ライフサイエンスコーパス: cystic

1 17.2% of perfluorodecalin eyes; outer retina cystic alterations were found in 39.6% of PFO eyes and 1

2 none of perfluorodecalin eyes; inner retina cystic alterations were found in 58.3% of PFO eyes and 1

3 Human cystic and alveolar echinococcosis are among the priorit

4 cludes three distinct life stages: adherent; cystic; and aggregative [13].

5 n (n = 20), or heterogeneous mass with solid-cystic appearance (n = 2).

6 Recurrent or metastatic adenoid cystic carcinoma (R/M ACC) is a malignant neoplasm of pr

7 rgets for precision therapies.FUNDINGAdenoid Cystic Carcinoma Research Foundation, Pershing Square So

8 mising candidates to be tested on human PKD1 cystic cells.

9 In cystic cholangiocytes UDCA-HDAC6i #1 restored primary ci

10 ed perifoveal outer retinal layers loss with cystic degeneration.

11 pplies only to patients with typical diffuse cystic disease (class 1).

12 lacement or replacement of cytoplasmic gross cystic disease fluid protein-15 and CK 7-positive tonofi

13 rotein-3 (Tulp3) as a key regulator of renal cystic disease from a forward genetic screen in the mous

14 Cystic echinococcosis (CE) is an important public health

15 ation in Sary-Kamysh (Jalal-Abad region) for cystic echinococcosis and 246 per 100 000 population in

16 was 13.1 per 100 000 population per year for cystic echinococcosis and 3.02 per 100 000 population pe

17 stem reported 2359 primary surgical cases of cystic echinococcosis and 546 primary surgical cases of

18 ntry incidence and geographical variation of cystic echinococcosis and alveolar echinococcosis at a h

19 The incidence of both cystic echinococcosis and alveolar echinococcosis has in

20 untry variation in the surgical incidence of cystic echinococcosis and alveolar echinococcosis in Kyr

21 We mapped all confirmed surgical cases of cystic echinococcosis and alveolar echinococcosis report

22 ld be targeted to reduce the burden of human cystic echinococcosis and alveolar echinococcosis.

23 Significant hotspots of cystic echinococcosis were found in four regions: Osh (f

24 asonographic features, such as predominantly cystic echogenic composition and the presence of a perin

25 asopressin type-2 receptor (V2R) activity in cystic epithelial cells can stimulate interstitial myofi

26 ched normal human CD cells, CD-derived renal cystic epithelial cells from patients with autosomal rec

27 imilarly, conditioned media from human ADPKD cystic epithelial cells increased myofibroblast activati

28 d media from primary cultures of human ADPKD cystic epithelial cells on myofibroblast activation.

29 sults demonstrate a novel mechanism by which cystic epithelial cells stimulate myofibroblasts in the

30 an ERK1/2-dependent mechanism in human ADPKD cystic epithelial cells.

31 le: Despite therapeutic progress in treating cystic fibrosis (CF) airway disease, airway inflammation

32 important implications in disorders such as cystic fibrosis (CF) and asthma.

33 ied differentiated primary cultures of human cystic fibrosis (CF) and non-CF airway epithelia.

34 ve therapeutic approach for the treatment of cystic fibrosis (CF) and other mucoobstructive diseases.

35 Mutations in these genes cause cystic fibrosis (CF) and sickle cell disease (SCD), resp

36 Over the past 30 years, a range of cystic fibrosis (CF) animal models have been generated f

37 Animal models of cystic fibrosis (CF) are essential for investigating dis

38 ned survival in patients with advanced-stage cystic fibrosis (CF) are not included in the lung alloca

39 dministration, such as pulmonary delivery in cystic fibrosis (CF) disease, remains a significant chal

40 Patients with cystic fibrosis (CF) do not respond with increased urina

41 om a 1993-1997 cohort from the United States Cystic Fibrosis (CF) Foundation Patient Registry to asse

42 en Pseudomonas aeruginosa from patients with cystic fibrosis (CF) frequently contain mutations in the

43 ress in the development of new therapies for cystic fibrosis (CF) has benefited from therapeutically

44 Adults with cystic fibrosis (CF) have been reported to be at five to

45 Patients with cystic fibrosis (CF) have increased risk of vitamin D de

46 Most infants with cystic fibrosis (CF) have pancreatic exocrine insufficie

47 bination recently approved for patients with cystic fibrosis (CF) homozygous for the Phe508del mutati

48 Cystic fibrosis (CF) is a genetic disease caused by muta

49 Cystic fibrosis (CF) is a genetic disorder of the epithe

50 Rationale: Cystic fibrosis (CF) is a life-shortening, multisystem h

51 Cystic fibrosis (CF) is a life-threatening autosomal rec

52 Cystic fibrosis (CF) is a life-threatening chronic infla

53 Cystic fibrosis (CF) is a monogenic disorder caused by m

54 Cystic fibrosis (CF) is a multiorgan disease caused by m

55 Cystic fibrosis (CF) is a multisystem disorder, but prog

56 Cystic fibrosis (CF) is an autosomal recessive disorder

57 Cystic fibrosis (CF) is caused by mutations in the CF tr

58 Cystic fibrosis (CF) is caused by mutations in the cysti

59 Cystic fibrosis (CF) is characterized by chronic bacteri

60 creasing life expectancy of individuals with Cystic Fibrosis (CF) is likely to be associated with new

61 The leading cause of cystic fibrosis (CF) is the deletion of phenylalanine 50

62 Cystic fibrosis (CF) lung disease is characterized by an

63 e characteristics, onset, and progression of cystic fibrosis (CF) lung disease.

64 ause severe lung infections in patients with cystic fibrosis (CF) or chronic granulomatous disease (C

65 airway pathogens to enter the circulation of cystic fibrosis (CF) patients during chronic infective s

66 Cystic fibrosis (CF) patients experience heightened leve

67 is increasingly recognized as a colonizer of cystic fibrosis (CF) patients, but the role that A. xylo

68 at causes pulmonary disease, particularly in cystic fibrosis (CF) patients.

69 species are opportunistic lung pathogens of cystic fibrosis (CF) patients.

70 In cystic fibrosis (CF) pigs, loss of cystic fibrosis trans

71 Rationale: Cystic fibrosis (CF) pulmonary disease is characterized

72 their abundance and functional relevance in cystic fibrosis (CF) remain poorly understood.

73 Cystic fibrosis (CF) remains the most common life-shorte

74 ator (CFTR) associated with a severe form of cystic fibrosis (CF) reveal the importance and heterogen

75 udomonas aeruginosa infection, especially in cystic fibrosis (CF) sufferers.

76 Diabetes is a common complication of cystic fibrosis (CF) that affects approximately 20% of a

77 Improvements in management of cystic fibrosis (CF) through specialist centres in the U

78 The role of epithelial cystic fibrosis (CF) transmembrane conductance regulator

79 Protein interactions that stabilize the cystic fibrosis (CF) transmembrane conductance regulator

80 formation in neutrophils from patients with cystic fibrosis (CF) was normal during early phagocytosi

81 the morbidity and mortality associated with cystic fibrosis (CF), a condition that predisposes patie

82 Cystic fibrosis (CF), a most deadly genetic disorder, is

83 nt localization to the plasma membrane cause cystic fibrosis (CF), an inherited and eventually lethal

84 thogen in burn patients and individuals with cystic fibrosis (CF), and a leading cause of nosocomial

85 is increasingly observed in patient sputa in cystic fibrosis (CF), and while existing epidemiology in

86 Conclusion In patients with cystic fibrosis (CF), automated quantification of lung M

87 Cystic fibrosis (CF), caused by mutations to CFTR, leads

88 ted with Pseudomonas aeruginosa infection in cystic fibrosis (CF), non-CF bronchiectasis (BE), and ch

89 Background In patients with cystic fibrosis (CF), pulmonary structures with high MRI

90 Background In cystic fibrosis (CF), recurrent imaging and pulmonary fu

91 Autosomal recessive diseases, such as cystic fibrosis (CF), require inheritance of 2 mutated g

92 on in some early infections in children with Cystic Fibrosis (CF), suggesting these isolates may have

93 els that underlie long QT syndrome (LQT) and cystic fibrosis (CF).

94 lent respiratory infections in children with cystic fibrosis (CF).

95 side-induced nephrotoxicity in children with Cystic Fibrosis (CF).

96 rotein that is defective in individuals with cystic fibrosis (CF).

97 s of growing clinical concern in people with cystic fibrosis (CF).

98 c obstructive pulmonary disease, asthma, and cystic fibrosis (CF).

99 used to improve lung health in patients with cystic fibrosis (CF).

100 y diarrheas, whereas CFTR mutations underlie cystic fibrosis (CF).

101 epithelial cells derived from subjects with cystic fibrosis (DeltaF508/DeltaF508 and DeltaF508/-) ba

102 hildren: infective pulmonary exacerbation of cystic fibrosis (n=2), gastroenteritis viral (n=1), and

103 le ion channels can restore host defences in cystic fibrosis airway epithelia via a mechanism that is

104 upregulated in response to P. aeruginosa by cystic fibrosis airway epithelia.

105 s and Main Results: Ceramide is increased in cystic fibrosis airway epithelium owing to differential

106 enesis of T(H) 1-directed lung diseases like cystic fibrosis and acute lung injury.

107 olated from the sputum of an individual with Cystic Fibrosis and assembled in a fully factorial desig

108 as putative treatments for diseases such as cystic fibrosis and cancer.

109 le for significant morbidity in persons with cystic fibrosis and chronic granulomatous disease, repre

110 elastase (NE) activity in tissues, including cystic fibrosis and chronic obstructive pulmonary diseas

111 s: To investigate sphingolipid metabolism in cystic fibrosis and the effects of treatment with recomb

112 ts in a large burden of care for people with cystic fibrosis and their families.

113 le: Chronic azithromycin is commonly used in cystic fibrosis based on short controlled clinical trial

114 ble gap in health outcomes for patients with cystic fibrosis between high-income countries, and low-i

115 Rationale: Non-cystic fibrosis bronchiectasis is characterized by airwa

116 rtonic saline inhalation acutely reduced non-cystic fibrosis bronchiectasis mucus concentration by 5%

117 Studies in patients with cystic fibrosis bronchiectasis were excluded.

118 recommended for long-term management of non-cystic fibrosis bronchiectasis with frequent exacerbatio

119 In patients with non-cystic fibrosis bronchiectasis, lung infection with Pseu

120 le for fragment-based drug discovery and the cystic fibrosis C2-corrector clinical candidate ABBV-322

121 iratory Medicine Commission on the future of cystic fibrosis care was established at a time of great

122 study of children aged 6-16 years at five US cystic fibrosis centres, using culture methods sensitive

123 r necrosis factor receptor 1 is increased in cystic fibrosis epithelia and activates NF-kappaB signal

124 ll tolerated in children aged 2-5 years with cystic fibrosis for 24 weeks.

125 ic Registry of Transplant Recipients and the Cystic Fibrosis Foundation Patient Registry.

126 his retrospective cohort study used the U.S. cystic fibrosis Foundation Patient Registry.

127 er, although life expectancy for people with cystic fibrosis has increased substantially, the disease

128 FTR corrector and potentiator in people with cystic fibrosis homozygous for the F508del mutation.

129 cal studies suggest that airway infection in cystic fibrosis initiates with Staphylococcus aureus and

130 Cystic fibrosis is a condition caused by mutations in th

131 Cystic fibrosis is characterized by dehydration of the a

132 Since the main organ that is affected by cystic fibrosis is the lung, the delivery of drugs direc

133 Using the cystic fibrosis lung as an example, we cultured an avera

134 dase ameliorates the two pivotal features of cystic fibrosis lung disease, inflammation and infection

135 rom biofilm-associated infections, including cystic fibrosis lung infection(4), as well as medical de

136 rincipal pathogens associated with wound and cystic fibrosis lung infections.

137 Culture-independent studies of cystic fibrosis lung microbiota have provided few mechan

138 (desert soil biocrust wetting) and clinical (cystic fibrosis lung) examples, our ability to recover m

139 ough morphotypes of M. abscessus However, in cystic fibrosis neutrophils, wortmannin inhibited killin

140 dies in the past two decades have shown that cystic fibrosis occurs and is more frequent than was pre

141 duces pulmonary exacerbations in people with cystic fibrosis older than age 6 years.

142 uses on pulmonary disease in adults (without cystic fibrosis or human immunodeficiency virus infectio

143 Patients with bronchiectasis due to cystic fibrosis or traction bronchiectasis associated wi

144 d in this way to measure CFTR function using cystic fibrosis patient-derived iPSC lines before and af

145 as of a nonresistance strain isolated from a cystic fibrosis patient.

146 evaluated on respiratory specimens from non-cystic fibrosis patients and compared to the mycobacteri

147 ude exhaled breath condensate collected from cystic fibrosis patients as well as in vitro-cultured hu

148 model, and in sputum samples recovered from cystic fibrosis patients that contain multiple mixed bac

149 gladioli strains isolated from the lungs of cystic fibrosis patients were found to produce unusual l

150 Eight cystic fibrosis patients with A. xylosoxidans were treat

151 and BCC1622, both isolated from the lungs of cystic fibrosis patients.

152 um abscessus are increasing in prevalence in cystic fibrosis patients.

153 within the extracellular DNA of sputum from cystic fibrosis patients.

154 ctions and are the leading cause of death in cystic fibrosis patients.

155 aracteristics of this pathogen among the non-cystic fibrosis population and the importance of early r

156 ently, Food and Drug Administration-approved cystic fibrosis protein trafficking chaperone, lumacafto

157 63% lower, a respiratory domain score on the Cystic Fibrosis Questionnaire-Revised (range, 0 to 100,

158 s were absolute change in sweat chloride and Cystic Fibrosis Questionnaire-Revised respiratory domain

159 untreated neutrophils from either healthy or cystic fibrosis subjects.

160 lian Respiratory Early Surveillance Team for Cystic Fibrosis surveillance program between 2000 and 20

161 Rationale: In cystic fibrosis the major cause of morbidity and mortali

162 creting goblet cells, motile ciliated cells, cystic fibrosis transmembrane conductance regulator (CFT

163 The Cystic Fibrosis Transmembrane Conductance Regulator (CFT

164 fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT

165 d chloride channels (TMEM16A), including the cystic fibrosis transmembrane conductance regulator (CFT

166 In cystic fibrosis (CF) pigs, loss of cystic fibrosis transmembrane conductance regulator (CFT

167 noz and Yu et al. explored the role that the cystic fibrosis transmembrane conductance regulator (CFT

168 (-) drinking test to assess the role of the cystic fibrosis transmembrane conductance regulator (CFT

169 The cystic fibrosis transmembrane conductance regulator (CFT

170 The cystic fibrosis transmembrane conductance regulator (CFT

171 is is a condition caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT

172 acterizations of three nonsense mutations of cystic fibrosis transmembrane conductance regulator (CFT

173 Cigarette smoke decreased AMPhi cystic fibrosis transmembrane conductance regulator (CFT

174 ultiorgan disease caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFT

175 Loss-of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFT

176 The cystic fibrosis transmembrane conductance regulator (CFT

177 proved methods are needed to reliably assess Cystic Fibrosis Transmembrane Conductance Regulator (CFT

178 Cystic fibrosis transmembrane conductance regulator (CFT

179 irst nucleotide-binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFT

180 opment of therapies targeting defects in the cystic fibrosis transmembrane conductance regulator (CFT

181 (-) secretion, through the chloride channels cystic fibrosis transmembrane conductance regulator (CFT

182 hannels involved in Cl(-) extrusion, such as cystic fibrosis transmembrane conductance regulator (CFT

183 A pathway for cystic fibrosis transmembrane conductance regulator (CFT

184 onogenic disorder caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFT

185 demonstrated that VX-809, a corrector of the cystic fibrosis transmembrane conductance regulator (CFT

186 irst nucleotide-binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFT

187 The cystic fibrosis transmembrane conductance regulator (CFT

188 Reduced expression of cystic fibrosis transmembrane conductance regulator and

189 ain whether an acidic pH produced by loss of cystic fibrosis transmembrane conductance regulator anio

190 hase 1, sodium/glucose co-transporter-1, and cystic fibrosis transmembrane conductance regulator in t

191 that CF is caused by mutations in the CFTR (cystic fibrosis transmembrane conductance regulator) gen

192 Rationale: Lumacaftor-ivacaftor is a CFTR (cystic fibrosis transmembrane conductance regulator) mod

193 ut does not replicate a human-relevant CFTR (cystic fibrosis transmembrane conductance regulator) var

194 Rationale: Enhancing non-CFTR (cystic fibrosis transmembrane conductance regulator)-med

195 n essential cargo for lumen formation, CFTR (cystic fibrosis transmembrane conductance regulator).

196 n 19, epithelial cellular adhesion molecule, cystic fibrosis transmembrane conductance regulator, and

197 cal resistance (TEER) (>400 Ohms.cm(2)), and cystic fibrosis transmembrane conductance regulator-medi

198 ed efficiency and specificity to correct the cystic fibrosis transmembrane regulator (CFTR) function

199 ly lower expression of the gene encoding the cystic fibrosis transmembrane regulator characteristic o

200 c Reticulum-associated degradation (ERAD) of Cystic fibrosis transmembrane-conductance regulator (CFT

201 or in patients 12 years of age or older with cystic fibrosis with Phe508del-minimal function genotype

202 air respiratory host defences in people with cystic fibrosis(1-3).

203 CFTR mutations cause cystic fibrosis, a lethal incurable disease.

204 show that in cystic fibrosis, airway gland mucus gels form under cond

205 management of lung diseases such as asthma, cystic fibrosis, and chronic obstructive pulmonary disea

206 a of asthma, chloride channel dysfunction of cystic fibrosis, and ciliary defects of primary ciliary

207 s, contribute to airway mucus obstruction in cystic fibrosis, and facilitate tumor metastasis after d

208 prevalent in chronic lung disease, including cystic fibrosis, and infections are characterized by neu

209 a variety of human diseases, such as cancer, cystic fibrosis, and inflammatory bowel diseases.

210 genetic testing supporting the diagnosis of cystic fibrosis, and the development of therapies target

211 coronary artery disease, multiple sclerosis, cystic fibrosis, asthma, cancer, neurological disorders,

212 circulations have been identified in asthma, cystic fibrosis, chronic thromboembolism and primary car

213 se of serious infections in individuals with cystic fibrosis, compromised immune systems, or severe b

214 fic therapeutic targets include scleroderma, cystic fibrosis, dermatomyositis, and lupus, all of whic

215 ry airway diseases such as asthma, COPD, and cystic fibrosis, novel strategies are needed to avoid ke

216 nicity of this bacterium in individuals with cystic fibrosis, our results highlight that the O(2)-ind

217 nce of Mendelian inheritance, for example in cystic fibrosis, primary ciliary dyskinesia (PCD), and s

218 in mucoinflammatory airway diseases, such as cystic fibrosis, remain unknown.

219 g to develop sgNIPTs of sickle cell disease, cystic fibrosis, spinal muscular atrophy, alpha-thalasse

220 However, in cystic fibrosis, stimulating submucosal glands has the o

221 haled antibiotics is the standard of care in cystic fibrosis, there is insufficient evidence to suppo

222 Conclusion In lungs with cystic fibrosis, ultrashort echo time oxygen-enhanced MR

223 essing and gating defects of the predominant cystic fibrosis-causing mutation.

224 ucus obstruction and related phenotypes in a cystic fibrosis-like lung disease model (i.e., Scnn1b-Tg

225 enic (Scnn1b-Tg(+)) mice, which recapitulate cystic fibrosis-like mucoinflammatory airway disease, de

226 Cystic fibrosis-related diabetes (CFRD) worsens CF lung

227 y epithelial cells cultured from people with cystic fibrosis.

228 gy of chronic lung infections in people with cystic fibrosis.

229 tract, such as inflammatory bowel disease or Cystic Fibrosis.

230 y within a few breath holds in patients with cystic fibrosis.

231 patients with inflammatory bowel disease or cystic fibrosis.

232 ch as pulmonary hypertension, hypoxemia, and cystic fibrosis.

233 constipation including that associated with cystic fibrosis.

234 rm decline of lung function in patients with cystic fibrosis.

235 s in patients with bronchiectasis not due to cystic fibrosis.

236 t often infects open wounds or patients with cystic fibrosis.

237 al for its mucolytic action in patients with cystic fibrosis.

238 t unique host-pathogen interactions exist in cystic fibrosis.

239 unocompromised individuals and patients with cystic fibrosis.

240 h underlying diseases including HIV/AIDS and cystic fibrosis.

241 few options for a cure for all patients with cystic fibrosis.

242 e with burns, surgical wounds or people with cystic fibrosis.

243 olding are transforming the clinical care of cystic fibrosis.

244 resemble the airway defects associated with cystic fibrosis.

245 stone disease, urinary tract infection, and cystic fibrosis.

246 rane regulator characteristic of the disease cystic fibrosis.

247 d 36-72 months; had a confirmed diagnosis of cystic fibrosis; were able to comply with medication use

248 Clinical, EUS and pancreatic cystic fluid (PCF) data were prospectively registered.

249 of the corpus callosum with hydrocephalus to cystic formations, abnormal hippocampi, and polymicrogyr

250 decrease hyperproliferation, leading to non-cystic harmonious hyper growth of kidneys.

251 leural or pericardial effusions, skin edema, cystic hygroma, increased nuchal translucency, or a comb

252 beta-catenin stability and are predominantly cystic in appearance.

253 Based on kidney-to-body-weight ratio, cystic index, and epithelial proliferation in developing

254 t target dysregulated signalling pathways in cystic kidney and liver are needed.

255 snd (alias Barttin) as a genetic modifier of cystic kidney disease in Joubert syndrome, using a Cep29

256 fewer patients have simple cysts or acquired cystic kidney disease.

257 patient affected with progressive medullary cystic kidney disease.

258 Conditional Mks6 mutants have a variable cystic kidney phenotype along with severe retinal degene

259 parental mouse strain phenocopied the severe cystic kidney phenotype.

260 it resulted in a massive infiltration of the cystic kidneys by macrophages and T cells, precluding an

261 ar localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice.

262 tion mutations in NOTCH2 are associated with cystic kidneys in Hajdu-Cheney syndrome patients.

263 Cystic kidneys showed increased mitogen-activated protei

264 phron-specific Tulp3 knockout mice developed cystic kidneys, while retaining intact cilia.

265 ation (EUS-FNA) is recommended in pancreatic cystic lesions (PCLs) with worrisome features (size >= 3

266 ects primarily males and is characterized by cystic lesions of the inner retina, decreased visual acu

267 h standard deviation of greyscale values for cystic lesions was 1208.375 +/- 93 and for that of the t

268 ain elastography of the non-vascular and non-cystic lesions was performed and strain ratios were calc

269 l large cysts.Measurements and Main Results: Cystic lung areas averaged larger Vts than noncystic lun

270 e pulmonary interstitial space that leads to cystic lung destruction and spontaneous pneumothoraces.

271 mphangioleiomyomatosis (LAM) is a rare fatal cystic lung disease due to bi-allelic inactivating mutat

272 Vt of any analyzed lung region.Conclusions: Cystic lung has greater normalized Vt when compared with

273 volumes in total lung, noncystic lung, total-cystic lung, and individual large cysts.Measurements and

274 time does not correlate with Vt of normal or cystic lung.

275 t enhancement in 19 patients or thick-walled cystic mass (n = 4).

276 ltrasound biomicroscopy revealed a partially cystic mass adjacent to the ciliary body between the 5 a

277 lary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms (MCNs) are non-invasive neoplasms that

278 is to provide a real-life picture of serous cystic neoplasms (SCNs) management once a presumptive di

279 cursor lesions, new findings in premalignant cystic neoplasms, and recently updated staging criteria

280 al papillary mucinous neoplasms and mucinous cystic neoplasms, while pancreatic intraepithelial neopl

281 sociated neoplasms pleuropulmonary blastoma, cystic nephroma, and nasal chondromesenchymal hamartoma)

282 med with histopathological reports depicting cystic or tumour-like lesions were included in the study

283 ar LH secretion may be the root cause of the cystic ovarian phenotype with similarities to PCOS.

284 d signaling causes episodic LH secretion and cystic ovary.

285 acterize an international cohort of resected cystic pancreatic neuroendocrine neoplasms (cPanNENs) an

286 The characteristics of cystic pancreatic neuroendocrine neoplasms (cPanNENs) ar

287 tion of Cdk1 with Pkd1 markedly improved the cystic phenotype and kidney function compared with inact

288 ion mutations in PKHD1 also recapitulate the cystic phenotype associated with autosomal recessive pol

289 Hepatocystic triangle and cystic plate visualization was achieved more often in lo

290 ls with numerous, large mitochondria and are cystic precursors to pancreatic ductal adenocarcinoma (P

291 revalent form of renal insult may accelerate cystic progression and investigated tubular crystal depo

292 imaging was used to test the hypothesis that cystic regions of the lung will exhibit a quantifiable V

293 LAM causes cystic remodeling of the lung and progressive respirator

294 Cystic renal cell carcinoma (RCC) is almost certainly ov

295 defined categories, including congenital or cystic renal disease (127 of 531 patients [23.9%]) and n

296 n used to stratify the risk of malignancy in cystic renal masses.

297 eneity seen in PDAC with similar phenotypes (cystic-solid).

298 Cystic spaces in the ICM (46.67%), schisis-like spitting

299 nal incision on the right side, an uncertain cystic structure was found in the hernial sac, and sever

300 le cells, laminin, and elastin in airway and cystic walls using immunofluorescence staining, we found