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M Shibuya

Publications and source records attributed to M Shibuya.

At least 487 records · Page 27Linked to original sources
PubMed1982

Effect of pyridoxine-deficiency on the syntheses of aspartate aminotransferase in rat liver and muscle in vivo.

The rates of synthesis of aspartate aminotransferase isozymes in the liver and skeletal muscle in pyridoxine-deficient rats were examined. The rates of synthesis were compared in rats given pyridoxine-deficient diet ad libitum, rats given control diet ad libitum and rats pair-fed with those on the deficient diet. The rates of incorporation of 3H-L-leucine by both cytosolic and mitochondrial enzymes were highest in pair-fed controls. Incorporation of radioactivity into the cytosolic enzyme was higher in deficient rat liver than in that of controls fed ad libitum, but the rate of incorporation into the mitochondrial enzyme was similar in these two groups. In muscle the rates of incorporation of labeled leucine into both isozymes were similar in all groups when expressed relative to total protein synthesis. It was suggested that increase of glucocorticoid receptor might result in increased synthesis of cytosolic aspartate aminotransferase in pyridoxine-deficient rat liver.

Animals↗
PubMed1982

Effect of pyridoxine deficiency on activities and amounts of aspartate aminotransferase isozymes in rat tissues.

The enzyme and antigen activities of aspartate aminotransferase [EC 2.6.1.1] isozymes in several tissues of rats fed on pyridoxine-deficient or control diet for 4 weeks were determined. The enzyme activities in liver (supernate, mitochondria), heart (supernate), brain (mitochondria), and muscle (mitochondria) preparations of the deficient rats were abnormally low, whereas those in other tissue preparations were similar to those of control rats. In liver and heart preparations, the antigen activities of the deficient rats were similar to those in controls, but in brain and muscle mitochondria they were abnormally low. These findings suggest that the activity and the amount of this enzyme are regulated in different ways in different tissues, and suggest that the coenzyme level affects metabolic regulation of the enzyme molecule.

Animals↗
PubMed1982

Cellular sequences related to three new onc genes of avian sarcoma virus (fps, yes, and ros) and their expression in normal and transformed cells.

Two onc genes of avian sarcoma viruses unrelated to the src gene have recently been identified: fps of Fujinami sarcoma virus/PRCII/UR1 and yes of Y73/Esh sarcoma virus. In the first part of this study we demonstrated that UR2, the most recently isolated avian sarcoma virus, contains in its genome a unique sequence, ros, nonhomologous to src, fps, and yes sequences or to transforming genes of avian acute leukemia viruses. Using cDNAs specific to the inserts of avian sarcoma virus genomes, we examined the existence and the transcription of cellular nucleotide sequences related to the three new onc genes of avian sarcoma virus (fps, yes and ros) in various cells. The progenitor cellular sequences for these onc genes (c-onc) were present in uninfected chicken DNA in one or few copies per haploid genome. These c-onc sequences were detectable in cellular DNA of a wide variety of vertebrates, and the homology between viral and cellular onc was inversely related to the phylogenetic distance of animal species. The pattern of expression of these c-onc genes in different tissues of chickens was found to be unique to each gene. The expression of c-fps and c-ros genes was generally repressed in many tissues, but c-fps was expressed at higher levels in bone marrow (2.5 copies per cell) and lung (1.1 copies per cell), whereas c-ros was mainly transcribed in kidney (2.5 copies per cell). On the other hand, c-yes transcripts were easily detectable in all tissues analyzed and were found at high levels in kidney (26 copies per cell). These c-onc expressions were unaffected by infection with avian sarcoma viruses that contained other onc genes. In a few cultures of chicken and quail transformed cells derived from tumors induced by chemical carcinogens, we found that the levels of transcription of the four c-onc genes remained unaltered, compared with that in normal tissues.

Alpharetrovirus↗
PubMed1982

Molecular cloning of the Fujinami sarcoma virus genome and its comparison with sequences of other related transforming viruses.

Full-length proviral DNA of Fujinami sarcoma virus (FSV) of chickens was molecularly cloned and characterized. An analysis of FSV DNA integrated in mammalian cells showed that restriction endonuclease SacI has a single cleavage site on FSV DNA. Unintegrated closed circular FSV DNA obtained from newly infected cells was linearized by digestion with SacI and cloned into lambdagtWES.lambdaB. The following three different molecules were isolated: FSV-1 (4.4 kilobases [kb]) and FSV-2 (4.7 kb), which appeared to be full-length FSV DNA molecules containing either one or two copies of the long terminal repeat structure, and FSV-3 (6 kb), which consisted of part FSV DNA and part DNA of unknown origin. An analysis of the structure of cloned FSV-1 and FSV-2 DNA molecules by restriction endonuclease mapping and hybridization with appropriate probes showed that about 2.6 kb of the FSV-unique sequence called FSV-fps is located in the middle of the FSV genome and is flanked by helper virus-derived sequences of about 1.3 kb at the 5' end and 0.5 kb at the 3' end. The long terminal repeats of FSV were found to have no cleavage site for either EcoRI or PvuI. Upon transfection, both FSV-1 DNA and FSV-2 DNA were able to transform mammalian fibroblasts. Four (32)P-labeled DNA fragments derived from different portions of the FSV-fps sequence were used for hybridization to viral RNAs. We found that sequences within the 3' half of the FSV-fps gene are homologous to RNAs of PRCII avian sarcoma virus and the Snyder-Theilen strain of feline sarcoma virus, both of which were previously shown to contain transforming genes related to FSV-fps. These results suggest that the 3' portion of the FSV-fps sequence may be crucial for the transforming activity of fps-related oncogenic sequences.

Alpharetrovirus↗
PubMed1982

[Phase II study of vindesine in patients with carcinoma of the lung and metastatic pulmonary tumor].

A phase II study of Vindesine (VDS) was carried out in 20 patients with carcinoma of the lung (14 adenocarcinomas, 3 squamous cell carcinomas, 2 large cell carcinomas and 1 small cell carcinoma), and in 18 patients with metastatic pulmonary tumor (primary organ: 4 colons, 2 uteri, 2 lungs, one each tongue, pharynx, maxillary sinus, esophagus, mediastinum, bile duct, pancreas, kidney, rectum and sarcoma). VDS was given weekly by i. v. push at a dose of 3 mg/m2. Patients should be given at least three times of VDS for eligibility. Of 18 evaluable patients with carcinoma of the lung, 3 patients with adenocarcinoma showed a partial response. Response rates were 17% for patients with carcinoma of the lung, and 25% for 12 patients with adenocarcinoma. Two responders (uterine cervical carcinoma and mediastinal embryonal carcinoma) were observed in 14 evaluable patients with metastatic pulmonary tumor. In addition, one patient with metastatic maxillary sinus tumor showed a minor response. Major hematologic toxicities of VDS were leukopenia (less than 4000 cells/mm3--92%, less than 2000 cells/mm3--28%), anemia (less than 10.0 g/dl, 38%) and thrombocytopenia (less than 10 X 10(4) cells/mm3, 11%). Major non-hematologic toxicities were numbness (24%), constipation (11%), anorexia (21%), fever (16%) and liver dysfunction (21%). The dose limiting factor of VDS was leukopenia.

Adenocarcinoma↗
PubMed1982

Effects of BCG and cyclophosphamide on the spontaneous and antibody-dependent cell-mediated cytotoxicity of peritoneal and spleen lymphocytes of ACI/N rats.

The effects of BCG and cyclophosphamide on the antibody-dependent cell-mediated cytotoxicity (ADCC) and natural killer (NK) activity of spleen and peritoneal lymphocytes were serially examined after treatment. The changes of ADCC and NK activity were different in peritoneal and spleen lymphocytes according to the route and timing of administration. The decrease of NK activity induced by cyclophosphamide is not marked, and the degree of decrease depends on the timing of cyclophosphamide administration. The ADCC and NK activity of peritoneal lymphocytes after intravenous BCG administration were elevated 7 days after treatment, but the NK activity of spleen lymphocytes was decreased. On the other hand, the NK activities of peritoneal and spleen lymphocytes were elevated in rats given intraperitoneal BCG. Spleen lymphocytes and peritoneal lymphocytes from rats given intravenous BCG suppressed tumor growth in the Winn test during the early tumor-bearing stage. The spleen lymphocytes with low NK activity in rats given intravenous BCG strongly suppressed the NK activity of normal spleen lymphocytes.

Animals↗
PubMed1981

Biochemical evidence of dysfunction of brain neurotransmitters in the Lesch-Nyhan syndrome.

Different brain regions were removed post mortem from three patients with the Lesch-Nyhan syndrome and were examined for alterations in hypoxanthine-guanine phosphoribosyl transferase (HGPRT), adenine phosphoribosyl transferase, and biochemical indexes of norepinephrine, dopamine, serotonin, gamma-aminobutyric acid (GABA), and acetylcholine neuron function, as compared with age-matched controls. The level of HGPRT activity in the material from patients with the Lesch-Nyhan syndrome was less than 1 per cent of control levels, whereas adenyl phosphoribosyl transferase was not significantly altered. All biochemical aspects of the function of dopamine-neuron terminals in the striatum (except dihydroxyphenylacetic acid levels) were decreased to 10 to 30 per cent of the control values. Serotonin and 5-hydroxyindoleacetic acid levels were increased, striatal choline acetyltransferase levels were low, and striatal glutamic acid decarboxylase and guanylate cyclase activities were unaltered. The disruption of the balance between the functions of GABA, dopamine, and acetylcholine neurons in the extrapyramidal system probably accounts for some of the symptoms observed in the Lesch-Nyhan syndrome (e.g., choreoathetosis).

Acetylcholine↗
PubMed1981

Transcription of the E. coli tufB gene: cotranscription with four tRNA genes and inhibition by guanosine-5'-diphosphate-3'-diphosphate.

The transcription of the tufB gene by purified RNA polymerase holoenzyme was studied using the transducing phage lambda rifd 18 DNA and the hybrid plasmid pTUB1 DNA (Miyajima et al. 1979) as templates. The size of tufB mRNA synthesized in this system was about 1,700 nucleotides, and the same strand as for rrnB was transcribed. By electron microscopic examination of the R-loop formed between lambda fus3 DNA and tufB mRNA synthesized under the direction of pTUB1 DNA, it was found that the untranslated sequence of about 500 nucleotides is at the 5' end of tufB mRNA. The sequencing of the 5' region of tufB mRNA synthesized on the truncated template has revealed that the tufB gene is cotranscribed with its upstream genes for four tRNAs (thrU, tyrU, glyT, and thrT). The synthesis of this mRNA molecule is completely abolished by low concentrations of ppGpp. Neither pppGpp, ppGp, nor pGpp was effective as inhibitor in this cell-free system.

Depression, Chemical↗
PubMed1981

Genetic structure, transforming sequence, and gene product of avian sarcoma virus UR1.

We analyzed the genetic structure and gene products of the newly isolated avian sarcoma virus UR1, which recently has been shown to be replication defective and to contain no sequences homologous to the src gene of Rous sarcoma virus. The sizes of the genomic RNAs of UR1 and its associated helper virus, UR1AV, were determined to be 29S and 35S (5.9 and 8.5 kilobases), respectively, by gel electrophoresis and sucrose gradient sedimentation. RNase T1 oligonucleotide mapping of purified viral RNAs indicated that UR1 RNA contains eight unique oligonucleotides in the middle of the genome and shares four 5'-terminal and three 3'-terminal oligonucleotides with UR1AV RNA. The unique sequences of UR1 and Fujinami sarcoma virus were found to be closely related to each other by molecular hybridization of UR1 RNA with DNA complementary to the unique sequence of Fujinami sarcoma virus RNA, but minor differences were found by oligonucleotides fingerprinting. In the regions flanking the unique sequences, UR1 and Fujinami sarcoma viral RNAs contain distinct oligonucleotides, which are shared with oligonucleotides of the respective helper viral RNAs. Cell transformed with UR1 produce a single 29S RNA species which contains a UR1 unique sequence; this species is most likely the mRNA coding for the transforming protein. In UR1-transformed cells, a phosphoprotein fo 150,000 daltons (p150) was detected by immunoprecipitation with antiserum against gag proteins. p150 was associated with a protein kinase activity that was capable of phosphorylating p150 itself, immunoglobulin G of antiserum, and a soluble substrate, alpha-casein. This enzyme transferred phosphate exclusively to tyrosine residues of substrates in vitro, but p 150 labeled in vivo with 32P contained both phosphoserine and phosphotyrosine. The in vitro kinase reaction was not affected by the presence of cyclic AMP or cyclic GMP and strongly preferred Mn2+ over Mg2+. Thus, the properties of UR1 protein are almost identical to those of Fujinami sarcoma virus protein.

Alpharetrovirus↗
PubMed1981

Some biological properties of two new avian sarcoma viruses.

The new avian retroviruses UR1 and UR2 were isolated from spontaneous tumors of chickens by cocultivation of tumor material with susceptible chicken embryo fibroblasts. In vitro, UR1 induced formation of small foci of round and fusiform cells. On the other hand, cells infected by UR2 assumed an extremely elongated morphology. In vivo, both viruses induced fibrosarcomas and myxosarcomas with short latencies. Infectivity assays with and without mitomycin C showed that both viruses were defective for replication, but transformed nonproducing cell clones were obtained only with UR1. UR1-infected transformed nonproducing clones did not release particles detectable by reverse transcriptase assays, and fusion of transformed nonproducing cells with quail cells chronically infected with Rous sarcoma virus (a Bryan strain) failed to rescue infectious virus. This suggested that UR1 does not code for functional envelope glycoproteins. In this regard, UR1 appeared to be similar to Fujinami, PRCII, and Y73 viruses. The helper viruses of partially purified stocks of UR1 and UR2 appeared to belong to subgroup A, but these helper viruses were distinguishable from each other, as shown by host range experiments and neutralization tests. Hybridization studies with DNA complementary to the src gene of Rous sarcoma virus and RNAs extracted from both UR1 and UR2 showed no homology between the genomes of the new isolates and the transforming gene of Rous sarcoma virus.

Alpharetrovirus↗
PubMed1981

Effects of CDP-choline on striatal dopamine level and behavior in rats.

To further assess the effects of CDP (cytidine diphosphate)-choline on Parkinsonian symptoms, striatal dopamine (DA) was measured fluorometrically in rats after injection of CDP-choline. CDP-choline (300 mg/kg, i.p.) increased the DA content in the striatum (p less than 0.05) one hour after injection. The behavioral effect of CDP-choline was then tested in rats in which the unilateral nigro-striatal DA neurons had degenerated following an intranigral injection of 6-hydroxydopamine (6-OHDA). CDP-choline alone did not produce behavioral changes in these rats. However, pretreatment with a single dose of CDP-choline (900 mg/kg, i.p.) suppressed both the apomorphine-induced contralateral and the d-amphetamine-induced ipsilateral circling. The same dose of CDP-choline suppressed the number of treadmill revolutions in mice. On the other hand, a 7-day consecutive treatment with 300 mg/kg of CDP-choline enhanced the apomorphine-induced contralateral circling (by 42%, p less than 0.05). The same treatment with CDP-choline raised the striatal DA content by 29% (p less than 0.05) on the intact side, but not on the 6-OHDA injected side. These results indicate that CDP-choline has either a direct nor an indirect DA agonistic effect. The increase in DA content, decrease in locomotion and enhancement of the effect of apomorphine can be explained on the hypothesis that CDP-choline may act as an antagonist on the DA neurons and receptors. The validity of this apparently paradoxical use of CDP-choline with antagonistic effect on DA neurons in the treatment of Parkinson's disease is discussed.

Animals↗