Cell kinetics of the erythroid precursors was investigated in normal mice and rats by ³H- thymidine labeling method with or without simultaneous administration of colchicine, and the following results were obtained : 1) DNA synthesis time (S-time) of the erythroid precursors assessed by the labeled mitosis method was 7 hours in mice and 7.5 hours in rats, G₂- and M-time were 1.5 hours and 1.0 hour, respectively, in both animal species. 2) S-time of basophilic erythroblasts of mice assessed by the ³H-thymidine labeling method with colchicine was 7 hours and that of the polychromatic erythroblasts was 8 hours. In rats, S-time of both basophilic and polychromatic erythroblasts was equally 7 hours. G₁-time of basophilic erythroblasts was 2 hours both in rats and mice. Time for remaining in G₁-phase of the polychromatic erythroblasts was 6 hours in mice and from 7 to 10 hours in rats. 3) Three percent of the basophilic erythroblasts and 7% of the polychromatic erythroblasts were in non-proliferating fraction in mice during 6-7 hours' observation period. Moreover, labeled mitosis curve of the erythroid precursors was different between mice and rats. In rats, the rate of labeled mitoses of the erythroid precursors increased rapidly and attained to 100% 3 hours after the first administration of ³H-thymidine, while in mice the maximum rate was about 80%. These findings may indicate the difference in erythroblastkinetics between two animal species. From the above results, cytokinetics of erythroid precursors was discussed.

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Diphenylthiohydantoin (DPTH) is a potent goitrogenic compound and produces a large goiter in rats. Like methimazole, DPTH depresses plasma thyroxine (T₄) and triiodothyronine (T₃) concentrations and elevates plasma TSH concentration. Unlike methimazole, however, DPTH does not suppress thyroidal radioiodine uptake and thyroid hormone synthesis. DPTH does not depress thyroidal radioiodine release nor augment the degradation of thyroid hormone. DPTH depresses an increase of plasma T₃ and T₄ in thyroidectomized, T₄- and T₃-maintained rats by augmenting fecal excretion of hormones. In addition, DPTH depresses peripheral conversion of T₄ to T₃ in vitro.
It is suggested that DPTH is an unique goitrogen which acts on 2 different extrathyroidal sites, viz. fecal loss of thyroid hormone and conversion of T₄ to T₃.

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This paper examined some of the relations between thyroid function and the hypothermia of the obese mouse after exposure to the cold. The fall in body temperature of obese mice treated with T₃ was less rapid than in untreated obese mice. In the lean mouse, the induction of hypothyroidism by pretreatment with PTU enhanced the rate of fall of body temperature of these mice while in the cold. Circulating levels of TSH were the same in lean and obese mice at 28 t and after exposure to 24°C, TSH in obese mouse was increased more than in lean mouse, but maximal response of TSH to cold at 4°C was same between lean and obese mouse.
The TSH response to TRH was significantly less in the obese mice. The thyroidal ¹²⁵I-uptake was also lower in the obese mouse. The lowered uptake was, however, accompanied by a higher turnover rate as indicated by the more rapid appearance of radioactivity in BEI. Pretreatment with TSH increased the size of the thyroid gland, the uptake of radioactive iodine, the concentration of T₄ and T₃ in the serum, but did not alter the rapid decline in body temperature of the obese mouse after exposure to the cold. The possibility of an impaired response to exogenous T₃ was examined by rendering lean and obese mice hypothyroid with injections of methimazole and then giving T₃. The level of plasma T₃ in obese mouse was higher than in lean mouse on daily supprement of T₃ 15mg and and the level of plasma TSH in obese mouse was lower on daily supprement of T₃ 50ng. However, not even the highest dose of T₃ in the obese mice prevented completely the fall in body temperature. These studies suggest that peripheral unresponsiveness to the actions of triiodothyronine may be a major reason for the hypometabolism and hypothermia in these animals.

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The usefulness of breast-feeding has been reappreciated, and its necessity is emphatically voiced. But nevertheless many mothers still adhere to bottle feeding. The present survey was conducted to find out, in the actual state surrounding the pregnancy and delivery and attitude toward the nursing, the factors which impede breast-feeding. The chief findings were as follows :
1) Breast-feeding is gradually decreasing with advance in month of age, while the bottle-feeding is conversely increasing.
2) Until 7 days after delivery, almost all the mother (94.6%) practiced breast-feeding regardless of the place of delivery and method of nutrition.
3) Infants fed on processed milk before given colostrum accounted for more than a half (68.9%). When probable or unspecified cases are added, the percentage becomes 80.9%. Those not given processed milk before colostrum constitute only 19.1%.
4) For 74.4% of mothers who changed breast-feeding to bottle-feeding, the reason of the change was poor secretion of their own milk.
5) Those who had firmly decided breast-feeding during pregnancy, practiced it at a high per cent. But those who had considered to try it if possible, or who had not any special consideration about it, performed it at a low rate.
6) Those attending the mothers' class accounted for only 1/3 of the surveyed. Those not attending it because of no knowledge of its opening were in most cases mothers remaining at home. When the reason for no attendance was for work, they were mostly workers away from their homes.
It seemed necessary for the promotion of breast-feeding to deepen the understanding and knowledge about this feeding method on the occasion of mothers' education during or before pregnancy. However, the rate of attendance to such education is not always satisfactory. It is considered important that not only health centers but also medical institutions and all the members of the community should cooperate for the prevalence of breast-feeding.

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It has been postulated that dopamine, the metabolite of L-dopa, may play a role in the regulation of secretion of anterior pituitary hormones. However, many investigators reported that L-dopa had no effect on circulating TSH levels in humans and experimental animals. In attempt to study hypothalamo-pituitary system in thyrotoxic patients, the effect of L-dopa on serum TSH levels was tested.
A single oral administration of L-dopa failed to show discernible changes of serum TSH in euthyroid subjects and in untreated thyrotoxic patients. Serum TSH response to synthetic TRH was also negligible in thyrotoxic patients, while a significant increase in serum TSH was observed in euthyroid subjects. Exaggerated TSH response to TRH, associated with elevated basal TSH levels, was shown in patients with hypothyroid state during antithyroid drug therapy for hyperthyroidism. All patients with elevated basal TSH levels responded to L-dopa with 40% drop from the basal level. A similar phenomenon was also observed with a drip infusion of L-dopa.
These observations suggest that hypothalamo-pituitary system in thyrotoxic patients is maintained intact and provide evidence that dopamine affect TSH secretory mechanism, particularly in a situation in which TSH secretion is stimulated.

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In order to assess the diagnostic value of the Q-K intervals as a measure of left ventricular performance, the present investigation was carried out on ischemic heart disease.
The systolic and the diastolic values of the Q-K intervals were designated as Q-K_s and Q-K_d respectively.
Although there was a significant relationship between the Q-K intervals and the systolic time intervals in ischemic heart disease, the correlation was more remarkable in Q-K_d than in Q-K_ss. On the other hand, the negative correlation with the cardiac output was more obvious in Q-K_s than in Q-K_d.
The above results suggest that the measurement of the Q-K intervals is of great importance for noninvasive evaluation of the left ventricular performance.

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On the isolated frog's S-A node is investigated the relationship between dominant pacemaker potentials and applied transmembrane current by use of two barrels glassmicroelectrodes. namely, the dominant pacemaker potentials are recorded with one electrode, while the transmembrane current is simultaneously applied to the same cell through the other electrode. The direction of transmembrane current is alternated and the KCl solution with which is filled in the other electrode is also exchanged for many other solutions. The following results are obtained.
1) Two notches which show the phase boundary of excitation appear on the plateau when the transmembrane current is applied to true or latent pacemaker cell. The one is at the site of 150-200 msec. from the upstroke of action potential, the other at the site of 400 msec.
2) Applying the outward current, the notches project upward, and make the plateau increase. On the contrary, the inward current, the notches depress downward and make the plateau decrease.
3) When the transmembrane current is applied through the microelectrode filled with 2M-NaCl solution instead of 3M-KCl, it is difficult to get these notches. On that occasion the prepotentials show slight changes.
4) Changes above mentioned can not be. seen on the ordinary cardiac muscle fibre.
5) Even if the microelectrode for transmembrane current is filled with acetylcholine or epinephrine solution instead of 3M-KCl, the rhythm during and after the transmembrane current is not changed.
6) Mechanical movement in the pacemaker cell shows the similar change as the pacemaker potential timely, but variations of action potential induced by transmembrane current are independent mechanogram.
The main conclusions to be drawn from these resluts are as follow.
a) The dominant pacemaker rhythm is not changed even if one cell of the dominant pacemaker is stimulated.
b) The phase boundary of excitation of the pacemaker cell is clearly shown by applying subthreshold transmembrane current to the exciting cell.
c) It is needless to say that there is a fundamental difference between pacemaker potential and its mechanical movement in view of the fact that the variations of action potential induced by transmembrane current are independent of mechanogram.

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In order to clarify morphological differences of arteriosclerosis in various visceral arteries, the cerebral, coronary and renal arteries were morphometrically and histologically investigated.
1. Hypertension enhanced the grade of arteriosclerosis of the major cerebral arteries as well as that of the intracerebral small arteries. The enhancement was markedly observed in cases over age 40.
2. Morphological findings of intracerebral arteriosclerosis were more varied than those in other organs. They were cellulofibrous intimal thickening, atherosclerosis, intimal lipoidosis, intimal edema and fibro-nodular arterial lesions, and others in hypertensive brains.
3. The grade of coronary sclerosis was also increased by hypertension. The effect of hypertension on the coronary arteries was more slight than that on the cerebral arteries.
4. Newly formed capillaries in the thickened intima were found more frequently in the coronary arteries than the other arteries. They might play a role in exacerbation of atherosclerosis.
5. Morphological pictures of intramyocardial coronary sclerosis were cellulofibrous intimal thickening and mucoid degeneration. For the pathogenesis of the latter not only hypertension but also hypoxia was considered responsible.
6. Histological characteristics of intrarenal arteriosclerosis were intimal laminated elastosis and arteriolar hyalinosis. The severity of the former was increased with hypertension and aging. It was suggested that the elastic fibers in the elastosis were produced by intimal smooth muscle cells. Hyaliosis of arterioles in the kidney had a close relation to hypertension. There was a positive parallelism between the grade of the hyalinosis and cerebral arteriosclerosis.
7. It could be concluded that the differences in histological features and development-grade of arteriosclerosis among various visceral organs were induced by the differences of arterial wall architecture and of hemodynamics, both of them depending on the characteristic organ functions.

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