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Biomedical subjects

K Onari

Publications and source records attributed to K Onari.

At least 19 recordsLinked to original sources

Mapping of the gene for Machado-Joseph disease within a 3.6-cM interval flanked by D14S291/D14S280 and D14S81, on the basis of studies of linkage and linkage disequilibrium in 24 Japanese families.

The gene locus of Machado-Joseph disease (MJD) has recently been mapped within a 29-cM subregion of 14q chromosome. We did a linkage study of 24 multigenerational MJD Japanese pedigrees, in an attempt to narrow the candidate region of this gene. Pairwise and multipoint linkage analysis, together with haplotype segregation analysis, led to the conclusion that the MJD gene is located at the 6.8-cM interval between D14S256 and D14S81 (Zmax = 24.78, multipoint linkage analysis). D14S291 and D14S280, located at the center of this interval, showed no obligate recombination with the MJD gene (Zmax = 5.93 for D14S291 and 9.99 for D14S280). A weak, but significant, linkage disequilibrium of MJD gene was noted with D14S81 (P < .05) but not with D14S291 or D14S280. These results suggest that a 3.6-cM interval flanked by D14S291/D14S280 and D14S81 is the most likely location of the MJD gene and that it is closest to D14S81.

Adult

Exercise intensity determines the magnitude of IOP decrease after running.

The effects of the intensity, duration and quantity (intensity x duration) of exercise on the reduction of intraocular pressure (IOP) in healthy and physically fit individuals were studied. Five minutes after 15 minutes of exercise at 70%, 55% and 40% of maximum exercise load (%HRmax) the IOP decreased 4.3 +/- 0.7 mmHg, 2.2 +/- 0.7 mmHg and 0.6 +/- 0.5 mmHg, respectively. The magnitude of IOP reduction increased with exercise load. Running for 7.5 minutes at 70%HRmax decreased IOP comparable to 15 minutes of running at the same exercise load (4.4 +/- 0.6 mmHg). Twenty-five minutes of running at 40%HRmax is almost the same quantity of exercise as 15 minutes of running at 70%HRmax. However, the former did not result in IOP reductions to equal the latter (2.3 +/- 0.5 vs 4.4 +/- 0.6 mmHg). The amount of IOP reduction after short-term exercise seems to depend on the intensity of exercise, not on the duration of exercise or the quantity of exercise.

Adult

Evaluation of a new bronchodilator, Formoterol, using biochemical parameters.

The authors administered orally 40, 60 and 80 micrograms of Formoterol which was developed as a new bronchodilator and 4 mg of Salbutamol which is considered to be a beta 2-selective drug, to healthy adults. Pulse rate, blood pressure and blood levels of cyclic GMP, free fatty acid, cyclic AMP, glucose and lactic acid were measured in order to evaluate efficacy and dosage of Formoterol and to compare efficacy of this drug with that of Salbutamol. As a result, it is considered that Formoterol has a strong dose dependent beta 2-effect with 40 micrograms of Formoterol almost as high as 4 mg of Salbutamol in beta 2-effect. In addition, Formoterol has almost no alpha-effect and its beta 1-effect can be considered negligible in the doses of 60 micrograms and 80 micrograms.

Adult

Differential effects of age on mitotically active and inactive bone marrow stem cells and splenic T cells in mice.

Young and old BALB/c mice and thymectomized young mice were subjected to continuous exposure of 6-thioguanine (6-TG), and the numbers of their bone marrow spleen colony-forming units (CFU-S) and in vitro culture colony-forming units (CFU-C) and the number and mitogen-induced proliferative activity of their splenic T cells were determined at various time intervals. The results indicated that (a) old mice have seven times more 6-TG-resistant (6-TGr) CFU-S than young mice, (b) the mitogen-induced proliferative activity of 6-TGr T cells is comparable to that of 6-TG-sensitive (6-TGs) T cells of both young and old mice, and (c) 6-TGr CFU-S and T cells are resistant to 6-TG because they are mitotically inactive and not because they are drug-resistant mutants.

Aging

Immune function in aging atomic bomb survivors residing in the United States.

Immunologic parameters were studied among survivors of the 1945 atomic bombs who now reside in the United States. Of all known survivors living in the U.S., about 40% (n = 189) participated in this study. Of those survivors on whom radiation exposure information was available (n = 168), 96% were exposed to less than 50 rad at the time of the bomb (ATB). Survivors were divided into two groups; those exposed to varying low doses of radiation (S+ group, exposed at less than or equal to 2500 m from the hypocenter) were compared with those exposed to "O rad" (S0 group, exposed at greater than 2500 m from the hypocenter). Of the former group, 92% were exposed to less than 100 rad and 89% to less than 50 rad ATB. Cellular immune responses, including natural cell-mediated cytotoxicity (NCMC), interferon production, and the mitogenic response to PHA, tended to be higher among S+ individuals, although only the difference for NCMC was statistically significant. This was suggestive of a trend which was consistent with the higher serum interferon levels and lower frequencies of detectable immune complexes and antimitochondrial antibodies among the S+ group, although these differences were not statistically significant. Other immunologic parameters which showed no trend included frequency of antinuclear antibodies, rheumatoid factor, levels of serum immunoglobulins, levels of isoantibodies and heteroantibodies, and the magnitude of the mixed lymphocyte reaction.

Adolescent

Changes in natural killer cell, antibody-dependent cell-mediated cytotoxicity and interferon activities with administration of Nocardia rubra cell wall skeleton to subjects with high risk of lung cancer.

Changes in natural killer (NK) cell, antibody-dependent cell-mediated cytotoxicity (ADCC) and interferon activities after administration of Nocardia rubra cell wall skeleton (N-CWS) to a group of subjects with high risk of lung cancer (retired workers of the Okunojima poison gas factory) were studied. No difference in NK cell activity against K-562 derived from chronic myelogeneous leukemia was observed among normal controls, non N-CWS-injected workers and N-CWS-injected workers. None of the normals or N-CWS-injected retired workers showed low NK cell activity (less than 10% cytotoxicity), but among the non N-CWS-injected workers 6.3% showed reduced activity. Following injection of N-CWS, NK cell activity against K-562 and T-24 derived from bladder cancer was significantly elevated by the second week and then gradually reverted to the preinjection level. When a second injection was administered at the twelfth week, a similar elevation was noted. Further, a significant increase was noted in ADCC activity two weeks after N-CWS injection. There was a significant elevation of interferon at the second week after N-CWS injection. It was considered that N-CWS affects the NK cell activity enhancement by serum interferon.

Adjuvants, Immunologic

Metabolism, 45Ca uptake and insulin releasing capacities of glucose and mannose.

A detailed dose-response study relating mannose and glucose oxidation with the induction of 45Ca uptake and insulin release was performed using in vitro incubation of collagenase digested rat islets of Langerhans. The threshold value for 14C-U-D-glucose oxidation, glucose-stimulation of 45Ca uptake, and insulin release was about 5.5 mM. The half maximal response for these 3 parameters occurred at 13.4 mM, 11.6 mM, and 12.2 mM, respectively. Their maximal responses were obtained at approximately 20 mM. The threshold level for mannose oxidation, induction of 45Ca uptake and insulin release was about 11.0 mM, with half maximal responses obtained at 24.6 mM, 20.5 mM, and 22.2 mM, respectively. The maximum response of the 3 parameters to mannose was obtained at 38.8 mM and appeared to reach the same level obtained for glucose. These results suggest that hexose degradation has a significant role in controlling Ca uptake and subsequent insulin release. A lower rate of mannose oxidation appeared to account for its weaker stimulating efficacy for Ca uptake and insulin release.

Animals

Alloxan inhibits glucose oxidation in the pancreatic islets.

The effects of alloxan on glucose oxidation and the protection by anomers of D-glucose from alloxan inhibition of glucose oxidation in the pancreatic islets were investigated using in vitro incubation of rat isolated islets. The pretreatment by alloxan (5-30 mg/dl) for 6 minutes inhibits significantly 14CO2 formation from 14C-U-D-glucose (10 mM) and the addition of alpha-anomer of D-glucose (8.3 mM) to alloxan (20 mg/dl) completely reverses alloxan inhibition of glucose oxidation. These findings seem to be incompatible with the recent view that alloxan acts at the glucose receptor on the plasma membrane of pancreatic beta-cells without affecting glucose metabolism in the pancreatic islets.

Alloxan