{'fraction_non_alphanumeric': 0.014164305949008499, 'fraction_numerical': 0.0028328611898017, 'mean_word_length': 4.891666666666667, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Teratogenesis of acetazolamide in the CBA/J and SWV strains of mice. II. Genetic control of the teratogenic response.

Three independently segregating loci appear to control the difference in response of CBA and SWV mouse embryos to the ectrodactyly-inducing effect of acetazolamide. Response of the CBA embryo appears to depend on recessive genes for sensitivity being present in the homozygous condition at all 3 loci, and resistance to be conferred by the presence of a dominant allele at any one of the 3 loci. The genetic variability for the ectrodactyly response of the mouse is discussed in the light of the reported physiological factors necessary for acetazolamide-induced ectrodactyly in the rat.