Pathways through which health influences early retirement: a qualitative study

Background: Due to the aeging of the population, there is a societal need for workers to prolong their working lives. In the Netherlands, many employees still leave the workforce before the official retirement age of 65. Previous quantitative research showed that poor self-perceived health is a risk factor of (non-disability) early retirement. However, little is known on how poor health may lead to early retirement, and why poor health leads to early retirement in some employees, but not in others. Therefore, the present qualitative study aims to identify in which ways health influences early retirement. Methods. Face-to-face semi-structured interviews were conducted with 30 employees (60-64 years) who retired before the official retirement age of 65. Participants were selected from the Study on Transitions in Employment, Ability and Motivation. The interviews were transcribed verbatim, a summary was made including a timeline, and the interviews were open coded. Results: In 15 of the 30 persons, health played a role in early retirement. Both poor and good health influenced early retirement. For poor health, four pathways were identified. First, employees felt unable to work at all due to health problems. Second, health problems resulted in a self-perceived (future) decline in the ability to work, and employees chose to retire early. Third, employees with health problems were afraid of a further decline in health, and chose to retire early. Fourth, employees with poor health retired early because they felt pushed out by their employer, although they themselves did not experience a reduced work ability. A good health influenced early retirement, since persons wanted to enjoy life while their health still allowed to do so. The financial opportunity to retire sometimes triggered the influence of poor health on early retirement, and often triggered the influence of good health. Employees and employers barely discussed opportunities to prolong working life. Conclusions: Poor and good health influence early retirement via several different pathways. To prolong working life, a dialogue between employers and employees and tailored work-related interventions may be helpful

Epigenetic Regulation of a Murine Retrotransposon by a Dual Histone Modification Mark

Large fractions of eukaryotic genomes contain repetitive sequences of which the vast majority is derived from transposable elements (TEs). In order to inactivate those potentially harmful elements, host organisms silence TEs via methylation of transposon DNA and packaging into chromatin associated with repressive histone marks. The contribution of individual histone modifications in this process is not completely resolved. Therefore, we aimed to define the role of reversible histone acetylation, a modification commonly associated with transcriptional activity, in transcriptional regulation of murine TEs. We surveyed histone acetylation patterns and expression levels of ten different murine TEs in mouse fibroblasts with altered histone acetylation levels, which was achieved via chemical HDAC inhibition with trichostatin A (TSA), or genetic inactivation of the major deacetylase HDAC1. We found that one LTR retrotransposon family encompassing virus-like 30S elements (VL30) showed significant histone H3 hyperacetylation and strong transcriptional activation in response to TSA treatment. Analysis of VL30 transcripts revealed that increased VL30 transcription is due to enhanced expression of a limited number of genomic elements, with one locus being particularly responsive to HDAC inhibition. Importantly, transcriptional induction of VL30 was entirely dependent on the activation of MAP kinase pathways, resulting in serine 10 phosphorylation at histone H3. Stimulation of MAP kinase cascades together with HDAC inhibition led to simultaneous phosphorylation and acetylation (phosphoacetylation) of histone H3 at the VL30 regulatory region. The presence of the phosphoacetylation mark at VL30 LTRs was linked with full transcriptional activation of the mobile element. Our data indicate that the activity of different TEs is controlled by distinct chromatin modifications. We show that activation of a specific mobile element is linked to a dual epigenetic mark and propose a model whereby phosphoacetylation of histone H3 is crucial for full transcriptional activation of VL30 elements

Effect of Tobacco Smoking on The Clinical, Histopathological, and Serological Manifestations of Sjögren’s Syndrome

The authors wish to thank Dr. A. Darise Farris for her critical review of the cellular immune response discussion.Objectives To assess the association of smoking habits with the clinical, serological, and histopathological manifestations of Sjögren’s syndrome (SS) and non-Sjögren’s sicca (non-SS sicca). Methods Cross-sectional case-control study of 1288 patients with sicca symptoms (587 SS and 701 non-SS sicca) evaluated in a multi-disciplinary research clinic. Smoking patterns were obtained from questionnaire data and disease-related clinical and laboratory data were compared between current, past, ever, and never smokers. Results Current smoking rates were 4.6% for SS patients compared to 14.1% in non-SS sicca (p = 5.17x10E-09), 18% in a local lupus cohort (p = 1.13x10E-14) and 16.8% in the community (p = 4.12x10E-15). Current smoking was protective against SS classification (OR 0.35, 95%CI 0.22–0.56, FDR q = 1.9E10-05), focal lymphocytic sialadenitis (OR 0.26, 95%CI 0.15–0.44, FDR q = 1.52x10E-06), focus score ≥1 (OR 0.22, 95%CI 0.13–0.39, FDR q = 1.43x10E-07), and anti-Ro/SSA(+) (OR 0.36, 95%CI 0.2–0.64, FDR q = 0.0009); ever smoking was protective against the same features and against anti-La/SSB(+) (OR 0.52, 95%CI 0.39–0.70, FDR q = 5.82x10E-05). Duration of smoking was inversely correlated with SS even after controlling for socioeconomic status, BMI, alcohol and caffeine consumption. Conclusions Current tobacco smoking is negatively and independently associated with SS, protecting against disease-associated humoral and cellular autoimmunity. The overall smoking rate amongst SS patients is significantly lower than in matched populations and the effects of smoking are proportional to exposure duration. In spite of the protective effects of tobacco on SS manifestations, it is associated with other serious comorbidities such as lung disease, cardiovascular risk and malignancy, and should thus be strongly discouraged in patients with sicca.Yeshttp://www.plosone.org/static/editorial#pee