Effects of an Internet Delivered Behavioral Activation Program on Improving Work Engagement Among Japanese Workers: A Pretest and Posttest Study.

OBJECTIVE: The aim of the study is to examine the effect of a newly developed Internet-delivered behavioral activation (iBA) program on work engagement and well-being among Japanese workers with elevated psychological distress. METHODS: Participants were recruited via an Internet survey company ( N = 3299). The eligibility criteria were as follows: (1) Japanese employees aged 20 to 59 years, (2) having psychological distress, and (3) not self-employed. This iBA program was a 3-week web-based training course using behavioral activation techniques. Work engagement, psychological distress, and eudemonic well-being at work were measured at baseline and postintervention period. A paired sample t test was conducted to assess the intervention effect. RESULTS: Of the 568 eligible participants, 120 were randomly selected. A total of 108 participants completed the baseline survey and received the iBA program. Eighty respondents completed the postintervention survey and were included in analyses. The iBA program did not show a significant intervention effect on work engagement ( P = 0.22, Cohen d = 0.14), while psychological distress ( P < 0.01, d = -0.40) and role-oriented future prospects ( P = 0.02, Cohen d = 0.27) were significantly improved. CONCLUSIONS: The effect of the iBA program on work engagement may be limited.

Hindbrain Adenosine 5-Triphosphate (ATP)-Purinergic Signaling Triggers LH Surge and Ovulation via Activation of AVPV Kisspeptin Neurons in Rats.

Ovulation disorders are a serious problem for humans and livestock. In female rodents, kisspeptin neurons in the anteroventral periventricular nucleus (AVPV) are responsible for generating a luteinizing hormone (LH) surge and consequent ovulation. Here, we report that adenosine 5-triphosphate (ATP), a purinergic receptor ligand, is a possible neurotransmitter that stimulates AVPV kisspeptin neurons to induce an LH surge and consequent ovulation in rodents. Administration of an ATP receptor antagonist (PPADS) into the AVPV blocked the LH surge in ovariectomized (OVX) rats treated with a proestrous level of estrogen (OVX + high E2) and significantly reduced the ovulation rate in proestrous ovary-intact rats. AVPV ATP administration induced a surge-like LH increase in OVX + high E2 rats in the morning. Importantly, AVPV ATP administration could not induce the LH increase in Kiss1 KO rats. Furthermore, ATP significantly increased intracellular Ca2+ levels in immortalized kisspeptin neuronal cell line, and coadministration of PPADS blocked the ATP-induced Ca2+ increase. Histologic analysis revealed that the proestrous level of estrogen significantly increased the number of P2X2 receptor (an ATP receptor)-immunopositive AVPV kisspeptin neurons visualized by tdTomato in Kiss1-tdTomato rats. The proestrous level of estrogen significantly increased varicosity-like vesicular nucleotide transporter (a purinergic marker)-immunopositive fibers projecting to the vicinity of AVPV kisspeptin neurons. Furthermore, we found that some hindbrain vesicular nucleotide transporter-positive neurons projected to the AVPV and expressed estrogen receptor α, and the neurons were activated by the high E2 treatment. These results suggest that hindbrain ATP-purinergic signaling triggers ovulation via activation of AVPV kisspeptin neurons.SIGNIFICANCE STATEMENT Ovulation disorders, which cause infertility and low pregnancy rates, are a serious problem for humans and livestock. The present study provides evidence that adenosine 5-triphosphate, acting as a neurotransmitter in the brain, stimulates kisspeptin neurons in the anteroventral periventricular nucleus, known as the gonadotropin-releasing hormone surge generator, via purinergic receptors to induce the gonadotropin-releasing hormone/luteinizing hormone surge and ovulation in rats. In addition, histologic analyses indicate that adenosine 5-triphosphate is likely to be originated from the purinergic neurons in the A1 and A2 of the hindbrain. These findings may contribute to new therapeutic controls for hypothalamic ovulation disorders in humans and livestock.