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T Horiuchi

Publications and source records attributed to T Horiuchi.

At least 433 records · Page 24Linked to original sources
PubMed1987

[A case of cerebral embolism caused by atrial myxoma--superselective fibrinolytic therapy].

A 37-year-old man was admitted to our clinic 3 hours after the onset of cerebrovascular accident with right hemiparesis and total aphasia. On admission, we started combined administration of mannitol, vitamin E, phenytoin (Sendai Cocktail) and perfluorochemicals to protect ischemic brain. Left cerebral angiography revealed occlusion of the left middle cerebral artery involving its perforating arteries. Following the performance of angiography, vascular balloon catheter was introduced into the embolus, and fibrinolytic agent (urokinase) was continuously injected. Soon after the injection of 240,000 unit urokinase, recanalization of left middle cerebral artery was shown by repeated cerebral angiography performed 5.5 hours after the onset. On his clinical course, left hemiparesis and aphasia were improved step by step, and 1 week later, he could walk by himself with minor neurological deficits. Further examination revealed that myxoma was located on left atrium by echocardiography. Within 1 week, the patient was transferred to cardio-surgical unit, and myxoma was successfully removed. Now he is in good health and has returned to his job. Usually cerebral embolisms result from atrial myxoma cause severe cerebral infarction. Here we reported a case of cerebral embolism by myxoma and recanalized using fibrinolytic agent by balloon catheter injection. The damage will be reduced if the duration of occlusion is limited, so this method will be helpful to treat cerebral embolism.

Adult↗
PubMed1986

Involvement of sulfatide in activation of protein kinase C by tumor promoters.

Sulfatide (cerebroside sulfate) activated protein kinase C to the same extent as phosphatidylserine did with the tumor promoters, 12-O-tetradecanoylphorbol-13-acetate (TPA), teleocidin and debromoaplysiatoxin. Sulfatide and phosphatidylserine both induced specific binding of [3H]TPA to protein kinase C, although the ratios of specific to non-specific [3H]TPA binding to protein kinase C with the two were not the same. It is concluded that sulfatide is involved in activation of protein kinase C by tumor promoters in a slightly different way from phosphatidylserine.

Animals↗
PubMed1986

Absence of phosphorylation of retinoid-binding proteins by protein kinase C in vitro.

Cellular retinol-binding protein, cellular retinoic acid-binding protein, and fetal cellular retinol-binding protein were purified to homogeneity and each polypeptide had a molecular weight of 16,000. Their apoproteins were not phosphorylated under the same conditions. Their holoproteins did not inhibit the phosphorylation of histone III-S by protein kinase C. Each of these observations is contrary to the results reported by Cope et al. (Biochem. Biophys. Res. Commun., 120, 593-601, 1984).

Animals↗
PubMed1986

Structure and function of dnaQ and mutD mutators of Escherichia coli.

The nucleotide sequences of the recessive dnaQ49 and the dominant mutD5 mutator were determined. The dnaQ49 mutator has a single base substitution in the dnaQ gene, thus causing one amino acid change, 96Val (GTG)----Gly (GGG), in the DnaQ protein (epsilon subunit of DNA polymerase III holoenzyme). The mutD5 mutator possesses two base substitutions in the same gene, resulting in two amino acid changes, 73Leu (TTG)----Trp (TGG) and 164Ala (GCA)----Val (GTA), which were designated the mutD52 and mutD51 mutations, respectively. Construction of chimaeric genes carrying one or two of these mutations revealed: either mutD51 or mutD52 alone causes the dominant mutator phenotype when present in a multi-copy plasmid; mutator phenotype when present in a low-copy plasmid; the dominant mutD51 mutator activity is suppressed by the dnaQ49 mutation when both mutations are present in the same gene. Based on these findings, we devised a model for the action of these mutators.

Amino Acid Sequence↗
PubMed1986

Ammonium ion as a possible regulator of the commencement of rRNA synthesis in Xenopus laevis embryogenesis.

Recently, we have shown that ammonium salts and amines at an external concentration of 3 mM selectively inhibit rRNA synthesis in Xenopus disaggregated neurula cells. We studied here the change in the amount of ammonia within the embryo and its inhibitory action on the commencement of rRNA synthesis which normally occurs at the blastula stage of development. Ammonia exists at ca. 50 ng/egg (or ca. 3.0 mM at an intra-egg concentration) in the unfertilized egg. This level was maintained during cleavage and then sharply decreased during the blastula stage to the level of ca. 20 ng/embryo (or 1.2 mM) in postblastular stages. Ammonia was extracted from cleavage embryos in a form of ammonium chloride and confirmed to selectively inhibit rRNA synthesis in neurula cells. With authentic ammonium chloride, ammonia was found to be promptly incorporated into cells and to inhibit rRNA synthesis within 1 hr after treatment. In blastula cells, ammonium salts reversibly inhibited the commencement of the synthesis of rRNA, but not hnRNA, 5 S RNA and U1, U2, and U5 snRNAs. The inhibition was at the step of transcription of 40 S pre-rRNA but not the processing or degradation of the processed rRNA. Ammonium salts did not inhibit DNA synthesis, protein synthesis, cell division, and cellular reaggregation. These observations suggest that ammonium ion may be involved in the regulation of the commencement of rRNA synthesis in Xenopus embryogenesis, although it is not yet clear if the ammonium ion exerts its effect directly upon the rDNA transcription system.

Ammonium Chloride↗
PubMed1986

Palytoxin is a non-12-O-tetradecanoylphorbol-13-acetate type tumor promoter in two-stage mouse skin carcinogenesis.

Palytoxon, which is a toxin with a molecular weight of 2681 daltons isolated from a marine coelenterate, is a potent skin irritant. However, it did not induce ornithine decarboxylase in mouse skin, or adhesion of human promyelocytic leukemia cells (HL-60). Moreover, it did not inhibit the specific binding of [3H]12-O-tetradecanoylphorbol-13-acetate (TPA) to a mouse skin particulate fraction or activate protein kinase C isolated from mouse brain in vitro. Since palytoxin showed strong irritation on mouse ear in one short-term screening test for a promoter, it was examined in a two-stage carcinogenesis experiment. The incidence of tumors in a group of mice treated with 7,12-dimethylbenz[a]anthracene plus palytoxin was 62.5% in week 25. These tumors were identified histologically as seven papillomas and one carcinoma. This paper reports the potent tumor-promoting activity of palytoxin, which is classified as a non-TPA-type tumor promoter.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Purification and properties of intracellular clotting factor, factor B, from horseshoe crab (Tachypleus tridentatus) hemocytes.

An intracellular clotting factor, factor B, which is closely associated with the hemolymph coagulation system of horseshoe crab (Tachypleus tridentatus), was purified and characterized. The purified preparation gave a single band (Mr = 64,000) on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) in the absence of 2-mercaptoethanol, while three bands (Mr = 64,000, 40,000, and 25,000) were detected on SDS-PAGE after reduction. This preparation was converted by limulus clotting factor C to an activated form, factor B, with Mr = 56,000 consisting of a heavy chain (Mr = 32,000) and a light chain (Mr = 25,000) bridged by disulfide linkage(s). The factor B, which was produced separately by treating the partially purified factor B with factor C, was also purified. It gave a single band on unreduced SDS-PAGE and two bands on reduced SDS-PAGE. The purified factor B had Mr of 56,000 consisting of a heavy chain (Mr = 32,000) and a light chain (Mr = 25,000). These results indicated that the purified factor B zymogen is a mixture of single-chain and two-chain forms, both of which have the same molecular weight of 64,000, and that these two forms are converted to factor B by factor C. The diisopropyl phosphorofluoridate-sensitive site of factor B was found in the heavy chain. The reconstitution studies using purified factor C, factor B, proclotting enzyme and coagulogen in the presence of lipopolysaccharide indicated that factor B is an essential component to complete sequential activation of the limulus clotting system, and that it specifically activates proclotting enzyme to the active clotting enzyme.

Amino Acids↗
PubMed1986

camR, a negative regulator locus of the cytochrome P-450cam hydroxylase operon.

A 4.27-kilobase insert from a HindIII DNA library of Pseudomonas putida carrying the CAM plasmid allowed coordinate expression of genes camD and camC under control of camR, an upstream regulator. The camC gene specifies cytochrome P-450cam, and camD specifies the 5-exo-alcohol dehydrogenase. A 1.38-kilobase deletion from the insert results in the constitutive expression of genes camC and camD; transformation in trans restores the substrate control, indicating that camR is a negative regulator.

Alcohol Dehydrogenase↗
PubMed1986

Granulomatous pneumonitis induced by bacille Calmette-Guérin in the mouse and its treatment with cyclosporin A.

Granulomatous pneumonitis was induced intravenously by an injection of BCG, and changes in the population of cells from bronchoalveolar lavage (BAL) fluid were examined. Increased lymphocytes in BAL fluid, especially Lyt-1 positive T-lymphocytes, were observed after the development of granulomatous pneumonitis. Cyclosporin A (Cy A) administered for 5 days before and for 5 days after BCG injection clearly suppressed development of the granuloma. The BAL cell count and cell population became almost the same as those in naive animals. The increase in the number of Lyt-1 positive T cells was abrogated by Cy A treatment. These results suggested the important role of Lyt-1 positive T cells in the development of granulomas and the possible beneficial effect of Cy A in human granulomatous lung diseases.

Animals↗
PubMed1986

Pulmonary vascular disease in secundum atrial septal defect with pulmonary hypertension.

Histopathologic and morphometric studies of small pulmonary arteries were performed in 16 cases of secundum atrial septal defect (ASD) and severe pulmonary hypertension. Besides typical plexogenic arteriopathies found in six cases, organized microthrombi and what we call "musculoelastosis," that is, proliferation of longitudinal smooth muscle bundles and elastic fibers, were seen in small pulmonary arteries in three and four cases, respectively. These changes were observed co-existing in the remaining three cases. Thrombi of the small pulmonary arteries and musculoelastosis were the forms of pulmonary vascular disease characteristically found in the older patients with both ASD and pulmonary hypertension. Yamaki's index of pulmonary vascular disease, though effective in describing severity of plexogenic arteriopathy, proved to be less so for the intimal lesions in old microthrombi and for musculoelastosis. Among the cases with plexogenic arteriopathy, there was a positive significant correlation between the medial thickness of small pulmonary arteries and peak arterial pressure, which, however, was not demonstrated when all the cases of ASD were included.

Adult↗
PubMed1986

A method for measurement of total circulating blood volume using indocyanine green.

A method of measuring total circulating blood volume (TBV) using indocyanine green (ICG) dye was investigated in 7 dogs and 16 patients. Since concentration of injected ICG decreases exponentially from the circulating system after recirculation, concentration of the dye at the time of appearance (Cta) can be extrapolated by extending the slope of the dye dilution curve transcribed to a semi-logarithmic graph. TBV was calculated using the following formula: TBV = I/Cta, where I is the amount (mg) of ICG injected. Repeat measurements of TBV using ICG demonstrated good reproducibility (average coefficient of variation, 2.0%) and when compared to measurements made with Evans blue dye resulted in a correlation coefficient of 0.98 or more. We conclude that assessment of TBV using ICG is reliable and experimentally and clinically feasible.

Adolescent↗
PubMed1986

Determination of safe interval of circulatory arrest from the cerebral metabolic aspect.

To determine the safe interval of hypothermic total circulatory arrest, the cerebral metabolic state was evaluated in 30 dogs. Surface cooling was achieved by deep ether anesthesia and the animals were assigned to three equal groups. Group I: 30 min circulatory arrest and surface rewarming. Group II: 60 min circulatory arrest and surface rewarming. Group III: 60 min circulatory arrest and perfusion rewarming. Brain tissue gas tension was monitored and cerebral O2 consumption was calculated. Cerebral O2 consumption reduced with cooling, parallel to the decrease in cerebral blood flow. Rapid increase in Po2, elevation of PCO2, and decrease of pH in the brain tissue were observed during circulatory arrest. Brain tissue PO2 increased significantly after circulatory arrest in Group I, but it remained low during rewarming in Groups II and III. Cerebral O2 consumption was at reduced levels in all groups during rewarming and it remained at 29% of the precooling control level in Group II at the end of rewarming, whereas it recovered to 71% and 57% of the precooling levels in Groups I and III, respectively. It was estimated that cerebral metabolism may be recovered after 30 min circulatory arrest, despite a transient reduction in cerebral O2 consumption. On the other hand, after 60 min circulatory arrest, the recovery of cerebral metabolism was delayed in Group II and organic failure might have occurred in this group. However, even after circulatory arrest for 60 min, cerebral metabolism was recovered in Group III. The safe period of circulatory arrest is considered to be prolonged by use of extra-corporeal circulation.

Animals↗