and doctors to track health results and identify candidates for clinical trials. gene therapy gene therapy has been explored as a potential cure for cf. results from clinical trials have shown limited success as of 2016, and using gene therapy as routine therapy is not suggested. a small study published in 2015 found a small benefit. 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. to prevent the lung manifestations of cf, only 5–10% the normal amount of cftr gene expression is needed. multiple approaches have been tested for gene transfer, such as liposomes and viral vectors in animal models and clinical trials. 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. there has been a functional repair in culture of cftr by crispr/cas9 in intestinal stem cell organoids of cystic fibrosis patients. phage therapy phage therapy is being studied for multidrug resistant bacteria in people with cf. gene modulators a number of small molecules that aim at compensating various mutations of the cftr gene are under development. cftr modulator therapies have been used in place of other types of genetic therapies. these therapies focus on the expression of a genetic mutation instead of the mutated gene itself. modulators are split into two classes: potentiators and correctors. potentiators act on the cftr ion channels that are embedded in the cell membrane, and these types of drugs help open up the channel to allow transmembrane flow. correctors are meant to assist in the transportation of nascent proteins, a protein that is formed by ribosomes before it is morphed into a specific shape, to the cell surface to be implemented into the cell membrane. most target the transcription stage of genetic expression. one approach has been to try and develop medication that get the ribosome to overcome the stop codon and produce a full-length cftr protein. about 10% of cf results from a premature stop codon in the dna, leading to early termination of protein synthesis and truncated proteins. these drugs target nonsense mutations such as g542x, which consists of the amino acid glycine in position 542 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. future research for these modulators is focused on the cellular targets that can be effected by a change in a gene's expression. otherwise, genetic therapy will be used as a treatment when modulator therapies do not work given that 10% of people with cystic fibrosis are not affected by these drugs. elexacaftor/ivacaftor/tezacaftor was approved in the united states in 2019 for cystic fibrosis. this combination of previously developed medicines is able to treat up to 90% of people with cystic fibrosis. this medications restores some effectiveness of the cftr protein so that it can work as an ion channel on the cell's surface. ecological therapy it has previously been shown that inter-species interactions are an important contributor to the pathology of cf lung infections. examples include the production of antibiotic degrading enzymes such as β-lactamases and the production of metabolic by-products such as short-chain fatty acids (scfas) by anaerobic species, which can enhance the pathogenicity of traditional pathogens such as pseudomonas aeruginosa. due to this, it has been suggested that the direct alteration of cf microbial community composition and metabolic function would provide an alternative to traditional antibiotic therapies. society and culture salt in my soul: an unfinished life a posthumous memoir by mallory smith, a californian with cf sick: the life and death of bob flanagan, supermasochist, a 1997 documentary film 65 redroses, a 2009 documentary film breathing for a living, a memoir by laura rothenberg every breath i take, surviving and thriving with cystic fibrosis, book by claire wineland five feet apart, a 2019 romantic drama film starring cole sprouse and haley lu richardson orla tinsley: warrior, a 2018 documentary film about cf campaigner orla tinsley the performance art of martin o'brien continent chasers, a traveller and cf patient documenting travel and cf blogs, continentchasers.com notes the cystic fibrosis foundation recommends a diagnosis of cystic fibrosis for anyone suspected of cystic fibrosis (positive newborn screen, symptoms of cystic fibrosis, or a family history of cystic fibrosis) with sweat chloride above 60 millimoles/liter. those with less than 30 millimoles/liter sweat chloride are unlikely to develop cystic fibrosis. for people with intermediate sweat chloride between 30 and 59 millimoles/liter, they recommend additional genetic testing.