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4 s derived faithfully retained their parental cystic and spiky morphologies and were termed CC (cystic
6 tic kidney rats by 35%; in contrast, hepatic cystic areas were decreased by 45% in TGR5-deficient TGR
8 ing squamous cell carcinoma (HNSCC), adenoid cystic carcinoma (ACC), and other salivary and cutaneous
9 cteristics included: adenocarcinoma, adenoid cystic carcinoma, meningioma, chondrosarcoma and fibromy
14 ition behavior, almost completely eliminates cystic cavities in a clinically relevant rat spinal cord
15 ition behavior, almost completely eliminates cystic cavities in a clinically relevant rat spinal cord
16 ipheral nerve graft bridge (PNG) through the cystic cavity and treated the graft/host interface with
17 ate tissue repair following CNS injuries.The cystic cavity that develops following injuries to brain
20 es such as fluorescein-negative intraretinal cystic changes, choroidal neovascularization, serous ret
21 vitro were decreased by approximately 30% in cystic cholangiocytes after treatment with SBI-115 alone
24 ic knockdown of ILK strikingly reduced renal cystic disease and fibrosis and extended the life of pcy
30 They are major pathogens in patients with cystic fibrosis (CF) and can cause severe necrotizing pn
31 urkholderia dolosa caused an outbreak in the cystic fibrosis (CF) clinic at Boston Children's Hospita
32 erimental measurements made using normal and cystic fibrosis (CF) cultured human airway epithelium.
35 es are reminiscent of the pathophysiology of cystic fibrosis (CF) in which loss-of-function mutations
36 progression of lung disease in children with cystic fibrosis (CF) indicates that sensitive noninvasiv
40 B-OprM efflux system, naturally occurring in cystic fibrosis (CF) isolates, have been previously show
43 lize a panel of P. aeruginosa burn wound and cystic fibrosis (CF) lung isolates to demonstrate that P
44 respiratory virus infections predispose the cystic fibrosis (CF) lung to chronic bacterial colonizat
45 bacteria rarely reported in patients without cystic fibrosis (CF) or immunocompromising conditions.
46 es chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-co
49 e been implemented for health care visits by cystic fibrosis (CF) patients in an attempt to prevent t
50 with pulmonary exacerbations, especially in cystic fibrosis (CF) patients, and the importance of thi
52 the effects of NBD2 mutations identified in cystic fibrosis (CF) patients, demonstrating that mutant
58 n strategies to prevent lung damage in early cystic fibrosis (CF) requires objective outcome measures
61 . aeruginosa lung infections associated with cystic fibrosis (CF) will be advanced by an improved und
62 Akt signaling is suppressed in patients with cystic fibrosis (CF), a disease characterized by hyper-i
63 ole in chronic inflammatory diseases such as cystic fibrosis (CF), and targeting ER stress may be use
64 rane conductance regulator (CFTR) gene cause cystic fibrosis (CF), but are not good predictors of lun
65 sweat is an important diagnostic marker for cystic fibrosis (CF), but the implementation of point-of
66 tracellular pathogen killing is defective in cystic fibrosis (CF), despite abundant production of rea
67 ), which is defective in the genetic disease cystic fibrosis (CF), forms a gated pathway for chloride
68 rin in inflammatory lung diseases, including cystic fibrosis (CF), perhaps by regulation of airway su
69 ion of universal newborn screening (NBS) for cystic fibrosis (CF), the timing and magnitude of growth
70 in sepsis, pneumonia, wound infections, and cystic fibrosis (CF), which is caused by mutations of th
88 TTs), respectively, in pancreatic-sufficient cystic fibrosis (PS-CF), PI-CF, and normal control subje
89 of lumacaftor and ivacaftor in patients with cystic fibrosis aged 6-11 years homozygous for F508del-C
90 A longitudinal cohort study of patients with cystic fibrosis aged 6-21 years was conducted using the
92 sms fail in CFTR(-/-) swine, suggesting that cystic fibrosis airways do not respond to inhaled pathog
95 ic rhinosinusitis, and exacerbations of both cystic fibrosis and chronic obstructive pulmonary diseas
97 R) activity and lung function in people with cystic fibrosis and G551D-CFTR mutations but does not re
98 nts in patients aged 12 years and older with cystic fibrosis and homozygous for F508del-CFTR, but it
99 ible if they were at least 12 years old with cystic fibrosis and homozygous for the F508del-CFTR muta
101 teractions in A. fumigatus and patients with cystic fibrosis and the ongoing validation of novel labo
102 48 patients 12 years of age or older who had cystic fibrosis and were heterozygous for the Phe508del
103 in patients 12 years of age or older who had cystic fibrosis and were homozygous for the CFTR Phe508d
104 in patients 12 years of age or older who had cystic fibrosis and were homozygous for the CFTR Phe508d
109 ombinations may have therapeutic efficacy in cystic fibrosis caused by the W1282X mutation, although
111 ormation of the temperature-sensitive mutant cystic fibrosis channel (F508-CFTR) at the plasma membra
113 o reducing the detrimental health effects of cystic fibrosis could be the identification of proteins
114 studies were performed in the context of the cystic fibrosis diagnosis and preliminary investigation
120 ian Cystic Fibrosis Registry (CCFR) and U.S. Cystic Fibrosis Foundation Patient Registry (CFFPR) betw
122 sits in the first 12 months of life at 28 US Cystic Fibrosis Foundation-accredited Care Centers from
123 r mutant cells were grown as biofilms on the Cystic Fibrosis genotype bronchial epithelial cells.
126 al therapies that target the basic defect in cystic fibrosis have recently been developed and are eff
127 ed studies and patients aged 6-11 years with cystic fibrosis homozygous for F508del-CFTR in an open-l
129 cacy in patients aged 12 years or older with cystic fibrosis homozygous for F508del-cystic fibrosis t
131 Median age of survival in patients with cystic fibrosis increased in both countries between 1990
134 to tissue remodeling and respiratory disease.Cystic fibrosis is caused by mutations in the CFTR chlor
139 nome analyses of B. cenocepacia infection in cystic fibrosis lungs and serves as a valuable resource
143 gladioli BCC0238, a clinical isolate from a cystic fibrosis patient, led to the discovery of gladiol
144 directed approach, we were able to generate cystic fibrosis patient-specific iPSC-derived airway org
146 ed the elevated sweat electrolyte content of cystic fibrosis patients compared with that of healthy c
147 coccus aureus-specific serum IgG compared to cystic fibrosis patients despite recurrent S. aureus inf
148 ed autophagy has previously been reported in cystic fibrosis patients with the common F508del-CFTR mu
149 tant strains of P. aeruginosa (isolated from cystic fibrosis patients) indicating a potential therape
150 ed Burkholderia cenocepacia isolates from 16 cystic fibrosis patients, spanning a period of 2-20 yr a
154 e (+0.15; 95% CI, 0.08 to 0.22; P < 0.0001), Cystic Fibrosis Questionnaire-Revised respiratory domain
155 Scores on the respiratory domain of the Cystic Fibrosis Questionnaire-Revised, a quality-of-life
159 the median age of survival of patients with cystic fibrosis reported in the United States was 36.8 y
163 To use a standardized approach to calculate cystic fibrosis survival estimates and to explore differ
166 vious work indicates that ivacaftor improves cystic fibrosis transmembrane conductance regulator (CFT
167 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
169 e expression, stability, and function of the cystic fibrosis transmembrane conductance regulator (CFT
171 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
172 n autosomal recessive disorder affecting the cystic fibrosis transmembrane conductance regulator (CFT
173 modifies the local translation speed of the cystic fibrosis transmembrane conductance regulator (CFT
174 d selectivity against other proteins such as cystic fibrosis transmembrane conductance regulator (CFT
175 ase is caused by the loss of function of the cystic fibrosis transmembrane conductance regulator (CFT
176 letion of phenylalanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFT
179 is (CF), which is caused by mutations of the cystic fibrosis transmembrane conductance regulator (Cft
181 antivirals and as correctors of the F508del-cystic fibrosis transmembrane conductance regulator (CFT
182 kA), the alginate transporter (AlgE) and the cystic fibrosis transmembrane conductance regulator (CFT
185 cond nucleotide-binding domain (NBD2) of the cystic fibrosis transmembrane conductance regulator (CFT
186 ch are homologous to the gating mutations of cystic fibrosis transmembrane conductance regulator (CFT
187 ed phenylquinoxalinone CFTRact-J027 (4) as a cystic fibrosis transmembrane conductance regulator (CFT
189 t is in part regulated by apically expressed cystic fibrosis transmembrane conductance regulator (CFT
190 (IL-8) secretion and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFT
191 not dependent upon special properties of the cystic fibrosis transmembrane conductance regulator (CFT
192 e determined the amino acids inserted at the cystic fibrosis transmembrane conductance regulator (CFT
194 diseases.The F508 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFT
195 and specific domain interaction between the cystic fibrosis transmembrane conductance regulator (CFT
197 ism of action of modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFT
198 with cystic fibrosis homozygous for F508del-cystic fibrosis transmembrane conductance regulator (CFT
200 ystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFT
201 nstrate that mice carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFT
202 as I507-ATC-->ATT, in deletion of Phe508 in cystic fibrosis transmembrane conductance regulator (Del
203 d hydrostatic pressure resulted in decreased cystic fibrosis transmembrane conductance regulator acti
205 a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhi
206 n, an effect which was partially reversed by cystic fibrosis transmembrane conductance regulator pote
208 To determine the feasibility of using a cystic fibrosis transmembrane conductance regulator pote
210 d lower expression of chloride channel 2 and cystic fibrosis transmembrane regulator in diabetic corn
212 timal colonoscopy strategy for patients with cystic fibrosis who never received an organ transplant;
213 timal colonoscopy strategy for patients with cystic fibrosis who never received an organ transplant;
214 RCTs)-TRAFFIC and TRANSPORT-in patients with cystic fibrosis who were aged 12 years or older and homo
215 aftor alone was efficacious in patients with cystic fibrosis who were heterozygous for the Phe508del
216 ion therapy in patients aged 6-11 years with cystic fibrosis who were homozygous for F508del-CFTR.
217 s to be safe in children aged 2-5 years with cystic fibrosis with a gating mutation followed up for 2
218 t was seen predominantly in patients without cystic fibrosis with MAC and was sustained 1 year after
219 lso to treat conformational diseases such as cystic fibrosis, and Alpha-1 antitrypsin deficiency.
221 Neutrophilic airway diseases, including cystic fibrosis, are characterized by excessive neutroph
225 t least 15 kg, with a confirmed diagnosis of cystic fibrosis, percent predicted forced expiratory vol
226 retion in wild-type but not in pig models of cystic fibrosis, suggesting an impaired response to path
250 nerated zebrafish mutants for pkd1 and noted cystic kidney and mTOR activation in pkd1a mutants, sugg
251 an aminopeptidase XPNPEP3 is associated with cystic kidney disease and TNF-TNFR2 cellular signaling.
252 al manifestation of JBTS is a juvenile-onset cystic kidney disease, known as nephronophthisis, typica
253 d long term and developed slowly progressive cystic kidney disease, renal fibrosis, and hydronephrosi
259 ockout mice resulted in development of multi-cystic kidneys and cardiac hypertrophy in some mice.
261 c-Myc upregulates miR-17 approximately 92 in cystic kidneys, which in turn aggravates cyst growth by
267 mucinous neoplasias (IPMNs) are precancerous cystic lesions that can develop into pancreatic ductal a
268 7 patients underwent resection of pancreatic cystic lesions, and 349 (20.9%) had an MCN (310 women [8
271 to lymphatic channels and likely drives the cystic lung remodeling that often culminates in respirat
272 morbidities, such as angle closure glaucoma, cystic macular edema, and exudative retinal detachment.
273 re categorized into four groups as malignant cystic, malignant solid, benign cystic and benign solid.
276 In Six2cre;Frs2alpha(Fl/Fl) mice, a renal cystic model, ectopic p-Creb stained proximal tubule-der
279 al papillary mucinous neoplasms and mucinous cystic neoplasms, have the potential to progress to panc
280 er tumors often are associated with mucinous cystic neoplasms, which are hypothesized to share a hist
283 diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mu
284 entricular hemorrhage grade of 3 or greater, cystic periventricular leukomalacia, surgical necrotizin
287 luded in the differential diagnosis of solid-cystic pituitary masses along with clinical correlation,
289 5 subunit of NF-kappaB, leading to increased cystic renal epithelial cell proliferation and survival.
291 tic liver disease (PCLD) is characterized by cystic replacement of the hepatic parenchyma, leading to
292 topic p-Creb stained proximal tubule-derived cystic segments that lost the differentiation marker lot
294 showed a heterogeneous lesion that contained cystic-solid components and millimetric calcifications i
297 ive increase in the number and size of these cystic structures and tissue opacities that gradually ex
300 onal CT images following treatment, such as: cystic transformation of lesions, enlargement of lesions
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