ライフサイエンスコーパス: dysplasia

1 stic cases and five patients with high-grade dysplasia.

2 n with the development of colitis-associated dysplasia.

3 acute deregulation of SOX2 drives bronchial dysplasia.

4 e to build an organotypic model of bronchial dysplasia.

5 rmal dysplasia with anhidrosis, and muscular dysplasia.

6 er with characteristic intestinal epithelial dysplasia.

7 n in the pre-cancerous stages of colitis and dysplasia.

8 ated lymphoid tissue (MALT) hyperplasia, and dysplasia.

9 ) in order to accurately assess the grade of dysplasia.

10 ocopy human X-linked hypohidrotic ectodermal dysplasia.

11 ppression of autophagy in cases with typical dysplasia.

12 o detect recurrent intestinal metaplasia and dysplasia.

13 ralogy of Fallot, and 1 with pulmonary valve dysplasia.

14 dy cysts in a patient with oculodentodigital dysplasia.

15 s imperfecta (OI) is a collagen-related bone dysplasia.

16 ypical AGW that harbored different grades of dysplasia.

17 never expanded to the point of dominance or dysplasia.

18 o manage in a patient with oculodentodigital dysplasia.

19 important in patients with oculodentodigital dysplasia.

20 e inheritance of an uncharacterized skeletal dysplasia.

21 d space results in the formation of cortical dysplasia.

22 l papillary mucinous neoplasm had high-grade dysplasia.

23 nset severe developmental delay and skeletal dysplasia.

24 and 0.43 (95% CI, 0.36-0.46) for high-grade dysplasia.

25 o the human disorder hypohidrotic ectodermal dysplasia.

26 pical changes suggestive of bronchopulmonary dysplasia.

27 ent in FAP-adenoma but is not present in IBD-dysplasia.

28 and diffuse megalencephaly without cortical dysplasia.

29 hizencephaly, heterotopia, or focal cortical dysplasia.

30 mpling bias and the subjective assessment of dysplasia.

31 h are responsible for Schimke immuno-osseous dysplasia.

32 51 were non-dysplastic and 14 had high-grade dysplasia.

33 ft ventricular arrhythmogenic cardiomyopathy/dysplasia.

34 sulfate sodium to induce colitis-associated dysplasia.

35 orectal cancer, but not in patients with IBD-dysplasia.

36 increased bone growth, and reduced skeletal dysplasia.

37 low in human lung tumors and in progressive dysplasias.

38 s including arrhythmogenic right ventricular dysplasia 3.

39 -3.3 to 4.5; P = .70), and bronchopulmonary dysplasia (4.4% vs 5.1%; 95% CI of risk difference, -3.9

40 ) and 2 of 45 samples that were negative for dysplasia (4.4%).

41 or CRC was 4.4% for patients with SSA/P with dysplasia, 4.5% for patients with TSAs, and 2.3% for pat

42 years among patients with baseline low-grade dysplasia (95% CI 1.5-7.2), and 7.3 per 100 person-years

43 ears among patients with baseline high-grade dysplasia (95% CI 4.2-12.5).

44 ears among patients with baseline high-grade dysplasia (95% CI 8.8-20.7).

45 years among patients with baseline low-grade dysplasia (95% CI, 4.9-14.0), and 13.5 per 100 person-ye

46 clin analogue iloprost reduces endobronchial dysplasia, a premalignant lung lesion.

47 n in Ig20 reportedly cause frontometaphyseal dysplasia, a skeletal disorder with unknown pathogenesis

48 ments, associated renal lesions - congenital dysplasia, acquired scarring or both - are a common caus

49 a (FMD) is a progressive sclerosing skeletal dysplasia affecting the long bones and skull.

50 subsequent development of colitis-associated dysplasia after in situ fluorination of inflammatory mac

51 Ablation of Intestinal Metaplasia Containing Dysplasia (AIM) trial.

52 ubsequent commensal dysbiosis and epithelial dysplasia along the GI tract.

53 ewborn, surfactant use, and bronchopulmonary dysplasia also occurred significantly less frequently in

54 hythmogenic right ventricular cardiomyopathy/dysplasia, although their cellular and molecular pathome

55 istered in the US Registry for Fibromuscular Dysplasia, an observational disease-based registry of pa

56 Of these, 376 had no dysplasia and 22 had high-grade dysplasia or intramucosa

57 ] age, 47.3 [11.1] years) harboring areas of dysplasia and 22 patients who were HIV- (5 women, 17 men

58 V+ MSM with AGWs (n = 38) harboring areas of dysplasia and 22 patients who were HIV-negative (HIV-) w

59 ft ventricular arrhythmogenic cardiomyopathy/dysplasia and a high incidence of adverse cardiac events

60 of TWIST1, in two subjects with frontonasal dysplasia and additional malformations.

61 l evolution in the absence of significant BM dysplasia and blast cells can be difficult to address in

62 rogression of esophageal mucosal metaplasia, dysplasia and carcinoma.

63 se of severe immune deficiency with skeletal dysplasia and developmental delay and underline a crucia

64 ess likely with a diagnosis of fibromuscular dysplasia and extracoronary vascular abnormalities (42%

65 t hypermobility, contractures, mild skeletal dysplasia and high myopia.

66 colony-stimulating factor with myeloid cell dysplasia and ineffective hematopoiesis.

67 ndromes (MDSs) share features of cytological dysplasia and ineffective hematopoiesis.

68 ts of their rates of complete eradication of dysplasia and intestinal metaplasia and adverse events i

69 -dependent progressive anemia, megakaryocyte dysplasia and loss of hematopoietic stem cell (HSC) quie

70 g up the competing risks of bronchopulmonary dysplasia and neurodevelopmental harm.

71 l disorders such as cranio-lenticulo-sutural dysplasia and osteogenesis imperfect, caused by mutation

72 (such as hemimegalencephaly, focal cortical dysplasia and polymicrogyria).

73 t of degree of prematurity, bronchopulmonary dysplasia and postnatal sepsis.

74 icity and burden, protection from high-grade dysplasia and significantly reduced colitis.

75 of the NU/J strain progressed to high grade dysplasia and to carcinoma in situ.

76 agnetic resonance imaging (MRI) detection of dysplasia and to contribute to the presurgical imaging e

77 eas GAC repeats are associated with skeletal dysplasias and expand from the normal five to a maximum

78 (SMDs) comprise a diverse group of skeletal dysplasias and often manifest as short stature, growth-p

79 f 110 (32%) patients had recurrence of BE or dysplasia, and 19 (17%) had dysplasia recurrence.

80 tubular adenomas >/=10 mm or with high-grade dysplasia, and conventional adenomas with villous histol

81 ynostosis, cardiac septal defects with valve dysplasia, and deafness with inner ear malformations.

82 Eed haploinsufficiency induced hematopoietic dysplasia, and Eed heterozygous mice were susceptible to

83 e, cervical artery dissection, fibromuscular dysplasia, and hypertension.

84 minal erythroid maturation defect, erythroid dysplasia, and long-term hematopoietic stem cell (LT-HSC

85 SOX2 deregulation drives dysplasia, and loss of tumor promoter 53 is a cooperatin

86 crocephaly, craniofacial anomalies, skeletal dysplasia, and neonatal lethality.

87 yers acrofacial dysostosis, cranioectodermal dysplasia, and oral-facial-digital syndrome, altogether

88 of patients who were HIV- showed no signs of dysplasia, and p16INK4a-staining was always negative.

89 marrow cells had intestinal inflammation and dysplasia, and reduced expression of cytokines produced

90 with inherited arrhythmogenic cardiomyopathy/dysplasia, and the functional study showed an abnormal g

91 of postesophagectomy columnar metaplasia and dysplasia, and the timescale over which it develops.

92 early event in the pathogenesis of bronchial dysplasia; and (3) to use the model for studies on patho

93 In the absence of fucosylation, dysplasia appeared and progressed to adenocarcinoma in u

94 Several definitions of bronchopulmonary dysplasia are clinically used; however, their validity r

95 Early neoplastic features in oral epithelial dysplasia are first evident at the basal epithelium posi

96 Measures to reduce bronchopulmonary dysplasia are not always effective or have important adv

97 scribed, but incidence and the potential for dysplasia are uncertain, and the clinical relevance uncl

98 Skeletal dysplasias are a clinically and genetically heterogeneou

99 ed by low-risk HPV-types, whereas anogenital dysplasias are potential cancer precursors associated wi

100 eletal disorders, such as spondyloepiphyseal dysplasias, are linked to mutations in type II collagen

101 hythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) varies depending on study cohort and

102 owth hormone deficiency, and mild ectodermal dysplasia as previously described.

103 joint contractures, muscle weakness and bone dysplasia as well as high myopia, with evidence of clini

104 ied as having physiological bronchopulmonary dysplasia, as compared with 269 (43.9%) of the 613 infan

105 The effects of skeletal dysplasia associated mutations of the structure and mech

106 ombined outcome of death or bronchopulmonary dysplasia at 36 weeks' postmenstrual age and respiratory

107 with nondysplastic BE (or BE with low-grade dysplasia) at their index endoscopy and at least a 3-yea

108 Bronchopulmonary dysplasia based on a clinical definition occurred in 53.

109 ting in a high incidence of bronchopulmonary dysplasia (BPD) and chronic respiratory morbidity.

110 ted with increased risk for bronchopulmonary dysplasia (BPD) and respiratory disease during early chi

111 ncreases the risk of AA and bronchopulmonary dysplasia (BPD) in children and animal models.

112 utor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preve

113 Bronchopulmonary dysplasia (BPD) is characterized by lifelong obstructive

114 Bronchopulmonary dysplasia (BPD) occurs in approximately 40% of infants b

115 utor to the pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity t

116 iratory outcomes, including bronchopulmonary dysplasia (BPD), in preterm infants.

117 Bronchopulmonary dysplasia (BPD), the main consequence of prematurity, ha

118 ngth of stay increased with bronchopulmonary dysplasia (BPD; 1.77), whereas total cost increased with

119 to improve survival without bronchopulmonary dysplasia but its safety with regard to neurodevelopment

120 d, might reduce the risk of bronchopulmonary dysplasia, but appropriately designed trials are lacking

121 nd reduces the incidence of bronchopulmonary dysplasia, but its effects on respiratory function in la

122 mTOR pathway was activated, as in cases with dysplasia, but the immunoreactivities of nucleoporin p62

123 ncluding systemic inflammation and cartilage dysplasia, but the mechanisms of skeletal manifestations

124 Defining bronchopulmonary dysplasia by the use of oxygen alone is inadequate becau

125 cause Larsen syndrome and Frontometaphyseal dysplasia can affect the structure and therefore functio

126 dates for malignant potential and high-grade dysplasia/cancer were identified by an explorative prote

127 stem-cell antigen could identify high-grade dysplasia/cancer with an accuracy of 96% (95% CI, 90% to

128 s with arrhythmogenic right ventricular (RV) dysplasia/cardiomyopathy (ARVD/C) and the relationship o

129 c course of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).

130 rised 27 non-dysplastic and eight high-grade dysplasia cases, whereas the high-risk group (8% of the

131 ps: patients with highly asymmetric cortical dysplasia caused by the common p.E17K mutation, and pati

132 Cleidocranial dysplasia (CCD) is an autosomal dominant human disorder

133 samples resected from patients with cortical dysplasia (CD), which was correlated with duration of ep

134 e is highly consistent with craniodiaphyseal dysplasia (CDD; OMIM 122860), we propose activation of t

135 airless dog breeds show a form of ectodermal dysplasia characterised by a lack of hair and abnormal t

136 hropathy; and Winchester syndromes, skeletal dysplasias characterized by carpal/tarsal and epiphyseal

137 syndrome is an autosomal-recessive skeletal dysplasia, characterized by short stature and postaxial

138 chondrocalcinosis (CCAL2), craniometaphyseal dysplasia (CMD), mental retardation, deafness and ankylo

139 Dysplasia-containing AGW tissue of HIV+ MSM were compare

140 The 38 dysplasia-containing AGWs of HIV+ MSM harbored low-grade

141 Various traditional bronchopulmonary dysplasia criteria based on respiratory status at differ

142 Severe bronchopulmonary dysplasia/death rates at 36 weeks' postmenstrual age wer

143 The primary outcome was bronchopulmonary dysplasia, defined on a physiological basis (with the us

144 r severely shortened upper limbs (upper limb dysplasia), despite some variability, could perceive, an

145 This review chronicles the evolution of dysplasia detection and management in inflammatory bowel

146 lds and in blind spots, which might increase dysplasia detection.

147 dysfunction of filamin and frontometaphyseal dysplasia disease.

148 ntify loci significantly associated with hip dysplasia, elbow dysplasia, idiopathic epilepsy, lymphom

149 x-2 expression was associated with increased dysplasia, epithelial cell Cox-2 expression and submucos

150 tructural patterns in type II focal cortical dysplasia (FCD) have been studied to explain the differe

151 epsy, one of each pair having focal cortical dysplasia (FCD) IIa.

152 Focal cortical dysplasia (FCD), a local malformation of cortical develo

153 y (FLE) that is distinct from focal cortical dysplasia (FCD).

154 mistry in the core of type II focal cortical dysplasias (FCD-II), at the FCD boundary (perilesion), a

155 Focal cortical dysplasias (FCDs) are malformations of cortical developm

156 nflammatory bowel disease and flat low-grade dysplasia (fLGD) in the colon.

157 d a strong association between fibromuscular dysplasia (FMD) and spontaneous coronary artery dissecti

158 Fibromuscular dysplasia (FMD) is a heterogeneous group of non-atherosc

159 Fibromuscular dysplasia (FMD) is a noninflammatory arterial disease th

160 Frontometaphyseal dysplasia (FMD) is a progressive sclerosing skeletal dys

161 nial aneurysm in patients with fibromuscular dysplasia (FMD) is uncertain.

162 ECTI contour differentiated dysplasia from control/benign mucosa with higher sensiti

163 luorescently labelled lectins to distinguish dysplasia from normal tissue when sprayed on to the lumi

164 cribed in the ANO5 gene for gnathodiaphyseal dysplasia (GDD, OMIM: 166260), and multiple recessive mu

165 Gnathodiaphyseal dysplasia (GDD; MIM#166260) is an autosomal dominant syn

166 ndings were tumours (n=33, 50%), followed by dysplasia, gliosis (n=11, each) and hippocampus sclerosi

167 history of prematurity and bronchopulmonary dysplasia have a high risk of asthma and viral-induced e

168 Whilst >450 skeletal dysplasias have been reported, 30% are genetically uncha

169 Hypohidrotic ectodermal dysplasia (HED) results from mutation of the EDA, EDAR o

170 in Eda or Edar cause hypohidrotic ectodermal dysplasia (HED), a condition characterized by malformati

171 protecting against cervical cancer, cervical dysplasia, herpes simplex virus type 2, chlamydia, and s

172 pancreatic cancer (P = 0.027) and high-grade dysplasia (HGD) (P = 0.003) were independent risk factor

173 tt's esophagus for progression to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC).

174 aining low-grade dysplasia (LGD), high-grade dysplasia (HGD) or carcinoma (C), with 81% sensitivity,

175 ociated with later development of high-grade dysplasia (HGD) or colorectal cancer.

176 rs associated with progression to high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC) in pa

177 ttle is known about their risk of high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC).

178 ssue microarrays, containing EAC, high grade dysplasia (HGD), low grade dysplasia (LGD), Barrett's es

179 g nuclear factor 2 (TIN2) and adrenocortical dysplasia homolog (ACD) were identified in dyskeratosis

180 interaction between POT1 and adrenocortical dysplasia homolog (ACD), which is a part of the telomere

181 SOX9 expression and causes a human skeletal dysplasia, identifying a mechanism that regulates chondr

182 icantly associated with hip dysplasia, elbow dysplasia, idiopathic epilepsy, lymphoma, mast cell tumo

183 Some of the ciliopathies display skeletal dysplasias, implying the important role of primary cilia

184 grade dysplasia in 6 cases (16%), high-grade dysplasia in 31 cases (81%), and areas of invasive anal

185 ntaining AGWs of HIV+ MSM harbored low-grade dysplasia in 6 cases (16%), high-grade dysplasia in 31 c

186 robial diversity in patients with high-grade dysplasia in comparison to control patients, as measured

187 to Improve Survival without Bronchopulmonary Dysplasia in Extremely Preterm Infants) randomized clini

188 birth to the development of bronchopulmonary dysplasia in extremely preterm infants.

189 rmalities have been associated with skeletal dysplasia in humans, and our findings present opportunit

190 timately, causes growth plate and epiphyseal dysplasia in mice.

191 We compared FUSE vs FVC in the detection of dysplasia in patients with IBDs.

192 The presence of high-grade dysplasia in serrated lesions was uncommon when compared

193 e-specific development of colitis-associated dysplasia in the descending colon showed good correlatio

194 following esophagectomy, but the absence of dysplasia in this large cohort is reassuring.

195 Dexamethasone to prevent bronchopulmonary dysplasia in very preterm neonates was associated with a

196 We recapitulated human bronchial dysplasia in vitro.

197 Mutation associated to Frontometaphyseal dysplasia, in turn, transforms 16-17 fragment from compa

198 treatment for Barrett's esophagus (BE) with dysplasia is complete eradication of intestinal metaplas

199 increase Fzd9 expression, and progression of dysplasia is inhibited.

200 Adenocarcinoma or high-grade dysplasia is present in 14.9% of resected pancreatic MCN

201 expansions in the COMP gene lead to skeletal dysplasias is poorly understood.

202 mos, microphthalmia or anophthalmia, retinal dysplasia, keratitis, corneal neovascularization, catara

203 ncreased risk of developing bronchopulmonary dysplasia, leading to significant respiratory morbidity.

204 in the diagnosis and management of low-grade dysplasia (LGD) in Barrett's esophagus patients.

205 pathologists, in the diagnosis of low-grade dysplasia (LGD) in patients with Barrett's esophagus (BE

206 pathologists, in the diagnosis of low-grade dysplasia (LGD) in patients with Barrett's esophagus (BE

207 rett's esophagus, the diagnosis of low-grade dysplasia (LGD) is subjective, and reported outcomes var

208 g EAC, high grade dysplasia (HGD), low grade dysplasia (LGD), Barrett's esophagus (BE), columnar cell

209 tinguished from regions containing low-grade dysplasia (LGD), high-grade dysplasia (HGD) or carcinoma

210 ped markedly craniofacial dysplasia, scapula dysplasia, long bone length shortage and body weight dec

211 nclude that colorectal cancer prevention and dysplasia management for patients with inflammatory bowe

212 oise ratio was found at sites that developed dysplasia (mean, 0.58 +/- 0.09 [standard deviation]) as

213 showed cell-autonomous anaemia and erythroid dysplasia, mimicking dyserythropoiesis in MDS.

214 cting for per-unit withdrawal time, the mean dysplasia miss rate per subject was significantly lower

215 The primary end point was dysplasia missed by the first colonoscopy detected by th

216 e, a predisposing factor to bronchopulmonary dysplasia, modulates the innate immune response, produci

217 s in the genetic diseases short-rib thoracic dysplasia, Mohr-syndrome and amyotrophic lateral scleros

218 Villous adenomas (n = 545; 3.6 %), dysplasia (n = 49; 0.4 %), and invasive carcinoma (n = 2

219 n = 36; tubulovillous adenoma with low grade dysplasia, n = 27; sessile serrated adenoma, n = 4; tubu

220 n = 4; tubulovillous adenoma with high grade dysplasia, n = 3; villous adenoma, n = 3), and 20 cases

221 of death, brain injury, or bronchopulmonary dysplasia (neonatal), and a standardised cognitive score

222 al cavernous malformation, a cerebrovascular dysplasia occurring in up to 0.5% of the population.

223 for malignancy (adenocarcinoma or high-grade dysplasia) occurring in the setting of an MCN.

224 Oculodentodigital dysplasia (ODDD) is a rare genetic disease that affects

225 Intraepithelial dysplasia of the oral mucosa typically originates in the

226 atients with CID, anhidrosis, and ectodermal dysplasia of unknown etiology.

227 ogeneity characterizes a variety of skeletal dysplasias often due to interacting or overlapping signa

228 presence and the border of type II cortical dysplasia on MRI, a quantitative ROI-based analysis (coe

229 d with multiple sclerosis, one with cortical dysplasia, one with pineal hemorrhage and one with a bra

230 The development of dysplasia or cancer selected for attenuated virulence ph

231 te outcome of physiological bronchopulmonary dysplasia or death before 36 weeks of postmenstrual age

232 ents, AGWs of HIV+ MSM may harbor high-grade dysplasia or even invasive squamous cell carcinoma.

233 alterations were associated with subsequent dysplasia or GC; conversely patients exhibiting normal-l

234 00) and the probability of having high-grade dysplasia or intramucosal adenocarcinoma was 0% (0-4).

235 whereas the probability of having high-grade dysplasia or intramucosal adenocarcinoma was 87% (73-95)

236 , 376 had no dysplasia and 22 had high-grade dysplasia or intramucosal adenocarcinoma.

237 Malignant disease was defined as high-grade dysplasia or invasive adenocarcinoma on results of surgi

238 Malignancies (high-grade dysplasia or invasive neoplasm) developed after 5 years

239 omas (villous or tubulovillous or high grade dysplasia or size > 1 cm or > 3 adenomatous polyps) were

240 with villous histologic findings, high-grade dysplasia, or cancer) during follow-up.

241 as development of bronchiectasis, anogenital dysplasia, or invasive cancer.

242 or abdominal complications, bronchopulmonary dysplasia, or retinopathy of prematurity).

243 th the skeletal phenotypes Frontometaphyseal dysplasia, Otopalatodigital, and Melnick-Needles syndrom

244 d frequent bone fractures and florid osseous dysplasia (p.Cys356Tyr), while one Chinese family with t

245 with inherited arrhythmogenic cardiomyopathy/dysplasia phenotype with variable disease severity expre

246 e families with Progressive Pseudorheumatoid Dysplasia (PPD).

247 Neither BE nor dysplasia recurred at a constant rate.

248 tinued; our study did not identify any BE or dysplasia recurrence after 4 years of surveillance.

249 The incidence rate of dysplasia recurrence was 5.2 per 100 person-years overal

250 urrence of BE or dysplasia, and 19 (17%) had dysplasia recurrence.

251 otential therapeutic approaches for skeletal dysplasias related to over-activation of human FGFR3, an

252 These mice developed markedly craniofacial dysplasia, scapula dysplasia, long bone length shortage

253 Shohat-type spondyloepimetaphyseal dysplasia (SEMD) is a skeletal dysplasia that affects ca

254 cluded perinatal mortality, bronchopulmonary dysplasia, sepsis, intraventricular haemorrhage, periven

255 turity reduces the rates of bronchopulmonary dysplasia, severe retinopathy, and neurodevelopmental di

256 enome-wide association analyses for skeletal dysplasia (short limbs) within a single breed (PBonferro

257 Spondylometaphyseal dysplasias (SMDs) comprise a diverse group of skeletal d

258 features of human cerebrofaciothoracic (CFT) dysplasia spectrum, a developmental disorder linked to T

259 ade in endoscopic diagnosis and treatment of dysplasia (squamous and Barrett's), and early esophageal

260 el to compute the conditional probability of dysplasia status.

261 egalencephaly) as well as segmental cortical dysplasia (such as hemimegalencephaly, focal cortical dy

262 A to the luminal surface epithelium in human dysplasia suggests that these lectins may enable more se

263 FR2 mutations that are germline in bent bone dysplasia syndrome (BBDS), we reveal a mechanistic conne

264 tions in EXTL3 cause a neuro-immuno-skeletal dysplasia syndrome, and to gain insight into the pathoge

265 studied three patients with severe skeletal dysplasia, T cell immunodeficiency, and developmental de

266 lower risk of physiological bronchopulmonary dysplasia than a control emulsion among preterm infants

267 ECTI contour was higher in dysplasia than control or inflamed specimens, indicating

268 pimetaphyseal dysplasia (SEMD) is a skeletal dysplasia that affects cartilage development.

269 y the optimal definition of bronchopulmonary dysplasia that best predicts respiratory and neurodevelo

270 moking, length of BE, and baseline low-grade dysplasia that identified patients with BE at low, inter

271 1) To develop an in vitro model of bronchial dysplasia that recapitulates key molecular and phenotypi

272 When adjusted for bronchopulmonary dysplasia, the difference in flow rates between groups d

273 When categorized based on degree of dysplasia, the kappa value was 0.22 (95% CI, 0.11-0.29)

274 r follow-up analysis of patients with BE and dysplasia treated by radiofrequency ablation (RFA) in th

275 Participants for the AIM Dysplasia trial (18-80 years old) were recruited from 19

276 Of 127 patients in the AIM Dysplasia trial, 119 received RFA and met inclusion crit

277 ysis of prospective cohort data from the AIM Dysplasia trial, we found BE to recur after CEIM by RFA

278 Using a mouse model of Thanatophoric Dysplasia Type II (TDII) we show that both HDAC6 deletio

279 uantitated alterations in ECTI topography in dysplasia using in vivo volumetric multiphoton autofluor

280 e risk; the probability of having high-grade dysplasia was 14% (9-21).

281 al intensity in mice with colitis-associated dysplasia was compared with that in control mice with a

282 Dysplasia was diagnosed by an expert gastrointestinal pa

283 Fibromuscular dysplasia was present in 62.7%, connective tissue disord

284 The presence and degree of dysplasia was separately recorded for each biopsy and cl

285 l diagnosis among adults, and focal cortical dysplasia was the most common diagnosis among children.

286 ortical development in 19.8% (focal cortical dysplasia was the most common type, 52.7% of cases of wh

287 SSA/Ps with cytology markers of dysplasia were associated with a particularly high OR (4

288 and various degrees of bile duct paucity and dysplasia were identified.

289 ngth of BE, and baseline-confirmed low-grade dysplasia were significantly associated with progression

290 samples of LGD, and 34 samples of high-grade dysplasia) were identified, randomly assigned to 7 patho

291 n without hands (individuals with upper limb dysplasia), who use tools with their feet.

292 ft ventricular arrhythmogenic cardiomyopathy/dysplasia with a high incidence of adverse clinical even

293 NEMO mutations result in X-linked ectodermal dysplasia with anhidrosis and immunodeficiency, also ref

294 intestinal disease in addition to ectodermal dysplasia with anhidrosis and immunodeficiency.

295 kindreds with CID, autoimmunity, ectodermal dysplasia with anhidrosis, and muscular dysplasia.

296 reported patients with anhidrotic ectodermal dysplasia with immunodeficiency caused by mutations in t

297 esenting a new form of anhidrotic ectodermal dysplasia with immunodeficiency that is distinct from pr

298 al forward-viewing colonoscopy (FVC) detects dysplasia with low levels of sensitivity.

299 cted at the pre-invasive stage of high-grade dysplasia with the novel Cytosponge device.

300 A 6-year old girl with oculodentodigital dysplasia, with progressive chronic angle- closure glauc

301 r results emphasize the role of keratinocyte dysplasia within dysplastic nevi.