Acceleration and circadian rhythm of eruption rates in the rat incisor.
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Biomedical subjects
Publications and source records attributed to M Chiba.
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The effect of heat treatment on erythrocyte delta-aminolevulinic acid dehydrase (ALAD) activity in the blood of human subjects was examined in relation to their lead exposure.
Activity of 5-aminolevulinate hydrolyase (delta-aminolevulinic acid dehydrase, ALAD, EC 4.2.1.24) in the blood was determined in relation to age in humans and rats, and the following findings were obtained: (1) In the group which consisted of 47 women (mean age 46, ranged 24 to 62 years) living in a rural district, where the atmospheric lead concentration was 0.5 micron/m3, a significant negative correlation between ALAD activity and age was observed statistically (r = -0.54). However, in the group which consisted of 53 women of similar age group living in an urban district, where the atmospheric lead concentration was 1.9 microng/m3, showed a lower level of the ALAD activity than that of the former group and no correlation was found r = -0.01) between ALAD activity and age. (2) The ALAD activity of intact rats showed a decrease with age. The decrease proceeds rapidly within 8 weeks of age and becomes stable after reaching 25 weeks of age or 300 g of body weight. The value of the activity after 25 weeks of age was about one tenth of that at 5 weeks of age or 100 to 130 g of body weight. (3) Fifteen intact rats weighing 240 to 705 g were divided into three groups according to their body weight and were injected with lead acetate solution equivalent to 1 mg Pb/kg intraperitoneally in order to examine the sensitivity to lead in rats that have variation of ALAD activity by age or by body weight. The ALAD activity of these rats fell to the same level in all groups independently of the activity or the body weight before injection.
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CD-3400 developed by Nippon Chemiphar Co. Ltd., is a new antihypertensive agent belonging to the class of rauwolfa alkaloids. Influence of the agent on gastric mucosa, healing process of acetic acid-induced gastric ulcer and gastric juice in rats was investigated and compared with effects of reserpine and rescinnamine. CD-3400-induced gastric lesions were fewer in number than those produced with reserpine and rescinnamine in fasted rats. After a three day treatment of CD-3400 to fed rats, however, there were few gastric lesions, while reserpine- and rescinnamine-induced gastric lesions were aggravated to a greater extent that when a single administration was given to fasted rats. Influence of CD-3400, reserpine and rescinnamine on the healing process of acetic acid-induced ulcer was insignificant, but treatment with high doses of reserpine and rescinnamine resulted in death. Pretreatment with CD-3400 and reserpine produced a decrease in gastric acid and K+, and an increase in Na+. Repeated administration of reserpine for 5 days resulted in a decrease of both gastric volume and acid, while such was not seen with CD-3400. Treatment with anticholinergic agents such as atropine sulfate and atropine methylbromide inhibited CD-3400- and reserpine-induced gastric lesions. From these results, it would appear that cholinergic factors play a role in the pathogenesis of CD-3400-induced gastric lesions, as in the case with reserpine, and that the responses of these lesions to reserpine and CD-3400 correlate with changes of ionic fluxes in gastric juice.
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Eight normal subjects and ten diabetic patients were studied to compare the response of plasma insulin to glucagon with that to glucose and tolbutamide. Oral glucose tolerance test, glucagon test and tolbutamide-glucagon test were performed at intervals of several days. In glucose tolerance test, insulin response was reduced in the patients with severe diabetes. Plasma insulin increased and reached the peak 3 min after glucagon injection (glucagon I) in the normal controls, while plasma insulin response was reduced in diabetic patients, especially in the severe diabetics. In the normal controls plasma insulin rose and reached the peak 6 min after the tolbutamide injection and thereafter fell to the initial level. Glucagon injection following tolbutamide (glucagon II) caused the rise in insulin in the control subjects. In diabetics insulin response to either tolbutamide or glucagon I was reduced. Tolbutamide or glucagon II caused a significant difference in plasma insulin response in all the diabetic groups compared with the normal subjects, while glucose or glucagon I showed a significant increment of plasma insulin between the normal subjects and the severe diabetics. These results suggest that injection of tolbutamide as well as glucagon II provides a definite discrimination of insulin response in diabetics from the normal controls. The usefulness of the tolbutamide-glucagon test in the diagnosis of diabetes mellitus was discussed. -- glucose tolerance test; glucagon test; tolbutamide-glucagon test; plasma insulin.
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