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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 433 records · Page 24Linked to original sources
PubMed1990

Anticholinergic action of disopyramide in intestinal smooth muscle of the guinea pig: inhibition of muscarinic receptors (M1 and M2).

Antimuscarinic actions of disopyramide were investigated by measuring the contractile responses of intestinal smooth muscles and ligand binding in cardiac and intestinal membrane preparations. Disopyramide caused a parallel shift of the dose-response curves for acetylcholine, McN-A-343, and carbachol to the right in the guinea pig taenia caeci; pA2 values were 5.4 for acetylcholine, 5.5 for McN-A-343 and 5.9 for carbachol. In the guinea pig ileum, disopyramide competitively antagonized acetylcholine in the contractile responses, having the pA2 value of 6.1. In microsomal fractions of the guinea pig taenia caecum and heart, disopyramide was capable of replacing 3H-QNB; K1 values were 7 x 10(-6) M for the taenia and 2 x 10(-6) M for the heart. These results suggest that disopyramide exerts antimuscarinic action through M1 and M2 receptors with a potency approximately 3 times greater for M2 than M1.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1990

Effects of extraneuronal accumulation of isoprenaline on cAMP production in perfused rat heart.

The effects of extraneuronal accumulation of isoprenaline on the level of cAMP in perfused rat hearts were investigated. When catechol-O-methyl transferase (COMT) was intact, perfusion with isoprenaline (10(-6) M) for 5 min and 30 min (low accumulation of isoprenaline in the heart) enhanced the cAMP level. Propranolol (10(-6) M) significantly decreased the high level of cAMP produced by the perfusion with isoprenaline for 5 min and 30 min (low accumulation of isoprenaline). When COMT was inhibited by tropolone, perfusion with isoprenaline (10(-6) M) for 5 min (slight accumulation of isoprenaline in the heart) slightly increased the level of cAMP, while perfusion for 30 min (high accumulation of isoprenaline in the heart) did not increase the level of cAMP. Propranolol (10(-6) M) significantly decreased the cAMP level produced by 5 min perfusion with isoprenaline, but did not change the level by 30 min perfusion. The perfusion length (5 min and 30 min) and COMT inhibition by tropolone (10(-4) M) in the absence of isoprenaline did not affect cAMP levels. These results suggest that extraneuronally accumulated isoprenaline may inhibit the adenylate cyclase in perfused rat hearts.

Animals↗
PubMed1990

Inhibition of proliferative responses and interleukin 2 productions by salazosulfapyridine and its metabolites.

Mixed lymphocytes reactions (MLR) and concanavalin A (Con A)- or phytohemagglutinin (PHA)-stimulated proliferative responses were dose-dependently inhibited by salazosulfapyridine (SASP) and cyclosporin A (CsA) in the concentration ranges of 1 x 10(-5) -5 x 10(-4) M and 10-1000 ng/ml, respectively. Such a significant inhibition was not observed with metabolites of SASP, sulfapyridine (SP) and 5-aminosalicylic acid (5-ASA). In addition, SASP and CsA inhibited the production of interleukin 2 (IL-2) from splenocytes in these experiments. The inhibitory effect of CsA on IL-2 production practically correlated with that on proliferative responses, whereas SASP showed a less marked inhibitory effect on IL-2 production than on proliferative responses. Neither SP nor 5-ASA inhibited the IL-2 production. In the Con A-induced proliferative response, SASP showed a full inhibition even when added after 4-8 hr of culture, but CsA did not. The splenocytes that were pulsed with Con A for 4 hr could proliferate in response to Con A-supernatant or purified IL-2. CsA exhibited the inhibitory activity only when present during the time of Con A-pulsing, while SASP acted on the subsequent stage of the response, exerting its inhibitory effect. These findings suggest that SASP down-regulates the immune response by a mechanism apparently distinct from that of CsA.

Aminosalicylic Acids↗
PubMed1990

Effects of nitroglycerin on stable thromboxane A2 analogue-induced, nifedipine-resistant contraction in canine basilar artery.

The stable thromboxane A2 analogue, STA2, caused concentration-dependent contractions in the canine basilar artery. In Ca2(+)-free medium containing EGTA (0.1 mM) and nifedipine (10(-6) M), the addition of Ca2+ (2.5 mM) in the presence of STA2 (10(-8) M) caused a tonic contraction (nifedipine-resistant Ca2(+)-induced contraction). In the basilar artery, nitroglycerin did not significantly affect such nifedipine-resistant Ca2(+)-induced contractions, but nearly abolished the contraction in the coronary artery. The present experiments suggest that the regulatory mechanism of mobilized Ca2+ for the nifedipine-resistant Ca2(+)-induced contraction produced by STA2 in the basilar artery is different from that in the coronary artery.

Animals↗
PubMed1990

Cooking losses of thiamin in food and its nutritional significance.

To clarify the discrepancy between values of thiamin intake reported in national nutrition survey in Japan and judgment which was concluded by medical and biochemical examination in our field survey, thiamin of various daily foods were analyzed pre and post cooking in the various cooking methods, the following results were obtained. (1) The thiamin contents in cooked daily meals were 50-60 percent of the calculated values on an average. (2) The cooking losses of thiamin were particularly large in rice and green vegetables. (3) The loss of thiamin largest in boiling, followed by baking, parching and frying. (4) High temperature, pH, and chlorine on the public water accelerated thiamin losses. (5) The decrease of thiamin in cooked foods is caused by both of getting away of thiamin from foods and cleavage of thiamin of foods.

Chlorine↗
PubMed1990

Limiting-dilution analysis of the frequency of myelin basic protein-reactive T cells in Lewis, PVG/c and BN rats. Implication for susceptibility to autoimmune encephalomyelitis.

Susceptibility to experimental autoimmune encephalomyelitis (EAE), which is an autoimmune disease inducible by immunization with a brain-specific antigen in complete Freund's adjuvant (CFA), is different among strains. In an attempt to resolve the immune mechanisms by which the difference in susceptibility to EAE is regulated, we re-estimated susceptibility of several strains of rats, and the frequency of antigen-reactive T cells in each strain was determined by limiting-dilution analysis. EAE was induced in Lewis (LEW), PVG/c and BN rats using four different methods: (i) active immunization with guinea-pig myelin basic protein (GPBP) in CFA; (ii) immunization with GPBP in CFA that had been further supplemented with Mycobacterium tuberculosis H37Ra (supplemented CFA); (iii) adoptive transfer of GPBP-activated spleen cells into syngeneic rats; and (iv) transfer of a GPBP-specific T-cell line. The LEW strain was susceptible to all four methods. The PVG/c strain was resistant to immunization with GPBP in conventional CFA (GPBP/conv. CFA), but was susceptible to immunization with GPBP in supplemented CFA (GPBP/suppl. CFA) and to transfer of activated spleen cells. The BN strain was resistant to all methods. Limiting-dilution analysis using T cells from LEW, PVG/c or BN rats has revealed that each strain of rat displays a different pattern of frequencies of GPBP-reactive or the 68-88 sequence (GP68-88)-reactive T cells. LEW rats showed relatively high frequencies of GPBP-reactive and GP68-88-reactive T cells after immunization with either GPBP/conv. CFA or GPBP/suppl. CFA, symptomatic rats showing higher values than asymptomatic rats. In asymptomatic PVG/c rats, the frequency of GP68-88-reactive T cells was lower than that of GPBP-reactive T cells. In PVG/c rats with clinical EAE, however, GP68-88-reactive T cells increased in frequency and were almost the same as GPBP-reactive T cells. BN rats, on the other hand, responded very poorly not only to the GP68-88 sequence but also to the whole GPBP molecule, even after immunization with GPBP/suppl. CFA. These findings, obtained by limiting-dilution analysis, strongly suggest that the development of EAE in LEW, PVG/c and BN rats is closely related to the frequency of GPBP-reactive T cells. Furthermore, it is shown that resistance to EAE found in PVG/c and BN rats may be generated by different immune mechanisms.

Animals↗
PubMed1990

[Coronary circulation, myocardial metabolism and cardiac catecholamine flux in patients with syndrome X].

To clarify the pathogenesis of syndrome X (Sx), hemodynamics, coronary circulation, myocardial lactate metabolism and cardiac catecholamine flux were studied before and during bicycle ergometry in 25 patients (pts) and these data were compared with those in 15 with effort angina (EA) and in eight controls. The results were as follows: 1. The cardiac index during exercise decreased in EA pts probably due to their coronary lesions, while those in the controls and Sx were well preserved. 2. An increase of coronary blood flow during exercise, both in Sx and EA pts, was significantly impaired and the myocardial extraction ratio of lactic acid was significantly lower compared with those in the controls. The cardiac norepinephrine release during exercise was markedly higher in Sx, compared with that in controls and in EA. These results suggested that in Sx, excessive sympathoadrenergic stimulation may play an important role in restricting coronary reserve and in accelerating myocardial anaerobic metabolism.

Angina Pectoris↗
PubMed1990

The Na(+)-dependent release of endogenous dopamine and noradrenaline from rat brain synaptosomes.

The involvement of intrasynaptosomal-free Ca++ concentration [( Ca++]i) in Na(+)-dependent release of endogenous dopamine and noradrenaline from rat brain synaptosomes was studied. The release of endogenous dopamine and noradrenaline from rat whole brain synaptosomes were measured using high-performance liquid chromatography with electrochemical detector. The change of [Ca++]i was measured fluorometrically using a Ca++ indicator, Quin-2. Whether extracellular Ca++ was present or not, 30 microM veratridine, a Na(+)-ionophore, increased the release of endogenous dopamine and noradrenaline. In the presence of 1.25 mM Ca++, 30 microM veratridine increased [Ca++]i. In contrast, in the absence of extracellular Ca++, veratridine did not affect [Ca++]i. Ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) increased the release of dopamine and noradrenaline in Ca-Mg-free medium. This stimulatory effect of EGTA seemed to be the result of an increase in the influx of Na+ through Ca++ channels in the absence of divalent cation. In Ca-Mg-free medium, EGTA caused a slight decrease in [Ca++]i. The EGTA-stimulated release of dopamine and noradrenaline was blocked by La which also significantly blocked the decrease in [Ca++]i observed after the addition of EGTA. These results suggest that the Na(+)-dependent release of dopamine and noradrenaline may not depend on a change in [Ca++]i. Veratridine (30 microM)-induced release of dopamine and noradrenaline were detected simultaneously. However, the time needed to induce the maximal stimulatory effect of veratridine on the release of dopamine was apparently shorter than that of noradrenaline. This delay might suggest that the Na(+)-dependent release process of dopamine is not similar to that of noradrenaline.

Amiloride↗
PubMed1990

[Dental findings in a case of Chondrodysplasia Punctata].

Chondrodysplasia Punctata is a disease belonging to the metaphysia syndrome. This disease is characterized by endochondral punctata calcification of epiphysis or apophysis, short legs and hands, arthrogryposis, saddle nose, ichthyosis, cataract and mental retardation. This report concerns a case of Chondrodysplasia Punctata (Rhizomeric form) in a 4 year 1 month old girl. Observations were made from the dental point of view, and the findings were as follows: 1) The mesio-distal and bucco-lingual lengths of all primary teeth were smaller than the standard size. 2) Measuring the dental cast, the width of the dental arch was found to be larger, but the length of the arch was found to be smaller than the standard size. 3) The value of the palatal height was slightly smaller, compared with that of the normal children. 4) According to X-ray cephalometric analysis, the growth of the mandible was insufficient. 5) An enlargement of the angles of the teeth axes of the upper and lower central incisors was found. 6) The growth of the basal arches of the maxilla and mandible were shown to be retarded in the anterior portion. 7) Measurement of the area of the tubella sella triangle, revealed the posterior parts to be large and almost standard in the mesofacial part, and small in the mandibulo-facial parts.

Child, Preschool↗
PubMed1990

[Coronary reserve of the hypertensive heart: relationship to left ventricular hypertrophy].

We investigated the relationship between electrocardiographic left ventricular hypertrophy with ST-changes, and coronary circulation and myocardial metabolism in 25 patients with essential hypertension (systolic blood pressure greater than or equal to 160 mmHg, diastolic blood pressure greater than or equal to 95 mmHg). No patients had abnormal coronary arteriograms. They were categorized in two groups: non-hypertrophy group; cases with no hypertrophy on echocardiograms (interventricular septum and posterior wall thickness less than or equal to 11 mm), and hypertrophy group; cases with hypertrophy (wall thickness greater than or equal to 12 mm). Supine bicycle ergometry (50 watts, 50 rpm, 15 min) was performed during coronary sinus catheterization and electrocardiography. For cardiac hemodynamics, the coronary circulation and myocardial metabolism were observed at rest and during exercise. There was no significant difference in unit coronary blood flow (coronary blood flow per 100 gm) before exercise between the two groups. Unit coronary blood flow was significantly greater in the non-hypertrophy group after exercise. However, total coronary blood flow (coronary blood flow per 100 gm x left ventricular mass) showed no significant difference between the two groups. Coronary vascular resistance per 100 gm was higher in the hypertrophy group during exercise, though there was no significant difference at rest. Myocardial oxygen extraction O2 (A-C) was not different between the two groups at rest and during exercise, but unit myocardial oxygen consumption (MVO2) during exercise was higher in the non-hypertrophy group than in the hypertrophy group. The lactate extraction ratio tended to decrease in the hypertrophy group during exercise, and tended to increase in the non-hypertrophy group. Myocardial potassium flux tended to increase in the hypertrophy group during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Endothelium-dependent contraction induced by platelet-derived substances in canine basilar arteries.

The supernatant obtained from platelet-suspension incubated with thrombin caused contractions in both intact and endothelium-removed canine basilar arteries. Cyproheptadine (5 x 10(-7) M), which reduced the serotonin-induced contraction to about 20%, attenuated the supernatant-induced contraction to 51% in intact arteries and to 24% in endothelium-removed arteries. In both absence and presence of cyproheptadine, the supernatant-induced contraction of intact arteries was significantly larger than that of endothelium-removed arteries. The cyproheptadine-resistant contraction by the supernatant of intact arteries was attenuated by aspirin, OKY-046 (a thromboxane A2 synthetase inhibitor) and ONO-3708 (a thromboxane A2 antagonist), whereas such contraction of endothelium-removed arteries was not affected by these agents. The concentrations of serotonin, ATP and ADP in the supernatant used here were approximately 3, 67 and 44 micrograms/ml, respectively. The mixed solution of serotonin, ATP and ADP, at the same concentrations as the supernatant, also induced cyproheptadine-resistant, endothelium-dependent contractions in intact arteries. The contraction induced by the mixed solution in intact arteries was also attenuated by aspirin, OKY-046 and ONO-3708. The present experiments indicate that the supernatant causes endothelium-dependent contraction in canine cerebral arteries and that platelet-derived ATP and ADP contribute to this contraction.

Adenosine Diphosphate↗
PubMed1990

[A case of herpes zoster ophthalmicus with complete ophthalmoplegia].

A 58-year old man with herpes zoster ophthalmicus developed complete ophthalmoplegia, dissemination of herpetic lesions and meningitis. Eye movements improved two month after the onset of zoster. Five months later, eye movements recovered completely, but his sight was disturbed severely due to corneal ulcer.

Herpes Zoster Ophthalmicus↗
PubMed1990

[Long-term cultures of marrow cells from the patients with aplastic anemia].

Long-term marrow cultures were established from 35 patients with aplastic anemia (AA) and the adherent stromal cell layers were assessed. Cultures from 23 of the 35 patients grew scanty stromal cell layers or did not produce any adherent cells. Long-term cultures from the remaining patients formed adherent cell layers that appeared to be morphologically normal. Cultures from 7 patients that grew apparently normal adherent cell layers were examined for expression of intermediate filament proteins using antibodies CGA-7 and HHF, which respectively recognize actin epitopes expressed in smooth muscle and normal marrow stromal cells. Cells from 4 of the 7 patients expressed vimentin (antibody 43 beta E8) but did not react with CGA-7 or HHF. It thus appears that most patients with AA have quantitative or qualitative abnormalities in the adherent cell layers from long-term marrow cultures, suggesting a defect in the hematopoietic microenvironment.

Anemia, Aplastic↗
PubMed1989

Ascorbic acid suppresses the deconjugation of noradrenaline but not dopamine in plasma.

The characteristics of hydrolysis of sulfoconjugated noradrenaline (NA) and dopamine (DA) in plasma using sulfatase were investigated. Ascorbic acid has been used as an antioxidant during the hydrolysis of conjugated NA or DA. Hydrolysis of NA sulfates was considerably inhibited by adding ascorbic acid (0.5-10 mM), and slightly inhibited by adding dithiothreitol (1-10 mM). In contrast, the hydrolysis of DA sulfates was not affected after either ascorbic acid or DTT treatment. On the basis of these findings, the levels of NA sulfates previously reported are found to be markedly lower than the actual levels of NA sulfates in human plasma.

Ascorbic Acid↗
PubMed1989

Relationship of calcium and adenylate cyclase messenger systems in rat brain synaptosomes.

The effects of cyclic AMP on the rise in cytosolic free calcium concentration, [Ca2+]i, after stimulation with 15 mM K+ in rat brain synaptosomes were investigated. The fluorescent chelating agent Quin-2 was employed to monitor alterations of K+-evoked [Ca2+]i. Under normoxic conditions, clonidine (1, 10 microM), an alpha 2-adrenoceptor agonist, decreased the 15 mM K+-evoked [Ca2+]i. Although yohimbine (1, 10 microM), an alpha 2-adrenoceptor antagonist, had little or no effect on K+-evoked [Ca2+]i, the inhibitory effects of clonidine were blocked by yohimbine. 8-Bromo cyclic AMP, a cyclic AMP analogue, (50-500 microM), increased K+-evoked [Ca2+]i in a dose-dependent manner. The addition of cyclic AMP analogues subsequent to clonidine treatment reversed the clonidine-induced suppression of K+-evoked [Ca2+]i. On the other hand, under hypoxic conditions, K+-evoked [Ca2+]i was reduced by about 50-60%. 8-Bromo cyclic AMP and the adenylate cyclase activators, yohimbine (1-10 microM) and isoproterenol, a beta-adrenoceptor agonist, (0.1-10 microM), transiently reversed the reduction of the K+-evoked [Ca2+]i caused by hypoxia. These results indicate that the activation of alpha 2-adrenoceptor produces a rapid, sustained decrease in [Ca2+]i which may be due to a decrease in the levels of intracellular cyclic AMP. In addition, the increase in cellular levels of cyclic AMP reversed the reduction of the Ca2+ response to high K+ stimulation caused by hypoxia. If this is so, there is the possibility that increased cyclic AMP might improve the hypoxic damage.

Adenylyl Cyclases↗
PubMed1989

Purification of the thromboxane A2/prostaglandin H2 receptor from human blood platelets.

S-145 (5Z-7-(3-endo-phenylsulfonylamino-(2.2.1.)-bicyclohept -2-exo-yl) heptenoic acid) is a potent and selective antagonist for thromboxane A2/prostaglandin H2 receptor. Using this compound as an immobilized ligand for affinity chromatography and [3H]S-145 as a radioligand, we have purified the thromboxane A2/prostaglandin H2 receptor from the membranes of human blood platelets. The purification procedures consisted of solubilization of the receptor with 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS), affinity chromatographies on columns of S-145 affinity gel, wheat germ agglutinin agarose and red agarose, and repeated gel filtration high performance liquid chromatography on a TSK gel G-3000SW column. On the second gel filtration high performance liquid chromatography, the [3H]S-145 binding activity was eluted as a symmetrical peak which overlapped exactly with a peak of ultraviolet absorption at 280 nm. By these procedures, the receptor was purified about 8700-fold from the solubilized extract with a recovery of 6%. The final preparation showed a broad protein band at Mr 57,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis and maximally bound 19.2 nmol of [3H]S-145/mg protein with a Kd of 29.8 nM. The [3H]S-145 binding to the purified receptor was specifically displaced by several thromboxane A2/prostaglandin H2 analogues.

Binding, Competitive↗
PubMed1989

cDNA cloning of Gb, the substrate for botulinum ADP-ribosyltransferase from bovine adrenal gland and its identification as a rho gene product.

A 1.5 kilobase cDNA coding for the complete amino acid sequence of Gb, the substrate for ADP-ribosyltransferase in C1 and D botulinum toxins from bovine adrenal gland, has been isolated from a cDNA library of bovine adrenal gland. This cDNA encodes a polypeptide of 21,770 Da consisting of 193 amino acid residues, and the deduced amino acid sequence contains all the partial amino acid sequences reported previously (Narumiya, S., Sekine, A., and Fujiwara, M. (1988) J. Biol. Chem., 263, 17255-17257). Sequence comparison revealed that Gb is identical with the product of human rho clone 12 (rho A). The present results also confirmed our suggestion that the ADP-ribosylation occurs at Asn41 in the putative effector domain of the rho gene product.

Adrenal Glands↗