Biomedical subjects

M Umezawa

Publications and source records attributed to M Umezawa.

11 recordsLinked to original sources

PubMed1990

Effects of dietary restriction on age-related immune dysfunction in the senescence accelerated mouse (SAM).

The effects of age and dietary restriction on immune response were investigated using an animal model of accelerated senescence (senescence accelerated mouse, SAM). The experimental groups consisted of control (ad libitum fed) and restricted groups (fed 60% of energy intake of the controls). Spleen weight and total number of splenic cells were significantly lower in the food-restricted group at 8 mo of age. Percentages of T (Thy-1.1+) and B (surface Ig+) cells in the splenic cells were not significantly different between the two groups. The number of direct hemolytic plaque-forming cells per 10(6) spleen cells 4 d following immunization with sheep red blood cells and dinitrophenyl-Ficoll was significantly greater in the 8-mo-old mice in the food-restricted group than in the control group. In the latter group, antibody responses Progressively decreased with age. Mitogen responses to concanavalin A and lipopolysaccharide were maintained in the food-restricted group but were depressed in the control group at 8 mo. In addition, though autoantibody to single-stranded DNA increased in the control group with advancing age, there was a steady decrease in the food-restricted group until 8 mo. Serum immunoglobulin (IgA and IgM) concentrations were significantly lower in the food-restricted group than in controls at 8 mo of age. Therefore, our results suggest that when senescence accelerated mice are subjected to food restriction, there may be a modulatory effect on the immune dysfunction associated with advancing age.

Aging↗

PubMed1989

Decreased endosteal formation during cortical bone modelling in SAM-P/6 mice with a low peak bone mass.

Inter-strain differences in bone mass and density during growth were followed in three strains of mice: SAM-P/2, SAM-R/1 and SAM-P/6 (a murine model of senile osteoporosis, Matsushita et al., Am J Pathol 1986;125:276-283). Photometrically, the inter-strain disparities first appeared in mice at about age 28 days and increased until age 60 days. During this period, tetracycline labelling revealed significant strain differences regarding rate of the appositional formation at the endosteal surface but not at the periosteal surface. The order coincided with results of the photometrical assay, that is, highest in SAM-P/2, followed by SAM-R/1 and SAM-P/6, respectively. Therefore, strain differences, especially the osteopenic state of SAM-P/6, occur, at least in part, by disparities in endosteal formation rates during cortical bone modelling.

Aging↗

PubMed1989

Spontaneous spongy degeneration of the brain stem in SAM-P/8 mice, a newly developed memory-deficient strain.

A spontaneous spongy degeneration of the brain stem and spinal cord was discovered in a murine model of accelerated senescence (SAM), cared for under both conventional (SAM-P/8) and specific pathogen-free (SAM-P/8/Ta) conditions. SAM-P/8 and SAM-P/8/Ta showed no clinical neurological abnormalities, yet there was a deterioration in learning and memory abilities. Light microscopic examination revealed a spongy degeneration in the brain stem and spinal cord, in the reticular formation, and proliferation of hypertrophic astrocytes in the spongy area. The spongiform degeneration progressed with advancing age from four to eight months, after which the entire brain was involved. Astrocytosis increased with advancing degeneration. Ultrastructurally, mild dendritic swelling occurred at one month of age. At two months of age, moderate postsynaptic swelling and a widening of intracellular membrane structure were observed, and at age five months there were large vacuoles circumscribed by membranous lamellae, identifiable as myelin. Vacuoles in SAM-P/8 proved to be swollen neuronal processes and oligodendroglial processes. These SAM-P/8 and SAM-P/8/Ta strains of mice are new memory-deficient strains with spontaneous spongy degeneration associated with aging.

Animals↗

PubMed1972