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T Murayama

Publications and source records attributed to T Murayama.

At least 163 records · Page 9Linked to original sources
PubMed1997

[Isolation and structure elucidation of cirensenosides Q and R].

Two new saponins (cirensenoside Q and R) were isolated from the leaves of Oplopanax elatus. Their structures were elucidated as follows: Q, gypsogenin 3-O-beta-glucopyranosyl-28-O-alpha-L-rhamnopyranosyl(1-->4)-beta-D- glucopyranosyl(1-->6)-beta-D-glucopyranoside; R, 3 beta-hydroxylup-20(29)-ene-23-al-28-oic acid 3-O-beta-D-glucopyranosyl-28-O-alpha-L-rhamnopyranosyl(1-->4)-beta-D- glucopyranosyl(1-->6)-beta-D-glucopyranoside, respectively.

Magnoliopsida↗
PubMed1997

[2 cases of lung disease caused by Mycobacterium avium complex occurred in middle-aged women without underlying disorders, which we observed for more than 30 years].

We reported 2 cases of Mycobacterium avium complex lung disease occurred in middle-aged women without underlying disorders, which we could observe for more than 30 years. One case was a 42-year-old woman started with bloody sputum, and the other was a 43-year-old woman with cough and sputum. In both cases, chest X ray films were normal on their first visit. More than 15 years after their first visit, Mycobacterium avium complex was isolated from their sputum or bronchial washing. During the observation, a cluster of small nodules in the periphery of the lung and bronchiectasis appeared and deteriorated, and excretion of the bacilli increased gradually. Their past history and family history were normal. Since lung disease caused by Mycobacterium avium complex progresses very slowly, long-time observation would be necessary to consider its pathogenesis.

Adult↗
PubMed1997

Transient rise in serum cytokines during coronary artery bypass graft surgery.

In order to examine the specificity of cytokine production during coronary artery bypass graft (CABG) surgery, we serially measured serum levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta) and tumor necrosis factor (TNF), in twenty patients between 52 and 80 years of age, during surgery and 2 days afterwards. Serum MCP-1, as well as IL-8 and IL-6, increased significantly during the surgery (P < 0.05), while IL-1 beta and TNF did not. MCP-1, IL-8 and IL-6 concentrations were not different in the sera of three patients tested at three different sites, i.e., the hepatic vein, pulmonary artery and radial artery. They increased in parallel in each patient, although the actual timing of the increase relative to the surgical step varied among individuals. In complicated patients, MCP-1, IL-8 and IL-6 showed higher peaks and persisted longer than in patients without complications. The universal and simultaneous appearance of MCP-1, IL-8 and IL-6 could indicate that these three cytokines may be stimulated by a yet undiscovered stimulus (or stimuli) which occurs systemically despite the independent pathways of production.

Aged↗
PubMed1997

[Evaluation of mycobacteria growth indicator tube (MGIT) for drug susceptibility testing of Mycobacterium tuberculosis isolates].

Fifty six clinical isolates of Mycobacterium tuberculosis were tested for drug susceptibility in Mycobacteria Growth Indicator Tube (MGIT) containing 0.1 microgram/ml of INH, 1.0 microgram/ml of RFP, 3.5 micrograms/ml of EB and 0.8 microgram/ml of SM. These results were compared with those obtained by testing the same M.tuberculosis isolates by the absolute concentration method using 1% Ogawa egg slant containing 0.1 microgram/ml of INH, 10 micrograms/ml of REP, 2.5 micrograms/ml of EB and 20 micrograms/ml of SM. Fifty six isolates consisted of 18 pansensitive strains, 27 multidrug resistant strains and 11 single drug resistant strains. The results of individual drugs showed excellent agreement between the MGIT and the Ogawa methods, and overall agreement rate of the two methods were 96.4%. The results were just the same for all drugs in 48 out of 56 strains studied. The drug resistance could be observed much earlier by the MGIT method (mean 5.9 days) than by the Ogawa method (more than 21 days). In conclusion, the MGIT system could be a promising new drug susceptibility test which might become available in Japan replacing the Ogawa method.

Antitubercular Agents↗
PubMed1996

P2 purinoceptor-mediated stimulation of adenylyl cyclase in PC12 cells.

PC12 pheochromocytoma cells have P2 purinoceptors which are activated by ATP and coupled to Ca2+ influx and catecholamine release. Also PC12 cells have adenosine receptors coupled positively to adenylyl cyclase, and cyclic AMP regulates cell functions such as catecholamine release. The effects of ATP and ATP analogs on cyclic AMP accumulation in PC12 cells were investigated in this study. ATP and adenosine 5'-0-(3-thiotriphosphate) stimulated cyclic AMP accumulation at low concentrations up to 300 microM but showed inhibitory effects above this concentration. 2',3'-O-(4-Benzoyl)benzoyl ATP and 2-methylthio ATP showed similar effects, although the responses were very limited. Addition of adenosine 5'-O-(2-thiodiphosphate) (ADP beta S) or beta, gamma-methylene ATP, but not alpha, beta-methylene ATP, stimulated cyclic AMP accumulation markedly without causing an inhibitory phase. The effects of ATP, ADP beta S and beta, gamma-methylene ATP were not inhibited by adenosine deaminase or specific antagonists to A1 and A2 adenosine receptors. Neither ADp beta S nor beta, gamma-methylene ATP showed any effect on Ca2+ influx or noradrenaline release. Suramin, a P2 receptors antagonists, had no inhibitory effect against ATP analog-stimulated cyclic AMP accumulation, although reactive blue 2 inhibited the beta, gamma-methylene ATP-stimulated reaction but not that up-regulated by ADP beta S. These findings suggest that the pharmacological characteristics of these ATP receptors coupled to adenylyl cyclase are clearly different from those of ligand-gated ion channels defined by P2X purinoceptors, which have been cloned and shown to be coupled to Ca2+ influx and catecholamine release in PC12 cells. The existence of a new type of P2 purinoceptor-mediating stimulation of adenylyl cyclase is proposed in PC12 cells.

Adenosine Triphosphate↗
PubMed1996

Autocrine loop through cholecystokinin-B/gastrin receptors involved in growth of human leukemia cells.

The cholecystokinin (CCK)-B/gastrin receptor binds two brain-gut hormones, CCK and gastrin, with high affinities. These peptides have a trophic effect on gastrointestinal cells expressing the receptor in vivo as well as in vitro. Recently, this receptor mRNA was reported to be expressed in immunocytes localized in the lamina propria of normal rat stomach mucosa. Here, we studied the receptor expression in human hematopoietic cells in order to determine whether they play a role in cell growth. The CCK-B/gastrin receptor mRNA was detectable in the polymorphonuclear (PMN) cells but not in the mononuclear cells of normal peripheral white blood cells by reverse transcription-polymerase chain reaction. The receptor transcript was, however, expressed in human leukemia cell lines (14 of 18 cell lines tested) derived from not only myeloid, but also T- and B- lymphoid lineages. The CCK-B/gastrin receptors on several leukemia cell lines were shown to be biologically active by demonstrating ligand-dependent cell proliferation in serum-deprived medium. Interestingly, a human CCK-B/gastrin receptor specific antagonist, YM022, but not its stereotype isoform, selectively inhibited the DNA synthesis of THP-1, MOLT-16, MOLT-14, and CCRF-CEM in the absence of exogenous peptide ligands. Further investigation revealed that these leukemia cell lines and normal PMN cells also expressed gastrin mRNA. These results suggest that growth of human leukemia cells is promoted by an autocrine mechanism through the CCK-B/gastrin receptors.

Cell Division↗
PubMed1996

Sodium nitroprusside stimulates noradrenaline release from rat hippocampal slices in the presence of dithiothreitol.

It is becoming apparent that nitrogen monoxide (NO) such as nitric oxide has regulatory roles for neuronal cell functions. We examined the role of NO using NO donors on [3H]noradrenaline (NA) release from prelabeled rat hippocampal slices. Sodium nitroprusside (SNP), which had no effect by itself, stimulated [3H]NA release in a dose-dependent manner (ED50 = 0.5 mM) in the presence of dithiothreitol (DTT). The stimulatory effect of SNP with DTT, but not high K+, was observed in an extracellular Ca(2+)-free buffer. The maximal effect of SNP was obtained after incubation for 1-2 h with DTT in buffer at physiological pH (7.4). The simultaneous addition of SNP and DTT to the slices induced a small effect, and the effect of SNP declined after 3.5 h. SNP stimulated cyclic GMP accumulation in the slices without DTT. NaNO2 and 1-hydroxy-2-oxo-3,3-bis(2-aminoethyl)-1-triazene (a generator of nitric oxide), which stimulated cyclic GMP accumulation by themselves, did not stimulate [3H]NA release in the presence and absence of DTT. 3-Morpholinosydnonimine HC1 (a generator of peroxynitrite) had no effect on the release. The stimulatory effect of SNP and DTT on NA release was inhibited 40% by nitric oxide scavengers such as oxyhemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxy-3-oxide, although cyclic GMP accumulation induced by NO donors was completely inhibited. These findings suggest that SNP reacts with DTT to produce unknown active species, and that cyclic GMP is not a mediator for SNP-stimulated NA release.

Animals↗
PubMed1996

G(o) protein does not regulate ATP-stimulated [Ca2+]i elevation or noradrenaline release in PC12 cells.

The roles of G(o), a heterotrimeric GTP binding (G) protein with a 40-kDa alpha subunit and which is localized predominantly in neuronal cells, in exocytosis have been discussed recently. PC12 pheochromocytoma cell line is a convenient model in which to study the Ca(2+)-dependent mechanisms of the neurosecretory process. The stimulation of ATP receptors or addition of KCl stimulated an elevation of cytosolic free Ca2+ concentration ([Ca2+]i) and [3H]noradrenaline (NA) release in PC12 cells. In this study, we investigated the roles of G(o) in ATP- and KCl-stimulated reactions. Nerve growth factor treatment for 2 days and transfection of PC12 cells with cDNA of subunit of (G(o alpha) had no effect on ATP-stimulated [3H]NA release, although both treatments increased levels of the G(o alpha) and its trimeric form by about twofold over those in unstimulated cells. The [Ca2+]i rise induced by ATP in NGF-treated cells was similar to that in control cells, although the maximal response was slightly smaller. Cholera toxin treatment for 2 days inhibited ATP- and KCl-stimulated NA release, although this treatment caused an approximately twofold increase in the level of G(o). Pertussis toxin treatment, which ADP ribosylated over 90% of endogenous G proteins such as G(o), had no effect on ATP-stimulated reactions. These findings show that G(o) does not directly regulate ATP-stimulated Ca2+ channels or the NA release process in PC12 cells. Cholera toxin-sensitive protein(s) may regulate exocytosis.

Adenosine Triphosphate↗
PubMed1996

A 11.5-kb 5'-terminal cDNA sequence of chicken breast muscle connectin/titin reveals its Z line binding region.

A partial 5'-region cDNA (11.5 kb) of chicken breast muscle connectin/titin encoding 3752 amino acids was sequenced. The predicted amino acid sequence contains 31 immunoglobulin C2 motifs and 10 interdomains. The sequence suggests a skeletal muscle type of connectin isoforms. Immunoelectron microscopic studies using antisera raised against several products of the cDNA fragments expressed in E. coli revealed that a region of some 800 amino acids from the N terminus of connectin is involved in its binding to the Z line in a sarcomere.

Animals↗
PubMed1996

Cholecystokinin-B/gastrin receptors mediate rapid formation of actin stress fibers.

Specific receptors for brain-gut peptide hormones, cholecystokinin (CCK) and gastrin, are expressed in a variety of human tumor cells. CCK and gastrin promote the growth of NIH3T3 cells into which the CCK-B/gastrin receptor had been introduced via a eukaryotic expression vector. In this study, we have examined the effect of CCK-8 on the actin cytoskeleton by using two mouse fibroblast cell lines expressing human CCK-B/gastrin receptors. Treatment with very low concentration of CCK-8 (10(-10) M) induced the formation of actin stress fibers within one minute. Stress fiber formation increased for 30 min. In contrast, a potent mitogen for fibroblasts, platelet-derived growth factor (PDGF), initially induced membrane ruffling and, later, a weak formation of stress fibers. Microinjection of rho GDP dissociation inhibitor or Clostridium botulinum ADP-ribosyltransferase C3 which is known to impair the function of a small GTP-binding protein, rho p21, inhibited the stress fiber formation by CCK-8 as well as by PDGF. These results indicate that CCK-B/gastrin receptor could regulate stress fiber formation in a rho p21-dependent manner. The signals from CCK-B/gastrin receptor might affect cell growth as well as cell motility or adhesion by regulating the actin cytoskeleton.

3T3 Cells↗
PubMed1996

Properties of Ryr3 ryanodine receptor isoform in mammalian brain.

Although the RNA for the third isoform (Ryr3) of ryanodine receptor (RyR), a Ca2+ release channel, is detected in specific regions of mammalian brain, little is known about the protein. We investigated Ryr3 in rabbit brain, using an antibody raised against the synthetic peptide corresponding to amino acid sequence 4375-4387 of rabbit Ryr3, the homologue of bullfrog beta-RyR. The antibody which reacted with bullfrog beta-RyR, but not with the other isoforms, Ryr1 or Ryr2, specifically precipitated a single polypeptide from rabbit brain microsomes having a size similar to beta-RyR. Sucrose gradient ultracentrifugation revealed that Ryr3 forms a homotetramer, as true of the other isoforms. Being consistent with the distribution of its RNA, Ryr3 was abundantly expressed in hippocampus, corpus striatum, and diencephalon. Ryr3 demonstrated Ca2+-dependent [3H]ryanodine binding, and caffeine increased its Ca2+ sensitivity. The Ca2+ sensitivity of Ryr3 was also enhanced in a medium containing 1 m NaCl, as observed with beta-RyR. [3H]Ryanodine binding gave an estimate of Ryr3 which would be only 2% or less of total RyR in rabbit brain. These results confirm the expression of functional Ryr3 in mammalian brain which is similar to nonmammalian beta-RyR.

Amino Acid Sequence↗
PubMed1996

Similar Ca2+ dependences of [3H]ryanodine binding to alpha- and beta-ryanodine receptors purified from bullfrog skeletal muscle in an isotonic medium.

To understand the functions of the two ryanodine receptor isoforms (alpha- and beta-RyRs) in nonmammalian skeletal muscles, we determined [3H]ryanodine binding to these isoforms purified from bullfrog skeletal muscle. In 0.17 M-NaCl medium both isoforms demonstrated similar Ca2+ dependent ryanodine binding activities, while the Ca2+ sensitivity for activation of beta-RyR was increased in 1 M-NaCl medium. This enhancement in Ca2+ sensitivity depended on the kinds of salts used. These results imply that alpha- and beta-RyRs may have similar properties as Ca2+-induced Ca2+ release channels in bullfrog skeletal muscle.

Adenosine Triphosphate↗
PubMed1996

NO donors stimulate noradrenaline release from rat hippocampus in a calmodulin-dependent manner in the presence of L-cysteine.

Nitrogen oxides (NO) such as nitric oxide have been suggested to potentiate neurotransmitter release in a variety of neuronal cells. In this study, we showed that NO donors stimulate the release of noradrenaline (NA) from rat hippocampus both in vivo and in vitro. Co-addition of NO donors (sodium nitroprusside [SNP] or S-nitroso-N-acetylpenicillamine [SNAP]) and thiol compounds (dithiothreitol [DTT] or L-cysteine) stimulated [3H]NA release from prelabeled hippocampal slices. Microdialysis in freely moving rats was used to ascertain the role of NO in control of NA release from the hippocampus in vivo. Co-addition of SNAP and L-cysteine stimulated endogenous NA release within 30 min. The concentration of NA peaked between 30-60 min to almost 3 times basal level. Another thiol compound, glutathione, had no effect on [3H]NA release in the presence of SNP or SNAP. In the presence of SNAP, the effect of L-cysteine was much higher than that of the D-isomer, although SNAP did not show stereospecificity. The effect of SNAP/L-cysteine was rapid and the maximal increase in [3H]NA release was attained 0-1 min after application, which was similar in time course to the effect of KCI. Unlike the release by KCI, SNAP/L-cysteine-stimulated NA release was independent of extracellular CaCl2. However, pretreatment with the calmodulin antagonists W-7 or trifluoperazine significantly reduced the SNAP/L-cysteine-stimulated [3H]NA release. Formation of nitric oxide and activation of guanylate cyclase by nitric oxide were not responsible for SNAP/L-cysteine-stimulated NA release. These findings suggest that NO donors stimulate NA release from the hippocampus in the presence of thiol compounds such as L-cysteine in vivo and in vitro in a calmodulin-dependent, Ca(2+)-and cyclic GMP-independent manner. The physiological roles of thiol compounds such as L-cysteine or glutathione as intermediates of NO are discussed.

Animals↗
PubMed1996

Pertussis toxin-insensitive effects of mastoparan, a wasp venom peptide, in PC12 cells.

Recent studies have shown that mastoparan, an amphiphilic peptide derived from wasp venom, modifies the secretion of neurotransmitters and hormones from a variety of cell types. Mastoparan interacts with heterotrimeric guanine nucleotide-binding proteins (G proteins) such as Gi and G(o), which are ADP-ribosylated by pertussis toxin (PTX) and thereby uncoupled from receptors. Previously, some of the effects of mastoparan including secretion were reported to be modified selectively by PTX but not by cholera toxin (CTX). In the present study, we examined the influence of bacterial toxins on the effects of mastoparan in PC12 cells. Mastoparan stimulated [3H]noradrenaline (NA) release from prelabeled PC12 cells in the absence of CaCl2, although high K+ or ATP-stimulated the release in a Ca(2+)-dependent manner. Pretreatment with CTX, not PTX, for 24 h inhibited mastoparan-stimulated [3H]NA release. Mastoparan inhibited forskolin-stimulated cyclic AMP accumulation in a dose-dependent manner, although mastoparan had no effect by itself. Pretreatment with PTX completely abolished the inhibitory effect of carbachol via Gi on cyclic AMP accumulation and partially reduced the effect of mastoparan. However, the inhibitory effect of 20 microM mastoparan was not modified by pretreatment with PTX. Thus, we investigated the effect of mastoparan on CTX-catalyzed [32P]ADP-ribosylation of proteins in PC12 cells. A subunit of CTX (CTX-A) catalyzed [32P]ADP-ribosylation of many proteins in the cytosolic fraction of PC12 cells. One of these was a 20 kDa protein, named ADP-ribosylating factor (ARF). The addition of mastoparan to assay mixtures inhibited ADP-ribosylation of many proteins including ARF and CTX-A in the presence of the cytosolic fraction. In the absence of the cytosolic fraction, however, mastoparan slightly enhanced ADP-ribosylation of bovine serum albumin and auto-ADP-ribosylation by CTX-A. Mastoparan did not inhibit ADP-ribosylation of the alpha subunit of Gs in the membrane fraction. These findings suggest that 1) mastoparan interacts with PTX-insensitive and CTX-sensitive factor(s) to stimulate NA release, and 2) mastoparan interacts with ARF inhibiting its activity to enhance the ADP-ribosylation reaction by CTX. ARF may be an exocytosis-linked G protein.

ADP-Ribosylation Factors↗
PubMed1996

Refractory thrombocytopenia with chromosome 11q23 abnormality.

Although cytopenia is a common manifestation of myelodysplastic syndrome (MDS), isolated thrombocytopenia is rare. The term "refractory thrombocytopenia" (RTC) has been proposed as a counterpart of refractory anemia. We describe here a case of RTC associated with chromosome abnormality on 11q23. A 59-year-old man was admitted because of severe thrombocytopenia. A bone marrow examination revealed an increased number of micromegakaryocytes and the absence of normal-sized megakaryocytes without obvious dysplasia in either the myeloid or the erythroid lineage. A remarkable increase of GPIIb/IIIa (CD41a)-positive precursor cells in the bone marrow was observed. Cytogenetic examination detected the chromosome abnormality, an addition on chromosome 11q23. Translocation of the HRX gene was not detectable by Southern blot analysis. The diagnostic problems of isolated thrombocytopenia and possible participation of gene(s) on chromosome 11q23 in megakaryocytopoiesis as well as early hematopoiesis are discussed.

Biopsy, Needle↗
PubMed1996

Changes of GTP binding proteins, not neurofilament-associated proteins, in the brain of the neurofilament-deficient quail, "Quiver".

A neurofilament (NF)-deficient mutant of the Japanese quail was named "Quiver", as it showed generalized quivering as a clinical sign. NF consists of three major subunits; low, middle and high. We previously reported that the noradrenaline and 5-hydroxytryptamine content in the neostriatum of the Quiver's brain was different from that in the normal quail, although disappearance of the three NF proteins occurred in all areas of the Quiver's brain. Thus, NF-related proteins may show considerable changes in the specific sites of Quiver's brain. In this study, an examination was made of the changes in NF-related proteins in the Quiver, by immunoblotting analysis. The amounts of cyclin-dependent kinase 5 (cdk5), which phosphorylates NF proteins, and tau which is a substrate of cdk5, in the neostriatum of the Quiver, were essentially the same as those in the normal quail, although NF proteins could not be detected in the Quiver. The amount of alpha-tubulin in the Quiver's brain was similar to that in the normal quail. Next, we investigated the changes of GTP binding (G) proteins in the Quiver's brain, because cytoskeletal components such as tubulin and F-actin bind with G proteins. [32P]ADP-ribosylation of G proteins (Gs by cholera toxin and Gi/G0 by pertussis toxin) in the neostriatum of the Quiver increased significantly, although alpha subunits of G proteins showed no change by immunoblotting analysis. The ratios of the trimer form in G proteins thus appear to increase more in the NF-deficient Quiver brain than in the brain of the normal quail. The G proteins-mediated adenylate cyclase activities were the same in the brain of both the Quiver and the normal quail. Possible interactions between NFs and G proteins are discussed.

Adenosine Diphosphate Ribose↗