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Crack is produced by dissolving powdered cocaine in a mixture of water and ammonia or sodium bicarbonate (baking soda). The mixture is boiled until a solid substance forms. The solid is removed from the liquid, dried, and then broken into the chunks (rocks) that are sold as crack cocaine.
People can manage lactose intolerance by not drinking as much milk and eating fewer dairy products. Most can eat a small amount of dairy. But they need to eat it with other foods that don't contain lactose and not eat too much dairy at once.
You may find that other dairy products, such as yogurt and cheeses, are easier to digest than milk. Lactose-free milk is also a great way to get calcium in the diet without the problems. It can also help to keep a food diary to learn which foods you can or can't tolerate.
Amlodipine and olmesartan medoxomil tablets contain amlodipine besylate, USP, a white to off-white crystalline powder, and olmesartan medoxomil, USP a white to light yellowish-white powder or crystalline powder. The molecular weights of amlodipine besylate, USP and olmesartan medoxomil, USP are 567.1 and 558.59, respectively. Amlodipine besylate, USP is slightly soluble in water and sparingly soluble in ethanol. Olmesartan medoxomil, USP is practically insoluble in water and sparingly soluble in methanol.
In rats, olmesartan crossed the blood-brain barrier poorly, if at all. Olmesartan passed across the placental barrier in rats and was distributed to the fetus. Olmesartan was distributed to milk at low levels in rats.
There are no data on the presence of tadalafil and/or its metabolites in human milk, the effects on the breastfed child, or the effects on milk production. Tadalafil and/or its metabolites are present in the milk of lactating rats at concentrations approximately 2.4-times that found in the plasma. When a drug is present in animal milk, it is likely that the drug will be present in human milk.
The transition from pregnancy to lactation is a critical event in the survival of the newborn since all the nutrient requirements of the infant are provided by milk. While milk contains numerous components, including proteins, that aid in maintaining the health of the infant, lactose and milk fat represent the critical energy providing elements of milk. Much of the research to date on mammary epithelial differentiation has focused upon expression of milk protein genes, providing a somewhat distorted view of alveolar differentiation and secretory activation. While expression of milk protein genes increases during pregnancy and at secretory activation, the genes whose expression is more tightly regulated at this transition are those that regulate lipid biosynthesis. The sterol regulatory element binding protein (SREBP) family of transcription factors is recognized as regulating fatty acid and cholesterol biosynthesis. We propose that SREBP1 is a critical regulator of secretory activation with regard to lipid biosynthesis, in a manner that responds to diet, and that the serine/threonine protein kinase Akt influences this process, resulting in a highly efficient lipid synthetic organ that is able to support the nutritional needs of the newborn.
Over the past 12 years our understanding of the regulation of milk protein gene expression has improved dramatically. One important advance was the discovery of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway; prolactin (PRL)-induced activation of JAK2 and STAT5 is required to induce expression of most, if not all, milk protein genes [1, 2]. Recent advances suggest that the transcription factor Elf5 and the ubiquitin ligase Socs2 (suppressor of cytokine signaling) are important mediators of PRL action. Loss of Socs2, which negatively regulates the PLR receptor (PRLR), or forced expression of the Elf5 transcription factor can restore lactation in mice that fail to lactate due to the loss of one or both alleles encoding the PRL receptor . These findings led the investigators to suggest that Elf5 is encoded by one of the master controller genes that regulate alveolar differentiation (recently termed the alveolar switch in a review by Oakes and colleagues  in this series of reviews). Despite these advances, our understanding of the molecular changes that underlie alveolar differentiation and secretory activation (the lactation switch) is relatively unsophisticated. In this review we identify changes that are known to occur in the mouse as a means to identify questions and challenges for the coming decade and suggest that sterol regulatory element binding protein (SREBP)-1c and the serine/threonine protein kinase Akt1 play a major role in the lactational switch.
The morphological changes that occur in the mammary gland during puberty, pregnancy and lactation are well established . A rudimentary mammary ductal structure is established in utero  and all subsequent developmental events occur after birth. Ductal elongation and branching occur primarily after the onset of puberty under the influence of estrogen, epidermal growth factor, and insulin like growth factor (IGF)-1 [7, 8]. The terminal end bud is the primary proliferative structure that directs ductal elongation, which appears to occur maximally between three to six weeks of age. By ten to twelve weeks of age the ducts have reached the margins of the fat pad, the terminal end buds regress to form terminal ducts, and ductal elongation ceases. In contrast to humans, in which ten to fifteen branching ducts connect to the nipple, in the mouse a single primary duct, which can be identified by its proximity to the nipple and the thick sheath of connective tissue, serves as a conduit for the passage of milk to the suckling young. Secondary and tertiary ducts, which contain a single layer of cuboidal luminal epithelial cells surrounded by a layer of basal cells, are formed by branching off the primary duct. Formation of lateral and alveolar buds occurs in the post-pubertal mammary gland following initiation of the estrous cycle [9, 10]. These lateral buds are often termed side branches and represent the origin of the alveoli that are the milk producing cells in the lactating mammary gland .
Alveolar differentiation, for example, the formation of lobuloalveolar structures capable of milk production, occurs during pregnancy and is also stimulated by PRL [16, 17]. Transcription profiling studies indicate that PRL stimulates transcription of Wnt4 , RankL , and cyclin D1 via induction of IGF-2 [19, 20]. PRL also induces the expression of two other transcription factors of note: the ETS transcription family member Elf5  and SREBP1 . Harris and colleagues  demonstrated that forced expression of Elf5 in mammary epithelial cells from PRLR knockout mice is able to restore morphological differentiation and production of milk proteins. In these experiments it could not be determined whether Elf5 induced a functional restoration since the transfected mammary epithelial cells were transplanted into a recipient host and lactation does not occur in these mice due to the lack of ductal connections with the teat. The role of SREBP1 will be discussed below as it regulates the expression of a number of key lipid metabolism genes .
Histological changes in mammary gland morphology in the mouse during pregnancy and lactation are shown in Figure 1. Initial changes observed during pregnancy include an increase in ductal branching and the formation of alveolar buds (Figure 1a); this phase of differentiation is characterized by the largest increase in DNA synthesis and cellular proliferation during pregnancy . The latter half of pregnancy is characterized by the expansion of alveolar buds to form clusters of lobuloalveolar units, followed by the differentiation of these structures into pre-secretory structures. By day 12 of pregnancy there is a readily apparent increase in the size of the epithelial compartment compared to the adipose compartment (Figure 1c), and expansion of the epithelium continues until the epithelial compartment predominates by late pregnancy (Figure 1e). The luminal space is clearly evident by late pregnancy, filled with a proteinaceous substance whose identity is not clear but may represent milk proteins, glycoproteins such as Muc1, lactoferrin, and possibily immunoglobulins (Figure 1f). Large lipid droplets are also present in the cytoplasm of the alveolar epithelial cells and, to some extent, in the luminal space (Figure 1f). Following parturition, the secretory lobuloalveolar structures become more apparent as the luminal space expands, and the epithelial cell layer becomes more prominent against the adipocytes (Figure 1g). The large lipid droplets, which were present at day 18 of pregnancy, are not present, having been replaced by small lipid droplets at the apical surface of the epithelial cells (Figure 1h), and although the luminal space may contain proteinaceous material when it has not been lost during fixation and sectioning, it stains much more lightly than during late pregnancy (Figure 1i versus 1b). By day nine of lactation in the mouse, the mammary gland is producing copious amounts of milk. Examination of the histology of the mammary gland at this stage reveals prominent luminal structures and ducts; however, few adipocytes are visible at this time (Figure 1i). This change is thought to reflect delipidation of adipocytes rather than a decrease in their number .
Lactation is defined as the continuous production of milk by the dam. In most species there are two phases: a colostral phase in which the milk contains large amounts of immunoglobulins and other immune defense proteins , and the mature secretion phase characterized by the production of large volumes of milk that support the growth of the newborn. Although the colostral phase has not been well-characterized in the mouse, preliminary evidence from the Neville laboratory suggests that it is brief in this species (Neville MC, unpublished data). Mouse milk contains about 12% proteins (the different caseins, α-lactalbumin, whey acidic protein (WAP), lactoferrin, secretory immunoglobulin A, and others), 30% lipid, and 5% lactose, a disaccharide that is unique to milk. With the closure of the tight junctions there is no transfer of sugars from the blood to the milk. Synthesis of lactose takes place in the Golgi compartment, where the required synthetic enzymes are located. In both mice and rats, lactose is not detected in the mammary gland until the day before parturition [51, 52], and thus lactose synthesis may be considered a marker of secretory activation. Furthermore, mice with a null mutation of the gene for α-lactalbumin, an essential co-factor for lactose synthesis, fail to lactate . 2b1af7f3a8