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Biomedical subjects

A Watanabe

Publications and source records attributed to A Watanabe.

At least 757 records · Page 42Linked to original sources
PubMed1988

Wakefulness during the induction with high-dose fentanyl and oxygen anesthesia.

The purpose of this study was to investigate the state of wakefulness during the induction of anesthesia with high-dose fentanyl using the isolated forearm technique. Ten patients scheduled for elective cardiovascular surgery were premedicated with morphine (0.15 mg/kg) and scoploamine (0.3-0.4 mg) intramuscularly one hour before induction. The induction of anesthesia was performed by intravenous administration of 100 micro g/kg of fentanyl in 15 min or over. The pneumatic tourniquet applied on the left upper arm was inflated to 220-240 mmHg after 10 micro g/kg of fentanyl was given and then pancuronium was administered. Verbal commands were given to the patient after 25, 50, 75 and 100 micro g/kg of fentanyl was administered. Eight patients out of 10 responded to the verbal commands after administration of 25 micro g/kg of fentanyl. Six patients also responded after administration of 100 micro g/kg of fentanyl and diazepam 5 mg was given to prevent tachycardia and rigidity during endotracheal intubation. Muscle rigidity and tachycardia were noticed in three and four patients respectively. These complications disappeared by diazepam administration. It was noted that wakefulness frequently occurred during the induction by high-dose fentanyl and oxygen anesthesia. To prevent such wakefulness therefore, it is necessary to use anesthetic supplements which do not cause cardiovascular depression.

Journal Article↗
PubMed1988

Synthesis and assembly of H+-ATPase complex by isolated "rough" thylakoids.

The synthesis and assembly of chloroplast H+-ATPase complex were studied by analyzing the incorporation of [35S]methionine into the constituent subunits with isolated intact chloroplasts and with thylakoid membranes that had been prepared from the chloroplasts so that they would retain ribosomes. The complex was isolated from thylakoids after labeling and identified by immunoprecipitation with an antiserum specific to CF1. The mechanism for the assembly of the complex was demonstrated to be active in the isolated chloroplasts by the following observations: the plastid genome-regulated subunits (alpha, beta, epsilon, I, and III) were labeled by in organello translation and recovered with the complex, and three other subunits (gamma, delta, and II) were labeled when intact chloroplasts were incubated with translation products from polyadenylated RNA. The two largest subunits, alpha and beta, were translated on thylakoid-bound ribosomes when the thylakoid membranes were incubated with soluble factors from Escherichia coli. They were recovered with the H+-ATPase complex, suggesting that they are translated on the bound ribosomes in the chloroplast, and that the isolated membranes retain the ability to assemble a complete complex. Provided that these observations are the result of de novo assembly of the complex, the imported and processed nuclear-coded subunits are presumed to be pooled not in stroma but on the membrane.

Cell Fractionation↗
PubMed1988

Amino acid neurotransmitters and their receptors in the brain synaptosomes of acute hepatic failure rats.

Ammonia contents in the brain stem and prosencephalon markedly increased in a rat model of acute hepatic failure induced by partial hepatectomy following CCl4 intoxication. In hepatic failure rats, synaptosomal glutamic acid (excitatory amino acid neurotransmitter) contents decreased significantly in the prosencephalon, and GABA (inhibitory amino acid neurotransmitter) contents decreased significantly in the brain stem. The molar ratio of glutamic acid to glutamine significantly diminished in the brain stem. Glutamic acid decarboxylase activity in the synaptosomes and the binding of [3H]glutamic acid and [3H]GABA to synaptosomal membrane preparations were unchanged in acute hepatic failure rats. These results indicate than an insufficiency of both excitatory and inhibitory neurotransmitter amino acids is induced by high ammonia contents in the synaptosomes of the brain stem during acute hepatic failure.

Acute Disease↗
PubMed1988

Increase in urinary beta-phenylethylamine preceding the switch from mania to depression: a "rapid cycler".

beta-Phenylethylamine (PEA), an endogenous amphetamine-like substance, is known to increase central catecholamine metabolism and has been hypothesized to have an etiological importance in affective disorders. A case of a "rapid cycler" who showed increased PEA excretion before the switch from mania into depression was reported. In order to evaluate whether the patient's cycle of moods could be prevented by modulating PEA metabolism, carbidopa (peripheral dopa decarboxylase inhibitor) and safrazine (monoamine oxidase inhibitor) were administered during the manic and depressive periods of the patient, respectively. Carbidopa exacerbated the manic symptoms, although it decreased PEA excretion. Safrazine induced the increase of PEA without any beneficial effect on the depressive symptoms. These findings may suggest that PEA plays the role of a biochemical trigger in the switch mechanism of a rapid cycler, especially in the switch from mania to depression.

Adult↗
PubMed1988

Senescence-specific increase in cytosolic glutamine synthetase and its mRNA in radish cotyledons.

Changes in the levels of cytosolic and chloroplastic isoforms of glutamine synthetase were examined in senescing radish (Raphanus sativus L. cv Comet) cotyledons by immunoblotting analysis using antibodies raised separately against maize glutamine synthetase isoforms. Translatable mRNAs for these isoforms were also examined by analyzing translation products from poly(A)(+) RNA in a wheat germ system with the antibodies. The relative content of cytosolic isoform (GS(1)) increased twofold in the cotyledons that were placed in the dark for 72 hours to accelerate senescence, while that of chloroplastic isoform (GS(2)) declined to half of its initial level. The dark-treatment also increased the relative level of translatable mRNA for GS(1) sevenfold after 72 hours, and decreased rapidly that for GS(2) and for other nuclear-coded chloroplast proteins as well. Cotyledons also accumulated GS(1) mRNA when they became senescent after a lengthy growth period under continuous light. These observations suggested that GS(1) genes were activated, while those for GS(2) were repressed, and eventually the population of the enzyme was altered in senescent cotyledonary cells. The role of increased cytosolic enzyme is discussed in relation to the nitrogen metabolism in senescent leaves.

Journal Article↗
PubMed1988

Quinone derivatives lower blood and liver acetaldehyde but not ethanol concentrations following ethanol loading to rats.

A rise in blood and liver acetaldehyde concentrations following an intragastric administration of ethanol to rats was significantly inhibited when the quinone derivatives 2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone (ubidecarenone, coenzyme Q10), 4,5-dihydro-4,5-dioxo-1H-pyrrolo[2,3-f]quinoline-2,7,9-tricarboxylic acid (pyrroloquinoline quinone, PQQ) and 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone) were injected intraperitoneally, prior to ethanol load, at a dose of 10, 11.5 and 30 mg/kg of body weight, respectively. When acetaldehyde was incubated in vitro with 1,4-benzoquinone (3.7-13.0 mM) or PQQ (1.4-4.9 mM) at 0 and 40 degrees C, the acetaldehyde concentrations slowly decreased with incubation time at 40 degrees C. The results suggest that low acetaldehyde concentrations following ethanol load are due to an accelerated oxidation of acetaldehyde by PQQ in the liver and the circulating blood.

Acetaldehyde↗
PubMed1988

Type IV collagen-degrading enzyme activity in human serum.

Type IV collagen-degrading enzyme activity was detected in human serum. Serum was preincubated with 4-aminophenylmercuric acetate and trypsin to activate the enzyme prior to assay. Type IV collagen, purified from human placentas and radiolabeled with [1-14C] acetic anhydride, was used as the substrate. The enzyme activity was measured at pH 7.5 and inhibited by treatment with ethylenediaminetetraacetic acid or heat. The assay of type IV collagen-degrading enzyme in human serum might be useful for estimating the degradation of type IV collagen.

Blood Proteins↗
PubMed1988

Effect of branched-chain amino acid on 15N incorporation into liver and skeletal muscle proteins following [15N]-ammonium chloride administration to carbon tetrachloride-intoxicated rats.

The effect of branched-chain amino acid (BCAA) on protein synthesis and nitrogen metabolism in liver and skeletal muscle was evaluated by an intraperitoneal injection of [15N]ammonium chloride (15NH4Cl) to carbon tetrachloride (CCl4)-intoxicated rats. The 15NH4Cl was bolusly injected at a dose of 6 mg/100 g body weight one hour after an amino acid solution containing leucine and valine (150 mM each, abbreviated as BCAA), phenylalanine and alanine (150 mM each, PA), 120 mM leucine and 30 mM valine (Leu-rich) or 120 mM valine and 30 mM leucine (Val-rich) was administered intragastrially at a dose of 2.5 ml each/100 g body weight. The 15N-enrichment in the protein fraction of the liver was higher in CCl4-BCAA group than CCl4-PA group. The Leu-rich solution was found more effective in enhanced incorporation of 15N into liver and skeletal muscle proteins. The disappearance rate of [15N]urea from the plasma, which was influenced by the synthesis from 15NH3 and the excretion into urine, was much faster in the CCl4-BCAA group than CCl4-PA group. In Leu-rich group, both 15N incorporation into non-protein fraction of skeletal muscle and disappearance rate of plasma urea-15N were greater than those in Val-rich group. The results suggest that BCAA, particularly leucine, has beneficial effects on protein synthesis and ammonium detoxification in liver-injured rats.

Amino Acids, Branched-Chain↗
PubMed1988

Exposure of platelet fibrinogen receptors by a monoclonal antibody to CD9 antigen.

We found that a monoclonal antibody to CD9 antigen, PMA2, induces fibrinogen binding to platelets and examined the mechanism for this. That PMA2 recognized the CD9 antigen was confirmed by its immunoblot-reactivity with a 24,000-dalton protein, reactivity with platelets and common acute lymphoblastic leukemia (ALL) cells, and competitive binding with the ALB6 antibody known as the CD9 antibody. At saturation, PMA2 bound to approximately 46,000 sites per platelet. The binding of 125I-fibrinogen to platelets occurred in a PMA2 concentration-dependent manner and was blocked by EDTA or an anti-glycoprotein (GP)IIb-IIIa monoclonal antibody. PMA2-stimulated platelets caused ATP secretion and thromboxane B2 synthesis under non-stirred conditions. The role of secreted ADP and thromboxane in fibrinogen-binding and subsequent platelet aggregation was studied using creatine phosphate/creatine phosphokinase (CP/CPK) and aspirin. CP/CPK or aspirin alone reduced fibrinogen binding to 20% to 30%; however, this binding was sufficient to support full platelet aggregation. Combined treatment with CP/CPK and aspirin abolished fibrinogen binding and aggregation. These results demonstrate that the binding of IgG molecules to the CD9 antigen exposes fibrinogen receptors through both secreted ADP and thromboxane and that either one of both can expose the receptors to an extent sufficient to aggregate platelets.

Animals↗