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Biomedical subjects

M Takada

Publications and source records attributed to M Takada.

At least 631 records · Page 35Linked to original sources
PubMed1985

Differentiation of the active sodium transport system during metamorphosis in Rana catesbeiana skin in relation to cadmium- and amiloride-induced responses.

The differentiation of the sodium active transport system across Rana catesbeiana skin during metamorphosis was investigated and the system was analyzed by the effects of Cd2+ and amiloride. Active transport of Na in the frog skin first appeared at stage XXI of the tadpole, indicated by the appearance of a potential difference (PD) and a short circuit current (SCC) across the skin. The effects of epidermal application of Cd2+ and amiloride on the various indicators of active Na transport were as follows: (1) Cd2+ increased PD and SCC after stage XXII; (2) Cd2+ also increased the skin resistance (RM) from stage B to XXIII, but decreased it after stage XXV; and (3) amiloride decreased PD and SCC but increased RM after stage XXI. The adult frog skin can be expressed as an equivalent circuit by three parameters: ENa, the electromotive force of the active Na current, and RNa and R sigma, corresponding to the resistance to the active Na current and the resistance of the shunt pathway, respectively. These three parameters were calculated from the amiloride effect on PD and SCC. ENa was almost null and RNa was infinite until stage XX. ENa then gradually increased, while RNa was fairly constant between 10 and 20 k omega . cm2 after stage XXI. R sigma gradually increased during metamorphosis. These data suggest that there is not an active Na pathway but a passive one in the early stage of metamorphosis of the tadpole, and that the active Na transport system suddenly appears at stage XXI and gradually develops thereafter.

Amiloride↗
PubMed1985

Redox levels of intravenously administered [14C]coenzyme Q10 and coenzyme Q10-reducing activity in subcellular fractions of guinea pig liver.

The blood level of [14C]coenzyme Q10 and the redox levels of [14C]coenzyme Q10 in the liver and heart were measured after intravenous injection of [14C]coenzyme Q10 solubilized in multilamellar liposomes into guinea pigs. The blood level of radioactivity declined biexponentially with half-lives of 11.5 min and 15.6 h in the first and second phases, respectively. The levels of reduced [14C]coenzyme Q10 in the liver and heart reached 55.8 and 46.4%, respectively, of the labeled compound in the tissues at 30 min after the injection. Coenzyme Q10-reducing activity in cytosol, microsomes and mitochondria was also investigated. This activity was found in all the fractions. The total activity was the highest in the liver cytosol. Moreover, the results of experiments using a purified enzyme suggested that one of the coenzyme Q10-reducing enzymes was NAD(P)H: quinone oxidoreductase [EC 1.6.99.2, DT-diaphorase]. These results are discussed in relation to the protective effect of reduced coenzyme Q10 against lipid peroxidation in membranes.

Animals↗
PubMed1985

[Phase II study of cis-dichlorodiammineplatinum (II) for non-small cell lung cancer].

A phase II study of cis-dichlorodiammineplatinum (II) (CDDP) was performed in 83 patients with inoperable non-small cell lung cancer (21 squamous cell carcinomas, 57 adenocarcinomas and 5 large cell carcinomas). CDDP was given by i.v. infusion at a dosage of 50 mg/m2 (low-dose regimen) or 80-100 mg/m2 (high-dose regimen) every 3 to 4 weeks. Seventy-nine out of 83 patients were evaluable for tumor response. Sixteen of these evaluable patients achieved complete or partial response, and the overall response rate was 20.3%. The response rates were 27.8% in patients with squamous cell carcinoma and 19.6% in those with adenocarcinoma. None of the patients with large cell carcinoma responded. The high-dose regimen was superior to the low-dose regimen in response rate (25.6% versus 5.8%). The responders survived significantly longer than patients with NC (p = 0.02) or PD (p = 0.003). Leukopenia of less than 3000/mm3 occurred in 12.1% of cases, and thrombocytopenia of less than 7 X 10(4)/mm3 occurred in 7.6%. A transient elevation of serum creatinine value was observed in 9 patients (10.8%). Moderate to severe nausea and/or vomiting occurred in almost all patients. It was therefore considered that CDDP was one of the most effective agents for non-small cell lung cancer with tolerable toxic effects.

Adenocarcinoma↗
PubMed1985

[Studies on the endocrinological metabolism of the parathyroid. I. The production of renal calcinosis by cyclic AMP injection in rat].

We found that a few patients with urolithiasis had normal parathyroid hormone levels but high cyclic AMP excretion. The purpose of this paper was to study the endocrinological mechanism. Male rats were given intraperitoneally dibutyryl cyclic AMP (DBcAMP), a derivative of cyclic AMP, per 100 gm of body weight for 50 days. Feed and water were supplied ad libitum. Crystal formation or calcification in mainly the dystal tubules and collecting system were found in 3 out of 10 rats, and renal calcium stones in 2 rats. The cyclic AMP of the renal parenchyma, especially the renal medulla, was elevated by more than 100 times after DBcAMP administration. Serum calcium levels, urinary calcium and phosphate excretion, and the adrenaline levels of the renal parenchyma were significantly increased. Serum parathyroid hormone was slightly enhanced, but vitamin D and the noradrenaline levels of the renal parenchyma were not changed. Based on these findings, it is suspected that stone formation in rats injected DBcAMP occurs through the action of DBcAMP on the renal tubules to increase urinary calcium excretion and to make renal stones as a form of primary hyperparathyroidism.

Animals↗
PubMed1985

[Studies on the endocrinological metabolism of the parathyroid. II. Influence of ACTH on parathyroid function and calcium metabolism].

Parathyroid hormone (PTH) is strongly concerned with the pathogenesis of urinary stones. PTH is mainly regulated by the serum calcium concentration and not by other hormones, as is usually the case. We studied whether PTH is also regulated by adrenocorticotrophic hormone (ACTH) or not. ACTH (0.25 mg) was injected intravenously to 17 patients with primary hyperparathyroidism PHP, 7 patients with urolithiasis, 7 patients with malignant hypercalcemia, and 6 control subjects. Serum calcium was significantly increased in only PHP. The serum calcium increase rate showed a significant positive correlation with serum alkaline phosphatase, and a negative correlation with the preinjected serum calcium. PTH was slightly increased in all four groups. Serum cortisol and ACTH concentrations were not significantly different among the groups. PTH concentration in a culture medium of parathyroid tissues increased after ACTH addition. Serum calcium was significantly increased after ACTH injection in an adrenalectomized rat, and decreased in a parathyroidectomized rat. From our data and those of others, it appears that ACTH acts on the adrenal glands to decrease the serum calcium concentration, and might act directly on the parathyroid gland or bones to increase it.

Adrenocorticotropic Hormone↗