PubMed Health⌕ Search

Biomedical subjects

A Kohno

Publications and source records attributed to A Kohno.

At least 73 records · Page 4Linked to original sources
PubMed1986

Age-related changes of beta-adrenoceptors in spleen lymphocytes and cerebral cortex of NZB/BIN mice.

The density (Bmax) of beta-adrenoceptors in splenic lymphocytes of NZB/BIN mice decreased up to an age of about 40 weeks and then levelled out. The Bmax in cerebral cortex, on the other hand, increased in the first half of life and then changed relatively little. The dissociation constant of the ligand (Kd) was larger in the cortex than the spleen and showed relatively little age-dependent change.

Aging↗
PubMed1986

Purification and characterization of a senile amyloid-related antigenic substance (apoSASSAM) from mouse serum. apoSASSAM is an apoA-II apolipoprotein of mouse high density lipoproteins.

Two putative serum precursors which cross-react with antiserum against murine senile amyloid protein (ASSAM) were isolated from the high density lipoprotein (HDL) of normal mouse serum. Apolipoproteins designated "apoSASSAM-1" and "apoSASSAM-2" have the same molecular weight as tissue amyloid fibril protein. ApoSASSAM-1 and apoSASSAM-2 migrate to an intermediate position between apoA-I and apoC on alkaline-urea polyacrylamide gel electrophoresis and are present mainly in HDL apoproteins and to a slight extent in very low density lipoprotein apoproteins when compared to apoC. ApoSASSAM-1 and apoSASSAM-2 are polymorphic; there are two apparent isoproteins of apoSASSAM-1 with isoelectric points of 4.72 and 4.79 and two major isoproteins of apo-SASSAM-2. Subunit bands of ASSAM separated by alkaline-urea polyacrylamide gel electrophoresis and that migrated to the same positions as apoSASSAM-1 and apoSASSAM-2 were labeled by anti-apoSASSAM-1 antiserum. The amino acid compositions of apoSASSAM-1 and apoSASSAM-2 were much the same and closely resembled those of ASSAM and mouse apoA-II. Sequence analysis of apoSASSAM and ASSAM revealed a blocked amino terminus. ApoSASSAM is considered to be a mouse apoA-II and probably transforms to amyloid fibril "ASSAM" in tissues through a process yet to be clarified.

Amino Acids↗
PubMed1986

Naturally occurring antibody response to DNA is associated with the response to retroviral gp70 in autoimmune New Zealand mice.

The spontaneous occurrence of retroviral gp70 immune complexes (ICs) in the blood of autoimmune New Zealand black and (New Zealand black X New Zealand white)F1 ([NZB X NZW]F1) mice is determined by a single dominant locus of the NZB strain (provisionally designated Agp-1). A combined effect of 2 unlinked dominant NZB loci (Ads-1 and Ads-2) is required for the production of anti-double-stranded DNA (anti-dsDNA) antibodies in these mice. The present genetic studies using (NZB X NZW)F1 X NZW backcross mice and their second through fourth generation progeny revealed that Agp-1 and Ads-1 exist in common or are closely linked on chromosome 17 of NZB mice and are related to the occurrence of renal disease. The renal disease and the serum level of both anti-dsDNA antibodies and gp70 ICs were more intense in (NZB X NZW)F1 hybrids than in NZB mice, indicating the contribution of NZW genes. In (NZB X NZW)F1 mice, a single dominant locus from the NZW strain, Agp-3, intensified the magnitude of gp70 IC formation, and a combined effect of 2 unlinked dominant loci from the NZW strain, Ads-3 and Ads-4, acted to increase the serum titers of anti-dsDNA antibodies. This study clearly indicates that the NZW loci Agp-3 and Ads-3 exist in common or are tightly linked on chromosome 17, are closely linked to the H-2 complex, and are associated with the severity of renal disease in (NZB X NZW)F1 hybrids.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1986

Age-related changes in beta-adrenoceptors of lymphocytes.

The density of adrenoceptors (Bmax) is greater on B than on T splenocytes. It decreases more or less rapidly on membranes of both populations, as animals age. The exception, we have observed in this respect, is an increase in Bmax on B cells of SJL mice, between the 6th and 25th week of life.

Aging↗
PubMed1986

Age-related changes of beta-adrenoceptors in aging inbred mice.

The density (Bmax) and antagonist dissociation constant (KD) of beta-adrenoceptors were determined on spleen and brain of three different inbred strains of mice--BALB/cJ, C3H/HeJ, and C57BL/6J. Receptor densities (Bmax) differed with strain and declined in both spleen and cortical receptor populations as mice became older. Age-related changes in KD were found on spleen cells of BALB/cJ and in the cortex of C3H/HeJ and C57BL/6J. Bmax and KD in different organs of the same strain changed at different rates. changed at different rates.

Aging↗
PubMed1986

A measurement of galvanic current and electrical potential in extracted human teeth.

When opposing teeth with amalgam and gold restoration are in contact, current flows in the mouth at the instant the dissimilar metals touch. In this study, this condition was simulated by use of resistors and extracted human teeth with amalgam and MOD gold inlay restorations. When both teeth were in contact in a physiological saline solution, we measured current and electrical potential generated in each pulp chamber. Galvanic current generated in the tooth with amalgam was always larger (as much as 18.2 times at the instant of contact) than that in the tooth with gold. Electrical potential generated in the tooth with amalgam was always larger (as much as 9.7 times at the instant of contact) than that in the tooth with gold. It should be emphasized that the larger current generated in the tooth with amalgam was caused mainly by its larger electrical potential. These results correspond well with the clinical phenomenon of galvanic pain, which occurs in the tooth with amalgam rather than in the tooth with gold.

Dental Amalgam↗
PubMed1986

Age-related changes in bone mass in the senescence-accelerated mouse (SAM). SAM-R/3 and SAM-P/6 as new murine models for senile osteoporosis.

Age-related changes of the femoral bone mass in several strains of the senescence-accelerated mouse (SAM) were investigated. Microdensitometrically, all strains exhibited essentially the same patterns of age changes, that is, bone mass corrected by the diameter of the shaft reached the peak value when the mice were 4 or 5 months of age and then fell linearly with age up to over 20 months of age. Two strains, SAM-R/3 and SAM-P/6, which originated from the same ancestry on pedigree, had a significantly lower peak bone mass than other strains (SAM-R/1, SAM-R/2, SAM-P/1, and SAM-P/2). On the other hand, the strains with a low peak bone mass had the same rate of decrease as other strains. Mineral and collagen contents per dry weight of bone showed little difference among the strains. Histologic studies of tibia, femur, and lumbar spine revealed that the osteopenia was not due to osteomalacia but, rather, to osteoporosis. The elderly mice in these two strains were prone to fracture, thus should be important models for study of senile osteoporosis seen clinically.

Aging↗
PubMed1985

Pathogenesis of lupus dermatoses in autoimmune mice. IV. Association between cutaneous immunoglobulin deposition and anti-single-stranded DNA antibodies in sera.

The skin of New Zealand, MRL and BXSB mice was immunohistopathologically examined in order to study the appearance of skin immunoglobulin (Ig) deposition and its correlation with the occurrence of anti-single-stranded (ss) DNA antibodies in sera. Our studies revealed Ig deposition at the dermoepidermal junction (DEJ) in non-lesional skin and a significant age-related correlation between skin Ig deposition and serum anti-ssDNA antibodies. However, immunofluorescent study of autoimmune mice using anti-ultraviolet-irradiated DNA antiserum failed to demonstrate DNA antigens at the DEJ.

Aging↗
PubMed1985

Immune response, tolerance circumvention and autoantibodies in aging MRL/Mp-lpr and MRL/Mp-+ mice.

Isotype distribution was analyzed, as a function of age in MRL/Mp-lpr and MRL/Mp-+ mice. The mice were tested for: (1) "spontaneous" response to nucleic acid (2) induced response to alum-precipitated phosphorylcholine-rabbit gamma globulin (PC-RGG) (immunized animals) and (3) induced response to alum-precipitated PC-RGG after pretreatment with aggregate-free RGG (tolerized-immunized animals). "spontaneous" nucleic acid antibodies of isotypes, other than IgM, increased as animals became older. The quantity of RGG antibody declined as a function of the age at which animals were immunized. Young tolerized-immunized animals made less antibody of all isotypes than did immunized animals. In later life, resistance against tolerance induction developed. Aggregate-free RGG sensitized older animals and, thus, augmented the response to alum-precipitated PC-RGG. Up to the age of 20 weeks, spontaneous antibody and antibody of tolerized-immunized animals showed striking similarities in age- and strain-dependent changes of IgG2b and IgA isotypes. Results were discussed in terms of: (1) a defect in down regulation of immune responsiveness, which contributes to the initiation of autoimmunity and age-dependent resistance to tolerance induction; (2) regulatory mechanisms for isotype switching, which contribute to resistance to tolerance induction, whether naturally occurring or experimentally induced; and (3) age-related immunological changes which are inherent in the MRL/Mp genome, the mutant gene, lpr/lpr, accelerating the changes.

Aging↗
PubMed1985

Chronic food restriction modulates the advance of senescence in the senescence accelerated mouse (SAM).

The effects of chronic food restriction on grading scores of senescence, deposition of senile amyloid (ASSAM), mean life span and 10th decile were investigated by using animal models for accelerated senescence (SAM-P/1) and for normal aging (SAM-R/1). The experimental groups consisted of control (ad libitum fed), 80% (fed 80% of control intake), and 60% (fed 60% of control intake) groups. The grading score of SAM-P/1 mice was significantly improved in the 60% group, but not in the 80% group, compared to the control group. The grading score of SAM-R/1 mice, however, was significantly less than that in the control group in both the 60 and 80% groups. In SAM-P/1 mice liver, skin and testis, the severity of senile amyloid deposition was significantly less with 40% food restriction (60% group) than in the control group. A restriction of 20% (80% group) had no influence on amyloid deposition. A definite tendency to prolong mean life span (24.3%) and 10th decile (65.9%, mean life span of the last 10th of survivors of a group) was observed in the 60% group of SAM-P/1 mice, but the changes were not statistically significant. In the 80% group of SAM-P/1 mice and also in either restriction group of SAM-R/1 mice, however, such a tendency was not evident. These results indicate that 40% food restriction modulates the advance of senescence in these mice.

Aging↗