall II and between 36% and 50% in UK Biobank. In two well-characterised cohort studies, up to one third of the social inequalities in incidence of dementia was attributable to cardiovascular health factors. Promotion of cardiovascular health in midlife may contribute to reducing social inequalities in risk of dementia, in addition to cardiovascular diseases and all-cause mortality. This study used adult measures of SEP, further research is warranted using lifecourse measures of SEP. 10.13039/100000002 NIH (RF1AG062553)

INTRODUCTION: Our main objective was to investigate whether retinal neurodegeneration, estimated from lower thickness of inner retinal layers, was associated with incident all‐cause dementia and Alzheimer's disease (AD).METHODS: We performed an individual participant data meta‐analysis using unpublished data from four prospective cohort studies with a total of 69,955 participants (n = 1087 cases of incident all‐cause dementia; n = 520 cases incident AD; follow‐up time median [interquartile range] 11.3 [8.8–11.5] years).RESULTS: General baseline characteristics of the study population were mean (standard deviation) age, 58.1 (8.8) years; 47% women. After adjustment, lower baseline macular retinal nerve fiber layer thickness was significantly associated with a 10% and 11% higher incidence of all‐cause dementia and AD, respectively. Lower baseline macular ganglion cell‐inner plexiform layer thickness was not significantly associated with these outcomes.DISCUSSION: These findings suggest that retinal neurodegeneration precedes the onset of clinical dementia. Retinal imaging tools may be informative biomarkers for the study of the early pathophysiology of dementia.

Background: Microvascular dysfunction (MVD) is an important contributor to major clinical disease such as stroke, dementia, depression, retinopathy, and chronic kidney disease. Alcohol consumption may be a determinant of MVD. Objective: Main objectives were (1) to study whether alcohol consumption was associated with MVD as assessed in the brain, retina, skin, kidney and in the blood; and (2) to investigate whether associations differed by history of cardiovascular disease or sex. Design: We used cross-sectional data from The Maastricht Study (N = 3,120 participants, 50.9% men, mean age 60 years, and 27.5% with type 2 diabetes [the latter oversampled by design]). We used regression analyses to study the association between total alcohol (per unit and in the categories, i.e. none, light, moderate, high) and MVD, where all measures of MVD were combined into a total MVD composite score (expressed in SD). We adjusted all associations for potential confounders; and tested for interaction by sex, and history of cardiovascular disease. Additionally we tested for interaction with glucose metabolism status. Results: The association between total alcohol consumption and MVD was non-linear, i.e. J-shaped. Moderate versus light total alcohol consumption was significantly associated with less MVD, after full adjustment (beta [95% confidence interval], -0.10 [-0.19; -0.01]). The shape of the curve differed with sex (P_interaction = 0.03), history of cardiovascular disease (P_interaction < 0.001), and glucose metabolism status (P_interaction = 0.02). Conclusions: The present cross-sectional, population-based study found evidence that alcohol consumption may have an effect on MVD. Hence, although increasing alcohol consumption cannot be recommended as a policy, this study suggests that prevention of MVD may be possible through dietary interventions.

Late-life depression is a debilitating disease that may be caused by neurodegeneration.^1,2 Clinically, late-life depression is associated with a high comorbidity of psychiatric and physical diseases including neurodegenerative diseases such as Alzheimer disease.³ Mechanistically, neurodegeneration in brain regions involved in reward, salience, and cognitive function is thought to lead to disturbances in mood, cognition, and motoric behavior, all of which are clinical symptoms of late-life depression.¹