We examined the effects of active learning education on arterial stiffness and physical activity of community-dwelling older adults with low health literacy. This study is a secondary analysis of randomized controlled trial of 60 participants aged 65 and older with low health literacy. The intervention group (n=30) participated in a weekly 90-minute active learning program session for 24 weeks, which addressed health promotion in older age. The control group (n=30) attended a 90-minute health education class in a didactic manner. The outcomes were measured at baseline and in week 24. The degree of arterial stiffness was assessed based on the cardio-ankle vascular index (CAVI) using the VS-1500 device (Fukuda Denshi Co., Ltd., Tokyo, Japan). The shortened version of the self-reported International Physical Activity Questionnaire was used to assess the amount of total physical activity determined by the metabolic equivalent hours per week. Selleckchem CP-690550 We used analysis by intention-to-treat, with multiple imputation for missing data. Seven participants (11.7%) dropped out prior to the post-intervention assessment. The multiple imputation analysis revealed that the intervention group showed significant improvement in CAVI [between-groups difference (95% confidence interval)=-0.78 (-1.25 to -0.31), Cohen's d=0.82] and physical activity [32.5 (0.3 to 64.7), Cohen's d=0.57] as compared with the control group. The sensitivity analysis for the complete cases showed similar results. Active learning health education may be effective in improving arterial stiffness and physical activity in older adults with low health literacy.Active learning health education may be effective in improving arterial stiffness and physical activity in older adults with low health literacy.Administration of cisplatin and methotrexate significantly increased 5-hydroxytryptamine (5-HT) release from intestinal tissues isolated at 72 h after administration in rats. Daily administration with nafamostat mesilate, a potent serine protease inhibitor, significantly inhibited the release of 5-HT induced by methotrexate, but not by cisplatin, in a dose-dependent manner. When applied to isolated ileal tissues in vitro, nafamostat mesilate also significantly inhibited the release of 5-HT induced by methotrexate, but not by cisplatin, in a concentration-dependent manner. These results suggest that serine proteases are involved in the mechanism of the methotrexate-induced release of 5-HT from the rat small intestine.The vomeronasal organ (VNO) is an accessory olfactory device related to reproductive behavior. The soft tissue of the tubular organ is composed of sensory/non-sensory epithelia and a highly developed vasculature, which in the latter the dilation and contraction of blood vessels are thought to contribute to pumping in and out luminal fluid or air, like penile erectile tissue. The present histological observation of the murine VNO revealed a more complicated vasculature than previously evaluated ones with large differences along the rostro-caudal axis. An immunohistochemical study for vasoactive substances displayed extremely dense innervation by cholinergic nerves containing nitric oxide synthase and VIP/PHI in the thick smooth muscle layer surrounding venous sinuses at light and electron microscopic levels. Furthermore, the differential distribution of cholinergic nerves and adrenergic nerves may provide a novel insight into the pumping mechanism of VNO.Xeroderma pigmentosum (XP) involves a defect in the initial step of nucleotide excision repair (NER) and consists of eight genetic complementation groups (groups A-G and a variant). XP group A (XPA) patients have a high incidence of UV-induced skin tumors, immature testicular development, and neurological symptoms. In an earlier study, we have shown that XP group A (Xpa) gene-knockout mice (Xpa-/- mice) were highly sensitive to UV-induced skin carcinogenesis with a defect in NER and were highly susceptibility to spontaneous tumorigenesis with impaired spermatogenesis. However, the pathology of impaired spermatogenesis in Xpa-/- mice is unknown. To unravel the underlying pathology, we made a concerted effort using the testis of 3-month-old Xpa-/- mice. We found many large vacuoles in the seminiferous tubules of 3-month old Xpa-/- mice, while there were no large vacuoles in that of Xpa+/+ mice. Immunohistochemistry of microtubule-associated protein 1 light chain 3 (LC3), an autophagosome marker, showed degenerating cells with intense signal of LC3 in the seminiferous tubules, and immunoblotting revealed induction of LC3-II in the 3-month-old Xpa-/- mice. The results of the present study suggest autophagy induction as the possible mechanism underlying the impaired spermatogenesis in Xpa-/- mice. Therefore, Xpa-/- mice could be a useful model for investigating aging and male infertility with low expression of XPA.Diabetes mellitus induces skeletal muscle dysfunction, such as decreased metabolic activity and capillarization. This study aimed to investigate the effects of aerobic low intensity exercise training on metabolic oxidative capacity and capillarization in skeletal muscle of non-obese diabetic rats. Eleven to twenty-five week-old male non-obese Spontaneous Diabetic Torii (SDT) rats (n = 11) and age-matched healthy male Sprague-Dawley SD rats (n = 11) were randomly assigned to either exercise or sedentary groups. The exercise training was performed on a low-speed motorized treadmill (15 m min-1) for 60 min per session, 5 sessions per week for 14 weeks in exercised groups. Sedentary SDT rats resulted in hyperglycemia, reduction of metabolic oxidative enzyme, and low percentage of oxidative fibers in the skeletal muscles. The low-intensity exercise training inhibited the growth-related increase in glucose level, and increased the muscle oxidative enzyme in exercised SDT rats compared with sedentary SDT rats. In addition, the exercise program prevented capillary regression in the skeletal muscle of diabetic rats. These results suggest that low-intensity exercise training may be an effective treatment to counter the detrimental effects of type 2 diabetes mellitus on the oxidative capacity and the capillary network of skeletal muscles.