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Biomedical subjects

S Eto

Publications and source records attributed to S Eto.

At least 181 records · Page 10Linked to original sources
PubMed1989

[Changes in gastric mucosal blood flow after selective proximal vagotomy; an experimental study in rats].

The effect of selective proximal vagotomy (SPV) on gastric mucosal blood flow (MBF) was studied in rats using hydrogen gas clearance technique. The following results were obtained. 1) Resting MBF of the corpus decreased significantly from 106.3 +/- 9.8 ml/min/100g to 74.5 +/- 15.5 ml/min/100g at 12 weeks after SPV (p less than 0.01). Resting MBF of the antrum did not decrease. 2) Tetragastrin, betazol-HCl and 2-deoxy-d-glucose (2DG)-stimulated acid outputs were reduced following SPV for more than 12 weeks after operation. 3) The increase of corporal MBF after tetragastrin, betazol-HCl and 2DG stimulation was less significant with accompanying reduction of acid output. 4) The increase of antral MBF after tetragastrin or betazol-HCl stimulation was less significant after SPV. But, the increase after 2DG stimulation was as much as after SPV.

Animals↗
PubMed1988

Production of B cell-stimulating factors by B cells in patients with systemic lupus erythematosus.

The production of B cell-stimulating factors (BSF) by B cells in patients with systemic lupus erythematosus (SLE) was studied in vitro. B cells from SLE patients markedly proliferated and differentiated into Ig-producing cells by in vitro culture without any stimulation. The culture supernatant of these B cells contained BSF activity that stimulated Staphylococcus aureus Cowan I-treated normal B cells to proliferate and differentiate into Ig-producing cells. By a Percoll gradient density centrifugation, BSF-producing cells were enriched in the higher density fraction, but were reduced in the lower density fraction. The BSF also stimulated the proliferation and the differentiation of SLE B cells. By a Percoll gradient density centrifugation, SLE B cells responsive to the BSF were enriched in the higher density fraction, but were reduced in the lower density fraction. The Mr of the BSF was estimated as about 18,000 Da by Sephacryl S-200 column chromatography. The BSF fraction did not possess IL-2 and IFN activity, but possessed IL-1 activity, which stimulated murine thymocyte proliferative responses. The BSF activity was partially, but not completely, absorbed by an anti-IL-1 alpha antibody. Furthermore, the BSF possessed IL-4 activity, which induced not only the proliferative responses of normal B cells stimulated with B cell mitogens, but also the expression of low affinity Fc epsilon R/CD23 on normal B cells. The BSF also possessed IL-6 activity, which induced the proliferative responses of IL-6-dependent hybridoma cells, MH-60 BSF2. Moreover, human rIL-1, rIL-4, and rIL-6 stimulated SLE B cells. These results suggest that SLE B cells spontaneously produce the BSF such as IL-1 alpha, IL-4, and IL-6 and express their receptors on their surface, and the interaction between the BSF and their receptors stimulates SLE B cells to spontaneously proliferate and differentiate into Ig-producing cells as an autocrine mechanism.

Animals↗
PubMed1988

[The effect of purified mouse GM-CSF on CFU-C colony growth in serum-free cultures].

We investigated the effect of the ingredients in serum-free cultures, in which serum was completely replaced by albumin, cholesterol and transferrin, on the growth of murine granulocyte/macrophage progenitor cells (colony forming unit in culture: CFU-C) stimulated by serum-free PWM-SCM and the influences of purified granulocyte-macrophage colony stimulating factor (GM-CSF) in serum-free cultures. The results were as follows: 1) The number of CFU-C colonies reached a peak after 4 days of incubation. 2) A linear relationship was observed between the number of CFU-C colonies and the number of inoculated bone marrow cells. 3) Serum-free cultures could support CFU-C colony growth to the same degree as that in serum-containing cultures. Also, no significant differences were found in the types of colonies grown in both cultures. 4) Bovine serum albumin (BSA) and cholesterol were considered to play the most important roles among the ingredients in serum-free cultures. 5) Purified GM-CSF supported CFU-C colony growth in serum-free cultures and more than a half of the colonies formed were GM-colonies. These results showed the usefulness of our serum-free cultures for studying the granulopoiesis in vitro without the influences of various substances in the serum.

Animals↗
PubMed1988

Production of bone-resorbing activity corresponding to interleukin-1 alpha by adult T-cell leukemia cells in humans.

The physicochemical properties and relationship of bone-resorbing activity and interleukin 1 (IL-1) produced by adult T-cell leukemia (ATL) cells and cell line were studied in vitro. The culture supernatant of ATL cell line, MT2, and peripheral blood lymphocytes freshly obtained from ATL patients had both IL-1 activity detected by the stimulation of murine thymocyte-proliferative responses and bone-resorbing activity detected by the stimulation of 45Ca release from prelabeled murine fetal bones. By Sephacryl S-200 column chromatography, both activities were eluted as a single peak at approximately Mr 15,000. By the chromatofocusing technique, the isoelectric point values of both activities were estimated as pH 4.8 and 5.2. Furthermore, both activities were absorbed with rabbit anti-IL-1 alpha antiserum, but not with anti-IL-1 beta antiserum. These results suggest that ATL cells and cell line produce bone-resorbing activity which corresponds to IL-1 alpha and that this IL-1 alpha is one of the most important causes of hypercalcemia in ATL patients.

Biological Assay↗
PubMed1988

Inhibitory effect of anti-class II antibodies on human B-cell activation.

The role of class II antigens for B-cell activation was analyzed using purified human B cells and anti-class II monoclonal antibodies. The stimulation of purified B cells with Staphylococcus aureus Cowan I induced proliferation and differentiation into immunoglobulin-producing cells in the presence of interleukin-1 and T-cell-derived factors (B-cell growth factor and B-cell differentiation factor). The addition of anti-class II monoclonal antibodies inhibited B-cell responses. However, anti-class I monoclonal antibody did not inhibit B-cell responses. When mitomycin C and cycloheximide-treated B cells were added to the induction culture of B cells as the stimulator, B-cell responses were enhanced in a dose-dependent manner. Furthermore, the stimulator B cells also partially restored the suppressed B-cell responses which were induced by the pretreatment of B cells with anti-class II antibody. This enhancing effect of stimulator B cells on B-cell responses was inhibited by the pretreatment of stimulator B cells with anti-class II antibody. The treatment of B cells with anti-class II antibody and complement depleted the activity of both responder B cells and stimulator B cells. These results suggest that cellular interaction among B cells exists in the B-cell activation induced with Staphylococcus aureus, Cowan I and anti-class II antibody inhibits B-cell activation by interfering in this cellular interaction.

B-Lymphocytes↗
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

[Estrogen receptors in human gastric, hepatocellular, and gallbladder carcinomas and normal liver tissues].

Steroid binding assay using the dextran coated charcoal (DCC) method was applied to human tissues including tumors of the digestive organs, and the results were compared with those of enzymeimmunoassay (EIA) and immunocytochemical assay (ICA) with monoclonal antibody against human estrogen receptor of MCF-7 breast cancer cells. Using the DCC method, estrogen receptor activity was detected in 6 of 26 cases (23.1%) with gastric carcinoma, 3 of 16 hepatocellular carcinoma cases (18.8%), 1 of 3 gallbladder carcinoma cases (33.3%), and both of the 2 cases (100%) with normal liver tissue. However, using EIA, no ER activity was detected in any case. Moreover, ER positive cells were not found by immunohistochemical staining in the gastric carcinoma cases or in normal liver tissue, both of which showed ER activity by the DCC method. These results suggest that the estrogen receptor like material exists in cytosol of the human digestive tumors and normal liver tissue, but that the specificity of the antibodies against estrogen receptor molecules in these tumors may be different from that of the breast tumors.

Breast Neoplasms↗
PubMed1987

[Circulating HLA-DR (Ia) positive T cells and T cell activation by thyroglobulin, thyroid microsome and TSH-receptor in autoimmune thyroid diseases].

HLA-DR antigens are not expressed on normal circulating T lymphocytes, but recently it has become apparent that HLA-DR antigens are expressed on immunologically activated T lymphocytes, as well as monocytes, macrophages, and B lymphocytes. Namely, the HLA-DR antigens are considered to be one of the activated T cell antigens. It is apparent from the previous studies that increased numbers of HLA-DR positive T cells frequently appear in the circulation in systemic autoimmune diseases, such as RA and SLE. Furthermore, in such diseases, it is reported that the variations in circulating HLA-DR positive T cells are related to the activity of the diseases. In this communication, we examined the variations in HLA-DR positive T cells in the peripheral blood of the patients with autoimmune thyroid diseases. HLA-DR positive T cells were detected by cytotoxicity test using anti HLA-DR mouse monoclonal antibody (Leu-HLA-DR antibody) and rabbit complement. The results indicate that; 1) The percentage of HLA-DR positive T cells were increased in the patients with autoimmune thyroid diseases. 2) The changes of HLA-DR positive T cells accompanied with the stimulation by non-specific mitogens in vitro in autoimmune thyroid diseases did not differ from those in the normal controls. 3) The percentage of HLA-DR positive T cells increased by the stimulation of TSH-receptor and thyroid microsome in Graves' disease, on the other hand, it occurred by the stimulation of thyroglobulin and thyroid microsome in Hashimoto's thyroiditis. 4) The percentage of HLA-DR positive T cells were correlated with TRAb (TSH receptor Ab assayed by Smith's kit) in Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Circulating monocyte (macrophage)-specific antibodies in patients with autoimmune thyroid diseases].

We investigated the presence of circulating monocyte-specific antibodies (monocytotoxic activities) by cytotoxicity tests and also the relationships between these monocytotoxic activities and the clinical data in autoimmune thyroid diseases. Subjects of this investigation include 16 patients with Graves' disease, 20 patients with Hashimoto's thyroiditis and 10 normal controls. To obtain monocyte-rich population, peripheral blood mononuclear cells of type 0 healthy donor were incubated on culture dishes for 12 hours and dish adherent cells were separated by pipetting. These monocyte-rich population were incubated with sample sera which were previously absorbed by lymphocytes of many different kinds of HLA types to eliminate anti-lymphocyte antibodies, and thereafter cytotoxicity tests were performed by adding rabbit complements. The monocytotoxic activities were expressed by %cytotoxicities and the value of %cytotoxicity over 3.9% (mean + 4SD of %cytotoxicities of normal controls) was considered to be positive in monocytotoxic activity. The results indicate that; 1) 8 patients (50%) of Graves' disease and 10 patients (50%) of Hashimoto's thyroiditis had positive values of monocytotoxic activity. 2) These positive values of monocytotoxic activity were markedly decreased after absorption of sample sera by monocytes, and these patients who had positive values of monocytotoxic activities to allogenic monocytes also had positive values of monocytotoxic activities to autologous monocytes. 3) Patients who had positive monocytotoxic activities also had high levels of TSH receptor antibody (TRAb) and anti-microsomal antibody, besides, monocytotoxic activity was significantly correlated with levels of TRAb in Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
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↗