Associations between combinations of job demands and job control among 6,16,818 people aged 55-64 in paid work with their labour market status 11 years later: a prospective cohort study.

BACKGROUND: Given current discussions about extending working lives, more knowledge is needed on working conditions associated with labour market status in older age. OBJECTIVE: To explore associations between combinations of job demands and job control among workers aged 55-64 years and their labour market status 11 years later. METHODS: A population-based prospective cohort study using nationwide register data. The 616,818 individuals in Sweden aged 55-64 who in 2001 were in paid work were categorised using a job exposure matrix based on tertiles (reference = medium control/medium demands). Participants were followed up in 2012 regarding their main labour market status (paid work, old-age pension, no income/social assistance, sickness absence/disability pension, emigrated, dead; reference = old-age pension) using multinomial logistic regression for odds ratios (OR) and 95% confidence intervals (CI). The fully adjusted analyses included adjustment for sociodemographic factors and unemployment or sickness absence/disability pension for more than half the year in 2001. RESULTS: Those in occupations with low job control at baseline were less likely to be in paid work at follow-up (OR low demands/low control 0.74, CI 0.71-0.78; high demands/low control 0.81, CI 0.75-0.87). Those in occupations with baseline high demands were less likely to have no income/social assistance at follow-up (OR high demands/low control 0.71, CI 0.52-0.96; high demands/high control 0.59, CI 0.47-0.75). CONCLUSION: Job demands and control when aged 55-64 were associated with labour market status 11 years later: high control was associated with greater chance of being in paid work, and high demands were associated with lower risk of no income/social assistance

Sick leave among people in paid work after age 65: A Swedish population-based study covering 1995, 2000, 2005 and 2010

AIMS: Extending working life into older age groups is discussed in many countries. However, there is no knowledge about how this affects rates of sick leave. The aim of this work was to investigate rates of sick leave among people in paid work after retirement age and if such rates have changed over time. METHODS: Swedish nationwide register data on people aged >65 years and living in Sweden in 1995, 2000, 2005 and 2010 were analysed. All people with a sufficiently high work income to be eligible for public sick leave benefits were included. The proportions in paid work and compensated rates of sick leave for people aged 66-70 and ≥71 were analysed by sex, educational level, country of birth, living area, and employment type and sector. RESULTS: The percentage of people in paid work at ages 66-70 years increased from 65 years were lower in 2010 than in 1995, despite much higher rates of labour market participation in 2010

Contribution of income and job strain to the association between education and cardiovascular disease in 1.6 million Danish employees

AIMS: We examined the extent to which associations between education and cardiovascular disease (CVD) morbidity and mortality are attributable to income and work stress. METHODS AND RESULTS: We included all employed Danish residents aged 30-59 years in 2000. Cardiovascular disease morbidity analyses included 1 638 270 individuals, free of cardiometabolic disease (CVD or diabetes). Mortality analyses included 41 944 individuals with cardiometabolic disease. We assessed education and income annually from population registers and work stress, defined as job strain, with a job-exposure matrix. Outcomes were ascertained until 2014 from health registers and risk was estimated using Cox regression. During 10 957 399 (men) and 10 776 516 person-years (women), we identified 51 585 and 24 075 incident CVD cases, respectively. For men with low education, risk of CVD was 1.62 [95% confidence interval (CI) 1.58-1.66] before and 1.46 (95% CI 1.42-1.50) after adjustment for income and job strain (25% reduction). In women, estimates were 1.66 (95% CI 1.61-1.72) and 1.53 (95% CI 1.47-1.58) (21% reduction). Of individuals with cardiometabolic disease, 1736 men (362 234 person-years) and 341 women (179 402 person-years) died from CVD. Education predicted CVD mortality in both sexes. Estimates were reduced with 54% (men) and 33% (women) after adjustment for income and job strain. CONCLUSION: Low education predicted incident CVD in initially healthy individuals and CVD mortality in individuals with prevalent cardiometabolic disease. In men with cardiometabolic disease, income and job strain explained half of the higher CVD mortality in the low education group. In healthy men and in women regardless of cardiometabolic disease, these factors explained 21-33% of the higher CVD morbidity and mortality

Epigenetics and Malaria Susceptibility/Protection: A Missing Piece of the Puzzle

A better understanding of stable changes in regulation of gene expression that result from epigenetic events is of great relevance in the development of strategies to prevent and treat infectious diseases. Histone modification and DNA methylation are key epigenetic mechanisms that can be regarded as marks, which ensure an accurate transmission of the chromatin states and gene expression profiles over generations of cells. There is an increasing list of these modifications, and the complexity of their action is just beginning to be understood. It is clear that the epigenetic landscape plays a fundamental role in most biological processes that involve the manipulation and expression of DNA. Although the molecular mechanism of gene regulation is relatively well understood, the hierarchical order of events and dependencies that lead to protection against infection remain largely unknown. In this review, we propose that host epigenetics is an essential, though relatively under studied, factor in the protection or susceptibility to malaria

Work stress and loss of years lived without chronic disease : an 18-year follow-up of 1.5 million employees in Denmark

We aimed to examine the association between exposure to work stress and chronic disease incidence and loss of chronic disease-free life years in the Danish workforce. The study population included 1,592,491 employees, aged 30-59 in 2000 and without prevalent chronic diseases. We assessed work stress as the combination of job strain and effort-reward imbalance using job exposure matrices. We used Cox regressions to estimate risk of incident hospital-diagnoses or death of chronic diseases (i.e., type 2 diabetes, coronary heart disease, stroke, cancer, asthma, chronic obstructive pulmonary disease, heart failure, and dementia) during 18 years of follow-up and calculated corresponding chronic disease-free life expectancy from age 30 to age 75. Individuals working in occupations with high prevalence of work stress had a higher risk of incident chronic disease compared to those in occupations with low prevalence of work stress (women: HR 1.04 (95% CI 1.02-1.05), men: HR 1.12 (95% CI 1.11-1.14)). The corresponding loss in chronic disease-free life expectancy was 0.25 (95% CI - 0.10 to 0.60) and 0.84 (95% CI 0.56-1.11) years in women and men, respectively. Additional adjustment for health behaviours attenuated these associations among men. We conclude that men working in high-stress occupations have a small loss of years lived without chronic disease compared to men working in low-stress occupations. This finding appeared to be partially attributable to harmful health behaviours. In women, high work stress indicated a very small and statistically non-significant loss of years lived without chronic disease.Peer reviewe

The Chromatin Remodelling Complex B-WICH Changes the Chromatin Structure and Recruits Histone Acetyl-Transferases to Active rRNA Genes

The chromatin remodelling complex B-WICH, which comprises the William syndrome transcription factor (WSTF), SNF2h, and nuclear myosin 1 (NM1), is involved in regulating rDNA transcription, and SiRNA silencing of WSTF leads to a reduced level of 45S pre-rRNA. The mechanism behind the action of B-WICH is unclear. Here, we show that the B-WICH complex affects the chromatin structure and that silencing of the WSTF protein results in a compaction of the chromatin structure over a 200 basepair region at the rRNA promoter. WSTF knock down does not show an effect on the binding of the rRNA-specific enhancer and chromatin protein UBF, which contributes to the chromatin structure at active genes. Instead, WSTF knock down results in a reduced level of acetylated H3-Ac, in particular H3K9-Ac, at the promoter and along the gene. The association of the histone acetyl-transferases PCAF, p300 and GCN5 with the promoter is reduced in WSTF knock down cells, whereas the association of the histone acetyl-transferase MOF is retained. A low level of H3-Ac was also found in growing cells, but here histone acetyl-transferases were present at the rDNA promoter. We propose that the B-WICH complex remodels the chromatin structure at actively transcribed rRNA genes, and this allows for the association of specific histone acetyl-transferases