[Gonadal sex chromatin and psychic sex in several cases of adrenal virilization].
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Sex chromatin counts of subcultured cells of both female human mammary tumor and female rabbit kidney show a considerable drop from an initial high level. Cultures in which sex chromatin persists also retain the viral insensitivity of their source material.
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Like mammals, Lepidoptera possess female-specific sex chromatin. In a compilation of new and published data, 81% of the 238 investigated Lepidoptera species display one or more heterochromatin bodies in female somatic interphase cells, but not in male cells. In contrast with the similar phenomenon in mammals, this sex-specific heterochromatin does not function as a dosage compensation mechanism. Most Lepidoptera have a WZ/ZZ sex chromosome mechanism, and the sex chromatin is derived from the univalent W sex chromosome. Sex chromatin is regarded as an indicator of an advanced stage of W chromosome evolution. In species with a Z/ZZ sex chromosome mechanism, loss of the W chromosome is accompanied by loss of the female-specific heterochromatin. Since sex chromatin can be discerned easily in interphase nuclei, and especially so in the highly polyploid somatic cells, it is a useful marker for diagnosing chromosomal sex of embryos and larvae, and of identifying sex chromosome aberrations in mutagenesis screens. All species with sex chromatin belong to the Ditrysia, the main clade of Lepidoptera that contains more than 98% of all extant species. Sex chromatin has not been reported for clades that branched off earlier. The nonditrysian clades share this character with Trichoptera, a sister group of the Lepidoptera. We propose that Lepidoptera originally had a Z/ZZ sex chromosome mechanism like Trichoptera; the WZ/ZZ sex chromosome mechanism evolved later in the ditrysian branch of Lepidoptera. Secondary losses of the W chromosome account for the sporadically occurring Z/ZZ sex chromosome systems in ditrysian families. The lepidopteran sex chromatin, therefore, appears to mirror the full evolutionary life cycle of a univalent sex chromosome from its birth through heterochromatinization to sporadic loss.
The incidence of sex-chromatin-positive cells during the first five days of life was investigated in buccal smears stained with aceto-orcein in three groups of newborn females: 51 term infants, 17 small-for-date prematures and 9 prematures with birth weight appropriate for gestational age. In addition, single buccal smears were obtained from a control group of 50 older female children. No significant difference was found in the number of sex-chromatin positive cells between the three groups of infants. The mean incidence of sex-chromatin-positive cells in the neonatal period was lower than that of the older control girls, as has been reported by previous workers. The mean incidence of sex-chromatin-positive cells on the fifth postnatal day never reached 17% which was the mean frequency of sex-chromatin positive cells in older controls. This contrasts with the findings of other workers who reported the rise of sex-chromatin positive cells to occur on the second or third days of life.
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The incidence of sex chromatin in tumour cell nuclei was estimated in twenty five cases each of carcinoma and fibroadenoma breast using haematoxylin and eosin, thionine, aceto-orcein and Papanicolaou's stains on imprint-smears. The sex chromatin incidence in fibroadenoma was found similar to that of normal breast tissue but the incidence markedly decreased in carcinoma breast. Undifferentiated tumours with histologic grade III, nuclear grade I, no lymphocytic infiltrate and involvement of overlying skin, nipple and areola were more often associated with low sex chromatin incidence. No relationship was observed between sex chromatin incidence and tumour size or axillary lymph node metastasis.