[The application of computed radiography to lateral cephalograms].
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Adult↗
Biomedical subjects
Y Takata
Publications and source records attributed to Y Takata.
Interaction of complement solubilized complexes with mouse peritoneal macrophages and their clearance and tissue uptake.
To clarify the biological activity of complement solubilized immune complexes, we studied their interaction with mouse peritoneal macrophages. The solubilized complexes lost their binding affinity for C3b receptor and Fc receptor but still bound to MPM mainly via the C3bi receptor (CR3). When solubilized immune complexes were injected into mice, they were more rapidly removed from the circulation than antigen excess soluble complexes and taken up by the liver Kupffer cells. Therefore, the solubilized complexes could be catabolized by the reticuloendothelial system, mainly in the liver. Probably, CR3 plays an important role in this process.
Animals↗
Bronchodilating and cardiovascular effects of intraduodenally and orally administered clenbuterol in dogs.
The bronchodilating and cardiovascular effects of intraduodenally and orally administered 4-amino-alpha-[tert-butylamino)methyl]-3,5-dichlorobenzylalcohol hydrochloride (clenbuterol, NAB 365) in anesthetized and conscious dogs were investigated and compared with those of salbutamol, isoprenaline (isoproterenol) and (4-amino-3,5-dichlorophenyl) glycolic acid (M-7), a metabolite of clenbuterol. In pentobarbitalized dogs, clenbuterol, 3-100 micrograms/kg i.d., inhibited the increase in airway resistance induced by histamine in a dose-related manner; clenbuterol was approximately 2 and 100 times more potent than salbutamol and isoprenaline, respectively. The plasma level of clenbuterol increased within 15 min and reached the maximum level within 60 to 90 min, which lasted for over 4 h after administration. The inhibitory effect was abolished by pretreatment with propranolol. M-7 showed no significant effect. In anesthetized dogs, clenbuterol and salbutamol, 10 and 100 microgram/kg i.d., decreased arterial blood pressure and increased heart rate and maximum rate of rise of left ventricular pressure. Isoprenaline, 10 and 100 micrograms/kg i.d., caused no marked changes in these parameters. In conscious dogs, clenbuterol, 10 and 100 micrograms/kg p.o., and salbutamol, 100 micrograms/kg p.o., increased heart rate; the maximum responses were observed 1 to 2 h after administration and lasted for over 3 h. No marked effects were observed after salbutamol, 10 micrograms/kg p.o., isoprenaline, 10 and 100 micrograms/kg p.o., and M-7, 100 micrograms/kg p.o.(ABSTRACT TRUNCATED AT 250 WORDS)
Airway Resistance↗
5'-[p-(Fluorosulfonyl)benzoyl]adenosine-mediated inactivation of S-adenosylhomocysteinase.
Rat liver S-adenosylhomocysteinase (EC 3.3.1.1) is inactivated by 5'-[p-(fluorosulfonyl)benzoyl]adenosine following pseudo-first-order kinetics. A plot of the apparent first-order rate constant for inactivation vs. the 5'-[p-(fluorosulfonyl)benzoyl]adenosine concentration exhibits a hyperbolic curve indicative of the formation of a reversible enzyme-reagent complex prior to the inactivation. Values of 71.0 +/- 7.7 microM and 0.14 +/- 0.01 min-1 are estimated for Kd and k, respectively, at pH 8.25 and 25 degrees C. The substrate adenosine and a competitive inhibitor adenine completely protect the enzyme against inactivation. Values of dissociation constant for these ligands calculated from the protection experiments agree well with those obtained by other means, indicating that 5'-[p-(fluorosulfonyl)benzoyl]adenosine competes with these ligands for the same binding site. The inactivation is not reversed by dialysis against phosphate buffer or tris(hydroxymethyl)aminomethane hydrochloride buffer, but a full enzyme activity is regained by treatment with dithiothreitol. The inactivation is not accompanied by covalent attachment of the reagent but is correlated with the loss of two sulfhydryl groups per enzyme subunit. Thus, the inactivation appears to result from a reagent-mediated formation of a disulfide between two cysteine residues in close proximity. The 5'-[p-(fluorosulfonyl)benzoyl]adenosine-modified enzyme which is not capable of catalyzing the overall reaction can still catalyze the partial reactions such as the oxidation of the 3'-hydroxyl and the abstraction of the 4'-proton of adenosine.
Adenosine↗
Determination of urea in whole blood using a urea electrode with an immobilised urease membrane.
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Electrodes↗
In vitro effects of glucocorticoid on glucose transport in rat adipocytes: evidence of a post-receptor coupling defect in insulin action.
The in vitro effect of glucocorticoid on insulin binding and glucose transport was studied with rat adipocytes. Isolated rat adipocytes were incubated with or without 0.70 microgram/ml (1.9 mumol) of hydrocortisone in TCM 199 medium at 37 degrees C, 5% CO2/95% air (v/v), pH 7.4, for 2, 4, and 8 h, and then fat cell insulin binding and insulin-stimulated 3-O-methylglucose transport were measured. Hydrocortisone did not affect insulin binding in terms of affinity or receptor number. Glucose transport in the absence of insulin was significantly decreased at the incubation time of 2 h and continued to decrease up to 8 h of incubation with hydrocortisone. Decreased insulin sensitivity of glucose transport (i.e., a right-ward shift of the dose response curve) was also demonstrated after 2 h incubation with hydrocortisone, and the ED50 of insulin was maximally increased at 4 h of incubation (0.53 ng/ml for treated vs. 0.22 ng/ml for control cells). Maximal insulin responsiveness was also significantly decreased in treated cells after 8 h incubation with hydrocortisone. When percent maximum glucose transport was expressed relative to receptor-bound insulin, the ED50 values of treated and control cells were 10.5 and 7.2 pg of bound insulin, per 2 X 10(5) cells, respectively. Thus, it was evident that glucocorticoid induced a post-receptor coupling defect in the signal transmission of insulin-receptor complex.
3-O-Methylglucose↗
Effects of Ca antagonists on the norepinephrine release and contractile responses of isolated canine saphenous veins to transmural nerve stimulation.
Effects of verapamil, diltiazem and nicardipine on tritium overflow and contraction evoked by transmural nerve stimulation (TNS) were evaluated using canine saphenous vein strips preincubated with [3H]norepinephrine. External Ca2+ was required for both tritium overflow and contraction evoked by TNS. All the Ca antagonists tested significantly increased the spontaneous overflow of tritium in a concentration-dependent manner with no changes in basal tension. Verapamil in concentrations lower than 10(-5) M significantly enhanced the TNS-evoked tritium overflow, but reduced it at 3 X 10(-5) M, while this drug at 3 X 10(-6)-3 X 10(-5) M concentration-dependently inhibited the TNS-evoked contraction. Verapamil, 3 X 10(-5) M, inhibited the TNS-evoked contraction more strongly than the evoked tritium overflow. On the other hand, diltiazem and nicardipine in concentrations higher than 10(-5) M significantly inhibited both tritium overflow and contraction evoked by TNS. There was no significant difference between inhibitions of the TNS-evoked tritium overflow and contraction by either diltiazem or nicardipine. Neither increase in the spontaneous tritium overflow nor inhibitions of the TNS-evoked tritium overflow and contraction by nicardipine appeared to be related to its phosphodiesterase inhibiting activity. These results suggest that diltiazem and nicardipine may inhibit the TNS-evoked contraction mainly by inhibiting Ca2+-dependent transmitter release from the adrenergic nerve endings, whereas verapamil may inhibit it by restricting the availability of Ca2+ at the postsynaptic sites and in the highest concentration used, by additional inhibition of transmitter release.
Adrenergic Fibers↗
Interaction of C3 with antigen-antibody complexes in the process of solubilization of immune precipitates.
The binding properties of activated C3 to immune complexes were studied by using solubilization phenomenon as a model system. IgG or F(ab')2 immune precipitates were solubilized by the six isolated alternative pathway proteins, and the solubilized complexes were analyzed by SDS-PAGE. As a result of solubilization, we observed some high m.w. bands. Under reducing conditions, the bands with m.w. of 150,000 and 115,000 appeared in the case of IgG and F(ab')2 complexes, respectively. Two-dimensional SDS-PAGE revealed that hydroxylamine treatment resulted in the dissociation of the 150,000-m.w. polypeptide into the C3 alpha-65 and the heavy chain of IgG. Similarly, the 115,000-m.w. polypeptide was dissociated into the C3 alpha-65 and the Fd chain. Therefore, it is likely that iC3b binds covalently to the Fd region of the heavy chain of IgG via an ester bond. Under nonreducing conditions, iC3b-IgG and iC3b-F(ab')2 complexes had apparent m.w. of 340,000 and 270,000, respectively, corresponding to one iC3b molecule bound to one antibody molecule. In addition, a considerable amount of iC3b also binds to antigen molecules via an ester bond. The findings that C3 binds to the F(ab')2 molecules and bovine serum albumin, which contain only a small amount of carbohydrate, suggest that C3 may not bind to the carbohydrate moiety of antibody molecules. Indeed, various carbohydrate molecules did not inhibit the solubilization even at high concentrations. In contrast, acetyl tyrosine having an aromatic ring and a hydroxyl group produced the best inhibition of the solubilization. Furthermore, we demonstrated that generation of C3b in the presence of 3H-tyrosine resulted in covalent binding of the tyrosine specifically to the C3 alpha' chain, indicating that the inhibition of solubilization may be due to the competition between tyrosine and immune complexes for the covalent binding of C3. Thus, it could be concluded that C3 binds covalently to the amino acid residues of antigen and antibody molecules during solubilization.
Amines↗
Simplified method for purification of mouse beta 1H.
A simple three-step method was described for purification of murine beta 1H, one of the essential regulatory proteins of complement system. The method consists of heparin-Sepharose affinity chromatography; gel filtration on a Sepharose 6B column, and DNA-cellulose affinity chromatography. By this method over 10 mg of beta 1H can be purified by more than 200-fold from 100-ml of EDTA serum of various strains. Overall yield of beta 1H was about 45%. The purified beta 1H was homogeneous as judged by SDS-polyacrylamide gel electrophoresis and immunoelectrophoresis. The purified mouse beta 1H showed physicochemical properties very similar to those described for human beta 1H: mouse beta 1H is a beta-globulin consisting of a single polypeptide chain of molecular weight of 160,000. Purified mouse beta 1H retained its functional activity as the essential cofactor for the cleavage of fluid-phase human C3b by the human C3b inactivator. Immunization of rabbits with the purified mouse beta 1H resulted in the production of the potent and monospecific antibody.
Animals↗
Mechanisms of converting enzyme inhibition: studies in experimental animals.
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3-Mercaptopropionic Acid↗
[A case report of a 1st and 2nd branchial arch syndrome].
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Branchial Region↗
Inhibition of immune precipitation by complement.
Normal human complement serum (NHS) inhibited precipitin reactions between tetanus toxoid and human or rabbit anti-tetanus toxoid IgG antibody, between bovine serum albumin (BSA) and rabbit anti-BSA IgG antibody, and between hen egg albumin and rabbit anti-egg albumin IgG antibody. Ethylene-diaminetetraacetic acid (EDTA) prevented this inhibition. Mg-ethyleneglycol-bis(aminoethyl)-tetra-acetic acid-(EGTA) also prevented the inhibition except with lower concentrations of antibody and antigen. Therefore, the inhibition of immune precipitation seemed to occur mainly through the classical pathway of complement activation. The alternative pathway was usually dispensable, but it augmented the inhibition. Guinea pig complement serum (NGS) was less effective than NHS in inhibiting immune precipitation. Guinea pig serum deficient in C4 (C4DGS) did not inhibit the immune precipitation. Mouse complement serum was effective for inhibiting precipitation, and C5-deficient serum was as effective as normal serum. Therefore, the inhibition of immune precipitation is considered to occur by activation of complement up to the step of C3. The size of the soluble immune complexes formed in the presence of NHS varied depending on the concentrations of antibody and antigen, even when the ratio of antigen to antibody was constant. On incubation at 37 degrees C immune precipitation was inhibited by 1/2 dilution of NHS for 2 to 3 hr and then gradually increased to the level in the absence of complement. When the immune complexes were formed in the presence of serum containing complement, fragments of C4 and C3 were incorporated into the soluble immune complexes. The C3 fragments incorporated into the soluble complexes were C3b, iC3b, C3c, and C3d, some of which were bound covalently with heavy chains of IgG antibody molecules. Some of the covalent linkages between C3 fragments and IgG seemed to be destroyed by alkali treatment, but not by hydroxylamine treatment. The formation of covalent bonds between IgG and C3 and probably C4 was essential for inhibition of immune precipitation, because inhibitors of their formation, such as putrescine, cadaverine, and salicylhydroxamic acid, effectively prevented the inhibition of precipitation. When antigen and antibody reacted in the presence of mixtures of various combinations of isolated complement components, C1, C4, C2, and C3 showed maximal inhibition of immune precipitation, whereas factors I and H had little effect.
Animals↗
Chemical modification of arginine residues of rat liver S-adenosylhomocysteinase.
Rat liver S-adenosylhomocysteinase (EC 3.3.1.1) is inactivated by phenylglyoxal following pseudo-first order kinetics. The dependence of the apparent first order rate constant for inactivation on the phenylglyoxal concentration shows that the inactivation is second order in reagent. This fact together with the reversibility of inactivation upon removal of excess reagent and the lack of reaction at residues other than arginine as revealed by amino acid analysis and incorporation of phenylglyoxal into the protein indicate that the inactivation is due to the modification of arginine residue. The substrate adenosine largely but not completely protects the enzyme against inactivation. Although the modification of two arginine residues/subunit is required for complete inactivation, the relationship between loss of enzyme activity and the number of arginine residues modified, and the comparison of the numbers of phenylglyoxal incorporated into the enzyme in the presence and absence of adenosine indicate that one residue which reacts very rapidly with the reagent compared with the other is critical for activity. Although the phenylglyoxal treatment does not result in alteration of the molecular size of the enzyme or dissociation of the bound NAD+, the intrinsic protein fluorescence is largely lost upon modification. The equilibrium binding study shows that the modified enzyme apparently fails to bind adenosine.
Adenosylhomocysteinase↗
What stimulates the renin-angiotensin system in rats with two-kidney renal hypertension?
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Animals↗
Captopril potentiates the vasodepressor action of Met-enkephalin in the anaesthetized rat.
The transient vasodepressor action of Met-enkephalin (10-80 micrograms kg-1, i.v.) in anaesthetized rats was significantly potentiated by the angiotensin-converting enzyme inhibitor, captopril (2 mg kg-1, i.v.); at this dose, it failed to modify the transient vasodepressor action of the non-specific vasodilator, nitroprusside (2.5, 5.0, 10 micrograms kg-1, i.v.). Captopril (2 mg kg-1, i.v.) caused a slow, progressive fall in the blood pressure of anaesthetized spontaneously hypertensive (SH) rats when compared to vehicle-treated controls. Pretreatment with naloxone (1.5 mg kg-1, i.v.) 30 min earlier failed to alter significantly the hypotensive action of captopril in anaesthetized SH rats. It was concluded that although captopril potentiated the vasodepressor action of Met-enkephalin in anaesthetized normotensive rats, potentiation of endogenous opioids does not appear to be involved in the hypotensive action of captopril in anaesthetized SH rats.
Anesthesia↗
Antihypertensive effect of diltiazem in young or adult rats of genetically hypertensive strains.
The antihypertensive effects of diltiazem were investigated in three different strains of genetically hypertensive rats, i.e. spontaneously hypertensive rats (SHR), stroke prone SHR (SHR-sp) and genetically hypertensive rats (GHR) compared to their respective controls, normotensive Wistar-Kyoto (NT-WKY) and New Zealand strain (NT-NZ). Either adult (3-6 months) or young (4 weeks), conscious rats were used. In adult SHR, SHR-sp and GHR, the percent decrease in blood pressure produced by diltiazem (10, 30 and 100 mg/kg orally (p.o.) or 0.1, 0.3, 1.0 and 3.0 mg/kg intravenously (i.v.)) was greater than in NT-WKY or NT-NZ, while no difference was detected in case of hydralazine (5 mg/kg p.o.). In contrast, the reactivity to diltiazem was not different between the young rats bred from the normotensive and hypertensive rats of both the Japanese and the New Zealand strains. It is concluded that diltiazem is a more effective antihypertensive agent in the hypertensive rats than in the normotensive rats. However, the increased reactivity to this compound in the adult hypertensive rats cannot be readily explained by the known pathogenetic factors leading to their hypertension.
Age Factors↗
Exaggerated hypotensive responses to calcium antagonists in spontaneously hypertensive rats.
The hypotensive effects of intravenous injection and infusion of diltiazem, l- and d-verapamil were investigated in conscious and anaesthetized rats with spontaneous hypertension (SHR) and normal blood pressure (NT-WKY). The inhibitory actions of these calcium-influx blockers on the pressor responses to angiotensin II (AII) and noradrenaline (NA) were also examined in anaesthetized SHR and NT-WKY. The intravenous injections of these three drugs (0.03, 0.1, 0.3, 1.0 mg/kg) lowered mean arterial pressure (MAP) in a dose related manner in conscious NT-WKY and SHR. The small dose of the blockers administered by intravenous infusion (0.02 mg/kg per min) also decreased MAP in both groups. The potency of the antihypertensive action was in the order l-verapamil greater than d-verapamil = diltiazem. The fall in blood pressure expressed as percentage of the initial MAP produced by the compounds was significantly enhanced in SHR compared to NT-WKY. The pressor responses to AII (0.03, 0.1, 0.3, 1.0 micrograms/kg i.v.) were suppressed by the intravenous infusion of 20 micrograms/kg per min with l-verapamil but not with d-verapamil, diltiazem and vehicle in NT-WKY, while no calcium blocker significantly diminished the vasopressor action of AII in SHR. The pressor effects of NA (0.3, 1.0, 3.0, 10.0 micrograms/kg i.v.) were inhibited by the same doses of l-verapamil and diltiazem but not with d-verapamil and vehicle in NT-WKY. Diltiazem reduced the response to NA in SHR but the other compounds (l- and d-verapamil) did not alter the pressor response to NA in SHR. The pressor responses to arginine vasopressin (3, 10, 30 and 100 mU/kg i.v.) were not altered by diltiazem infusion in either SHR or NT-WKY. It is concluded that these compounds are different in the potency of their hypotensive action and also the inhibition of the pressor responses to AII and NA. Calcium entry blockers are more effective antihypertensive agents in SHR than in NT-WKY. It appears that their inhibitory effects on the responses to AII and NA do not explain the exaggerated hypotensive responses in SHR.
Action Potentials↗
Effects of prolonged administration of indenolol in hypertensive rats.
The effects of 4-week administration and subsequent 2-week withdrawal of indenolol, 50 mg/kg/day p.o., were investigated in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR) and DOCA-salt hypertensive rats (DHR) at established stage, and compared with those of propranolol, 100 mg/kg/day p.o. Indenolol and propranolol caused a marked decrease in heart rate in SHR, RHR and DHR without showing a pronounced antihypertensive activity. Both drugs did not affect the body weight gain in RHR and DHR. On the other hand, the drugs suppressed the body weight gain in SHR, which recovered during 2-week withdrawal period. Weights of the heart, kidney, liver, spleen and adrenals were not affected by the drugs. Indenolol and propranolol markedly lowered the plasma renin activity (PRA) in SHR, RHR and DHR. PRA in RHR and DHR recovered to the control level during 2-week withdrawal period, while that in SHR did not. The results indicate that indenolol produces essentially the same effect as propranolol in SHR, RHR and DHR. Prolonged administration of indenolol to SHR, RHR and DHR with established hypertension produces a marked suppression of cardiac performance and PRA with showing antihypertensive activity.
Adrenergic beta-Antagonists↗