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Biomedical subjects

T Obata

Publications and source records attributed to T Obata.

At least 217 records · Page 12Linked to original sources

[Studies on antimicrobial concentrations of flomoxef in serum, pelvic dead space exudate, and pelvic organs/tissues].

To women undergoing radical and total hysterectomy, flomoxef (FMOX, 6315-S) in a dose of 2 g was administered by intravenous drip infusion over 1 hour and drug concentrations in serum and pelvic dead space exudate as well as pelvic organs/tissues were determined over time. The following results were obtained: 1. Serum concentrations of FMOX after intravenous infusion showed the peak value of 92.86 +/- 17.05 micrograms/ml at the end of infusion and then gradually decreased to 29.00 +/- 10.49 micrograms/ml in 1 hour and 1.16 +/- 1.08 micrograms/ml in 6 hours. 2. Concentrations in pelvic dead space exudate, which were 6.54 +/- 3.21 micrograms/ml at the end of intravenous infusion, gradually increased to 31.28 +/- 12.69 micrograms/ml in 30 minutes, and the peak of 35.21 +/- 13.29 micrograms/ml in 1 hour. Exudate concentrations gradually decreased to 11.10 +/- 6.64 micrograms/ml at 6 hours after infusion. 3. The serum concentration at the ligature of uterine artery was 103.21 +/- 51.69 micrograms/ml. Among concentrations in pelvic organ/tissues 37.17 +/- 18.20 micrograms/ml in uterine cervix was the highest, followed by 35.77 +/- 7.68 micrograms/g in portio vaginalis, 26.35 +/- 14.15 micrograms/g in tube, 21.62 +/- 12.15 micrograms/g in ovary, 20.56 +/- 9.82 micrograms/g in myometrium, and 16.45 +/- 8.10 micrograms/g in endometrium, in this order. 4. From an analysis of the two-compartment model, the maximum serum concentration was 92.81 micrograms/ml, which was very high. The time of 50% reduction of concentration in beta phase was 1.21 hours. In the pelvic dead space exudate, the maximum concentration was 32.38 micrograms/ml and the time of 50% reduction was 2.44 hours. The AUC was 147 micrograms.hr/ml in serum and 201 micrograms.hr/ml in the pelvic dead space. The shift to the pelvic dead space was 137% when AUC's were used as the basis of the comparison. 5. Clinically, FMOX was excellently effective against adnexitis caused by Peptostreptococcus asaccharolyticus, intrauterine infection caused by Staphylococcus aureus, cystitis caused by Klebsiella and Escherichia coli, vaginal stump infection caused by Streptococcus and E. coli and many other infections.

Adult↗

The effect of benzodiazepines and beta-carbolines on GABA-stimulated chloride influx by membrane vesicles from the rat cerebral cortex.

Benzodiazepine agonists such as diazepam, flunitrazepam and clonazepam enhanced GABA (30 microM)-stimulated 36Cl- uptake in membrane vesicles from the rat cerebral cortex. The rank order of potencies was flunitrazepam greater than diazepam = clonazepam. beta-Carboline-3-carboxylate esters beta-CCM, beta-CCE and DMCM inhibited GABA-stimulated 36Cl- uptake. The rank order of inhibitory potencies was DMCM greater than beta-CCM greater than beta-CCE. The benzodiazepine antagonist Ro15-1788 antagonized the enhancement of flunitrazepam and the inhibition of DMCM on GABA-stimulated 36Cl- uptake in a competitive inhibitory manner. These results suggest that benzodiazepine receptors regulate GABA-stimulated 36Cl- uptake and there is a functional coupling between the GABA and benzodiazepine receptors, and chloride channels in membrane vesicles from the rat cerebral cortex.

Animals↗

[Studies on antimicrobial concentration of clindamycin phosphate in serum, pelvic dead space exudate, and pelvic organs/tissues].

In women undergoing radical and total abdominal hysterectomy, clindamycin phosphate (CLDM-P) in a dose of 1,200 mg was administered by intravenous drip infusion over 1 hour and the drug concentrations in serum and pelvic dead space exudate, as well as pelvic organs/tissues, were determined over time. The following results were obtained: The serum concentration of clindamycin (CLDM) after intravenous infusion showed the peak value of 24.54 +/- 7.02 micrograms/ml at the end of infusion and then gradually decreased to 3.87 +/- 0.70 micrograms/ml in 6 hours. Concentration in pelvic dead space exudate, which was 2.82 +/- 3.90 micrograms/ml at the end of intravenous infusion, gradually increased to the peak value of 13.49 +/- 6.62 micrograms/ml in 1 hour. Two hours after infusion, the level of 12.43 +/- 5.56 micrograms/ml outstripped serum concentration. Continuously in excess of serum concentration, the exudate concentration gradually decreased to 6.65 +/- 2.27 micrograms/ml at 6 hours after infusion. Cubital venous serum concentration (16.36 +/- 3.68 micrograms/ml) was almost equal to uterine arterial serum concentration (16.36 +/- 4.05 micrograms/ml) of CLDM at uterine removal. In the pelvic organ/tissue concentrations, 15.71 +/- 3.86 micrograms/g in endometrium was highest, followed by 15.19 +/- 3.80 micrograms/g in oviduct, 14.80 +/- 3.52 micrograms/g in myometrium, 14.74 +/- 4.02 micrograms/g in ovary, 14.09 +/- 2.90 micrograms/g in portio vaginalis. The concentration was lowest (11.49 +/- 1.44 micrograms/g) in cervix uteri. Clinically, combined treatment with CLDM-P and ceftizoxime was excellently effective for endometritis induced by P. asaccharolyticus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Molecular weight of mitochondrial type B MAO in various organs of guinea pig].

Molecular weights of mitochondrial type B monoamine oxidase (MAO) in guinea pig brain, liver and kidney were estimated, and their identities and multiplicity were studied. We ascertained what concentration of 3H-pargyline bound to type B MAO specifically from the inhibition curve toward serotonin (5-HT) and beta-phenylethylamine (beta-PEA) by pargyline. Pargyline irreversibly binds to FAD in MAO at a one to one molecular ratio. 3H-pargyline bound to type B MAO specifically and irreversibly by incubation for 5 hr at 37 degrees C, and SDS-disc electrophoresis was carried out using 3H-pargyline as a tracer. The molecular weight of MAO was estimated after specific binding of pargyline was corrected for non-specific binding. The molecular weight of type B MAO in every organ was found to be 60,000, giving a single peak after solubilization with 6% SDS, but several peaks at higher molecular weight were found in each organ after solubilization with 2% SDS. In the brain, there appeared to be a peak of 100,000, and it was suggested that the MAO existed as a dimer which was composed of a FAD containing subunit and a low molecular weight subunit containing no FAD. In the liver, there appeared to be peaks of 120,000 and 240,000, and it was suggested that the MAO existed as a dimer and tetramer. In the kidney, there appeared to be a peak of 180,000, and MAO was suggested to exist as a trimer.

Animals↗

Gate mechanism in breathlessness caused by chest wall vibration in humans.

The effects of bilateral alternating out-of-phase vibrations were studied in 10 normal healthy subjects and five asthmatic patients. The second or third intercostal spaces were vibrated during expiration, and the seventh to ninth intercostal spaces were vibrated during inspiration. Most subjects sensed breathlessness during such vibrations, and 100 Hz was most effective. The degree of breathlessness correlated positively with increased respiratory rate. Respiratory rate increased from 14.1 +/- 3.78 (mean +/- SD) to 22.3 +/- 7.14 breaths/min (P less than 0.05) during relatively severe breathlessness and to 20.39 +/- 5.66 breaths/min (P less than 0.05) during less uncomfortable sensation. Slight or negligible breathlessness induced no significant increase in rate (15.33 +/- 4.19 breaths/min). All asthma patients described the sensations during vibration as similar to those during asthma attacks, and their respiratory rates increased 20.7 +/- 11.03% during 100 Hz vibration (P less than 0.01). It is suggested that the uncomfortable sensation of breathlessness may be induced by muscle spindles in the intercostal muscles being activated out of phase with the respiratory cycle. The central mechanism that receives the intercostal afferents may have a certain gate that operates in relation to the sensation of breathlessness.

Adult↗

Enzymic and molecular characteristics of a new form of monoamine oxidase, distinct from form-A and form-B.

The present study was undertaken to clarify the enzymic and molecular properties of monoamine oxidase (MAO) in carp brain. In particular, its sensitivities to selective MAO inhibitors, kinetic properties and molecular weight were compared with those of the enzyme in carp liver. The selective and potent MAO-A and MAO-B inhibitors FLA 788(+), FLA 336(+), MD 780236 and benzylcyanide caused dose-dependent inhibitions of MAO activity in both carp brain and liver; the inhibition curves were all single-sigmoidal, and the degrees of inhibition of the activities towards 5-hydroxytryptamine (5-HT, selective MAO-A substrate), tyramine (substrate for both forms of MAO) and beta-phenylethylamine (PEA, selective MAO-B substrate) were similar. This was also the case for inhibition of activity in carp brain by the irreversible and selective MAO-A and MAO-B inhibitors clorgyline and I-deprenyl, indicating the presence in both preparations of a single MAO which differs from either form of MAO. Studies on the substrate specificities and Km values for these three substrates and the inhibitory effects of some compounds suggested that the enzymic characters of MAO in carp preparations were similar and that these enzymes might be FAD-containing enzymes, like MAO in various mammals. By labelling the preparations with radioactive pargyline and then subjecting them to sodium dodecyl sulfate electrophoresis, the apparent molecular weights of carp brain and liver MAO were estimated as 60,000 daltons. The same value was also obtained for rat brain and liver mitochondrial MAO-B. These results indicate that by the present definitions of MAO-A and MAO-B, MAO in carp brain and liver is similar to, but distinct from, both these forms of MAO.

Animals↗

Potentiating activity of rat serum extract on ACTH-induced corticosteroidogenesis in isolated rat adrenal cells.

ACTH potentiating activity was found in rat serum. The extract, obtained from ACTH-free rat serum by the QUSO G 32 adsorption method, potentiated ACTH1-24-induced corticosterone production in isolated rat adrenal cells. In our assay system, the maximal potentiation was observed with the extract of 0.5 ml of rat serum. With the extract, the log dose response curve for ACTH1-24 shifted to the side of lower doses of ACTH1-24. The potentiating substance was stable in the serum: the activity was hardly decreased even after leaving the serum stand for six days at room temperature. On Sephadex G-100 gel filtration of the extract, the most of activity was found between about 40,000 to 9,000 in molecular weight and a small portion of the activity was in the range of lower molecular weight. After hypophysectomy, the potentiating activity found in the fractions was markedly decreased, but a part of the activity still remained 30 days after the operation. This result suggests that the potentiating substance is produced mainly by the pituitary, but also produced by the other organ(s). SDS polyacrylamide gel electrophoresis of the active fractions revealed five peptides which were decreased quantitatively by hypophysectomy.

Adrenal Glands↗

Nonicteric liver damage with a gamma-glutamyl transpeptidase level of 5,609 units/l in a renal-transplant recipient receiving azathioprine.

A 26-year-old male with renal allograft, who received immunosuppressive treatment with azathioprine, presented marked elevations of serum biliary tract enzymes, such as gamma-glutamyl transpeptidase (5,609 units/l) and alkaline phosphatase (60.5 Bessey-Lowry units), 14 months after transplantation. Two months later the patient became icteric; he died of respiratory failure 19 months after the renal allograft. Postmortem examination revealed intrahepatic cholestasis with minimal inflammatory cell infiltration, indicating drug hepatotoxicity.

Adult↗