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Physical exercise is usually part of outpatient care for people with cystic fibrosis. The prognosis for cystic fibrosis has improved due to earlier diagnosis through screening and better treatment and access to health care. In , the median age of survival of children with CF in the United States was six months. Chronic illnesses can be very difficult to manage. CF is a chronic illness that affects the "digestive and respiratory tracts resulting in generalized malnutrition and chronic respiratory infections". According to Schmitz and Goldbeck , CF significantly increases emotional stress on both the individual and the family, "and the necessary time-consuming daily treatment routine may have further negative effects on quality of life".
Exercise is promoted to increase lung function. Cystic fibrosis is the most common life-limiting autosomal recessive disease among people of European heritage.
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In Canada, about 4, people have CF. Although technically a rare disease, CF is ranked as one of the most widespread life-shortening genetic diseases.
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It is most common among nations in the Western world. An exception is Finland , where only one in 80 people carries a CF mutation.
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In contrast, only one in 15, African American children suffered from it, and in Asian Americans, the rate was even lower at one in 32, Cystic fibrosis is diagnosed in males and females equally. For reasons that remain unclear, data have shown that males tend to have a longer life expectancy than females,   but recent studies suggest this gender gap may no longer exist perhaps due to improvements in health care facilities,   while a recent study from Ireland identified a link between the female hormone estrogen and worse outcomes in CF.
The distribution of CF alleles varies among populations. CF is known to occur in only 20 families pedigrees in Finland. Other common autosomal recessive diseases such as sickle-cell anemia have been found to protect carriers from other diseases, an evolutionary trade-off known as heterozygote advantage.
Resistance to the following have all been proposed as possible sources of heterozygote advantage:. CF is supposed to have appeared about 3, BC because of migration of peoples, gene mutations, and new conditions in nourishment. In the 19th century, Carl von Rokitansky described a case of fetal death with meconium peritonitis , a complication of meconium ileus associated with CF. Meconium ileus was first described in by Karl Landsteiner. She was the first to describe the characteristic cystic fibrosis of the pancreas and to correlate it with the lung and intestinal disease prominent in CF.
In , Paul di Sant'Agnese discovered abnormalities in sweat electrolytes; a sweat test was developed and improved over the next decade. Riordan on the seventh chromosome. Subsequent research has found over 1, different mutations that cause CF. Because mutations in the CFTR gene are typically small, classical genetics techniques had been unable to accurately pinpoint the mutated gene. Chromosome-walking and -jumping techniques were then used to identify and sequence the gene. CF represents a classic example of how a human genetic disorder was elucidated strictly by the process of forward genetics.
Gene therapy has been explored as a potential cure for CF. Results from clinical trials have shown limited success as of [update] , and using gene therapy as routine therapy is not suggested. The focus of much CF gene therapy research is aimed at trying to place a normal copy of the CFTR gene into affected cells.
Transferring the normal CFTR gene into the affected epithelium cells would result in the production of functional CFTR protein in all target cells, without adverse reactions or an inflammation response. However, both methods were found to be relatively inefficient treatment options,  mainly because very few cells take up the vector and express the gene, so the treatment has little effect. Additionally, problems have been noted in cDNA recombination, such that the gene introduced by the treatment is rendered unusable.
Phage therapy is being studied for multidrug resistant bacteria in people with CF. A number of small molecules that aim at compensating various mutations of the CFTR gene are under development. One approach is to develop drugs that get the ribosome to overcome the stop codon and synthesize a full-length CFTR protein.
These drugs target nonsense mutations such as GX, which consists of the amino acid glycine in position being replaced by a stop codon. Aminoglycoside antibiotics interfere with protein synthesis and error-correction. In some cases, they can cause the cell to overcome a premature stop codon by inserting a random amino acid, thereby allowing expression of a full-length protein. From Wikipedia, the free encyclopedia. Autosomal recessive disease.
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Play media. See also: List of people diagnosed with cystic fibrosis. Cystic Fibrosis. CRC Press. Archived from the original on Paediatric Respiratory Reviews. Cystic fibrosis 3rd ed. London: Hodder Arnold. Molecular diagnostics fundamentals, methods, and clinical applications 2nd ed. Philadelphia: F. Davis Co. Clinical Medicine. Am J Dis Child. Respir Care. Consultant for Pediatricians. March Robbins basic pathology. The New England Journal of Medicine. The Cochrane Database of Systematic Reviews.
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Clinics in Chest Medicine Review. J Bras Pneumol. Human Reproduction Update. Fetal and maternal outcome". Retrieved Bibcode : Natur. Human Anatomy and Physiology. Pearson Education.
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