Lactogenesis and the effects of insulin-dependent diabetes mellitus and prematurity.

The initiation of lactation (lactogenesis II) by the mother must be synchronized to the delivery of the infant, permitting the transition of the newborn from continuous nourishment from the umbilical cord to comparable but intermittent life support from its mother's breasts. The onset of lactogenesis II can be adversely affected by a variety of factors. Over 80% of women who have delivered prematurely and are expressing milk for their infant had a compromised initiation of lactation, that is one or more lactogenesis II markers (lactose, citrate, sodium and total protein) in their milk > 3 SD from the mean of the full-term women on d 5 postpartum. Similarly, the lactogenesis II markers (lactose, citrate and total nitrogen) in the milk of women with insulin-dependent diabetes mellitus take an additional 24 h to attain the concentrations of normal women. The mechanisms that lead to the development of delayed or compromised onset of lactogenesis II in women are poorly understood and require additional research.

Computerized breast measurement from conception to weaning: clinical implications.

The CBM system has enabled our laboratory to measure breast growth and demonstrate the importance of the short-term local control of milk synthesis in lactating women. Although the specific mechanism by which the short-term control of milk synthesis occurs has yet to be fully understood, it is now apparent that the interaction between storage capacity, degree of fullness, and frequency of milk removal plays a significant role. These factors demonstrate that the breastfeeding mother can take comfort in the individuality of her breast development and feeding pattern, which is uniquely adapted to suit the physiology of her breasts and the developmental requirements of her infant.

Membrane potassium channels and human bladder tumor cells: II. Growth properties.

These experiments were done to determine the effect of glibenclamide and diazoxide on the growth of human bladder carcinoma (HTB-9) cells in vitro. Cell growth was assayed by cell counts, protein accumulation, and 3H-thymidine uptake. Glibenclamide added at 75 and 150 microM for 48 hr reduced cell proliferation. Dose-inhibition curves showed that glibenclamide added for 48 hr reduced cell growth at concentrations as low as 1 microM (IC50 = 73 microM) when growth was assayed in the absence of added serum. This microM-effect on cell growth was in agreement with the dose range in which glibenclamide decreased open probability of membrane KATP channels. Addition of glibenclamide for 48 hr also altered the distribution of cells within stages of the cell cycle as determined by flow cytometry using 10(-5) M bromodeoxyuridine. Glibenclamide (100 microM) increased the percentage of cells in G0/G1 from 33.6% (vehicle control) to 38.3% (P < 0.05), and it reduced the percentage of cells in S phase from 38.3% to 30.6%. On the other hand, diazoxide, which opens membrane KATP channels in HTB-9 cells, stimulated growth measured by protein accumulation, but it did not increase the cell number. We conclude that the sulfonylurea receptor and the corresponding membrane KATP channel are involved in mechanisms controlling HTB-9 cell growth. However, KATP is not rate-limiting among the signaling mechanisms or molecular switches that regulate the cell cycle.