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Biomedical subjects

H Tezuka

Publications and source records attributed to H Tezuka.

At least 37 records · Page 2Linked to original sources
PubMed1991

[A case of adrenomyeloneuropathy with marked spinal cord atrophy on magnetic resonance imaging].

A 29-year-old man complained of increasing paraplegia and sphincter disturbances. On admission, he was 23 years old. He had moderate pigmentation of the skin, and his neurological examinations revealed spastic paraplegia, hyperreflexia of both legs with Babinski's signs, a pinprick sensation deficit below the L-1 level, loss of vibration sense in the lower extremities and horizontal nystagmus on lateral gaze. Endocrinological examinations revealed adrenocortical insufficiency. CSF, EEG, EMG, brain-CT and myelography did not show any abnormalities, but metrizamide CT myelography at the low thoracic spinal cord revealed decreased cord diameter. Nerve conduction velocities showed impairment in the tibial and peroneal motor fibers. Auditory brain-stem response revealed elongated III-V interval. A cystometrogram disclosed a reflex neurogenic bladder. In the analysis of the fatty acid component of plasma sphingomyelin, the C26/C22, C25/C22, C24/C22 ratios were found to be increased, and the diagnosis of adrenomyeloneuropathy (AMN) was confirmed. The patient's mother was also found to be asymptomatic carrier of AMN on the basis of long chain fatty acid plasma levels. The MRI performed in his age of 29 years, showed marked spinal atrophy from low cervical to low thoracic regions and mild cerebellar atrophy. This findings seems to correspond with chronic progressive demyelination of spinal white matter such as pyramidal tract and fasciculus gracilis.

Adrenoleukodystrophy↗
PubMed1990

Phenotypic characterization of lymphocytes infiltrating synovial tissue from patients with rheumatoid arthritis: analysis of lymphocytes isolated from minced synovial tissue by dual immunofluorescent staining.

The phenotypic markers of mononuclear cells in synovial tissue from 19 patients with active rheumatoid arthritis (RA) were identified by a dual immunofluorescent method. The mononuclear cells were isolated from synovial tissue by mechanical disaggregation and an enzymatic digestion technique. The results revealed a marked reduction in CD4+2H4+ cells (suppressor inducer T cells) and an increment in CD4+4B4+ cells (helper T cells) among CD4+ cells in synovial tissue. The percentage of CD8+CD11b+ cells (suppressor effector T cells) was significantly lower in synovial tissue than in peripheral blood from patients with RA, resulting in an increased percentage of CD8+CD11b-- cells (cytotoxic T cells). The synovial tissue had higher percentages of pan B cells (B1+ cells), differentiated B cells (B1+B2-- cells) and plasma cells (PCA-1+ cells). These findings suggest that a combination of the increment in helper T cells, the reduction in suppressor T cells, and the increment in differentiated B cells may lead to excessive production of autoantibodies.

Adult↗
PubMed1990

Inhibitory effects of gold sodium thiomalate on the proliferation and interferon-gamma induced HLA-DR expression in human endothelial cells.

Our study was undertaken to investigate the effects of gold sodium thiomalate (GSTM) on the proliferation and HLA-DR antigen expression of human umbilical vein endothelial cells (EC). The proliferation of the EC was determined by 3H-thymidine incorporation into the EC. The expression of HLA-DR antigen on the surface of the EC was detected by an indirect immunofluorescent method using a fluorescent flow cytometer. When GSTM was added at the start of the EC culture, GSTM at a low concentration could inhibit the proliferative response of the EC to endothelial cell growth supplement. Furthermore, when the EC were cultured with recombinant interferon-gamma (rIFN-gamma) and GSTM, GSTM was also able to suppress the HLA-DR antigen expression on the surface of EC induced by rIFN-gamma. On the time-kinetic study of the effects of GSTM on the HLA-DR antigen expression induced by rIFN-gamma, the pretreatment of GSTM was able to suppress the HLA-DR antigen expression, whereas GSTM did not affect the HLA-DR antigen expression already induced by rIFN-gamma. Our findings suggest that the therapeutic effects of gold compounds in patients with rheumatoid arthritis may be attributed to the interference of the proliferation and HLA-DR antigen expression of the EC.

Antigens, Surface↗
PubMed1990

[Multiple myeloma causing obstructive jaundice by extramedullary plasmacytoma after Bence Jones protein loss--an autopsy case report].

A 63-year-old man was admitted to our hospital with a chief complaint of general malaise in March 1986. A diagnosis of Bence Jones protein (kappa) type of multiple myeloma was made from increased atypical plasma cells in the bone marrow, urinary BJP (kappa) and osteolytic lesions. Urinary BJP (kappa) was decreased by MP and VENP therapies. In April 1987, he visited us again with the complaint of pain on the left shoulder. An examination revealed multiple osteolytic lesions and bilateral pleural effusion containing atypical plasma cells. Jaundice was developed at the end of July 1987. An ultrasound examination revealed a hypoechoic mass in the area of pancreatic head. The effusion was gradually increased without response to the treatment. He died of respiratory failure on July 31, 1987. On autopsy, extramedullary plasmacytoma was found in the head of pancreas. It was a rare case of multiple myeloma in which pleural effusion and multiple plasmacytomas, and finally obstructive jaundice were developed although urinary BJP (kappa) was reduced by treatment.

Bence Jones Protein↗
PubMed1990

[Two cases of abdominal bronchogenic cyst].

Two cases of abdominal bronchogenic cyst were reported. In the first case, the cyst was communicated with gastric fundus and existed as gastric abscess. In the second case, the cyst showed high CT number and chemical analysis of the contents revealed high range of Ca, Fe and Amylase levels.

Adult↗
PubMed1989

Increment in the Ta1+ cells in the peripheral blood and thyroid tissue of patients with Graves' disease.

The present study utilized the anti-Ta1 mAb to characterize the cell surface phenotypes of peripheral blood and intrathyroidal lymphocytes in patients with Graves' disease. We found an increase in PBL bearing the Ta1 Ag in untreated patients. The euthyroid patients in remission, induced by antithyroidal drugs, radioisotope therapy, and subtotal thyroidectomy, had lower percentages of Ta1+ cells than did untreated patients. An increased percentage of Ta1+ cells in untreated patients was found in both CD4+ cells and CD8+ cells. The ratio of CD4+Ta1+ cells to CD8+Ta1+ cells in untreated patients was significantly higher than that of normal subjects. There was a positive correlation between the percentage of Ta1+ cells and the level of anti-TSH receptor antibody. In this prospective study, the proportion of Ta1+ cells was decreased in parallel with the reduction in anti-TSH receptor antibody and free T3 levels. In the chronically treated patients, the proportion of Ta1+ cells in the thyroid tissue was, yet similar to that in the peripheral blood, markedly increased in comparison to that of normal subjects. In contrast to Ta1+ cells, the thyroid tissue had a significantly higher percentage of HLA-DR+ T cells than did the paired peripheral blood. The proliferative responses of the Ta1+ cell-enriched population isolated from untreated patients toward thyroglobulin and microsomal Ag were markedly higher than those in a Ta1+ cell-depleted population, but both populations were able to respond equally to PHA. These results suggest that the Ta1+ cells may include Ag-triggered memory cells that are reactive with thyroid-specific Ag. Furthermore, monitoring such cells may provide an objective measure of abnormal immunologic activity.

Adolescent↗
PubMed1989

Interleukin-1 production and action in thyroid tissue.

This study was undertaken to determine the effects of interleukin-1 (IL-1) on human thyroid epithelial cells (thyrocytes) and whether thyrocytes produce IL-1. The supernatants of cultured peripheral blood monocytes stimulated with lipopolysaccharide (LPS) increased [3H]thymidine incorporation into thyrocytes from normal subjects and patients with Grave's disease. The IL-1 levels of cultured supernatants of monocytes were measured by a thymocyte costimulation assay and a solid phase sandwich immunoenzymometric assay. The supernatants of monocyte cultures stimulated with LPS contained significant amounts of IL-1 bioactivity and IL-1 alpha and IL-1 beta immunoactivity. Recombinant IL-1 beta (rIL-1 beta) also stimulated [3H]thymidine incorporation into thyrocytes from normal subjects and patients with Graves' disease, and it increased the proportion of thyrocytes in the S phase of the cell cycle. Furthermore, thyrocytes stimulated with rIL-1 beta for 24 h produced significant amounts of prostaglandin E2. Indomethacin inhibited completely the rIL-1 beta-stimulated prostaglandin E2 production and increased markedly [3H]thymidine incorporation. IL-1-like activity also was detected in the cultured supernatants of lipopolysaccharide (LPS)-stimulated thyrocytes from Graves' and normal thyroid glands, but the amount of IL-1-like activity secreted by thyrocytes was significantly less than that secreted by circulating monocytes. The kinetics of the release of IL-1-like activity by thyrocytes were similar to those of its production by circulating monocytes. Pretreatment of thyrocytes with interferon-gamma failed to enhance the release of IL-1-like activity. Moreover, IL-1 alpha or IL-1 beta immunoreactivity could not be detected in the supernatants of LPS-stimulated thyrocytes, despite the presence of IL-1-like bioactivity. No IL-1 alpha mRNA was detected in unstimulated thyrocytes or thyrocytes stimulated with LPS and phorbol myristate acid. These findings demonstrate that thyrocytes produce an IL-1-like substance(s), but not IL-1, when stimulated by LPS. We conclude that IL-1 may regulate the proliferation of thyrocytes and that local production of IL-1 by infiltrating monocytes may contribute to the development of goiter in patients with autoimmune thyroid diseases.

Biological Availability↗
PubMed1989

Abnormal B lymphocyte function in thyroid glands from patients with Graves' disease.

Thyroid-infiltrating B lymphocytes from patients with Graves' disease were investigated in regard to their phenotypic profiles, cell size, cell cycle status, proliferative response to Staphylococcus aureus Cowan 1 (SAC), and spontaneous production of immunoglobulin G (IgG) and antithyroidal autoantibodies. Thyroid tissues and peripheral blood were obtained at the time of subtotal thyroidectomy of 27 Graves' patients who had been treated with thionamide drugs and iodide before operation. Two intrathyroidal mononuclear cell populations were obtained from these thyroid tissues. One cell population was isolated from the supernatants after mechanical disaggregation of the tissues and was defined as TG-1 cells. Another cell population, defined as TG-2 cells, was isolated from the supernatants of overnight cultures of the thyroid debris after enzymatic digestion. The percentages of B lymphocytes bearing activated markers and plasma cells (CD20+CD21-, IgM+IgD-, CD20+ transferrin receptor+, PCA-1+) were significantly higher in the TG-1 and TG-2 cell populations than in peripheral blood from Graves' disease patients and normal subjects. These phenotypic changes were accompanied by increased thyroid gland B lymphocyte cell size from patients with Graves' disease. The proliferative response of B lymphocytes to SAC was markedly lower in TG-1 and TG-2 cell populations than in peripheral blood cells from Graves' disease patients and normal subjects. B lymphocytes isolated from thyroid glands secreted significantly more IgG and antithyroidal autoantibodies than those from peripheral blood. Based on the findings of abnormalities in thyroid-infiltrating B lymphocytes, we suggest that activated B lymphocytes may induce the excessive production of antithyroidal autoantibodies in thyroid glands from patients with Graves' disease.

Adult↗
PubMed1989

[Two cases of ectopic prostatic tissue in the prostatic urethra].

Two cases of ectopic prostatic tissue or adenomatous polyps with prostatic type epithelium in the prostatic urethra were reported. They were 30-and 33-year-old males suffering from gross-hematuria and from urethral pain on urination with terminal gross-hematuria. Endoscopic examination revealed papillary lesions from the dilated orifice of the prostatic utricle. Biopsied pathology demonstrated a tissue similar to that of the prostatic gland. PSA (prostatic specific antigen) stain using immunohistochemical methods was positive. Histogenesis and the importance of this lesion particularly as a cause of hematuria in the young male adult were discussed.

Adult↗
PubMed1989

Cytotoxic activity of interleukin-2 (IL-2) activated killer cells toward thyroid epithelial cells.

We investigated the sensitivity of thyroid epithelial cells (thyrocytes) to IL-2 activated killer cells. The thyrocytes were lysed by autologous and allogeneic IL-2-activated killer cells; there were no differences in sensitivity to the killer cells between normal thyrocytes and thyrocytes from patients with Graves' disease. When thyrocytes were pretreated with recombinant interferon (rIFN) gamma or alpha, the IL-2-activated killer cell-mediated cytotoxicity was depressed and varied inversely with the cell surface expression of class I HLA gene products. The rIFN-gamma pretreatment did not alter the kinetics of thyrocytes lysis by IL-2-activated killer cells. Using cold target competition analysis, rIFN-gamma-pretreated thyrocytes clearly competed less effectively than did untreated cells for lysis of untreated target cells. These results suggest that rIFN-gamma or IFN-alpha pretreatment of thyrocytes may reduce their ability to be recognized by effector cells. These findings suggest that destruction of thyrocytes in autoimmune thyroiditis may be, in part, due to IL-2-activated killer cells and may be regulated by IFN.

Cells, Cultured↗
PubMed1989

Increment of Tal positive cells in peripheral blood from patients with rheumatoid arthritis.

Recently it was demonstrated that the Tal antigen is a marker for activated T cells and the population of Tal+ cells includes memory T cells. Our study was undertaken to analyze Tal+ cells in peripheral blood from patients with rheumatoid arthritis (RA) and examine the correlation between the proportion of Tal+ cells and disease activity. Using a dual immunofluorescent method, T cell subsets were analyzed in peripheral blood from 46 patients with RA, 10 patients with osteoarthritis (OA) and 10 healthy subjects. Patients with RA had a significantly higher percentage of T cells bearing the Tal antigen than patients with OA and healthy subjects. Furthermore, the percentage of CD3+Tal+ cells in peripheral blood from patients with RA was significantly correlated with disease activity including erythrocyte sedimentation rate, morning stiffness and the Lansbury index, whereas CD3+ HLA-DR+ cells did not correlate. In serial observations in patients with RA, the percentage of CD3+ Tal+ cells decreased in accordance with the improvement of disease activity. Thus, we suggest that the percentage of Tal+ cells may be a marker of the disease activity in patients with RA.

Aged↗
PubMed1989

Elevation of a tumor associated antigen CA 19-9 levels in patients with rheumatic diseases.

We investigated the incidence and characteristics of an elevated tumor associated antigen CA 19-9 in patients with rheumatic diseases. Serum concentration of CA 19-9 was increased in 13 of 39 patients (33.3%) with definite or classical rheumatoid arthritis (RA), in 6 of 19 patients (31.6%) with systemic lupus erythematosus (SLE), in 3 of 9 patients (33.3%) with progressive systemic sclerosis (PSS) and in 9 of the other 35 patients (25.7%). Malignant neoplasm was not detected in any of the patients with rheumatic diseases. Pretreatment of mouse serum with patients' sera did not reduce the measured CA 19-9 values obtained by the conventional assay. The CA 19-9 antigen found in sera from patients with RA was present in a non-IgG fraction, and had the same molecular weight as that in one patient with pancreatic cancer, as determined by gel filtration. These results demonstrated that serum CA 19-9 levels were increased in some patients with rheumatic diseases.

Adult↗
PubMed1989

[A case of progressive systemic sclerosis accompanied with rheumatoid arthritis].

A 37-year old man was suffered from Raynaud's phenomenon, sclerodactyly, and polyarthritis involving knees, shoulders, and hands. Recurrent skin ulcers were present in finger tips. Laboratory studies showed positive RA test, antinuclear antibody (nucleolar type), and anti-Scl 70 antibody. So diagnosis of progressive systemic sclerosis (PSS) was made. Progressed destructive arthritis with rheumatoid nodules developed in the patient. The joint destruction was severe and he was satisfied with the criteria of the American Rheumatism Association (ARA). This patient appears to be an overlapping case of PSS and rheumatoid arthritis (RA).

Adult↗
PubMed1989

[A case of alternating Tolosa-Hunt syndrome].

A 50-year-old woman developed third, fourth, and fifth cranial nerve palsies in the right associated with frontal pain in the ipsilateral side. Oral administration of prednisolone (30 mg/day) was initiated. The painful ophthalmoplegia improved dramatically following this treatment. Three months later, the patient developed the third, fourth, and fifth cranial palsies in the left which was contralateral to the previous episode. The patient had pain in the left frontal region. The corticosteroid therapy was again effective. Cavernous sinus and orbital venographies demonstrated a constriction of the right superior ophthalmic vein in the first and third parts, with a partial filling of the cavernous sinus. The left superior vein and cavernous sinus were normal. A left carotid arteriogram showed a slight deformity of the carotid siphon in the left. The glucose tolerance test demonstrated a mild diabetic pattern. Diabetic ophthalmoplegia can also be suspected in this case, however, the finding of a partial filling of the right cavernous sinus was indicative of Tolosa-Hunt syndrome. Therefore this case was diagnosed as Tolosa-Hunt syndrome. Alternating relapsing Tolosa-Hunt syndrome involving the third, fourth and fifth cranial nerve as seen in this case is very rare. There are many diseases which may demonstrate similar symptoms; i.e. parasellar tumor, aneurysm, diabetic ophthalmoplegia, multiple cranial neuropathy, etc. The pathologic process involved in Tolosa-Hunt syndrome is poorly understood and it appears that the clinical entity of this syndrome should be questioned. We believe that it is necessary to clarify the precise pathologic process involved in this syndrome and its relation with other similar syndromes exhibiting similar symptoms.

Female↗
PubMed1989

Reproducible establishment of hemopoietic supportive stromal cell lines from murine bone marrow.

Stromal cell lines, designated MS-1, -2, -3, -4, -5, -6, and -7 were established by irradiating the adherent cells in long-term bone marrow cultures with 900-rad x-rays. Two of the cell lines, MS-1 and MS-5, have the capacity to support the growth of hemopoietic stem cells (spleen colony-forming cells and granulocyte-macrophage colony-forming cells) for greater than 2 months in vitro. These two cell lines were alkaline phosphatase-, peroxidase-, and factor VIII-negative and positive for periodic acid-Schiff and nonspecific esterase. Extracellular matrix proteins such as fibronectin, laminin, and collagen type I were produced by these two cell lines. Neither MS-1 cell- nor MS-5 cell-conditioned medium supported the growth of hemopoietic stem cells, and hemopoietic stem cells were found preferentially to be under and on MS-1 and MS-5 layers rather than in suspension. Close contact with the MS-1 cell layer or the MS-5 cell layer appears to be essential in maintaining hemopoiesis in vitro. Conditioned media from MS-1 cells and MS-5 cells stimulated granulocyte colony formation from murine bone marrow cells in semisolid culture.

Animals↗
PubMed1988

Establishment of a hemopoietic stimulating factor producing murine leukemia cell lines: pathogenesis of granulocytosis in L8313 bearing mice.

Thy 1.2+ cells of L8313 leukemia bearing mice were previously shown to produce granulocyte macrophage colony stimulating activity (GM-CSA) and interleukin-3 (IL-3). Cell lines with the Thy 1.2+ phenotype were established from spleen cells of the leukemic mice, and were designated STIL-3 C5 and STIL-3 D10. They produced and released GM-CSA and IL-3 activities in culture supernatant. C5 cells were phenotypically Thy 1.2+ and Lyt 2.1+ with rearrangement of the T-cell receptor beta chain gene also being identified. D10 was Thy 1.2+ and L3T4+ with T-cell receptor beta chain gene rearrangement not detectable. Since the same sized rearranged bands were observed between C5 and L8313 leukemic mouse spleen cells, it is indicated that C5 cells are derived from the leukemic cells. Inoculation of these cells into mice induced granulocytosis. These results indicated that L8313, which was thought to be a "granulocytic leukemia", is actually a T-cell leukemia, whose granulocytosis is a leukemoid reaction induced by normal hemopoietic cells responding to the hemopoietic stimulating factors, GM-CSA and IL-3, produced by the leukemic T cells. Thus, L8313 should be known as a T-cell leukemia associated with granulocytosis.

Animals↗