Takashi Tanimura

Myeloschisis in early human embryos.

Four early human embryos with open myeloschisis are reported. These are a thoracolumbar myeloschisis in Carnegie developmental stage 12, a cervical myeloschisis in stage 13, and two lumbosacral myeloschisis in stage 14. All of them are the smallest human embryos with this type of malformation ever reported. In these embryos, the neuroectodermal junction is smooth and there is no microscopic evidence that the neural tube is forced open after its proper closure. The presence of the lesion in such early embryos, especially in one of stage 12, implies that the lesion evolved from the neural plate which never closed. Cellular polarity and the limiting membrane in the lesion are generally well preserved in spite of apparent overgrowth of the neural tissue. These findings do not support the hypothesis of LEMIRE et al. that the defective external limiting membrane predisposes to a loss of cellular polarity and resultant neural overgrowth.

Teratogenesis study of tolnaftate, an antitrichophyton agent

Abstract Tolnaftate did not affect average litter size, fetal mortality, or sex ratio of mouse fetuses surviving to term. The mean body weight of live fetuses from mothers treated with 1000 mg/kg subcutaneously was slightly lower than that of the control. A few external malformations were observed in every group including the control. No significant difference in their incidence, however, was detcted between the control and treated groups. They may be considered as incidental, and not attributable to administration of the drug. Examination of rat fetuses at term in the treated groups revealed no differences in average litter size, fetal mortality, and sex ratio of survivors from the control. A slight decease in mean body weight was noted in the fetuses from mothers treated with 500 mg/kg of tolnaftate. External gross malformations were not observed in either the control or the treated groups. Investigation of cleared skeletons stained with Alizarin Red S showed no significant difference in incidence of malformations in the treated groups of either species as compared to their respective controls. Retardation of ossification, however, was noticed in some portions of the skeleton in the fetuses of treated rats, but not in other parts. Therefore, it cannot be determined whether tolnaftate had played a role in that finding. Postnatal development of the young of both species was quite satisfactory. It is concluded that tolnaftate did not exert a deleterious effect upon the fetal and postnatal development of mice and rats under the experimental conditions of the present studies.