Suchergebnisse

AIMS. People with severe mental illness (SMI) have a high risk of living socially excluded from the mainstream society. Policy initiatives and health systems aim to improve the social situation of people who suffer from mental health disabilities. The aim of this study was to explore the extent of social exclusion (employment and income, social network and social activities, health problems) of people with SMI in Switzerland. METHODS. Data from the Swiss Health Survey 2012 were used to compare the social exclusion magnitude of people with SMI with those suffering from severe physical illness, common mental illness and the general population. RESULTS. With the exception of Instrumental Activities of Daily Living, we found a gradient of social exclusion that showed people with SMI to be more excluded than the comparison groups. Loneliness and poverty were widespread among people with SMI. Logistic regression analyses on each individual exclusion indicator revealed that people with SMI and people with severe physical illness were similarly excluded on many indicators, whereas people with common mental illness and the general population were much more socially included. CONCLUSIONS. In contrast to political and health system goals, many people with SMI suffer from social exclusion. Social policy and clinical support should increase the efforts to counter exclusionary trends, especially in terms of loneliness and poverty.

Genome wide association studies (GWAS) for type 2 diabetes (T2D) have identified genetic loci that often localise in non-coding regions of the genome, suggesting gene regulation effects. We combined genetic and transcriptomic analysis from human islets obtained from brain-dead organ donors or surgical patients to detect expression quantitative trait loci (eQTLs) and shed light into the regulatory mechanisms of these genes. Pancreatic islets were isolated either by laser capture microdissection (LCM) from surgical specimens of 103 metabolically phenotyped pancreatectomized patients (PPP) or by collagenase digestion of pancreas from 100 brain-dead organ donors (OD). Genotyping (> 8.7 million single nucleotide polymorphisms) and expression (> 47,000 transcripts and splice variants) analyses were combined to generate cis-eQTLs. After applying genome-wide false discovery rate significance thresholds, we identified 1,173 and 1,021 eQTLs in samples of OD and PPP, respectively. Among the strongest eQTLs shared between OD and PPP were CHURC1 (OD p-value=1.71 × 10 -24 ; PPP p-value = 3.64 × 10 -24 ) and PSPH (OD p-value = 3.92 × 10 -26 ; PPP p-value = 3.64 × 10 -24 ). We identified eQTLs in linkage-disequilibrium with GWAS loci T2D and associated traits, including TTLL6, MLX and KIF9 loci, which do not implicate the nearest gene. We found in the PPP datasets 11 eQTL genes, which were differentially expressed in T2D and two genes (CYP4V2 and TSEN2) associated with HbA1c but none in the OD samples. eQTL analysis of LCM islets from PPP led us to identify novel genes which had not been previously linked to islet biology and T2D. The understanding gained from eQTL approaches, especially using surgical samples of living patients, provides a more accurate 3-dimensional representation than those from genetic studies alone.

Cardiovascular disease (CVD) prevention is defined as a coordinated set of actions, at the population level or targeted at an individual, that are aimed at eliminating or minimizing the impact of CVDs and their related disabilities.1 CVD remains a leading cause of morbidity and mortality, despite improvements in outcomes. Age-adjusted coronary artery disease (CAD) mortality has declined since the 1980s, particularly in high-income regions.2 CAD rates are now less than half what they were in the early 1980s in many countries in Europe, due to preventive measures including the success of smoking legislation. However, inequalities between countries persist and many risk factors, particularly obesity3 and diabetes mellitus (DM),4 have been increasing substantially. If prevention was practised as instructed it would markedly reduce the prevalence of CVD. It is thus not only prevailing risk factors that are of concern, but poor implementation of preventive measures as well.5,6 Prevention should be delivered (i) at the general population level by promoting healthy lifestyle behaviour7 and (ii) at the individual level, i.e. in those subjects at moderate to high risk of CVD or patients with established CVD, by tackling unhealthy lifestyles (e.g. poor-quality diet, physical inactivity, smoking) and by optimising risk factors. Prevention is effective: the elimination of health risk behaviours would make it possible to prevent at least 80% of CVDs and even 40% of cancers.