Biomedical subjects
Publications and source records attributed to N Terada.
Although associations of a variety of developmental abnormalities of the brain and the spinal cord with neurofibromatosis have been reported, association of a cerebral arachnoid cyst with neurofibromatosis is extremely rare. We report the second case of this association in an 8-year-old Japanese boy.
To ascertain whether abnormalities in testicular binding of follicle stimulating hormone (FSH) are related with spermatogenic impairment found in idiopathic male infertility, we measured FSH receptors in testicular tissues obtained by biopsy from 37 infertile men. Since there had been few reports on the characterization of human testicular FSH receptor, we first established conditions for FSH receptor assay in small amounts of human testicular tissues taken by biopsy. Thirty-seven infertile men were divided into 3 groups by histological grading using Johnsen's score count, and testicular FSH receptors among these groups were compared. Although 6 of 12 infertile men with low Johnsen's score count and 3 of 9 men with middle score count had no obvious FSH binding sites with high affinity, all 16 men with high score count had high affinity FSH binding sites. The present findings demonstrate that the decrease in testicular high affinity binding sites for FSH is related with the degree of spermatogenic impairment found in idiopathic male infertility.
Intravenous administration of leucine-enkephalin (30 micrograms/kg) caused significant decreases in mean blood pressure, cardiac output, and left ventricular dP/dt in intact dogs. However, cardiovascular effects of leucine-enkephalin (30-120 micrograms/kg) did not occur in the heart-lung preparation uninfluenced by extracardiopulmonary factors. These results provide no evidence of a direct cardiac action of leucine-enkephalin.
In anesthetized dogs, intravenous infections of 30 micrograms/kg of leucine- and methionine-enkephalin (L- and M-enk respectively) produced a significant reduction of mean blood pressure (MPB) and heart rate (HR). The peak decreases in MBP and HR occurred within 1 min after injection and recoveries to pre-injection levels within 3 min. The depressor responses to both L-enk and M-enk were abolished by intracisternal pretreatment with yohimbine (0.5 mg/kg) but not with prazosin (0.1 mg/kg). Pretreatment with either drug did not alter the bradycardia. All cardiovascular effects of both L-enk and M-enk were prevented by intravenous pretreatment with naloxone (2 mg/kg). These results suggest that central alpha 2-adrenoceptors may participate in the central actions of enkephalins on blood pressure regulation. HR responses to enkephalins may be elicited by a different mechanism.
As a tracer, biotin was bound to the amino group of newly synthesized 6-ethylenediamino-17-beta-estradiol. Two competitive methods were developed by using the tracer (E2-B). Method I, E2-B, sample, and anti E2 antibody conjugated with horse radish peroxidase were mixed, and the mixture was added to the avidin immobilized on a microplate to separate free and bound tracer. Then the enzyme activity which remained after washing was measured by using H2O2 and o-phenylenediamine. E2 was quantified from 75 pg/ml to 9.6 ng/ml; (II) E2-B and the samples were added to the anti E2 adsorbed on a microplate. After washing, the avidin conjugated with HRP was put into the immune complex plate, and the enzyme activity which remained was determined to calculate E2. The standard curve indicated E2 from 75 pg/ml to 19.2 ng/ml. The E2 values obtained by the new methods correlated with those by 3H-RIA and the EIA was useful in monitoring the induction of ovulation.
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Bilateral tubular adenomas develop spontaneously in ovaries of WB X C57BL/6 F1-Sl/Slt mice after exponential loss of oocytes. We investigated the ability of this tumor to produce sex steroids. Incubation of tubular adenoma tissue with [3H] progesterone resulted in production of [3H]androstenedione and [3H]-testosterone. The amount of androgens produced by the tumor tissue was much greater than that produced by the normal ovarian tissue. The concentration of testosterone in the serum of the Sl/Slt mice bearing tubular adenomas, measured by radioimmunoassay, was about five times as high as the value in the serum of the congenic +/+ mice. Although incubation of the tumor tissue with [3H]androstenedione resulted in production of 3H-estrogens, the aromatase activity of the tumor tissue was about one-fifth of that of the normal ovarian tissue. Therefore, the major sex steroid secreted by tubular adenomas seemed to be testosterone. These endocrinological features of tubular adenomas were consistent with the following pathological features of the Sl/Slt mice with the tumors: (a) although the weight of uterus of the Sl/Slt mice was about one-half of the value observed in the +/+ mice, it decreased markedly after oophorectomy; and (b) submandibular glands of the Sl/Slt mice were significantly heavier than those of the +/+ mice.
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Addition of cortisol at concentrations above 300 nM selectively inhibited the synthesis of alpha-lactalbumin and the accumulation of its mRNA in the mouse mammary gland cultured in the presence of insulin and prolactin, whereas the same treatment augmented casein synthesis and the accumulation of casein mRNA. Prostaglandin E2 or F2 alpha reversed the inhibitory effects of cortisol in a dose-dependent manner, without affecting casein production. The levels of prostaglandin E2 or F2 alpha in tissue explants cultured with insulin and prolactin increased about 2.6-fold over those in uncultured tissue, and the addition of cortisol decreased these levels approximately 2-fold. These results indicate the ability of prostaglandins to counteract the inhibitory effect of cortisol on the alpha-lactalbumin gene expression in the mouse mammary gland.
Diethylstilbestrol (DES) pellets were implanted in female golden hamsters on day 22 after birth. Hamsters with or without the DES pellet were hypophysectomized on day 23. Starting from day 26, the hypophysectomized hamsters were injected daily with 2.3-40 micrograms NIH-LH-S19, 6 or 18 micrograms NIAMD-oFSH-13, 50 micrograms NIAMD-Rat-FSH-B-1, or saline for 3 days. Ovarian homogenates from these hamsters on day 29 were incubated with [14C]-4-androstene-3,17-dione and enzyme activity (nmol/g/h) was estimated. The 5 alpha- and 5 beta-reductase activities decreased significantly following hypophysectomy. In the hypophysectomized hamster ovary, a distinct response to LH but not to FSH or DES in the 5 alpha-reductase activity was found. On the other hand, the 17 beta-ol-dehydrogenase activity was stimulated by FSH but not by LH or DES. The 5 beta-reductase activity was stimulated by DES, FSH or 2.3 micrograms LH but not by 7-40 micrograms LH. In the DES-treated, hypophysectomized hamster ovary, LH and FSH stimulated the 5 alpha-reductase and 17 beta-ol-dehydrogenase activities, respectively, but FSH or LH treatment had no significant effect on the 5 beta-reductase activity. These results show that the 5 alpha-reductase activity is regulated by LH, while the 17 beta-ol-dehydrogenase activity is stimulated by FSH in immature golden hamster ovary. The 5 beta-reductase activity seems to be regulated predominantly by FSH but the effect of FSH is largely mediated by estrogen.
We have reported [1,2] in immature golden hamster testis that 5 beta-reductase is localized in the seminiferous tubules, while 5a-reductase is present in the interstitial tissue and that the 17 beta-ol-dehydrogenase activity is found predominantly in the seminiferous tubules. In the present study, we show the intratubular localization of these enzymes. The left testis of golden hamster was irradiated with 2000R or 8000R of X-rays at 22 days of age. The hamsters were killed at 28 days of age. Homogenates of the left irradiated and right intact testes were incubated with [14C]-4-androstone-3,17-dione and NADPH, and enzyme activity was estimated. Both testes were also examined histologically. The X-irradiation of the testis resulted in an almost complete disappearance of germ cells with a significant decrease in testis weight, but the interstitial tissue and tubular nongerm cells including Sertoli cells remained almost unchanged. However, the activities of 5 beta-reductase and 17 beta-ol-dehydrogenase expressed as nmol formed/testis/h did not decrease at all. These results show that 5 beta-reductase is localized in the tubular nongerm cells including the Sertoli cells and 17 beta-ol-dehydrogenase is present in the tubular nongerm cells and interstitial tissue in immature golden hamster testis.
Cortisol 21-mesylate, an alkylating derivatives of cortisol, was previously shown to exert an anti-glucocorticoid action in rat hepatoma cell culture (Simons, Thompson and Johnson 1980). In this study the effect of cortisol 21-mesylate on milk protein synthesis induced in cultured mouse mammary gland by glucocorticoid, insulin, and prolactin was investigated. Addition of cortisol 21-mesylate at concentrations ranging from 10(-8) M to 10(-6) M produced no inhibition of casein synthesis that was induced by glucocorticoid, insulin and prolactin in mammary explants from midpregnant mice. On the other hand, cortisol 21-mesylate in combination with insulin and prolactin stimulated casein synthesis in cultured tissue. The potency of cortisol mesylate was about 1/10 to 1/30th of that of cortisol. Cortisol 21-mesylate, like cortisol, also augmented the accumulation of alpha-lactalbumin in midpregnant rat mammary tissue cultured in the presence of insulin and prolactin. A cell-free competition study of glucocorticoid receptors using cytoplasmic extracts from mouse mammary tissue showed that cortisol 21-mesylate competitively inhibited the binding of dexamethasone on glucocorticoid receptors. The apparent affinity of cortisol 21-mesylate for glucocorticoid receptors is about 1/10th of that of cortisol. These results indicate that cortisol 21-mesylate acts as a glucocorticoid but not as an antiglucocorticoid in the mammary gland.
The effect of ethanol on maternal and neonatal hepatic heme and drug metabolizing systems was determined. Ethanol (16%, w/v) was administered orally as drinking solution to pregnant or lactating rats at different pre- and post-natal stages. The dams and pups were sacrificed on days 7, 14 and 21 after parturition, respectively. Ethanol administration to lactating rats from just after birth caused an appreciable decrease in the maternal and neonatal body and liver weights. In addition, the activities of nicotinamide adenine dinucleotide phosphate-cytochrome c reductase, nicotinamide adenine dinucleotide-cytochrome b5 reductase and heme oxygenase were significantly enhanced in the livers of neonates whose mothers were exposed to the ethanol during only first week of lactation, but those activities were not altered in the maternal livers. However, no remarkable alterations were observed in the contents of cytochrome P-450 and b5, and the activities of aminopyrine demethylase, aniline hydroxylase and delta-aminolevulinic acid synthetase in the livers of neonates from mothers who had received ethanol during lactation period or last week of gestation, although the activities of aminopyrine demethylase and aniline hydroxylase were enhanced significantly in lactating dams by ethanol consumption for 14 d after parturition.
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Previous studies of cultured mammary gland from mid-pregnant mice showed that addition of cortisol at concentrations ranging from 3 X 10(-8) to 3 X 10(-6) M caused progressive increases in casein accumulation but marked decreases in alpha-lactalbumin accumulation in tissue cultured in the presence of insulin and prolactin (Ono, M., and Oka, T. (1980) Cell 19, 473-480). The present studies showed that the addition of prostaglandin (PG) E2 blocked the inhibitory effect of cortisol on the synthesis and accumulation of alpha-lactalbumin without affecting casein production. The effect of PGE2 was observed at a concentration as low as 6.6 X 10(-8) M and was maximal at 2.8 X 10(-6) M. Among various prostaglandins tested, PGE2 and PGE1 were most potent and other prostaglandins were also active with the potency decreasing in the following order: PGF1 alpha greater than or equal to PGF2 alpha greater than or equal to PGA2 greater than or equal to PGB2 greater than PGA1 greater than or equal to PGB1. Arachidonic acid was also effective, but only at very high concentrations, 6.6 X 10(-5)-1.6 X 10(-4) M. The ability of prostaglandins to allow a maximal formation of the two milk proteins suggests a possible modulatory role of prostaglandins in hormonal control of milk-protein synthesis.
Ovarian homogenates from 10-, 23- 128- and 60-day-old golden hamsters were incubated with [14C]-4-androstene-3,17-dione or [7-3H]-progesterone in the presence of NADPH and enzyme activities and metabolism of progesterone were estimated. A rapid increase in uterine weight was found around 28 days of age. The activity of 5 alpha-reductase was very high in the ovaries of 23-day-old hamsters (647 +/- 117 (SD) nmol/g tissue/h), high in those of 28-day-old hamsters (135 +/- 4) and low in those of 10- and 60-day-old animals (20 +/- 16, 39 +/- 11). However, the activity of 5 beta-reductase was high in all ovaries of golden hamsters at different stages of development (84-132 nmol/g tissue/h). The major C-21-17-hydroxysteroids and C19-steroids formed from progesterone by the ovaries of 23-day-old hamsters were 5 alpha-steroids such as 3 alpha, 17-dihydroxy-5 alpha-pregnan-20-one and androsterone, whereas those by the ovaries of 28- and 60-day-old hamsters were 4-ene-3-ketosteroids and 5 beta- and 5 alpha-steroids such as 17-hydroxy-4-pregnene-3,20-dione. 3 alpha, 17-dihydroxy-5 alpha- and 5 beta-pregnan-20-one, 4-androstene-3,17-dione, testosterone and androsterone. The formation of oestradiol-17 beta and oestrone from progesterone was found only in the ovaries of 38- and 60-day-old hamsters. These results show that similarly high levels of 5 beta-reductase are present in all ovaries from suckling, immature and adult golden hamsters and that high levels of 5 alpha-reductase are formed only in ovaries from immature hamsters, especially those with small uterus. The active 5 alpha-reduction of 4-ene-3-ketosteroids may be responsible for the decrease in the formation of oestrogens in immature hamster ovaries.
Testes of 28- and 70-day-old golden hamsters were separated into seminiferus tubules and interstitial tissue by wet dissection. Homogenates of the tissues and subcellular fractions were incubated with [14C]androstenedione, and NADPH and enzyme activity (nanomoles per 100 mg protein/h) was estimated. In immature testes, the 5 beta-reductase activity was largely confined to the seminiferous tubules, while 5 alpha-reductase was localized in the interstitial tissue. The activity of 17 beta-ol-dehydrogenase was found to be equally distributed between tubules and interstitial tissue. Although the activities of 5 beta- and 5 alpha-reductases were approximately 10 times greater in immature than adult testes, the 17 beta-ol-dehydrogenase activity in adult testes was approximately 10 times that in immature testes. In the immature testes, most 5 alpha-reductase and 17 beta-ol-dehydrogenase were localized in microsomes, whereas 5 beta-reductase was wholly localized in cytosol. These results indicates that 5 beta-reduction of delta 4-3-ketosteroids takes place largely in cytosol of tubular cells, while 5 alpha-reduction occurs in microsomes of interstitial cells in the testis of the immature golden hamster.
In the present study, the effects of maternal ethanol intake during pregnancy on microsomal cytochrome contents and on enzyme activities in the developing fetus were investigated. Ethanol intake to pregnant females did not affect the maternal body weight or number of fetuses, but tended to reduce the mean fetal body weight, especially the fetuses from a litter of mother who were treated with ethanol during day zero to 20 of gestation showed significant decreases in the body and liver weights. No significant changes were observed in the contents of cytochrome P-450 and b5 and the activities of NADPH-cytochrome c reductase and heme oxygenase in the livers of fetuses whose mothers were exposed to ethanol during pregnancy when compared with that of untreated pregnant rats. However, NADH-cytochrome b5 reductase activity in the fetal livers was found to significantly decrease by maternal ethanol intake during pregnancy.