The relative distribution of somatostatin- and calcitonin-containing cells in thyroid glands from various mammalian species was investigated by immunoperoxidase staining, and the concentration of immunoreactive somatostatin by radioimmunoassay. In the thyroid glands of guinea pigs and rabbits, most of the calcitonin cells were also immunoreactive to the somatostatin antiserum, and high concentration of immunoreactive somatostatin was obtained. On the other hand, in the thyroids of other animal species--rats, dogs, pigs, cows, goats, cats, monkeys, mice, and hamsters--only a few C cells revealed the immunoreaction for somatostatin, and the concentration of somatostatin was low. In all animal species studied, the somatostatin was present in the same cells that contain calcitonin, though in guinea pigs and rats there were some C cells containing a large number of reaction products for somatostatin but very few for calcitonin. Thus, it was concluded that there was a considerable variation in somatostatin immunoreactivity of thyroid C cells from species to species.
Highly enantioselective catalytic asymmetric [2+2] cycloadditions of cyclic α-alkylidene β-oxo imides with ynamides are described. The high reactivity of the cyclic α-alkylidene β-oxo imide allows the [2+2] cycloadditions of a hindered substrate with unreactive ynamides at low temperature. The X-ray crystallographic analysis of the product suggests that the enantioselectivity of the [2+2] cycloaddition can be well explained by the chelate model comprising the intramolecular hydrogen bond, wherein the cyclic α-alkylidene β-oxo imide coordinates with Cu(II) through the two imide carbonyls. The imide group in the product can be transformed to amide, nitrile, and ester groups; moreover, it is removable.
Five healthy adult men were given metoclopramide (10 and 20 mg) iv, and in repeated tests almost always developed transient restlessness lasting from 10-30 min. The effects of L-dopa and dexamethasone on metoclopramide-induced increases in cortisol concentration were determined. These response values were compared with those of a control. After an injection of 10 mg metoclopramide, the cortisol level increased significantly only at 40 min; the ACTH level did not change. The cortisol rise was suppressed by dexamethasone pretreatment. Pretreatment with 0.5 g L-dopa resulted in a decrease in the PRL level from -20 min to 20 min, and the increase in cortisol seen at 40 min was cancelled. The ACTH level did not change. After injecting 20 mg metoclopramide, the ACTH level increased significantly from 20 min to 60 min and the cortisol level showed a significant increase from 20 min to 120 min. Pretreatment with dexamethasone resulted in a decrease in these hormones. The L-dopa pretreatment did not reduce even the rise in the PRL level which resulted from the administration of 20 mg metoclopramide. These findings suggest that the ACTH and cortisol response to metoclopramide is a stress-mediated effect. Plasma cortisol responses to 20 mg metoclopramide and insulin-induced hypoglycemia were studied and compared in seven volunteers and found to be similar.
Highly enantioselective catalytic asymmetric reactions of rationally designed R-alkylidene β-keto imides are described. The [4 þ 2] cycloadditions and HosomiÀSakurai reactions of R-alkylidene β-keto imides proceed with high enantioselectivity and yield. The [4 þ 2] cycloadditions of the imides with various dienes afford products bearing an all-carbon quaternary stereogenic center at the ring junction. R-Alkylidene β-keto imides should be useful for the enantioselective total synthesis of natural products and other catalytic asymmetric applications.
The development of immunoreactive somatostatin in thyroid C cells of dogs and guinea pigs from early fetuses to adults was investigated by the use of immunoperoxidase histochemistry and radioimmunoassay. The time of appearance and developmental patterns of immunoreactive somatostatin in the C cells were completely different in both species. In guinea pig thyroids, the somatostatin immunoreactivity appeared later than the calcitonin immunoreactivity and the number of somatostatin-positive cells was very small during fetal periods. The somatostatin immunoreactivity rapidly increased during neonatal periods. A large population of the somatostatin cells and a high concentration of somatostatin immunoreactivity were observed in mature animals. On the other hand, in dog fetuses somatostatin immunoreactivity appeared very early, at the same time as the calcitonin immunoreactivity. The largest population of somatostatin cells was found at the stage when the primordial follicles were vigorously formed throughout whole thyroid parenchyma. At this stage almost all of calcitonin-positive cells were also somatostatin-positive. The somatostatin cells progressively decreased as the development proceeded, in contrast to the calcitonin cells which increased with gestational age. In postnatal dogs only a few C cells revealed the immunoreaction for somatostatin, and the concentration of somatostatin was very low. These findings suggest that the function of somatostatin in dog thyroid C cells may be different from that in guinea pig C cells.
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