ライフサイエンスコーパス: palate

1 null mice both have clefts of the secondary palate.

2 for fusion to occur to establish the primary palate.

3 latory protein (Esrp1) develop cleft lip and palate.

4 s is conserved in ferret, pig and human soft palate.

5 ular keratinocyte differentiation, and cleft palate.

6 lformations such as dental defects and cleft palate.

7 tterning, hydrocephalus incidence, and cleft palate.

8 syndrome, 2 syndromic forms of cleft lip and palate.

9 aniofacial defects including cleft secondary palate.

10 us membrane, the retromolar triangle and the palate.

11 on and non-surgical correction of cleft soft palate.

12 most common syndromic form of cleft lip and palate.

13 ratory failure, neonatal lethality and cleft palate.

14 ssively enlarging ulcerated mass on the hard palate.

15 rmal oral periderm and 17% developed a cleft palate.

16 ssue interactions, resulting in a cleft soft palate.

17 sis and bilateral cleft of the soft and hard palate.

18 growth resulted in clefting of the secondary palate.

19 ly affects the physiological function of the palate.

20 models exhibit an isolated cleft in the soft palate.

21 ppropriate than tissue transplanted from the palate.

22 that of Tgfbr2 mutant mice, as well as cleft palate.

23 osynostosis, mandibular hypoplasia and cleft palate.

24 a median cleft in the upper lip and primary palate.

25 a median cleft in the upper lip and primary palate.

26 he regularly spaced transverse ridges of the palate.

27 asal symmetry in patients with cleft lip and palate.

28 reatment trajectories, such as cleft lip and palate.

29 se at the midline, forming the hard and soft palate.

30 e palatal mesenchyme, exhibit isolated cleft palate.

31 abnormal oral epithelial adhesions and cleft palate.

32 and these patients often have cleft lip and palate.

33 hich resulted in an absence of the secondary palate.

34 ry acquisition of the mandible and secondary palate.

35 poplasia, cardiovascular anomalies and cleft palates.

36 ation defect in both Tgfbr2 and Smad4 mutant palates.

37 re; Tgfbr2(fl/fl) and Osr2-Cre; Smad4(fl/fl) palates.

38 s (0.6%), hydrocephalus (0.6%), cleft lip or palate (0%), and obstetric fistula (0%).

39 of any of these processes could cause cleft palate, a common birth defect that significantly affects

40 Among these is high arched palate, a condition that affects speech and quality of l

41 e virus, we demonstrate that the ferret soft palate, a tissue not normally sampled in animal models o

42 ed all cells (up to approximately 20,000 per palate), allowing the quantification of cell shape and p

43 row nasal bridge, a tented upper lip, a high palate, an open mouth, tightly adherent skin, an aged ap

44 having exencephaly, pericardial edema, cleft palate and abnormal limb development, phenotypes not obs

45 that loss of Dlx5 leads to a shortened soft palate and an absence of the levator veli palatini, pala

46 mal-dominant disorder characterized by cleft palate and congenital contractures of the hands and feet

47 ses of developmental disorders such as cleft palate and congenital heart disease.

48 ies, including microcephaly, cleft secondary palate and dental hypoplasia.

49 osome Xq22.1 associates with epilepsy, cleft palate and developmental defects in heterozygous female

50 cle-associated epithelium of the dorsal soft palate and dorsal nasopharynx in persistently infected c

51 E. coli's hardiness, versatility, broad palate and ease of handling have made it the most intens

52 However, despite of formation of cleft palate and ectopic cartilage, forced expression of a con

53 exposure to inhaled beta2-agonists for cleft palate and gastroschisis and found a potential new signa

54 formed on a subject with micrognathia, cleft palate and hypotonia that harbored a de novo, balanced c

55 f multiple genes genetically linked to cleft palate and identify AP-2alpha (TFAP2A) as a co-regulator

56 were harvested in the anterior and posterior palate and in areas close to (marginal) and distant from

57 naling and osteoblast differentiation in the palate and increased osteogenesis in FGF mutants, indica

58 with different malformations, such as cleft palate and limb deformation, resembling the human congen

59 that mutations in IRF6 lead to cleft lip and palate and mandibular abnormalities.

60 Vax1 is not expressed in the developing palate and mutant palatal shelves elevate above the tong

61 to PNH associated with toe syndactyly, cleft palate and neurodevelopmental delay.

62 y phenotypes, including cystic kidney, cleft palate and polydactyly.

63 n the base of oral cavity as compared to the palate and posterior tongue.

64 al defects including bilateral cleft lip and palate and tongue agenesis, following the loss of the pr

65 ttal view which can be used to differentiate palate and tongue obstructions, and this can be helpful

66 Clefts of the palate and/or lip are among the most common human cranio

67 ar defects were also found, along with cleft palates and ectopically located thymi, in Wnt1-Cre alpha

68 ia, temporomandibular joint ankylosis, cleft palate, and a characteristic "question-mark" ear malform

69 defects, excencephaly, hyperterlorism, cleft palate, and a striking loss of many NC and paraxial meso

70 pigmentation, blue pigmentation on the hard palate, and black pigment deposits on the conjuctivae.

71 trimester, mothers of limb deficiency, cleft palate, and cleft lip cases were, respectively, 1.8 (95%

72 es, hypospadias, hydrocephalus, cleft lip or palate, and club foot.

73 estes, hypospadias, hydrocephalus, cleft lip/palate, and clubfoot) was determined by physical examina

74 n between the nasal septum and the secondary palate, and higher levels of phosphorylated SMAD1 and SM

75 apular descending eruption, petechiae on the palate, and hyperemic sclerae in a 44-year-old man retur

76 anal atresia, hearing loss, cleft lip and/or palate, and other craniofacial dysmorphisms.

77 such as throat, tonsils, tongue dorsum, hard palate, and saliva.

78 re seen in children with microcephaly, cleft palate, and selected eye, cardiac, and renal defects.

79 including anophthalmia, microcephaly, cleft palates, and mandibular malformations.

80 egregating with deafness and with dental and palate anomalies to Xq24-27.

81 , coarctation of the aorta, cleft lip, cleft palate, anorectal atresia/stenosis, and limb reduction (

82 ified associations with cleft lip with cleft palate (aOR = 1.23) and anorectal atresia/stenosis (aOR

83 long nose, small mouth, micrognathia, cleft palate, arachnodactyly and intellectual disability.

84 s--affecting the eyes, face, jaw, tongue, or palate--are an under-recognised feature of patients with

85 late p57(Kip2) expression in the prospective palate area to allow adequate levels of cell proliferati

86 mutants that may be relevant to human cleft palate as well.

87 hypoplasia that leads to agnathia and cleft palate at birth.

88 rkers to stain oral epithelial sheets of the palate, base of oral cavity, and posterior tongue.

89 morphologies, such as clefts of the primary palate, because there appears to be little opportunity f

90 olydactyly, heart defects, hypomastia, cleft palate/bifid uvula, progressive scoliosis, and structura

91 he denture was observed by week 4 and on the palate by week 6 postinoculation.

92 e genes for genetic disorders (cleft lip and palate, certain forms of cancer) or solute uptake and ef

93 uld decrease cleft lip with or without cleft palate (CL +/- P) risk and that menstrual regulation sup

94 Cleft lip and/or palate (CL/P) are common structural birth defects in hum

95 ndromic (NS) cleft lip with or without cleft palate (CL/P) is a common disorder with a strong genetic

96 Cleft lip with or without cleft palate (CL/P) is one of the most common congenital malfo

97 the risk of cleft lip with or without cleft palate (CL/P) or cleft palate (CP).

98 on-syndromic cleft lip with or without cleft palate (CL/P), are among the most common birth defects i

99 commonly found in individuals with cleft lip/palate (CL/P), we used four large cohorts to evaluate if

100 cial clefting, including cleft lip and cleft palate (CL/P).

101 le underlying the international practice of 'palate cleansing'.

102 re to inhaled steroids were confirmed (cleft palate, cleft lip, anal atresia, and hypospadias).

103 niofacial defects, middle-ear defects, cleft palate, cleft lip, limb defects, limb-reduction defects,

104 are shown by the genetic rescue of secondary palate clefts in Pax9(-/-)Dkk1(f/+);Wnt1Cre embryos.

105 , Wnt3a and Wnt11; an increased frequency of palate closure defects is observed with Vangl2; and earl

106 he murine palatal shelves at E12.5, prior to palate closure.

107 cell biological pathways that contribute to palate closure.

108 Cleft lip with or without palate (CLP) and isolated cleft palate (CP) are common h

109 wider de novo deletions among cleft lip and palate (CLP) cases than seen among cleft palate (CP) and

110 Patients with cleft lip/palate (CLP) have been reported, in some studies, to exh

111 ommon diseases, isolated cleft lip and cleft palate (CLP), hypothyroidism and thyroid cancer all map

112 pina bifida, cleft lip with or without cleft palate (CLP), or cleft palate only.

113 Patients with cleft lip and/or palate (CLP), who undergo numerous medical interventions

114 yndromic and nonsyndromic forms of cleft lip/palate (CLP).

115 lated cleft lip only (CLO) and cleft lip and palate (CLP).

116 treatable conditions (breast mass, cleft lip/palate, club foot, hernia or hydrocele [adult and paedia

117 fective therapies for the treatment of cleft palate conditions and other single-gene disorders affect

118 and palate (CLP) cases than seen among cleft palate (CP) and cleft lip (CL) cases.

119 h or without palate (CLP) and isolated cleft palate (CP) are common human developmental malformations

120 Cleft palate (CP) is a common birth defect occurring in 1 in 2

121 IRF6 was also associated with cleft palate (CP) with impaction of permanent teeth (p<10(-6))

122 with or without cleft palate (CL/P) or cleft palate (CP).

123 rmal development (including cleft lip and/or palate, craniosynostosis and facial dysostoses), compris

124 t years, in vitro cell-based assays, ex vivo palate cultures, and genetically engineered animal model

125 s of relative tissue composition in the hard palate, DE-harvested CTG contains much larger amounts of

126 mental disorders with increased incidents of palate defects among the patients.

127 todysplasin (Eda) pathway, can resolve cleft palate defects in Pax9(-/-) embryos in utero.

128 enhancers near the genes implicated in human palate defects through functional assays.

129 a novel connection between the initiation of palate development and a cell cycle inhibitor via LHX.

130 nt signaling and its regulation in secondary palate development are not well understood.

131 shelf morphogenesis partly rescued secondary palate development in Pax9-deficient embryos.

132 critical regulator of upper lip and primary palate development in Xenopus laevis.

133 ore, understanding the molecular genetics of palate development is important from both scientific and

134 ells from embryonic mouse embryos at various palate development stages.

135 complex nature of the upper lip and primary palate development which will lead to important insights

136 tifying a large number of genes required for palate development, recent studies have begun to unravel

137 ell proliferation and thereby promote normal palate development.

138 lecular genetic pathway downstream of Lhx in palate development.

139 sms involving these transcription factors in palate development.

140 t it may be involved in key processes during palate development.

141 he mesenchyme-epithelium interactions during palate development.

142 anchial arch are integral to lip and primary palate development.

143 nowledge of the genetic control of secondary palate development.

144 hways, including BMP and Sema3 signaling, in palate development.

145 ole in Pax9-mediated regulation of secondary palate development.

146 the dynamic behavior of epithelia during lip/palate development.

147 upported a crucial requirement for Golgb1 in palate development.

148 c Fuz mutant mouse, we find that high arched palate does not, as commonly suggested, arise from midfa

149 brafish, untreated pdgfra mutants have cleft palate due to defective neural crest cell migration, whe

150 erozygosity for the deletion manifests cleft palate, early postnatal lethality, postnatal growth dela

151 ilure in midline fusion resulting in a cleft palate, ectopia cordis, and a large omphalocele.

152 dactyly, ectodermal dysplasia, and cleft lip/palate (EEC) syndrome is caused by single point mutation

153 dactyly, ectodermal dysplasia, and cleft lip/palate (EEC) syndrome patients with p63 mutations as an

154 ectodermal dysplasia-ectrodactyly-cleft lip/palate (EEC) syndrome, comprising SHFM.

155 ates that several gene combinations regulate palate elevation and extension during development.

156 ptured confocal stacks of entire fixed mouse palate epithelia throughout the mid-gestation growth per

157 by a subset of taste cells on the tongue and palate epithelium that respond to acids with trains of a

158 aste receptor cells (TRCs) on the tongue and palate epithelium.

159 n, and that wnt5b and wnt9a are required for palate extension in the anteroposterior and transverse a

160 in sustained colonization of the denture and palate for 8 weeks postinoculation.

161 The upper lip and primary palate form an essential separation between the brain, n

162 Recent data suggest that the risk of cleft palate formation after in-utero glucocorticoid exposure

163 aniofacial development with special focus on palate formation, using mouse embryos with a complete kn

164 rst trimester may increase the risk of cleft palate formation.

165 n TGFbeta signaling and IRF6 activity during palate formation.

166 anial neural crest cell proliferation during palate formation.

167 ne expression profiles of embryonic day 14.5 palates from Tgfbr2(fl/fl);Wnt1-Cre mice and previously

168 cell intercalation and cell extrusion during palate fusion and suggest a general mechanism for tissue

169 However, individuals with isolated cleft palate had increased health risks and mortality.

170 Although the embryology of the palate has long been studied, the past decade has brough

171 , and patients with the common cleft lip and palate have a higher prevalence of dental caries and gin

172 e fusion of tissues, often manifested in the palate, heart or neural tube.

173 Individuals with isolated cleft palate (ie, without cleft lip) had increased mortality (

174 he Golgb1 gene that co-segregated with cleft palate in a new mutant mouse line.

175 ng growth factor alpha (TGFA) gene and cleft palate in an Irish study.

176 1), and with SNP rs3923086 and cleft lip and palate in Asian populations (p = 0.004).

177 ein, SATB2, result in micrognathia and cleft palate in both humans and mice.

178 hway have been associated with cleft lip and palate in humans and mice, the mechanisms involving cano

179 have been linked to clefts of the lip and/or palate in humans, and ablation of PDGF-C in 129/Sv backg

180 craniofacial malformations, including cleft palate in mice (Tgfbr2(fl/fl);Wnt1-Cre mice).

181 st an indirect mechanism for secondary cleft palate in Nog mutants that may be relevant to human clef

182 Cleft palate in these mice was associated with delay/failure o

183 Development of the palate in vertebrates involves cranial neural crest migr

184 ies that can either prevent or correct cleft palates in humans.

185 ause craniofacial deformities, such as cleft palate, in mice.

186 ndividuals with isolated cleft lip and cleft palate, increased risks of intellectual disability (rela

187 is believed to be the initial report of hard-palate infection caused by Blastomyces dermatitidis.

188 e developmental disorder manifested by cleft palate, intellectual disability, and skeletal abnormalit

189 Development of the mammalian secondary palate involves highly dynamic morphogenetic processes,

190 Cleft palate is a common birth defect caused by disruption of

191 Cleft palate is a common birth defect in humans.

192 Cleft palate is a common major birth defect for which currentl

193 High arched palate is also a prevalent feature of fibroblast growth

194 tening of the snout and widening of the hard palate is common to brachycephalic dogs and is a welfare

195 of the genome play in the etiology of cleft palate is not well studied.

196 Cleft palate is one of the most common birth defects in humans

197 Cleft palate is one of the most common human birth defects and

198 Cleft lip with or without cleft palate is the most common congenital malformation of the

199 ociated with cognitive defects and cleft lip/palate, its role in mammalian development and physiology

200 by a winemaker's panel, to have an increased palate length and body.

201 derived from the 4th PA mesoderm in the soft palate, likely via interactions between CNC-derived and

202 rather than repression and formation of the palate, lip, and characteristic folds of the closed Anti

203 identified as genetic risk factors for cleft palate, little is known about the relationship between T

204 n normal airways, the secreted protein short palate lung and nasal epithelial clone 1 (SPLUNC1) effec

205 ly of innate immune genes, particularly with palate, lung and nasal epithelial clone (PLUNC) members

206 The short palate, lung and nasal epithelial clone 1 (SPLUNC1) prot

207 natural regulation of ENaC activity by short palate, lung, and nasal epithelial clone 1, known as SPL

208 clone 1 (SPLUNC1) protein is a member of the palate, lung, and nasal epithelium clone (PLUNC) family,

209 The short palate, lung, and nasal epithelium clone (SPLUNC)1 prote

210 The short palate, lung, nasal epithelium clone (PLUNC) 1 (SPLUNC1)

211 oband presented with bilateral cleft lip and palate, malformed auricles, and bilateral ectrodactyly o

212 Wnt1-Cre;Erk2(fl/fl) mice exhibited cleft palate, malformed tongue, micrognathia and mandibular as

213 capacity for bone formation in the expanded palate, more than 80% of the patient population experien

214 ), bypassing the role of the gene in lip and palate morphogenesis and thus ensuring survival to adult

215 This work presents a mechanistic analysis of palate morphogenesis in a clinically relevant context.

216 ist of canonical Wnt signaling, also rescued palate morphogenesis in Pax9-deficient mice.

217 ough a Pax9(Osr2KI) allele rescued posterior palate morphogenesis in the absence of Pax9 protein func

218 factors Wls, Gpc4 and Frzb in the context of palate morphogenesis in zebrafish.

219 During palate morphogenesis, defective cranial neural crest cel

220 ing in acting downstream of Pax9 to regulate palate morphogenesis.

221 e mutants also show complete secondary cleft palate, most likely due to inhibition of posterior palat

222 ing 14 specialties (ophthalmology, cleft lip/palate, multidisciplinary teams, orthopaedics, cardiac,

223 rgical specialties (ophthalmology, cleft lip/palate, multidisciplinary teams, orthopaedics, cardiac,

224 naling in the palatal epithelium led to soft palate muscle defects in Tgfbr2(fl/fl);K14-Cre mice.

225 (n = 6), scleral (n = 9), iris (n = 3), and palate (n = 1) melanocytosis.

226 a vestibuloplasty with either a FGG from the palate (n = 7) or the CM (n = 7).

227 an X-linked lethal disorder involving cleft palate, neonatal seizures, contractures, central nervous

228 on-syndromic cleft lip with or without cleft palate (NS CL/P).

229 Nonsyndromic cleft lip with/without cleft palate (nsCL/P) and nonsyndromic cleft palate only (nsCP

230 nonsyndromic cleft lip with or without cleft palate (NSCL/P) in populations of Asian and European anc

231 Nonsyndromic cleft lip and/or palate (NSCL/P) is a prevalent birth defect of complex e

232 Nonsyndromic cleft lip with or without cleft palate (nsCL/P) is among the most common human birth def

233 nonsyndromic cleft lip with or without cleft palate (NSCL/P).

234 on-syndromic cleft lip with or without cleft palate (NSCL/P).

235 Non-syndromic cleft lip and/or palate (NSCLP) is a common congenital malformation with

236 Nonsyndromic Cleft Lip and/or Palate (NSCLP) is regarded as a multifactorial condition

237 Non-syndromic cleft lip with palate (NSCLP) is the most serious sub-phenotype of non-

238 Clefting of the soft palate occurs as a congenital defect in humans and adver

239 (fl/fl);K14-Cre mice, although the secondary palate of Irf6(+/R84C) and Smad4(fl/fl);K14-Cre mice for

240 hibitor, was up-regulated in the prospective palate of Lhx6(-/-);Lhx8(-/-) mutants.

241 atenin signaling, is upregulated in the soft palate of Tgfbr2(fl/fl);K14-Cre mice, and WNT-beta-caten

242 tion and differentiation defects in the soft palate of Tgfbr2(fl/fl);K14-Cre mice.

243 isted of inserting a needle through the bony palate of the oral cavity.

244 cally, muscle mass was decreased in the soft palates of Tgfbr2 mutant mice, following defects in cell

245 expression of both cyclins D1 and D3 in the palates of Tgfbr2(fl/fl);Wnt1-Cre mice, consistent with

246 GFBR2 expression levels were elevated in the palates of these miR transgenic embryos at embryonic day

247 al fusion, failure of which results in cleft palate, one of the most common birth defects in humans.

248 Unfortunately, for patients with cleft palate-one of the most common of congenital birth defect

249 s known about the genetic etiology for cleft palate only (CPO).

250 cleft palate (nsCL/P) and nonsyndromic cleft palate only (nsCPO) are the most frequent subphenotypes

251 some loci with NSCL/P and nonsyndromic cleft palate only (NSCPO) in cohorts from Africa (Ghana, Ethio

252 Nonsyndromic cleft palate only (nsCPO) is a facial malformation that has a

253 table that is shared with nonsyndromic cleft palate only (nsCPO).

254 ina bifida, 277 with CLP, and 117 with cleft palate only in addition to 785 controls.

255 was observed for the fetal NOG1 SNP on cleft palate only, opposite in direction to the effect on CLO.

256 with or without cleft palate (CLP), or cleft palate only.

257 Cleft palate (OR, 1.63; 95% CI, 1.05-2.52) and gastroschisis (

258 hypospadias, cleft lip with or without cleft palate, or hydrocephalus.

259 15 cleft lip and palate organisations totalled 26% of both revenue and ex

260 We found that cleft palate pathogenesis in Pax9-deficient embryos is accompa

261 he motoneuronal cell groups innervating soft palate, pharynx, and larynx as well as diaphragm, interc

262 innervating the dilator muscles of the soft palate, pharynx, and larynx, but abnormal respiratory me

263 ax9(-/-) mouse model with a consistent cleft palate phenotype to test small-molecule Wnt agonist ther

264 nt1-Cre mice and previously identified cleft palate phenotypes in genetically engineered mouse models

265 of the CNC-derived mesenchyme in the lip and palate region in mice and is a strong candidate as an or

266 etiology of cleft lip with or without cleft palate, relatively little is known about the genetic eti

267 d cellular mechanism of clefting of the soft palate remains unclear because few animal models exhibit

268 Median CERs of cleft lip or palate repair ($47.74 per DALY), general surgery ($82.32

269 itarian surgical organisations provide cleft palate repair for patients without access to surgical ca

270 hypoplastic maxilla and mandible, and cleft palate resulting from a failure of palatal shelves to ap

271 ns: buccal mucosa, keratinized gingiva, hard palate; saliva, tongue, tonsils, throat; sub- and supra-

272 of 20p12 are variably associated with cleft palate, short stature, and developmental delay.

273 ompanied by intellectual disability, a cleft palate, short stature, and dysmorphic features.

274 he palatal mesenchyme, did not display cleft palate, suggesting that palatal clefting in Wnt1-Cre;Erk

275 ein (BMP) downstream targets in Smad4 mutant palates, suggesting that the reduction in cell prolifera

276 as ophthalmology (88, 28%) and cleft lip and palate surgery (70, 22%) were also frequently performed.

277 at ophthalmology, followed by cleft lip and palate surgery.

278 were more prevalent in cleft lip with cleft palate than other cleft types.

279 the development of therapies for human cleft palates that arise from single-gene disorders.

280 ects in the anterior and posterior secondary palate, these phenotypes were less severe than those see

281 date genes for nonsyndromic cleft lip and/or palate through genome-wide linkage analysis.

282 ontribution to nonsyndromic cleft lip and/or palate through the analysis of family pedigrees.

283 ng and proper muscle development in the soft palate through tissue-tissue interactions, resulting in

284 Histological analysis of palate tissue demonstrated progressively increasing infl

285 a consistent phenotype of a secondary cleft palate, to test a novel therapeutic.

286 quence and highlights the interconnection of palate, tongue and mandible development.

287 proteins were not expressed on MEE cells of palates treated with SB431542, an inhibitor of TGFbeta s

288 f anterior-posterior obstruction of the soft palate, uvular (94%) and velar (6%), and three types of

289 evelopment of the neural crest such as cleft palate, ventricular septal defect, abnormal development

290 The oronasal anatomy (premaxilla-palate-vomer architecture) is similar to other Australop

291 Cleft palate was observed in both conditional knockout and ove

292 The initial outgrowth of the palate was severely impaired in the mutant embryos, due

293 The presence of cleft palate was significantly associated with c.8057G>A (Fish

294 pharyngeal fat pads, lateral walls, and soft palate) was similar between subjects with OSAS and obese

295 ffected siblings with isolated cleft lip and palate, we discovered that they share a novel missense m

296 ients with complete unilateral cleft lip and palate were prospectively recruited.

297 stula presentation among three cohorts whose palates were repaired between April, 2005, and November,

298 tion and was remarkably enriched in the soft palate, where long-chain alpha2,6-linked sialic acids pr

299 kles, sorbets, wines, and teas 'cleanse' the palate while eating.

300 exhibit VSDs with ~50% penetrance and cleft palate with less than 10% penetrance; and Fz2(-/-);Fz7(-