The present study performed a cross-sectional survey to investigate sleep habits and sleep health in Japanese women aged 40 to 69 years with and without a habit of exercise. A standardized questionnaire evaluating sleep was administered to two subject groups. One was the “exercise group” who habitually performed aerobic exercise at mild to moderate intensity with a frequency of ≥2 times/week and duration of ≥30 minutes/one session (n=207) . The other was the age-matched “non-exercise group” who had no exercise habit (n=567) . Two-way ANOVA was employed for com paring the two subject groups and examining the effects of exercise on aging. Regarding sleep habits, as bed time significantly advanced with advancing age, sleep habits (bed time, waking time and sleep duration) were significantly more regular in the exercise group than in the non-exercise group. Concerning independent sleep health risk factors consisting of sleep initiation, sleep maintenance, sleep apnea, parasomnia, and waking-up, the factor score for sleep maintenance significantly deteriorated with advancing age; and was significantly better in the exercise group than in the non-exercise group. These results suggest that an exercise habit may improve sleep health in middle-aged and older Japanese women among which a higher prevalence of sleep problems has been reported.

Recently, arterial keton body ratio (AKBR) has attracted attention as a new indicator of liver function which is in equibilium with the ratio between oxidized and reduced forms of free nicotinamide-adenine dinucleotides (free NAD⁺/NADH ration) in the mitochondria. There are few reports on whether AKBR contributes to the hepatic energy charge in the open heart surgery with extra corporeal circulation (ECC) or not. This study was undertaken to clarify the contribution of AKBR to the hepatic energy charge during ECC and the relationship between AKBR and hepatic blood flow. AKBR was determined before, during and after ECC in the open heart surgery for 14 patients. Furthermore, the blood flow in hepatic artery, portal vein and liver microcirculation was measured before, during and after ECC in canine models. Finally, the pulsatile perfusion was performed in canine models and compared with the conventional non-pulsatile perfusion for the blood flow and AKBR. In clinical cases, AKBR was decreased in all cases during the ECC. AKBR which was measured at 2 or 3hr after weaning from the ECC was negatively correlated to the total perfusion time with -0.57 as the correlation coefficient. Six patients who were on the ECC over 180min did not show a good recovery of the AKBR after weaning from the ECC. Especially, three patients presented a clinical picture of acute hepatic failure with jaundice, elevation of the serum levels of transaminase and direct hyperbililubinemia, but only one showed hypoglycemia. These patients showed no improvement in clinical data and AKBR. The patient with improved AKBR recovered clinically. In our experiment, the blood flow in the hepatic artery, portal vein was measured by electromagnetic blood flow meter and the liver microcirculation was measured by laserdoppler flowmeter. The blood flow was decreased remakably in the non-pulsatile group at all sites of measurement: it recovered after ECC in hepatic artery and portal vein, but liver microcirculation did not improve well. AKBR was decreased during ECC and did not recover after ECC in the non-pulsatile perfusion. When the pulsatile perfusion was performed, liver circulation was maintained well, and AKBR recovered well after ECC. The above results suggest that AKBR reflects the liver microcirculation and pulsatile perfusion is beneficial to the liver microcirculation. Pulsatile circulation, however, involves several problems, hemolysis, the decrease of platelets, and so on, but these problems have been improved gradually. We think that the pulsatile perfusion will be used in clinical operations to maintain the good hepatic circulation.

Metaxin, a mitochondrial outer membrane protein, is critical for TNF-induced cell death in L929 cells. Its deficiency, caused by retroviral insertion-mediated mutagenesis, renders L929 cells resistance to TNF killing. In this study, we further characterized metaxin deficiency-caused TNF resistance in parallel with Bcl-X(L) overexpression-mediated death resistance. We did not find obvious change in mitochondria membrane potential in metaxin-deficient (Met(mut)) and Bcl-X(L)-overexpressing cells, but we did find an increase in the release rate of the mitochondrial membrane potential probe rhodamine 123 (Rh123) that was preloaded into mitochondria. In addition, overexpression of a function-interfering mutant of metaxin (MetaΔTM/C) or Bcl-X(L) in MCF-7.3.28 cells also resulted in an acquired resistance to TNF killing and a faster rate of Rh123 release, indicating a close correlation between TNF resistance and higher rates of the dye release from the mitochondria. The release of Rh123 can be controlled by the mitochondrial membrane permeability transition (PT) pore, as targeting an inner membrane component of the PT pore by cyclosporin A (CsA) inhibited Rh123 release. However, metaxin deficiency and Bcl-X(L) overexpression apparently affect Rh123 release from a site(s) different from that of CsA, as CsA can overcome their effect. Though both metaxin and Bcl-X(L) appear to function on the outer mitochondrial membrane, they do not interact with each other. They may use different mechanisms to increase the permeability of Rh123, since previous studies have suggested that metaxin may influence certain outer membrane porins while Bcl-X(L) may form pores on the outer membrane. The alteration of the mitochondrial outer membrane properties by metaxin deficiency and Bcl-X(L) overexpression, as indicated by a quicker Rh123 release, may be helpful in maintaining mitochondrial integrity.
Animals ; Apoptosis ; Cell Line, Tumor ; Cell Membrane Permeability ; Humans ; Membrane Potential, Mitochondrial ; physiology ; Mice ; Mitochondrial Membrane Transport Proteins ; physiology ; Mitochondrial Membranes ; metabolism ; Mutation ; Necrosis ; Proteins ; genetics ; metabolism ; Reactive Oxygen Species ; metabolism ; Rhodamine 123 ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology ; physiology ; bcl-X Protein ; metabolism