Prospective register-based study of the impact of immigration on educational inequalities in mortality in Norway

Background: Differences in mortality with regard to socioeconomic status have widened in recent decades in many European countries, including Norway. A rapid upsurge of immigration to Norway has occurred since the 1990s. The article investigates the impact of immigration on educational mortality differences among adults in Norway. Methods: Two linked register-based data sets are analyzed; the first consists of all registered inhabitants aged 20–69 in Norway January 1, 1993 (2.6 millions), and the second of all registered inhabitants aged 20–69 as of January 1, 2008 (2.8 millions). Deaths 1993–1996 and 2008–2011, respectively, immigrant status, and other background information are available in the data. Mortality is examined by Cox regression analyses and by estimations of age-adjusted deaths per 100,000 personyears. Results: Both relative and absolute educational inequality in mortality increased from the 1993–1996 period to 2008–2011, but overall mortality levels went down during these years. Immigrants in general, and almost all the analyzed immigrant subcategories, had lower mortality than the native majority. This was due to comparatively low mortality among lower educated immigrants, while mortality among higher educated immigrants was similar to the mortality level of highly educated natives. Conclusions: The widening of educational inequality in mortality during the 1990s and 2000s in Norway was not due to immigration. Immigration rather contributed to slightly lower overall mortality in the population and a less steep educational gradient in mortality

A framework to assess welfare mix and service provision models in health care and social welfare: case studies of two prominent Italian regions

BACKGROUND: The mechanisms through which the relationships among public institutions, private providers and families affect care and service provision systems are puzzling. How can we understand the mechanisms in these contexts? Which elements should we explore to capture the complexity of care provision? The aim of our study is to provide a framework that can help read and reframe these puzzling care provision mechanisms in a welfare mix context. METHODS: First, we develop a theoretical framework for understanding how service provision occurs in care systems that are characterised by a variety of relationships between multiple actors, using an evidence-based approach that looks at both public and private expenditures and the number of users relative to the level of needs coverage and compared with declared values and political rhetoric. Second, we test this framework in two case studies built on data from two prominent Italian regions, Lombardy and Emilia-Romagna. We argue that service provision models depend on the interplay among six conceptual elements: policy values, governance rules, resources, nature of the providers, service standards and eligibility criteria. RESULTS: Our empirical study shows that beneath the relevant differences in values and political rhetoric between the case studies of the two Italian regions, there is a surprising isomorphism in service standards and the levels of covering the population’s needs. CONCLUSION: The suggested framework appears to be effective and feasible; it fosters interdisciplinary approaches and supports policy-making discussions. This study may contribute to deepening knowledge about public care service provision and institutional arrangements, which can be used to promote more effective reforms and may advance future research. Although the framework was tested on the Italian welfare system, it can be used to assess many different systems

The alkyl side chain of PACA nanoparticles dictates the impact on cellular stress responses and the mode of particle-induced cell death

AbstractFor optimal exploitation of nanoparticles (NPs) in biomedicine, and to predict nanotoxicity, detailed knowledge on the cellular responses to cell-bound or internalized NPs is imperative. The outcome of NP-cell interaction is dictated by the type and magnitude of the NP insult and the cellular response. Here, we have systematically studied the impact of minor differences in NP composition on cellular stress responses and viability by using highly similar poly(alkylcyanoacrylate) (PACA) particles. Surprisingly, PACA particles differing only in their alkyl side chains; butyl (PBCA), ethylbutyl (PEBCA), or octyl (POCA), respectively, induced different stress responses and modes of cell death in human cell lines. POCA particles induced endoplasmic reticulum stress and apoptosis. In contrast, PBCA and PEBCA particles induced lipid peroxidation by depletion of the main cellular antioxidant glutathione (GSH), in a manner depending on the levels of the GSH precursor cystine, and transcription of the cystine transporter SLC7A11 regulated by ATF4 and Nrf2. Intriguingly, these particles activated the recently discovered cell death mechanism ferroptosis, which constitutes a promising alternative for targeting multidrug-resistant cancer stem-like cells. Of the two, PBCA was the strongest inducer. In summary, our findings highlight the cellular sensitivity to nanoparticle composition and have important implications for the choice of PACA monomer in therapeutical settings.</jats:p

Danish and Norwegian hospital social workers’ cross-institutional work amidst inter-sectoral restructuring of health and social welfare

Starting in the 2000s, Denmark and Norway have under gone extensive restructuring of the ir health - related social benefit programmes , including how they are governed . Several reforms have sought to enhance inter - sectoral collaboration . Aiming at ensuring patients’ faster return to work , policy makers have ins tituted economic incentives to both individual s and the health and welfare organisation s who handle them . Through an institutional logics approach , t his paper explores how h ospital social workers in these countries are experiencing the se changes . The ‘ social ’ part of post - treatment care and rehabilitation receives more attention in the Norwegian institutional set - up than in the Danish , and whilst challenges are experienced in both countries, in group interviews Danish social workers in particular expres s concerns about the implications of the accelerated return - to - work focus . In both countries, they report increasing difficulties in ‘ making their way through ’ the state - municipal bureaucracy . However, by d rawing on the formal health knowledge derived from medical settings and the symbo lic capital it bestows on them, they often manage to negotiate the work - and - welfare services , and t hereby transforming the social context for the patient

Brain change trajectories in healthy adults correlate with Alzheimer’s related genetic variation and memory decline across life

Throughout adulthood and ageing our brains undergo structural loss in an average pattern resembling faster atrophy in Alzheimer’s disease (AD). Using a longitudinal adult lifespan sample (aged 30-89; 2–7 timepoints) and four polygenic scores for AD, we show that change in AD-sensitive brain features correlates with genetic AD-risk and memory decline in healthy adults. We first show genetic risk links with more brain loss than expected for age in early Braak regions, and find this extends beyond APOE genotype. Next, we run machine learning on AD-control data from the Alzheimer’s Disease Neuroimaging Initiative using brain change trajectories conditioned on age, to identify AD-sensitive features and model their change in healthy adults. Genetic AD-risk linked with multivariate change across many AD-sensitive features, and we show most individuals over age ~50 are on an accelerated trajectory of brain loss in AD-sensitive regions. Finally, high genetic risk adults with elevated brain change showed more memory decline through adulthood, compared to high genetic risk adults with less brain change. Our findings suggest quantitative AD risk factors are detectable in healthy individuals, via a shared pattern of ageing- and AD-related neurodegeneration that occurs along a continuum and tracks memory decline through adulthood

Constitutive Activation of Chaperone-mediated Autophagy in Cells with Impaired Macroautophagy

Three different types of autophagy—macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA)—contribute to degradation of intracellular components in lysosomes in mammalian cells. Although some level of basal macroautophagy and CMA activities has been described in different cell types and tissues, these two pathways are maximally activated under stress conditions. Activation of these two pathways is often sequential, suggesting the existence of some level of cross-talk between both stress-related autophagic pathways. In this work, we analyze the consequences of blockage of macroautophagy on CMA activity. Using mouse embryonic fibroblasts deficient in Atg5, an autophagy-related protein required for autophagosome formation, we have found that blockage of macroautophagy leads to up-regulation of CMA, even under basal conditions. Interestingly, different mechanisms contribute to the observed changes in CMA-related proteins and the consequent activation of CMA during basal and stress conditions in these macroautophagy-deficient cells. This work supports a direct cross-talk between these two forms of autophagy, and it identifies changes in the lysosomal compartment that underlie the basis for the communication between both autophagic pathways