ライフサイエンスコーパス: palate

1 and knockout animals develop an overt cleft palate.

2 ations in the occiput, jaw articulation, and palate.

3 levation delay and clefting of the secondary palate.

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

5 us membrane, the retromolar triangle and the palate.

6 growth resulted in clefting of the secondary palate.

7 osynostosis, mandibular hypoplasia and cleft palate.

8 asal symmetry in patients with cleft lip and palate.

9 te development and the pathogenesis of cleft palate.

10 reatment trajectories, such as cleft lip and palate.

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

12 e palatal mesenchyme, exhibit isolated cleft palate.

13 abnormal oral epithelial adhesions and cleft palate.

14 and these patients often have cleft lip and palate.

15 tered jaw skeletal differentiation and cleft palate.

16 abnormal palate rugae but did not show cleft palate.

17 hich resulted in an absence of the secondary palate.

18 ry acquisition of the mandible and secondary palate.

19 null mice both have clefts of the secondary palate.

20 have fully penetrant bilateral cleft lip and palate.

21 for fusion to occur to establish the primary palate.

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

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

24 ular keratinocyte differentiation, and cleft palate.

25 lformations such as dental defects and cleft palate.

26 tterning, hydrocephalus incidence, and cleft palate.

27 aniofacial defects including cleft secondary palate.

28 ically for nonsyndromic cleft lip with cleft palate.

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

30 ial anomalies such as micrognathia and cleft palate.

31 various skeletal deformities including cleft palate.

32 abnormalities, dysmorphic features and cleft palate.

33 tion delay with incompletely penetrant cleft palate.

34 mineralization of the bones of the secondary palate.

35 ute myeloid leukaemia and development of the palate.

36 esulted in undersized bones of the secondary palate.

37 ns affecting the upper lip and hard and soft palate.

38 5 mm deep, were created on both sides of the palate.

39 rs to differentiate into muscles in the soft palate.

40 ital diseases such as spina bifida and cleft palate.

41 al rugae and palatal epithelium in the fused palate.

42 poplasia, cardiovascular anomalies and cleft palates.

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

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

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

46 a, with a short posterior border of the soft palate, abnormal tonsillar pillars, and velopharyngeal i

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

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

49 iations in this gene underlie not only cleft palate and BCD but may be expanded to a broader velocard

50 implicated in human diseases including cleft palate and blepharocheilodontic (BCD) syndrome albeit on

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

52 nd deletion of Rbfox2 in NCCs leads to cleft palate and defects in craniofacial bone development.

53 the oral bacterial microbiota of the tongue, palate and denture-fitting surface was characterised usi

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

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

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

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

58 th craniofacial dysmorphisms including cleft palate and hypodontia, as well as congenital cardiac ano

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

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

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

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

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

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

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

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

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

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

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

70 Seven patients presented a cleft palate and two also had an omphalocele, reproducing the

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

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

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

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

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

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

77 Foxf 2 is expressed in the posterior mouse palate, and knockout animals develop an overt cleft pala

78 Nonsyndromic clefts of the lip and palate are common birth defects resulting from gene-gene

79 In humans, ankyloglossia and cleft palate are common congenital craniofacial anomalies, and

80 nsformations of the adductor musculature and palate-are thought to have permitted greater mobility of

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

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

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

84 rticipating in fusion of the lip and primary palate, as well as formation of the nasolacrimal groove,

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

86 Has2(f/f);Osr2-Cre mutant mice exhibit cleft palate at complete penetrance, the Has2(f/f); Wnt1-Cre f

87 ficant differences in the perception of wine palate attributes were observed, with dealcoholized wine

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 etiology of cleft lip and clefts of the hard palate, but study of the underlying etiology of soft pal

92 al cells underlies formation of the face and palate, but the basic molecular events mediating this cr

93 xpression of BMP2 and FGF9 in cultured human palate cells and Fgf9 and Pdgfra in cultured mouse palat

94 cells and Fgf9 and Pdgfra in cultured mouse palate cells.

95 CP, was investigated in both human and mouse palate cells.

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

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

98 ate only (CPO) and cleft lip with or without palate (CL/P) with ~17 million markers in sub-Saharan Af

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

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

101 l clefts and with syndromic cleft lip and/or palate (CL/P).

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

103 1, and Tbx22, have been associated with soft palate clefting in humans and mice, suggesting that they

104 Soft palate clefting leads to muscle misorientation and oroph

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

106 but study of the underlying etiology of soft palate clefts is an emerging field.

107 ng molecular and cellular mechanisms of soft palate clefts.

108 s of either induces a low penetrance of mild palate closure defects, while loss of both causes severe

109 cell biological pathways that contribute to palate closure.

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Cleft palate (CP) is one of the most common craniofacial birth

124 Cleft palate (CP) is the second most common congenital birth d

125 Cleft palate (CP), one of the most common congenital condition

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

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

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

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

130 nce of distinguishing specific types of soft palate defects in patients and developing relevant anima

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

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

133 s and spleen, as well as atretic trachea and palate defects were observed in the homozygous mutant em

134 of Kabuki Syndrome, including microcephaly, palate defects, abnormal ear development, and cardiac de

135 These mutants developed median cleft lip and palate demonstrating a previously undocumented cell auto

136 hways that are essential for normal face and palate development - the disruption of which leads to or

137 Irf6 and Esrp1 are important for palate development across vertebrates.

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

139 ular processes supports their involvement in palate development and the pathogenesis of cleft palate.

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

141 nal target genes mediating Foxf2 function in palate development in mice.

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

143 Secondary palate development is a complex, multistep process that

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

145 lar signaling pathways at critical phases of palate development is necessary to pioneer novel prenata

146 evidence for a requirement of hyaluronan in palate development is still lacking.

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

148 Recent advances in the understanding of soft palate development suggest that it may be regulated by d

149 3 plays a critical role in regulating murine palate development, and Tgf-beta3 null mutants develop c

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

151 play important regulatory roles during soft palate development.

152 standing of the regulatory mechanism of soft palate development.

153 tanding of the molecular network controlling palate development.

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

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

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

157 upported a crucial requirement for Golgb1 in palate development.

158 ell proliferation and thereby promote normal palate development.

159 lecular genetic pathway downstream of Lhx in palate development.

160 nvestigate the regulatory mechanisms of soft palate development.

161 tinct pathways from those implicated in hard palate development.

162 e identified a novel mouse mutant (cleft lip/palate, edema and exencephaly; Clpex) with a hypo-morphi

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

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

165 GT/DeltaC510 compound heterozygotes showed a palate elevation delay with incompletely penetrant cleft

166 Together, our data indicate that palate elevation is sensitive to deficiency of SPECC1L d

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

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

169 located in taste buds across the tongue and palate epithelium.

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

171 ae (transverse ridges) in the mammalian oral palate, focusing on multiple previously implicated pathw

172 The mammalian lip and primary palate form when coordinated growth and morphogenesis br

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

174 from partial reduction of ADAMTS9 and cleft palate from loss of ADAMTS20 and partially reduced ADAMT

175 Significant correlations were found between palate fullness and macromolecular fractions and beer co

176 Palate fullness and mouthfeel of beer are key attributes

177 s fractions influence sensory perceptions of palate fullness and mouthfeel.

178 be used as a guideline by brewers to control palate fullness and mouthfeel.

179 tered into groups differing significantly in palate fullness intensity and macromolecular distributio

180 are regression (PLS) analysis to predict the palate fullness intensity in beers (R(2)(C) = 0.7993).

181 uating analytical data of beer compositions, palate fullness, and mouthfeel descriptors.

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

183 , and is likely to have an important role in palate fusion.

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

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

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

187 scles compresses the tongue between the hard palate, hyoid and mouth floor, squeezing the midline ton

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

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

190 anisms leading to cleft lip as well as cleft palate in both existing and new Esrp1 mutant mouse model

191 mutations in FOXF2 are associated with cleft palate in humans and mice and that Foxf2 acts in a Shh-F

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

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

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

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

196 es previously implicated in cleft lip and/or palate, including components of multiple signaling pathw

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

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

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

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

201 Cleft palate is a common birth defect in humans.

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

203 Cleft palate is a common major birth defect resulting from dis

204 Cleft palate is among the most common structural birth defects

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

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

207 Clefting of the secondary palate is one of the most common congenital anomalies, a

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

209 Gad1-/- mice die neonatally of severe cleft palate, it has not been possible to determine any potent

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

211 mental and epileptic encephalopathies, cleft palate, joint contractures and/or omphalocele.

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

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

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

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

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

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

218 TX mutation, including fully penetrant cleft palate, mandible hypoplasia and deficits in cranial base

219 lts in micrognathia, glossoptosis, and cleft palate, mimicking the phenotype of Pierre Robin sequence

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

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

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

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

224 During palate morphogenesis, defective cranial neural crest cel

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

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

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

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 with or without cleft palate (NSCL/P) is a common birth defect with a complex

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

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

234 nonsyndromic 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 ip only (NSCLO), nonsyndromic cleft lip with palate (NSCLP), and nonsyndromic cleft palate only (NSCP

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

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

241 olyacrylamide gel was injected into the soft palate of the rabbits to induce OSAHS.

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

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

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

245 d genome-wide association analyses for cleft palate only (CPO) and cleft lip with or without palate (

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

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

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

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

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

251 with palate (NSCLP), and nonsyndromic cleft palate only (NSCPO).

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

253 ther anterior-, lateral-, superficial-, deep-palate or the maxillary tuberosity) can affect the graft

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

255 15 cleft lip and palate organisations totalled 26% of both revenue and ex

256 xpression of SULT2A1 in mesenchymal cells in palate, palatal rugae and palatal epithelium in the fuse

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

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

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

260 XF2 function, which may account for the rare palate phenotype observed.

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

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

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

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

265 taC510/DeltaC510 homozygotes showed abnormal palate rugae but did not show cleft palate.

266 e nectin-afadin axis is essential for proper palate shelf elevation and fusion.

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

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

269 s Media with Effusion in Children with Cleft Palate study scoring system; risk of bias and study qual

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

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

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

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

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

275 izures, dysmorphic facial features and cleft palate through an unknown mechanism.

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

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

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

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

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

281 rgeries that individuals with isolated cleft palate undergo are associated with major costs and morbi

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

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

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

285 Every hemi-palate was assigned to receive the trap-door harvesting

286 nvolvement of the buccal mucosa, tongue, and palate was more common in this group than in the group w

287 Cleft palate was observed in both conditional knockout and ove

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

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

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

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

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

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

294 ol levels exhibit increased 'hotness' on the palate, which is generally considered to negatively impa

295 tic underpinnings of ankyloglossia and cleft palate will be an important step toward rational treatme

296 This resulted in ankyloglossia and cleft palate with 100% penetrance in embryos examined after em

297 nt, and Tgf-beta3 null mutants develop cleft palate with 100% penetrance.

298 vested from the maxillary tuberosity or from palate with different approaches that can have an impact

299 andible size and about 50% of them had cleft palate with disruption of palatal shelf elevation.

300 rs is large, suggesting they possess a broad palate with respect to sensing.