Programmed cell death (PCD) of mammary alveolar cells during involution commences within hours of the end of suckling. Locally, milk accumulates within alveolar lumens; systemically, levels of lactogenic hormones fall. Four experimental models were used to define the role of local factors as compared with systemic hormones during the first and second stages of involution. In three models, milk release was disrupted in the presence of systemic lactogenic hormones: (i) sealing of the teats, (ii) mammary gland transplants that cannot release milk due to the absence of a teat connection, and (

Forty Holstein heifer calves were assigned to two treatments. Control calves (n = 20) were fed milk replacer in open buckets, and calves that were allowed to suckle (n = 20) were paired and suckled the same dam three times daily. Treatments were conducted during the first 6 wk following birth; thereafter, all calves received the same management, and weaning was at 60 d of age. During treatment, calves that were allowed to suckle had significantly higher average daily gains than did control calves. However, at 12 wk of age, calves that were allowed to suckle had significantly lower body weights (BW) than did control calves. Age at conception was significantly lower, and BW at conception and conception rate tended to be higher, for calves that were allowed to suckle. Calving age was significantly earlier for heifers that had been allowed to suckle as calves, and BW at calving also tended to be higher. Height at the withers after calving was also significantly higher for those heifers. Milk production during first lactation tended to be higher for the heifers that had been allowed to suckle as calves. Our results indicated that heifer calves that suckled milk during the first 42 d of age had higher average daily gains, higher height at the withers, an earlier age at calving, and a tendency for greater milk production than did calves fed milk replacer.

Bcl-2 is an anti-apoptotic and anti-proliferative protein over-expressed in several di erent human cancers including breast. Gain of Bcl-2 function in mammary epithelial cells was superimposed on the WAP-TAg transgenic mouse model of breast cancer progression to determine its e ect on epithelial cell survival and proliferation at three key stages in oncogenesis: the initial proliferative process, hyperplasia, and cancer. During the initial proliferative process, Bcl-2 strongly inhibited both apoptosis and mitotic activity. However as tumorigenesis progressed to hyperplasia and adenocarcinoma, the inhibitory e ects on mitotic activity were lost. In contrast, anti-apoptotic activity persisted in both hyperplasias and adenocarcinomas. These results demonstrate that the inhibitory e ect of Bcl-2 on epithelial cell proliferation and apoptosis can separate during cancer progression. In this model, retention of anti-apoptotic activity with loss of anti-proliferative action resulted in earlier tumor presentation.