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T Tamura

Publications and source records attributed to T Tamura.

At least 1,009 records · Page 56Linked to original sources
PubMed1989

[Long-term evaluation of the superior vena cava-pulmonary artery anastomosis in cyanotic heart disease].

We followed up thirty-three patients, to whom the superior vena cava-pulmonary artery anastomosis (Glenn procedure) was undergone between April 1966 and March 1988. There were eighteen patients with single ventricle and nine with tricuspid atresia, two with pulmonary atresia with intact ventricular septum and four with other complex anomalies. Seven patients (21%), including six with single ventricle, died 0.3 to 14.9 years after operation. Regurgitation of common atrioventricular valve was the cause of death in three patients. Serum hemoglobin level fell down from 19.3 +/- 2.2 g/dl preoperatively to 15.3 +/- 1.9 g/dl after operation but increased gradually to the preoperative level about ten years later. The actuarial survival rate at ten years is 80%. Reoperation was performed in 9 patients and reoperation free rate at 10 years is 78%. This analysis suggests that Glenn procedure is still good palliative operation for ten years, although some patients will be necessitated the second operation in future.

Adolescent↗
PubMed1989

[Report of a case of an atypical huge patent ductus arteriosus].

An atypical huge patent ductus arteriosus (PDA) associated with extreme pulmonary hypertension in a 6-month old female infant was reported. The left 3rd intercostal thoracotomy revealed huge PDA which has an appearance of pulmonary-ductus-descending aorta-trunk (PDDT) on the left side. The right side of the ductus continued to the aortic arch without demarcation between the ductus and the aorta. The median sternotomy clarified the ascending aorta, normal aortic arch, and main pulmonary artery. However, the top of the main pulmonary artery seemed to be fused with the aortic arch. The diagnosis of distal type of aortopulmonary window with wide communication was made and the total circulatory arrest with deep hypothermia and the intracavitary patching for separation of systemic and pulmonary blood flow seemed to be required for the complete repair. Total repair was decided to be postponed one week later and the chest was closed. The patient died of multi-organ failure originating from acute respiratory failure 23 days after exploratory thoracotomy without being repaired. Postmortem examination revealed a huge PDA freely communicating with the ascending aorta and the aortic arch. This is a report of an atypical huge PDA rarely seen and the conventional division or ligation is unfeasible. The circulatory arrest with deep hypothermia and intracavitary patching are obligatory for the surgical repair.

Ductus Arteriosus, Patent↗
PubMed1989

[Successful mitral valve repair and myocardial revascularization in an infant with anomalous origin of the left coronary artery from the pulmonary artery].

An 8-month-old girl of anomalous origin of the left coronary artery from the pulmonary artery associated with severe mitral regurgitation underwent radical operation. She had been in serious cardiac and respiratory failure. Aorto-left coronary arterial continuity was established by intrapulmonary arterial tunnel using Takeuchi's technique. Mitral annulus was plicated by modified Kay's technique. Post-operative course was uneventful.

Coronary Vessel Anomalies↗
PubMed1989

Potential bile acid metabolites. 14. Hyocholic and muricholic acid stereoisomers.

The complete set of the eight theoretically possible stereoisomeric 3,6,7-trihydroxy-5 beta-cholanic acids, four of which are new, related to hyocholic and muricholic acids were prepared from chenodeoxycholic acid. The principal reactions used were 1) cis-dihydroxylation of delta 6-compounds with osmium tetroxide/N-methylmorpholine N-oxide; 2) trans-dihydroxylation of 6 alpha, 7 alpha-epoxy compounds with boron trifluoride etherate in N,N-dimethyl-formamide; 3) inversion of equatorial 3 alpha-hydroxylated compounds to the corresponding 3 beta-epimers with diethyl azodicarboxylate/triphenylphosphine/formic acid; and 4) stereoselective reduction of 7-keto derivatives with zinc borohydride (or sodium borohydride) and by metallic potassium/tert-amyl alcohol.

Bile Acids and Salts↗
PubMed1989

Control of cisplatin-induced delayed emesis with metoclopramide and dexamethasone: a randomized controlled trial.

Forty-two patients with advanced lung cancer undergoing chemotherapy containing cisplatin (80 mg/m2) were submitted to a randomized controlled trial to evaluate the effect of the combination of metoclopramide and dexamethasone for the treatment of delayed cisplatin-induced emesis occurring more than 24 hours after cisplatin administration. All patients received intravenously (i.v.) high-dose metoclopramide and dexamethasone on the day of cisplatin treatment. Excellent emetic control (no emesis during the 24 hours following cisplatin administration) was achieved in 30 out of 41 patients (73%) with this combination. Patients treated i.v. with metoclopramide and dexamethasone on days 2-7 experienced less delayed emesis, nausea and anorexia compared to those treated with a placebo (delayed emesis, 25 vs 50%, respectively, P = 0.105; more than four days of nausea, 10 vs 35%, respectively, P = 0.059; less than three days of anorexia, 80 vs 50%, respectively, P = 0.048). Although the results of the study showed no statistically significant advantage with the combination of i.v. metoclopramide and dexamethasone for patients treated with cisplatin, in view of the short duration of anorexia and the marginal reduction in nausea. Female patients tended to have more emetic episodes and extrapyramidal side effects (except akathisia) than male patients, but the differences were not statistically significant except for acute emesis (P less than 0.005).

Adult↗
PubMed1989

Blood vitamin and trace metal levels in epidermolysis bullosa.

Plasma or erythrocyte levels of ten nutrients (vitamins A, C, B12 and B6; folate; thiamine; riboflavin; zinc; copper; iron) were assayed in 73 patients with various forms of inherited epidermolysis bullosa (EB). Whereas the mean level for each nutrient was within its normal range, deficient levels were noted in individual EB subsets for selected nutrients. Notable abnormalities included low levels of plasma iron and zinc (in junctional EB and recessive dystrophic EB), vitamin C (primarily in EB simplex), vitamin A (in junctional and recessive dystrophic EB), vitamin B12 (primarily in EB simplex), and vitamin B6 (especially in recessive dystrophic EB). With the exception of low plasma iron and zinc levels in junctional and recessive dystrophic EB, however, only a minority of patients in any of the EB subsets had low levels of most of the other nutrients, and an apparent correlation with malabsorption was possible with only selected nutrients.

Adolescent↗
PubMed1988

Analysis of transcription control elements of the mouse myelin basic protein gene in HeLa cell extracts: demonstration of a strong NFI-binding motif in the upstream region.

Promoter elements of the mouse myelin basic protein (MBP) gene were analyzed by in vitro transcription using HeLa cell extracts. We demonstrated the MBTE (MBP transcription element), GC-box core and TATA-box elements, at -130, -93 and -34, respectively. The TATA-box was indispensable for the promoter function. The GC-box was suggested to function co-operatively with far upstream sequences including the MBTE. The MBTE was crucial to direct maximal transcription, and also functioned with a heterologous promoter irrespective of its orientation. We identified a ubiquitous binding factor which interacted specifically with the MBTE and activated transcription. Intensive foot-printing studies demonstrated that the MBTE had a NFI-binding sequence. The MBTE was considered to be one of the strongest NFI-binding motif among known cellular genes. Interestingly, similar strong NFI-binding motifs were suggested to be present in the enhancer of JC virus whose gene is expressed like the MBP gene, in the nervous system.

Animals↗
PubMed1988

Enhancer of human polyoma JC virus contains nuclear factor I-binding sequences; analysis using mouse brain nuclear extracts.

Neurotrophic human JC virus carries a 98 bp duplicate enhancer responsible for tissue-specific gene expression. DNase I footprinting studies using mouse brain nuclear extracts revealed weak (pseudo NFI motif) and strong (NFI motif) nuclear factor I-binding sequences just upstream (at 229) and in the middle (at 156 and 58) of the enhancer, respectively. In vitro transcription driven in brain extracts demonstrated that the NFI motif is a possible transcription control element. Together with previous observations (Khalili, K., Rappaport, J. and Khoury, G. (1988) EMBO J. 7, 1205-1210 (20], the NFI motif is suggested to play an important role in early gene expression of JCV.

Animals↗
PubMed1988

Increase of histidine decarboxylase activity in murine myelomonocytic leukemia cells (WEHI-3B) in parallel to their differentiation into macrophages.

When cells of mouse myelomonocytic leukemia cell line, WEHI-3B, were cultured in the presence of actinomycin D plus the serum which was obtained from mice injected with bacterial endotoxin, i.e., lipopolysaccharide, their histidine decarboxylase (L-histidine carboxy-lyase, EC 4.1.1.22) (HDC) activity increased about 100-fold with a peak at 48 h. According to the increase in HDC activity, the expression of surface antigens associated with macrophages, such as Mac II, Mac III and Iad, increased markedly on WEHI-3B cells as well as their morphological changes to macrophages. Histamine levels in the culture medium increased concomitantly with the increase in the HDC activity in WEHI-3B cells, whereas the histamine contents inside the cells did not increase remarkably. Furthermore, the addition of lipopolysaccharide to the culture medium caused an additional 2-fold increase in the HDC activity of WEHI-3B cells. These results indicate that the increase in HDC activity in WEHI-3B cells may represent an event in the process of the differentiation to macrophages.

Animals↗
PubMed1988

The superoxide-generating respiratory burst oxidase of human neutrophil plasma membrane. Phosphatidylserine as an effector of the activated enzyme.

The superoxide-generating respiratory burst oxidase is an integral membrane enzyme found in the plasma membrane of polymorphonuclear leukocytes (neutrophils). NADPH-dependent superoxide generation is seen in isolated plasma membranes and in their detergent extracts following activation of the intact cells with phorbol myristate acetate. We have herein examined the effects of phospholipids on the activity of the solubilized oxidase. Solubilization of plasma membranes with 0.5% each of Tween 20 plus deoxycholate resulted in an approximately 2-fold enhancement of activity. Inclusion of phospholipids in the extraction medium resulted in further activation. At 1.0 mg/ml the order of effectiveness was phosphatidylserine (PS) greater than cardiolipin greater than phosphatidylethanolamine greater than phosphatidylinositol; phosphatidylcholine and phosphorylated inositol lipids were not effective. The concentrations required for half-maximal activation by PS and phosphatidylethanolamine were 85 and 200 micrograms/ml, respectively. When PS was used at a maximally activating concentration (0.5 mg/ml), the activity was enhanced 3-5-fold. Detergent solubilization alone elevated the Km of the oxidase for NADPH from 68 microM in intact plasma membranes to 123 microM, but inclusion of PS with detergent restored the Km to near or below that seen in intact membranes. PS also increased the Vmax by a factor of 2-3, but had no effect on the pH optimum. A plot of the activity versus enzyme concentration was linear when membranes were used, but activity showed a quadratic dependence on concentration in solubilized membrane, with lower than expected activity at lower enzyme concentration. PS restored linearity of the concentration-activity plot. The activation by PS was not influenced by the addition of Ca2+, EGTA, or dioctanoylglycerol, indicating that activation was not dependent on protein kinase C. These results implicate phosphatidylserine as a direct effector of the NADPH-oxidase.

Cell Membrane↗
PubMed1988

ATP-driven Ca2+ pump in the basolateral membrane of rat kidney cortex catalyzes an electroneutral Ca2+/H+ antiport.

An ATP-driven Ca2+ pump in the basolateral membrane of rat kidney cortex pumps Ca2+ out of the cell at the expense of MgATP (Km = 0.191 mM). This pump has a high affinity for free Ca2+ (26 nM). Vanadate, lanthanum, N-ethylmaleimide and calmodulin inhibitor R24571 inhibited this pump activity. Dimethyl[2-14C]oxazolidine-2,4-dione [( 14C]DMO) was entrapped in the vesicles in association with the ATP-driven Ca2+ influx. The ATP-driven Ca2+ influx was stimulated by the intravesicular acid pH and an upper convex Lineweaver-Burk reciprocal plot suggested two possible kinetics; one is that this Ca2+ pump is an allosteric enzyme with more than 1.72 H+ binding sites and another is the presence of two Ca2+ pumps with different affinities for H+. Valinomycin study indicated that the ATP-dependent Ca2+ transport by the BLMV was electroneutral and voltage independent. These results strongly suggest that the ATP-driven Ca2+ pump in the renal basolateral membrane catalyzes an electroneutral Ca2+/H+ antiport.

Adenosine Triphosphate↗
PubMed1988

Membrane integration and intracellular transport of the coronavirus glycoprotein E1, a class III membrane glycoprotein.

The E1-glycoprotein (Mr = 26,014; 228 amino acids) of mouse hepatitis virus A59 is a class III membrane glycoprotein which has been used in this study as a model system in the study of membrane integration and protein transport. The protein lacks an NH2-terminal cleavable signal sequence and spans the viral membrane three times. Hydrophobic domains I and III could serve as signal sequences for cotranslational membrane integration. Domain I alone was sufficient to translocate the hydrophilic NH2 terminus of E1 across the membranes as evidenced by glycosylation of a newly introduced N-glycosylation site. The COOH-terminal part of E1 involving amino acids Leu124 to Thr228 was found to associate tightly with membranes at the post-translational level, although this part of the molecule lacks pronounced hydrophobic sequences. Membrane protection assays with proteinase K showed that a 2-kDa hydrophilic fragment was removed from the COOH terminus of E1 indicating that the protein is largely embedded into the membrane. Microinjection of in vitro transcribed capped and polyadenylated mRNA into CV-1 cells or into secretory AtT20 pituitary tumor cells showed that the E1-protein accumulated in the Golgi but was not detectable at the plasma membrane or in secretory granules. The 28 NH2-terminal hydrophilic amino acid residues play no role in membrane assembly or in intracellular targeting. Various NH2-terminal portions of E1 were fused to Ile145 of the cytoplasmic N-protein of mouse hepatitis virus. The resulting hybrid proteins were shown to assemble into membranes in vitro and were detected either in the rough endoplasmic reticulum or transient vesicles of microinjected cells.

Amino Acid Sequence↗
PubMed1988

In vivo antitumor activity of multiple injections of recombinant interleukin 2, alone and in combination with three different types of recombinant interferon, on various syngeneic murine tumors.

We have used several transplantable experimental murine tumors to evaluate the potentiation of antitumor activity by a combination of human recombinant interleukin 2 (rHIL2) and recombinant interferons (rIFNs). The combination of rHIL2 and either human hybrid recombinant alpha-interferon A/D (rIFN-alpha A/D) or mouse recombinant beta-interferon (rIFN-beta) induced the s.c. adenocarcinoma 755, which had been established for 8 days, to regress, although rHIL2 or the rIFNs alone hardly inhibited the tumor's growth. Eight injections of the rHIL2-rIFN-alpha A/D combination cured 38% of the tumor-bearing mice. The rHIL2-rIFN-beta combination achieved a complete cure only when given in more than 13 injections. The administration of rHIL2 and mouse recombinant gamma-interferon (rIFN-gamma) markedly inhibited tumor growth of the s.c. established adenocarcinoma 755, but did not cure any of the mice. Other tumors, B16-F10 melanoma, and colon tumors 38 and 26 responded almost as well to a rHIL2-rIFN-alpha A/D or -beta combination, but not to a rHIL2-rIFN-gamma combination. The growth of Lewis lung carcinoma was inhibited to a lesser extent by all combinations, for which there were no long-term survivors. The combination therapy of rHIL2 and rIFN-beta produced a marked regression of the tumor in beige mice which have low natural killer activity, suggesting the activated natural killer cells not to be responsible for the therapeutic effect. And T-cell immunity may be important in the regression of s.c. established tumors, because of the lesser potentiation of antitumor activity in athymic mice. These results demonstrate that combination therapies of rHIL2 and rIFN-alpha A/D or -beta can function synergistically in the various s.c. established murine tumor systems and give further evidence in support of their clinical potential.

Animals↗
PubMed1988

Gene organization and transcription of duplicated MBP genes of myelin deficient (shi(mld)) mutant mouse.

A hereditary dysmyelinating mutation, named myelin deficient (shi(mld)), is characterized by reduced expression of myelin basic protein (MBP). In shi(mld), the MBP gene is duplicated and its reduced expression is mainly determined by the level of mRNA. We have characterized the structure and function of the promoter regions of the duplicated MBP genes in shi(mld). Among the lambda clones containing promoter regions of the duplicated MBP genes in shi(mld), one (gene 1) had the same restriction enzyme pattern as that in control mice, but another (gene 2) had a rearrangement on a distal part of the promoter. A 712-bp nucleotide sequence upstream of the first exons of both of the duplicated MBP genes of shi(mld) was completely consistent with that of the control. Promoter activities of 1.3-kb 5'-flanking regions from respective genes of shi(mld) measured by in vitro run-off assay using HeLa whole-cell extracts were indistinguishable from that of the control MPB gene. Chromosomal mapping by in situ hybridization suggested that the duplicated MBP genes were located closely to each other at the distal part of chromosome 18. A recombinational event including the inversion seemed to have occurred within gene 1 and its possible relationship to the reduced expression of MBP is discussed.

Animals↗