PubMed HealthSearch

Biomedical subjects

T Sakurami

Publications and source records attributed to T Sakurami.

At least 19 recordsLinked to original sources

Tumor necrosis factor-beta in the serum of adult T-cell leukemia with hypercalcemia.

Serum tumor necrosis factor-beta (TNF-beta) from patients with adult T-cell leukemia (ATL) was studied by a sandwich enzyme-linked immunosorbent assay (ELISA) developed in our laboratory using biotinylated monoclonal anti-TNF-beta and recombinant TNF-beta. Seven of eight patients with hypercalcemia showed elevation of serum TNF-beta. On the other hand, TNF-beta could not be detected by the ELISA in 28 patients without hypercalcemia. The lower detection limit in this assay was 100 pg/mL, corresponding to 500 pg/mL by the conventional method. In two patients serum TNF-beta level decreased after treatment in association with the level of serum calcium. Furthermore, immuno-staining using anti-TNF-beta and avidin-biotin complex showed the presence of cytoplasmic TNF-beta in not only human T-cell leukemia virus type I infected cell lines, but also freshly isolated cells from ATL patients with hypercalcemia. The actual biologic activity of TNF-beta in serum was confirmed by a conventional bioassay in a patient with hypercalcemia, and its cytotoxic activity was inhibited by the addition of anti-TNF-beta antibody in the assay. These results suggested that serum TNF-beta might be one of the factors contributing to the hypercalcemia, at least in patients with ATL.

Adult

An enzyme-linked immunosorbent assay for immune complex of HTLV-I.

A sandwich enzyme-linked immunosorbent assay (ELISA) for immune complexes of human T cell leukemia virus type I (HTLV-I) was developed using monoclonal antibody (MoAb) 3G1 which recognizes a different epitope on HTLV-I to that with which natural human anti-HTLV-I antibody binds. The assay was capable of titrating artificial immune complexes not only at antigen-antibody equivalence but also at antibody excess. Although the antigen-antibody ratios could not be determined in the individual sera from patients with overt ATL, the level of immune complexes in three out of four sera was estimated to be 250 +/- 36 ng/ml. Immune complexes of HTLV-I could not be identified in sera obtained from one patient with overt ATL, three healthy HTLV-I carriers and three normal human controls.

Adult

[Classification of asymptomatic autoimmune thyroiditis by thyrotropin-releasing hormone loading].

Thyrotropin-releasing hormone loading was performed on 91 patients with asymptomatic autoimmune thyroiditis. Four women had no response to this loading test and had high levels in serum total and free thyroxine (TT4, FT4) and in serum total and free triiodothyronine (TT3, FT3). These patients might be classified as subclinical hyperthyroidism (Group G). Twenty-four patients had normal levels of both basal and peak thyrotropin after loading and were classified as Group I. There were no significant differences between 45 controls (Group C) and Group I patients in serum thyroid hormone levels. Patients with normal basal and high peak levels of thyrotropin were included in Group II. The number of patients in this group was 53. The mean levels of basal and peak thyrotropin were 4.8 microU/ml and 39.6 microU/ml, respectively, and were significantly higher than in Group C and Group I (P less than 0.005). In 10 patients classified as Group III with high levels of both basal and peak thyrotropin, serum concentrations of TT4, FT4 and FT3 were significantly lower than in the other groups (P less than 0.025); however, significant differences in TT3 could not be seen among them. Serum cholesterol levels gradually increased from Group C to Group III. There were significant differences between Group C and Group II (P less than 0.05).

Aged

[Immunohistochemical localization of cytoskeletal proteins and thyroglobulin in the follicular cells of Hashimoto's thyroiditis].

Using antisera against three kinds of cytoskeletal proteins (keratin proteins, actin protein and myosin protein) and thyroglobulin, immunoperoxidase staining was performed on the follicular cells of 30 patients with Hashimoto's thyroiditis. These patients were subdivided into three types by Woolner's classification: 9 patients of lymphoid type (L-type), 12 patients of oxiphilic cell type (O-type), and 9 patients of pronounced epithelial destruction type (P-type). The results obtained were as follows: (1) In three-ninths to seven-twelfths of the patients of O-type and P-type, the cytoskeletal proteins were identified in the epithelial cells forming degenerating or atrophic thyroid follicles. In the patients of L-type, however, the cytoskeletal proteins which form large follicles containing much colloid were not found in the epithelium. (2) In some patients of O-type, keratin proteins were abundantly present in the epithelial cells with squamous cell metaplasia. (3) In the patients of L-type, thyroglobulin was found in most of the epithelium forming large follicles, but it was not found in those forming degenerating or atrophic follicles in the patients of O-type and P-type.

Adult

Islet cell antibodies in the Japanese population and subjects with type 1 (insulin-dependent) diabetes.

Islet cell antibodies were studied in 1,112 non-diabetic adults, 473 normal school children and 162 Type 1 (insulin-dependent) diabetic patients in a Japanese population. The prevalence of islet cell antibodies was 0.5%, 0.4% and 32%, respectively. Most islet cell antibodies positive subjects with Type 1 diabetes had short duration of the disease. No patients who had over 10 years from the onset had islet cell antibodies. Six non-diabetic adults with islet cell antibodies were followed for 4 years. Only one with Hashimoto's thyroiditis showed a diabetic pattern in her oral glucose tolerance test. However, none developed overt insulin-dependent diabetes until 1984. Two out of these six subjects continued to be positive for both islet cell antibodies and antithyroid antibodies or antinuclear antibodies. Islet cell antibodies in the remaining four patients disappeared during the second year. It is difficult to predict the onset of Type 1 diabetes by islet cell antibodies in non-diabetic individuals because they may be transient.

Adult

HLA-DRW4 antigen linkage in patients with hypertrophic obstructive cardiomyopathy.

To determine the association of histocompatibility (HLA) genes in patients with hypertrophic cardiomyopathy, we determined HLA-A, HLA-B, HLA-C, and HLA-DR specificities in 33 Japanese patients (15 with the obstructive type off hypertrophic cardiomyopathy, and 18 with the nonobstructive type). HLA-DRW4 was found in 73% of patients with hypertrophic obstructive cardiomyopathy, as compared to 33% of 144 normal controls (p < 0.005). HLA-DRW4 occurred in 33% of those with hypertrophic nonobstructive cardiomyopathy, and there was no significant difference as compared with controls. Thus, hypertrophic obstructive cardiomyopathy is associated with genes in the HLA-DR region and immunogenetic factors linked to HLA appear to play a role in the pathogenesis. This work is the first attempt at demonstration of HLA-DR antigen in hypertrophic cardiomyopathy.

Adult

[In vitro stimulation of peripheral blood lymphocytes with allogeneic lymphocytes or phytomitogens in patients with insulin-dependent diabetes mellitus (author's transl)].

The lymphocyte transformation response to the allogeneic lymphocytes (mixed lymphocyte culture, MLC) was determined in nineteen well-controlled insulin-dependent diabetics (IDD) and nineteen matched normal subjects. All possible combinations between lymphocytes from the patients and controls were mixed in both one-way and two-way MLC. From the results of one-way MLC, the stimulatory capacity (SC) and responding capacity (RC) of IDD lymphocytes were compared with those of normal lymphocytes as follows: (1) Nm leads to N: 10,538 +/- 3,937 N; normal lymphocytes (2) Nm leads to D: 8;466 +/- 5,387 D; IDD lymphocytes (3) Dm leads to N: 7,562 +/- 3,088 m; mitomycin-treated stimulating lymphocytes (4) Dm leads to D: 7,102 +/- 4,873 (leads to; stimulatory direction, results; M +/- SD cpm) IDD lymphocytes showed a marked depressive function as stimulators (SC, (1) -- (3)), but the RC of IDD lymphocytes was unchanged ((1) -- (2)). Phytomitogen-response was studied simultaneously for the same responding lymphocytes (N, D) of MLC. IDD lymphocytes exhibited significantly decreased responses to phytohemagglutinin P, pokeweed mitogen and concanavalin A.

Adult

The effect of thoracic duct drainage on lymphocyte dynamics and clinical symptoms in patients with rheumatoid arthritis.

Thoracic duct drainage (TDD) was performed in 4 patients with severe rheumatoid arthritis. Clinical effects were apparent in all during drainage, but the term of TDD and the cumulative number of lymphocytes drained had no direct relation to the improvement of clinical symptoms. The number of lymphocytes in the peripheral blood increased despite discharge of lymphocytes from the thoracic duct in the very early stage of drainage, suggesting that lymph drainage from thoracic duct accelerates migration of lymphocytes from lymphocyte pools to the blood stream. Biopsy specimens of synovial membranes obtained post-TDD showed marked decrease of mononuclear cell infiltration as compared to the specimens obtained preoperatively. These findings suggest that clinical effectiveness may be due not only to systemic immunosuppression induced by lymphocyte depletion but also to accelerated migration of inflammatory cells from the synovial tissues to the blood stream occurring with dynamic change of lymph flow during TDD.

Adult

HL-A and hypertrophic cardiomyopathy.

HL-A antigens were determined in 26 unrelated Japanese patients with hypertrophic cardiomyopathy. Several antigens were more common in patients compared with controls, but statistically significant differences were not evidenced. We also studied two families in which many had a hypertrophic cardiomyopathy. All the affected individuals revealed HL-A-A9 and B7, while none among the unaffected family members had HL-A-B7. Our findings suggest that the HLA-A system may play some role in the pathogenesis of hypertrophic cardiomyopathy with familial occurrence.

Adolescent

HLA in hypertrophic cardiomyopathy and rheumatic heart disease.

1. HLA antigens were determined in 30 Japanese patients with hypertrophic cardiomyopathy. Several antigens were more common in patients compared with controls, but statistically significant differences were not evidenced. In families one and two, six of seven kindred who inherited HLA-A9 and B7 had the disease. None of five kindred lacking HLA-B7 showed evidence of the disease. In families three and four, affecting family members had HLA-A2 and BW-35. Our finding suggest that the HLA system may play some role in the pathogenesis of hypertrophic cardiomyopathy with familial occurrence. 2. Twenty patients with rheumatic valvular heart disease were also studied. There was no significant difference in frequencies of HLA antigens between patients and controls.

Adolescent

Thyroglobulin and microsomal antibodies in patients with insulin dependent diabetes mellitus and their relatives.

The sera for 88 parents and 9 siblings of 73 patients with insulin dependent diabetes mellitus in childhood and 437 controls matched in age and sex, were tested by the thyroglobulin and microsome-coated tanned red cell hemagglutination test (Fuji-Zoki Co. Tokyo). None of 73 children with diabetes mellitus had antithyroglobulin antibodies, whereas twelve (16.4%) had antimicrosomal antibodies compared with the incidence of 0.4% and 1.1%, respectively, in 437 controls. In the parents and siblings of these probands, thyroid antibodies were also found in increased incidence. The incidence of antimicrosomal antibodies in the 68 mothers was significantly higher than in controls matched for age and sex, but the incidence of the positive thyroid antibodies in the 20 fathers and 9 siblings was not significantly different from that in control populations. The incidence of thyroid antibodies tended to be higher, though not significant, in parents and siblings of diabetic children with positive thyroid antibodies than in those of diabetics with negative ones. These findings suggest that immunogenetic factors may be responsible for the pathogenesis of some cases of diabetes mellitus in childhood.

Adolescent

Circulating immune complexes in the serum of diabetes mellitus in childhood by a modified 125I-C1q binding test.

The 125I-C1q binding test for the detection of soluble immune complexes in native unheated human serum was applied to the study of sera from 52 patients with diabetes mellitus in childhood. This radiolabeled C1q binding test is more sensitive and reproducible among the various methods proposed for the detection of immune complexes. The 125I-C1q binding activity in 52 sera from diabetes mellitus in childhood was 9.47 +/- 0.36% compared to 6.94 +/- 0.74% in normal controls. 125I-C1q binding values in diabetes mellitus in childhood were significantly higher than normal controls. Slight high values were seen in 3 patients with positive anti-DNA-antibodies in diabetes mellitus in childhood. 125I-C1q binding was not significantly increased in patients with positive antithyroid antibodies and insulin antibodies. There was no significant correlation between the duration of diabetes and 125I-C1q binding activity.

Adolescent

Antimicrosomal antibodies, gastric parietal cell antibodies and antinuclear factors in insulin dependent diabetes mellitus.

Thyroid antimicrosomal antibodies, gastric parietal cell antibodies (PCA) and antinuclear factors were studied in 208 insulin dependent diabetic (IDD) according to the duration of diabetes and patient's age at the time of testing. Antimicrosomal antibodies were found in 11 out of 47 (23.4%) IDD with the duration of less than one year, however this value declined to 13.1% at 1 to 3 years, 15.3% at 4 to 5 years, 10.8% at 6 to 10 years and 5.8% at more than 10 years. Of the 47 IDD, 7 (14.8%) were positive for gastric parietal cell antibodies. The prevalence of PCA declined with increasing duration of diabetes. However, this decrease in the prevalence of antimicrosomal antibodies and PCA was not so extreme as that of pancreatic islet cell antibodies. Antinuclear factors did not reveal a significant correlation with the duration of diabetes. In normal controls, the prevalence of antimicrosomal antibodies, PCA and the antinuclear factors increased progressively with age. In IDD, the prevalence of the antinuclear factors was also progressively greater with age. However, the prevalence of antimicrosomal antibodies in IDD decreased with age and those of PCA showed the lowest percent in the 40-69 year-age group.

Adolescent