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Biomedical subjects

T Nishimoto

Publications and source records attributed to T Nishimoto.

At least 145 records · Page 8Linked to original sources
PubMed1991

[Main pulmonary artery injury caused by golf-swing].

A 87-year-old man suddenly complained of dyspnea and fell into shock just after tee-shot. UCG revealed a large amount of pericardial effusion and good wall motion of the heart. Enhanced CT scan didn't prove any intimal flaps in the aorta. With cardiopulmonary bypass stand-by, we opened the pericardium and found a small laceration in the main pulmonary artery. The site of the laceration corresponded to a hard and sharp pericardial reflection ridge. We speculated that the difference of deceleration power between body and the heart resulted in pendulous or torsional motion of his heart. Supposedly the mutual actions between sharp pericardial reflection ridge and strange motion of the heart injured his main pulmonary artery.

Aged↗
PubMed1991

[Multiple coronary aneurysms due to Kawasaki disease in young man--successful triple coronary bypass grafting by utilizing the right gastroepiploic artery, internal thoracic artery and saphenous vein].

A 28-year-old man developed acute anteroseptal myocardial infarction. Emergency coronary angiography revealed multiple coronary aneurysms, associated with complete obstruction of left anterior descending artery (LAD) and 50 to 99% stenosis of the right and the circumflex coronary artery (CX). Coronary artery bypass graftings were performed seven weeks after successful emergency intracoronary thrombolysis. The saphenous vein graft was anastomosed to CX, the internal thoracic artery to LAD, the right gastroepiploic artery to RCA just above the bifurcation. Post-operative course was uneventful. On sixth post operative week cardiac catheterization was performed. The study showed all three bypass grafts and native coronary artery to be patent. The patient is now followed up under anticoagulant therapy.

Adult↗
PubMed1990

Okadaic acid, a potent inhibitor of type 1 and type 2A protein phosphatases, activates cdc2/H1 kinase and transiently induces a premature mitosis-like state in BHK21 cells.

When BHK21 cells synchronized in early S phase were exposed to okadaic acid (OA), an inhibitor of protein phosphatases 1 and 2A, mitosis specific events such as premature chromosome condensation, the production of MPM-2 antigens, dispersion of nuclear lamins and the appearance of mitotic asters were induced, and then disappeared upon further incubation. These mitosis specific events occurred even in the presence of cycloheximide. Within 1 h of exposure to OA, cdc2/histone H1 kinase activity rose 10-fold compared with untreated controls, but returned to the control level upon further incubation. Using antibodies against either p34cdc2 or cyclin B it was found that p34cdc2 complexed with cyclin B was dephosphorylated after OA treatment concomitant with the activation of cdc2 kinase, and that cyclin B was subsequently degraded concomitant with a decrease in cdc2 kinase activity, as in normal mitosis. In contrast, when cells in G1 phase were treated with OA no increase in cdc2 kinase activity was observed. Moreover when cells in pseudo-metaphase induced by nocodazole were treated with OA, cdc2 kinase was inactivated. These results suggest that OA sensitive protein phosphatases control both the activation and inactivation of the p34cdc2 kinase.

Animals↗
PubMed1990

Self suppression of phosphoinositide turnover and contraction by stimulating release of endogenous endothelium derived relaxing factor in vascular action of histamine.

STUDY OBJECTIVE: The aim of the study was to examine the relationship between phosphoinositide turnover and vascular contraction in response to histamine, and the role of endothelium derived relaxing factor (EDRF) in these activities. DESIGN: Thoracic aortic strips were studied under isometric tension in an organ bath. Phosphoinositide turnover was studied using [32P]Pi labelling. Cumulative concentration-response curves were obtained for histamine, and for histamine plus H1 and H2 antagonists. The effect of endothelial denudation was examined, as was that of removing Ca2+ from buffer medium, and of adding methylene blue, an inhibitor of EDRF. EXPERIMENTAL PREPARATIONS: Thoracic aortic rings were obtained from 81 male Japanese white rabbits, weight 2.0-2.4 kg. MEASUREMENTS AND MAIN RESULTS: Histamine (0.1 mumol-0.1 mmol.litre-1) caused concentration dependent contractions and increases of [32P]Pi incorporation into phosphatidylinositol (ED50 = 4.6 mumol.litre-1 and 4.0 mumol.litre-1 respectively). Diphenhydramine inhibited contractile response and phosphatidylinositol labelling by histamine. Cimetidine potentiated contractile response but had no effect on phosphatidylinositol labelling. Endothelial denudation potentiated maximum contraction by 15% and augmented phosphatidylinositol labelling at 0.1 mmol.litre-1 histamine by 30%. In intact aortic rings, methylene blue (10 mumol.litre-1), an inhibitor of EDRF, potentiated histamine induced phosphatidylinositol labelling, but had no influence on denuded rings. A-23187 (0.01 mumol.litre-1), which caused release of EDRF from intact endothelium, suppressed histamine induced phosphatidylinositol labelling in intact aortic rings. CONCLUSIONS: The results suggest that stimulation of the release of EDRF in response to histamine causes self suppression of phosphoinositide turnover and contraction.

Animals↗
PubMed1990

Cloning of Xenopus RCC1 cDNA, a homolog of the human RCC1 gene: complementation of tsBN2 mutation and identification of the product.

We isolated a cDNA clone from Xenopus cDNA libraries for the homolog of the human RCC1 gene, which is considered to be a regulator for the onset of chromosome condensation. The cloned Xenopus RCC1 cDNA encoded a protein of 424 amino acids which had the same seven homologous repeated domains of about 60 amino acids as found in human RCC1 cDNA. The overall identity of amino acid sequence between the human and Xenopus RCC1 protein was 76%. Specifically, in the repeated domain the amino acid sequence was highly conserved between both species. The identity of amino acids in this region was 82%. In the N-terminal region, albeit the overall identity was low (35%), some positively charged amino acids were conserved. The transcript for Xenopus RCC1 gene with the length of 2.2-kb was detected in both Xenopus oocytes and cultured somatic cells, A6. The antibody prepared against Xenopus RCC1 protein produced in E. coli recognized 45 and 46 kDa proteins not only in Xenopus oocytes and A6 cells, but also in human and hamster cells. Xenopus RCC1 cDNA complemented the tsBN2 mutation, depending on the amount of its product in transformants. Thus, the RCC1 protein was suggested to regulate the onset of chromosome condensation in the eukaryote from amphibian to mammalian cells.

Amino Acid Sequence↗
PubMed1990

Premature chromosome condensation is induced by a point mutation in the hamster RCC1 gene.

At the nonpermissive temperature, premature chromosome condensation (PCC) occurs in tsBN2 cells derived from the BHK cell line, which can be converted to the Ts+ phenotype by the human RCC1 gene. To prove that the RCC1 gene is the mutant gene in tsBN2 cells, which have RCC1 mRNA and protein of the same sizes as those of BHK cells, RCC1 cDNAs were isolated from BHK and tsBN2 cells and sequenced to search for mutations. The hamster (BHK) RCC1 cDNA encodes a protein of 421 amino acids homologous to the human RCC1 protein. In a comparison of the base sequences of BHK and BN2 RCC1 cDNAs, a single base change, cytosine to thymine (serine to phenylalanine), was found in the 256th codon of BN2 RCC1 cDNA. The same transition was verified in the RCC1 genomic DNA by the polymerase chain reaction method. BHK RCC1 cDNA, but not tsBN2 RCC1 cDNA, complemented the tsBN2 mutation, although both have the same amino acid sequence except for one amino acid at the 256th codon. This amino acid change, serine to phenylalanine, was estimated to cause a profound structural change in the RCC1 protein.

Amino Acid Sequence↗
PubMed1990

Cyclic adenosine monophosphate production and contractile response induced by beta-adrenoceptor subtypes in rabbit urinary bladder smooth muscle.

The spontaneous contractile force of muscle strips isolated from male rabbit urinary bladder dome [detrusor) and base (trigonal muscle) was dose dependently inhibited by isoproterenol, a non-specific beta-adrenoceptor agonist. The relaxant response to 10(-6) M isoproterenol in the detrusor muscle was completely blocked by butoxamine (10(-4) M), a selective beta-2-antagonist, and by propranolol (10(-6) M), a non-specific beta-antagonist, but not by metoprolol (10(-6) to 10(-4) M), a selective beta-1-antagonist. Relaxation of trigonal muscle induced by 10(-6) M isoproterenol was inhibited 30% by metoprolol (10(-5) M), 70% by butoxamine (10(-4)M), and 100% by propranolol (10(-6) M). Terbutaline, a selective beta-2-adrenoceptor agonist, also caused dose dependently a relaxant response in detrusor and trigonal muscle. The maximum relaxant responses to isoproterenol and terbutaline were significantly greater in detrusor than in trigonal muscle. Dobutamine, a relatively specific beta-1-adrenoceptor agonist, caused a small but significant relaxant response in trigonal, but no change in detrusor muscle. In trigonal muscle the relaxant response to dobutamine was less than that to terbutaline. Cyclic adenosine monophosphate accumulation in detrusor did not significantly increase after administration of dobutamine, but significantly increased after administration of terbutaline. On the other hand, not only terbutaline, but also dobutamine, markedly increased cyclic adenosine monophosphate accumulation in trigonal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1990

Changes in lipid composition and isoproterenol- and ethanol-stimulated adenylate cyclase activity in aging Fischer rat bladders.

In the aging rat bladder dome, changes are noted in membrane composition and in the activity of the membrane-bound enzyme, adenylate cyclase (AC). When bladder domes from 22 day and 22 to 24 month Fischer rats are compared, changes in composition include: a 25% decrease in percentage of protein [(milligrams of protein per milligram of wet weight) x 100]; an approximately 40% decrease in both the total phospholipid content and in the content of the major phospholipids, phosphatidylcholine and phosphatidylethanolamine; and a 69% increase in the cholesterol to phospholipid ratio. These changes are indicative of a more rigid lipid bilayer in the aged rat bladder. Changes in AC with aging include a decrease in basal and forskolin-activated AC and a loss of the ability of isoproterenol to activate AC in the aged (22-24 month) rat bladder dome homogenate. Activation by isoproterenol (ISO; 3 microM) is 55 and 72% over 5' guanylimidodiphosphate [Gpp(NH)p; 1 microM] controls in 22 day and 90 day rat bladder dome homogenates, respectively. Activation by AC by NaF and Gpp(NH)p does not decline with aging. Ethanol, an agent that increases membrane fluidity, stimulates AC to a much greater extent in homogenates from the 22 month than from the 22 day or 90 day rat bladder dome. The ethanol-induced activation occurs not only in basal AC but also in Gpp(NH)p- and ISO-plus Gpp(NH)p-activated AC. The observed changes in AC with aging in part may reflect changes in the membrane lipid environment.

Adenylyl Cyclases↗
PubMed1989

The RCC1 protein, a regulator for the onset of chromosome condensation locates in the nucleus and binds to DNA.

The RCC1 gene, a regulator for the onset of chromosome condensation was found to encode a protein with a molecular mass of 45 kD, determined using the antibody against the synthetic peptides prepared according to the amino acid sequence of the putative RCC1 protein. The p45 located in the nuclei was released from the isolated nuclei, either by DNase I digestion or by treatment with 0.3 M NaCl. Consistently, p45 bound to the DNA-cellulose column was eluted with 0.3 M NaCl. After sequential treatment with DNase I and 2 M NaCl, almost all of the RCC1 protein were released from the nuclei. Thus, RCC1 protein locates on the chromatin and is not a component of the nuclear matrix. In mitotic cells, p45 is dispersed into the cytoplasm. Presumably, RCC1 protein plays a role in regulating the onset of chromosome condensation, at the level of transcription or of mRNA maturation.

Amino Acid Sequence↗
PubMed1989

[Effects of tricyclic antidepressant drugs on receptor binding sites and Ca2+ binding to sarcoplasmic reticulum in rat heart].

The effects of tricyclic antidepressant drugs on cardiac receptor binding sites and Ca2+ binding to cardiac sarcoplasmic reticulum were investigated in rats. 1) Quinupramine was found to possess higher affinity for muscarinic cholinergic receptor binding sites in brain and heart, compared with imipramine. 2) Repeated quinupramine treatment induced a significant increase in the Bmax value in cardiac muscarinic cholinergic receptors. 3) In imipramine treated heart, isoproterenol-induced stimulation of ornithine decarboxylase activity was significantly decreased compared with that in the vehicle control. 4) Repeated quinupramine and imipramine treatment caused a significant reduction of Bmax of 45Ca2+ binding in cardiac sarcoplasmic reticulum fractions. 5) After single quinupramine treatment, its concentrations in heart were higher than those in brain and plasma. 6) After the repeated quinupramine treatment, its concentration in heart was 2.4 times higher than that after single treatment. These results demonstrate that repeated tricyclic antidepressant drug treatment caused a functional impairment in Ca2+ binding sites of cardiac sarcoplasmic reticulum and adaptive changes of receptor binding sites.

Animals↗
PubMed1989

X-ray-related potentially lethal damage expressed by chromosome condensation and the influence of caffeine.

Caffeine has been reported to induce premature chromosome condensation (PCC) in S-phase cells in the presence of an inhibitor of DNA synthesis. We found that when S-phase cells are treated with caffeine and hydroxyurea after X irradiation, substantially more potentially lethal damage (PLD) is expressed, but the addition of cycloheximide, which inhibits PCC induction in S-phase cells, in the presence of caffeine and hydroxyurea reduces the expression of PLD to the same level as seen with caffeine alone. This can be interpreted to mean that the expression of PLD seen with caffeine in the absence of an inhibitor of DNA synthesis is not associated with chromosome condensation. Evidence that PCC induction in S-phase cells and the influence of caffeine on PLD expression were suppressed by incubation at 40 degrees C of tsBN75 cells with a ts defect in ubiquitin-activating enzyme indicates the involvement of ubiquitin in these two processes. These observations as well as previous findings on ubiquitin suggest to us that caffeine induces changes in DNA-chromatin conformation, which are caused by induction of PCC or ubiquitination of chromosomal protein. Such changes occurring postirradiation would favor expression of PLD.

Caffeine↗
PubMed1989

[Coronary artery reoperation utilizing "free" gastroepiploic artery].

A 57-year-old female underwent coronary artery bypass reoperation successfully by utilizing the free gastroepiploic artery (GEA) graft in combination with the in situ left internal mammary artery (IMA) graft. The left IMA was anastomosed to the left anterior descending artery and the "free" GEA was anastomosed to the left IMA proximally and to the first diagonal branch distally. The patient recovered well with a disappearance of angina. Postoperative angiogram at 6 weeks showed good patency of both grafts and improvement of left ventricular contraction was obtained. Thus, GEA can be utilized not only as an "in situ" graft, but also as a "free" graft, effectively.

Arteries↗
PubMed1989

[Surgical management of stab wound of the chest].

During the past three and half years, we experienced eighteen patients with stab wound of the chest. Ten patients were homicidal victims and the remainders were suicides. According to our indications (Table 4), thoracotomy was done in eight patients (44%). The major reason for thoracotomy in this series was massive bleeding. Five pulmonary, four diaphragmatic, four intercostal-artery's and two pericardial injuries were repaired. In our series, six patients (33%) were accompanied with abdominal stab wound and laparotomy was done in five patients. Four liver's one stomach's, one spleen's, one intestine's and one omentum's injuries were repaired. There were three DOA's (dead on arrival). The causes of DOA's were massive bleedings from the heart in two patients and from the liver in one patients. Except for the DOA's, four patients (27%) were not operated on. In conclusion, three DOA's, could not be resuscitated, but all remainders (the thoracotomy's, the laparotomy's and the non-surgical patients) survived and had no complications.

Adolescent↗
PubMed1988

The gene coding a ubiquitin-activating enzyme may locate on X chromosome.

tsBN75 cells which have a ts defect in the S phase have a mutation linked to the gene of hypoxanthine phosphoribosyl transferase and cannot complement ts85 cells which have a ts defect in the ubiquitin-activating enzyme. The ubiquitin-activating enzyme may be required for completion of the S phase.

Animals↗