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The Human Lactation Research Group is under the direction of Professor Peter Hartmann. The group’s research aim is to gain a greater understanding of the synthesis and secretion of breastmilk as well as the mechanisms of removal of milk from the breast by either the suckling infant or by expression with an electric breast pump. The understanding of these mechanisms will facilitate successful breastfeeding by providing an evidence base for the clinical management of human lactation. Anatomy of the Human Lactating Breast Descriptions and diagrams of the anatomy of the human lactating breast has changed little over the last 160 years and are based on dissections of the breasts of lactating cadavers (Figure 1) by Sir Astley Cooper (1840). Using ultrasound imaging we studied 21 fully lactating women’s breasts. We found that there were approximately 9 main ducts that are about 2mm in diameter. All the ducts branched under the areolar radius close to the nipple and did not display large dilated areas. This suggests that the main function of the milk ducts is to transport, rather than store breastmilk. Since we have found the ductal anatomy of the breast to be different to previously believed (Figure 2) it has now led to the re-investigation of how the infant removes milk from the breast. Figure 1. Artist impression of the milk duct system of the lactating breast injected with coloured wax (Cooper, 1840) 
Figure 2. A drawing of the gross anatomy of the lactating breast based on ultrasound observations made of the milk duct system and distribution of different tissues within the breast Excretion of Lactose in Urine as a Measure of Increased Permeability of the Lactating Breast during Inflammation Mastitis is a significant problem for many lactating women causing fever, flu-like symptoms and localized inflammation of the breast. Both repeated bouts and increased severity of mastitis may also contribute to early weaning of the baby. While mastitis is known to change the composition of breastmilk (decreased lactose and increased sodium) it was hypothesized that these changes would be accompanied by an increase in lactose in the urine. Samples of breastmilk, blood, and 24-h urine were collected prospectively along with details of clinical symptoms from 26 mothers from Day 5 post partum to the end of their lactation. Indeed it was found that urine lactose was higher during mastitis, peaking at the beginning of the mastitis and decreasing with the resolution of symptoms. This was in keeping with changes in sodium, chloride and lactose in milk. In addition the increased severity of breast symptoms resulted in the increased excretion of lactose in urine. Therefore the measurement of 24-hour excretion of lactose in urine provided a reliable marker of the physiological changes occurring during mastitis.
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