ライフサイエンスコーパス: sacral

1 ebral block: cervical, thoracic, lumbar, and sacral.

2 nal segments, cervical, thoracic, lumbar and sacral.

3 the TPN lie in spinal segments trunk 17 and sacral 1 (T17-S1).

4 Fos-positive cells in the lumbar 6 (L6) and sacral 1 and 2 (S1, S2) segments, whereas no change was

5 cic (66 patients), lumbar (64 patients), and sacral (41 patients) spine.

6 ocalization in several additional hereditary sacral agenesis (HSA) families.

7 to 7q36 markers in two dominantly inherited sacral agenesis families.

8 Caudal regression syndrome (sacral agenesis), which impairs development of the cauda

9 pancreatic transcription factor HLXB9 causes sacral agenesis, our results implicate pancreatic transc

10 Sacral tumors involved body and sacral ala.

11 The activity of VF neurons and the sacral and lumbar CPGs was abolished when non-NMDA recep

12 nt to clarify the functional organization of sacral and lumbar networks and their linking pathways.

13 ing electrophysiological recordings from the sacral and lumbar spinal segments, we show that the moto

14 Sacral and pelvic floor magnetic stimulation have also b

15 e largely dispensable for the development of sacral and tail vertebrae (secondary body formation).

16 However, the sacral and tail vertebrae are only minimally affected in

17 the migration/signalling mechanisms used by sacral and vagal NCC, as transplanted vagal cells migrat

18 igate the possible interrelationship between sacral and vagal-derived neural crest cells within the h

19 Indeed, sacral application of atropine or the M2 -type receptor

20 k interface pressure between the skin at the sacral area and support surface in healthy volunteers.

21 e interface pressure between the skin of the sacral area and the bed with healthy volunteers.

22 The vertebral column in the sacral area has large anterior and posterior zygapophyse

23 Interface pressure profiles of the sacral area were obtained for the 0 degrees , 10 degrees

24 graphs showed sclerosis along the transverse-sacral articulation in only 8 (21%) of the 39 patients w

25 phy often indicates stress at the transverse-sacral articulation of young patients with low-back pain

26 patients with high uptake at the transverse-sacral articulation who underwent these examinations.

27 patients with high uptake at the transverse-sacral articulation, the lumbosacral transitional verteb

28 opically grafted neural crest cells from the sacral axial level to the thoracic level and vice versa

29 is of a transverse slice at the level of the sacral base produced mean, median, maximum, and minimum

30 Three of four sacral biopsies were adequate.

31 he hip and one with a stress fracture of the sacral bone.

32 nd caudal growth defects that resemble human sacral/caudal agenesis.

33 agal neural crest ablated chicks showed that sacral cells migrated along normal, previously described

34 migrated along pathways normally followed by sacral cells, but did so in much larger numbers, earlier

35 Thus, pharmacological manipulations of the sacral cholinergic system may be used to modulate the lo

36 ding novel insights into mechanisms by which sacral circuitry recruits lumbar flexors, and enhances t

37 Of the abdominal repairs, abdominal sacral colpopexy with mesh remains the gold standard.

38 iously we reported on adrenoceptor-dependent sacral control of lumbar flexor motoneuron firing in new

39 visceral nociceptive signals through the rat sacral cord by microdialysis administration of morphine

40 ences, HSV2-LAT-S1 DNA increased more in the sacral cord compared to its rescuant or HSV-2.

41 neurons using an in vitro preparation of the sacral cord from the G93A SOD1 mouse model of ALS.

42 to opioids induces a latent sensitization in sacral cord neurons that can be manifested as neuronal h

43 be the morphology of these VIP fibers in the sacral cord of the cat.

44 Histochemical and immunostaining of the sacral cord reveals expression of acetylcholinesterase a

45 -related motor pool activity migrates to the sacral cord segments, while the lumbar motoneurons are s

46 rong innervation of the caudal region of the sacral cord suggest that hypocretin may participate in t

47 The thoraco-sacral cord therefore has the neuronal machinery necessa

48 ne shows that postsynaptic DC neurons in the sacral cord transmit visceral nociceptive signals to the

49 No differences were recorded in the sacral cord.

50 The sacral coronal plane was best for the visualization of t

51 ing circuitry linking adrenoceptor-activated sacral CPGs and lumbar flexor motoneurons, thereby provi

52 We suggest that METH-activated sacral CPGs excite ventral clusters of sacral VF neurons

53 The capacity of noradrenergic-activated sacral CPGs to modulate the activity of lumbar networks

54 In contrast, when the sacral CPGs were activated by SCA stimulation, rhythmic

55 cral NMDA receptors were blocked by APV, the sacral CPGs were suppressed, VF neurons with nonrhythmic

56 CA to induce stepping can be enhanced by the sacral CPGs.

57 n which only the fluorescent protein-labeled sacral crest are present in the terminal colon.

58 We conclude that sacral crest cells enter the hindgut by advancing on ext

59 ENCCs reaches the terminal bowel, strands of sacral crest cells extend, and intersect with vagal cres

60 t an evolutionarily conserved model in which sacral crest cells first colonize the extramural ganglio

61 Because it is difficult to visualize sacral crest cells independently of vagal crest, the nat

62 Although Wnt1-lacZ-positive sacral crest cells populate pelvic ganglia in the mesenc

63 after neurulation, and the other states that sacral crest cells reside transiently in the extraenteri

64 We found that sacral crest cells were associated with extrinsic nerve

65 of vagal crest, the nature and extent of the sacral crest contribution to the enteric nervous system

66 s a route of entry for both rodent and avian sacral crest into the hindgut.

67 Sacral crest-derived cells along these fibers diminished

68 olons of ganglionated preparations and found sacral crest-derived cells associated with both extrinsi

69 Contribution of sacral crest-derived cells to the enteric nervous system

70 A small number of sacral crest-derived cells were found between the muscle

71 bodies, the migration and differentiation of sacral crest-derived cells.

72 nonablated control animals demonstrated that sacral-derived cells migrated into the gut and different

73 ficant expertise in laparoscopy required for sacral dissection and intracorporeal suturing can readil

74 ted direct multisegmental projections of the sacral dorsal root 4 (S4) afferent collaterals in Lissau

75 antly less HSV-2 genomic DNA detected in the sacral dorsal root ganglia compared with control animals

76 miR-I is also expressed in human sacral dorsal root ganglia latently infected with HSV-2.

77 Lumbar and sacral DRG neuronal subpopulations were immunoreactive (

78 ve non-rib-bearing lumbar vertebrae and five sacral elements, the same configuration that occurs moda

79 absence of cystic or adipose contents and of sacral erosion/destruction.

80 st for the visualization of the bony sacrum, sacral foramina, and proximal S-1 to S-4 nerve roots.

81 ions, while HSV-2 reactivates primarily from sacral ganglia causing recurrent genital lesions.

82 dl5-29 virus could not be detected by PCR in sacral ganglia from guinea pigs vaccinated intravaginall

83 sequencing of small RNAs isolated from human sacral ganglia latently infected with herpes simplex vir

84 that HSV establishes latency throughout the sacral ganglia.

85 multaneous viral reactivations from multiple sacral ganglia.

86 neonates, epidural catheters inserted at the sacral hiatus can easily be advanced to a lumbar or thor

87 distance between the greater trochanter and sacral hiatus.

88 0.62 Gy (blood-derived method) and 0.97 Gy (sacral image-derived method) to red marrow, and 0.57 Gy

89 rvous system from spinal nerves, thoracic to sacral inclusively.

90 tio 1.5; 0.7-3.1); immune suppression; prior sacral infections, and duration of total (or just parent

91 a, apophyseal and sacroiliac joint pain, and sacral insufficiency fractures.

92 Peak sacral interface pressures increased with large increase

93 al femoral metaphysis is identifiable in the sacral intermediolateral cell column and central autonom

94 at least two environmental conditions at the sacral level enhance ventral migration.

95 sis that neural crest cells derived from the sacral level have cell-autonomous migratory properties t

96 Our results show that the environment at the sacral level is sufficient to allow neural crest cells f

97 In these same ablated animals, the sacral level neural axis was removed and replaced with t

98 We suggest that variations in the sacral level of acetylcholine modulate the SCA-induced l

99 The long-term outcomes of sacral level patients show a surprising decline in adult

100 ut endoderm is more dorsally situated at the sacral level than at the thoracic level.

101 st pronounced differences were at the middle sacral level, which suggests that this may be the optima

102 The greatest differences were at the middle sacral level.

103 paralogous genes are expressed at lumbar and sacral levels of the developing neural tube and surround

104 posteriorization events at the thoracic and sacral levels of the skeleton, and showed sternal and pe

105 ce of descending pathways that finally reach sacral levels of the spinal cord housing motor neurons i

106 At the caudal thoracic, lumbar, and sacral levels there was a complete loss of neural crest

107 hen project along the dorsolateral column to sacral levels, giving rise to collaterals that project i

108 at superior, middle, and inferior transverse sacral levels.

109 ery, slightly misplaced from the site of the sacral lymph node in wild-type mice.

110 The sacral lymph node of the LT beta-deficient mice, as well

111 timulating a Th1 response were found in this sacral lymph node.

112 with symptomatic improvement one week after sacral magnetic stimulation has been demonstrated.

113 Hispanic patients with non-syndromic lumbar-sacral myelomeningocele.

114 hroughout the ENS, within a subpopulation of sacral NC-derived ENS precursors, and in the majority of

115 By E10, the stage at which sacral NCC begin to colonise the hindgut in large number

116 m the ENS; vagal NCC formed most of the ENS, sacral NCC contributed a limited number of ENS cells, an

117 ck grafting studies, suggests that vagal and sacral NCC have intrinsic differences in their ability t

118 We also found that over-expression of RET in sacral NCC increased their ENS developmental potential s

119 the entire gut, whereas the contribution of sacral NCC is mainly limited to the hindgut.

120 ength of the gastrointestinal tract, whereas sacral NCC migrate in an opposing caudorostral direction

121 r in development, thus promoting the fate of sacral NCC towards that of vagal NCC.

122 s, the nerve of Remak and a subpopulation of sacral NCC within hindgut enteric ganglia.

123 known to be essential for ENS formation, in sacral NCC within the chick hindgut.

124 NCC, Sox10, EdnrB, and Ret are expressed in sacral NCC within the gut.

125 rfold increase in expression in vagal versus sacral NCC.

126 rformed DNA microarray analysis of vagal and sacral NCC.

127 and in the majority of transplanted vagal-to-sacral NCC.

128 restore voiding in this group of patients - sacral nerve electrical stimulation therapy.

129 ence for the use of onabotulinum toxin A and sacral nerve neuromodulation for the treatment of overac

130 diarrhoea-predominant or mixed IBS subtypes sacral nerve stimulation (SNS) alleviates IBS-specific s

131 This study aimed to evaluate the outcome of sacral nerve stimulation (SNS) for fecal incontinence at

132 Sacral nerve stimulation (SNS) is an evolving treatment

133 : Stimulation amplitude used in sacral nerve stimulation (SNS) is at or just above the s

134 sical or transdermal electrical stimulation, sacral nerve stimulation and biofeedback therapy are und

135 who respond best to neuromodulation through sacral nerve stimulation are those with a primary disord

136 Long-term outcomes of sacral nerve stimulation for refractory OAB have been re

137 It is likely that sacral nerve stimulation has an indirect modulatory effe

138 Sacral nerve stimulation has been approved for use in tr

139 Experience of sacral nerve stimulation has increased over the past few

140 Sacral nerve stimulation has minimal risk and more durab

141 Sacral nerve stimulation has shown promising early resul

142 was to determine the safety and efficacy of sacral nerve stimulation in a large population under the

143 There has been growing interest in sacral nerve stimulation in the management of both overa

144 Sacral nerve stimulation significantly reduces symptoms

145 Sacral nerve stimulation using InterStim Therapy is a sa

146 antidiarrheal and laxative medications, and sacral nerve stimulation) require validation by randomiz

147 an inflatable artificial anal sphincter, and sacral nerve stimulation.

148 Since the body-stabilizing sacral networks can activate and modulate the limb-movin

149 found that methoxamine (METH) activation of sacral networks within the ventral aspect of S2 segments

150 ervous system (ENS) is formed from vagal and sacral neural crest cells (NCC).

151 rvous system (ENS) is derived from vagal and sacral neural crest cells (NCC).

152 Both vagal and sacral neural crest cells contribute to the enteric nerv

153 fate of a relatively fixed subpopulation of sacral neural crest cells may be predetermined as these

154 differentiate into enteric neurons and glia, sacral neural crest cells may require an interaction wit

155 Thus, sacral neural crest cells take a more direct path to the

156 First, sacral neural crest cells take a ventral rather than a m

157 rvous system (ENS) is derived from vagal and sacral neural crest cells that migrate, proliferate, and

158 dependence may also explain the inability of sacral neural crest cells to compensate for the lack of

159 een proposed to describe the contribution of sacral neural crest cells.

160 Sacral neural crest contributes to a subset of enteric g

161 molecular programs controlling vagal versus sacral neural crest development.

162 Sacral neural crest grafting in these vagal neural crest

163 the gut, so that earlier arrival assures the sacral neural crest of gaining access to the gut.

164 hindgut are derived from separate vagal and sacral neural crest populations.

165 , expansion and differentiation of vagal and sacral neural crest progenitor cells.

166 ed that a second region of the neuraxis, the sacral neural crest, also contributes to the enteric neu

167 ral crest-derived ENCCs express TNC, whereas sacral neural crest-derived cells do not.

168 ived enteric plexuses, as ganglia containing sacral neural crest-derived neurons and glia were small

169 However, the increase in numbers of sacral neural crest-derived neurons within the hindgut d

170 Results from this previous study showed that sacral neural crest-derived precursors colonised the gut

171 lopment; (2) vagal NCC transplanted into the sacral neuraxis extensively colonised the hindgut, migra

172 of 200 U of onabotulinumtoxinA (n = 192) or sacral neuromodulation (n = 189).

173 rgency urinary incontinence are treated with sacral neuromodulation and onabotulinumtoxinA with limit

174 presents the current evidence for the use of sacral neuromodulation and percutaneous tibial nerve sti

175 Both sacral neuromodulation and percutaneous tibial nerve sti

176 incontinence per day than did the 174 in the sacral neuromodulation group (-3.9 vs -3.3 episodes per

177 ss whether onabotulinumtoxinA is superior to sacral neuromodulation in controlling refractory episode

178 atment with onabotulinumtoxinA compared with sacral neuromodulation resulted in a small daily improve

179 oxin, percutaneous tibial nerve stimulation, sacral neuromodulation, and surgical procedures for stre

180 , 4.3 to 16.5; P < .001) than treatment with sacral neuromodulation.

181 Here we study the involvement of sacral neurons projecting rostrally through the ventral

182 the cellular environments of trigeminal and sacral neurons to promote the reactivation patterns char

183 drawal from morphine evokes hyperactivity of sacral neurons, particularly those involved in regions t

184 When sacral NMDA receptors were blocked by APV, the sacral CP

185 nsory neurons were significantly larger than sacral ones (1,112 +/- 624 mum(2) vs. 716 +/- 421 mum(2)

186 dition of one somite length of either vagal, sacral or trunk neural tube into embryos that had the ne

187 By every single one, the sacral outflow is indistinguishable from the thoracolumb

188 gent innervation may serve to coregulate the sacral parasympathetic nervous system and brain noradren

189 indicate that a lower activation of PVN and sacral parasympathetic nuclei in Lewis compared with Fis

190 ntermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1) and (4) in the la

191 ntermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (4) the late

192 eral and medial superficial dorsal horn, the sacral parasympathetic nucleus (SPN) and lamina X around

193 n in neurons in the dorsal commissure (DCM), sacral parasympathetic nucleus (SPN) as well as the medi

194 center (PMC) neurons send projections to the sacral parasympathetic nucleus (SPN) of the intermediola

195 nal sphincter response, included the area of sacral parasympathetic nucleus (SPN), the area medial to

196 X, and X of the lumbosacral cord; and in the sacral parasympathetic nucleus (SPN).

197 particularly in laminae I/II, X, and in the sacral parasympathetic nucleus (SPN).

198 ML) cell column of the thoracic cord and the sacral parasympathetic nucleus (SPN).

199 n L(6)-S(1), the cells were more numerous in sacral parasympathetic nucleus (SPN, 38.7%) and LDH (25.

200 se was lower by 32.0% in the PVN, and 63% in sacral parasympathetic nucleus in Lewis compared with Fi

201 g the lateral edge of the dorsal horn to the sacral parasympathetic nucleus in the L6-S1 spinal segme

202 activation of NADPHd-positive neurons in the sacral parasympathetic nucleus suggests a possible role

203 th the intermediolateral cell column and the sacral parasympathetic nucleus, as well as to regions of

204 ncluding the intermediolateral cell nucleus, sacral parasympathetic nucleus, dorsal grey commissure a

205 the locus coeruleus (LC) and projects to the sacral parasympathetic nucleus, is a source of afferent

206 were observed in the 5-HT innervation of the sacral parasympathetic nucleus, which was maintained, an

207 in the dorsal grey commissure and within the sacral parasympathetic nucleus.

208 population of PGN in the lateral band of the sacral parasympathetic nucleus.

209 g the central canal) and by nine-fold in the sacral parasympathetic nucleus.

210 The axons of sacral parasympathetic preganglionic neurons (PGNs) orig

211 s suggesting that they are interneurons, not sacral parasympathetic preganglionic neurons.

212 her, these data indicate that the lumbar and sacral pathways probably play different roles in sensory

213 In the adult, the lumbar and sacral patterns become more dissociated with shorter act

214 segments projecting nerve fibers through the sacral plexus to innervate the musculature of the hindli

215 ze afferent or efferent stimulation from the sacral plexus.

216 Accordingly, sacral preganglionic neurons are considered parasympathe

217 nd the supporting tissues laterally from the sacral promontory to the pelvic floor.

218 he ability of vagal NCC, transplanted to the sacral region of the neuraxis, to colonise the chick hin

219 when the vagal NC was transplanted into the sacral region of the neuraxis, vagal-derived ENS precurs

220 s restricted to the hindgut, arises from the sacral region of the neuraxis.

221 bia/fibula, as well as transformation of the sacral region to a lumbar phenotype.

222 om the last thoracic vertebrae to beyond the sacral region.

223 ar spine and a soft tissue mass in the lower sacral region.

224 hedgehog signal response in the thoracic to sacral regions correlating with the regions of morpholog

225 n this ganglion and others of the lumbar and sacral regions, 75% or more of such HE TRPV1 cells expre

226 ations, extending from the craniocervical to sacral regions.

227 ation by sacrocaudal afferent (SCA) input of sacral relay neurons projecting rostrally through the ve

228 ch as the lack of both an attachment for the sacral rib and an ischium.

229 ined to the iliac process of a hypertrophied sacral rib; fusion of these bones in tetrapods creates a

230 e of lumbar (L6) cord with more found in the sacral (S1) cord.

231 m different parts of the lumbar (L1, L2) and sacral (S1-S3) segments rose, peaked, and decayed in a r

232 exhibiting FLI were found bilaterally in the sacral (S1-S3) spinal cord and were localized to the lat

233 xtending from the lower lumbar (L3) to upper sacral (S2) cord.

234 s-like immunoreactivity throughout the first sacral segment, particularly in laminae I/II, X, and in

235 voked by intraspinal microstimulation of the sacral segments (S1-S2) in neurologically intact, chlora

236 ey were detected in the last trunk and first sacral segments (T17-S1).

237 vels of L1 expression detected in lumbar and sacral segments and the lowest in cervical spinal cord.

238 and cholinergic interneurons in thoracic and sacral segments are positioned normally.

239 to central canal cluster cells in lumbar and sacral segments of OEG- than media-injected rats.

240 SCA stimulation is enhanced by exposing the sacral segments of the neonatal rat spinal cord to the a

241 In the thoracolumbar and sacral segments of the spinal cord, SN-LI nerve fibers w

242 ventromedially located neurons of lumbar and sacral segments to the contralateral ventral gray matter

243 was abolished when non-NMDA receptors in the sacral segments were blocked by the antagonist CNQX.

244 l levels of the spinal cord from cervical to sacral segments, as studied in mouse, rat, and human spi

245 a higher overall activation of lumbar versus sacral segments, consistent with a rostrocaudal excitabi

246 f group II muscle afferents in midlumbar and sacral segments.

247 ferents terminating within the midlumbar and sacral segments.

248 Few cells were labeled in upper cervical or sacral segments.

249 oxide synthase immunoreactivity (NOS1-ir) in sacral somatic motor neurons of normal adult cats was co

250 ls from the vagal (somite level 1-7) and the sacral (somite level 28 and posterior) axial levels migr

251 and the parasympathetic nucleus of the lumbo-sacral spinal cord (L6-S1) in both Lewis and Fischer rat

252 toring Fos immunoreactivity in the brain and sacral spinal cord and fecal pellet output.

253 ain-type NMDAR1 was present in the brain and sacral spinal cord and not in the penis.

254 y from the pontine micturition center to the sacral spinal cord in the lateral medulla was responsibl

255 Unmyelinated sensory axons in the sacral spinal cord may play a role in bladder reflexes u

256 reganglionic neurons (PGN) obtained from the sacral spinal cord of the cat by intracellular injection

257 This study shows that in the sacral spinal cord of the cat, VIP terminals originate o

258 s in preganglionic neurons in the lumbar and sacral spinal cord of the female rat that may underlie i

259 ormation directly from cervical, lumbar, and sacral spinal cord segments to the hypothalamus.

260 e monitored Fos-like immunoreactivity in the sacral spinal cord to identify neurons that are likely t

261 rainstem, and cervical, thoracic, lumbar and sacral spinal cord).

262 ricle, Lamina X of the cervical, lumbar, and sacral spinal cord, and various hypothalamic and telence

263 rd, while HSV-2 DNA was more abundant in the sacral spinal cord, which may provide insights into the

264 strally to the brainstem and caudally to the sacral spinal cord.

265 ated dynorphin in the ipsilateral lumbar and sacral spinal cord.

266 lateral collateral pathway, a region of the sacral spinal dorsal horn important for the relay of pel

267 Interestingly, in the lower lumbar and upper sacral spinal dorsal horn, numerous TH-IR neurons were o

268 eonatal sciatic nerve and from the lumbar or sacral spinal roots of 10-day-old animals.

269 During sacrocolpopexy, placing the sacral suture at the promontory may put the L5-S1 interv

270 Sacral tumors involved body and sacral ala.

271 Lumbar and sacral UBT sensory neurons also showed different IB4 lab

272 Lumbar and sacral UBT sensory neurons expressed similar percentages

273 Stimulation of sacral ventral roots (S1-S3) revealed that the S2 effere

274 rtebral levels from the 12th thoracic to 1st sacral vertebra (identified on a sagittal section) for t

275 In the absence of Hox11 function, sacral vertebrae are not formed and instead these verteb

276 Sacral vertebrae beginning at the level of S2 exhibit ho

277 and ribs had abnormal morphology, lumbar and sacral vertebrae were malformed or completely absent, an

278 ire homeotic transformations from trunk into sacral vertebrae, or vice versa, and mutations toward su

279 apen, fused and reduced number of lumbar and sacral vertebrae, under-developed hind limb bones and a

280 tions of the cervical, thoracic, lumbar, and sacral vertebrae.

281 somitogenesis and the pathogenesis of lumbar/sacral vertebral anomalies.

282 s located at or below the level of the third sacral vertebral body in all 49 patients with isolated p

283 mechanisms and that the modified activity of sacral VF neurons in the presence of an acetylcholineste

284 modulate the activity of lumbar networks via sacral VF neurons provides a novel way to recruit rostra

285 Collectively, our studies indicate that sacral VF neurons serve as a major link between SCA and

286 vated sacral CPGs excite ventral clusters of sacral VF neurons to deliver the ascending drive require

287 nt proportions of fluorescently back-labeled sacral VF neurons.

288 ontitis and an intractable, deep, nonhealing sacral wound.