An intervention study to promote self-improvement of lifestyle in a Japanese community: a new health support program.

Objective: To assess the effectiveness of two health support programs developed to improve the lifestyle of community residents through exercise, nutrition-based health education, and group dynamics.

Methods: A total of 171 subjects were selected from community residents showing an abnormal result in at least one metabolic syndrome-related laboratory test. The subjects were divided into two groups: a group participating only in the 5-month initiation program (i.

TZDs reduce mitochondrial ROS production and enhance mitochondrial biogenesis.

Although it has been reported that thiazolidinediones (TZDs) may reduce cardiovascular events in type 2 diabetic patients, its precise mechanism is unclear. We previously demonstrated that hyperglycemia-induced production of reactive oxygen species from mitochondria (mtROS) contributed to the development of diabetic complications, and metformin normalized mt ROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating the PGC-1alpha pathway. In this study, we examined whether TZDs could inhibit hyperglycemia-induced mtROS production by activating the PGC-1alpha pathway.

Endothelial MnSOD overexpression prevents retinal VEGF expression in diabetic mice.

We previously proposed that hyperglycemia-induced mitochondrial ROS overproduction is a key event in the development of diabetic complications. In this study, we established a novel transgenic mouse (eMnSOD-Tg), which specifically expressed MnSOD in endothelial cells, by employing a Tie2 promoter/enhancer, and investigated the impact of mitochondrial ROS production on diabetic retinopathy in vivo. Using immunohistochemistry, overexpression of MnSOD in endothelial cells was confirmed in eMnSOD-Tg mice.

Chronic hepatitis B with flare due to co-infection of hepatitis delta virus during lamivudine therapy.

In 1997, a 27-year-old homosexual man contracted acute hepatitis B that developed into chronic hepatitis. Because of repeated flares, administration of lamivudine was started in March 2002. Hepatitis B virus (HBV) DNA immediately decreased, but the serum level of alanine aminotransferase gradually increased.