ライフサイエンスコーパス: cystic

1 once development is completed is retained in cystic adult kidneys.

2 , proximal tubules are predisposed to become cystic after cAMP stimulation.

3 as malignant cystic, malignant solid, benign cystic and benign solid.

4 s derived faithfully retained their parental cystic and spiky morphologies and were termed CC (cystic

5 c and spiky morphologies and were termed CC (cystic) and SC (spiky), respectively.

6 tic kidney rats by 35%; in contrast, hepatic cystic areas were decreased by 45% in TGR5-deficient TGR

7 of corpus luteum, and an increased number of cystic/atretic follicles.

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

10 Adenoid cystic carcinomas (ACC) are rare salivary gland cancers

11 Purpose Adenoid cystic carcinomas (ACCs) represent a heterogeneous group

12 d frequency of NOTCH1 alterations in adenoid cystic carcinomas compared with previous studies.

13 Cystic cavities are bridged by fibronectin-rich extracel

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

18 The cystic cavity that develops following injuries to brain

19 For women who have cystic changes on high-resolution computed tomography of

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

22 ) proteins was increased 2-fold to 3-fold in cystic cholangiocytes in vitro and in vivo.

23 The cystic-common bile duct junction was visualized before C

24 ic knockdown of ILK strikingly reduced renal cystic disease and fibrosis and extended the life of pcy

25 1beta regulates the transcription of several cystic disease genes.

26 xic bile acids into the duodenum through the cystic duct and common bile duct system.

27 yos, together with the appearance of ectopic cystic duct-like epithelia in their gallbladders.

28 In cystic fibrosis (CF) altered mucus properties impair muc

29 Chronic inflammation is a hallmark of cystic fibrosis (CF) and associated with increased produ

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.

33 leading to hyperinflammation, a hallmark of cystic fibrosis (CF) disease.

34 RATIONALE: Individuals with cystic fibrosis (CF) experience frequent acute pulmonary

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

37 Cystic fibrosis (CF) is an autosomal recessive disorder

38 Cystic fibrosis (CF) is caused by mutations in the gene

39 Cystic fibrosis (CF) is caused by mutations that disrupt

40 B-OprM efflux system, naturally occurring in cystic fibrosis (CF) isolates, have been previously show

41 Cystic fibrosis (CF) liver disease (CFLD), a leading cau

42 RATIONALE: Cystic fibrosis (CF) lung disease is caused by the loss

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

47 Growth failure in cystic fibrosis (CF) patients has been well-documented a

48 alence of fungi in the respiratory tracts of cystic fibrosis (CF) patients has risen.

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

51 In cystic fibrosis (CF) patients, chronic airway infection

52 the effects of NBD2 mutations identified in cystic fibrosis (CF) patients, demonstrating that mutant

53 CFTR, the chloride channel mutated in cystic fibrosis (CF) patients, is opened by ATP binding

54 pidly growing mycobacteria from the sputa of cystic fibrosis (CF) patients.

55 aeruginosa are a major cause of mortality in cystic fibrosis (CF) patients.

56 rged as a clinically significant pathogen in cystic fibrosis (CF) patients.

57 f the role of respiratory viral pathogens on cystic fibrosis (CF) pulmonary disease is needed.

58 n strategies to prevent lung damage in early cystic fibrosis (CF) requires objective outcome measures

59 Notably, females with cystic fibrosis (CF) suffer worse outcomes, particularly

60 In the liver, the cystic fibrosis (CF) transmembrane conductance regulator

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

71 Cystic fibrosis (CF)-related diabetes (CFRD) is thought

72 rt in the lung, pancreas and other organs in cystic fibrosis (CF).

73 (-) channel defective in the genetic disease cystic fibrosis (CF).

74 of morbidity and mortality in patients with cystic fibrosis (CF).

75 tantially increased survival of persons with cystic fibrosis (CF).

76 a (NTM) of special, international concern in Cystic Fibrosis (CF).

77 by protein kinase A, but fails to operate in cystic fibrosis (CF).

78 d gene whose loss-of-function variants cause cystic fibrosis (CF).

79 mation characterize the chronic lung disease cystic fibrosis (CF).

80 (ASL) pH has been proposed as a therapy for cystic fibrosis (CF).

81 P. aeruginosa isolates from individuals with cystic fibrosis (CF).

82 gic bronchopulmonary aspergillosis (ABPA) in cystic fibrosis (CF).

83 nosa causes lung infections in patients with cystic fibrosis (CF).

84 ve ventilation (QV) imaging in patients with cystic fibrosis (CF).

85 hogenesis and progression of lung disease in cystic fibrosis (CF).

86 fibrin gels and in sputum from patients with cystic fibrosis (CF).

87 Patients with pancreatic-insufficient cystic fibrosis (PI-CF) are at increased risk for develo

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

91 Chr11p13 that is implicated as a modifier of cystic fibrosis airway disease.

92 sms fail in CFTR(-/-) swine, suggesting that cystic fibrosis airways do not respond to inhaled pathog

93 r developing new drugs for disorders such as cystic fibrosis and asthma.

94 ammation, and lung function in subjects with cystic fibrosis and chronic airway infections.

95 ic rhinosinusitis, and exacerbations of both cystic fibrosis and chronic obstructive pulmonary diseas

96 proved clearance in airway diseases, such as cystic fibrosis and chronic rhinosinusitis.

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

100 ose that occur in the lungs of patients with cystic fibrosis and nonhealing ulcers.

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

105 BACKGROUND & AIMS: Individuals with cystic fibrosis are at increased risk of colorectal canc

106 BACKGROUND & AIMS: Individuals with cystic fibrosis are at increased risk of colorectal canc

107 RATIONALE: Individuals with cystic fibrosis are at risk for prolonged drops in lung

108 anadian cystic fibrosis clinics and 110 U.S. cystic fibrosis care centers.

109 ombinations may have therapeutic efficacy in cystic fibrosis caused by the W1282X mutation, although

110 f its functional mechanism and correction of cystic fibrosis causing mutants.

111 ormation of the temperature-sensitive mutant cystic fibrosis channel (F508-CFTR) at the plasma membra

112 42 Canadian cystic fibrosis clinics and 110 U.S. cystic fibrosis car

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

115 vels in artificial human sweat for potential cystic fibrosis diagnostic use.

116 An estimated 8%-10% of patients with cystic fibrosis experience this condition.

117 n model, we found screening of patients with cystic fibrosis for CRC to be cost effective.

118 n model, we found screening of patients with cystic fibrosis for CRC to be cost-effective.

119 a diagnosis of ABPA was the criteria of the Cystic Fibrosis Foundation Consensus Conference.

120 ian Cystic Fibrosis Registry (CCFR) and U.S. Cystic Fibrosis Foundation Patient Registry (CFFPR) betw

121 osis aged 6-21 years was conducted using the Cystic Fibrosis Foundation Patient Registry.

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.

124 SL secretion and whether this is abnormal in cystic fibrosis has never been tested.

125 Patients with cystic fibrosis have an increased incidence of hyperoxal

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

128 sus placebo in patients aged 6-11 years with cystic fibrosis homozygous for F508del-CFTR.

129 cacy in patients aged 12 years or older with cystic fibrosis homozygous for F508del-cystic fibrosis t

130 de clinical use for the chronic treatment of cystic fibrosis in patients.

131 Median age of survival in patients with cystic fibrosis increased in both countries between 1990

132 Cystic fibrosis is a common life-limiting autosomal rece

133 Cystic fibrosis is an autosomal recessive disease caused

134 to tissue remodeling and respiratory disease.Cystic fibrosis is caused by mutations in the CFTR chlor

135 Cystic fibrosis is caused by mutations in the gene encod

136 Cystic fibrosis liver disease (CFLD) in children causes

137 progress independently of CFTR activity once cystic fibrosis lung disease is established.

138 ile lifestyle to resilient biofilm as in the cystic fibrosis lung.

139 nome analyses of B. cenocepacia infection in cystic fibrosis lungs and serves as a valuable resource

140 s for 24 weeks in addition to their existing cystic fibrosis medications.

141 y aspergillosis occurs almost exclusively in cystic fibrosis or asthmatic patients.

142 ofilm formation, potentially contributing to cystic fibrosis pathogenesis.

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

145 l and chemical makeup of a human lung from a cystic fibrosis patient.

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

151 pathogen that infects immunocompromised and cystic fibrosis patients.

152 leading cause of morbidity and mortality in cystic fibrosis patients.

153 ssociated with more severe meconium ileus in cystic fibrosis patients.

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

156 Patients followed in the Canadian Cystic Fibrosis Registry (CCFR) and U.S. Cystic Fibrosis

157 ASL secretory response to the inhalation of cystic fibrosis relevant bacteria.

158 ric muco-obstructive airway diseases such as cystic fibrosis remains unclear.

159 the median age of survival of patients with cystic fibrosis reported in the United States was 36.8 y

160 Cystic fibrosis results from mutations in the cystic fib

161 g-resistant pulmonary pathogen especially in cystic fibrosis sufferers.

162 Differences in cystic fibrosis survival between Canada and the United S

163 To use a standardized approach to calculate cystic fibrosis survival estimates and to explore differ

164 Mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFT

165 Ivacaftor is a potentiator of the cystic fibrosis transmembrane conductance regulator (CFT

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

168 ABSTRACT: Cystic fibrosis transmembrane conductance regulator (CFT

169 e expression, stability, and function of the cystic fibrosis transmembrane conductance regulator (CFT

170 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

177 The cystic fibrosis transmembrane conductance regulator (CFT

178 Mutations in the cystic fibrosis transmembrane conductance regulator (CFT

179 is (CF), which is caused by mutations of the cystic fibrosis transmembrane conductance regulator (Cft

180 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

183 Combination treatment with the cystic fibrosis transmembrane conductance regulator (CFT

184 Macrophages (MPhis) with mutations in 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

188 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

193 KEY POINTS: 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

196 Inappropriate activation of 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

199 The 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

204 We used mice deficient in the cystic fibrosis transmembrane conductance regulator gene

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

207 Cystic fibrosis transmembrane conductance regulator pote

208 To determine the feasibility of using a cystic fibrosis transmembrane conductance regulator pote

209 W1282X is the fifth most common cystic fibrosis transmembrane regulator (CFTR) mutation

210 d lower expression of chloride channel 2 and cystic fibrosis transmembrane regulator in diabetic corn

211 Among patients with cystic fibrosis who had received an organ transplant, op

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.

220 te respiratory distress syndrome, pneumonia, cystic fibrosis, and bronchiectasis.

221 Neutrophilic airway diseases, including cystic fibrosis, are characterized by excessive neutroph

222 ulation leads to a range of diseases such as cystic fibrosis, Bartter's syndrome and epilepsy.

223 Patients with cystic fibrosis, chronic obstructive pulmonary disease,

224 In cystic fibrosis, deletion of phenylalanine 508 (F508del)

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

227 eral nutrition-associated liver disease, and cystic fibrosis-associated liver disease.

228 logy of many respiratory diseases, including cystic fibrosis.

229 l CRC screening strategies for patients with cystic fibrosis.

230 mbrane regulator (CFTR) mutation that causes cystic fibrosis.

231 sweat diagnostics with reliable detection of cystic fibrosis.

232 k and lower life expectancy in patients with cystic fibrosis.

233 yperoxaluria observed in this mouse model of cystic fibrosis.

234 Cystic fibrosis.

235 ss 23 sites of the lungs from a patient with cystic fibrosis.

236 6-mediated oxalate secretion is defective in cystic fibrosis.

237 underlying cause of disease in patients with cystic fibrosis.

238 del mutation, which is the dominant cause of cystic fibrosis.

239 ted with an aggressive clinical phenotype in cystic fibrosis.

240 k and lower life expectancy in patients with cystic fibrosis.

241 ts with hospital-acquired infections or with cystic fibrosis.

242 s of several respiratory diseases, including cystic fibrosis.

243 te stone formation observed in patients with cystic fibrosis.

244 of-function chloride channelopathies such as cystic fibrosis.

245 ision therapies for airway disorders such as cystic fibrosis.

246 ight be promising as co-adjuvant therapy for cystic fibrosis.

247 icted to be cost-effective for patients with cystic fibrosis.

248 tricted evidence available for patients with cystic fibrosis.

249 elopathies including cardiac arrhythmias and cystic fibrosis.

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

254 mplications toward mitochondrial fitness and cystic kidney disease.

255 ediator of cAMP signaling, in developing and cystic kidney models.

256 Flcn knockout mice did not rescue the multi-cystic kidney phenotype.

257 bit typical ciliopathy phenotypes, including cystic kidney, cleft palate and polydactyly.

258 e a promising treatment for SCLT1-associated cystic kidney.

259 ockout mice resulted in development of multi-cystic kidneys and cardiac hypertrophy in some mice.

260 ed misregulation of multiple pathways in the cystic kidneys of this model.

261 c-Myc upregulates miR-17 approximately 92 in cystic kidneys, which in turn aggravates cyst growth by

262 Purpose Pancreatic cystic lesions are common incidental findings on imaging

263 atic intraepithelial neoplasias (PanINs) and cystic lesions in Kras(G12D)-expressing mice.

264 Literature on the behavior of cystic lesions in pancreas transplants is scarce, and he

265 In this Review, we discuss the major cystic lesions of the pancreas and their underlying mole

266 Cystic lesions of the transplant pancreas developed in 2

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

269 entify premalignant and malignant pancreatic cystic lesions.

270 Lymphangioleiomyomatosis (LAM) is a rare cystic lung disease that primarily affects women.

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.

274 MRI revealed a solid-cystic mass involving the anterior lobe of the pituitary

275 MRI appearance of AH, presenting as a solid-cystic mass.

276 In Six2cre;Frs2alpha(Fl/Fl) mice, a renal cystic model, ectopic p-Creb stained proximal tubule-der

277 Mucinous cystic neoplasm-associated adenocarcinoma appears to hav

278 Pancreatic mucinous cystic neoplasms (MCNs) harbor malignant potential, and

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

281 There was conspicuous absence of cystic or adipose contents and of sacral erosion/destruc

282 Rat liver stem cells, which grow as cystic organoids, were characterized by high expression

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

285 tricular hemorrhage grade of 3 or greater or cystic periventricular leukomalacia.

286 vestigated their ability to rescue the multi-cystic phenotype of Flcn-deficient mouse kidneys.

287 luded in the differential diagnosis of solid-cystic pituitary masses along with clinical correlation,

288 ly accurate identification and assessment of cystic precursors to pancreatic adenocarcinoma.

289 5 subunit of NF-kappaB, leading to increased cystic renal epithelial cell proliferation and survival.

290 differentiation between benign and malignant cystic renal lesions.

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

293 ling marks dedifferentiated proximal tubular cystic segments.

294 showed a heterogeneous lesion that contained cystic-solid components and millimetric calcifications i

295 lumen, typically surrounded by intraretinal cystic spaces.

296 onsists of a trophic stage and an ascus-like cystic stage.

297 ive increase in the number and size of these cystic structures and tissue opacities that gradually ex

298 Cystic structures, but no teratomas, were observed in NT

299 Lowering cAMP in cystic tissues through the inhibition of the type-2 vaso

300 onal CT images following treatment, such as: cystic transformation of lesions, enlargement of lesions