In the calcification figure of the rabbit's incisor dentine, hematoxylin unstained hypocalcification layer was formed in the third trimester of pregnancy. Using this hypocalcification layer and the newborn in the fetal age as indicators, Miyahara reported in the 2nd report of a series of studies, the effects of calcium preparations and vitamin D have intimate relation with calcification of bone and tooth. In the present work, author used estradiol, estriol and progesterone, which are most deeply connected with pregnancy, and investigation was performed on their effects on the dentine calcification figure of mother rabbits and newborns in the fetal age, and on quantitative change in serum calcium and inorganic phosphate, which are closely related with calcification. The results were as follows :
1) Normal female rabbits were intramuscularly injected with 3mg/kg of estradiol, 1 mg/kg of estriol, and 5mg/kg of progesterone, and little effect was confirmed on the striped calcification figure or growth rate of dentine and quantitative changes in serum calcium and inorganic phosphate.
2) In the dentine calcification figure of mother rabbits, the hematoxylin unstained layer, formed in the third trimester of pregnancy was replaced by hematoxylin blue or deep blue stained layer after the administration of 0.001 mg/kg of estradiol, or 0.001 mg/kg of estriol, or 5 mg/kg of progesterone.
This action was exerted most strongly by estradiol and weakly by estriol and progesterone. The growth rate of dentine, which tended to decrease in the third trimeter of pregnancy, was restored by the administration of estradiol and progesterone, but hardly in any degree by estriol. Calcification in the fetal age was sometimes inhibited by any of these hormones, but most strongly by estradiol also in this case.
3) The tendency of decrease in serum calcium level in pregnancy could be inhibited by the administration of estradiol, but neither by estriol nor by progesterone. However, the tendency of inorganic phosphate to decrease was arrested by any of them, though with difference in degree.

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1. Blood group H activity against chicken and eel anti-H agglutinins of H substances from human stomach mucosa and ovarian cyst fluid was destroyed by partial alkaline hydrolysis with aqueous methanolic triethylamine. The triethylamine treated H substances lost H(Se) activity against eel anti-H(Se) preicpitin and Le^b activity by partial acid hydrolysis with hydrochloric acid.
2. Three oligosaccharides were isolated from the triethylamine hydolysis products of a H substance from human ovarian cyst. H active and fucose-containing trisaccharide was characterized as α-Fuc-(1→2)-β-Gal-(1→4)-GlcNTAc, which had type II chain.
3. Application of the hydrochloric acid to the partial hydrolysis of the H(Se) substance resulted in the liberation of H (Se) active sugar-peptides. Five oligosaccharides were isolated from the sugar-peptide pool by the treatment of alkaline sodium borohydride. Pentasaccharide containing a- (1→2) -fucosyl residue was characterized as a-Fuc-(1→2)-β-Gal-(1→3)-β-GlcNAc-(1→4)-β-Gal(1→3)-GalNAc, which had type I chain. The pentasaccharide with a β- (1→4) -linkage between N-acetylglucosamine and galactose has not been found in fucose containing oligosaccharides previously isolated and characterized from human blood-group substances. The pentasaccharide did not inhibit the precipitation of anti-H(Se) eel serum but inhibited the agglutination of eel and chicken anti-H. The serological results indicated that the H (Se) activity of the pentasaccharide structure displayed in sugar-peptide or H substance, and eel and chicken anti-H agglutinins could not differentiate α-Fuc-(1→2)-Gal structure of type I and type II oligosaccharides.

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The objective of the present study was to investigate the role of pancreatic lecithinase-A released into systemic circulation during shock involving the deterioration of alveolar surface activity. Mongrel dogs were led to hemorrhagic shock maintaining mean arterial blood pressure 40 mmHg until 40% of shed blood was spontaneously taken up. Then remaining blood was retransfused and the experiment was terminated when arterial pressure declined to 50 mmHg. The changes of lecithinase-A and lysosomal hydrolases in the pancreas and plasma were observed every hour through the experement. Pulmonary surface activity was determined on excised lobes at the terminal stage after retransfusion. Next, the effect of lecithinase-A infused intraveously on arterial blood oxgenation and pulmonary stability was assessed on anesthetized dogs.
The arterial blood oxygen tention decreased at the terminal stage following retransfusion in shocked animals. Plasma concentration of lecithinase-A increased markedly 120 minutes after the initiation of oligemic hypotention, being preceded by a rise in lecithin splitting enzyme of the pancreas. Pressure-volume curves of the excised lobes of dogs in hemorrhagic shock and lecithinase infusion showed significant shifts to the right, demonstrating the reduction in pulmonary surface activity. These results suggest that pancreatic lecithinase-A released into plasma may inactivates pulmonary surface active substances.

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To evaluate quantitatively and qualitatively iodine metabolism and thyroid function of the developing chick embryo, we measured total iodine contents and identified chemical nature of the main iodine components of the egg (white Leghorn) by an autoanalizer for PBI (Technicon) and other analytical methods.
The iodine was predominantly distributed in the yolk (21 μg, 74%) at first, while a small portion (0.9 μg) was found in the white. The contents in the shell (6 pig) and shell membrane (0.4 μg) remained constant during incubation but the latter increased to 1.5 pig on Day 18. After Day 10, when vascularization of the yolk was well developed and the thyroid started to accumulate iodide, yolk iodine decreased abruptly to Day 12 (6.2 pig), then gradually to Day 18 (0.9 μig), while iodine contents in the amniotic and allantoic fluids increased inversely from Day 10 to Macimally Day 15 (14.2 and 8.4 pig, respectively). On Day 18, however, the iodine in the two compartments, particularly in the amnion was reduced (3.9 and 6.9 pig, respectively).
In accordance with those changes, serum iodine in the embryo started to increase gradually from Day 10 (44 μg/ml), tliereafteir vigorously to Day 20 (1, 580 ng/ml). After hatching, serum iodine decreased dramatically probably via urine excretion.
Thyroidal iodine also increased from Day 10 (34 ng/gland) and rapidly from Day 15 (560 ng/gland) to Day 18 (2, 341 ng/gland). Serum T₄ level measured by RIA increased gradually to Day 19 (17 ng/ml), whereas T₃ showed no marked change.
We then extracted the iodine in the yolk, serum (Day 19) and the two fluids (Day 15) with CHCl₃ and MeOH (2:1) and found the iodine more than 80% in MeOH-H₂O layer and others were found as protein-bound and lipid-bound iodine. The iodine rich fraction was analyzed by five methods, i) Sephadex G 10 column, ii) Sephadex G 25 column, iii) thin-layer chromatography, iv) cation-exchange chromatography, and v) a fully automated amino acid analyzer. We identified two major components, as iodide and monoiodohistidine (MIH). Besides those, diiodotyrosine was also identified among other minor components. The two major components were identified in amniotic and allantoic fluids as well as in the yolk and serum.
We concluded from the present findings that laying hen ovary concentrates an excess amount of iodine mainly as iodine and MIH into the yolk, and iodide as active source for thyroid hormone synthesis and MIH as an inert iodine compound circulating in compartments of the developing chick embryo. Thus, a role of MIH in the closed environment might be a detoxication mechanism which was subservient to avoid the Wolff-Chaik off efect caused by excess iodide to inhibit thyroid functions.

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The antiandrogenic properties of AA560 (N- (2'-chloromethy1-2 '-hydroxypropionyl) -3, 4, 5-trichloroaniline) and the mechanism of its action were investigated. The following results were obtained.
1. The antagonistic effect of AA560 against exogeneous androgen was stronger than SCH 13521, cyproterone acetate or chlormadinone acetate.
2. The antagonistic affect of AA560 against endogeneous androgen was stronger than SCH13521 or chlormadinone acetate.
3. In intact male rats given AA560 orally there was significant increase of serum LH, FSH and testosterone levels.
4. In the in vivo experiment, the pretreatment with AA560 decreased the uptake of ³H-androgens in the nuclear fraction. On the other hand, 145°C of increase in the uptake of ³H-radioactivity in the cytosol fraction was observed.
5. It was observed in the in vitro displacement study that AA560 inhibited the formation of 5α-DHT-Receptor complex in the cytosol of rat ventral prostate.

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The relationship between plasma lysosomal enzyme levels and reticuloendothelial function was investigated in dogs subjected to hemorrhagic shock. 12 dogs were bled to a reservoir, maintaining mean arterial blood pressure 40 mmHg for two hours. They received shed blood after shock. Phagocytic indices were determined before and after shock using colloidal carbon as an indicator. Plasma β-glucuronidase levels were measured as a prototype of lysosomal enzymes according to Fishman's method before and after shock.
Phagocytic indices decreased significantly after shock and plasma β-glucuronidase elevated inversely after shock. A significant inverse correlation was observed between phagocytic index and plasma enzyme level.

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