Two critical windows in mammary development have been proposed. The first arises from observations in rodents that nutrition during fetal and neonatal periods can affect mammary ductular outgrowth, subsequent proliferative activity and, eventually, tumorigenesis, that is, potentially it could have a long-term effect on pathological outcome (breast cancer) in women. The second similarly involves early diet, but in this case the outcome is phenotypic, in that dairy heifers reared too quickly during the peripubertal period subsequently show impaired udder development and reduced milk yield persisting throughout life. Most mammary development occurs during pregnancy, but this period is usually thought of only in terms of the immediate outcome for the subsequent lactation; it is not believed to be a critical window, at least in terms of lifetime mammary productivity. This review examines the evidence underlying these various claims and attempts to define the mechanisms involved, and also considers whether derangements occurring earlier in life (prenatally) could also have long-term consequences for physiological or pathological mammary development.
CH Knight and A Sorensen
ROMMOM L. LAWSON and A. M. SORENSEN Jr.
It has been known for many years that in certain animals, particularly rodents, a firm coagulated mass forms in the vagina after copulation. It was called a vaginal plug or copulation plug by Moore & Gallagher (1930) who described the anterior lobes of the prostate as the source of the coagulating enzyme and called these `coagulating glands'. This anterior portion differs physiologically and histologically from the middle and posterior lobes. In the albino rat the coagulating glands lie on the margins of the seminal vesicles, extending from their extremity to the base near the prostate.
Scott & Dziuk (1959) concluded that the coagulating gland in the albino rat was a major obstacle to electro-ejaculation since the plug blocked the urethra and caused death from uraemic poisoning. These authors removed the seminal vesicles and the
U Bentin-Ley, T Horn, A Sjogren, S Sorensen, J Falck Larsen and L Hamberger
The interactions of seven human blastocysts with cultured endometrial cells were investigated by light microscopy and transmission electron microscopy. Trophoblastic-endometrial contact was observed at the lateral border of endometrial epithelial cells where trophoblast and endometrial epithelial cells shared apical junctional complexes and desmosomes. The first sign of penetration was invasion of a trophoblastic cytoplasmic protrusion between endometrial epithelial cells. In broad contact areas, lateral displacement of endometrial epithelial cells and formation of a peripheral pseudostratified epithelium were observed. When trophoblastic cells were interposed fully among endometrial epithelial cells, they formed a penetration cone and appeared to dislodge endometrial epithelial cells from the stromal compartment. A single penetration cone only was found in each specimen. Endometrial or trophoblastic degeneration was not observed. Formation of multinucleate (>/= three nuclei per cell) trophoblast cells was not observed, but many cells displayed areas with abrupt disappearance of well-defined plasma membranes, which is indicative of syncytium formation. In this study, adhesion and penetration occurred at the same time. The human blastocysts penetrated the endometrial surface epithelium by intrusive penetration. Epithelial penetration was achieved primarily by cellular syncytiotrophoblast-like cells and the first indications of syncytium formation were observed simultaneously with penetration of the epithelium.