ライフサイエンスコーパス: dysplasia

1 turity stage 3-5, or severe bronchopulmonary dysplasia).

2 uals with MAS but not in humans with fibrous dysplasia.

3 and in controls and foot in individuals with dysplasia.

4 elial cells (HMECs) is one of the indices of dysplasia.

5 ents with confirmed and persistent low-grade dysplasia.

6 t dysgenesis, retinal detachment and retinal dysplasia.

7 es, including mortality and bronchopulmonary dysplasia.

8 nt Barrett's esophagus (BE), with or without dysplasia.

9 perplastic polyps or adenomas with low-grade dysplasia.

10 st four pregnancies associated with skeletal dysplasia.

11 enes being targeted in early versus advanced dysplasia.

12 atal lung injury leading to bronchopulmonary dysplasia.

13 ons in 10 of 13 individuals with SPONASTRIME dysplasia.

14 g injury that may result in bronchopulmonary dysplasia.

15 ctors such has family history and high-grade dysplasia.

16 n discovered in individuals with SPONASTRIME dysplasia.

17 rom SCN and within PMNs predict the grade of dysplasia.

18 in a novel autosomal dominant human skeletal dysplasia.

19 mutation was associated with Schneckenbecken dysplasia.

20 to preterm infants without bronchopulmonary dysplasia.

21 asia (HHT) is an autosomal dominant vascular dysplasia.

22 y mucinous neoplasms with intermediate-grade dysplasia.

23 e to build an organotypic model of bronchial dysplasia.

24 r able to differentiate tumor from low-grade dysplasia.

25 izure freedom following surgery for cortical dysplasia.

26 ate deposition disease and craniometaphyseal dysplasia.

27 c arteriopathies, particularly fibromuscular dysplasia.

28 diseases, such as xerocytosis and lymphatic dysplasia.

29 o disrupted angiogenesis in bronchopulmonary dysplasia.

30 hologically defined as intimal fibromuscular dysplasia.

31 rted in patients with these lethal pulmonary dysplasias.

32 sive connective tissue disorder, geleophysic dysplasia 1 (GPHYSD1), which is characterized by short s

33 Twenty seven (26%) were negative for dysplasia, 46 were classified as AIN1 (44%), 14 as AIN2

34 hich is the causative gene of the ectodermal dysplasia 9 (ECTD9) in human patients.

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

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

37 ungs of infants with severe bronchopulmonary dysplasia, a chronic lung disease associated with preter

38 ation of alveoli results in bronchopulmonary dysplasia, a disease of prematurity.

39 E 1: In BE patients with confirmed low-grade dysplasia, a repeat examination with high-definition whi

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

41 red recovery from DSS induction and triggers dysplasia: a Schematic illustration of the experimental

42 cebo group survived without bronchopulmonary dysplasia (absolute difference, -5.0% [95% CI, -11.6% to

43 dicted this outcome defined bronchopulmonary dysplasia according to treatment with the following supp

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

45 elvis X-rays was used to identify persistent dysplasia after 9 months and walking age (after 18 month

46 plasma EV of the 11 patients with high-grade dysplasia alone, only 1 had high MUC5AC expression (sens

47 sive progression but some cases of low-grade dysplasia also progressed to cancer.

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

49 invasive SCCs than in hyperplasias and mild dysplasias, although mutations in p53, Notch1 and Fat1 o

50 (95% CI, 0.85-1.33) for low-grade/high-grade dysplasia and 0.14 (95% CI, 0.06-0.22) for GC.

51 Chronic colonic inflammation leads to dysplasia and cancer in patients with inflammatory bowel

52 ike receptor 4 (TLR4) in the pathogenesis of dysplasia and cancer.

53 ssion from sessile serrated adenoma (SSA) to dysplasia and carcinoma has not been elucidated.

54 disease (i.e., higher proportions in severe dysplasia and carcinoma than in less severe lesions).

55 genes reduce MSO fidelity, leading to tissue dysplasia and causing several diseases such as microceph

56 resentations with arterial involvement, bone dysplasia and characteristic dysmorphic features.

57 In contrast, the molecular bases of acinar dysplasia and congenital alveolar dysplasia have remaine

58 While all mice developed severe dysplasia and cystic papillary neoplasms, there existed

59 ould also lead to the diagnosis of treatable dysplasia and early cancer.

60 Barrett's esophagus (BE) can progress to dysplasia and esophageal adenocarcinoma (EAC), accompani

61 iferative subtype is enriched with bronchial dysplasia and exhibits up-regulation of metabolic and ce

62 reduced function of TONSL cause SPONASTRIME dysplasia and highlight the importance of TONSL in embry

63 We identified in an adult with ectodermal dysplasia and immunodeficiency a germline, gain-of-funct

64 nd in vitro in both animal models of fibrous dysplasia and in cultured cells from individuals with MA

65 fying the entire spectrum of oral epithelial dysplasia and oral squamous cell carcinoma.

66 To date, it remains unknown whether fibrous dysplasia and other symptoms of MAS, including neuropsyc

67 years between the development of high-grade dysplasia and pancreatic cancer.

68 t have been associated with HPV persistence, dysplasia and progression to ICC.

69 role in development of precancerous cervical dysplasia and progression to invasive cervical carcinoma

70 ion in patients with hypohidrotic ectodermal dysplasia and reveal the dynamic expression pattern of L

71 fied areas in basal ganglia, dentato-olivary dysplasia and severe hypoplasia/agenesis of the pyramida

72 papillary mucinous neoplasms with high-grade dysplasia and some enlarged pancreatic intraepithelial n

73 s with and without neonatal bronchopulmonary dysplasia and term-born control subjects at 19 years of

74 mour-suppressive mode, mutant p53 eliminated dysplasia and tumorigenesis in Csnk1a1-deficient and Apc

75 e female susceptibility to age-dependent gut dysplasia and tumorigenesis, thus potentially reducing l

76 L2-IL1B mice fed an HFD developed esophageal dysplasia and tumors more rapidly than mice fed the cont

77 patients with Barrett's esophagus (BE) with dysplasia and/or early cancer and appropriate follow-up

78 n rate of 100% (8/8) in detecting high-grade dysplasias and carcinomas over white-light detection alo

79 Mutational burden is higher in moderate dysplasias and invasive SCCs than in hyperplasias and mi

80 uently in human neoplasms, including myeloid dysplasias and leukemias, and less often in solid tumors

81 re occurrence of CRN (inclusive of low-grade dysplasia) and colectomy.

82 and without villous histology or high-grade dysplasia) and no neoplasia, respectively (log-rank P =

83 lenomegaly, thrombocytopenia, megakaryocytic dysplasia, and a propensity for chronic granulocytosis;

84 that include low-grade dysplasia, high-grade dysplasia, and adenocarcinomas.

85 alveolar spaces resembling bronchopulmonary dysplasia, and altered expression of genes associated wi

86 om patients with colitis, colitis-associated dysplasia, and CAC as well as in dysplastic tumors of C5

87 es at different disease stages, hyperplasia, dysplasia, and cancer, and their subsequent classificati

88 ontrols cellular dynamics and progression to dysplasia, and DSCs might contribute to cellular heterog

89 t in immunodeficiency, anhidrotic ectodermal dysplasia, and enamel defects.

90 jects (from eight families) with SPONASTRIME dysplasia, and four subjects (from three families) with

91 eristics (diameter, growth pattern, grade of dysplasia, and number of adenomas).

92 veins, acinar dysplasia, congenital alveolar dysplasia, and other unspecified primary pulmonary hypop

93 s were worse after neonatal bronchopulmonary dysplasia, and respiratory function differences were sim

94 essive inflammation, the presence of retinal dysplasia, and significant storage pathology in various

95 pression in VPGCs to result in inflammation, dysplasia, and tumor formation.

96 man ribosomopathy defined by a rare skeletal dysplasia, and we highlight the role of this ribosomal p

97 SSP without dysplasia, with any or low-grade dysplasia, and with high-grade dysplasia were 60.8 years

98 als and included hyperkeratoses, papillomas, dysplasias, and cancers.

99 MAS in a given individual, including fibrous dysplasia, are determined by the timing and location of

100 (DCM, 49%), arrhythmogenic right ventricular dysplasia (ARVD, 17%), postmyocarditis (14%), valvular h

101 inar tissue, and an increase in both ADM and dysplasia as disease progresses.

102 ing follow-up among HIV-positive MSM without dysplasia at baseline.

103 ing follow-up among HIV-positive MSM without dysplasia at baseline.

104 ndividuals with IM (including indefinite for dysplasia) at baseline, incidence rates per 100 person-y

105 reafter; and baseline diagnosis of low-grade dysplasia: at 1 and 3 years.

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

107 with an increased risk for bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) after pr

108 Preterm infants with bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) have acc

109 Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are

110 ey antecedent risk factors, bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP), wi

111 educes the rate of death or bronchopulmonary dysplasia (BPD) but may cause long-term adverse effects

112 is a known risk factor for bronchopulmonary dysplasia (BPD) in premature infants, a disease characte

113 Bronchopulmonary dysplasia (BPD) is a chronic disease of preterm babies w

114 Bronchopulmonary dysplasia (BPD) is a disease prevalent in preterm babies

115 Rationale: Bronchopulmonary dysplasia (BPD) is a leading complication of preterm bir

116 Bronchopulmonary dysplasia (BPD) remains a major respiratory illness in e

117 rongly associated with high bronchopulmonary dysplasia (BPD) risk in preterm infants.

118 e shown in a mouse model of bronchopulmonary dysplasia (BPD) that mesenchymal stem cells (MSC) protec

119 sted alveologenesis akin to bronchopulmonary dysplasia (BPD), a neonatal chronic lung disease.

120 a high risk for developing bronchopulmonary dysplasia (BPD), but its relationship with late respirat

121 s of prematurity, including bronchopulmonary dysplasia (BPD), cause mortality and morbidity later in

122 Rationale: Patients with bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH) h

123 Bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH) i

124 c lung disorders, including bronchopulmonary dysplasia (BPD).

125 th preterm birth, including bronchopulmonary dysplasia (BPD).

126 ng the most severe forms of bronchopulmonary dysplasia (BPD).

127 less than 5 years old with bronchopulmonary dysplasia (BPD).

128 pulmonary diseases (asthma; bronchopulmonary dysplasia (BPD); and chronic obstructive pulmonary disea

129 nic lung dysfunction termed bronchopulmonary dysplasia (BPD; also known as chronic lung disease).

130 disease of ECM remodeling (bronchopulmonary dysplasia [BPD]).

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

132 supplementation may prevent bronchopulmonary dysplasia, but evidence remains inconclusive.

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

134 e model of BE, we found that an HFD promoted dysplasia by altering the esophageal microenvironment an

135 signalling in chondrocytes leads to skeletal dysplasia by interfering with cellular bioenergetics and

136 The acceleration of dysplasia by the HFD in the L2-IL1B mice was associated

137 mTOR pathway genes, severe forms of cortical dysplasia can also result from activating mutations affe

138 neoplastic disease and those with high-grade dysplasia/cancer with 72.1% of cases correctly classifie

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

140 High-risk disease was defined as high-grade dysplasia/carcinoma.

141 te HIF-1alpha signalling results in skeletal dysplasia caused by collagen overmodification, an effect

142 morphisms, developmental delay, and skeletal dysplasia caused by pathogenic variants in XYLT1.

143 four unrelated individuals with a rare bone dysplasia causing severe short stature.

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

145 ormation, which could result in the skeletal dysplasia characteristic of HGPS.

146 RIME dysplasia is a rare, recessive skeletal dysplasia characterized by short stature, facial dysmorp

147 n autosomal-recessive spondyloepimetaphyseal dysplasia characterized by spine (spondylar) abnormaliti

148 Premature infants with bronchopulmonary dysplasia, characterized by interrupted postnatal alveol

149 Evidence for any dysplasia, colon segment resection, aneuploidy, male sex

150 ainst HPV have a lower incidence of cervical dysplasia compared to unvaccinated women.

151 s, they had brain malformations and skeletal dysplasia compatible to dysosteosclerosis (DOS) or Pyle

152 ic index of the severity of bronchopulmonary dysplasia.Conclusions: Most infants with bronchopulmonar

153 misalignment of the pulmonary veins, acinar dysplasia, congenital alveolar dysplasia, and other unsp

154 from the metaplastic cell line CP-A towards dysplasia (CP-B) and EAC (OE33 and OE19), confirmed by a

155 helium (EPC-1, EPC-2), metaplasia (CP-A) and dysplasia (CP-B) to esophageal adenocarcinoma (EAC) cell

156 sia as part of the hypoparathyroidism, renal dysplasia, deafness (HDR) syndrome that includes mesangi

157 eletions of SIX2 associated with frontonasal dysplasia defects.

158 n in pathways associated with human skeletal dysplasias facilitates ecologically important variation

159 s sclerosis complex (TSC) and focal cortical dysplasia (FCD) are epileptogenic cortical malformations

160 s sclerosis complex (TSC) and focal cortical dysplasia (FCD) are focal malformations of cortical deve

161 developmental disorder, human focal cortical dysplasia (FCD), focusing on chloride regulation driving

162 g as a major cause of type II focal cortical dysplasia (FCD), hemimegalencephaly (HME) and tuberous s

163 Feline hip dysplasia (FHD) is a debilitating condition affecting th

164 vascular anomalies, especially fibromuscular dysplasia (FMD) and a low prevalence of coincidental cas

165 d not significantly improve bronchopulmonary dysplasia-free survival at 36 weeks' postmenstrual age c

166 The primary outcome was bronchopulmonary dysplasia-free survival in infants at 36 weeks' postmens

167 nced histologic features (cancer, high-grade dysplasia, >=25% villous features), 3 or more diminutive

168 anogenital cancer or treatment for cervical dysplasia, had no hysterectomy, and were not pregnancy a

169 enetic syndromes featuring CP and ectodermal dysplasia have been linked to mutations in genes regulat

170 clusions: Most infants with bronchopulmonary dysplasia have impaired oxygenation quantified by a simp

171 Individuals with dysplasia have no prior experience acting with hands, al

172 of acinar dysplasia and congenital alveolar dysplasia have remained poorly understood.

173 ausative genetic alterations for SPONASTRIME dysplasia have yet been determined.

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

175 t colonic adenoma associated with high-grade dysplasia (HGD) colon polyps at baseline colonoscopy rem

176 , 95%CI 1.34-15.26; P = 0.02) and high-grade dysplasia (HGD) in the original resection (HR 3.60, 95%C

177 s at high risk for progression to high-grade dysplasia (HGD) or EAC are needed to improve outcomes an

178 ples collected from patients with high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC), from

179 R) and ablation for patients with high-grade dysplasia (HGD) or intramucosal adenocarcinoma (IMC) is

180 low-grade dysplasia (LGD) through high-grade dysplasia (HGD) to invasive cancer.

181 ed treatment for BE patients with high-grade dysplasia (HGD).

182 de of gastric lesions that include low-grade dysplasia, high-grade dysplasia, and adenocarcinomas.

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

184 c cortices presenting type II focal cortical dysplasia (IIa and b), hippocampi with or without hippoc

185 s a 2-pronged strategy to reduce the risk of dysplasia in colitis patients.

186 ts with Dup22q11.2, optic nerve coloboma and dysplasia in optic nerve.

187 simplification phenotype of bronchopulmonary dysplasia in premature human infants and suggest that st

188 in Dup22q11.2 syndrome, such as coloboma and dysplasia in the optic nerve, are reported here, contrib

189 g correlated with known locations of fibrous dysplasia in the periphery of individuals with MAS; no u

190 f advanced adenomas, diagnosis of high-grade dysplasia in the rectum or pouch, or progression of duod

191 nvolved in the initiation and progression of dysplasia in the serrated pathway are documented.

192 ve advantage and promotes the development of dysplasia in the setting of dietary carcinogens.

193 increased cAMP activity in areas of fibrous dysplasia in vivo.

194 l-based HPV immunization program on cervical dysplasia in women in British Columbia, Canada.

195 . decreased as severity of bronchopulmonary dysplasia increased.

196 based on adenoma size >=20 mm or high-grade dysplasia (instead of the current high-risk classificati

197 the mouse epidermis induces hyperplasia and dysplasia, involving high proliferation rates of keratin

198 Rationale: Bronchopulmonary dysplasia is a heterogeneous lung disease characterized

199 SPONASTRIME dysplasia is a rare, recessive skeletal dysplasia charac

200 SPONASTRIME dysplasia is an autosomal-recessive spondyloepimetaphyse

201 Dysplasia is considered a key transition state between p

202 mon lesions that may progress from low-grade dysplasia (LGD) through high-grade dysplasia (HGD) to in

203 hate deposition disease or craniometaphyseal dysplasia linked mutations: P5L, E490del and S375del, G3

204 le combinations of lymphedema, chorioretinal dysplasia, microcephaly and/or mental retardation.

205 and INS-GAS (Nod1-/-) mice developed gastric dysplasia more frequently compared with Nod1(+/+) mice.

206 nts suffering from nonsyndromic mitral valve dysplasia (MVD).

207 interstitial neonatal lung disorders: acinar dysplasia (n = 14), congenital alveolar dysplasia (n = 2

208 inar dysplasia (n = 14), congenital alveolar dysplasia (n = 2), and other lethal lung hypoplasias (n

209 ; and refractory cytopenia with multilineage dysplasia, n = 1).

210 -grade glioma, 3 cavernoma, 4 focal cortical dysplasia; NEL_INST: 11 patients, 33 lesions, all brain

211 current oxygen therapy: no bronchopulmonary dysplasia, no support (n = 773); grade 1, nasal cannula

212 92 (4.1%) vs 28/518 (5.4%); bronchopulmonary dysplasia occurred in 130/458 (28.4%) vs 126/485 (26.0%)

213 Bronchopulmonary dysplasia occurred in 41.7% of surviving infants in the

214 Dysplasia of corpus callosum with focal thinning of the

215 opoietic stem cell diseases characterized by dysplasia of one or more hematologic lineages and a high

216 Subjects with developmental dysplasia of the hip (DDH) often show early-onset osteoa

217 Tissues from dysplasias of L2-IL1B mice fed the HFD contained increas

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

219 ed to 16s sequencing data from patients with dysplasia or BE.

220 se who develop colitis-associated colorectal dysplasia or cancer, still require restorative proctocol

221 ) and no history of advanced CRN (high-grade dysplasia or colorectal cancer) or colectomy.

222 tissues from 164 patients, with and without dysplasia or EAC, enrolled in a multicenter study.

223 of lesions suspected of harboring high-grade dysplasia or early adenocarcinoma, a novel grasp and sna

224 n the treatment of patients with BE who have dysplasia or early EAC, from surgical resection to endos

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

226 in predicting advanced neoplasia [high grade dysplasia or invasive carcinoma (HGD/IC)] was determined

227 epithelium demonstrate intestinal metaplasia/dysplasia or subsquamous intestinal metaplasia, a repeat

228 (eg, only participants with bronchopulmonary dysplasia) or in which few participants were born very p

229 (eg, multicystic dysplastic kidney or cystic dysplasia), or manifest as bilateral cystic disease (eg,

230 noma with villous growth pattern, high-grade dysplasia, or >=10 mm in diameter).

231 development of pancreatic cancer, high-grade dysplasia, or clinically worrisome features, adjusting f

232 denomas with villous histology or high-grade dysplasia, or colorectal cancer [CRC]) and assessed whet

233 anced colorectal neoplasia (aCRN, high-grade dysplasia, or CRC) in patients with IBD.

234 necrotizing enterocolitis, bronchopulmonary dysplasia, or death or in the frequency of serious adver

235 e those with invasive carcinomas, high-grade dysplasia, or intestinal-type intraductal papillary muci

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

237 e incidence of pancreatic cancer, high-grade dysplasia, or worrisome features on pancreatic imaging w

238 causes of rare diseases, such as ectodermal dysplasias, orofacial clefts, and other craniofacial and

239 sk of SCAD in individuals with fibromuscular dysplasia (P = 0.021, OR = 1.82 [95% CI: 1.09-3.02]) and

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

241 rway samples and blood from bronchopulmonary dysplasia patients, the innate immune responses in this

242 p.W764*) presented a hypohidrotic ectodermal dysplasia phenotype.

243 ses, and they lead to a spectrum of skeletal dysplasia phenotypes with numerous extra-skeletal manife

244 re linked with Progressive Pseudo Rheumatoid Dysplasia (PPRD) a debilitating musculoskeletal disorder

245 (n = 29/338) had some degree of cytological dysplasia, primarily in the ascending colon (n = 6/42, 1

246 r phenotypic heterogeneity and mechanisms of dysplasia progression have not been elucidated.

247 ined functional roles for Kras activation in dysplasia progression using Selumetinib, a MEK inhibitor

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

249 ent diagnostic criteria for bronchopulmonary dysplasia rely heavily on the level and duration of oxyg

250 bral cavernous malformation, a neurovascular dysplasia resulting in dilated, thin-walled vessels that

251 ncluded a severe form of spondylo-epiphyseal dysplasia, sensorineural hearing loss, intellectual disa

252 reduced adduct formation, tumorigenesis, and dysplasia severity.

253 ] 2.07; 95% CI 1.40-2.93) or with high-grade dysplasia (SIR 0.79; 95% CI 0.39-1.41), whereas for indi

254 ons in DDR2 develop spondylo-meta-epiphyseal dysplasia (SMED), a rare, autosomal recessive disorder c

255 cause severe diseases, including campomelic dysplasia (SOX9), sex determination disorders (SOX8 and

256 ified as strong while evidence for low-grade dysplasia, strictures, primary sclerosing cholangitis, p

257 ic ameloblast-associated protein) and dentin dysplasia targets (Dentin matrix acidic phosphoprotein 1

258 ad fewer progenitor cells and developed less dysplasia than in L2-IL1 mice raised under standard cond

259 clusions: The definition of bronchopulmonary dysplasia that best predicted early childhood morbidity

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

261 ted to GPC6, which is associated with a bone dysplasia that has a phenotypic overlap with Keipert syn

262 ied, revised definitions of bronchopulmonary dysplasia that variably define disease severity accordin

263 heterogeneity may be a feature of those mild dysplasias that are likely to progress to more aggressiv

264 lformations (CCMs) are common brain vascular dysplasias that are prone to acute and chronic hemorrhag

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

266 pe was classified as a 'Schneckenbecken-like dysplasia.' The effect of the missense change was assess

267 m 10% among infants without bronchopulmonary dysplasia to 77% among those with grade 3 disease.

268 ences each stage in cancer development, from dysplasia to full-blown metastatic disease.

269 rm infants with and without bronchopulmonary dysplasia to grade disease severity and to identify dete

270 oplasia includes a spectrum of diseases from dysplasia to invasive squamous cell carcinoma (SCC) of t

271 erative for early detection and treatment of dysplasia to prevent further progression to invasive EAC

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

273 s were seen for patients with focal cortical dysplasia type I or mild malformation of cortical develo

274 m cellular atypia through various degrees of dysplasia, ultimately leading to invasive HNSCC, most pa

275 The primary outcome was the degree of dysplasia using the Graf alpha-angle at 6 months of age.

276 tumor number, burden, and risk of high-grade dysplasia vs. WT mice.

277 The range for proportions of SSPs with dysplasia was 3.7%-42.9% across studies, possibly reflec

278 Low-grade dysplasia was a risk factor for progression but various

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

280 or low-grade dysplasia, and with high-grade dysplasia were 60.8 years, 65.6 years, and 70.2 years, r

281 is, systemic infections and bronchopulmonary dysplasia were associated with altered metabolite concen

282 adenomas >=20 mm in diameter and high-grade dysplasia were associated with increased risk of colorec

283 expansion of peribiliary glands (PBGs), and dysplasia were observed in PSC.

284 eathing infants with severe bronchopulmonary dysplasia were reconstructed into end-inspiration and en

285 proliferation, and prostate hyperplasia and dysplasia, whereas Nkx3.1(S186A/-) mouse prostates had i

286 Moreover, our tool distinguishes ADM from dysplasia, which are not reliably distinguished with imm

287 included age, caffeine intake, and low-grade dysplasia while colonic adenomas trended towards signifi

288 le born without upper limbs-individuals with dysplasia-who use the feet to act, as they and typically

289 n humans: lipodystrophy, spondylometaphyseal dysplasia with cone-rod dystrophy (SMD-CRD), and isolate

290 pe of acinar-to-ductal metaplasia (ADM), and dysplasia with Dice coefficients of 0.79, 0.70, and 0.79

291 lasia (CHH), an autosomal recessive skeletal dysplasia with growth failure, immunodeficiency, and a h

292 disorders are characterized by hematopoietic dysplasia with increased proliferation of monocytes, neu

293 Rationale: Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV)

294 c studies in infants with alveolar capillary dysplasia with misalignment of the pulmonary veins have

295 y, they have been termed: alveolar capillary dysplasia with misalignment of the pulmonary veins, acin

296 e of varied severity and spondylometaphyseal dysplasia with or without immunologic and hematologic ab

297 The mean ages for detection of SSP without dysplasia, with any or low-grade dysplasia, and with hig

298 r risk focuses upon histologic assessment of dysplasia within endoscopic biopsies.

299 ions of mRNAs between areas with and without dysplasia within the same SSA polyps.

300 me measure for infants with bronchopulmonary dysplasia would facilitate clinical benchmarking and enh