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Biomedical subjects

T Akimoto

Publications and source records attributed to T Akimoto.

At least 217 records · Page 12Linked to original sources
PubMed1982

A complete selective C1q deficiency in a patient with discoid lupus erythematosus (DLE).

A 32 year old male patient with discoid lupus erythematosus (DLE) was found to have a complete, selective deficiency of C1q subcomponent of the complement assessed either by haemolytic assay or by protein determination. Addition of highly purified C1q completely restored the complement haemolytic activity of the patient's serum. Neither C1q precipitin nor anti-complementary activity was detected. Lymphocytes isolated from the patient's peripheral blood, however, bound as many C1q molecules as those of healthy control individuals. The patient is in good health except for skin lesions. A low level of circulating immune complexes was detected in his serum, but no C1q molecules were bound. Serum complement activities of the patient's mother and two other siblings were within the normal range. An impaired synthesis of C1q protein was strongly suggested as the cause of C1q deficiency in this patient's serum.

Adult↗
PubMed1981

Effect of furosemide in congestive heart failure.

The diuretic effect of furosemide was studied in 18 patients with congestive heart failure. Subjects were divided into two groups, group I consisting of eight patients with moderate and group II of 10 patients with advanced congestive heart failure. Six hours after bolus injection of furosemide (40 mg), mean urinary sodium was 120.5 +/- 36.7 mEq in group I and 68.2 +/- 25.8 mEq in group II (p less than 0.01), mean urine volume was 1,100 +/- 281 and 764 +/- 257 ml (p less than 0.05), mean urinary furosemide excretion was 28.08 +/- 2.60 and 24.00 +/- 0.74 mg (p less than 0.05), and mean furosemide renal clearance was 73.4 +/- 16.6 and 42.3 +/- 11.5 ml/min (p less than 0.001). Diuretic effect and furosemide renal clearance, as well as urinary furosemide excretion, correlated positively. The diuretic effect of furosemide with and without hydralazine (0.2 mg/kg) was compared in eight patients in group II. Urinary sodium excretion 6 hr after furosemide rose from 77.2 +/- 31.0 to 122.8 +/- 42.5 mEq after furosemide with hydralazine (p less than 0.01). Urine volume rose from 854 +/- 278 to 1,279 +/- 359 ml (p less than 0.001), urinary furosemide excretion rose from 23.64 +/- 2.03 to 26.94 +/- 2.30 mg (p less than 0.01), and furosemide renal clearance rose from 46.3 +/- 12.2 to 62.5 +/- 18.6 ml/min (p less than 0.01).

Adult↗
PubMed1980

Lack of induction of dominant lethal mutations in male mice by nalidixic acid.

Nalidixic acid (NA) in single or in 5 consecutive daily doses of 100 or 1000 mg/kg produced no dominant lethal mutational effects in male ddY strain mice during an 8-week mating schedule. Ethylmethanesulfonate (EMS), used as a positive control, produced dominant lethal mutations in the first and second weeks.

Animals↗
PubMed1979

Mutagenicity studies of 4-(2-carboxyethyl) phenyl trans-4-aminomethylcyclohexane carboxylate hydrochloride (DV-1006). A new antiulcer drug.

An antiulcer drug, 4-(2-carboxyethyl) phenyl trans 4-aminomethylcyclohexane carboxylate hydrochloride (DV-1006), was studied for mutagenicity using bacterial systems, in vitro and in vivo cytogenetics, and dominant lethal tests. No mutagenicity of DV-1006 was observed either in the rec-assay on Bacillus subtilis or in the Salmonella/microsome test (Ames test). In in vitro cytogenetics, DV-1006 had no effects on the chromosomes of chinese hamster cells at cytotoxic doses. Rats were treated singly or on 5 consecutive days orally with dose levels of 16, 160, or 1600 mg DV-1006/kg for detecting cytogenetic effects in vivo. As a result, no increase of the incidence of chromosomal aberrations in bone marrow cells was observed in any group of DV-1006. A single or 5 daily oral administration of DV-1006 (16 or 1600 mg/kg) to male mice and subsequent mating for 8 weeks produced no dominant lethal mutational effects. These results show that DV-1006 has no mutagenic potential.

Animals↗
PubMed1979

Metabolism of budralazine, a new antihypertensive agent, III.

1. [14C]Budralazine (I) administered orally to normotensive and spontaneously hypertensive rats showed no significant difference in metabolic fate between the two groups. 2. Peak plasma levels of 14C were 3.6 microgram equiv. of I per ml in both normotensive and hypertensive rats. Approx. 5% of total 14C in the plasma consisted of I within 4 h, but thereafter the parent drug was not detected. Approx. 15% of 14C in the plasma consisted of 1-hydrazinophthalazine within 16 h after the administration. 3. 45% and 37% of the dose of 14C was excreted into urine and faeces within 24 h, respectively. 4. A high retention of 14C in the aorta wall was found and the time course of 14C in the aorta wall was compatible with that of the reduction in blood pressure. The radioactive materials retained in the aorta wall were likely to be I or 1-hydrazinophthalazine, probably the latter, following macroautoradiography in hypertensive rats.

Animals↗
PubMed1978

On the chromaffin cells in dog adrenal medulla; with special reference to the small granule chromaffin cells (SGC cells).

Small granule chromaffin cells (SGC cells) were identified in the adrenal medulla of adult dogs. They were small in size and usually showed a high nucleo-cytoplasmic ratio. Cytoplasmic projections were occasionally observed in some of these cells. They contained a variable number of small secretory granules with diameters ranging from 70 to 300 nm, but mostly from 100 to 200 nm. The densities of the secretory granules were variable, ranging from highly dense to less dense. These adrenal SGC cells were rich in free ribosomes and polysomes, but were relatively poor in other cell organelles. Chromaffin cells which were intermediate in their characteristics (IM cells) between the SGC cells and the typical A and N cells were also identified. These IM cells contained both highly electron dense and less dense granules in various proportions. The IM cells were classified into two subgroups, according to the proportions of adrenaline type granules and noradrenaline type granules. One group resembled A cells (IM-A cells) and the other resembled N cells (IM-N cells). Light microscopic histochemical studies of A cells stained with the ammoniacal silver solution demonstrated that they contained a small number of darkly stained granules. Electron microscopic cytochemistry revealed that the electron dense granuls in the SGC cells, IM cells and A cells reacted positively with both the potassium dichromate solution at pH 4.1 and the ammoniacal silver solution.

Adrenal Medulla↗
PubMed1978

Acute, subacute and chronic toxicity of oxepinac.

The acute, subacute and chronic toxicity of 6,11-dihydro-11-oxodibenz[b,e]oxepin-3-acetic acid (oxepinac) was investigated in several animal species. The LD50 value was lower in rats than in rabbits, mice and dogs. The major cause of death was perforative ulcer in the gastrointestinal tract. Long-term study in rats revealed that oxepinac produced no hematological, blood chemical and pathological changes except for minor anemia and fatal ulcer formation occurring predominantly in females. Oxepinac proved to be less toxic than indometacin in chronic toxicity in rats.

Acetates↗
PubMed1978

Teratogenicity study of oxepinac in mice and rabbits.

Teratogenic effects of 6,11-dihydro-11-oxodibenz[b,e]oxepin-3-acetic acid (oxepinac) were examined in mice and rabbits. Oxepinac was orally given to pregnant animals during the organogenesis period at 3, 30 and 90 mg/kg/day for mice, and at 3, 10 and 20 mg/kg/day for rabbits. It can be concluded that oxepinac has no teratogenic effect on fetuses in mice and rabbits. In addition, the medication of oxepinac to pregnant mice does not adversely affect the postnatal development of their pups.

Acetates↗
PubMed1977

Prostaglandin synthetase systems in rat and rabbit renal medulla and inhibition by non-steroidal anti-inflammatory drugs.

The properties of prostaglandin synthetase systems (PSSs) in the renal medulla of the rat and rabbit, and inhibition by ketoprofen, indomethacin, ibuprofen, phenylbutazone and aspirin were investigated in relation to their anti-inflammatory, analgesic, antipyretic and ulcerogenic activities. Rat and rabbit PSSs produced prostaglandin (PG)E and PGF from arachidonic and dihomo-gamma-linolenic acids and had an optimal pH of 8.5 and 7.5 for PGE formation, respectively. Only a slight loss of activity occurred with lyophilization. In the rat PSS, all drugs tested were inhibitory in the order of ketoprofen, ibuprofen, indomethacin and aspirin, respectively. In the rabbit PSS, the same potency relationship was also found. Drug sensitivity of the rat PSS was remarkably lower than that of the rabbit PSS. Significant correlations were noted between the inhibitory potencies of the drugs against both PSSs and other in vivo pharmacological activities within the same species.

Animals↗