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 ive, with nine cervicals, 15 dorsals and two sacrals, a pattern present also in their closest extinct

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

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

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

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

11 Sacral tumors involved body and sacral ala.

12 acral spine to lymphatic vessels, leading to sacral and iliac LNs.

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

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

15 s which interact with higher centers and the sacral and lumbar spinal cord to coordinate complex void

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

17 Sacral and pelvic floor magnetic stimulation have also b

18 Wedged sacral and posterior dorsal vertebrae cause the presacra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Three of four sacral biopsies were adequate.

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

36 mplete homeotic transformations at the lumbo-sacral border in fast-running mammals, while slower, amb

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 No differences were recorded in the sacral cord.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 Sacral crest-derived cells along these fibers diminished

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

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

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

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

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

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

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

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

80 Lumbar and sacral DRG neuronal subpopulations were immunoreactive (

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

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

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

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

85 multaneous viral reactivations from multiple sacral ganglia.

86 that HSV establishes latency throughout the sacral ganglia.

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

88 distance between the greater trochanter and sacral hiatus.

89 0.62 Gy (blood-derived method) and 0.97 Gy (sacral image-derived method) to red marrow, and 0.57 Gy

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

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

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 his study was to assess the effectiveness of sacral nerve modulation (SNM) in a large cohort of patie

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

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

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

133 Sacral nerve stimulation (SNS) is an evolving treatment

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

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

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

137 in real time to demonstrate that electrical sacral nerve stimulation can activate colonic enteric ne

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

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

140 Sacral nerve stimulation has been approved for use in tr

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

142 Sacral nerve stimulation has minimal risk and more durab

143 Sacral nerve stimulation has shown promising early resul

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

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

146 Sacral nerve stimulation significantly reduces symptoms

147 One example is sacral nerve stimulation to treat overactive bladder, ur

148 Sacral nerve stimulation using InterStim Therapy is a sa

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

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

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

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

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

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

155 In birds, sacral neural crest cells (sNCCs) first give rise to an

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

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

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

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

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

161 ENS cells originate from vagal and sacral neural crest cells that are initially located at

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

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

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

165 Sacral neural crest contributes to a subset of enteric g

166 molecular programs controlling vagal versus sacral neural crest development.

167 Sacral neural crest grafting in these vagal neural crest

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

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

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

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

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

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

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

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

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

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

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

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

180 Both sacral neuromodulation and percutaneous tibial nerve sti

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

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

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

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

185 , 4.3 to 16.5; P < .001) than treatment with sacral neuromodulation.

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

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

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

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

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

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

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

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

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

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

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

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

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

199 cord segments L5-S2 were concentrated in the sacral parasympathetic nucleus (SPN), dorsal horn lamina

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 ze afferent or efferent stimulation from the sacral plexus.

220 Accordingly, sacral preganglionic neurons are considered parasympathe

221 t of osteomyelitis in patients with stage IV sacral pressure ulcers is controversial.

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

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

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

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

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

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

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

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

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

231 ations, extending from the craniocervical to sacral regions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 ferents terminating within the midlumbar and sacral segments.

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

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

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

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

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

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

259 lateral collateral pathway, a region of the sacral spinal cord horn that receives visceral sensory a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 ominantly from intravertebral regions of the sacral spine to lymphatic vessels, leading to sacral and

275 The first phase generates pre-sacral structures (the so-called primary body) through t

276 witches to generate the secondary body (post-sacral structures), which depends on axial progenitors i

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

278 nted ganglia and cryosections of DRG and the sacral sympathetic ganglia (SSG) from latently infected

279 Sacral tumors involved body and sacral ala.

280 is the first crown-crocodylian to have three sacrals, two true sacral vertebrae and one non-pathologi

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

282 Lumbar and sacral UBT sensory neurons expressed similar percentages

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

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

285 -crocodylian to have three sacrals, two true sacral vertebrae and one non-pathological and functional

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

287 Sacral vertebrae beginning at the level of S2 exhibit ho

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

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

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

291 ls more readily tolerate intermediate lumbar/sacral vertebrae.

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

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

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

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

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

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

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

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

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