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1 r degeneration (AMD), diabetes mellitus, and cystic fibrosis).
2 logy of many respiratory diseases, including cystic fibrosis.
3 mbrane regulator (CFTR) mutation that causes cystic fibrosis.
4 sweat diagnostics with reliable detection of cystic fibrosis.
5 k and lower life expectancy in patients with cystic fibrosis.
6 yperoxaluria observed in this mouse model of cystic fibrosis.
7                                              Cystic fibrosis.
8 ss 23 sites of the lungs from a patient with cystic fibrosis.
9 6-mediated oxalate secretion is defective in cystic fibrosis.
10 underlying cause of disease in patients with cystic fibrosis.
11 del mutation, which is the dominant cause of cystic fibrosis.
12 ted with an aggressive clinical phenotype in cystic fibrosis.
13 k and lower life expectancy in patients with cystic fibrosis.
14  function decline and increased mortality in cystic fibrosis.
15  notably prevalent among young children with cystic fibrosis.
16  for further investigation as treatments for cystic fibrosis.
17 tation that is associated with mild forms of cystic fibrosis.
18 ch is associated with the pathophysiology of cystic fibrosis.
19 een increase airway surface liquid volume in cystic fibrosis.
20 ts with hospital-acquired infections or with cystic fibrosis.
21 ic validity of attenuating IL-17 activity in cystic fibrosis.
22 s of several respiratory diseases, including cystic fibrosis.
23 of-function chloride channelopathies such as cystic fibrosis.
24 te stone formation observed in patients with cystic fibrosis.
25 ision therapies for airway disorders such as cystic fibrosis.
26 ight be promising as co-adjuvant therapy for cystic fibrosis.
27 icted to be cost-effective for patients with cystic fibrosis.
28 tricted evidence available for patients with cystic fibrosis.
29 elopathies including cardiac arrhythmias and cystic fibrosis.
30 l CRC screening strategies for patients with cystic fibrosis.
31                                           In cystic fibrosis, abnormal glucose tolerance is associate
32 of lumacaftor and ivacaftor in patients with cystic fibrosis aged 6-11 years homozygous for F508del-C
33 A longitudinal cohort study of patients with cystic fibrosis aged 6-21 years was conducted using the
34 Chr11p13 that is implicated as a modifier of cystic fibrosis airway disease.
35 sms fail in CFTR(-/-) swine, suggesting that cystic fibrosis airways do not respond to inhaled pathog
36 g 8 kg or more with a confirmed diagnosis of cystic fibrosis and a CFTR gating mutation on at least o
37 r developing new drugs for disorders such as cystic fibrosis and asthma.
38 ammation, and lung function in subjects with cystic fibrosis and chronic airway infections.
39 ic rhinosinusitis, and exacerbations of both cystic fibrosis and chronic obstructive pulmonary diseas
40 proved clearance in airway diseases, such as cystic fibrosis and chronic rhinosinusitis.
41 R) activity and lung function in people with cystic fibrosis and G551D-CFTR mutations but does not re
42 nts in patients aged 12 years and older with cystic fibrosis and homozygous for F508del-CFTR, but it
43 ible if they were at least 12 years old with cystic fibrosis and homozygous for the F508del-CFTR muta
44 acrophages in human lungs from patients with cystic fibrosis and induced in mouse macrophages in resp
45 ose that occur in the lungs of patients with cystic fibrosis and nonhealing ulcers.
46 teractions in A. fumigatus and patients with cystic fibrosis and the ongoing validation of novel labo
47 48 patients 12 years of age or older who had cystic fibrosis and were heterozygous for the Phe508del
48 in patients 12 years of age or older who had cystic fibrosis and were homozygous for the CFTR Phe508d
49 in patients 12 years of age or older who had cystic fibrosis and were homozygous for the CFTR Phe508d
50 lso to treat conformational diseases such as cystic fibrosis, and Alpha-1 antitrypsin deficiency.
51 te respiratory distress syndrome, pneumonia, cystic fibrosis, and bronchiectasis.
52          BACKGROUND & AIMS: Individuals with cystic fibrosis are at increased risk of colorectal canc
53          BACKGROUND & AIMS: Individuals with cystic fibrosis are at increased risk of colorectal canc
54                  RATIONALE: Individuals with cystic fibrosis are at risk for prolonged drops in lung
55      Neutrophilic airway diseases, including cystic fibrosis, are characterized by excessive neutroph
56 eral nutrition-associated liver disease, and cystic fibrosis-associated liver disease.
57 onal and experimental approach to rescue the cystic-fibrosis-associated protein cystic fibrosis trans
58 ulation leads to a range of diseases such as cystic fibrosis, Bartter's syndrome and epilepsy.
59 anadian cystic fibrosis clinics and 110 U.S. cystic fibrosis care centers.
60 ombinations may have therapeutic efficacy in cystic fibrosis caused by the W1282X mutation, although
61 f its functional mechanism and correction of cystic fibrosis causing mutants.
62          The structure also reveals why many cystic-fibrosis-causing mutations would lead to defects
63                                          The cystic fibrosis (CF) airway surface liquid (ASL) provide
64                                           In cystic fibrosis (CF) altered mucus properties impair muc
65        Chronic inflammation is a hallmark of cystic fibrosis (CF) and associated with increased produ
66    They are major pathogens in patients with cystic fibrosis (CF) and can cause severe necrotizing pn
67 onization in chronic lung disease, including cystic fibrosis (CF) and chronic obstructive pulmonary d
68  mechanism in airways, and it is impaired in cystic fibrosis (CF) and other obstructive lung diseases
69 urkholderia dolosa caused an outbreak in the cystic fibrosis (CF) clinic at Boston Children's Hospita
70 erimental measurements made using normal and cystic fibrosis (CF) cultured human airway epithelium.
71  leading to hyperinflammation, a hallmark of cystic fibrosis (CF) disease.
72                  RATIONALE: Individuals with cystic fibrosis (CF) experience frequent acute pulmonary
73                                    CFTR, the cystic fibrosis (CF) gene, encodes for the CFTR protein
74 es are reminiscent of the pathophysiology of cystic fibrosis (CF) in which loss-of-function mutations
75 progression of lung disease in children with cystic fibrosis (CF) indicates that sensitive noninvasiv
76                                              Cystic fibrosis (CF) is a common genetic disease caused
77                                              Cystic fibrosis (CF) is a major lethal genetic disease c
78                                              Cystic fibrosis (CF) is an autosomal recessive disorder
79                                              Cystic fibrosis (CF) is caused by loss-of-function mutat
80                                              Cystic fibrosis (CF) is caused by mutations in the gene
81                                              Cystic fibrosis (CF) is caused by mutations that disrupt
82 teria (NTM) from the sputum of patients with cystic fibrosis (CF) is challenging due to overgrowth by
83                                              Cystic fibrosis (CF) is characterized by an excessive ne
84                                              Cystic fibrosis (CF) is characterized by chronic infecti
85                                              Cystic fibrosis (CF) is characterized by early structura
86 B-OprM efflux system, naturally occurring in cystic fibrosis (CF) isolates, have been previously show
87                                              Cystic fibrosis (CF) liver disease (CFLD), a leading cau
88 mains an important pathogen in patients with cystic fibrosis (CF) lung disease as well as non-CF bron
89                                   RATIONALE: Cystic fibrosis (CF) lung disease is caused by the loss
90 ommunity of three temperate phages active in cystic fibrosis (CF) lung infections, including the tran
91 lize a panel of P. aeruginosa burn wound and cystic fibrosis (CF) lung isolates to demonstrate that P
92  respiratory virus infections predispose the cystic fibrosis (CF) lung to chronic bacterial colonizat
93 y adaptation during chronic infection of the cystic fibrosis (CF) lung, including reduced production
94 bacteria rarely reported in patients without cystic fibrosis (CF) or immunocompromising conditions.
95 istic pathogen that persists in the lungs of cystic fibrosis (CF) patients and may be responsible for
96 es chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-co
97                            Growth failure in cystic fibrosis (CF) patients has been well-documented a
98 alence of fungi in the respiratory tracts of cystic fibrosis (CF) patients has risen.
99 e been implemented for health care visits by cystic fibrosis (CF) patients in an attempt to prevent t
100  with pulmonary exacerbations, especially in cystic fibrosis (CF) patients, and the importance of thi
101                                           In cystic fibrosis (CF) patients, chronic airway infection
102  the effects of NBD2 mutations identified in cystic fibrosis (CF) patients, demonstrating that mutant
103        CFTR, the chloride channel mutated in cystic fibrosis (CF) patients, is opened by ATP binding
104 pidly growing mycobacteria from the sputa of cystic fibrosis (CF) patients.
105 aeruginosa are a major cause of mortality in cystic fibrosis (CF) patients.
106 rged as a clinically significant pathogen in cystic fibrosis (CF) patients.
107 f the role of respiratory viral pathogens on cystic fibrosis (CF) pulmonary disease is needed.
108 n strategies to prevent lung damage in early cystic fibrosis (CF) requires objective outcome measures
109                   Clinical manifestations of cystic fibrosis (CF) result from an increase in the visc
110                        Notably, females with cystic fibrosis (CF) suffer worse outcomes, particularly
111                            In the liver, the cystic fibrosis (CF) transmembrane conductance regulator
112 . aeruginosa lung infections associated with cystic fibrosis (CF) will be advanced by an improved und
113 ma membrane of secretory epithelia and cause cystic fibrosis (CF) with variable disease severity.
114 Akt signaling is suppressed in patients with cystic fibrosis (CF), a disease characterized by hyper-i
115 flammatory responses in mice and humans with cystic fibrosis (CF), a life-threatening disorder of the
116 covery of the genetic defect responsible for cystic fibrosis (CF), a monogenic disorder.
117 ole in chronic inflammatory diseases such as cystic fibrosis (CF), and targeting ER stress may be use
118 rane conductance regulator (CFTR) gene cause cystic fibrosis (CF), but are not good predictors of lun
119  sweat is an important diagnostic marker for cystic fibrosis (CF), but the implementation of point-of
120 tly in the sputum of pediatric patients with cystic fibrosis (CF), by combining the high sensitivity
121 tracellular pathogen killing is defective in cystic fibrosis (CF), despite abundant production of rea
122 ), which is defective in the genetic disease cystic fibrosis (CF), forms a gated pathway for chloride
123  important global threat to individuals with cystic fibrosis (CF), in whom M. abscessus accelerates i
124 rin in inflammatory lung diseases, including cystic fibrosis (CF), perhaps by regulation of airway su
125 ion of universal newborn screening (NBS) for cystic fibrosis (CF), the timing and magnitude of growth
126  in sepsis, pneumonia, wound infections, and cystic fibrosis (CF), which is caused by mutations of th
127 e, but their potential role in patients with cystic fibrosis (CF)-associated lung disease remains unc
128                                              Cystic fibrosis (CF)-related diabetes (CFRD) is thought
129  of morbidity and mortality in patients with cystic fibrosis (CF).
130 tantially increased survival of persons with cystic fibrosis (CF).
131 a (NTM) of special, international concern in Cystic Fibrosis (CF).
132 by protein kinase A, but fails to operate in cystic fibrosis (CF).
133 d gene whose loss-of-function variants cause cystic fibrosis (CF).
134 mation characterize the chronic lung disease cystic fibrosis (CF).
135  (ASL) pH has been proposed as a therapy for cystic fibrosis (CF).
136 P. aeruginosa isolates from individuals with cystic fibrosis (CF).
137 cerbations of chronic lung diseases, such as cystic fibrosis (CF).
138  cause of pulmonary disease in patients with cystic fibrosis (CF).
139 gic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis (CF).
140 nosa causes lung infections in patients with cystic fibrosis (CF).
141 ve ventilation (QV) imaging in patients with cystic fibrosis (CF).
142 hogenesis and progression of lung disease in cystic fibrosis (CF).
143 fibrin gels and in sputum from patients with cystic fibrosis (CF).
144 rt in the lung, pancreas and other organs in cystic fibrosis (CF).
145 (-) channel defective in the genetic disease cystic fibrosis (CF).
146 tural lung abnormalities in individuals with cystic fibrosis (CF); however, the associations between
147  lung disease are characteristic features of cystic fibrosis (CF, OMIM #219700).
148                               In addition to cystic fibrosis, CFTR dysregulation has been implicated
149 ormation of the temperature-sensitive mutant cystic fibrosis channel (F508-CFTR) at the plasma membra
150                                Patients with cystic fibrosis, chronic obstructive pulmonary disease,
151                                  42 Canadian cystic fibrosis clinics and 110 U.S. cystic fibrosis car
152 o reducing the detrimental health effects of cystic fibrosis could be the identification of proteins
153                                           In cystic fibrosis, deletion of phenylalanine 508 (F508del)
154 138 mimic or siRNA against SIN3A to cultured cystic fibrosis (DeltaF508/DeltaF508) airway epithelia p
155 studies were performed in the context of the cystic fibrosis diagnosis and preliminary investigation
156 vels in artificial human sweat for potential cystic fibrosis diagnostic use.
157 t chloride is of interest as a biomarker for cystic fibrosis, electrolyte metabolism disorders, elect
158         An estimated 8%-10% of patients with cystic fibrosis experience this condition.
159 n model, we found screening of patients with cystic fibrosis for CRC to be cost effective.
160 n model, we found screening of patients with cystic fibrosis for CRC to be cost-effective.
161  a diagnosis of ABPA was the criteria of the Cystic Fibrosis Foundation Consensus Conference.
162 ian Cystic Fibrosis Registry (CCFR) and U.S. Cystic Fibrosis Foundation Patient Registry (CFFPR) betw
163 osis aged 6-21 years was conducted using the Cystic Fibrosis Foundation Patient Registry.
164 ood Institute/National Institutes of Health, Cystic Fibrosis Foundation, the University of Alabama at
165 sits in the first 12 months of life at 28 US Cystic Fibrosis Foundation-accredited Care Centers from
166 r mutant cells were grown as biofilms on the Cystic Fibrosis genotype bronchial epithelial cells.
167 muscular dystrophy, spinal muscular atrophy, cystic fibrosis, haemophilia and sickle cell disease.
168 SL secretion and whether this is abnormal in cystic fibrosis has never been tested.
169                                Patients with cystic fibrosis have an increased incidence of hyperoxal
170 al therapies that target the basic defect in cystic fibrosis have recently been developed and are eff
171 ed studies and patients aged 6-11 years with cystic fibrosis homozygous for F508del-CFTR in an open-l
172 sus placebo in patients aged 6-11 years with cystic fibrosis homozygous for F508del-CFTR.
173 cacy in patients aged 12 years or older with cystic fibrosis homozygous for F508del-cystic fibrosis t
174 recting CFTR-dependent chloride transport in cystic fibrosis human airway epithelium.
175 de clinical use for the chronic treatment of cystic fibrosis in patients.
176      Median age of survival in patients with cystic fibrosis increased in both countries between 1990
177                                              Cystic fibrosis is a common life-limiting autosomal rece
178                                              Cystic fibrosis is a fatal genetic disease, most frequen
179                                              Cystic fibrosis is an autosomal recessive disease caused
180 to tissue remodeling and respiratory disease.Cystic fibrosis is caused by mutations in the CFTR chlor
181                                              Cystic fibrosis is caused by mutations in the gene encod
182                                              Cystic fibrosis liver disease (CFLD) in children causes
183 nstrate the in vivo contribution of IL-17 in cystic fibrosis lung disease and the therapeutic validit
184 progress independently of CFTR activity once cystic fibrosis lung disease is established.
185 ocepacia is an opportunistic pathogen of the cystic fibrosis lung that elicits a strong inflammatory
186 ile lifestyle to resilient biofilm as in the cystic fibrosis lung.
187 nome analyses of B. cenocepacia infection in cystic fibrosis lungs and serves as a valuable resource
188 s for 24 weeks in addition to their existing cystic fibrosis medications.
189                                              Cystic fibrosis NBS has now moved on from the developmen
190 s cathepsin C inhibitor for the treatment of cystic fibrosis, noncystic fibrosis bronchiectasis, ANCA
191 y aspergillosis occurs almost exclusively in cystic fibrosis or asthmatic patients.
192 ofilm formation, potentially contributing to cystic fibrosis pathogenesis.
193  gladioli BCC0238, a clinical isolate from a cystic fibrosis patient, led to the discovery of gladiol
194  directed approach, we were able to generate cystic fibrosis patient-specific iPSC-derived airway org
195     The bronchial cells were obtained from a cystic fibrosis patient.
196 l and chemical makeup of a human lung from a cystic fibrosis patient.
197 ed the elevated sweat electrolyte content of cystic fibrosis patients compared with that of healthy c
198 coccus aureus-specific serum IgG compared to cystic fibrosis patients despite recurrent S. aureus inf
199 idly growing mycobacteria from the sputum of cystic fibrosis patients has recently been reported.
200 ed autophagy has previously been reported in cystic fibrosis patients with the common F508del-CFTR mu
201 tant strains of P. aeruginosa (isolated from cystic fibrosis patients) indicating a potential therape
202 ed Burkholderia cenocepacia isolates from 16 cystic fibrosis patients, spanning a period of 2-20 yr a
203  leading cause of morbidity and mortality in cystic fibrosis patients.
204 ssociated with more severe meconium ileus in cystic fibrosis patients.
205  pathogen that infects immunocompromised and cystic fibrosis patients.
206 t least 15 kg, with a confirmed diagnosis of cystic fibrosis, percent predicted forced expiratory vol
207 bably the most relevant structural change in cystic fibrosis) peribronchial thickening, mucous pluggi
208        Patients with pancreatic-insufficient cystic fibrosis (PI-CF) are at increased risk for develo
209 TTs), respectively, in pancreatic-sufficient cystic fibrosis (PS-CF), PI-CF, and normal control subje
210 dam Annotated Grid Morphometric Analysis for Cystic Fibrosis quantitative outcome measure.
211 e (+0.15; 95% CI, 0.08 to 0.22; P < 0.0001), Cystic Fibrosis Questionnaire-Revised respiratory domain
212      Scores on the respiratory domain of the Cystic Fibrosis Questionnaire-Revised, a quality-of-life
213 a well-established in vivo clinical test for cystic fibrosis, reflects transepithelial cation and ani
214            Patients followed in the Canadian Cystic Fibrosis Registry (CCFR) and U.S. Cystic Fibrosis
215               Of those, two met criteria for cystic fibrosis-related diabetes, two indeterminate glyc
216  ASL secretory response to the inhalation of cystic fibrosis relevant bacteria.
217 ric muco-obstructive airway diseases such as cystic fibrosis remains unclear.
218  the median age of survival of patients with cystic fibrosis reported in the United States was 36.8 y
219                                              Cystic fibrosis results from mutations in the cystic fib
220 morphological abnormalities in patients with cystic fibrosis, such as bronchiectasis (which is progre
221 g-resistant pulmonary pathogen especially in cystic fibrosis sufferers.
222 retion in wild-type but not in pig models of cystic fibrosis, suggesting an impaired response to path
223                               Differences in cystic fibrosis survival between Canada and the United S
224  To use a standardized approach to calculate cystic fibrosis survival estimates and to explore differ
225 3-CFTR interface might offer an approach for cystic fibrosis therapeutics.
226 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
227 n autosomal recessive disorder affecting the cystic fibrosis transmembrane conductance regulator (CFT
228  modifies the local translation speed of the cystic fibrosis transmembrane conductance regulator (CFT
229 d selectivity against other proteins such as cystic fibrosis transmembrane conductance regulator (CFT
230 ase is caused by the loss of function of the cystic fibrosis transmembrane conductance regulator (CFT
231 letion of phenylalanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFT
232                                          The cystic fibrosis transmembrane conductance regulator (CFT
233                             Mutations in the cystic fibrosis transmembrane conductance regulator (CFT
234                                              Cystic Fibrosis Transmembrane Conductance Regulator (CFT
235  antivirals and as correctors of the F508del-cystic fibrosis transmembrane conductance regulator (CFT
236 kA), the alginate transporter (AlgE) and the cystic fibrosis transmembrane conductance regulator (CFT
237               Combination treatment with the cystic fibrosis transmembrane conductance regulator (CFT
238        Macrophages (MPhis) with mutations in cystic fibrosis transmembrane conductance regulator (CFT
239 cond nucleotide-binding domain (NBD2) of the cystic fibrosis transmembrane conductance regulator (CFT
240 ed phenylquinoxalinone CFTRact-J027 (4) as a cystic fibrosis transmembrane conductance regulator (CFT
241 ch are homologous to the gating mutations of cystic fibrosis transmembrane conductance regulator (CFT
242                                              Cystic fibrosis transmembrane conductance regulator (CFT
243 t is in part regulated by apically expressed cystic fibrosis transmembrane conductance regulator (CFT
244 (IL-8) secretion and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFT
245 not dependent upon special properties of the cystic fibrosis transmembrane conductance regulator (CFT
246 e determined the amino acids inserted at the cystic fibrosis transmembrane conductance regulator (CFT
247                              KEY POINTS: The cystic fibrosis transmembrane conductance regulator (CFT
248 is (CF), which is caused by mutations of the cystic fibrosis transmembrane conductance regulator (Cft
249  diseases.The F508 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFT
250  and specific domain interaction between the cystic fibrosis transmembrane conductance regulator (CFT
251 reased intestinal permeability and decreased cystic fibrosis transmembrane conductance regulator (Cft
252              More than 2000 mutations in the cystic fibrosis transmembrane conductance regulator (CFT
253 tive degradation of the common mutant of the cystic fibrosis transmembrane conductance regulator (CFT
254              Two functional abnormalities of cystic fibrosis transmembrane conductance regulator (CFT
255 ector, rAAV2/HBoV1, expressing a full-length cystic fibrosis transmembrane conductance regulator (CFT
256 ent protein kinase (PKG), and opening of the cystic fibrosis transmembrane conductance regulator (CFT
257 cessfully to identify the interactome of the cystic fibrosis transmembrane conductance regulator (CFT
258              Inappropriate activation of the cystic fibrosis transmembrane conductance regulator (CFT
259 n genetic disease caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFT
260 irway epithelia partially restored DeltaF508-cystic fibrosis transmembrane conductance regulator (CFT
261 ng (PDE1), control of cell proliferation and cystic fibrosis transmembrane conductance regulator (CFT
262  caused by loss-of-function mutations of the cystic fibrosis transmembrane conductance regulator (CFT
263  (MRPs), and an ATP-gated anion channel, the cystic fibrosis transmembrane conductance regulator (CFT
264 ism of action of modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFT
265  with cystic fibrosis homozygous for F508del-cystic fibrosis transmembrane conductance regulator (CFT
266                                          The cystic fibrosis transmembrane conductance regulator (CFT
267 ystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFT
268 nstrate that mice carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFT
269                             Mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFT
270            Ivacaftor is a potentiator of the cystic fibrosis transmembrane conductance regulator (CFT
271 vious work indicates that ivacaftor improves cystic fibrosis transmembrane conductance regulator (CFT
272 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
273                                    ABSTRACT: Cystic fibrosis transmembrane conductance regulator (CFT
274 e expression, stability, and function of the cystic fibrosis transmembrane conductance regulator (CFT
275                                          The cystic fibrosis transmembrane conductance regulator (CFT
276  as I507-ATC-->ATT, in deletion of Phe508 in cystic fibrosis transmembrane conductance regulator (Del
277 d hydrostatic pressure resulted in decreased cystic fibrosis transmembrane conductance regulator acti
278 uodenal HCO3(-) secretion appears to require cystic fibrosis transmembrane conductance regulator and
279                We used mice deficient in the cystic fibrosis transmembrane conductance regulator gene
280  a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhi
281 n, an effect which was partially reversed by cystic fibrosis transmembrane conductance regulator pote
282                                              Cystic fibrosis transmembrane conductance regulator pote
283      To determine the feasibility of using a cystic fibrosis transmembrane conductance regulator pote
284 quently caused by the retention of the CFTR (cystic fibrosis transmembrane conductance regulator) mut
285 escue the cystic-fibrosis-associated protein cystic fibrosis transmembrane conductance regulator, whi
286 e within the airway as a result of defective cystic fibrosis transmembrane receptor (CFTR) expression
287              W1282X is the fifth most common cystic fibrosis transmembrane regulator (CFTR) mutation
288 d lower expression of chloride channel 2 and cystic fibrosis transmembrane regulator in diabetic corn
289                             Gene therapy for cystic fibrosis using non-viral, plasmid-based formulati
290 say for early identification of infants with cystic fibrosis was first recognised, the performance of
291 lidation cohort included adult patients with cystic fibrosis who had CT imaging performed between Jan
292                          Among patients with cystic fibrosis who had received an organ transplant, op
293 timal colonoscopy strategy for patients with cystic fibrosis who never received an organ transplant;
294 timal colonoscopy strategy for patients with cystic fibrosis who never received an organ transplant;
295 RCTs)-TRAFFIC and TRANSPORT-in patients with cystic fibrosis who were aged 12 years or older and homo
296 aftor alone was efficacious in patients with cystic fibrosis who were heterozygous for the Phe508del
297 ion therapy in patients aged 6-11 years with cystic fibrosis who were homozygous for F508del-CFTR.
298 s to be safe in children aged 2-5 years with cystic fibrosis with a gating mutation followed up for 2
299 rve for glucose and insulin in children with cystic fibrosis with control subjects.
300 t was seen predominantly in patients without cystic fibrosis with MAC and was sustained 1 year after

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