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Biomedical subjects

H A Bern

Publications and source records attributed to H A Bern.

At least 145 records · Page 8Linked to original sources
PubMed1979

Adenosis-like lesions and other cervicovaginal abnormalities in mice treated perinatally with estrogen.

Female mice from three inbred strains (BALB/cCrgl, C3H/Crgl, and C57BL/Crgl) and one noninbred stock [RU:NCS (RU)] were treated perinatally with estradiol benzoate (EB), diethylstilbestrol (DES), or sesame oil and were killed on postnatal days 30--36. A combined prenatal and neonatal regime of EB injections resulted in the abnormal presence of columnar epithelium in the vaginal fornices of some of the mice from each strain or stock. The same epithelial abnormalities were also present in the vaginal fornices of 30-day-old RU:NCS(RU) mice that had been treated only neonatally with EB or DES. The incidence of these lesions was 40--67% in the mice treated prenatally and neonatally with EB, 68% in the neonatal EB treatment group, and 100% in the neonatal DES treatment group. The columnar cells were arranged either as single layers in areas of the fornical lining epithelium or as glandlike or cystic structures in the subepithelial stroma. No cells of this type were detected in any of the samples from sesame oil-inoculated control mice. No comparable epithelial lesions were detected in the common cervical canal of the perinatally estrogen-treated animals, but this treatment consistently resulted in gross structural abnormalities at this site.

Animals↗
PubMed1979

Long-term effects of perinatal exposure to hormones on normal and neoplastic mammary growth in rodents: a review.

Exposure of mammals to hormones and drugs during pregnancy sometimes results in profound consequences in the offspring. In this review, the long-term effects of perinatal exposure to hormones on the mammary gland in female rodents at advanced ages are discussed as a model for possible human consequences of antenatal exposure to sex hormones. In general, antenatal hormone treatments may influence the development and growth of the mammary gland. Perinatal treatment with estrogen, androgen, progesterone, or even prolactin in some cases induces not only irreversible abnormality of mammary growth but also influences spontaneous and carcinogen-induced mammary tumorigenesis. Effects of neonatal hormone treatment on mammary tumorigenesis, which appear to be mainly due to the endogenous hormone imbalance produced, vary according to the time and period of the treatment and to the species and/or strain employed.

Animals↗
PubMed1979

Cervicovaginal and mammary gland abnormalities in BALB/cCrgl mice treated neonatally with progesterone and estrogen, alone or in combination.

Neonatal female BALB/cCrgl mice (mammary tumor virus unexpressed) were given a daily injection of estradiol and/or progesterone for 5 days, beginning within 36 hr after birth. About one-half of each group was ovariectomized when 40 days old, and all mice were killed when between 18.5 and 26 months of age. Neonatal progesterone leads to ovary-dependent persistent vaginal cornification and hyperplasia. In addition, 16 of the 24 progesterone-treated mice had genital tract lesions, and 4 of these showed predominantly glandular features. No such lesions were observed in either oil-treated or untreated mice. Lesions were also observed in both intact and ovariectomized mice treated with estrogen-progesterone combinations, but most of the lesions were not as severe as those seen in mice treated neonatally with progesterone alone, and they were predominantly squamous in appearance. Although mammary tumors were not observed in either the control or the neonatally steroid-treated intact mice, many in the latter groups possessed hyperplastic alveolar-like mammary nodules and other abnormalities.

Animals↗
PubMed1978

Histometric study of the pituitary in mice treated neonatally with steroids and the relationship between prolactin cells and mammary tumorigenesis.

Neonatal female mice of the BALB/cC3H/Crgl strain were given daily injections of 17 beta-estradiol, progesterone and prolactin, singly and in some combinations, for 5 days beginning within 36 hr after birth. Mice were killed at tumor age or by 12 months of age. Differential cell counts of the anterior pituitary showed that prolactin cells were more numerous in neomatally estrogen-treated mice and progesterone-treated intact mice than in control mice. Paired analysis of tumor-bearing and non-tumor-bearing mice of all groups revealed that the occurrence of prolactin cells was greater in the former than the latter. Counts of gonadotropes and thyrotropes did not show any significant correlation with mammary tumorigenesis. However, neonatal estrogen and/or progesterone treatment resulted in significantly decreased numbers of gonadotropes in intact mice. In ovariectomized mice, gonadotropes were significantly increased regardless of neonatal treatment. The present results support the suggestion that the stimulatory effects of neonatal steroid treatment of mammary tumorigenesis may be a consequence of increased prolactin secretion, resulting from sustained minimal estrogen secretion by the ovary.

Animals↗
PubMed1978

Alteration of sodium transport in mouse mammary epithelium associated with neoplastic transformation.

Using electrophysiological techniques we have examined the apical membrane ionic permeabilities of primary cell cultures of the mouse mammary gland in the midpregnant, preneoplastic, and neoplastic states. Membrane Na+ permeability changed with tumorigenesis, whereas K+ and Cl- permeabilities were unaltered. With tracer flux techniques the unidirectional efflux rate constant of 22Na was found to be greater in tumor cells than it is in normal cells. This increase in 22Na efflux was eliminated by the addition of ouabain. The results are interpreted as an increase in Na+ permeability and in Na+-K+-ATPase activity with the neoplastic transformation. The presence or absence of the virus in midpregnant cells does not seem to affect Na+ permeability.

Animals↗
PubMed1977

Histopathogenesis of 7,12-diemthylbenz(a)anthracene-induced rat mammary tumors.

The histopathogenesis and growth behavior of mammary tumors and dysplasias induced by a single intragastric dose of 7,12-dimethylbenz[a]anthracene in 50-day-old virgin female Lewis rats were examined both in situ and after transplantation into gland-free mammary fat pads of syngeneic hosts. Terminal mammary ductules are indicated as a site of origin of both ovarian hormone-dependent mammary tumors and spontaneously gegressing mammary tumors, and terminal ductule hyperplasia appears to be an early stage in mammary tumor formation. The precancerous nature of hyperplastic alveolar nodules induced by dimethylbenzanthracene in rats has been further examined, and our studies indicate that these nodules are not significantly preneoplastic.

9,10-Dimethyl-1,2-benzanthracene↗