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Biomedical subjects

J Yoshitake

Publications and source records attributed to J Yoshitake.

At least 73 records · Page 4Linked to original sources
PubMed1987

Neutrophils become refractory to phorbol myristate acetate when treated with Ca2+-ionophore and Ca2+.

Human neutrophils deprived of divalent cations by treatment with ionophore A23187 in the presence of ethylene glycol bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA) showed superoxide release when they were preincubated with calcium and then treated with the ionophore. The release was not observed when the ionophore was added first and then calcium was added more than 5 min later. The absence of the release in this case can be ascribed to a refractoriness of the cells to stimuli, because the cells did not release superoxide on stimulation with phorbol myristate acetate (PMA). The cells pretreated with either calcium or the ionophore alone did release superoxide on addition of PMA. The refractoriness of the cells to PMA depended on the concentrations of calcium and the ionophore and on the time interval between the two treatments. Calcium could be replaced with Cd2+ but not with Mg2+, Ba2+, or Sr2+. The release of granular enzymes was observed when the depleted cells were pretreated with the ionophore and then with calcium. These observations indicate that calcium has dual effects on the superoxide release of neutrophils, i.e., it stimulates the cells and makes them refractory to stimuli, depending on the time interval after the addition of the ionophore, and it also regulates the enzyme release by a different mechanism.

Aminoquinolines↗
PubMed1986

Calcium channel antagonist induced inhibition of superoxide production in human neutrophils. Mechanisms independent of antagonizing calcium influx.

Three calcium channel antagonists, verapamil, diltiazem and nisoldipine, inhibited superoxide production in human neutrophils that were stimulated by phorbol 12-myristate 13-acetate (PMA) in a buffered saline lacking calcium. Concentrations of these drugs giving 50% control activity (IC50) were 0.3, 0.45 and 0.01 mM respectively. This inhibition was also observed in the presence of ethylene glycol bis (beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) and was not reversed by the addition of calcium. This suggests that calcium channel antagonists inhibited superoxide production independently of extracellular calcium. These calcium channel antagonists inhibited the mobilization of membrane-associated calcium, and protein phosphorylation probably catalyzed by C-kinase, both of which are thought to be involved in the signal transmission for the induction of superoxide production. Calcium channel antagonists also inhibited NADPH oxidase, responsible for superoxide production, with IC50 = 0.5, 3 and more than 0.08 mM, respectively, for verapamil, diltiazem and nisoldipine. The results indicate that calcium channel antagonists inhibit superoxide production by affecting not only the catalytic activity by also the activation of NADPH oxidase. Inhibition of superoxide production by calcium channel antagonists suggests that these antagonists do not affect cell functions merely by affecting calcium influx.

Calcium↗
PubMed1986

Cinchocaine and amethocaine inhibit activation and activity of superoxide production in human neutrophils.

Local anaesthetics, cinchocaine and amethocaine, inhibited superoxide production in human neutrophils stimulated by phorbol ester, with IC50 (concentration of a drug giving 50% activity of control) values of 0.2 and 0.6 mmol litre-1, respectively. These anaesthetics inhibited protein (de)phosphorylation and mobilization of membrane-associated calcium, both of which are probable signal transmission mechanisms for the induction of superoxide production. Local anaesthetics also inhibited NADPH oxidase, responsible for superoxide production, with IC50 = 0.3 and 0.9 mmol litre-1, respectively. The results indicate that cinchocaine and amethocaine inhibit superoxide production in human neutrophils by affecting not only the catalytic activity, but also the activation, of NADPH oxidase.

Blood Proteins↗
PubMed1986

NADPH-dependent superoxide-forming oxidase in phagocytic vesicles of human monocytes.

Phagocytic vesicles with superoxide-forming NADPH oxidase activity were obtained from human monocytes phagocytosing oil droplets. The superoxide-forming activity in the monocyte vesicles increased for the first 5 min during incubation with oil droplets and remained constant for 30 min. NADPH-dependent activities of 2,6-dichlorophenol-indophenol (DCIP) reduction and ubiquinone-1 (Q1) reduction were found in the vesicles and the activities were closely associated with the superoxide-forming oxidase. The values of apparent Km for NADPH of these three activities were essentially the same and the activities were inhibited with a similar pattern by p-chloromercuribenzoate and a cationic detergent, cetyltrimethylammonium bromide. The activities were extremely labile and the DCIP reductase activity was most labile. The superoxide-forming oxidase and the Q1 reductase could be extracted with a mixture of deoxycholate and Tween-20. The extracted activities were not enhanced by the addition of FAD.

2,6-Dichloroindophenol↗
PubMed1986

Inhibition of superoxide production and Ca2+ mobilization in human neutrophils by halothane, enflurane, and isoflurane.

The inhibitory effects of three inhalation anesthetics, i.e., halothane, enflurane, and isoflurane, on superoxide production and the intracellular mobilization of calcium in human neutrophils were studied. The superoxide production induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) was inhibited by the anesthetics, but the binding of FML[3H]P to the cells and the superoxide-forming NADPH oxidase of the phagocytic vesicles were not inhibited. The inhibition of the cellular superoxide production was partially reversed by the addition of a calcium ionophore, A23187. The increase in intracellular free calcium monitored by a calcium-sensitive fluorescent probe, quin-2 and the release of calcium from hydrophobic environment monitored by chlortetracycline were inhibited dose dependently by the anesthetics. These observations suggest that decreased mobilization of intracellular Ca2+ is one of the mechanisms by which the anesthetics inhibited the superoxide production of human neutrophils stimulated by FMLP.

Calcimycin↗
PubMed1986

Differential count of 5,000 leukocytes for acute nonlymphocytic leukemia patients during remission.

In order to find the level of leukemic cells during remission a differential count of 5,000 leukocytes was made in 91 acute nonlymphocytic leukemia cases during their first complete remission. Patients were divided into three groups according to the level of leukemic cells, i.e., 0-1/5,000, 2-4/5,000 and 5-/5,000. A close correlation was observed between the survival of patients and the level of leukemic cells and their tendency to decrease or increase during remission. All patients in whom leukemic cells rose from 0-1/5,000 to a level higher than 8/5,000 suffered a documented relapse after 4-8 weeks. This method appears to be a good supportive examination for acute leukemia patients during remission.

Acute Disease↗
PubMed1985

Lack of effects of d-tubocurarine and pancuronium on the slow action potential of the guinea pig papillary muscle.

Inotropic effects of non-depolarizing muscle relaxants were examined with guinea pig ventricular papillary muscle depolarized to -47 mV in high K Ba-Tyrode solution. Field stimulation of 0.1 Hz elicited the slow action potential, a measure of the calcium current. The amplitude, the duration at 0 mV level and dV/dt of the action potential were monitored together with the contractile tension. Amelizol (3 mg X ml-1 d-tubocurarine (d-tc) and 5 mg X ml-1 chlorobutanol) depressed the four functions in a dose-dependent manner, while crystalline d-tc did not. Chlorobutanol (the antimicrobial preservative) had the same effects as Amelizol. Neither Mioblock (2 mg X ml-1 pancuronium and unpublished preservative) nor crystalline pancuronium altered the functions. These findings suggest that the negative inotropic effect of Amelizol is not due to d-tc but to chlorobutanol, which may exert its effect by depressing the calcium current. The lack of change in the slow action potential seen with pancuronium may indicate no direct effect on the calcium current, thereby further suggesting absent direct beta-adrenomimetic action of this agent.

Action Potentials↗
PubMed1985

The effects of ketamine on venous capacitance in rats.

The purpose of this study was to examine the effects of ketamine and pentobarbital on venous capacitance in rats. Venous capacitance was assessed by measuring the mean circulatory filling pressure (MCFP) at three levels of blood volume in conscious rats as well as during anesthesia with ketamine (125 mg/kg, ip) or pentobarbital (50 mg/kg, ip). MCFP was measured during brief periods of circulatory arrest produced by inflating an indwelling balloon in the right atrium. MCFP was maintained during ketamine anesthesia at a level similar to that measured in conscious animals, while it was decreased (P less than 0.01) during pentobarbital anesthesia both at normal blood volume and following hemorrhage. These results suggest that ketamine did not alter but pentobarbital increased venous capacitance. The slope of the regression line relating MCFP and blood volume was not altered by ketamine but was increased (P less than 0.05) by pentobarbital, which suggests that ketamine did not alter but pentobarbital decreased total vascular compliance. These results suggest that ketamine maintains but pentobarbital decreases venous tone.

Animals↗
PubMed1985

Reduction of the slow inward current of isolated rat ventricular cells by thiamylal and halothane.

The barbiturates and halothane exert a negative inotropic effect on the myocardium. A reduction in the slow inward current, carried mainly by calcium ions, is an important factor for the underlying mechanism because the calcium current during the action potential provides the calcium ions for accompanying contraction, supplies Ca ions to the sarcoplasmic reticulum for subsequent contractions, and induces Ca release from the store site. It has been suggested that reduction in the slow inward current caused by anesthetics is indicated by depression of the slow action potential of the partially depolarized myocardium. In order to assess directly the effect of anesthetics on the slow inward current, we carried out voltage clamp experiments with single isolated rat ventricular cells obtained by an enzymatic dissociation method. Thiamylal (10(-4) mol . l-1) and halothane (1%) decreased the slow inward current to 60 +/- 5% (mean +/- s.d., n = 8) and to 65 +/- 10% (mean +/- s.d., n = 8) of the control value, respectively, without changing the configuration of the current-voltage curve. The results provide further evidence for anesthetic reduction of the slow inward current of the myocardium, and suggest that the negative inotropic effect is at least partly due to the reduction in that current.

Action Potentials↗
PubMed1985

Cloning of a developmentally regulated element from alkalophilic Bacillus subtilis DNA.

An alkalophilic Bacillus DNA bank cloned in an expression probe plasmid, pGR71, was screened for the presence of developmentally regulated genetic elements. A 508-base pair HindIII fragment isolated from this bank in plasmid pGR71-5 expressed plasmid-encoded chloramphenicol resistance only during the sporulation phase of a Bacillus subtilis host grown on Schaeffer medium. This developmentally regulated expression was altered in spo0E and spo0H mutants which had very low levels of chloramphenicol acetyltransferase activity relative to the wild type or other spo0 mutants. We determined the nucleotide sequence of the entire 508-base pair fragment and located the site of regulated transcription initiation by high-resolution S1 nuclease mapping of the in vivo transcript. The deduced promoter sequences upstream from this start site were 5'C-G-A-A-T-C-A-T-G-A3' at -10 and 5' A-G-G-A-A-T-C3' at -35. This transcript was not detected in spo0E or spo0H mutants, indicating that the products of these genes control developmentally regulated chloramphenicol acetyltransferase expression at the level of transcription.

Acetyltransferases↗
PubMed1985

Association of second primary leukemias with the method of treatment of the first primary cancer.

A case-control study of the association between chemotherapy and/or radiotherapy for the first primary cancer and the second primary leukemia was made. All leukemia cases were collected from the cancer patients' file of the Osaka Cancer Registry which listed more than 220,000 cases during the 1965-82 period. Among the 2,765 leukemia patients, 46 had other (first) cancers. Two controls were selected from the cancer patients' file for each of the first primary cancers of 46 cases, with which they were matched in age, sex, cancer site, date of diagnosis, size of the treating hospital and survival period. Comparing the method of treatment of the first primary cancer in the cases and the controls, the proportion of patients treated by chemotherapy and/or radiotherapy was significantly higher among the cases than among the controls when the interval of the two primary cancers was 5 years or more.

Adolescent↗