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Understanding diet and energy balance as risk factors for breast, colon, and other cancers requires information on the contribution of each factor and of interactions among factors to cancer risk. Rodent models for breast cancer provide extensive data on effects of dietary fat and calories, energy balance, body weight gain, and physical activity on tumor development. Analyses of the combined data from many studies have shown clearly that quality and quantity of dietary fat and energy balance contribute independently to increased mammary gland tumorigenesis. These findings were seen in female rats fed diets high in fat (35-40% of calories) compared to rats fed control diets, with approximately 10% of calories as fat (Fay and Freedman, 1997, Breast Cancer Res. Treat. 46, 215-223). The methods used permit comparison of experimental and epidemiological data, and they may be useful in extrapolating between species and developing public health recommendations. In addition to the contributions of lifetime-diet composition, intake, energy balance, and physical activity to cancer risk, there are questions about the timing and duration of alterations in these factors and about the "dose-response" characteristics of cancer risk to the factors. Endocrine mechanisms may be significant in mammary gland tumor risk, but experimental and epidemiological data indicate that cancers at other sites, such as colon and liver, also are influenced by the factors listed. Other diet and lifestyle factors that influence energy, or specifically fat, metabolism may also affect risk for cancers that are promoted by increased intake of fat and calories. Studies of separate and interactive effects of dietary fat, black tea, weight gain, and mammary gland tumorigenesis (Rogers, et al, 1998, Carcinogenesis 19, 1269-1273) have been analyzed. Using adjustment of carcinogenesis endpoints for body weight, tumor burden, and latency, they were found to be related to weight gain within treatment groups in 2 of 3 experiments.   相似文献   
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The purpose of this study was to compare the effect of the nature and quantity of various dietary fibre (cellulose, hemicellulose, pectin, lignin) in diets on the binding capacity to pesticides azinphos-methyl (AZM), chlorpropham (CLP), chlorothalonil (CKL), permethrin (PER) as estimated by solubility under conditions of pH and temperature simulating those in the gastrointestinal tract (incubated at pH 2 for 30 min at 37°C, then at pH 7 for 60 min). The ratios of fibre to pesticides were determined in omnivorous diets. In this model, the binding capacity of lignin was equal to hemicellulose for PER, AZM and CLP, but it was significantly higher for CKL. Hemicellulose bound more CKL, AZM and CLP than did cellulose. Although pectin appreciably decreased all pesticides, its effect was lower than other fibres with one exception—cellulose-CKL. In the presence of equal amounts of fibre, lignin exerted the most significant effect on pesticide solubility. Hemicellulose and cellulose bind to the same extent PER and AZM. The effect of pectin was significant only on CKL and AZM when compared to the control.  相似文献   
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Successful pregnancy in a transfusion-dependent thalassaemic patient receiving subcutaneous desferrixaomine is reported. This is the first such case to be described.  相似文献   
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Three sibs all presented in the early neonatal period with a salt-losing syndrome. The salt-losing form of congenital adrenal hyperplasia was diagnosed and appropriate treatment with glucocorticosteroids, mineralocorticosteroids, and additional dietary salt started. Although early life was maintained with difficulty, with age all 3 children required decreasing amounts of replacement steroids to maintain normal plasma electrolyte balance. They were reinvestigated at the ages of 15 years and 8 years (twins), when cortisol synthesis and metabolism proved normal, but aldosterone synthesis was blocked by deficiency of 18-dehydrogenase. Rational treatment of these cases of a salt-losing syndrome in which aldosterone synthesis alone is blocked due to lack of the enzyme 18-dehydrogenase requires the administration of a mineralocorticosteroid drug only. Since deoxycorticosterone (acetate or pivalate) requires intramuscular administration, as life-long therapy oral fludrocortisone is preferable. Although fludrocortisone has glucocorticoid activity, the "hydrocortisone equivalent" effect of the small dosage used was unlikely to inhibit either pituitary corticotrophin or growth hormone production.  相似文献   
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