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Biomedical subjects

Y Morikawa

Publications and source records attributed to Y Morikawa.

At least 361 records · Page 20Linked to original sources

Effect of maternal malnutrition on matrix cell proliferation in the cerebrum of mouse embryo: an autoradiographic study.

Thirty pregnant mice were undernourished by providing low protein diets (PM) or providing approximately one-third their normal diets (PCM) for 9 days from the 8th to the 16th day of gestation. Another 15 pregnant mice, which were fed a normal diet, served as the control. On the 16th day of gestation, all animals were injected with a single does of [3H]thymidine and were killed one by one at 1- or 2-hr intervals. Mean litter size was statistically insignificant between the control group and two malnourished groups. There was, however, a significant difference in mean body weight between the control group and two malnourished groups (P less than 0.005). The cerebral cortex at this stage of development consisted of three different layers, i.e., the cortical plate, the migratory zone, and the matrix layer. The width of the cortical plate of the malnourished embryos was significantly smaller (P less than 0.001). There was, however, no significant difference in width of the migratory zone between the control and the malnourished groups. The width of the matrix layer in PM was significantly smaller (P less than 0.001), but that of PCM showed no significant difference from the control (P greater than 0.1). Coronal section of the brains of the embryos were processed for autoradiography. Labeled cells were found almost exclusively at the matrix layer surrounding the lateral ventricels. Labeling index counted in the matrix layer after 1 or 2 hr of [3H]thymidine injection indicated that more than 30% of the cells in this layer were always synthesizing DNA in each group of embryos. The generation times of the matrix cell, precursor of the neurons, in the matrix layer were approximately 18.5 hr in the control and 21.5 hr and 21.8 hr in the malnourished embryos, thus indicating about 3 hr of prolongation in the latter. DNA synthetic time was about 6.5 hr in the control and 7.0 hr and 7.0 hr in the two malnourished groups. The postduplication time was about 2.5 hr in the control and 3.0 hr and 3.5 hr in the malnourished. The preduplication time was about 8.8 hr in the control and 10.6 hr and 10.3 hr in the malnourished.

Animals↗

Rise of plasma corticosterone concentrations in rats immediately before and after birth and in fetal rats after the ligation of maternal uterine blood vessels or of the umbilical cord.

Just before normal vaginal delivery the plasma corticosterone concentration (PCC) in fetal rats increased markedly compared with that on day 22 of gestation. The PCC was elevated 2 h after birth and then declined until 12 h after birth, when it approached the level found on day 22 of gestation. Similarly, in premature newborn rats obtained by cesarean delivery on days 21 and 22 of gestation, the PCC increased 2 to 4 h after delivery and then declined. The PCC in 22-day-old fetal rats, 30 min after ligation of the maternal blood vessels running along a uterine horn, rose markedly compared with that in fetuses in the contralateral intact horn. A similar increase in PCC was not observed in either decapitated or encephalectomized fetuses, but observed in fetuses whose umbilical cords were ligated. The rise in fetal PCC after ligation of uterine blood vessels and of umbilical cords was considerably higher than that observed after various stresses reported by other investigators and also higher than that found 60 min after maternal adrenalectomy. The rise in PCC just before and just after birth and after the ligation should not be considered as the result of stress, parturition or ligation, but may be a result of the response to other factors.

Animals↗

Failure of estradiol benzoate given after birth to prevent the adrenal glands from shrinking in newborn rats.

Two hr after birth, newborn rats were given a subcutaneous injection of 0.01 mg estradiol benzoate dissolved in 0.05 ml sesame oil. Other siblings were given sesame oil alone. Autopsy was performed on days 1, 2 and 3 after birth. Gravimetric and histologic examinations of the adrenals from these animals and from normal littermate controls were made together with the determination of plasma corticosterone concentrations. In all the three groups of rats, estrogen-treated, oil-treated and non-treated, the weight of the adrenal glands declined with a concomitant decrease in the plasma corticosterone concentrations. The results indicate that estradiol benzoate, when given after birth, does not prevent the neonatal adrenal from shrinking.

Adrenal Glands↗

Changes in the weight of the adrenal glands and in the concentration of plasma corticosterone in perinatal rats after prenatal treatment with oestadiol benzoate.

On day 20 of gestation, foetal rats received a subcutaneous injection of 0-01 mg oestradiol benzoate dissolved in 0-05 ml sesame oil; foetuses in other litters were given sesame oil alone. Autopsy was performed on day 22 of gestation, at delivery or at various times after birth. Gravimetric and histological observations of the adrenals from oestradiol-treated, oil-treated and intact litter-mate control foetal and neonatal rats were performed together with determination of plasma corticosterone concentrations. Activity of 3 phi-ol dehydrogenase was also examined histochemically in the adrenals from these animals. The results indicated that oestradiol benzoate when given prenatally prevented the neonatal decline of adrenal weight and adrenocortical cell size. In normal or oil-treated rats, plasma corticosterone concentration was greatly increased during delivery and 2 h after birth, declining up to 12 h after birth. Oestradiol benzoate prevented this perinatal increase and suppressed the activity of 3 phi-ol dehydrogenase in the perinatal adrenal cortices.

Adrenal Glands↗

Granular cells in the juxtaglomerular apparatus in perinatal rats.

Granular cell indices (GCI; Dunihue and Robertson, '57) in kidneys of fetal and newborn rats were determined by examining sections stained with Bowie's technique. Some fetuses were delivered prematurely by Caesarean section a day earlier than the expected delivery, and were then nursed by a foster mother. Similarly, postmature Caesarean newborn rats were obtained; retention one day beyond the normal gestation was induced by maternal progesterone injections. The GCI was strikingly increased within a day after birth, followed by an immediate decrease therafter. This was also observed in both premature and postmature rats. It seems that this temporary increase of the GCI is not attributable solely to the age of rat, but follows only the separation from the maternal environment.

Animals↗

Ultrasonographic determination of the splenic size and its clinical usefulness in various liver diseases.

Contact ultrasonic tomography was employed to obtain the size of the spleen in vivo. The scanning was done parallel to the ribs, and the splenotomograms obtained by this method showed three basic patterns of enlargement: a soft, bulging spleen, splenic congestion, or a firm spleen. Of the 96 patients with liver disease studied by this technique, 95% gave evidence of splenic enlargement. Useful information on prognosis may be obtained by observing the changes in the sectional areas of the spleen.

Acute Disease↗

Hypothalamic control of the pituitary-testicular relation in fetal rats: measurement of collective volume of Leydig cells.

On the 20th day of gestation in pregnant rats, the male fetuses were subjected to surgical hypophysectomy by decapitation or to intracranial paraffin injection which compressed the fetal brain. Autopsy was done on the 22nd day of gestation. The collective volume of Leydig cells in the left fetal testis was estimated by Chalkley's method. Decapitation of a fetus caused a significant retardation in increase of the collective volume of Leydig cells 2 days later. In fetuses given an intracranial paraffin injection, the Leydig cell volume was increased significantly compared with normal fetuses on the 20th day of gestation but was far smaller than that in their intact littermates. This effect of paraffin compression was completely prevented by injections of LRH. The Leydig cell volume remained extremely small in decapitated fetuses given LRH. The observations suggest that in the male rat the hypothalamus begins to govern a pituitary gonadotropic function before birth.

Animals↗