1) Skeleton of the feet of 13 toad larvae with defective ,digital malformations and regressive spiracles induced by cultivation in aerated \vater at a high temperature of 30~ 10C were anatomically studied. 2) It was clarified that the defective digital malformations resulted mainly from severe reductive changes of the phalanges, and that the metatarsalia showed no marked regressive changes. 3) The cause of these skeletal anomlies was discussed.

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One mg/g monosodium glutamate (MSG) was given subcutaneouasly to neonate CF#1 mice on day 2 or 4 after birth according to Olney's procedure. They were examined in sections under a light microscope 3 or 6 hours after the treatment, and results similar to those shown by him were confirmed. Then, the same strain of the mouse was treated with 5 mg/g MSG on day 17 or 18 of pregnancy subcutaneously. Fetal brains were similarly examined 3, 6 and 24 hours after the treatment. Similar necrosis of the neural element was detected in groups administered. Frequency of the involvement seemed to be higher in group treated on day 18. Cellular necrosis was seen both in the ventromedial and arcuate nuclei. In those examined on day 17, lesions were more predominant in the ventromedial nucleus than in the arcuate nucleus. These lesions in the ependyma fronting the 3rd ventricle especially in the ventral part of it. In those observed 24 hours after the Injection, no cases showed the lesion in the medial ventromedial nucleus in those treatedon day 17 or 18. Whether the recovery process had taken place or no lesions had originally arisen was difficult to venture. Further, relationship between susceptibility of the brain tissue involved and the maturity of the cell also required further studies. Monosodium L-aspartate (MLA) caused similar lesions in the fetal brain. Generally, lesions caused by MSG or MLA present findings similar to those shown in adult mice by goldthioglucose (GTG).

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1. Wistar rats were treated with a single intraperitoneal injection of trypan blue solution on day 8 of pregnancy. Embryos and fetuses were removed surgically from mothers on days 10, 11, 12, 13, 14, 15, 17, and 20. After gross observations, fetuses were fixed with Bouin's solution for microscopic observations. 2. Embryonic mortality increased from day 10 to 13, and frequency of myeloschisis manifested declined gradually from day 10 to 13. Thereafter, both mortality and frequency of myeloschisis showed no difference among groups examined from days 13 to 20, respectively. 3. Cystic myeloschisis observed in the day 10-embryo appeared to be myelocystocele, and the cyst was filled with blood or fluid. This blood or fluid was gradually resorbed as the developmental stage advanced. Meanwhile, degenerative changes on the surface of the exposed neural tissue gradually exceeded both the development and differentiation of the involved region. Finally, on day 20, cystic myeloschisis was observed as spina bifida aperta. 4. Non-cystic myeloschisis was found in the embryos on day 11 and 12. Morphogenetic process of this type was different from that described above in the early stages of development. After day 13, there was no difference between the two types of myeloschisis in their external appearance. 5. The morphogenetic process of myeloschisis in the rat fetus due to trypan blue is not simple. Although the morphological features seemed to be similar when obseved in the later stages, two different processes were found in the earlier stages of development.

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The autopsy protocols of 25 cases with tumors were examined. Thyroid, ovary and intestinal cysts, lipoma, fibroadenoma, cervical polyp,papilloma of the skin, hemangioma, lymphangioma, hemangioendothelioma, neuroblastoma and struma comprised the subject of this study. Sixteen cases (64%) were associated with congenital malformations and 111 anomalies were found in the group with tumor. Lymphangioma was usually coincident with hypoplastic thoracic organs, non-structural heart anomalies, and urogenital anomalies, while the cases with chromosome aberration occurred with structural heart anomalies. In some cases, the definition of congenital tumors was difficult to determine, having no difference with non-tumorous pathologic changes of the cells in spite of macroscopical tumorous proliferation. It is suggested that some tumors might be included in the category of congenital anomalies. The significance of congenital tumor in relation to congenital anomalies was emphasized, but the sequene of the tumor in the postnatal period was difficult to evaluate at present.

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1) Mitotic frequency was estimated in the presumptive skeletal mesoderm of the hindlimb bud in toad larvae at limb bud stages, i.e. , at stages 3-5. 2) When the larva was reared at an optimal temperature of. 20±1 ℃, mitotic frequency was extremely high at stage 4. Thus, this stage seemed to be most sensitive to teratogenic agents. 3) In the larva reared at a high temperature of 30±1 ℃, not only mitotic frequency was lower than that in the larva reaed at 20±1 ℃, but also no increase of mitotic frequency was recognized at stage 4. 4) The cause of defective digital malformations produced by a high temperature of 30±1 ℃ was discussed in relation to decrease of mitotic frequency in the presumptive skeletal mesoderm.

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