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Biomedical subjects

K Takazawa

Publications and source records attributed to K Takazawa.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Coronary reoperation].

From 1884 to 1997, 24 patients (1.3%) underwent coronary reoperation in a mean of 10.18 +/- 3.35 ears after the first operation at Juntendo University. The mean age of the patients at reoperation was 60.7 +/- 8.0 years. Although 2 patients had received a left internal thoracic artery graft at the primary operation, both grafts were already occluded. At reoperation, 19 patients received at least one internal thoracic artery, and 2 received a gastroepiploic artery graft. The mean number of grafts was 1.96 +/- 0.67 at reoperation. One patient underwent reoperation combined with pseudoaneurysmectomy at the proximal anastomosis site, and one patient reoperation combined with mitral valve replacement. There were 2 in-hospital deaths. The use of an arterial graft to the LAD is recommended at reoperation because of its long-term superiority. Since transmyocardial laser revascularization (TMLR) and minimally invasive direct coronary artery bypass (MIDCAB) at reoperation have recently been reported, these strategies may be considered as useful methods in future.

Adult↗
PubMed1997

Structural identification of the myo-inositol 1,4,5-trisphosphate-binding domain in rat brain inositol 1,4,5-trisphosphate 3-kinase.

A series of key amino acids involved in Ins(1,4,5)P3 (InsP3) binding and catalytic activity of rat brain InsP3 3-kinase has been identified. The catalytic domain is at the C-terminal end and restricted to a maximum of 275 amino acids [Takazawa and Erneux (1991) Biochem. J. 280, 125-129]. In this study, newly prepared 5'-deletion and site-directed mutants have been compared both for InsP3 binding and InsP3 3-kinase activity. When the protein was expressed from L259 to R459, the activity was lost but InsP3 binding was conserved. Another deletion mutant that had lost only four amino acids after L259 had lost InsP3 binding, and this finding suggests that these residues (i.e. L259DCK262) are involved in InsP3 binding. To further support the data, we have produced two mutants by site-directed mutagenesis on residues C261 and K262. The two new enzymes were designated M4 (C261S) and M5 (K262A). M4 showed similar Vmax and Km values for InsP3 and ATP to wild-type enzyme. In contrast, M5 was totally inactive but had kept the ability to bind to calmodulin-Sepharose. C-terminal deletion mutants that had lost five, seven or nine amino acids showed a large decrease in InsP3 binding and InsP3 3-kinase activity. One mutant that had lost five amino acids (M2) was purified to apparent homogeneity: Km values for both substrates appeared unchanged but Vmax was decreased approx. 40-fold compared with the wild-type enzyme. The results indicate that (1) a positively charged amino acid residue K262 is essential for InsP3 binding and (2) amino acids at the C-terminal end of the protein are necessary to act as a catalyst in the InsP3 3-kinase reaction.

Amino Acid Sequence↗
PubMed1997

Comparison of lumen area after PTCA by IVUS and QCA.

The coronary lumen area just after percutaneous transluminal coronary angioplasty (PTCA) was assessed by intravascular ultrasonography (IVUS) with 4.3 F cardiovascular imaging systems (CVIS) and quantitative coronary angiography (QCA) with Kontron CARDIO 500. Altogether 34 lesions were divided into two groups by IVUS findings using Nissen's circular shape factor (CSF), which was defined by the (calculated perimeter/observed perimeter), expressing lumen eccentricity. The eccentric group (CSF < or = 0.92) was 22, and concentric group (CSF > 0.92) was 12. The minimum lumen diameter by IVUS and QCA (both edge-detection and densitometric methods) correlated in both the eccentric and concentric groups. As for the lumen area, only the QCA densitometric method in the concentric group correlated with the lumen area determined by IVUS. Despite using QCA, it is almost impossible for angiography to determine the lumen area just after PTCA if an eccentric lesion with a tear or dissection had occurred.

Aged↗
PubMed1996

Induction of persistent allograft tolerance in the rat by combined treatment with anti-leukocyte function-associated antigen-1 and anti-intercellular adhesion molecule-1 monoclonal antibodies, donor-specific transfusion, and FK506.

We previously reported that a short course of treatment with anti-LFA-1 and anti-ICAM-1 monoclonal antibodies (mAbs) led to a persistent acceptance of mouse cardiac allografts, which resulted from the induction of allospecific tolerance. In the present study, we tested the effect of anti-LFA-1 and anti-ICAM-1 mAbs on rat allograft rejection and analyzed the mechanisms underlying allograft tolerance. In sharp contrast to the mouse case, a short course of treatment with anti-LFA-1 and anti-ICAM-1 mAbs led to a persistent acceptance in only half of the treated rats when MHC was compatible but mismatched for minor antigens, and was virtually ineffective when MHC was fully incompatible. However, treatment with these mAbs combined with donor-specific transfusion and FK506 consistently led to a persistent acceptance, even when the MHC was fully incompatible. Donor-specific tolerance was induced by this treatment, as estimated by skin challenging. In the tolerant rats, proliferative response and CTL generation against donor-type alloantigen were severely impaired but partially restored by exogenous interleukin-2. Limiting dilution analysis demonstrated that the precursor frequency of CTL was decreased in the tolerant rats, as compared with the naive rats. These results suggest that donor-reactive T cells were partially deleted and rendered anergic in the periphery.

Animals↗
PubMed1995

CAM--a novel immunosuppressive agent.

This is an initial study of the immunosuppressive efficacy of CAM, a derivative of mycophenolic acid, in a rat heart allograft model when the major histocompatibility complex was fully incompatible, and its effect in improving heart allograft survival compared with mycophenolate mofetil (MMF, RS-61443). CAM or MMF was administered orally from day 1 following the allografting for 40 days. The median survival times (MST) were 6 days in rats with no immunosuppressive drug (control group; n = 6), 83 days with CAM 10 mg/kg (n = 6), and > 100 days with both 20 mg/kg (n = 7), and 30 mg/kg (n = 10). With MMF, in contrast, MST was 9, 17, 35, days with 10, 20, 30 mg/kg/day, respectively. All grafts in the CAM 30 mg/kg-treated group survived for more than 100 days after grafting, and, furthermore, CAM was also more effective than MMF in prolongation of the heart graft survival in rats at each dose. Rats with long-surviving cardiac allografts (30 mg/kg; CAM) accepted skin grafts from the donor-strain but rejected them from the third-party strain, suggesting that donor-specific tolerance was induced by CAM. In the tolerant rats, proliferative response against donor-type alloantigen was not impaired as compared with naive WKAH rats. In contrast, CML assay showed that T cells obtained from the rats bearing permanently accepted F344 heart grafts had less cytotoxic activity to the donor-type target, and the frequency of CTL precursor against donor-type alloantigen was also reduced.

Animals↗
PubMed1995

Changes in serum myosin light chain I following aortocoronary bypass operations.

The changes in myosin light chain I (MLC I) following aortocoronary bypass were studied in 31 patients and the curves of these changes were classified into three different patterns. A peak level of 14.7 +/- 1.54 ng/ml was seen in seven patients on postoperative day (POD) 2 which decreased suddenly to less than twice the normal value by POD 7 (group 1). Another 19 patients showed a peak level of 20.7 +/- 16.5 ng/ml on POD 5, which decreased slowly and was still high even by POD 7 (group 2). The remaining five patients developed only a slight increase in the MLC I level after the operation, with a peak value of 5.5 +/- 0.8 ng/ml (group 3). Creatine kinase myocardial band and glutamic oxaloacetic transaminase also remained low in this group. No correlation existed between the peak value of MLC I and the aortic cross-clamping time, or between the peak value of MLC I and the cardiopulmonary bypass time. Furthermore, the difference in cardiac output before and after the operation did not significantly differ among the three groups. These findings indicate that the measurement of MLC I is useful for diagnosing perioperative myocardial damage and may also be useful in the study of myocardial protection.

Adult↗
PubMed1995

Underestimation of vasodilator effects of nitroglycerin by upper limb blood pressure.

To determine why upper limb blood pressure measurement underestimates the vasodilator effects of nitroglycerin on lowering ascending aortic systolic pressure, we studied 24 patients (58 +/- 11 years, mean +/- SD). Ascending aortic pressure and radial artery pulse calibrated by cuff blood pressure measurement at the brachial artery were recorded simultaneously before and 5 minutes after sublingual administration of 0.3 mg nitroglycerin. Waves were analyzed by a signal processor, and the fourth derivative wave was used to find the early (S1) and late (S2) systolic shoulders (S1 corresponds to the second zero crossing and S2 to the third zero crossing). Before nitroglycerin administration, maximal systolic pressure in the ascending aorta (141 +/- 21 mm Hg) coincided with the late systolic peak in all patients, and in most patients (21 of 24) maximal systolic pressure in the radial artery (140 +/- 19 mm Hg) coincided with the early systolic peak. Maximal systolic pressure decreased more in the ascending aorta than in the radial artery (22 +/- 13 and 11 +/- 11 mm Hg, respectively; P < .001). However, the reduction in the shoulder of late systolic pressure in the radial artery (24 +/- 13 mm Hg) clearly indicated the reduction in maximal systolic pressure (late systolic peak) in the ascending aorta. The augmentation index of the ratio of the height of late systolic pressure to early systolic pressure fell proportionally (r = .74, P < .001) in the radial artery (from 0.88 +/- 0.13 to 0.60 +/- 0.11) and in the ascending aorta (from 1.57 +/- 0.25 to 1.26 +/- 0.24), which indicated the reduction in late systolic pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Desensitization to somatostatin analogue (Octreotide) observed in a patient with acromegaly.

We encountered a 33-year-old female patient with a pituitary growth hormone (GH)-secreting macroadenoma. The patient was treated with somatostatin analogue (Octreotide) in combination with bromocriptine for 2 months before a transsphenoidal adenomectomy was carried out. Octreotide (300-800 micrograms/day) in combination with bromocriptine was effective in reducing the size of the adenoma by 36%, but produced only a marginal decrease in serum GH. After the operation, bromocriptine alone (15 mg/day) did not lower the level of GH which was produced by residual adenoma tissue. When octreotide (200 micrograms/day) was resumed along with the bromocriptine one year after the operation, it effectively lowered serum GH for 6 months. Thereafter, octreotide therapy became ineffective with a concomitant rise in serum GH and somatomedin C, which was not accompanied by an increase in tumor size. This was a rare case of acromegaly that showed desensitization to octreotide after long-term treatment.

Acromegaly↗
PubMed1995

Inositol 1,4,5-trisphosphate 3-kinase activity in FRTL-5 cells: regulation of the enzyme activity by TSH.

Inositol 1,4,5-trisphosphate (InsP3) 3-kinase phosphorylates the Ca(2+)-mobilizing second messenger InsP3 to inositol 1,3,4,5-tetrakisphosphate (InsP4). InsP3 5-phosphatase dephosphorylates InsP3 to inositol 1,4-bisphosphate (InsP2). We compared the effects of TSH added to a culture of FRTL-5 thyroid cells on the activity of InsP3 5-phosphatase and InsP3 3-kinase. InsP3 3-kinase activity was decreased at a physiological concentration of TSH. Inhibition of this activity started after 3 h of incubation with TSH and was maximal after 24 h. In contrast, InsP3 5-phosphatase activity was not affected by TSH under the same conditions. The inhibitory effect of TSH on InsP3 3-kinase was characterized as follows: a) inhibition of activity was mimicked by both dibutyryl cyclic AMP and forskolin; b) activity obtained by mixing lysates of TSH-stimulated and non-stimulated cells was the sum of each activity measured separately; c) inhibition persisted after a crude lysate of TSH-stimulated cells had been subjected to SDS/polyacrylamide gel electrophoresis and the extraction of InsP3 3-kinase activity. The data suggest that TSH reduced the activity of InsP3 3-kinase in FRTL-5 cells either by a phosphorylation/dephosphorylation mechanism, or by affecting expression of the enzyme.

Animals↗
PubMed1994

Identification of high molecular weight forms of inositol 1,4,5-trisphosphate 3-kinase in rat thymus and human lymphocytes.

A soluble inositol 1,4,5-trisphosphate 3-kinase (InsP3 3-kinase) has been characterized from extracts of rat thymus. The enzyme was shown to have a molecular weight within the range 98,000-114,000 M(r) as determined by regeneration of enzyme activity from sodium dodecyl sulphate polyacrylamide gels. The enzyme phosphorylates inositol 1,4,5-trisphosphate (InsP3) to inositol 1,3,4,5-tetrakisphosphate (InsP4) with an apparent Km of 3.1 +/- 0.4 microM. The enzyme is stimulated 4-6-fold by Ca2+/calmodulin and is not recognised by polyclonal antisera raised against rat brain InsP3 3-kinase A. High levels of InsP3 3-kinase activity were also detected in soluble extracts of human lymphocyte preparations. The human lymphocyte enzyme was shown to have a molecular weight between 61,000 and 70,000 M(r) as judged by SDS-PAGE, and was stimulated approximately 10-fold in the presence of Ca2+/calmodulin. These results establish that InsP3 3-kinase from rat thymus and human lymphocyte preparations represent high molecular weight isoenzymes of the InsP3 3-kinase family.

Animals↗
PubMed1994

Involvement of apoptosis antigen Fas in clonal deletion of human thymocytes.

Apoptosis appears to play a major role in the differentiation and selection of T and B lymphocytes, but the mechanisms of clonal deletion of T cells in thymus are not well understood. We have prepared an anti-human Fas IgM mAb with associated apoptosis-inducing activity in Fas antigen-positive target cells including human T cells. We analyzed the expression of apoptosis antigen Fas on human thymocytes by cytofluorometry showing low, but significant amounts of Fas antigen on double-negative and double-positive undifferentiated thymocytes. On the contrary, most of the differentiated thymocytes (single-positive or CD3-brightest) expressed undetectable levels of Fas antigen. About 1-2% of thymocytes expressed high amounts of Fas antigen, and these cells, which were CD3-bright, were CD4-bright and CD8-low at the stage of late double-positive lineage. Immunohistological analysis shows these Fas-bright cells on the edge of the medulla. Stimulation through the TCR complex was shown to induce the expression of Fas antigen on thymocytes at the late double-positive stage and prolonged stimulation through the TCR complex rendered the Fas-bright thymocytes sensitive to apoptosis-inducing activity of anti-Fas. To show the involvement of the Fas system in the negative selection/clonal deletion of thymocytes, we organ-cultured human thymus in the presence of the superantigen, staphylococcus enterotoxin B (SEB), and new antagonistic anti-Fas mAb, which can inhibit the apoptosis-inducing activity of the original anti-Fas mAb. The SEB-reactive TCR complex on thymocytes was at first down-regulated by SEB, then the SEB-reactive clone was deleted by apoptosis, which was inhibited by an antagonistic anti-Fas mAb. Thus, Fas antigen is shown to be involved in the negative selection/clonal deletion of superantigen-reactive thymocytes.

Antibodies, Monoclonal↗
PubMed1994

Cardiac myxoma with Gamna-Gandy bodies: case report with MR imaging.

We describe a patient with a left atrial tumor that showed very unusual magnetic resonance (MR) imaging features. Postsurgical histologic examination showed characteristics of myxoma, and Gamna-Gandy bodies were found in the tumor. We believe that the unusual MR appearance was caused by the hemosiderin in the Gamna-Gandy bodies.

Aged↗