Effectiveness of a participatory physical and psychosocial intervention to balance the demands and resources of industrial workers: A cluster-randomized controlled trial

Objectives The aim of this study was to evaluate the effectiveness of a participatory physical and psychosocial workplace intervention (known as PIPPI) on work ability and recovery among industrial workers. Methods Eligible workers were cluster-randomized into intervention (N=193) and control (N=222) groups. Intervention group members participated in three workshops where they mapped positive and negative aspects of their physical and psychosocial work environment and developed action plans addressing the highlighted issues, which were subsequently implemented by the participants. Questionnaire-based data on work ability and recovery were collected at baseline and 8-, 10- and 12-month follow-up. Data on productivity, well-being, mental health, and physical demands and resources were collected at baseline and 12-month follow-up. Results The intervention was delivered and received as planned (100% planned workshops conducted, 69% [standard deviation (SD) 7%] participation in workshops) and with a response rate of 76% (SD 8%) to the questionnaires. No significant between-group improvements for any of the outcomes were found in intention-to-treat multi-level mixed models. On the contrary, tendencies were observed for poorer recovery and reduced work ability in the intervention compared to control group. Conclusion The intervention did not improve the outcomes. This result can have several explanations, such as a regression-toward-the-mean effect or that the intervention might have put an additional burden on the workers already facing high work demands. In addition, there may have been an insufficient match between the intervention components implemented and the predetermined outcomes, and implementation may have been unsuccessful. These potential explanations need to be investigated using process evaluation data

Population genomics of post-glacial western Eurasia.

Western Eurasia witnessed several large-scale human migrations during the Holocene <sup>1-5</sup> . Here, to investigate the cross-continental effects of these migrations, we shotgun-sequenced 317 genomes-mainly from the Mesolithic and Neolithic periods-from across northern and western Eurasia. These were imputed alongside published data to obtain diploid genotypes from more than 1,600 ancient humans. Our analyses revealed a 'great divide' genomic boundary extending from the Black Sea to the Baltic. Mesolithic hunter-gatherers were highly genetically differentiated east and west of this zone, and the effect of the neolithization was equally disparate. Large-scale ancestry shifts occurred in the west as farming was introduced, including near-total replacement of hunter-gatherers in many areas, whereas no substantial ancestry shifts happened east of the zone during the same period. Similarly, relatedness decreased in the west from the Neolithic transition onwards, whereas, east of the Urals, relatedness remained high until around 4,000 BP, consistent with the persistence of localized groups of hunter-gatherers. The boundary dissolved when Yamnaya-related ancestry spread across western Eurasia around 5,000 BP, resulting in a second major turnover that reached most parts of Europe within a 1,000-year span. The genetic origin and fate of the Yamnaya have remained elusive, but we show that hunter-gatherers from the Middle Don region contributed ancestry to them. Yamnaya groups later admixed with individuals associated with the Globular Amphora culture before expanding into Europe. Similar turnovers occurred in western Siberia, where we report new genomic data from a 'Neolithic steppe' cline spanning the Siberian forest steppe to Lake Baikal. These prehistoric migrations had profound and lasting effects on the genetic diversity of Eurasian populations

Splitting of the cyclotron resonance in two-dimensional electron systems

A large splitting of the cyclotron resonance line, observed in two different two-dimensional electron systems, remains unexplained. The splitting resembles an anti-level crossing with an unidentified mode of the semiconductor system. Here, we review our data on this splitting, and highlight some results of recent experiments

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)