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M Asano

Publications and source records attributed to M Asano.

At least 361 records · Page 20Linked to original sources
PubMed1990

Induction of interferon-alpha by interferon-beta, but not of interferon-beta by interferon-alpha, in the mouse.

The antigenicity of the interferon (IFN) produced in transgenic mice carrying an extra mouse IFN-beta gene under the control of mouse metallothionein-I enhancer-promoter was examined after induction with Cd2+. Unexpectedly, IFN-alpha in addition to IFN-beta was detected in the serum. Induction of IFN-alpha was also observed when recombinant mouse IFN-beta was injected into normal mice. IFN-alpha was first detected in the circulation 6-10 hr after the administration of IFN-beta, and after 12 hr, IFN-alpha became the major component of serum IFN. On the other hand, when IFN-alpha was injected, no production of IFN-beta was observed. Messenger RNAs specific for IFN-alpha and endogenous IFN-beta were detected in the spleen, though the amount of IFN-beta mRNA was much less than that of IFN-alpha mRNA. These mRNAs were not detected in other organs including the liver where exogenous IFN-beta gene was markedly expressed. These observations showed that the expression of IFN-alpha is inducible by IFN-beta in the mouse, and the spleen was suggested to be the main site of production. Possible mechanisms of the induction are discussed.

Animals↗
PubMed1990

In vivo characteristics of low molecular weight copolymers composed of L-lactic acid and various DL-hydroxy acids as biodegradable carriers for drug delivery systems.

Low molecular weight and amorphous copolyesters composed of 70 mol% L-lactic acid and 30 mol% DL-hydroxy acids such as DL-lactic acid, DL-alpha-hydroxy-n-butyric acid, DL-alpha-hydroxyisovaleric acid and DL-alpha-hydroxyisocaproic acid were synthesized by direct copolycondensation in the absence of catalysts, to evaluate their in vivo capabilities as biodegradable carriers for drug delivery systems. For this purpose, the copolyester was moulded into a small cylindrical specimen under melt-pressing technique and implanted subcutaneously in the back of male adult rats. The in vivo degradation pattern can be subdivided into three types: the formations of parabolic type (L-LA/DL-HBA copolymer), linear type (L-LA/DL-LA copolymer) and S type (L-LA/DL-HIVA and L-LA/DL-HICA copolymers). A luteinizing hormone-releasing hormone agonist, des-Gly10-(D-Leu6)-LH-RH ethylamide monoacetate (LH-RH agonist), was incorporated into the small cylinders of copolyester formulations, of which the strongest pharmacological influence was observed in a copoly(L-LA/DL-HICA) formulation system, resulting in the maintenance of effective pharmacological influence throughout an experimental period of 15 wk, at which the in vivo release rate of LH-RH agonist was held constant at approximately 45 micrograms/d.

Animals↗
PubMed1990

Extraction of diquat with 1-butanol from biological materials.

Diquat can be extracted with 1-butanol from high pH solution in the presence of several moderate reductants. The red colored reduced compound of diquat in water turns to a purple compound in 1-butanol. The absorption of the purple compound is 0.105 at 383 nm and 0.119 at 520 nm in 1 microgram diquat/ml 1-butanol. The latter value is a little higher than that of the red compound at 495 nm in water. The purple compound is much more stable than the red compound in water. More than 80% of 10 ppm diquat added can be extracted from serum, blood, tissues, urine and some drinks. The extraction with 1-butanol is useful for concentration of diquat contained in large volume. The lower limit of detection is 0.1 microgram/ml 1-butanol. Paraquat is insoluble in 1-butanol under the same condition. Therefore, this method is applicable for the determination of diquat when paraquat is also contained in the solution.

1-Butanol↗
PubMed1990

Evidence that pinacidil may promote the opening of ATP-sensitive K+ channels yet inhibit the opening of Ca2(+)-activated K+ channels in K(+)-contracted canine mesenteric artery.

1. The effects of cromakalim and pinacidil on contraction and 86Rb efflux were investigated in strips of canine mesenteric artery. 2. Cromakalim and pinacidil relaxed arterial strips precontracted with 20.9 mM K+ with pD2 values of 6.56 and 5.88, respectively. 3. High (above 10 microM) concentrations of pinacidil, but not cromakalim, relaxed arterial strips bathed by a medium containing 65.9 mM K+, and inhibited Ca2(+)-induced contractions in strips bathed by a medium containing 80 mM K+. These findings suggested that pinacidil may act as an inhibitor of Ca2+ influx. 4. In arterial strips preloaded with 86Rb, cromakalim and pinacidil increased the basal 86Rb efflux. 5. When the effects of cromakalim and pinacidil on 86Rb efflux were determined in arterial strips contracted with 65.9 mM K+, both drugs increased 86Rb efflux. The increase in 86Rb efflux induced by pinacidil was much smaller than that induced by cromakalim. Under the same conditions, nifedipine decreased 86Rb efflux. 6. After the addition of nifedipine to arterial strips contracted with 65.9 mM K+, pinacidil produced a greater increase in 86Rb efflux than in the absence of nifedipine, whereas the effects of cromakalim were the same for the two conditions. Therefore, the effects of pinacidil on 86Rb efflux may be the resultant of two opposing effects: an increased 86Rb efflux due to the opening of ATP-sensitive K+ channels, and a decreased efflux due to the closing of Ca2(+)-activated K+ channels. 7. In causing relaxation, cromakalim was competitively antagonized by glibenclamide with a pA2 value of 7.16. However, glibenclamide antagonism of pinacidil was not of the simple competitive type, suggesting that inhibition of Ca2 + influx may contribute to the relaxant action of pinacidil. 8. It may be concluded that although the ability of pinacidil to increase 86Rb efflux via ATP-sensitive K+ channel opening was similar to that of cromakalim, the inhibition of Ca2 + influx by pinacidil may reduce the opening of Ca2 +-activated K+ channels in K+-contracted arterial strips.

Adenosine Triphosphate↗
PubMed1990

A variant of calcifying epithelial odontogenic tumor with Langerhans cells.

A variant of calcifying epithelial odontogenic tumor (CEOT) with Langerhans cells is reported. Compared to a typical CEOT, the tumor islands of this case were thin and composed of a small number of polyhedral epithelial cells. Almost no calcification of homogeneous eosinophilic materials was observed. In addition, clear cells which structurally corresponded to Langerhans cell were intermingled in the epithelial islands. These cells stain positively for S-100 protein, lysozome, MT 1, LN-3 and OKT 6 antibodies, but not for keratin antibody. Electronmicroscopic examination revealed the rod-shaped and racket-shaped structures called Birbeck's granules in the cytoplasm of these clear cells. Our observations indicate a variant case of CEOT with Langerhans cells in tumor nests.

Adult↗
PubMed1990

Evidence that endogenous gamma interferon is produced early in Listeria monocytogenes infection.

It has been presumed that gamma interferon (IFN-gamma), which plays an essential role in antilisterial resistance, is produced late in Listeria monocytogenes infection. In the present study, however, IFN-gamma was detected in the bloodstreams and spleens of mice from days 1 to 4 of L. monocytogenes infection by both a double-sandwich enzyme-linked immunosorbent assay and an immunohistochemical technique, suggesting that endogenous IFN-gamma is produced early but not late in L. monocytogenes infection.

Animals↗
PubMed1990

Purification of a mouse nuclear factor that binds to both the A and B cores of the polyomavirus enhancer.

We have previously identified a protein factor, PEBP2 (polyomavirus enhancer-binding protein), in the nuclear extract from mouse NIH 3T3 cells which binds to the sequence motif, PEA2, located within the polyomavirus enhancer A element. Upon cellular transformation with activated oncogene c-Ha-ras, this factor frequently undergoes drastic molecular modifications into an altered form having a considerably reduced molecular size. In this study, the altered form, PEBP3, was purified to near homogeneity. The purified PEBP3 comprised two sets of families of polypeptides, alpha-1 to alpha-4 and beta-1 to beta-2, which were 30 to 35 kilodaltons and 20 to 25 kilodaltons in size, respectively. Both kinds of polypeptides possessed DNA-binding activities with exactly the same sequence specificity. Individual alpha or beta polypeptides complexed with DNA showed faster gel mobilities than did PEBP3. However, the original gel retardation pattern was restored when alpha and beta polypeptides were mixed together in any arbitrary pair. These observation along with the results of UV- and chemical-cross-linking studies led us to conclude that PEBP3 is a heterodimer of alpha and beta subunits, potentially having a divalent DNA-binding activity. Furthermore, PEBP3 was found to bind a second, hitherto-unnoticed site of the polyomavirus enhancer that is located within the B element and coincides with the sequence previously known as the simian virus 40 enhancer core homology. From comparison of this and the original binding sites, the consensus sequence for PEBP3 was defined to be PuACCPuCA. These findings provided new insights into the biological significance of PEBP3 and PEBP2.

Animals↗
PubMed1990

A polyomavirus enhancer-binding protein, PEBP5, responsive to 12-O-tetradecanoylphorbol-13-acetate but distinct from AP-1.

Element I, homologous to the adenovirus type 5 E1A enhancer core, is a 10-bp sequence in the A core of the polyomavirus enhancer and was shown previously to be responsive to 12-O-tetradecanoylphorbol-13-acetate (TPA). We found that element I by itself was capable of activating polyomavirus DNA replication in COP-5 cells which express the polyomavirus large T antigen. A nuclear factor, polyomavirus enhancer-binding protein 5 (PEBP5), which bound to the entire sequence of element I and was responsive to TPA was identified by an in vitro binding assay. Although the binding site of PEBP5 partly overlaps with that of PEBP1 (PEA1), a member of the AP-1 family, PEBP5 appears to be a distinct factor. Since we previously showed that element I alone was able to activate transcription, our present results suggest that PEBP5 is involved in the regulation of both transcription and replication of DNA. The amount of PEBP5 increased after F9 cells were induced to differentiate by retinoic acid. A relatively large amount of PEBP5 was detected in lymphoid and trophoblast cells.

Animals↗
PubMed1990

Quantitation of myosin light chain phosphorylation in intact smooth muscle.

An improved method for quantitating the extent of myosin light chain (P-LC) phosphorylation in small smooth muscle samples is described. Native myosin was isolated from other cellular proteins in a crude supernatant fraction prepared from a few milligrams of bovine tracheal smooth muscle by polyacrylamide gel electrophoresis (PAGE) in the presence of sodium pyrophosphate (PPi). When potassium iodide (KI, 0.6 M) was added to the crude supernatant fraction, myosin migrated into the gels during electrophoresis. Without adding KI, myosin remained at the top of the gel so that the myosin content in the gel was 20 times less than in the presence of KI. After the PPi-PAGE, myosin was subjected to isoelectric focusing (IEF) on polyacrylamide slab gels to separate the phosphorylated from the nonphosphorylated forms of the P-LC. The extent of P-LC phosphorylation was quantitated after densitometric scanning of silver-stained IEF gels. Examination of the temporal changes in carbachol-induced contraction and P-LC phosphorylation in tracheal smooth muscle strips exhibited a relatively transient change in the P-LC phosphorylation as shown in other smooth muscle preparations. This procedure is applicable to investigations on the role of Ca2+.calmodulin-induced activation of myosin light chain kinase and phosphorylation of smooth muscle myosin.

Animals↗
PubMed1990

Effects of the calmodulin antagonist W-7 on isometric tension development and myosin light chain phosphorylation in bovine tracheal smooth muscle.

Effects of N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) on isometric tension development and myosin light chain (P-LC) phosphorylation were determined in intact smooth muscle strips of bovine trachea. Addition of 10(-5) M carbachol resulted in a marked increase in the P-LC phosphorylation within 30 sec of stimulation. Subsequently, there was a gradual decrease in the P-LC phosphorylation. In contrast, steady-state contraction was not attained until 10 min of stimulation. In these strips, W-7 itself caused a contraction, probably due to the release of endogenous histamine that was blocked by pyrilamine. In the presence of W-7 and pyrilamine, the isometric tension development and P-LC phosphorylation during the initial 5-min stimulation period were inhibited. Concentrations of W-7 that caused a 50% inhibition were 145 and 125 microM, respectively, for tension and phosphorylation. N-(6-aminohexyl)-1-naphthalenesulfonamide (W-5), a weak calmodulin antagonist, produced no significant inhibition on the carbachol-induced isometric tension development and P-LC phosphorylation. After 10-min exposure to carbachol, W-7 inhibited the steady-state contraction without inhibition of the P-LC phosphorylation. These results suggest that 1) W-7 inhibits the smooth muscle contraction through the inhibition of the initial increase in the P-LC phosphorylation and 2) the maintenance of isometric tension (after 10 min exposure to carbachol) in unlikely to depend on the P-LC phosphorylation.

Animals↗
PubMed1990

Immunohistochemical study of high-grade endometrial stromal sarcoma. An autopsy report in comparison with carcinosarcoma, leiomyosarcoma and normal endometrium.

An autopsy case of high-grade endometrial stromal sarcoma (ESS) is reported. Immunohistochemical study of the ESS was done in comparison with carcinosarcoma (CS), leiomyosarcoma (LMS) and normal endometrium in the uterus in order to trace the origin of ESS, which is a point of some controversy. Co-expression of keratin and vimentin and/or desmin positivity in several elements of CS and LMS, and glandular or stromal tissues in normal endometrium made it difficult immunohistochemically to be certain of the origin of ESS.

Antigens↗
PubMed1990

Pharmacological profiles of YM-16151-1 and its optical isomers: a novel calcium entry blocking and selective beta-1 adrenoceptor blocking agent.

The pharmacological properties of YM-16151-1 [(+/-)-dimethyl 4-[2-[4-(2-hydroxy-3-phenoxypropylamino)butoxyl]-5-nitrop hen yl]-2,6- dimethyl-1,4-dihydropyridine-3,5-dicarboxylate hydrochloride] and its optical isomers were evaluated in in vitro studies and radioligand binding assay. In isolated tissues, YM-16151-1 produced a competitive antagonism of CaCl2-induced contraction in the isolated rabbit aorta with a pKca-1 value of 8.17, and also produced a competitive antagonism of isoproterenol-induced positive chronotropic responses in the isolated rat atria with a pA2 value of 8.47. In rat brain membrane preparations, YM-16151-1 produced dose-dependent inhibitions of [3H]nitrendipine and [3H]dihydroalprenolol bindings with pKi values of 7.21 and 8.07, respectively. Calcium entry blocking activity of YM-16151-1 was 7 times weaker and 3 times greater than nifedipine and diltiazem, respectively. Beta-1 adrenoceptor blocking activity of YM-16151-1 was 2 times weaker than that of propranolol. YM-16151-1 showed about 900-fold selectivity for beta-1 adrenoceptor. YM-16151-1 also showed a weak alpha-1 adrenoceptor blocking activity and its potency was about 13 times weaker than that of phentolamine. S-(-)- and R-(+)-isomers of YM-16151-1 showed the same potency of calcium entry blocking activity. However, in beta-1 adrenoceptor blocking activity, the S-(-)-enantiomer was about 13 to 22 times more potent than the R-(+)-enantiomer. Oral administration of YM-16151-1 produced a dose-dependent blood pressure lowering effect without increasing heart rate in conscious spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Possible involvement of ATP-sensitive K+ channels in the relaxant response of dog middle cerebral artery to cromakalim.

To determine the functions of ATP-sensitive K+ (KATP) channels in cerebral arterial smooth muscle, the effects of cromakalim, an opener of these channels, on tension and 86Rb efflux were investigated in endothelium-removed strips of dog middle cerebral arteries (MCAs). Cromakalim relaxed the strips that were precontracted with 20.9 mM K+ with a small maximum response. The relaxant responses to cromakalim were competitively antagonized by glibenclamide, a blocker of KATP channels. In strips precontracted with 65.9 mM K+, cromakalim failed to relax the strips. The addition of cromakalim to a resting strip caused a dose-dependent relaxation. In the resting strips of MCAs preloaded with 86Rb, cromakalim did not increase the 86Rb efflux. With 42K as the tracer ion, cromakalim still had no effect on the efflux from the resting strips. On the other hand, cromakalim increased the 86Rb and 42K efflux from the strips of dog coronary arteries (CAs). In 20.9 mM K(+)-contracted strips of MCAs, cromakalim significantly decreased the 86Rb efflux. However, after the inactivation of Ca(++)-activated K+ channels by the addition of 1 x 10(-7) M nifedipine to the 20.9 mM K(+)-contracted strips of MCAs, cromakalim produced a small but significant increase in the 86Rb efflux. Similarly, when the resting strips of MCAs were placed in the Ca(++)-free 12 mM-Mg(+)+ solution, cromakalim increased the 86Rb efflux. In 65.9 mM K(+)-contracted strips, cromakalim increased the 86Rb efflux from both arteries. However, the extent of the increase in 86Rb efflux was significantly smaller in the MCA than in the CA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

A tumor promoting phorbol ester, TPA, enhances polyomavirus DNA replication by activating the function of the viral enhancer.

The effect of tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA) on enhancer dependent polyomavirus (Py) DNA replication was examined in cells expressing Py large T antigen. The results showed that TPA enhanced Py DNA replication by stimulating the activity of the A element, one of the two cores of Py enhancer. Of the three subdomains of the A element, the biding sites of PEBP1 (PEA1), a member of AP1 family, and of PEBP5 were by themselves able to activate Py DNA replication. Furthermore, each binding site of PEBP1 and PEBP5 responded to TPA to enhance Py DNA replication. The results suggest that growth promoting signals could activate DNA replication directly via enhancer binding proteins.

Antigens, Polyomavirus Transforming↗
PubMed1990

Comparison of effects of cromakalim and pinacidil on mechanical activity and 86Rb efflux in dog coronary arteries.

Effects of two K+ channel openers, cromakalim and pinacidil, on mechanical activity and on 86Rb efflux were compared in strips of dog coronary arteries. Cromakalim and pinacidil produced the relaxation in 20.9 mM K(+)-contracted strips with a pD2 of 6.53 and 5.95, respectively. In 65.9 mM K(+)-contracted strips, high concentrations of pinacidil, but not cromakalim, produced relaxation. Ca+(+)-induced contractions in 80 mM K(+)-depolarized strips were also inhibited by pinacidil but not by cromakalim. Glibenclamide, a blocker of ATP-regulated K+ (KATP) channels, competitively antagonized the relaxant responses to cromakalim with a pA2 value of 7.62. However, the antagonism by glibenclamide of the relaxant responses to pinacidil was not a typical competitive type, suggesting the contribution of other effects than the KATP channel opening activity to the relaxant effects of pinacidil. In resting strips preloaded with 86Rb, cromakalim and pinacidil increased the basal 86Rb efflux in a dose-dependent manner. The increase in the 86Rb efflux induced by cromakalim was greater than that by pinacidil. When the effects of cromakalim and pinacidil on the 86Rb efflux were determined in the 20.9 or 65.9 mM K(+)-contracted strips, both drugs increased the 86Rb efflux. Under the same conditions nifedipine, a Ca(+)+ channel blocker, produced the relaxation that is accompanied by the decrease in 86Rb efflux. The increase in the 86Rb efflux induced by cromakalim was much greater than that by pinacidil.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Antiulcer effects of 3-[[[2-(3,4-dimethoxyphenyl)ethyl] carbamoyl]methyl]-amino-N-methylbenzamide in experimental gastric and duodenal ulcers.

Effects of 3-[[[2-(3,4-dimethoxyphenyl)ethyl]carbamoyl] methyl]-amino-N-methylbenzamide (DQ-2511), a newly synthesized compound, were evaluated using various types of experimental gastric and duodenal ulcers in rats. Pretreatment with DQ-2511, over the dose range 30-300 mg/kg p.o., resulted in a dose-related inhibition of water-immersion stress-, serotonin-, acetylsalicylic acid (ASA)-, indometacin-, ethanol-, and 2-deoxy-D-glucose(2DG) plus indometacin-induced gastric ulcers as well as cysteamine-induced duodenal ulcers. The antiulcer potencies of DQ-2511 were equal to or greater than those of H2-receptor antagonist cimetidine in these ulcer models except for ASA- and 2DG plus indometacin-induced ulcers. The rate of healing of chronic gastric ulcers induced by acetic acid was significantly accelerated by DQ-2511 (100 and 300 mg/kg p.o.) but not by the same doses of cimetidine. DQ-2511, at doses of 30 mg/kg p.o. and above, produced a significant decrease in gastric acid and pepsin output in pylorus-ligated rats. In anesthetized rats with acute gastric fistulae, 30 mg/kg i.v. of DQ-2511 significantly inhibited gastric acid secretion stimulated by 2DG, whereas it did not affect gastric hyperacidity evoked by either carbachol, histamine or pentagastrin. At effective antiulcer doses, this compound produced a sustained increase in gastric mucosal blood flow in conscious, restrained rats. Based on these observations, DQ-2511 is characterized as a new antiulcer compound with beneficial effects on both gastric aggressive and defensive factors. Furthermore, these results indicate a possible superiority of DQ2511 over cimetidine in regard to its antiulcer potency and spectrum.

Animals↗