DURING the past ten years we have been conducting a systematic study of hypoxia as a cause of intra-uterine deaths and congenital defects in mice for the purpose of determining biologic laws underlying the genesis of congenital malformations in mammals.1 A progress report on work done since 19522 and a formulation of basic principles, particularly those determining the development of skeletal anomalies in newborn mice brought about by maternal hypoxia during pregnancy, is given here. The first basic principle to emerge clearly confirmed from work done since 1935 on mammals3 is that a specific kind of defect may be caused . . .
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Ingalls et al. (1957) studied this question.
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