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Biomedical subjects

M Minami

Publications and source records attributed to M Minami.

At least 631 records · Page 35Linked to original sources

T cell allotypic determinants encoded by genes linked to the immunoglobulin heavy chain locus. I. Establishment of monoclonal antibodies against allotypic determinants.

Monoclonal alloantibodies for T cell allotypic determinants were obtained by hybridizing SP-2 tumor cells with BALB/c (H-2d, Igh-1a) spleen cells, which had been repeatedly immunized with Con A-stimulated CB-20 (H-2d, Igh-1b) spleen cells. It was found that these monoclonal anti-CB-20 antibodies detect the new allotypic determinants (distinct from the B cell Igh-C region determinant) expressed only on the augmenting or suppressor T cells. Genetic analysis of these antigenic determinants revealed these antibodies react with the gene products located on the telomeric side chromosome of the Igh variable region gene (Igh-V) cluster. These antibodies when given in vivo caused a modification of antibody production. The antibody activity was absorbed by Con A-stimulated B10.BR (H-2b, Igh-1b), C57BL/6 (H-2b, Igh-1b), CWB (H-2b, Igh-1b), CB-20 (H-2d, Igh-1b), and BAB-14 (H-2d, Igh-1b) spleen cells, but not by Con A-stimulated C3H.SW (H-2b, Igh-1j), BALB/c (H-2d, Igh-1a), A/Sn (H-2a, Igh-1e), and C.AL-20 (H-2d, Igh-1d) spleen cells. In addition, in vivo these monoclonal antibodies modified anti-SRBC antibody production only in Igh-1b allotype-bearing mice. One monoclonal antibody reacted with 4-hydroxy-3-nitrophenyl acetyl- (NP) hapten-specific augmenting T cells, and the other two batches of monoclonal antibodies reacted with NP-specific suppressor T cells of NP-mediated cutaneous responses. A mapping study with these recombinants limits the gene coding for the T cell-specific determinants to a gene within the variable region to the telomeric side of NP-VH and to the centromeric side of prealbumin. This segment is inclusive of all immunoglobulin genes, the region Owen named IgT-C, and a histocompatibility gene (H-Ig).

Animals↗

Mechanism responsible for the induction of I-J restriction on TS3 suppressor cells.

The mechanisms responsible for the induction of I-J restrictions on third-order suppressor T cells (TS3) were analyzed. The I-J phenotype of the antigen-coupled cells used for priming restricted the specificity of the TS3 population. Thus, TS3 cells were only generated after priming with antigen-coupled I-J homologous cells. Identity at the I-JM (and I-E) subregions was sufficient for TS3 induction. Furthermore, priming of H-2 heterozygous mice with antigen-coupled parental cells generated TS3 that were restricted to the parental haplotype used for priming. The splenic cell population responsible for antigen presentation and induction of TS3 cells was fractionated. The cells involved in antigen presentation were found in the splenic adherent population and were absent in the fraction containing splenic nonadherent T and B cells. The subsequent activation and interaction of TS3 cells is also restricted by genes in the H-2 complex. The results are discussed in terms of a general mechanism responsible for the induction of restrictions in T helper and TS3 cells.

Animals↗

I-J restrictions on the activation and interaction of parental and F1-derived TS3 suppressor cells.

An experimental system was developed to independently analyze the H-2 and Igh genetic restrictions at two steps of the 4-hydroxy-3-nitrophenylacetyl hapten (NP) suppressor cell pathway. This experimental system allowed genetic analysis of the activation of TS3 cells by hybridoma-derived TsF2 and independent analysis of the genetic restrictions that controlled the interaction of the TS3 cells with their target population. Thus, TS3 cells were activated in vitro with monoclonal H-2b or H-2k-derived TsF2. The activated TS3 cells were then adoptively transferred to TS3-depleted (cyclophosphamide-treated) recipients of various genotypes. When the TS3-containing lymph node population was activated in vitro for 2 h, suppressive activity was only noted in combinations of TSF2, TS3, and recipients that were matched at both the I-J and Igh gene complexes. The data indicate that TsF2 can activate TS3 cells and that both the activation and the interaction of TS3 cells are I-J and Igh restricted. Using (B10 x B10.BR)F1 mice as TS3 donors, we noted that H-2b-derived TsF2 activated these F1 TS3 cells to suppress NP-specific cutaneous sensitivity responses in H-2b but not in H-2k recipients. Reciprocal experiments using H-2k-derived TsF2 demonstrated that only an H-2k-restricted population was activated in the F1-derived TS3 cells. The simplest explanation to account for these observations is that two distinct populations, each of which is restricted to a parental I-J determinants, exists in the heterozygous F1 TS3 population. Furthermore, we demonstrated that both I-Jb and I-Jk determinants are expressed on F1-derived TS3 cells. These observations are discussed in terms of the mechanisms involved in immunoregulation.

Animals↗

Changes of the activities of superoxide dismutase after exposure to the fume of heavy metals and the significance of zinc in the tissue.

Pathological changes induced by cadmium aerosol had features common to the changes evoked by oxidants. Female rats were exposed to fumes of lead, antimony, zinc and cadmium (15-100 nmoles/m3). One hour after termination of exposure, superoxide dismutase (SOD) activity in erythrocytes of the exposed rats lowered by 15-40%. SOD activity of lung lavage fluid also lowered by 20-35% and the 2nd day after the exposure. The inverse value of SOD activity (l/SOD) in erythrocytes and of lung lavage fluid were proportional to the molar exposure level adjusted by the particle size (Dixon plot), irrespective of the difference of the exposed substance. The ratio of dry weight to wet weight of the lung was 4.3-26% lower than the control value on the later period after the exposure. With the heavy metal exposure, the uptake of the exposed metal was found to be proportional to the endogenous zinc concentration, which was correlated well with the change of SOD in the lung and in erythrocytes. Cadmium decreased the zinc concentration after the exposure.

Animals↗

Effects of clonidine and guanfacine on drinking and ambulation in spontaneously hypertensive rats.

Present experiment was undertaken to compare the effects of clonidine and guanfacine on water drinking behavior and ambulatory activity in spontaneously hypertensive rats (SHR). Equipotent hypotensive doses of clonidine and guanfacine, 150 micrograms/kg and 1500 micrograms/kg, respectively, given twice a day at 8:00 and 20:00, produced a triphasic pattern of behavioral changes; initial increase in water drinking and ambulation during the light period, decrease in water intake and ambulation at the beginning of the dark period, and a second increase in water drinking and ambulation at the end of the dark period. Guanfacine treated SHR showed less change in water drinking behavior and ambulation than the clonidine treated SHR.

Animals↗

Potentiation of toxicity and positive inotropic effect of ouabain by furosemide in guinea pig heart.

The present study was undertaken to elucidate the potentiation by furosemide of toxicity and positive inotropic effect of ouabain in guinea pigs. Arrhythmogenic responses to ouabain as well as the lowering of its lethal dose were potentiated by pretreatment with furosemide in guinea pigs. The potentiation of ouabain toxicity after furosemide administration was inhibited by pretreatment with potassium sparing diuretic, prorenoate. Furosemide-induced potentiations of contractile force and arrhythmogenic effect of ouabain were also observed in isolated guinea pig papillary muscle. However after pretreatment with furosemide, ouabain produced arrhythmias without any significant changes in either left ventricular or subcellular fractions binding of 3H-ouabain in guinea pigs. These findings suggest that furosemide-induced potentiation of ouabain toxicity is at least in part associated with the decreased intracellular potassium content of guinea pig heart. It was also demonstrated that the positive inotropic action induced by subtoxic dose of ouabain was potentiated by furosemide in guinea pig papillary muscle preparation.

Animals↗

[Clinical use of piperacillin on obstetrical and gynecological infections (Second report)].

We administered piperacillin (PIPC) to patients with obstetrical and gynecological infectious diseases and obtained the following results. 1. Sixteen patients were administered PIPC at a dose of 4 or 9 g by dripping infusion 2 or 3 times a day for a period of 4 approximately 14 days. Eight cases had cancer as their underlying disease (including cervical cancer etc.). The clinical effect was good in 3 of these 8 patients with cancer so that the efficacy rate was 37.5%. But the other 8 cases without cancer all responded effectively, so their efficacy rate was 100%. The efficacy was good in 11 out of 16 cases so the overall efficacy rate was 68.8%. 2. No side effect was observed. 3. No adverse reaction in laboratory findings (including hematological findings, hepatic function tests, renal function tests) was observed.

Adult↗