[A case report of bronchiolo-alveolar cell carcinoma involving the entire right lung asymptomatically].
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Biomedical subjects
Publications and source records attributed to Y Shimamoto.
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An inactive form of human urinary kallikrein (inactive HUK) was highly purified from fresh urine collected from healthy men. Inactive HUK was separated from the active kallikrein (HUK) initially presents in the urine by affinity chromatography on a column of aprotinin immobilized on Sepharose 4B and further purified by gel filtration, ion-exchange chromatography and immunoaffinity chromatography on an anti-HUK antibody immobilized Sepharose 4B column. Inactive HUK was rapidly activated by a trace amount of trypsin. While, plasmin, urokinase, thrombin and chymotrypsin caused no activation of inactive HUK. The molecular weights of inactive HUK and HUK were estimated to be 4.8 X 10(4) and 4.5 X 10(4), respectively. The molecular weight of active HUK generated from inactive HUK by the action of trypsin (HUK'') was almost the same as that of HUK. The mobility of inactive HUK was slightly slower than that of HUK on both immunoelectrophoresis and polyacrylamide gel disc electrophoresis. On the other hand, the electrophoretic mobility of HUKK'' was almost the same as that of HUK. These two types of active HUK had no significant difference in the Km values for H-Pro-Phe-Arg-MCA hydrolysis and inhibition profiles by various protease inhibitors and anti-HUK antibody. Inactive HUK was unable to be measured by the direct radioimmunoassay (RIA) but HUK" generated by the action of trypsin could be measured by the RIA.
The suppressive effects of Cyclosporin A (Cs A) on various types of T-dependent immune reactions, including delayed footpad reaction (DFR), plaque-forming cells (PFC), and cell-mediated cytolysis (CMC), were compared after intramuscular (i.m.) administration of this drug into mice immunized intraperitoneally (i.p.) with chicken erythrocytes (CRBC). A single injection with a high dosage of 500 mg/kg, at the time of the antigen administration suppressed only the PFC, but not the DFR and CMC. Three low dosage injections of 50 mg/kg the day before, on, and after the immunization also induced suppression of PFC. In this treatment, a dose of 100 mg/kg had a marked affect on PFC and CMC. DFR was slightly suppressed with a dose of 100 mg/kg, but markedly so with a dose of 200 mg/kg. This indicates that PFC is very sensitive to Cs A, CMC is moderately sensitive, and DFR is relatively resistant. The injections of Cs A close to the time of antigen administration are more effective than before or after. Thus it is indicated that the 3 types of reactions differ in their susceptibility to Cs A. It might be speculated that the susceptibility to Cs A varies among the types of T cells responsible for these 3 immune reactions, although this is only one of several possibilities.
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The effects of thymectomy at various times after birth, 1 and 7 days (Tx-1, Tx-7), on delayed footpad reactions, cell-mediated cytotoxicity (CMC), production of migration inhibitory factor (MIF), and graft-versus-host reactions (GVHR) against allogeneic antigens were determined by experiments with 8-week-old mice. Delayed footpad reactions were detected in Tx-1 mice, but CMC, production of MIF, and the ability to raise GVHR were not detected in such mice. CMC was detected in Tx-7 mice. However, the ability to raise GVHR and to produce MIF was abolished by thymectomy at 7 days after birth. These results suggest that the effector mechanism to mount a GVHR might be mediated by delayed-type hypersensitivity of tuberculin type rather than CMC to host antigens.
The thymus requirement for the development of immunological responsiveness was determined by estimation of immune responses raised to Listeria monocytogenes in athymic nude, neonatally thymectomized, and sham-operated mice at 6 weeks of age. Not only sham-operated mice, but also neonatally thymectomized mice could completely eliminate the bacteria from the spleen and liver, while athymic nude mice could not eliminate them and showed a persistent form of infection. A strong delayed footpad reaction and acquired cellular resistance could be raised in neonatally thymectomized mice just as well as in sham-operated mice, but not in athymic nude mice. The delayed footpad reaction could be induced in neonatally thymectomized mice without an accompanying ability to inhibit macrophage migration. These results suggest that T cells responsible for immunity against listerial infection require the presence of the thymus for only a very short period in their development.
The effect of neonatal thymectomy at various times after birth (Tx-1, Tx-7) on effector and suppressor T cells responsible for cell-mediated cytotoxicity (CMC) for allogenic antigens was determined. Following in-vitro primary mixed lymphocyte cultures, in the absence of T-cell growth factor (TCGF), alloreactive CMC was not detected in spleen cells of Tx-1 mice, but was detected in spleen cells of Tx-7 mice at as high levels as in those of sham-operated mice. However, in the presence of TCGF, as much alloreactive CMC was detected in spleen cells of Tx-1 mice as in those of Tx-7 mice. Furthermore, TCGF production was not detected in spleen cells of Tx-1 mice but was detected in those of Tx-7 mice. In in-vivo experiments, inhibition of allogeneic tumour growth and CMC in spleen cells showed the same pattern as in in-vitro experiments. These results support the concept that the reduction of CMC in Tx-1 mice might be due to a defect in helper function (TCGF-producing capacity) rather than to a defect in cytotoxic T lymphocytes and/or cytotoxic T lymphocyte precursors. Alloreactive suppressor T cells could not be induced in spleen cells of Tx-1 mice but were induced in spleen cells of Tx-7 mice. Therefore, it was suggested that alloreactive suppressor T cells require the presence of the thymus for 7 days after birth in their development.
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