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M Tsuboi

Publications and source records attributed to M Tsuboi.

At least 19 recordsLinked to original sources
PubMed1992

Mechanism of carbachol-stimulated diacylglycerol formation in rat parotid acinar cells.

We studied the relationship between phosphoinositide hydrolysis, phosphatidylcholine hydrolysis, and sn-1,2-diacylglycerol (DAG) formation in response to carbachol stimulation in rat parotid acinar cells. Previously, we demonstrated that DAG formation stimulated with 1 microM carbachol was biphasic: the first peak occurred at 5 min and the second one at 20 min. It was also demonstrated that the second peak was regulated in part by a calmodulin/protein kinase C-dependent mechanism. Based on the kinetic analysis of DAG formation and [32P]phosphoinositide breakdown, the first peak of carbachol (1 microM)-stimulated DAG accumulation was found to be related to the breakdown of [32P]phosphatidylinositol 4-monophosphate ([32P]PIP) and [32P]phosphatidylinositol 4,5-bisphosphate ([32P]PIP2). The second peak was found to be related to [32P]PIP2 breakdown. Carbachol stimulated the release of [3H]phosphocholine into the medium, indicating that the predominant pathway for phosphatidylcholine hydrolysis was via phospholipase C. Moreover, carbachol stimulated the release of [3H]choline metabolites in a time- and dose-dependent manner. This agonist slightly stimulated the release of [3H]ethanolamine metabolites. A calmodulin/protein kinase C-dependent mechanism was also studied and was found to be involved in carbachol-stimulated phosphatidylcholine hydrolysis; W-7, a calmodulin inhibitor and staurosporine, a protein kinase C inhibitor, inhibited the carbachol (1-microM)-induced release of [3H]choline metabolites at 20 min in a dose-dependent manner, but did not have inhibitory effects at 5 min. These results suggest that the first peak of DAG accumulation induced by carbachol is predominantly associated with the breakdown [32P]PIP and of [32P]PIP2 and that the second peak is predominantly associated with [32P]PIP2 breakdown and phosphatidylcholine hydrolysis.

Alkaloids↗
PubMed1992

Ca2+ potentiates corticotropin-induced, but not isoproterenol-induced, [3H]guanosine diphosphate release in rat adipocyte membranes.

EGTA abolished corticotropin (ACTH)-stimulated adenylate cyclase in rat adipocyte membranes. In contrast, the potency of guanosine triphosphate (GTP) stimulation of adenylate cyclase activated with ACTH was greater in the presence of Ca2+ (1 mmol/L). EGTA (1 mmol/L) powerfully inhibited ACTH-stimulated [3H]guanosine diphosphate (GDP) release from membranes prelabeled with [3H]GTP in the presence of isoproterenol (ISO) or ACTH, whereas Ca2+ significantly increased it. In contrast, neither EGTA nor Ca2+ affected ISO-stimulated [3H]GDP release. These data clearly show that Ca2+ is necessary for the binding of ACTH to its receptor, and that Ca2+ stimulates the interaction of the ACTH-occupied receptor with GTP-binding proteins.

Adenylyl Cyclases↗
PubMed1992

Effect of mammalian lignans on fMLP-induced oxidative bursts in human polymorphonuclear leucocytes.

We examined the effects of mammalian lignans, enterolactone, prestegane B and 2,3-dibenzylbutane-1,4-diol (DBB) on superoxide production and luminol-dependent chemiluminescence (LCL) response in human polymorphonuclear leucocytes (PMNs). The three lignans had no direct effect on the responses of human PMNs. DBB and prestegane B enhanced the superoxide production and LCL response induced by formylmethionyl-leucyl-phenylalanine (fMLP), but enterolactone inhibited fMLP-induced effects. The effects of DBB were stronger than those of prestegane B and the effects of DBB were inhibited by bromophenacyl bromide, mepacrine, N-(6-aminophenyl)-5-chloro-1-naphthalene, sulphonamide and trifluoroperazine, but not by gossypol, nordihydroguaretic acid, indomethacin, staurosporine, 1-(5-isoquinolinesulphonyl)-2-methylpiperazine dihydrochloride or (R,S)-2-methoxy-3-(octadecyl-carbamoyloxy)-propyl-2-(2-thiazoli o)-ethylphosphate. These results suggest that DBB primes the responses of human PMNs, and the priming effect is caused by the activation of phospholipase A2--and Ca(2+)-calmodulin-pathways, but not by the activation of lipoxygenase, cyclo-oxygenase and protein kinase C or by the release of platelet activating factor.

Humans↗
PubMed1992

Influence of melatonin on reproductive behavior in male rats.

The influence of melatonin on reproductive behavior was examined by administering it to pinealectomized male rats for 30 consecutive days. After the 30-d administration of melatonin or vehicle, each male rat was introduced into a female rat's cage on the day of proestrus and allowed to mate overnight. All rats administered the vehicle and the pinealectomized rats copulated; five of the twelve melatonin (8.0 mg/kg)-treated rats did not copulate. These findings suggest that melatonin inhibits the reproductive behavior of male rats.

Animals↗
PubMed1992

[Strain differences of mice in learning of swimming behavior and effect of hemicholinium and vasopressin. Observation by a simple water maze apparatus].

In order to determine the strain differences in learning of swimming behavior and to study the influence of vasopressin or its derivatives on hemicholinium-3-induced impairment of water maze learning in mice, we designed a new apparatus using water maze which has three panels in small fish breeding water bath (L60 x W30 x H36 cm). In the first swimming, six strains of adult male mice, ICR, ddY, ddN, C3H/He, BALB/C and C57BL were subjected to learn swimming behavior twice a day for 6 d in a straight course. Only ICR, ddN, C57BL and BALB/C strain mice were chosen for the next experiment. In the second swimming, mice (ICR, ddN, C57BL, BALB/C) were swum in the water maze apparatus. Scopolamine-induced impairment of water maze learning was produced only in ICR, BALB/C mice, but not in C57BL and ddN strain, which was recovered by physostigmine. Amnesia was not obtained by intracerebroventricular injection (i.c.v.) of cycloheximide and AlCl3 in mice (ICR). Hemicholinium-induced amnesia was improved by vasopressin and desmopressin. Lysine-vasopressin and oxytocin were without affecting hemicholinium-induced amnesia. Pretreatment with a vasopressin antagonist, ([1-(beta-mercapto-beta,beta-cyclopenta-methylene propionic acid), 2-(o-methyl)tyrosine arginine]-vasopressin) resulted in a reversible effect on the improvement of hemicholinium-induced amnesia by vasopressin. Of four different strain mice, ICR mice were the most preferable to the presently used test. They were also more responsive to hemicholinium and vasopressin than the other strains. These results suggest that the simple water maze apparatus may be useful for a pre-examination of nootropics or a study of learning of swimming behavior in mice.

Animals↗
PubMed1992

Ca2+ ionophore and phorbol ester stimulate diacylglycerol formation and phosphatidylcholine hydrolysis in rat parotid acinar cells.

We investigated the effects of A23187 and phorbol 12,13-dibutyrate (PDBu) on sn-1,2-diacylglycerol (DAG) accumulation and phosphatidylcholine (PC) hydrolysis in rat parotid acinar cells. Both A23187 and PDBu, in concentration ranges of 0.001-0.1 microM, stimulated DAG accumulation and PC hydrolysis in a time- and concentration-dependent manner. Treatment with A23187 and PDBu stimulated the release of [3H]choline and [3H]phosphocholine into the medium, indicating [3H]PC hydrolysis is due to the activation of phospholipases C and D; however, [3H]phosphatidylethanolamine hydrolysis was not indicated. These releases were unaffected by the addition of glucose 6-phosphate, a phosphatase inhibitor. Staurosporine, a protein kinase C inhibitor, significantly inhibited the DAG accumulation and the PC hydrolysis stimulated by these agents. Combinations of A23187 and PDBu potentiated the stimulatory effect which each of these agents alone had on DAG accumulation and PC hydrolysis. This mode of action was additive but not synergistic. These results suggest that DAG accumulation induced by A23187 and PDBu is related to the PC hydrolysis mediated via the activation of phospholipases C and D, and that it is not related to phosphatidylethanolamine hydrolysis.

Alkaloids↗
PubMed1992

Assignments of Raman tensors to Raman bands of nucleic acids: use of a single crystal of adenosine triphosphoric acid and DNA fibers.

A polarized laser (488.0 nm) Raman spectroscopic measurement has been made of a single crystal of adenosine triphosphoric acid trihydrate (ATP.3H2O), whose space group is P2(1)2(1)2(1), and whose dimensions are about 10 microns x 100 microns x 100 microns along the crystallographic a, b and c axes, respectively. For each Raman band in the 300-1800 cm-1 range, relative scattering intensities, Ibb and Icc, which correspond to the bb and cc components of the Raman tensor of the crystal, have been determined. In an aqueous solution of ATP, the depolarization ratio of each Raman band has also been determined. On the basis of these experimental results, some discussions are given of the shapes and orientations of the Raman scattering tensors localized in the base residue, ribose portion, and phosphodiester portions. A similar type of study has been made with a few DNA fibers.

Adenosine Triphosphate↗
PubMed1992

Phorbol ester alters carbachol-stimulated diacylglycerol formation in parotid acinar cells through the hydrolysis of phosphoinositides and phosphatidylcholine.

Incubation of rat parotid acinar cells with phorbol 12,13-dibutyrate (PDBu) resulted in inhibition of carbachol-stimulated formation of sn-1,2-diacylglycerol (DAG). PDBu pretreatment inhibited carbachol-induced turnover of phosphoinositides; this inhibition was indicated by phosphatidylinositol 4,5-bisphosphate breakdown. This pretreatment also attenuated the effect of carbachol on inositol phosphate generation and phosphatidylcholine hydrolysis. These results show that PDBu alters carbachol-stimulated DAG formation through the hydrolysis of phosphoinositides and phosphatidylcholine.

Animals↗
PubMed1992

[The local hyperthermochemotherapy for pleural carcinomatosis].

Local hyperthermochemotherapy was performed in 17 cases to control malignant effusion and intrathoracic disseminated lesions. Of these 15 patients, 11 cases primary lung cancer, 4 cases metastatic lung cancer had pleural carcinomatosis and 2 cases were malignant diffuse mesotheliomas. The procedure was radiofrequency hyperthermia (13.56 MHz) maintaining the peripleural temperature at 42-43 degrees C for 45-60 minutes, combined simultaneously with the intrathoracic administration of cisplatin (1-2 mg/m2, bolus) through a thoracic double lumen trocar tube. The treatment was repeated from 2 to 4 times at 7-day intervals. In 14 cases (87.5%) complete or partial response according to the criteria of the Japan Lung Cancer Society were obtained. There were 2 cases of no change and one case that was impossible to evaluate. In one lung cancer case, the disappearance of pleural disseminated lesions was confirmed by flexible thoracoscopy after the procedure. In 12 cases, there were abdominal complaints due to side effects of the hyperthermochemotherapy, such as vomiting and nausea, but these symptoms were milder than those caused by intravenous injection of anti-cancer agents, for example cisplatin, in conventional chemotherapy treatment. The median survival time and 2 years survival of the patients with the present procedure were 15 months and 41.7% respectively. Although distant metastases appeared in most cases, none had local recurrence and particularly noteworthy pleural effusion was well controlled. The above experience suggested that the local hyperthermochemotherapy is useful to control pleural effusion and can improve the quality of life of patients with pleural carcinomatosis.

Aged↗
PubMed1992

[Endoscopic surgery of airway lesions by Nd-YAG laser treatment].

Between April 1980 and November 1990, we treated 212 cases of airway lesion using an Nd-YAG laser via the fiberoptic bronchoscope. The Nd-YAG laser power output was usually 40 W (20-60 W) delivered in 2 sec. shots. The cases consisted of 98 primary lung cancer, 12 primary tracheal cancer, 53 metastatic airway lesion, 7 benign tumor, and 42 cicatricial and granulomatous lesions. The therapeutic effects of Nd-YAG laser treatment were evaluated based on alleviation of dyspnea, widening of airway, and curative vaporization for therapeutic purposes. Effectiveness was observed in 180 of a total of 212 cases (84.9%). Out of 75 emergency cases in which a lifesaving procedure was performed to widen the airway, effective results were obtained in 70 (93.3%) with dramatic improvement in condition. It was also effective in 90 of 109 cases (82.6%) in which the procedure was performed for staged (palliative) widening of airway. In 55 cases of advanced lung cancer (Stage III or IV, mainly non-small cell cancer) in which palliative widening procedure was performed, one year survival was 44%. In 13 of 18 cases (72.2%) in which the procedure was performed for curative vaporization of invasive cancer, successful results were obtained. In 7 cases of benign tumor in which vaporization was performed as a radical curative procedure, no recurrence was observed in any cases. In 53 cases of metastatic airway lesion, effective results were obtained 48 (90.6%). The primary lesions of these cases consisted of 14 cases of esophageal cancer, 9 cases of lung cancer, 7 cases of colo-rectal cancer, 7 cases of thyroid cancer, and 16 others.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchoscopy↗
PubMed1991

Substance P-induced diacylglycerol formation in rat parotid acinar cells.

The mechanisms underlying the ability of substance P, to stimulate the sn-1,2-diacylglycerol (DAG) formation were studied using rat parotid acinar cells. During a 60 s stimulation, 1 microM substance P caused a rapid rise in DAG accumulation at 5 s, whereas a low (0.1 microM) concentration of agonist did not. During long term stimulation for 30 min, DAG accumulation induced by 1 microM substance P reached near maximal levels at 5 min and remained elevated for at least 20 min. In contrast, DAG formation induced by 0.1 microM substance P exhibited a peak at 5 min, gradually declined and returned to near basal levels at 30 min. Furthermore, DAG accumulation in response to substance P at 5 and 20 min increased in a dose-dependent manner. The breakdown of both [32P]phosphatidylinositol 4-monophosphate ([32P]PIP) and [32P]phosphatidylinositol 4,5-bisphosphate ([32P]PIP2) stimulated by 1 microM substance P significantly increased from 5 to 20 min and returned to basal levels by 30 min; however, the breakdown of [32P]PIP2 was greater than that of [32P]PIP. At a low concentration of substance P, [32P]PIP2 breakdown reached maximal levels at 5 min followed by a progressive decrease and returned to basal levels at 30 min, whereas the breakdown of [32P]PIP reached maximal levels at 5 min and returned to near basal levels at 10 min. Both concentrations of substance P caused some [32P]phosphatidylinositol breakdown at 5 min. Changes in [3H]inositol trisphosphate induced by substance P were similar to those in [32P]PIP2. In addition, substance P (1 microM) did not stimulate the release of [3H]choline or [3H]ethanolamine metabolites into the medium. Substance P-induced DAG formation was not inhibited by staurosporine, a protein kinase C inhibitor. These results suggest that DAG formation caused by substance P is closely associated with the hydrolysis of phosphatidylinositides but not that of phosphatidylcholine or phosphatidylethanolamine, and is not regulated by protein kinase C-dependent mechanism(s).

Alkaloids↗
PubMed1991

Protein kinase C-dependent diacylglycerol formation is mediated via Ca2+/calmodulin in parotid cells.

The kinetics of carbachol-induced sn-1,2-diacylglycerol (DAG) formation and the underlying mechanism(s) involved in parotid acinar cells were investigated. Supramaximal concentrations of carbachol for amylase secretion (10 microM) caused a transient rise in DAG levels at 10 s. In contrast, this rapid rise was not elicited by 1 microM carbachol, which is the maximally effective concentration for amylase secretion. Carbachol (10 microM) also increased DAG levels linearly up to 20 min, which were sustained for up to a further 10 min. DAG formation stimulated by 1 microM carbachol was biphasic; the first peak was observed after 5 min and the second after 20 min. DAG formation induced by 0.01-0.1 microM carbachol was concentration-dependent and monophasic, peaking at 5 min. The second peak evoked by carbachol was partly inhibited by Ca2+ deprivation from the extracellular space, whereas the first peak was not. Similar results were obtained in experiments using Ca2+ antagonists such as verapamil and LaCl3. The protein kinase C inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and staurosporine, and a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), significantly inhibited the second DAG peak produced by 1 microM carbachol, but did not alter the first peak. The degree of inhibition of the second peak by these antagonists was comparable. Furthermore, the inhibitory effect of staurosporine and W-7 was concentration-dependent. The A23187-induced accumulation of DAG also was abolished by both staurosporine and W-7. These data indicate that a protein kinase C-dependent mechanism(s) is involved in mediating the second DAG accumulation peak induced by 1 microM carbachol and is mainly regulated by the Ca(2+)-calmodulin complex.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Effects of the mammalian lignan, 2,3-dibenzyl-butane-1,4-diol, on contraction and Ca2+ mobilization induced by noradrenaline in rat aorta.

1. In rat aorta, 2,3-dibenzylbutane-1,4-diol (DBB) inhibited noradrenaline (NA)-induced contraction in a concentration-dependent manner. The inhibitory effect of DBB was observed in verapamil-pretreated muscle, and did not differ from that in the high K+ solution containing verapamil (1.0 microM). 2. DBB inhibited not only contraction, but [Ca2+]i elevation induced by NA (10 microM) with the same potency. 3. The inhibitory effect of DBB on NA-induced contraction was reversed by methylene blue (3.2 microM) and enhanced by M&B 22,948 (10 microM). 4. DBB (100 microM) alone increased cyclic GMP levels. This effect was attenuated by methylene blue (3.2 microM) and augmented by M&B 22,948 (10 microM). 5. From these results, the inhibitory effects of DBB on NA-induced contraction in rat aorta may be caused by an increase of cyclic GMP levels.

Animals↗
PubMed1991

In vivo adaptive control of beta-receptors and adenylate cyclase during short-term heat exposure in rat parotid glands.

1. Adaptation of beta-adrenergic receptors (beta-AR) and adenylate cyclase (AC) in rat parotid glands during short-term heat exposure (33 degrees C) were studied. 2. Heat exposure reduced AC activity in response to isoproterenol (IPR). 3. The number of beta-AR on the cell surface significantly increased after 24 hr but returned to control level after 48 hr. 4. IPR-induced [3H]GDP release was significantly reduced throughout exposure. 5. The data suggest that the major factor which results in the desensitization of AC during short-term heat exposure is a blunted coupling between beta-AR and GTP binding protein(s).

Adaptation, Physiological↗
PubMed1991

Enhanced coupling of adenylate cyclase to lipolysis in permeabilized adipocytes from trained rats.

Digitonin-permeabilized adipocytes were used to study the coupling of adenylate cyclase (AC) to lipolysis in exercise-trained rats. Isoproterenol-(IPR) stimulated lipolysis in permeabilized cells was significantly greater in trained than in control rats. Under essentially identical conditions, the dose-response curve for IPR stimulation of AC activity in the absence of 3-isobutyl-1-methylxanthine was similar in trained and control rats. However, the potency of stimulation by IPR as a percentage of the basal level was greater in trained rats. AC activity and lipolysis in the presence of 3-isobutyl-1-methylxanthine were also significantly greater in trained than in control rats. Least-squares analysis by plotting the log AC vs. lipolysis values showed that the regression coefficient was about three-fold greater in trained than in control rats. The concentration of endogenous adenosine 3',5'-cyclic monophosphate (cAMP) needed to produce a half-maximal lipolytic response was 18.58 and 10.81 pmol.min-1.10(6) cells-1 in control and trained rats, respectively. Thus a positive relationship existed between lipolysis and AC activity, with a tighter coupling in trained rats. Lipolysis in response to exogenous cAMP tended to be greater in trained than in control rats, and the difference was statistically significant for 50 microM and 10 mM cAMP. Our finding support the concept that the major mechanism of enhanced lipolysis in trained rats was an increase in the activity of enzymatic step(s) distal to cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Effects of combination therapy with low-dose aspirin and warfarin on platelet functions after heart valve replacement.

To evaluate the efficacy and safety of combination therapy with aspirin and warfarin for preventing the development of thromboembolism, we compared the effects of low-dose aspirin (81 mg/day) on platelet functions to those of ticlopidine (300 mg/day) in heart valve replacement patients. Experiments were performed in two groups; the first group within 1 month after operation (the unstable period) and the second group between 3 months and 3 years after operation (the stable period). At the stable period, low-dose aspirin inhibited platelet aggregation induced by ADP, collagen, or arachidonic acid, and suppressed the increase in intracellular Ca2+ concentration [( Ca2+]i) induced by thrombin significantly. On the other hand, ticlopidine inhibited platelet aggregation induced by ADP or collagen, but did not suppress arachidonic acid-induced aggregation and the thrombin-induced [Ca2+]i increase. At the unstable period, the combination therapy of low-dose aspirin plus warfarin did not prolong the bleeding time compared to ticlopidine plus warfarin. And low-dose aspirin inhibited platelet aggregation induced by ADP, collagen or epinephrine, and especially blocked arachidonic acid-induced aggregation. Ticlopidine inhibited ADP-, collagen- or U-46619-induced aggregation, but did not affect on the increase in [Ca2+]i induced by thrombin. From the results in this study, we suggest that the combination therapy with low-dose aspirin (81 mg/day) and warfarin is safe as an antithrombotic medication in heart valve replacement, and results in the inhibition of platelet functions without any side effect calling for special mention at the early unstable period after operation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Priming effect of 2,3-dibenzylbutane-1,4-diol (mammalian lignan) on superoxide production in human neutrophils.

We investigated the effect of 2,3-dibenzylbutane-1,4-diol (DBB), a mammalian lignan, on superoxide production and [Ca2+]i mobilization in human neutrophils. DBB did not generate superoxide production by itself, but enhanced the FMLP or A23187-induced superoxide production in a dose dependent manner. DBB did not influence the OAG-induced superoxide production. The priming effect of DBB was inhibited by W-7 or trifluoroperazine, but not by H-7 or staurosporine. And the priming effect of DBB was observed in the presence or absence of extracellular Ca2+. DBB enhanced the low dose FMLP-induced [Ca2+]i mobilization. These results suggest that the priming effect of DBB in human neutrophils may be caused by the activation of the calcium-calmodulin pathway but not the protein kinase pathway.

Alkaloids↗