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S Kojima

Publications and source records attributed to S Kojima.

At least 973 records · Page 54Linked to original sources
PubMed1983

Immune response to Trichomonas vaginalis. IV. Immunochemical and immunobiological analyses of T. vaginalis antigen.

The immune response of patients with trichomoniasis vaginitis to Trichomonas vaginalis was examined by using passive hemagglutination assay and skin reactions. Trichomonas-specific immune responses could hardly be detected in the patients by these assay methods. In order to develop a simple and reliable assay for demonstration of T. vaginalis-specific immune responses in the patients, proliferation responses of peripheral mononuclear cells from the patients were examined. Lymphocytes obtained from the patients were shown to incorporate 3H-methyl-thymidine when stimulated with T. vaginalis antigen in vitro. Furthermore, immunochemical analysis of T. vaginalis antigen has been done by Sephadex chromatography and sodium dodecyl sulfate gel electrophoresis. The data revealed that the murine and human IgM antibodies specific to T. vaginalis recognize various antigens with a wide range of molecular weights (between 13,000 and 100,000 daltons), while human and murine IgG antibodies recognize molecules with a much narrower range of molecular weights (50,000-100,000 daltons).

Antibodies↗
PubMed1983

Presence of an intrastrain cross-reactive idiotype on A/J antibodies of the IgE class specific for the p-azophenylarsonate group.

An intrastrain cross-reactive idiotype, CRIA, is associated with a large proportion of the anti-p-azophenylarsonate (anti-Ar) antibodies of A/J mice. The present experiments, in which the methods of direct and reverse passive cutaneous anaphylaxis (RPCA) were used, indicate that IgE anti-Ar antibodies are produced in A/J mice upon stimulation with a protein-Ar conjugate and that a large proportion of these antibodies express CRIA. The use of monoclonal anti-CRIA for RPCA eliminated the strong nonspecific reactions previously observed. The results provide a basis for studying factors that regulate the switch to IgE biosynthesis during an immune response.

Animals↗
PubMed1982

Delay-related activity of prefrontal neurons in rhesus monkeys performing delayed response.

Activity of dorsolateral prefrontal cortical neurons was examined in rhesus monkeys while they performed a spatial delayed-response task with delays of 2, 4, 8 or 12 s interposed between cue and response. Of the 600 neurons recorded for at least 10 trials under each delay condition, 95 displayed a pattern of discharge during the delay period which was significantly different from neuronal firing before or after this period. Changes in the duration of the delay elicit two distinct patterns of activity in these neurons: some (59/95, 62%) exhibit a fixed pattern of discharge regardless of the duration of the ensuing delay; others (31/95, 33%) alter their pattern of activity in relation to the temporal changes. Although both types of delay-related neurons display a variety of discharge profiles, more than half of each class exhibit their highest activity in the early part of the delay period. A related finding concerns a small subclass of spatially selective neurons which fire significantly more when the cue is presented on the left than on the right or vice versa. A striking 80% of these spatially discriminative neurons exhibit peak activity in the first few seconds of the delay period. These findings provide cellular evidence that (1) prefrontal neurons are responsive to temporal as well as spatial features of the delayed-response task; and (2) the involvement of a subset of these is particularly critical in the first few seconds of the delay. The latter finding emphasizes that prefrontal neurons may play an important role in the registration process of spatial memory.

Animals↗
PubMed1982

Operant behavioral analysis of memory loss in monkeys with prefrontal lesions.

The effects of dorsolateral prefrontal cortical ablation were examined in rhesus monkeys preoperatively trained to perform two versions of an indirect spatial delayed-response task. In one task (DR I), the stimulus keys that signaled the position of the reward were accessible throughout a trial. Thus, the monkeys could orient to the positive side ('rehearse') by continuing to press the correct key during the delay. The other task, DR II, was designed to disrupt bodily orientation and to prevent 'rehearsal'. In this task the monkeys were required to press an extraneous upper key during the delay. After bilateral ablation of the prefrontal cortex, 3 out of the 4 monkeys easily regained preoperative levels of performance on the DR I task, but all subjects were markedly impaired in the DR II task on which they exhibited strong positive preferences. These deficits were ameliorated by eliminating the position biases through training with short delay intervals followed by gradual increments in delay length. Analysis of the location of key presses during each phase of delayed-response trials showed that the monkeys press the correct key in the cue period even when they subsequently made incorrect responses. A consistent finding was that operated monkeys shifted their response to the incorrect key early in the delay period regardless of its duration, whenever the correct side was the nonpreferred side. These results support the idea that delayed-response deficits in monkeys with prefrontal lesions may be due in part to a defect in registering or encoding the correct spatial position in memory rather than to a loss in storage or retrieval processes.

Animals↗
PubMed1982

Uptake of 67Ga in the heart of rats treated with isoproterenol.

Gallium-67 citrate (67Ga) accumulation and various enzyme activities during the repair of rat heart with infarct-like lesions induced by isoproterenol (ISP) treatment were measured for 10 days after treatment. Serum creatine phosphokinase (CPK) and glutamic oxalacetic transaminase (GOT) activities were increased immediately after ISP treatment, reaching maximum levels of activity of 545 +/- 64 U/ml and 542 +/- 94 KU/ml, respectively, within 12 h. Uptake of 67Ga in the rat heart was elevated 12 h after ISP treatment, reaching a maximum on day 1 (0.473 +/- 0.015% dose/g heart). This pattern was essentially similar to the pattern of uronic acid content in the 1.2 M NaCl fraction, which contained mainly heparan sulfate (HS). The activity of glucose-6-phosphate dehydrogenase (G-6-PDH), a marker enzyme for fibrogenesis of damaged tissues, was also elevated 12 h after the ISP treatment, reaching a maximum of approximately 2.47 times that of the control heart on day 1. On the other hand, there were no significant changes in the 67Ga uptake and uronic acid content in any of the fractions of the liver and kidneys. These findings suggested that HS might be an acceptor for 67Ga accumulation during the repair of rat heart with infarct-like lesions, in accord with our previous results on CCl4-damaged rat liver.

Animals↗
PubMed1982

A computerized model to analyze transcellular fluid shift during hemofiltration.

Using urea and inulin as markers, we have developed a simple method to calculate intracellular and extracellular fluid volume in patients before and after hemofiltration therapy. During conventional hemofiltration using substitution fluid with a Na+ concentration of 140 mEq/L, a decrease in extracellular fluid volume was noted whereas the intracellular fluid volume was unaltered. Furthermore, we have developed a computerized mathematical model to analyze transcellular fluid shifts during hemofiltration. This model also indicates a decrease in extracellular fluid volume only, the intracellular fluid volume remaining unchanged. High-Na+ hemofiltration using substitution fluid with an Na+ concentration of 160 mEq/L has enabled us to remove fluid from both intracellular and extracellular compartments. Thus, high-Na+ hemofiltration is expected to normalize the intracellular hydration in uremic patients, and to reduce the decrease in extracellular fluid volume during hemofiltration therapy. Our data therefore suggest that high-Na+ hemofiltration could prevent hypotension due to large decreases in extracellular fluid volume by inducing a transcellular fluid shift out of body cells. Our computerized model can be a useful tool in the prescription of the optimal Na+ concentration in substitution fluid for individualized hemofiltration therapy.

Adult↗
PubMed1982

The role of cytotoxic T lymphocytes in the pathogenesis of Vogt-Koyanagi-Harada disease.

Peripheral blood lymphocytes (PBL) were isolated from blood of 6 patients with Vogt-Koyanagi-Harada disease (VKH), and their cytotoxic activity was assayed using 51Cr release from the labelled cells; the cytotoxicity was expressed as percentage release in reference to the complete release using saponin. The PBLs from the patients showed a significant cytotoxic activity against P-36 human melanoma cells, and the specificity of the reaction was confirmed by the cold target inhibition test and also by the use of HeLa-S3 human cervical carcinoma cells and B-16 mouse melanoma cells, since no significant cytotoxicity was seen against these cells. The cytotoxic activity was greatly reduced by pretreatment of the PBLs with monoclonal antihuman Leu-1 antibody plus the rabbit complement. It was, therefore, thought that the cytotoxic activity against the melanoma cells is mainly due to T cells. In addition, the cytotoxic activity was specifically blocked by monoclonal antihuman Leu-2a antibody, the specificity of which is distributed on cytotoxic/suppressor T cell subset of normal human peripheral lymphocytes and normal human thymocytes. A possibility was discussed as regards the involvement of the cytotoxic T lymphocytes in the pathogenesis of VKH.

Adult↗