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Biomedical subjects

M Takei

Publications and source records attributed to M Takei.

At least 127 records · Page 7Linked to original sources
PubMed1991

Effect of NCDC, a protease inhibitor, on histamine release from rat peritoneal mast cells induced by anti-IgE.

NCDC dose-dependently inhibited histamine release from rat peritoneal mast cells induced by anti-IgE. Moreover, NCDC inhibited Ca(2+)-mobilization from intracellular Ca(2+)-stores as well as histamine release in mast cells activated by anti IgE, the effect on both of these phenomena being closely correlated. Anti-IgE induced a rapid increase in IP3 production from phosphoinositides in mast cells, with its production in 15 sec, followed to baseline levels within 1 min. Anti-IgE stimulated PLC activity on mast cells membrane preparation. NCDC dose-dependently inhibited the generation of IP3. These results suggest that the inhibitory effect of NCDC on the release of histamine induced by anti-IgE is due to, in part at least, the inhibition of PI-specific PLC and that the inhibitory effects of NCDC are involved in intracellular calcium store.

Animals↗
PubMed1991

Proliferation of natural suppressor cells in long-term cultures of spleen cells from normal adult mice.

Natural suppressor cells were induced by culturing spleen cells from normal adult mice for 2 to 3 wk. The suppressor cells were large in size, nonadherent and nonspecifically suppressed the plaque-forming cells response of fresh spleen cells to SRBC in vitro. The suppressive activity of the cells was not affected by treatment with indomethacin or anti-Thy-1, anti-Ig, anti-Ia, or anti-asialoGM1 plus complement. Phenotype analysis by FACS showed that Thy-1, L3T4, Ly-2, CD3-epsilon, TCR-alpha beta, Ig, B220, Ia, and asialoGM1 Ag were all absent in the suppressor cells, although they were wheat germ agglutinin receptor positive. The suppressor cells did not demonstrate cytotoxicity against either YAC-1 or P-815 cells. Enriched large cell populations from fresh normal spleens expressed the same phenotypes and also exhibited the suppressive activity. These findings suggest that a minor population of natural suppressor cells exist in the normal adult mouse spleen and they proliferate during the in vitro culture of spleen cells.

Animals↗
PubMed1991

Functional participation in M1 receptor subtype on chronotropic and dromotropic responses to vagus stimulation in anesthetized dogs.

We investigated blocking effects of pirenzepine, AF-DX 116 and atropine on the negative chronotropic and dromotropic responses to stimulation of the intracardiac vagus nerves in the anesthetized, open-chest dogs. Stimulation of the intracardiac vagus nerves to the sinoatrial nodal region (stimulation of the intracardiac parasympathetic nerves to the sinoatrial nodal region) or to the atrioventricular nodal region (stimulation of intracardiac nerves to the atriventricular region) selectively decreased heart rate or increased atrioventricular conduction time, respectively. Pirenzepine at lower doses (0.3-3 microgram/kg i.v.) attenuated the stimulation of the negative chronotropic response to the intracardiac parasympathetic nerves to the sinoatrial nodal region to 80% of the control response significantly but did not affect the negative dromotropic one. Similarly, higher doses (10-1000 micrograms/kg i.v.) of pirenzepine inhibited the chronotropic and dromotropic responses to each stimulation in a dose-dependent manner. AF-DX 116 (0.3-300 microgram/kg i.v.) inhibited the chronotropic and dromotropic responses to each stimulation in a similar dose-dependent manner. Atropine (1-30 microgram/kg i.v.) blocked the cardiac responses to each stimulation. However, the ID50 of atropine for the chronotropic response was less than that for the dromotropic one, although ID50s of pirenzepine and AF-DX 116 for the chronotropic and dromotropic responses were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of ecdysterone on histamine release from rat peritoneal mast cells.

Ecdysterone dose-dependently inhibited anti-IgE-induced histamine release from mast cells. Moreover, the rate and extent of histamine release from mast cells induced by Concanavalin A (Con A) are significantly diminished in samples incubated with ecdysterone. Ecdysterone inhibited both the initial and gradual rise in fluorescent response by anti-IgE and Con A. The effects of ecdysterone on the fluorescence response was correlated with the inhibition of histamine release. These results suggest the possibility that the inhibition of histamine release from rat mast cells by ecdysterone might be due to inhibition of Ca2+ mobilization from intracellular Ca2+ storage.

Animals↗
PubMed1991

Effect of dantrolene on histamine release from rat peritoneal mast cells.

Dantrolene strongly and dose-dependently inhibited histamine release from rat peritoneal mast cells induced by anti-IgE. Dantrolene inhibited Ca(2+)-mobilization from intracellular Ca(2+)-store as well as histamine release in mast cells activated by anti-IgE, the effect on both these phenomena being closely correlated. These results suggested that the effect of dantrolene on histamine release from rat mast cell might be due to the inhibition of Ca(2+)-release from intracellular Ca(2+)-store.

Animals↗
PubMed1991

A toxic substance from the sea urchin Toxopneustes pileolus induces histamine release from rat peritoneal mast cells.

A toxic substance (P-II fraction), fractionated from the pedicellariae of the sea urchin Toxopneustes pileolus, dose-dependently caused the histamine release from rat peritoneal mast cells. The histamine release induced by P-II fraction increased with time, while compound 48/80 caused a more rapid histamine release. The dose-response curve for P-II fraction was studied with concentration 0.03-2.0 mg/ml. This reaction was dependent on Ca2+ and temperature. When glucose (5.5 mM) was omitted during the incubation step, the histamine release induced by P-II fraction was significantly reduced as compared to that of compound 48/80. Pyruvate reversed this reduction. On the other hand, the histamine release induced by P-II fraction was effectively potentiated by the addition of glucose (11.0 mM), but not that by compound 48/80. These results suggest that P-II fraction-induced histamine release differs from that of compound 48/80 disregards to the effects of glucose, because this histamine release appears to be more sensitive to the glycolytic pathway than compound 48/80-induced histamine release.

Animals↗
PubMed1991

A case of Caroli's disease with hepatolithiasis, choledocholithiasis, and cholangiocarcinoma.

A 48-year-old woman with Caroli's disease accompanied by hepatolithiasis, choledocholithiasis, and cholangiocarcinoma is reported. Magnetic resonance imaging was useful for the diagnosis of the cholangiocarcinoma. The relationship between cholangiocarcinoma and hepatolithiasis, choledocholithiasis, and chronic cholangitis in Caroli's disease is discussed.

Adenoma, Bile Duct↗
PubMed1991

Effects of tetrodotoxin and imipramine on the cardiac responses to nicotine in isolated, blood-perfused canine heart preparations.

The effects of nicotine on the sinus rate and atrial or left ventricular contractile force were investigated in the isolated, blood-perfused dog right atrium and left ventricle. Nicotine (3-300 nmol) in the right atrium induced dose-dependent negative followed by positive chronotropic and inotropic responses, whereas nicotine caused only a positive inotropic response in the left ventricle. The negative responses to nicotine were blocked by atropine, hexamethonium (C6), and tetrodotoxin (TTX). The positive effects of nicotine were abolished by propranolol and C6. TTX significantly inhibited the positive responses to nicotine by about 50% in the atrial preparation and totally suppressed them in the left ventricle. Imipramine inhibited the positive cardiac responses to nicotine and tyramine, but potentiated the responses to noradrenaline (NA) in atrial and ventricular preparations. These results suggest that (a) nicotine induces negative and positive cardiac effects mediated by parasympathetic ganglionic nicotinic receptors and presynaptic nicotinic receptors of the postganglionic sympathetic nerves, respectively, in the dog heart; (b) there are few parasympathetic ganglionic cells in the dog left ventricle; (c) the positive cardiac responses to nicotine are caused by both TTX-sensitive and TTX-insensitive NA release mechanisms; and (d) imipramine inhibits the positive cardiac responses to nicotine at the presynaptic nicotinic receptor sites of the postganglionic sympathetic nerves.

Animals↗
PubMed1991

Synergistic nonuniform shortening of atrial refractory period induced by autonomic stimulation.

We investigated the nonuniform effects of autonomic nerve stimulation of the effective refractory period (ERP) of the right atrium in the anesthetized dog. Stimulation of the discrete intracardiac sympathetic nerves to the sinoatrial (SA) nodal region uniformly shortened ERPs at three sites in the right atrium after administration of atropine. Right ansa subclavia (RS) stimulation similarly shortened ERPs in the absence of atropine. Stimulation of the discrete intracardiac parasympathetic nerves to the SA nodal region (SAP stimulation) shortened ERPs of the right atrium in a nonuniform manner. Simultaneous RS and SAP stimulation additively shortened ERPs at each site and decreased sinus rate much more than SAP stimulation alone. Shortening of ERP induced by SAP stimulation was greater than that induced by RS stimulation at similar absolute changes in heart rate. These results suggest that simultaneous activation of sympathetic and parasympathetic nerves nonuniformly shortens the ERP in the right atrium as the algebraic sum of the individual responses to each stimulation. However, parasympathetics exert the principal neural control over atrial ERP.

Animals↗
PubMed1991

Differential intracardiac sympathetic and parasympathetic innervation to the SA and AV nodes in anesthetized dog hearts.

Stimulation of discrete intracardiac sympathetic nerves to the SA (SAS stimulation) or AV nodal region (AVS stimulation) increased the heart rate or decreased AV conduction time and caused an AV junctional rhythm, respectively, in anesthetized dogs treated with atropine. Topical application of tetrodotoxin (TTX) at the SAS or AVS stimulation locus totally inhibited the response to each stimulation, whereas each TTX treatment slightly attenuated the chronotropic response to the right ansa stimulation by 23 +/- 7.7% and the dromotropic response to the left ansa stimulation by 7 +/- 7.5%. TTX abolished AVS stimulation-induced one. Before atropine, topical application of hexamethonium at the locus for stimulation of intracardiac parasympathetic nerves to the SA (SAP stimulation) or AV nodal region (AVP stimulation) abolished almost totally negative chronotropic responses to SAP and cervical vagus stimulation or negative dromotropic responses to AVP and cervical vagus stimulation, respectively. These results demonstrate that activation of a very small population of intracardiac sympathetic nerves to target cells is enough to induced positive chronotropic and dromotropic responses in the heart in situ, and that SA and AV nodal pacemaker activity and AV conductivity are controlled multi-directionally by intracardiac sympathetic nerves in contrast with parasympathetic ones.

Anesthesia↗
PubMed1991

Correlations between IL-2 enhancing activity and clinical parameters in patients with rheumatoid arthritis and systemic lupus erythematosus.

In a previous paper (Tomura, K. et al. Tohoku J. Exp. Med., 1989, 159, 171-183), we discovered IL-2 enhancing factor(s) designated B cell derived-growth enhancing factor-2 (BGEF-2), which enhanced IL-2 dependent cell proliferation, and reported that BGEF-2 was produced by B cells of the patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) only when they were in the active stage of the disease. In this paper, we studied relationship between each IL-2 enhancing activity from B cell supernatant of the patients with these diseases and clinical parameters. IL-2 enhancing activities did not correlate with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), but correlated with plasma concentrations of gamma-globulin from the patients with RA and SLE in the active stages. IL-2 enhancing activities correlated with hypocomplementemia and leukocytopenia in the patients with SLE, and also correlated with RAHA titer in the patients with RA. Moreover, on several patients with RA or SLE in the active stages, diminution of IL-2 enhancing activity was found when they were in the remission stage after treatments. These findings suggested that IL-2 enhancing activity (i.e., BGEF-2 activity) correlated with activity of these diseases and supported the hypothesis that BGEF-2 played an important role in the polyclonal B cell activation and autoantibody production in patients with these diseases.

Adult↗
PubMed1991

Effects of the new anti-ulcer drug nizatidine on prostaglandins in the rat gastric mucosa.

The effects of nizatidine (N-[2-[[[2-[(dimethylamino)methyl]- 4-thiazolyl]methyl]thio]ethyl]-N'-methyl-2-nitro-1,1-ethenediamine , CAS 76963-41-2), a new histamine H2-receptor antagonist, on the content of prostaglandins (PGs) in the rat gastric mucosa at doses that inhibit basal gastric acid secretion were compared with those of two other histamine H2-receptor antagonists, cimetidine and ranitidine. Nizatidine did not inhibit basal gastric acid secretion at a dose of 0.4 mg/kg but showed dose-dependent inhibition at doses of 10, 30, and 100 mg/kg. This drug had no effects on the content of PG in the gastric mucosa when subcutaneously administered at doses of 0.4, 10, 30 and 100 mg/kg once daily for 5 days. Cimetidine and ranitidine administered at doses that markedly inhibit basal gastric acid secretion (250 and 100 mg/kg/d, respectively) had no effects on the content of PG in the gastric mucosa. On the other hand, nizatidine, cimetidine, or ranitidine at concentrations of 1-100 mumols/l did not inhibit in vitro PGE2 synthesis using sheep seminal vesicle microsomes. These results suggest that nizatidine did not affect in vitro PGE2 synthesis and even doses that markedly inhibit gastric acid secretion had no effects on the content of PGs in the gastric mucosa.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Differential inhibition of neuropeptide Y on the chronotropic and inotropic responses to sympathetic and parasympathetic stimulation in the isolated, perfused dog atrium.

Neuropeptide Y (NPY) inhibits the release of noradrenaline (NA) or acetylcholine (ACh) from nerve terminals in the heart. Thus, we differentiated the blocking effects of NPY on the negative and positive (atrial chronotropic and inotropic) responses to simultaneous stimulation of the intracardiac parasympathetic and sympathetic nerves in isolated, blood-perfused dog atria. NPY (0.1-3 nmol) injected into the sinus node artery decreased atrial contractile force slightly, but not sinus rate by itself. NPY inhibited the negative atrial responses to intracardiac autonomic nerve stimulation in a dose-dependent manner, whereas it rather augmented the positive responses. The inhibition on the negative chronotropic effect was more prolonged than that on the inotropic one. NPY also inhibited the negative responses to intracardiac parasympathetic nerve stimulation alone. However, NPY (3 nmol) did not change the positive responses to intracardiac sympathetic stimulation after atropine was given. NPY did not affect the atrial responses to exogenous ACh or NA. These results suggest that, under activation of autonomic nerves, NPY released from sympathetic nerves attenuates the negative chronotropic and inotropic responses to ACh released from parasympathetic nerves at the prejunctional sites more effectively than the positive responses to NA released from sympathetic nerves, and modifies the sympathetic-parasympathetic interactions in the dog heart.

Acetylcholine↗
PubMed1990

Inhibition of phospholipid methylation by an anti-allergic agent, NCO-650, during histamine release.

Antigen, anti-IgE and concanavalin A (Con A) induced an increase in both the incorporation of the 3H-methyl moiety into phospholipids and histamine release. Maximal incorporation of the 3H-methyl moiety into the lipid fraction of the cells was observed within 15 sec and 1 min after being challenged with antigen (100 micrograms/mL) and anti-IgE (200 micrograms/mL) respectively. However, the methylated phospholipid decreased rapidly. The addition of Con A (10 micrograms/mL) also increased phospholipid methylation, which reached a maximum at 5 min after challenge. Trans-4-guanidinomethylcyclohexanecarboxylic acid p-tert-butylphenyl ester hydrochloride (NCO-650; 27 microM) strongly inhibited the incorporation of the 3H-methyl moiety into phospholipid by antigen, anti-IgE and Con A. The IC50 values of NCO-650 for phospholipid methylation in response to antigen, anti-IgE and Con A were 1.5, 4.7 and 1.1 microM respectively. Although the Ca2(+)-ionophore A23187 did not induce phospholipid methylation, it caused histamine release.

Animals↗
PubMed1990

Cardiac responses to VIP and VIP-ergic-cholinergic interaction in isolated dog heart preparations.

Whereas i.v. administration of vasoactive intestinal peptide (VIP) to support dogs increased heart rate and decreased systemic blood pressure, sinus rate and contractile force increased in isolated right atria perfused with blood from the support dogs. VIP injected intraarterially into isolated atria induced dose-dependent positive chronotropic and inotropic effects. Intracardiac parasympathetic nerve stimulation attenuated the positive cardiac responses to VIP, but neither propranolol, imipramine, nor tetrodotoxin influenced the responses to VIP. VIP given to isolated left ventricles also increased the contractile force in a dose-dependent manner. However, VIP induced a greater maximum atrial contractility than ventricular contractility. This may indicate that VIP receptor density in the ventricle was lower than in the atrium, as it has recognized that VIP-ergic nerves innervate the right atrium more densely than the left ventricle. We therefore suggest that the positive cardiac responses to VIP, together with the VIP-ergic innervation in dog hearts and vagal activation, attenuate the VIP-mediated responses at site(s) in the cyclic AMP cascade.

Animals↗
PubMed1990

Anti-peptide antibodies detect a lupus-related interspecies idiotype that maps to H chain CDR2.

Antibodies to the small nucleoprotein Sm occur spontaneously in human and murine systemic lupus erythematosus. Human and mouse monoclonal anti-Sm autoantibodies designated 4B4 and Y2 share an idiotype (Id) determinant located on the Ig H chain. To understand the molecular basis of this cross-reactivity, the VH regions of both antibodies were sequenced and analyzed for homology. The antibodies showed only 49.6% homology. The second complementary determining region (CDR2) was the most likely candidate for the Id site. To investigate this possibility, rabbit antiserum was made against a peptide corresponding to the CDR2 of 4B4. This antiserum was specific for the immunizing peptide and reacted weakly to a peptide corresponding to the CDR2 of Y2. Anti-CDR2 antibody bound to 4B4 and Y2 but not to other human and mouse mAb. Binding was directed at the H chain when analyzed by Western blots. Anti-CDR2 antibody blocked anti-Id antibody binding to 4B4 and Y2 by 58% and 24%, respectively. These studies suggest that this interspecies Id maps to the H chain CDR2 and that a conserved Id can occur within molecules that are otherwise radically different.

Amino Acid Sequence↗
PubMed1990

Inhibition of histamine release from rat peritoneal mast cells by MY-1250, an active metabolite of Repirinast (MY-5116).

MY-1250, an active metabolite of Repirinast (MY-5116), strongly and dose-dependently inhibited the in vitro histamine release from rat peritoneal mast cells induced by antigen. The IC50 value of MY-1250 for histamine release was in the order of 0.3 microM. Moreover MY-1250 strongly inhibited calcium ion mobilization from the intracellular Ca2+ store. In the presence of 3.6 x 10(-5) M of MY-1250, the initial rise in [Ca2+]i reached a maximum of only 13 nM, and the inhibitory effect was 81% for the initial rise. The IC50 value for this event was 0.25 microM. The inhibitory effect of MY-1250 on the initial rise in [Ca2+]i was closely correlated with that on histamine release.

Animals↗