ライフサイエンスコーパス: orofacial

1 Neither C3H/HeJ nor C3H/HeOuJ mice exhibited orofacial abscess development or infection dissemination

2 kout mice, which lack T and B cells, develop orofacial abscesses and disseminated infections followin

3 After 21 days, a high incidence (5/10) of orofacial abscesses was observed in SCID mice mono-infec

4 us on brainstem circuits that drive rhythmic orofacial actions.

5 t has made possible 3D and 4D examination of orofacial anatomy and function.

6 dorsal root ganglia (DRG) to cause recurrent orofacial and genital herpes, respectively.

7 ls affected by BBS due to abnormal embryonic orofacial and tooth development.

8 cient "asymptomatic" vaccine against ocular, orofacial, and genital herpes.

9 In addition to orofacial angio-oedema, painless swellings affect periph

10 rves collecting sensory information from the orofacial area synapse on second-order neurons in the do

11 l muscles during different types of rhythmic orofacial behavior in macaque monkeys, finding that the

12 emporal relationship between GC activity and orofacial behaviors by performing paired single-neuron a

13 mals perform a multitude of well-coordinated orofacial behaviors such as breathing, sniffing, chewing

14 l principles that have evolved to coordinate orofacial behaviors.

15 nsiently and purposely synchronize different orofacial behaviours.

16 one marrow (BMMSCs), mouse MSCs derived from orofacial bone have not been isolated due to technical d

17 They have been used for orofacial bone regeneration and autoimmune disease treat

18 Although human orofacial bone-marrow-derived mesenchymal stem cells sho

19 loped techniques to isolate and expand mouse orofacial bone/bone-marrow-derived MSCs (OMSCs) from man

20 Additional expressions of orofacial cancer pain include distant tumor effects, inv

21 As a presenting symptom of orofacial cancer, pain is often of low intensity and dia

22 mily; we propose to name this locus "OFC11" (orofacial cleft 11).

23 be born with a congenital heart defect or an orofacial cleft are reviewed in this paper.

24 iews with mothers of 731 (84.7% of eligible) orofacial cleft case infants and with mothers of 734 (78

25 we reanalyze data from a previously reported orofacial cleft study, to now investigate both fetal and

26 Orofacial cleft, low birth weight, preterm delivery, fet

27 aternal topical corticosteroid exposure with orofacial cleft, low birth weight, preterm delivery, fet

28 aternal topical corticosteroid exposure with orofacial cleft, preterm delivery, fetal death, low Apga

29 , can lead to nearly identical phenotypes of orofacial cleft.

30 devastating consequences resulting in severe orofacial clefting and extreme microphthalmia.

31 f multiple ectodermal appendages, as well as orofacial clefting and limb defects.

32 including SET and CCT3, for diseases such as orofacial clefting and micrognathia.

33 e dosage in humans may increase the risk for orofacial clefting and oligodontia.

34 t palate (CL/P) and 19 individuals with both orofacial clefting and tooth agenesis.

35 an der Woude syndrome, an autosomal dominant orofacial clefting disorder.

36 gion in mice and is a strong candidate as an orofacial clefting gene in humans.

37 get gene Msx1 in families with both forms of orofacial clefting has implicated Bmp signaling in both

38 This study offers evidence that the risk for orofacial clefting in infants may be influenced by mater

39 A common syndromic form of orofacial clefting is Van der Woude syndrome (VWS) where

40 c allele manifests an incompletely penetrant orofacial clefting phenotype.

41 RF6 and RTK signaling pathway genes in human orofacial clefting populations.

42 umans, mutations in IRF6 cause two mendelian orofacial clefting syndromes, and genetic variation in I

43 tested the hypothesis that individuals with orofacial clefting with or without tooth agenesis have M

44 oding mutations in MSX1 are not the cause of orofacial clefting with or without tooth agenesis in thi

45 ts of children with a specific birth defect, orofacial clefting, and discuss areas for future researc

46 1 has been considered a strong candidate for orofacial clefting, based on mouse expression studies an

47 al morphogenesis is disrupted, the result is orofacial clefting, including cleft lip and cleft palate

48 To dissect the function of Bmp signaling in orofacial clefting, we conditionally inactivated the typ

49 oss, intellectual disability, hematuria, and orofacial clefting.

50 d in ectodermal dysplasia, limb defects, and orofacial clefting.

51 and SPRY2, also contribute risk for isolated orofacial clefting.

52 is of both Mendelian and idiopathic forms of orofacial clefting.

53 hould be considered a candidate for isolated orofacial clefting.

54 ntiguous autosomal deletions associated with orofacial clefting.

55 success in defining the loci responsible for orofacial clefting.

56 variants identified to date for nonsyndromic orofacial clefting.

57 and GRHL3 also contribute risk for isolated orofacial clefting.

58 to understanding the phenotypic spectrum of orofacial clefting.

59 Orofacial clefts (cleft lip, cleft palate) are among the

60 most serious sub-phenotype of non-syndromic orofacial clefts (NSOFC), which are the most common cran

61 Orofacial clefts (OFCs) are congenital dysmorphologies o

62 Orofacial clefts (OFCs), which include non-syndromic cle

63 hat can be caused by maternal smoking (e.g., orofacial clefts and asthma) or adult smoking (e.g., cer

64 Nonsyndromic orofacial clefts are a common complex birth defect cause

65 Orofacial clefts are among the most common birth defects

66 Orofacial clefts are common birth defects with a known g

67 Orofacial clefts are congenital structural anomalies of

68 atogenic origins; the non-syndromic forms of orofacial clefts are more common and are likely due to s

69 Most orofacial clefts are nonsyndromic, isolated defects, whi

70 Nonsyndromic orofacial clefts are one of the most common birth defect

71 Orofacial clefts are well known for their complex etiolo

72 Orofacial clefts have been associated with maternal ciga

73 at increased risk of delivering infants with orofacial clefts have been mixed, and recently a gene-en

74 association studies (GWASs) for nonsyndromic orofacial clefts have identified multiple strongly assoc

75 review describes genes that are involved in orofacial clefts in humans and animal models and explore

76 The etiology of orofacial clefts is complex, including multiple genetic

77 e occurrence of congenital heart defects and orofacial clefts is reported, we will have additional su

78 he authors investigated whether the risks of orofacial clefts or conotruncal heart defects were influ

79 on plays a prominent role in the etiology of orofacial clefts, a frequent birth malformation.

80 tive system anomalies, 97.6% (95.9-98.6) for orofacial clefts, and 66.2% (61.5-70.5) for nervous syst

81 Dysregulation of palatogenesis results in orofacial clefts, which represent the most common struct

82 mportant insights into the etiology of human orofacial clefts.

83 abnormalities can result in various forms of orofacial clefts.

84 icillin in pregnancy was not associated with orofacial clefts.

85 rnal smoking is a recognized risk factor for orofacial clefts.

86 provide evidence that multivitamins prevent orofacial clefts.

87 e occurrence of congenital heart defects and orofacial clefts.

88 ractions that constitute the many factors of orofacial clefts.

89 an increased risk for having offspring with orofacial clefts.

90 sCPO) are the most frequent subphenotypes of orofacial clefts.

91 f known genetic alternations associated with orofacial clefts; so, it is not surprising that CL/P is

92 the prevention and management of dental and orofacial conditions as those processes emerge in people

93 he trigeminal transition zone in response to orofacial deep injury.

94 n zone plays an important role in processing orofacial deep input.

95 ar nucleus involved in central processing of orofacial deep noxious input.

96 totopically organized nociceptive responses, orofacial deep tissue injury also is coupled to somatovi

97 The Vi/Vc-RVM pathway is activated after orofacial deep tissue injury and plays a critical role i

98 gration and descending pain modulation after orofacial deep tissue injury.

99 geminal Vi/Vc transition zone in response to orofacial deep tissue injury.

100 mmation of the masseter muscle, an injury of orofacial deep tissue, results in a widespread change in

101 athways by directly comparing the effects of orofacial deep vs. cutaneous tissue inflammation on brai

102 ate that haploinsufficiency of IRF6 disrupts orofacial development and are consistent with dominant-n

103 Mutations in IRF6 disrupt orofacial development and cause cleft palate in humans.

104 or the spatial patterning of bone, cartilage orofacial development and, in mammals, teeth.

105 ical abnormalities were related to brain and orofacial development, consistent with the known roles o

106 ew their contribution to normal and abnormal orofacial development.

107 2, encode transcription factors critical for orofacial development.

108 romes, each affecting a protein critical for orofacial development.

109 al adhesions at a critical time point during orofacial development.

110 es the use of mouse models to study and cure orofacial diseases.

111 upregulation of neurotransmitters within the orofacial division of the trigeminal ganglia and in deve

112 athway distribution may correlate with acute orofacial dysfunction with spared pathways contributing

113 n being pyrexia (16 [16%] of 101 events) and orofacial dyskinesia (ten [10%]).

114 lycol(5)]-enkephalin (DAMGO) also stimulated orofacial dyskinesia when infused into the globus pallid

115 hin-1 in the globus pallidus of rats induced orofacial dyskinesia.

116 characterized by delayed onset of persistent orofacial dyskinesias in a sub-group of subjects chronic

117 exhibited limb and truncal stereotypies and orofacial dyskinesias upon weaning sedation.

118 l movements, including myoclonus, tongue and orofacial dyskinesias, and opsoclonus.

119 Identified FOXP2 mutations cause orofacial dyspraxia accompanied by abnormalities in cort

120 In addition, affected members have a severe orofacial dyspraxia, and their speech is largely incompr

121 use a severe form of language impairment and orofacial dyspraxia, while single-nucleotide polymorphis

122 ditioning and affective hedonic and aversive orofacial expressions of taste-elicited "liking" and "di

123 sal, as well as in nuclei that contribute to orofacial function and mastication, including the facial

124 most distressing symptom, leading to loss of orofacial function and poor quality of life.

125 aw time in a dolognawmeter indicates reduced orofacial function.

126 Mastication is one of the most important orofacial functions.

127 ly from a gingival inflammation to grotesque orofacial gangrene.

128 We present a case study of a paradigmatic orofacial "gesture," namely tongue protrusion and retrac

129 According to Keven & Akins (K&A), infant orofacial gestures may not reflect imitative responses.

130 dest and deepest understanding of dental and orofacial growth and development and the prevention and

131 ry and plays a critical role in facilitating orofacial hyperalgesia.

132 CCI-ION caused orofacial hypersensitivity that correlated with Cavalpha

133 e oligodeoxynucleotides led to a reversal of orofacial hypersensitivity, supporting an important role

134 m underlying trigeminal nerve injury-induced orofacial hypersensitivity, we used a rat model of chron

135 pelling alternative to the case for neonatal orofacial imitation, offered by Meltzoff and Moore.

136 steolytic gingival infection that results in orofacial implant failures.

137 Following orofacial infection, HSV establishes latency in innervat

138 are rapidly upregulated in TG neurons after orofacial inflammation and increase the capacity of TG n

139 Orofacial inflammation is associated with prostaglandin

140 g the turpentine-induced model of unilateral orofacial inflammation we also show that both the basal

141 Orofacial injury activates two distinct regions in the s

142 To understand the functional significance of orofacial injury-induced neuronal activation, this study

143 dalis (Vi/Vc) transition zone in response to orofacial injury.

144 ecifically related to the processing of deep orofacial input.

145 But sucrose taste fails to elicit higher orofacial "liking" reactions from mutant mice in an affe

146 , hydroxyapatite/tricalcium phosphate; OMSC, orofacial mesenchymal stem cell; OVX, ovariectomized.

147 The orofacial modules in lateral cortex resemble similar mod

148 or the imaging and reconstruction of dynamic orofacial morphology by use of 3D and four-dimensional (

149 mon relay pool for relaying JMSA to multiple orofacial motoneurons.

150 measure intercortical coherence between the orofacial motor (MIo) and somatosensory (SIo) areas of c

151 ucleus accumbens and substantia innominata), orofacial motor control (retrorubral area), thalamocorti

152 columns in the prospective Broca's area and orofacial motor cortex.

153 white matter injury is often accompanied by orofacial motor dysfunction, but little is known about t

154 self-initiated vocal production and nonvocal orofacial motor movement, we identified a subpopulation

155 t from other nonvocal motor activity such as orofacial motor movement.

156 t JMSA may coordinate activities of multiple orofacial motor nuclei, including Vmo, VII, XII and Amb

157 tractography efforts to localize descending orofacial motor pathways.

158 that generate and coordinate these and other orofacial motor patterns remain largely uncharacterized.

159 n of the parietal lobe; and (ii) a mosaic of orofacial motor programs located in the anterior and cen

160 unction with spared pathways contributing to orofacial motor recovery.

161 lei, the neuroendocrine system, and midbrain orofacial motor-related regions.

162 s: cerebral nuclei, behavior control column, orofacial motor-related, humorosensory/thirst-related, b

163 roduce novel sounds by configuring different orofacial movement patterns and these sounds are used in

164 r suppressed by vocal production, but not by orofacial movement.

165 as activated by vocal production, but not by orofacial movement.

166 in areas that appear to be critical for both orofacial movements and sequential articulation, leading

167 imed to contrast brachiomanual gestures with orofacial movements and vocalizations in the natural com

168 gion of the motor cortex where the mouth and orofacial movements are controlled.

169 ntral pattern generator circuits controlling orofacial movements are located.

170 ns these findings may assist in interpreting orofacial movements evoked during deep brain stimulation

171 n two phases: (1) from the onset of isolated orofacial movements in utero to the postnatal mastery of

172 y relative to the other, such as when visual orofacial movements precede a vocalization.

173 Stimulation of PMV elicited forelimb and orofacial movements, but not hindlimb movements.

174 tion of regions for motor control, including orofacial movements, in the primate brain.

175 imb cortex evoked shoulder stump, trunk, and orofacial movements, whereas stimulation in the deeffere

176 ticostriatal circuitry controlling voluntary orofacial movements.

177 C pathway in the Vc is involved in mediating orofacial muscle hypersensitivity under acute inflammato

178 g to overcontraction of the hands, feet, and orofacial muscles and other joints of the body.

179 ary motor cortical region that represent the orofacial musculature.

180 ance imaging, we found that individuals with orofacial neuropathic pain have increased infra-slow osc

181 this study, we report that individuals with orofacial neuropathic pain show altered functional conne

182 alpha2delta1 up-regulation may contribute to orofacial neuropathic pain states through abnormal excit

183 Orofacial neuropathic pain was associated with significa

184 nerves may contribute to the pathogenesis of orofacial neuropathic pain.

185 trigeminal nucleus in subjects with chronic orofacial neuropathic pain.

186 ial involvement in presynaptic inhibition of orofacial nociception.

187 To better understand developing orofacial nociceptive circuits and to provide a baseline

188 l connectivity with the region that receives orofacial nociceptor afferents, the spinal trigeminal nu

189 To provide a description of the orofacial nuclei of the adult mouse and to ascertain the

190 showed no systemic clinical signs (skeletal, orofacial, or auditory) usually associated with Stickler

191 are costs of those suffering from persistent orofacial pain (POFP).

192 r-year follow-up, of whom 229 (54%) reported orofacial pain and 195 (46%) did not report such pain.

193 mmation comprises a highly prevalent type of orofacial pain and is mediated by the generation of endo

194 on of arthritis prevented the development of orofacial pain and joint dysfunction, and reduced the de

195 ch in the etiology and clinical treatment of orofacial pain and temporomandibular disorders are revie

196 The treatment of orofacial pain and temporomandibular disorders has evolv

197 espread body pain, and taking medication for orofacial pain at baseline.

198 e clinical presentation of cancer-associated orofacial pain at various stages: initial diagnosis, dur

199 tion, and it affects numerous aspects of the orofacial pain experience, including pain intensity, pai

200 We aimed to describe the natural course of orofacial pain in a general population sample over a fou

201 Orofacial pain is often persistent, but it is not clear

202 MC1R variants may influence orofacial pain perception and, in turn, predispose indiv

203 ting an important role of Cavalpha2delta1 in orofacial pain processing.

204 and female patients with chronic neuropathic orofacial pain show increased functional connectivity be

205 he overall analysis indicates that rats with orofacial pain states had increased numbers and decrease

206 pathways, contributing to the development of orofacial pain states.

207 Persistent orofacial pain was associated with females, older age, p

208 regulation, particularly among persons with orofacial pain who also have high levels of PTSD symptom

209 nd pain-related functioning in patients with orofacial pain, a retrospective review was conducted of

210 dentification and treatment of patients with orofacial pain.

211 pation rate 74%), of whom 646 (26%) reported orofacial pain.

212 f smoking cessation efforts in patients with orofacial pain.

213 croglial signaling in chronic trigeminal and orofacial pain.

214 ation in pain chronification, especially for orofacial pain.

215 hogenesis of chronic pain, including chronic orofacial pain.

216 In 2006, the OPPERA project (Orofacial Pain: Prospective Evaluation and Risk Assessme

217 We used data from the Orofacial Pain: Prospective Evaluation and Risk Assessme

218 eletion of Panx1 in a mouse model of chronic orofacial pain; in this model, trigeminal ganglion Panx1

219 Thus orofacial parafunctional habits may influence brain circ

220 Other persistent adverse events were orofacial paresthesia (4 events [20%]), finger paresthes

221 The orofacial part was immersed in the bath throughout scann

222 In order to understand more about how orofacial patterning is controlled we have investigated

223 ew these advances in relation to somatic and orofacial persistent pain conditions.

224 S; OMIM 119500) is a disorder with a similar orofacial phenotype that also includes skin and genital

225 as one involving sequential articulation and orofacial praxis.

226 ity and whether these changes differ between orofacial primary motor (MIo) and somatosensory (SIo) co

227 f a Wnt signaling reporter is blocked in the orofacial primordia by Lrp6 deletion in mice.

228 in BMP signaling within developing limbs and orofacial primordia regulate proliferation and different

229 the mutants, which prevents the outgrowth of orofacial primordia, especially in the fusion site.

230 ary and partially overlapping regions of the orofacial prominences that fate mapping revealed contrib

231 We mapped changes in affective orofacial reactions of "liking"/"disliking" elicited by

232 s in hedonic "liking" (assessed by affective orofacial reactions to sucrose taste) versus "wanting" (

233 ctions are known to enhance positive hedonic orofacial reactions to the taste of sucrose ('liking' re

234 cted the nociceptive neurons innervating the orofacial region by causing increased expression of infl

235 The orofacial region is a major focus of chronic neuropathic

236 Aergic projections to the deep layers of the orofacial region of the lateral tectum (superior collicu

237 ory of the corticobulbar projection from the orofacial region of the primary (M1), ventrolateral (LPM

238 is expressed in the developing bones and the orofacial region.

239 llowing nerve injury and inflammation in the orofacial region.

240 ynamic peaks were detected in the homuncular orofacial region: the first peak during the nonpainful p

241 ts revealed a dramatic reorganization of the orofacial representation in SI.

242 , and delayed somatosensory input related to orofacial responses (more than approximately 1.0 sec).

243 lavored saccharin solution elicited aversive orofacial responses that predicted early-session cocaine

244 In contrast to studies that analyze orofacial responses, we found that lick cluster size was

245 Rats produce robust, highly distinctive orofacial rhythms in response to taste stimuli-responses

246 that governs the selection of taste-induced orofacial rhythms.

247 d taste-specific (i.e., consumption-related) orofacial rhythms.

248 midbrain and brainstem targets implicated in orofacial sensorimotor control, and consist of a mix of

249 t to multiple brainstem nuclei implicated in orofacial sensorimotor control.

250 The orofacial sensorimotor cortex is known to play a role in

251 of each breath initiates a "snapshot" of the orofacial sensory environment.

252 uggest, particularly for the case of primate orofacial signals, that they derive by ritualization of

253 l factors may lead to abnormal growth of the orofacial skeleton, affecting the overall structure of t

254 units (79%) received additional inputs from orofacial skin.

255 infections, trauma, or tumor resection, how orofacial stem/progenitor cells contribute to tissue dev

256 s the current status of our understanding of orofacial stem/progenitor cells, identifies gaps in our

257 Orofacial stereotypies are critical to optimizing food r

258 If correct, orofacial stereotypies are crucial to the maturation of

259 Like other orofacial stereotypies, TP/R emerges in the first phase

260 ary afferent fibers innervating extracranial orofacial structures (such as the cornea, nose, tongue,

261 Because sensory information from head and orofacial structures is processed by all subnuclei of th

262 To avoid deformation of the delicate orofacial structures, a water bath with an acoustic wind

263 esponsive to tactile inputs from surrounding orofacial structures, including the contralateral upper

264 hy; this possibility should be considered in orofacial surgery management.

265 nts developed severe toxic keratopathy after orofacial surgery on the left side with general anesthes

266 of comorbid health conditions and nonpainful orofacial symptoms.

267 rgone oral radiography and presented with no orofacial syndromes or defects.

268 The human orofacial system is richly endowed with low-threshold, s

269 he primary somatosensory cortex may underlie orofacial tactile sensitivity issues and sensorimotor st

270 ematically examine the effects of persistent orofacial tissue injury on prolonged neuronal activation

271 ulated in response to RARgamma inhibition in orofacial tissue, and uncovered homeobox genes lhx8 and

272 Orofacial tissues constantly receive mechanical forces a

273 Postnatal orofacial tissues harbor rare cells that exhibit stem ce

274 subclass of nociceptors and is found in many orofacial tissues, including dental pulp.

275 aired Hh signaling in skeletal, cardiac, and orofacial tissues.