Ubiquinol-10 supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice.

Aim: The present study was conducted to define the relationship between the anti-aging effect of ubiquinol-10 supplementation and mitochondrial activation in senescence-accelerated mouse prone 1 (SAMP1) mice.

Results: Here, we report that dietary supplementation with ubiquinol-10 prevents age-related decreases in the expression of sirtuin gene family members, which results in the activation of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a major factor that controls mitochondrial biogenesis and respiration, as well as superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2), which are major mitochondrial antioxidant enzymes. Ubiquinol-10 supplementation can also increase mitochondrial complex I activity and decrease levels of oxidative stress markers, including protein carbonyls, apurinic/apyrimidinic sites, malondialdehydes, and increase the reduced glutathione/oxidized glutathione ratio.

Exome sequencing of senescence-accelerated mice (SAM) reveals deleterious mutations in degenerative disease-causing genes.

Background: Senescence-accelerated mice (SAM) are a series of mouse strains originally derived from unexpected crosses between AKR/J and unknown mice, from which phenotypically distinct senescence-prone (SAMP) and -resistant (SAMR) inbred strains were subsequently established. Although SAMP strains have been widely used for aging research focusing on their short life spans and various age-related phenotypes, such as immune dysfunction, osteoporosis, and brain atrophy, the responsible gene mutations have not yet been fully elucidated.

Results: To identify mutations specific to SAMP strains, we performed whole exome sequencing of 6 SAMP and 3 SAMR strains.

Dysfunction in ABCB1A has only a weak effect on susceptibility to dextran sulfate sodium-induced colitis in SAM strains.

Genetic alterations in the gene for ATP-binding cassette, sub-family B (MDR/TAP), member 1A (ABCB1A) determine susceptibility to colitis in mice and humans. We investigated the influence of ABCB1A dysfunction on susceptibility to dextran sulfate sodium (DSS)-induced colitis by using Senescence-Accelerated Mouse (SAM) strains with a loss-of-function mutation in the Abcb1a gene (SAMR1, SAMP1, and SAMP6). Susceptibility to DSS colitis was different among SAM strains but on the whole was not different from other mouse strains with normal ABCB1A function.

Information-sharing system for disaster recovery of dialysis therapy in Japan.

If a natural disaster or other event causes damage that makes dialysis therapy impossible, what steps should be taken? Many actions will be required, including disaster recovery activities in the affected area as well as the performance of dialysis at substitute dialysis facilities outside the affected area. The Japanese Association of Dialysis Physicians (JADP), in collaboration with the Japan Association for Clinical Engineering Technologists (JACET), operates an "information sharing system" that will be essential when carrying out post-disaster activities. This system consists of a website and mailing lists on the Internet, and it has been used in 11 disasters so far.

Senescence-accelerated mouse (SAM) with special references to neurodegeneration models, SAMP8 and SAMP10 mice.

The SAM strains, a group of related inbred strains consisting of senescence-prone inbred strains (SAMP) and senescence-resistant inbred strains (SAMR), have been successfully developed by selective inbreeding of the AKR/J strain of mice donated by the Jackson laboratory in 1968. The characteristic feature of aging common to the SAMP and SAMR is accelerated senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains of mice manifest various pathobiological phenotypes spontaneously.

Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice.

The SAMP1 strain is a mouse model for accelerated senescence and severe senile amyloidosis. We determined whether supplementation with coenzyme Q10 (CoQ10) could decelerate aging in SAMP1 mice and its potential role in aging. Plasma concentrations of CoQ10 and CoQ9 decreased with age in SAMP1 but not in SAMR1 mice.

Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse.

Senescence-accelerated mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-II) amyloid fibril (AApoAII) deposits. This study was undertaken to investigate the effects of dietary fats on AApoAII deposits in SAMP1 mice when purified diets containing 4% fat as butter, safflower oil, or fish oil were fed to male mice for 26 weeks. The serum HDL cholesterol was significantly lower (P < 0.