Cystic Fibrosis Foundation - http://www.cff.org/facts.htm
The disease itself is caused by the presence of two defective CF genes. Carriers only have one defective gene. Thus, if two carriers have children, each child has a 25% chance of having CF , a 50% chance that they will be a carrier of the disease and a 25% chance that they will not inherit a defective gene at all (non-carrier).
The CF gene manufactures a protein caled CFTR. This protein helps the flow of sodium chloride ions (salt) across the membranes of cells lining organs such as the lungs and pancreas. The inability to transport the ions creates a thick, sticky mucus which forms on the organ linings. This mucus is hard to remove and provides a breeding ground for bacterial infections. Many CF patients suffer from pnuemonia coughing, and wheezing.
CF also affects the digestive system. The mucos produced in CF patients often builds up in the pancreas and prevents important digestive enzymes from reaching the intestines. Thus, CF patients have difficulty breaking down food. The patients suffer from excessive appetite, poor weight gain and bulky stools.
CF can be identified by the sweat test where doctors measure the amount of salt in a patients sweat. High salt levels indicate CF. The previously discussed symptoms are also good indicators of the disease.
Currently, the life expectancy of CF patients has grown from 8 yrs to around 30 yrs of age. New treatments are concentrating on the cause of the disease instead of the symptoms. (i.e. Instead of treating the infections with antibiotics, drugs have been developed to prevent the build up of the thick mucos which causes the infections.)
In order to construct this model we will concentrate on three compartments
Mold = 0
Pollen = 0
Dust graph
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LI graph
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Mold graph
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MS graph
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Pollen Graph
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