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Biomedical subjects

H Noguchi

Publications and source records attributed to H Noguchi.

At least 397 records · Page 22Linked to original sources

High-performance liquid chromatographic determination of prifinium quaternary ammonium ion in human serum and urine.

A simple, sensitive method for the determination of the prifinium ion, a quaternary ammonium ion, in human serum and urine is described. The method is based on extraction of the test solution with chloroform in the presence of saturated potassium bromide solution and normal-phase high-performance liquid chromatography using aqueous methanol as the mobile phase at pH 10. To prevent the dissolution of silica from the analytical column, the mobile phase is pre-saturated with silica by using a silica saturation column. Quantitation is possible down to 0.5 ng/ml of prifinium ion using 2 ml of serum and down to 5 ng/ml using a 1 ml of urine. The coefficients of variation of the method are less than 1.3% in both serum and urine. Serum levels and urinary excretion data obtained with this method are given for three healthy volunteers who had received a 60-mg oral dose of prifinium bromide.

Chromatography, High Pressure Liquid↗

Practical enzyme immunoassay for prolactin in human serum.

We have developed a competitive enzyme immunoassay for prolactin in human serum. Serum samples were incubated at 4 degrees C for 48 h with anti-prolactin antibodies and prolactin labeled with beta-D-galactosidase. The antibody-bound form of labeled prolactin was separated from the unbound form by a method based on the thiol-disulfide interchange reaction. By measuring the enzyme activity, serum prolactin could be determined. Sensitivity of the assay was 2.5 ng/ml, and the assay was as sensitive as radioimmunoassay. There was a good correlation between the values obtained by the enzyme immunoassay and those obtained by a radioimmunoassay (r = 0.98, slope = 1.26, y-intercept = - 12.8 ng/ml).

Humans↗

Depside as potent inhibitor of prostaglandin biosynthesis: a new active site model for fatty acid cyclooxygenase.

Forty depsides and depsidones, the esters of phenolcarboxylic acids, were examined for their inhibitory effect against prostaglandin biosynthesis with rabbit renal microsomes. 4-0-Methylcryptochlorophaeic acid was the most active inhibitor so far tested and its IC50 value was 0.34 muM. Kinetic investigation has shown that this depside acts competitively with respect to arachidonic acid as most of the non - steroidal antiinflammatory drugs. X-Ray analysis has revealed that 4-0-methylcryptochlorophaeic acid maintains its rigid conformation by forming a strong hydrogen bond between the hydroxyl and methoxyl groups. Comparison of CPK models between 4-0-methylcryptochlorophaeic acid and non-steroidal antiinflammatory drugs revealed that the carboxyl group and the two rings of these drugs are almost superimposable to those of the depside. This finding led us to propose a new active site model based on the three dimentional structure of the depside.

Animals↗

Breath-by-breath VCO2 and VO2 required compensation for transport delay and dynamic response.

Both transport delay (DELAY) and dynamic response (RESPONSE) of a mass spectrometer would theoretically result in considerable errors in the breath-by-breath calculation of VCO2 and VO2. However, curiously, the contribution of RESPONSE has been ignored. The purpose of this study is to quantify the error caused by RESPONSE. We found that RESPONSE of a mass spectrometer was regarded as a first-order response. We determined DELAY and time constant (T) of RESPONSE and compensated the on-line calculation for both DELAY and RESPONSE and for DELAY only. With T of 150 and 100 ms, deviations of VCO2 from the gas-collection method were 8 +/- 6 and 8 +/- 6 ml/min with compensation for both DELAY and RESPONSE, and 69 +/- 10 and 50 +/- 5 ml/min with compensation for DELAY only, respectively (mean +/- SD). Similar results were obtained with VO2. A computer simulation of error caused by RESPONSE disclosed that the error linearly increased with increasing T. We conclude that to be accurate within +/- 5% of the exact value, compensation should be made when T exceeds 25 ms.

Biological Transport↗

Metabolism of tiaramide in vitro. II. Oxidation of piperazineethanol group in tiaramide by 105 000 g supernatants from monkey and rat liver.

1. The piperazineethanol group in tiaramide was metabolized to the corresponding piperazineacetic acid group by monkey- and rat-liver preparations. 2. Formation of the piperazineacetic acid by soluble fractions from monkey and rat livers was faster with NAD+ than with NADP+ and was inhibited by pyrazole and disulfiram. 3. Tiaramide treatment did not impair ethanol elimination from blood of rats, but pyrazole pretreatment caused a drastic decrease of the piperazineacetic acid metabolite in the liver and serum of rats treated with tiaramide. 4. These results, and studies on partially purified liver enzymes, indicate that in monkey and rat liver, oxidation of the piperazineethanol moiety in tiaramide to piperazineacetic acid is catalysed by alcohol and aldehyde dehydrogenase.

Alcohol Dehydrogenase↗

Urinary metabolite profile of tiaramide in man and in some animal species.

1. The metabolism of tiaramide, 4-[(5-chloro-2-oxo-3(2H)-benzothiazolyl)acetyl]-1-piperazineethanol, was studied in healthy male volunteers and experimental animals. 2. Tiaramide was extensively metabolized in human with only 1.5% excreted unchanged. 3. Urinary metabolites were identified by FD, CI and EI mass spectral comparison with authentic standards. The major urinary metabolites in human were 4-[(5-chloro-2-oxo-3(2H)-benzothiazolyl)acetyl]-1-piperazineacetic acid (TRAA), 4-[(5-chloro-2-oxo-3(2H)-benzothiazolyl)acetyl]-1-piperazineacetic acid 1-oxide (TRAO) and the O-glucuronide of tiaramide. 4. TRAO, a new metabolite identified in human urine, was also present in mouse, rat, guinea-pig and monkey, but in smaller amounts than for human. 5. Sex differences in the excretion of sulphate of tiaramide were noted only in the rat.

Adult↗

Metabolism of tiaramide in vitro. I. Oxidative metabolism of tiaramide by human and rat liver microsomes.

1. N-Dealkylation and N-oxidation of tiaramide and of its major metabolite, TRAA, by human and rat liver microsomes were investigated. 2. With human liver microsomes, N-oxidation of tiaramide was 1.5-8.0 times faster than N-dealkylation. N-Oxidation of the metabolite, TRAA, by human liver microsomes was much slower than that of tiaramide. The high recovery of tertiary amine N-oxides in human urine after tiaramide dosing reflects the high activity of N-oxidation of tiaramide by human liver microsomes. 3. Phenobarbital treatment of rats caused an increase in the liver microsomal N-dealkylation of tiaramide in vitro, but had little effect on N-oxidation. 3-Methylcholanthrene treatment of rats caused decrease of both reactions. 4. Metyrapone added to rat liver microsomes inhibited N-dealkylation more strongly than N-oxidation. Tetrahydrofuran and 7,8-benzoflavone inhibited N-dealkylation but had little effect on N-oxidation. Addition to the microsomal incubations of antisera against NADPH-cytochrome c reductase caused marked inhibition of N-dealkylation and slight inhibition of N-oxidation.

Animals↗

[The cushion ability of lining materials for the setting and heating expansion of plaster bonded investment in casting ring. Part I: For casting mold cavity of inlay type (author's transl)].

We measured the dimensional change of mold cavity in casting ring and casting accuracy for inlay type casting using two kinds of lining materials in various conditions. These lining materials were asbestos ribbon and ceramic fiber. In the comparison of cushion ability for the expansion of investment in casting ring of these two lining materials, following results were obtained. 1. Compressibility of ceramic fiber was twice as much as asbestos. And, two sheets of ceramic fiber ribbons had enough ability for free expansion of investment in casting ring. 2. More than two sheets of asbestos ribbons in dry state had the ability of compensation for casting shrinkage in heating process. 3. Asbestos ribbon in wet state made a setting expansion of investment larger, but had not any ability of cushion for heating expansion of investment. 4. If the cushion ability of lining materials was not enough, the mold cavity shrank. The order of this shrinking inclination were no lining material state, two sheets, one sheet of wet asbestos, and one sheet of dry asbestos. 5. This shrinking inclination of smaller cavity was greater than that of larger cavity. That meant that the larger thickness of investment in ring made this shrinking inclination greater. 6. In case of without mold cavity, the heating expansion of the investment toward the casting ring were same value at any position in casting ring.

Chemical Phenomena↗

Effect of hepatic microsomal mixed-function oxidase activities in rats pretreated with Nocardia rubra cell wall skeleton.

Hepatic microsomal mixed-function oxidase activities such as aniline hydroxylase and aminopyrine demethylase activities decreased to about 50% of the control levels 1 day after i.v. injection of 4.0 mg/kg Nocardia rubra cell wall skeleton (N-CWS) to rats. These levels recovered gradually, and returned to almost the same levels as the control 6 days after injection. Cytochrome P-450 content and NADPH-cytochrome c reductase activity showed almost the same temporal changes as the mixed-function oxidase activities; cytochrome b5 content ws less affected than the others by the treatment. The enzyme activities and contents decreased less 1 and 3 days after i.v. injection of 0.4 and 0.04 mg/kg N-CWS than after the 4.0 mg/kg injection. These levels recovered gradually as well as the 4.0 mg/kg group. Three days after i.p., s.c. and p.o administration of 4.0 mg/kg N-CWS to rats, aniline hydroxylase activity and cytochrome b5 content decreased significantly to 82 and 92% of the control, respectively, in the s.c. pretreated group, but the others did not change significantly.

Animals↗