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Biomedical subjects

S Gotoh

Publications and source records attributed to S Gotoh.

At least 145 records · Page 8Linked to original sources
PubMed1984

[The effects of DDP on the seminiferous epithelium of rats].

Adult male rats were injected intraperitoneally with 2 mg, 4 mg and 6 mg Cis-diamminedichloroplatinum (DDP) per kg body weight. The animals were then sacrificed on the 7th, 24th or 35th day. Two specimens of testis from each rat were stained by H.E. technique, then the Pachytene primary spermatocytes and Sertoli cells in the cross sectioned tubules at stage IV-V, IX-X and XIII-XIV were counted. Significant decrease of Pachytene/Sertoli(P/S) valueinstage IX-X tubules on the 24th day (p less than 0.01) suggests that DDP has a cytotoxic effect on early differentiated type A spermatogonia (A1).

Animals↗
PubMed1983

Effect of captopril on renal vascular resistance, renin, prostaglandins and kinin in the isolated perfused kidney.

Vasodilatory and natriuretic effects of captopril were studied in the isolated hog kidney perfused with modified Krebs-Ringer solution. Renal arterial infusion of captopril caused increases in releases of renin, prostaglandins (PGE2, 6-keto-PGF1 alpha and PGF2 alpha) and kinin, and was accompanied by a decrease in the renal vascular resistance and an increase in urinary sodium excretion. Indomethacin administered with captopril diminished the saluretic effect of captopril and evoked an increase in kinin, but was associated with a marked decrease in prostaglandin and renin releases, while renal vascular resistance remained decreased. Indomethacin alone did not alter vascular resistance and kinin; however, renin and prostaglandin releases were decreased. Aprotinin administered with captopril showed a decrease in releases of prostaglandins, renin and kinin without any change in vascular resistance. These results suggest that increased release of kinin induced by captopril contributes to a reduction in renal vascular resistance. Increased prostaglandin release after captopril administration may be caused by an increase in kinin without direct involvement of captopril in prostaglandin synthesis. Renal prostaglandins may enhance sodium excretion and mediate renin secretion in captopril perfusion.

Animals↗
PubMed1983

Screening for carcinogens by DNA-synthesis inhibition test using mouse L-cells.

Bacterial test systems for potential carcinogens sometimes give false negative results. To overcome this problem, several short term test systems have been described. One of them is the DNA-synthesis inhibition test described by Painter (1977). Our DNA-synthesis inhibition test system using mouse L-cells gave positive results when monocrothaline, phenacetin and thioacetamide, which were negative in the Ames test, were tested.

Animals↗
PubMed1983

Establishment of a human diploid cell strain.

A new human diploid fibroblast-like cell strain has been established from dermal tissue of a 2 months old female embryo. This cell strain showed diploid karyotype and has a finite life span of 95-100 generations. No spontaneous transformation was observed during the whole life span in vitro. This cell strain is susceptible to SV40 infection and can be transformed easily by it.

Cell Line↗
PubMed1983

One-trial long-lasting food-aversion learning in wild Japanese monkeys (Macaca fuscata).

We examined how Japanese monkeys in the wild formed an aversion to food which had been paired with poison. Ten monkeys of various ages and both sexes were chosen as subjects from 105 members of the Shiga-A1 troop at Jigokudani in Shiga Heights in Japan. We gave almond nuts to each subject. Once a monkey ate 10-20 almond nuts, he was captured and moved into an injection cage. Seven experimental subjects were injected intravenously with cyclophosphamide (20 mg/kg). Three control subjects received the same treatment except that they were injected with physiological saline. About 1 hour later, all subjects were released into the troop. The tests for conditioned aversions were conducted during the next 2 days. In the tests, the experimental subjects would not eat almond nuts, while the control subjects showed no hesitation in eating them. Five of the seven experimental subjects retained perfectly the aversion to almond nuts in tests conducted 1 month and 3 months later. The one-trial long-lasting food-aversion learning shown by the wild Japanese monkeys is discussed in terms of their feeding strategy. These results also suggest that food-aversion conditioning has potential as a nonlethal method for controlling crop-raiding monkeys.

Animal Population Groups↗
PubMed1983

Levels of plasma 6-keto-PGF1 alpha in normotensive and essential hypertensive males with and without a family history of hypertension.

Prostacyclin may act physiologically as an antihypertensive hormone. It remains uncertain, however, whether prostacyclin may be involved in the etiology of primary hypertension. As an index of prostacyclin production, we measured the levels of venous plasma 6-keto-PGF1 alpha by specific radioimmunoassay after silicic acid column chromatographic purification in 31 normotensive and 36 hypertensive males. The subjects were grouped according to the presence or absence of a family history of hypertension, and matched for age and blood pressure. Levels of 6-keto-PGF1 alpha in normotensive males with a family history of hypertension (12.0 +/- 1.7 pg/ml; mean +/- SEM; n = 18) were lower than in normotensive males without a family history of hypertension (17.7 +/- 2.0 pg/ml; n = 13) (p less than 0.01). Levels of plasma 6-keto-PGF1 alpha in hypertensive males with a family history of hypertension (10.2 +/- 1.2 pg/ml; n = 15) were lower than in hypertensive males without a family history of hypertension (20.5 +/- 1.5 pg/ml; n = 21) (p less than 0.005). The levels of plasma 6-keto-PGF1 alpha in males with a family history of hypertension may be decreased genetically. The decrease in production of prostacyclin in males with a family history of hypertension may be a factor in the etiology of hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Effect of aging on 6-keto-PGF1 alpha levels in normotensive and essential hypertensive males.

Prostacyclin (PGI2) is produced in the vessel wall and acts as a vasodilator hormone. Measurement of plasma 6-keto-PGF1 alpha is considered to be an index of PGI2 production. In the present study the effects of aging on the plasma 6-keto-PGF1 alpha levels were studied in 64 normotensive and 48 essential hypertensive males. The subjects were divided into 3 groups, i.e., young (24-39 years), middle-aged (40-55 years) and elderly (over 56 years) groups. Plasma 6-keto-PGF1 alpha was measured by specific radioimmunoassay after silicic acid column chromatographic purification. The 6-keto-PGF1 alpha levels were lower in elderly normotensive males (10.3 +/- 1.4 pg/ml, mean +/- SE, n = 12) than in normotensive young males (15.3 +/- 2.3, n = 30, p less than 0.05). The plasma 6-keto-PGF1 alpha levels in hypertensive elderly males (10.6 +/- 1.3 pg/ml, n = 10) is lower than in hypertensive young males (19.8 +/- 2.2, n = 17, p less than 0.01). These results indicate that the plasma 6-keto-PGF1 alpha levels decreased with age in both normotensive and hypertensive groups. Thus, PGI2 production may decrease with age.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

[Combination chemotherapy with bleomycin, vincristine and methotrexate for stage I non-seminomatous germ cell testicular tumors].

Ten patients with Stage I non-seminomatous germ cell testicular tumors underwent orchiectomy and combination chemotherapy with bleomycin, vincristine and methotrexate with CF rescue (BOM) as an induction therapy followed by cyclophosphamide, vincristine and methotrexate as a maintenance therapy (COM). The results were as follows: BOM seemed to be effective as a further treatment for Stage I non-seminomatous germ cell testicular tumor patients. All 10 patients are alive and disease-free for a period from 1 year and 6 months to 5 years and 3 months (mean: 3 years and 9 months). The chemotherapy should be continued at least for a year, since relapse occurred in 2 of 4 patients who received only induction therapy. However, they completely responded to other chemotherapy regimens (BVP and BOAM ). BOM and COM therapy were scarcely toxic and no serious side effects were recognized. From the above results, it was considered that combination chemotherapy (BOM and COM) can be an alternative treatment to the conventional retroperitoneal node dissection and radiation therapy for Stage I non-seminomatous germ cell tumors.

Adult↗
PubMed1982

Effect of prostacyclin infusion on active and inactive renin release in the isolated perfused kidney.

The effect of prostacyclin infusion into the renal artery of the isolated perfused hog kidney on the release of active and inactive renin was investigated. Infusion of prostacyclin at a rate of 0.1 microgram/min resulted in a significant increase (p less than 0.01) in active renin and a significant fall (p less than 0.01) in inactive renin. Prostacyclin also increased urinary kallikrein excretion (p less than 0.05). The results indicate that the kidney secretes not only active renin but also inactive renin, and suggest that prostacyclin stimulates the conversion of inactive renin to the active form through the activation of the renal kallikrein system.

Animals↗
PubMed1982

Effect of three angiotensin II antagonists, [Sar1, Thr8]-, [Sar1, Ile8]- and [Sar1, Ala8]angiotensin II on blood pressure and endocrine factors in normal subjects.

The biological effects of 1-Sarcosine, 8-Threonine angiotensin II ([Sar1, Thr8]ANG II) on blood pressure, plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were investigated in six normal subjects on an unrestricted diet, and compared with those of 1-Sarcosine, 8-Isoleucine ANG II ([Sar1, Ile8]ANG II) and 1-Sarcosine, 8-Alanine ANG II ([Sar1, Ala8]ANG II). All three ANG II analogues (AIIA) showed agonistic pressor activity, that of [Sar1, Ile8]ANG II being greater than that of [Sar1, Thr8]ANG II or [Sar1, Ala8]ANG II. The antagonistic effect of [Sar1, Thr8]ANG II on blood pressure was less than [Sar1, I1e8]ANG II or [Sar1, Ala8]ANG II. Both [Sar1, Ile8]ANG II and [Sar1, Ala8]ANG II increased PAC and blocked the steroidogenic action of ANG II, while [Sar1, Thr8]ANG II showed little effect on PAC. All three AIIA caused similar suppression of PRA and showed no inhibitory effect on the decrease in PRA produced by ANG II. These results indicate that [Sar1, Thr8]ANG II is an AIIA with weak agonistic pressor action and that it has vascular selective properties. It is also suggested that ANG II receptors in a variety of target organs are heterogeneous.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1982

Responses of active and inactive plasma renin and changes in urinary kallikrein and plasma prekallikrein to various conditions in normal subjects.

Little is known about changes in inactive plasma renin in various conditions or the in vivo activation mechanism of inactive renin. The effects of various factors known to stimulate or suppress renin release on active and inactive PRA were examined in normal subjects. Inactive PRA was determined as the difference between the total PRA after trypsin activation and active PRA. Concurrent measurements of urinary kallikrein excretion and plasma prekallikrein activity were performed to assess the possible role of renal or plasma kallikrein in in vivo activation of inactive renin. Short term stimulation with iv furosemide and ambulation, infusion of isoproterenol, and administration of captopril increased active PRA, but had little or no effect on inactive PRA. Sodium restriction and sodium loading, each for 4 days, induced parallel changes in active and inactive PRA. The administration of propranolol for 4 days decreased active PRA but did not change inactive PRA. There were no significant correlations between the changes in urinary kallikrein excretion and those in active PRA or in the proportion of active to total PRA after any short term treatments, except furosemide administration. Plasma prekallikrein activity was correlated with the proportion of active renin only during the long term sodium balance study. The present data suggest that the mechanisms ofr the control of inactive and active renin are different. Neither renal nor plasma kallikrein seems to be consistently involved in the in vivo activation of inactive renin.

Adult↗
PubMed1982

Release of prostaglandin I2 from hog kidney by propranolol.

Prostaglandin I2 (PGI2) decreases blood pressure. Perfusion of isolated hog kidney by propranolol in modified Krebs-Ringer solution resulted in a significant increase in 6-keto-prostaglandin F1 alpha, the major metabolite of PGI2. Prostaglandin E2 and renin activity remained unchanged. Because the concentration of PGI2-like substance in the renal vein has been shown to be greater than in the renal artery after bradykinin infusion, a contribution of PGI2 to the regulation of blood pressure was proposed. Isoproterenol has been shown to augment urinary kallikrein, but the effect of urinary kallikrein on propranolol is unclear. With a modified Krebs-Ringer solution free of plasma kininogen, a renin substrate, it was concluded that propranolol (1) induces PGI2 release from the kidney, which may contribute to a direct antihypertensive action of this beta-adrenergic blocking agent, and (2) decreases urinary kallikrein.

Animals↗