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Biomedical subjects

T Mino

Publications and source records attributed to T Mino.

53 records · Page 3Linked to original sources
PubMed1995

Phosphorylation of calponin mediated by protein kinase C in association with contraction in porcine coronary artery.

Calponin is an actin-associated regulatory protein in smooth muscle. We report that both endothelin-1 (ET-1) and phorbol 12, 13-dibutyrate (PDBu) caused a significant increase in phosphorylation of calponin during contraction of porcine coronary artery, while high levels of KCl were ineffective. This phosphorylation was predominantly catalyzed by activation of protein kinase C(PKC). In addition, the level of phosphorylation of calponin increased closely in association with the size of the contractile force induced by PDBu. Thus, the phosphorylation of calponin in vivo by PKC might modulate in part the contraction of smooth muscle that occurs in response to ET-1 or PDBu.

Animals↗
PubMed1994

Application of the desulfurization of phenothiazines for a sensitive detection method by high-performance liquid chromatography.

A simple and sensitive high-performance liquid chromatographic (HPLC) method for the determination of phenothiazine (PHE) is described. PHE is converted to diphenylamine (DIP) by desulfurization with Raney nickel catalyst. DIP is highly sensitive to electrochemical detection. The calibration graph for PHE quantification after desulfurization was linear between 0.1 and 2.0 ng per injection. The detection limit (signal-to-noise ratio = 3) of PHE after desulfurization was 10 pg, which is twenty times higher than that of the parent compound PHE. The proposed desulfurization technique was applied to other PHE-related compounds. The structural confirmation of the desulfurized product of PHE was carried out by LC-MS using atmospheric pressure chemical ionization.

Calibration↗
PubMed1993

Calponin phosphatase from smooth muscle: a possible role of type 1 protein phosphatase in smooth muscle relaxation.

Smooth muscle myosin bound phosphatase (MBP) purified from chicken gizzard, which is a holoenzyme of type 1 delta protein phosphatase and dephosphorylated intact myosin, catalyzed the dephosphorylation of calponin phosphorylated by protein kinase C (PK-C). The Km of MBP for calponin was 0.6 microM and the Vmax was 350 nmol/min/mg. All of the multiple sites of phosphorylation by PK-C of calponin were completely dephosphorylated by MBP. Functionally, calponin dephosphorylated by MBP recovered its inhibitory effect on the actin-activated Mg(2+)-ATPase activity of myosin. Therefore, these results suggest that a type 1 delta protein phosphatase causes relaxation of smooth muscle by the dephosphorylation not only of myosin but also of calponin.

Animals↗
PubMed1993

Identification of the regulatory site in smooth muscle calponin that is phosphorylated by protein kinase C.

F-actin and tropomyosin inhibited the phosphorylation of calponin by protein kinase C, and the phosphorylation reduced the binding of calponin to F-actin and tropomyosin. Labeled phosphate from [gamma-32P]ATP was retained both on the chymotryptic NH2-terminal 22-kDa fragment, which contains the actin-, tropomyosin-, and calmodulin-binding regions, and on the COOH-terminal 12-kDa fragment. Fractionation of tryptic 32P-labeled peptides by high performance liquid chromatography allowed isolation of three phosphopeptides (designated T1, T2, and T3), each of which was located in three repeating amino acid motifs of calponin. Both the relative initial rates and extent of phosphorylation decreased in the order T2 > T3 > T1. Both serine and threonine residues were phosphorylated in T1 (GASQAGMTAPGTK), and only a threonine residue was phosphorylated in T2 (FASQQGMTAYGTR) and in T3 (GASQQGMTVYGLPR). As the 22-kDa fragment contained only T2, the phosphorylation site in T2 appeared to regulate the binding of calponin to F-actin and tropomyosin. The amino acid sequence of T2 indicates that protein kinase C phosphorylates Thr184. Thus Thr184 is the preferred site of phosphorylation and is functionally the most important of the sites phosphorylated by protein kinase C in smooth muscle calponin.

Actins↗
PubMed1989

The usefulness of systemic administration of recombinant human tissue-type plasminogen activator in femoral arterial thrombolysis of rabbits.

The thrombolytic effect of locally or systemically administered recombinant human tissue-type plasminogen activator (rt-PA) was investigated in comparison with the effect of tissue culture urokinase (TCUK), using a model of femoral artery thrombosis in rabbits. An 125I-labeled fibrinogen thrombus was formed in the femoral artery following injury of the intima by diluted sulfuric acid, and thrombolytic activity was evaluated one hour after the end of infusion of the agents. Local infusion of rt-PA (500-10,000 IU/kg) and TCUK (10,000 IU/kg) induced a marked thrombolysis. When rt-PA and TCUK were injected systemically in a high dose (200,000 IU/kg), rt-PA but not TCUK had a significant thrombolytic activity. In these cases, rt-PA was not accompanied by systemic activation of the fibrinolytic system, as evaluated by unaltered levels of alpha 2-antiplasmin in the plasma, while TCUK led to a substantial decrease in the alpha 2-antiplasmin level. These results suggest that systemically administered rt-PA but not TCUK induce a significant thrombolysis without systemic activation of the fibrinolytic system in cases of peripheral artery thrombosis.

Animals↗
PubMed1983

Changes of lipid peroxidation in mouse brain crude synaptosomal preparations in relation to the development and disappearance of tolerance to ethanol.

A single dose of ethanol induced a bimodal increase of Fe++- and ascorbic acid-stimulated lipid peroxidation in mouse brain crude synaptosomal preparations. This effect of ethanol was lost in preparations from ethanol tolerant animals and reappeared when the animals recovered from tolerance after withdrawal from ethanol treatments. The parallel changes in lipid peroxidation of brain crude synaptosomal preparations with the development and disappearance of tolerance to ethanol imply that the effect of ethanol on brain lipid may be directly associated with its mechanism in the CNS.

Animals↗
PubMed1982

[Studies on the physical dependence liability to guanabenz].

The physical dependence liability of guanabenz, a hypotensive agent with central noradrenergic alpha 2-agonistic activity, was investigated. 1) Guanabenz showed a potent analgesic effect nearly equipotent to morphine by the modified Haffner's method, and repeated p.o. treatment resulted in the development of tolerance to the effect. 2) In the combined treatment of guanabenz with morphine or hexobarbital, it potentiated morphine analgesia and prolonged hexobarbital hypnosis in a dose dependent manner. 3) The natural withdrawal signs appearing in morphine or barbital dependent mice was suppressed by guanabenz; however, the effect was accompanied by a marked loss of body weight and weakness of the animals, and especially the dose required for the suppression of barbital withdrawal signs was extremely high and was even lethal in some cases. A substitution test in barbital dependent mice showed that guanabenz could not substitute for barbital. In the primary dependence test after 30 days oral treatment with guanabenz, no appreciable withdrawal signs were observed after discontinuation of the administration. Thus, from the results obtained in the present experiments, it is revealed that guanabenz possesses no physical dependence liability of the morphine or barbital type.

Analgesics↗
PubMed1982

Effect of phospholipase C on lipid peroxidation of rat liver mitochondria.

Effect of phospholipase C on lipid peroxidation in rat liver mitochondria was studied. The lipid peroxidation of mitochondria in the presence of ascorbic acid and Fe2+ (FeSO4) was inhibited by approximately 45% after pretreatment of phospholipase C for 30 min. However, when phosphatidylcholine instead of mitochondria was used for the peroxidation, phospholipase C showed no inhibition on lipid peroxidation. Therefore, it may be considered that phospholipids in mitochondria are modified in diglyceride structure after digestion with phospholipase C, and the diglyceride is poor substrate for lipid peroxidation in mitochondria.

Animals↗
PubMedDate not supplied

Longitudinal growth study of male Japanese junior high school athletes.

The aim of this study was to establish the pattern of adolescent growth in height of male Japanese athletes, and to compare their growth with appropriate controls. The sample consisted of 126 baseball, 39 basketball, 83 soccer, and 53 volleyball players, and 36 nonathletes. The data were collected retrospectively in six public schools in Fukui Prefecture of Western Japan between 1970 and 1987. All subjects were measured at yearly intervals between the age of 6 and 18 years. The total number of measurement occasions for the 337 subjects amounted to 4,134. Athletes trained between 13 and 18 h/week. Individual growth patterns were determined by fitting Preece Baines model I to each individual's serial data. Various biological parameters were derived from the fitted curves. The results indicated that the average growth pattern of these adolescent athletes did not differ substantially from the control group. Volleyball players were significantly taller at 18 years (+3 cm) than the nonathletes (Student's t-test, P < 0.05). Soccer players showed a slight tendency towards late maturation with age at take-off and at peak velocity about half a year later than in nonathletes (Student's t-test, P < 0.05). The 2.3 cm gain in body height due to the later onset of the pubertal growth spurt in soccer players was counterbalanced by a 0.7 cm smaller prepubertal height and a 0.9 cm smaller adolescent gain, so that they ended up slightly, but not significantly, taller than the controls (+0.7 cm). The small differences in growth pattern observed between the nonathletes and the various sports suggest that, in contrast with top-level athletes, body size and maturation rate were not important selective factors in the various groups of athletes of the present study.

Adolescent↗
PubMedDate not supplied

PHA production by activated sludge.

The production of polyhydroxyalkanoate by anaerobic-aerobic activated sludge was reviewed concentrating on the biochemical mechanisms and on the trials to increase polyhydroxyalkanoate (PHA) content in activated sludge. The anaerobic aerobic activated sludge system selects microorganisms with the capabilities to couple glycolysis, polyphosphate degradation, and PHA accumulation for anaerobic substrate uptake. Some of the PHA-related metabolisms observed there have not been seen in pure cultures so far. Such metabolisms are the formation of PHA containing 3-hydroxy-2-methylvalerate, and '3-hydroxyvalerate fermentation' in which glucose or glycogen is converted to 3-hydroxyvalerate-rich PHA while yielding energy. The PHA content of activated sludge can be increased up to 62% by applying a microaerophilic-aerobic activated sludge process. PHA production by activated sludge is worth investigation.

Aerobiosis↗