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Biomedical subjects

T Ota

Publications and source records attributed to T Ota.

At least 271 records · Page 15Linked to original sources
PubMed1988

Mechanism of spontaneous activation of B cells in patients with systemic lupus erythematosus. Analysis with anti-class II antibody.

The mechanism of spontaneous activation of B cells in patients with systemic lupus erythematosus (SLE) was analyzed by using anti-class II monoclonal antibodies in vitro. B cells from SLE patients showed enhanced proliferation and Ig production by in vitro culture without any stimulation. The number of Ig-producing cells increased during a 5-day culture period, but the addition of anti-class II antibodies such as anti-HLA-DR, DQ, or DP monoclonal antibodies inhibited these B cell responses in a dose-dependent manner. Anti-class I and anti-B1 antibody gave no effect. The inhibitory effect of anti-class II antibodies on B cell responses became more remarkable when B cells were cultured on a longer period. By a Percoll gradient density centrifugation, Ig-producing cells were enriched in the lower density fraction, but became depleted in the higher density fraction. However, B cells of the higher density fraction developed into Ig-producing cells after 5 days of culture and anti-class II antibodies inhibited this development. When mitomycin C- and cycloheximide-treated B cells were added to the in vitro culture of B cells as a stimulator, B cell responses were enhanced in a dose-dependent manner. T cells treated with mitomycin C and cycloheximide had no enhancing effect on B cell responses. Furthermore, the enhancing effect of the stimulator B cells was inhibited by the pretreatment of stimulator B cells with anti-class II antibodies. These results suggest that in patients with SLE the abnormality exists in B precursor cells which are easily activated by interacting with other B cells to differentiate into Ig-producing cells and anti-class II antibodies inhibit the B cell activation by interfering with this cellular interaction.

Antibodies, Monoclonal↗
PubMed1988

Cell surface analysis of purified protein derivative-induced cytotoxic cells in tuberculous pleurisy.

High NK cell activity was observed in tuberculous pleural effusions from which mycobacterium tuberculosis was cultured. Further we observed that cytotoxicity against K562 was augmented by purified protein derivative (PPD). We have now performed the surface analysis of the cells in PPD-induced cytotoxicity using various monoclonal antibodies (mAb) (anti-Leu 1, anti-Leu 7, anti-Leu 11, anti-HLA-DR). Leu 11+ cells have essential cytotoxicity in PPD-induced cytotoxicity, but neither Leu 1+ nor Leu 7+ cells have such cytotoxicity. The PPD-induced cytotoxicity eliminated by the treatment with anti-HLA-DR mAb plus complement was reconstituted by adding either interferon (IFN)-alpha or beta. From these data it was suggested that Leu 11+ cells could be activated through either IFN-alpha or beta derived from HLA-DR+ cells in tuberculous pleural effusion.

Adult↗
PubMed1988

Purified protein derivative induced cytotoxicity in carcinomatous and tuberculous pleurisy.

We have found that natural killer (NK) cells were very active in pleural effusions containing Mycobacterium tuberculosis. Cytotoxicity against K562 and Raji was augmented when the mononuclear cells were cocultured for 18 hr with purified protein derivative (PPD) derived from M. tuberculosis culture supernatants. In pleural effusions of cancer patients, PPD-activated mononuclear cells were less cytotoxic than their counterparts in peripheral blood. However, in the same patients, interferon and interleukin-2 production was greater in pleural effusions than in peripheral blood. On the other hand, in tuberculosis patients there was no significant difference in cytotoxicity between peripheral blood and pleural effusion mononuclear cells, but the production of interferon and interleukin-2 was higher in pleural effusions than in peripheral blood. Neither group of patients consistently demonstrated a correlation between production of interferon or interleukin-2 in peripheral blood and cytotoxicity. Both PPD-induced cytotoxicity and the production of interferon and interleukin-2 were lower in mononuclear cells of carcinomatous than tuberculous pleural effusion. These results indicate that peripheral blood and pleural effusion mononuclear cells differ in cytotoxicity as well as in interferon and interleukin-2 production. Further, these activities also differ in tuberculous and carcinomatous pleural effusions.

Adult↗
PubMed1988

[A new method quantifying tricuspid regurgitant volume by two-dimensional color and continuous wave Doppler echocardiography].

To determine appropriate surgical management of secondary tricuspid regurgitation (TR), we attempted to quantify TR volume by using two-dimensional color Doppler echocardiography (2-DD) and continuous wave Doppler echocardiography (CW). Thirty patients with TR associated with acquired valvular disease were selected for the study. 1. The new quantitative method: TR was observed from two right-angled cross-sections in 2-DD (one; the parasternal long-axis view of the right ventricular inflow tract, and another; the apical four-chamber view or short-axis view at the level of the aortic valve). The width of the regurgitant jet (a and b) was measured at the position just below the tricuspid valve, and the cross-sectional area (S) of TR was calculated as an ellipse where the major and minor axes were a and b (pi/4.ab). The CW is recorded from the center of the regurgitant jet. The regurgitant volume of one unit area (Vp) was calculated by integrating a parabolic flow velocity signal during ejection phase (2/3.vt, where v = peak velocity, t = regurgitant time). Assuming that the fluid figure of TR flow is oval, the regurgitant volume per one beat (VTR) was calculated by the formula: 1/3.S.Vp = pi/18.abvt. 2. Thirty patients were classified into three groups according to VTR: Group 1, less than 10 cc (n = 12); Group 2, 10-20 cc (n = 12); and Group 3, greater than or equal to 20 cc (n = 6). Compared with pulsed Doppler echocardiography and right ventriculography, our classification was much more practical. Namely, in Group 1, the VTR decreased postoperatively with no surgical intervention for the tricuspid valve; in Group 2, 11 underwent tricuspid annuloplasty (TAP) while one received no surgical intervention, and all showed a decrease (less than 10 cc) in the VTR, in Group 3, five underwent TAP while one patient received tricuspid valve replacement (TVR), and three of the five showed 10-20 cc postoperative VTR. 3. There was a significant correlation between the preoperative VTR and tricuspid annular diameter (TAD) at end-diastole, right atrial mean pressure and right ventricular end-diastolic pressure. In three patients of Group 3 with the residual postoperative VTR of 10-20 cc, preoperative right ventricular systolic pressure and pulmonary capillary pressure were lower; and the preoperative systolic pressure gradient across the tricuspid valve was less than or equal to 20 mmHg and the TAD was greater than 50 mm.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Plant-glycoside modulation of cell surface related to control of differentiation in cultured B16 melanoma cells.

We have shown that the ginsenosides Rh1 and Rh2, which are plant glycosides with a dammarane skeleton resembling a steroid skeleton as an aglycone, control the phenotypic expression of mouse B16 melanoma cells in different ways. The effects of Rh1 and Rh2 on the cell surface were studied to clarify the relationship between the control of phenotypic expression and modification of the cell surface in B16 melanoma cells. Rh2, which has the capacity to inhibit the growth of and to stimulate melanogenesis in B16 melanoma cells, causes flattening of the cells cultured in a collagen gel, leading to organized, nonoverlapping monolayers. Cell-to-cell adhesiveness and cell-to-substrate adhesiveness were markedly increased in the B16 melanoma cells treated with Rh2. In Rh2-treated cells, the binding of peanut agglutinin on the cell surface was also increased, whereas no marked changes were observed in the binding of concanavalin A or wheat germ agglutinin. In contrast, Rh1, which showed no effect on cell growth, but did stimulate melanogenesis, did not cause morphological changes of the cells and exerted no effect on cell adhesiveness or cell surface lectin binding. 1,6-Diphenyl-1,3,5-hexatriene polarization values markedly decreased in cells treated with either Rh1 or Rh2. Rh2 was found to be incorporated in the lipid fraction of the B16 melanoma cell membrane. In contrast, Rh1 was not detected in the lipid fraction of B16 melanoma cells. However, novel lipid components were found.

Agglutination↗
PubMed1987

Expression of interleukin 1 receptors on human peripheral T cells.

The expression of interleukin 1 receptors (IL 1R) on human peripheral T cells was studied by the binding assay with 125I-labeled recombinant human interleukin 1 (IL 1) alpha and IL 1 beta and by the flow cytofluorometry with the fluorescein isothiocyanate (FITC)-conjugated IL 1 alpha. Peripheral blood lymphocytes expressed only few IL 1R without any stimulations. When they were stimulated with concanavalin A (Con A), IL 1R-positive cells began to increase by 4 hr, reached the maximum level at 48 hr, and then gradually decreased. The kinetics of the expression of IL 1 alpha R and IL 1 beta R showed the same pattern. Furthermore the binding of 125I-labeled IL 1 alpha to IL 1R on T cells was inhibited by the addition of either cold IL 1 alpha or IL beta, but not by interleukin 2 or interferons. The similar results were observed in the binding of 125I-labeled IL 1 beta. These results suggest that IL 1R on human peripheral T cells reactive for IL 1 alpha and IL 1 beta were identical. By Scatchard plot analysis, the numbers of IL 1R were estimated as 40 and 350 molecules per cell before and after Con A stimulation, respectively, and their Kd values were 3.1 X 10(-10) M and 2.8 X 10(-10) M. When purified T cells alone were stimulated with Con A, IL 1R were only marginally expressed. However, by the addition of monocytes, IL 1R were expressed on T cells in a dose-dependent manner. The maximum response was induced in the presence of 10% monocytes. The maximum IL 1R-positive T cells were approximately 30% by the detection of the flow cytofluorometry with FITC-conjugated IL 1 alpha. This enhancing activity of IL 1R expression on T cells by monocytes was inhibited by the addition of an anti-HLA-DR antibody or by the treatment of monocytes with the anti-HLA-DR antibody and complement. Furthermore T cell proliferative responses induced with IL 1 and Con A were also enhanced by the addition of HLA-DR-positive monocytes. These results suggest that IL 1R are expressed as the result of monocyte-T cell interaction in the early stage of T cell activation, and the expression of IL 1R on T cells and the responsiveness of T cells for IL 1 require the accessory function of HLA-DR-positive monocytes.

Antigen-Presenting Cells↗
PubMed1987

Treatment resistant chronic psychopathology and CT scans in schizophrenia.

In order to examine the relationship between the neuroleptic resistant chronic psychopathology and CT findings in schizophrenia, 25 schizophrenics who had been treated well and were in a stable condition were assessed for positive and negative symptoms, CT findings, medication, and the clinical course of illness. Correlational analysis showed that there was a group of patients who had comparatively small ventricles and presented treatment resistant positive symptoms, and another group of patients who had larger ventricles and lacked positive symptoms. Negative symptoms showed a tendency toward positive correlation with atrophic CT changes of cortices. Literature on CT findings and symptomatology was critically reviewed. The importance of the more chronic positive symptoms correlating to CT findings in schizophrenia were discussed.

Adolescent↗
PubMed1985

[Clinical significance of serum sialic acid in rheumatoid arthritis and systemic lupus erythematosus].

A study of the clinical significance of serum sialic acid (SA) in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) is presented in this paper. Because a definite correlation (n = 30, r = 0.74, P less than 0.001) between SA and erythrocyte sedimentation rate (ESR) and a good reflection of SA to disease activity in clinical course were revealed in RA patients, we were able to use SA in place of ESR as a marker of disease activity and a guide to treatment. On the other hand, although a good correlation (n = 22, r = 0.62, P less than 0.01) between SA and ESR was revealed in SLE patients, SA was inapplicable as a marker of disease activity in SLE because of a poor correlation between SA and anti-DNA antibody or serum complement which is mainly used as a marker of disease activity and a guide to treatment.

Antibodies, Antinuclear↗