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 rade viral tracing from muscles that control orofacial actions shows that these premotor nuclei segre

5 us on brainstem circuits that drive rhythmic orofacial actions.

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

7 The observation of animal orofacial and behavioral reactions has played a fundamen

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

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

10 DMF network is to exert cognitive control of orofacial and vocal acts and, in the language dominant h

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

12 dystonia with predominant cervical, bulbar, orofacial, and upper limb involvement.

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

14 Harnessing these assays in the orofacial area during gene manipulation should assist in

15 ntifiable behavioral assessment in the mouse orofacial area remains a major bottleneck in uncovering

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

17 n) is involved in the cognitive selection of orofacial, as well as, speech and nonspeech vocal respon

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

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

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

21 l principles that have evolved to coordinate orofacial behaviors.

22 nsiently and purposely synchronize different orofacial behaviours.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Mutations in human MSX1 have been linked to orofacial clefting and we show here that Msx1 deficiency

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

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

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

45 velopment - the disruption of which leads to orofacial clefting in human patients.

46 Orofacial clefting includes several distinct anatomic ma

47 The etiology of orofacial clefting is multifactorial, including genetic

48 Orofacial clefting is the most common congenital craniof

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

50 c allele manifests an incompletely penetrant orofacial clefting phenotype.

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

52 Mutations in IRF6, TFAP2A and GRHL3 cause orofacial clefting syndromes in humans.

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

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

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

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

57 1 has been considered a strong candidate for orofacial clefting, based on mouse expression studies an

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

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

60 variants identified to date for nonsyndromic orofacial clefting.

61 to understanding the phenotypic spectrum of orofacial clefting.

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

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

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

65 ntiguous autosomal deletions associated with orofacial clefting.

66 and GRHL3 also contribute risk for isolated orofacial clefting.

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

68 hould be considered a candidate for isolated orofacial clefting.

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

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

71 types observed in patients with nonsyndromic orofacial clefts (NSOFCs) are nonsyndromic cleft lip onl

72 Orofacial clefts (OFCs) are congenital dysmorphologies o

73 DNMs have not been fully explored regarding orofacial clefts (OFCs), one of the most common human bi

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

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

76 Orofacial clefts and their management impose a substanti

77 en identified in patients with rare atypical orofacial clefts and with syndromic cleft lip and/or pal

78 Nonsyndromic orofacial clefts are a common complex birth defect cause

79 Orofacial clefts are among the most common birth defects

80 Orofacial clefts are common birth defects with a known g

81 Orofacial clefts are common developmental disorders that

82 Orofacial clefts are congenital structural anomalies of

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

84 Most orofacial clefts are nonsyndromic, isolated defects, whi

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

86 Orofacial clefts are well known for their complex etiolo

87 ranslated into human trials that can correct orofacial clefts at earlier stages of development.

88 Orofacial clefts have been associated with maternal ciga

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

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

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

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

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

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

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

96 are diseases, such as ectodermal dysplasias, orofacial clefts, and other craniofacial and dental anom

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

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

99 mportant insights into the etiology of human orofacial clefts.

100 abnormalities can result in various forms of orofacial clefts.

101 icillin in pregnancy was not associated with orofacial clefts.

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

103 provide evidence that multivitamins prevent orofacial clefts.

104 e occurrence of congenital heart defects and orofacial clefts.

105 ractions that constitute the many factors of orofacial clefts.

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

107 Here, we aimed to identify orofacial conditions that can serve as potential risk ma

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

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

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

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

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

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

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

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

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

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

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

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

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

121 ew their contribution to normal and abnormal orofacial development.

122 2, encode transcription factors critical for orofacial development.

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

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

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

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

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

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

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

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

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

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

133 cortex and is involved in the development of orofacial dyskinesias, involuntary chewing-like movement

134 mpromised Kv3 channel function and VLS-based orofacial dyskinesias.

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

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

137 multiple system atrophy (red flag features: orofacial dystonia, disproportionate antecollis, camptoc

138 lapping Irf6 and Esrp1/2 expression in mouse orofacial epithelium.

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

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

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

142 most painful cancers, which interferes with orofacial function including talking and eating.

143 aw time in a dolognawmeter indicates reduced orofacial function.

144 Mastication is one of the most important orofacial functions.

145 ly from a gingival inflammation to grotesque orofacial gangrene.

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

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

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

149 CCI-ION caused orofacial hypersensitivity that correlated with Cavalpha

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

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

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

153 steolytic gingival infection that results in orofacial implant failures.

154 Following orofacial infection, HSV establishes latency in innervat

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

156 Orofacial inflammation is associated with prostaglandin

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

158 Orofacial injury activates two distinct regions in the s

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

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

161 ecifically related to the processing of deep orofacial input.

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

163 clude that neighboring projection neurons in orofacial MCtx form parallel pathways to distinct pools

164 uced a significant reduction in hind paw and orofacial mechanical withdrawal thresholds as a surrogat

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

166 The orofacial modules in lateral cortex resemble similar mod

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

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

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

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

171 How do neurons in orofacial motor cortex (MCtx) orchestrate behaviors?

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

173 We identify an orofacial motor cortical region and, via a series of per

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

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

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

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

178 tractography efforts to localize descending orofacial motor pathways.

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

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

181 unction with spared pathways contributing to orofacial motor recovery.

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

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

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

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

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

187 iculations of varying complexity, non-speech orofacial movements and speech listening, in a cohort of

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

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

190 ntral pattern generator circuits controlling orofacial movements are located.

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

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

193 an spiking hundreds of milliseconds prior to orofacial movements linked to sound presentation and rew

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

195 function control skilled forelimb behavior, orofacial movements, and locomotion.

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

197 Whisking involves coordinated orofacial movements, so mechanoreceptors innervating fac

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

199 ticostriatal circuitry controlling voluntary orofacial movements.

200 isorder involving difficulties in sequencing orofacial movements.

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

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

203 ary motor cortical region that represent the orofacial musculature.

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

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

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

207 Orofacial neuropathic pain was associated with significa

208 trigeminal nucleus in subjects with chronic orofacial neuropathic pain.

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

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

211 en different types of motor actions: manual, orofacial, nonspeech vocal, and speech vocal actions.

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

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

214 These data suggest that OXT via orofacial OXTR may play a peripheral role to modulate se

215 questionnaire from a case-control cohort of orofacial pain (n = 1,607).

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

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

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

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

220 ase of the joint that can produce persistent orofacial pain as well as functional and structural chan

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

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

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

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

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

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

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

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

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

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

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

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

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

234 separately investigated inflammation-driven orofacial pain, acute activity of the trigeminal nerve,

235 ooth agenesis, cancers of the head and neck, orofacial pain, temporomandibular disorders, and craniof

236 ation in pain chronification, especially for orofacial pain.

237 hogenesis of chronic pain, including chronic orofacial pain.

238 dentification and treatment of patients with orofacial pain.

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

240 f smoking cessation efforts in patients with orofacial pain.

241 croglial signaling in chronic trigeminal and orofacial pain.

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

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

244 Data were from the Orofacial Pain: Prospective Evaluation and Risk Assessme

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

246 Thus orofacial parafunctional habits may influence brain circ

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

248 The orofacial part was immersed in the bath throughout scann

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

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

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

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

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

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

255 ateral subfield of the striatum (VLS) is the orofacial projection field of the sensorimotor cortex an

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

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

258 nt in controlling the timing of stereotyped, orofacial reactions to aversive tastants during consumpt

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

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

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

262 The orofacial region is a major focus of chronic neuropathic

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

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

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

266 llowing nerve injury and inflammation in the orofacial region.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 opmental syndromes that are characterized by orofacial, skin and genital abnormalities result when th

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

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

284 Orofacial stereotypies are critical to optimizing food r

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

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

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

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

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

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

291 of comorbid health conditions and nonpainful orofacial symptoms.

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

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

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

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

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

297 Orofacial tissues constantly receive mechanical forces a

298 Postnatal orofacial tissues harbor rare cells that exhibit stem ce

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

300 a and ectopic pain originating from adjacent orofacial tissues.

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