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Biomedical subjects

I Takei

Publications and source records attributed to I Takei.

68 records · Page 4Linked to original sources
PubMed1984

A clinical profile of insulin-dependent diabetes with islet cell cytoplasmic and cell surface antibodies.

Both islet cytoplasmic and cell surface antibodies (ICA and ICSA) were studied from the onset of diabetes to the honeymoon in an insulin-dependent diabetic patient. The patient, a 24-year-old male, was admitted to the hospital because of ketoacidotic hyperglycemic precoma. Continuous subcutaneous infusion of a small dose of insulin was carried out for a couple of days followed by NPH-insulin injection. The dose was gradually decreased and on the 45th day after the onset, an oral hypoglycemic agent was substituted for insulin. The patient was followed up after discharge from the hospital and his disease was controlled well by diet and a hypoglycemic agent until he caught a common cold. He was then admitted again to the hospital because of hyperglycemia, and insulin injection was performed. Both ICA and ICSA were found independently of each other during the course of the disease. The ICSA, which was quantitatively determined by immunoassay using 125I-protein A, closely paralleled the clinical profile. However, the levels of quantitative ICSA were higher than normal, even though the patient's diabetes reached the honeymoon stage. These results suggest that quantitative ICSA has a strong association with the clinical profile in IDDM, and it may be a "marker" of islet cell damage during the diabetic period or a parameter for diabetic prognosis.

Adult↗
PubMed1984

Activation of acceptor-suppressor hybridoma with antigen-specific suppressor T cell factor of two-chain type: requirement of the antigen- and the I-J-restricting specificity.

The molecular mechanisms of activation of immunoregulatory T cells were characterized by using two complementary suppressor T cell hybridoma systems: the KLH-specific monoclonal suppressor factor (KLH-TsF), and the inducible acceptor-suppressor hybridoma line with anti-idiotypic receptor for KLH-TsF. It was demonstrated that the identity of the KLH specificity and genetic specificity was required for the TsF-acceptor interaction. These specificities were found to be mediated by the two polypeptide chains of TsF: KLH-binding, Ct-bearing heavy chain and I-J+ light chain. These two chains were essential for stimulation of the acceptor hybridoma. The results were also confirmed by the findings that the mixture of the 11S and 13S mRNA translation products reconstituted the active TsF to stimulate the acceptor hybridoma. Furthermore, the genetic restriction observed was found to be mediated by the I-J+ light chain and to be governed by the gene linked to the H-2 complex but not to the Igh genes. The gene controlling the restriction specificity was strongly suggested to be in the intra-H-2 complex, but not outside of the H-2 complex.

Animals↗
PubMed1983

Acceptor-suppressor T cell hybridoma with a receptor recognizing antigen-specific suppressor factor.

An acceptor hybridoma with a receptor that recognizes the keyhole limpet hemocyanin (KLH)-specific suppressor T cell factor (KLH-TsF) was established after the fusion of C57BL/6 splenic T cells enriched with KLH-coated petri dishes. The cloned hybridoma (34S-281) could be specifically activated by stimulation with the conventional KLH-TsF or monoclonal KLH-TsF from three different hybridomas in the absence of the relevant antigen (KLH) and it started to produce another factor that suppresses the antibody response against DNP-KLH in a KLH-specific fashion. The KLH specificity of the TsF was required for activation. The new factor was found not to bind the KLH but to be absorbed with the KLH-TsF-producing hybridoma. It is thus strongly suggested that the acceptor site has a complementary structure (antiidiotype) for the KLH-TsF. Moreover, the idiotypic determinant on KLH-TsF was found to have a structure similar to that on some of the anti-KLH antibodies, since the acceptor hybridoma was specifically killed by the conventional anti-KLH antibodies and complement. Drawing on the above results, the idiotype-antiidiotype network in the conventional antigen system is discussed.

Animals↗
PubMed1981

Monoclonal antibodies that recognize the product controlled by a gene in the I-J subregion of the mouse H-2 complex.

The B cell hybridomas producing monoclonal antibodies (E10, D7, F4, H6, and D4) were established by the fusion of P3U1 or NS-1 murine myeloma cell lines and spleen cells of B10.A(5R) mice hyperimmunized with mitomycin C-treated B10.A(3R) spleen and thymus cells. Two types of monoclonal antibodies specific for the products controlled by a gene in the I-Jb subregion of the H-2 complex were characterized: one specific for the private type of I-Jb determinant, the other recognizing the cross-reactive determinant between the I-Jb and I-Jd products. By using these monoclonal reagents, the I-J-encoded product on the antigen-specific suppressor T cells was found to be expressed on their soluble suppressor factors. Furthermore, the I-Jb products were successfully detected not only on the T cell hybridoma with suppressor activity specific for keyhole limpet hemocyanin (KLH), but also on KLH-primed suppressor T cells enriched by antigen-coated petri dishes and concanavalin A-induced thymocyte blasts of C57BL/6 mice by complement-dependent cytotoxic assays and membrane fluorescence techniques.

Animals↗
PubMed1981

Presence of interchain disulfide bonds between two gene products that compose the secreted form of an antigen-specific suppressor factor.

The secreted form of the suppressor T cell factor specific for keyhole limpet hemocyanin derived from the hybridoma 34S-704 was found to consist of the two distinct polypeptide chains, i.e., the antigen-binding and the I-J-encoded chains. They were linked in covalent association with disulfide bonds. The two chains were cleaved by the reduction with dithiothreitol and were easy to reconstitute the active form of TsF. The association of the two distinct chains was suggested to be essential for the expression of the TsF activity.

Animals↗
PubMed1980

Functional and molecular organisation of an antigen-specific suppressor factor from a T-cell hybridoma.

Thymus-dependent (T) lymphocytes have been shown to have antigen specificity. The antigen receptor on T lymphocytes, in contrast to that on B lymphocytes, does not appear to be of the conventional immunoglobulin (Ig) type. Studies on the antigen-specific factors derived from helper and suppressor T cells (Ts) demonstrated that they possess determinants with antigen binding affinity and products of genes in the H-2 complex (MHC). Furthermore, antibodies against the variable region of Ig heavy chains or idiotypes have been shown to react with T-cell antigen receptors as well as antigen-specific helper and suppressor T-cell factors (TsF). It is, therefore, conceivable that at least two gene products are involved in the structural entity of these receptors: one each coded for by genes in either. To establish the molecular nature of the recognition component of T cells we have used homogeneous TsF from a T-cell hybridoma with a specific function. We report here that the antigen binding and I-J coded molecules on TsF are independently synthesised in the cytoplasm, and are secreted as an associated form of the two molecules; this association is required for antigen-specific suppression of antibody response.

Animals↗
PubMed1980

Murine autoimmune interstitial nephritis and associated antigen: purification of a soluble tubular basement membrane antigen from mice kidneys.

A soluble tubular basement membrane (TBM) antigen has been purified from murine kidneys. The isolated fibers were trypsinized and subjected to zone electrophoresis, Sephadex G-200 gel filtration, and DEAE-cellulose chromatography eluted with linear NaCl concentration gradient while monitoring the TBM antigen activity with specific antihuman TBM antigen. The molecular weight of TBM antigen was estimated to be 30,000 daltons by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The purified TBM antigen gave a single precipitin line against the specific antiserum and cross-reacted with the TBM antigen similarly purified from other animals such as goat, guinea pig and also with human TBM antigen in an immunodiffusion plate. BALB/c, C3H/He and C57BL/6 mice were immunized twice at 2 weeks' interval with the TBM antigen and adjuvant. Histologically typical interstitial nephritis occurred in BALB/c mice, whereas no nephritis developed in other strains of mice. The inflammatory changes were characterized by intense mononuclear cell infiltration, tubular destruction, and interstitial and periglomerular fibrosis. The serum-stained basement membrane of normal tubules and Bowman's capsules, and no antiglomerular basement membrane activity was detectable in the serum by immunofluorescence. This system provides a simple and useful model in interstitial nephritis in mice produced with a purified TBM antigen.

Animals↗
PubMedDate not supplied

Influence of glycemic control and hypertension on urinary microprotein excretion in non-insulin-dependent diabetes mellitus.

In order to evaluate the influence of glycemic control and hypertension on the development of diabetic nephropathy, we measured urinary excretion of albumin (AER) and other microproteins in non-insulin-dependent diabetes mellitus (NIDDM), and reexamined the 103 patients who had had AER less than 300 micrograms/min at the initial study 12-18 months later. AER in the patients with HbA1c greater than or equal to 7.5% increased significantly in both the normoalbuminuric (AER less than 30 micrograms/min) and microalbuminuric (30-300 micrograms/min) groups, whereas no significant change in AER was observed in the patients with HbA1c less than 7.5%. In the microalbuminuric group, AER in both hypertensive and normotensive patients increased significantly. In this group, the change in AER correlated positively with the change in alpha 1-microglobulin (alpha 1M). These results indicate that glycemic control has a greater influence on the development of nephropathy in its early stage than hypertension and that alpha 1M is as a good predictor of nephropathy as albumin.

Acetylglucosaminidase↗
PubMedDate not supplied

Secretion of GIP in responders to acarbose in obese Type 2(NIDDM) patients.

Acarbose has been shown to reduce postprandial hyperglycemia and to improve lipid parameters in diabetics via its inhibitory effects on intestinal alpha-glucosidases. Response to acarbose may therefore be dependent upon gastric or pancreatic hormone function. To test this hypothesis, we treated 27 mild type 2 (NIDDM) Japanese diabetics who were mildly obese with low-dose acarbose (150 mg/day) for 3 months. We then performed a responder analysis to determine specific hormonal responses that may be associated with a good response to acarbose. At the end of the treatment period, a total of 15 evaluable patients was grouped as responders (n=6) and nonresponders (n=9) based on an effective decrease in postprandial glucose levels (>30 mg/day) and glycosylated hemoglobin (HbA1c) levels (>0.5%). There were no differences between the two groups in demographic variables or mean postprandial glucose levels at baseline. There was a small but significant increase in postprandial cholecystokinin (CCK) in responders, and fasting gastric inhibitory peptide (GIP) levels were significantly increased in responders and all patients after treatment. Serum leptin levels were reduced by treatment in our mildly obese responders and this was associated with a significant decrease in body weight. These results suggest that treatment with low-dose acarbose may reduce hyperglycemia in mild type 2 Japanese patients and may improve metabolic control by regulating hormones involved in glycemic control and digestive absorption. Acarbose may provide a safe adjunct to help treat insulin resistance in type 2 patients.

Acarbose↗