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The current study examines the efficacy of two treatments to help children with cystic fibrosis (CF) meet their dietary calorie requirements of 120% to 150% of the recommended daily allowance of energy and the effect of these treatments on weight gain and maintenance. One treatment provides children with CF and their parents nutrition education about the best foods for meeting their dietary needs. The second treatment gives children with CF and their families similar nutritional information plus behavioral parenting methods for motivating children to eat the recommended foods. Children with CF and their families are seen weekly for 7 treatment sessions across 9 weeks for the active phase of treatment. Families are then followed for 2 years after treatment in order to better understand how long the treatments are effective and to determine the health benefits of better nutrition status and weight gain.
Primary Purpose: Prevention
University of Florida
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Published on BioPortfolio: 2014-08-27T03:57:26-0400
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An autosomal recessive genetic disease of the EXOCRINE GLANDS. It is caused by mutations in the gene encoding the CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR expressed in several organs including the LUNG, the PANCREAS, the BILIARY SYSTEM, and the SWEAT GLANDS. Cystic fibrosis is characterized by epithelial secretory dysfunction associated with ductal obstruction resulting in AIRWAY OBSTRUCTION; chronic RESPIRATORY INFECTIONS; PANCREATIC INSUFFICIENCY; maldigestion; salt depletion; and HEAT PROSTRATION.
A chloride channel that regulates secretion in many exocrine tissues. Abnormalities in the CFTR gene have been shown to cause cystic fibrosis. (Hum Genet 1994;93(4):364-8)
A strain of mice widely studied as a model for cystic fibrosis. These mice are generated from embryonic stem cells in which the CFTR (cystic fibrosis transmembrane conductance regulator) gene is inactivated by gene targeting. As a result, all mice have one copy of this altered gene in all their tissues. Mice homozygous for the disrupted gene exhibit many features common to young cystic fibrosis patients, including failure to thrive, meconium ileus, and alteration of mucous and serous glands.
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