ライフサイエンスコーパス: spinal

1 Patients with either brain or spinal (43.4pg/ml, IQR = 25.2-65.3) or both brain and sp

2 facilitation of both tactile and nociceptive spinal activity in the first three postnatal weeks.

3 s antihyperalgesic in primed mice exposed to spinal administration of a D1/D5 agonist.

4 Single spinal afferent axons bifurcated many times upon enterin

5 The majority of spinal afferent nerve endings were CGRP-immunoreactive.

6 ugh the location of the nerve cell bodies of spinal afferents is well known to reside in dorsal root

7 and location of peripheral nerve endings of spinal afferents that transduce sensory stimuli into act

8 in our laboratory to selectively label only spinal afferents.

9 Spinal and bulbar muscular atrophy (SBMA) is a neuromusc

10 Spinal arachnoiditis is under-recognized, since diagnosi

11 dominal hypersensitivity caused by augmented spinal astroglial and microglial activity.

12 ssociation impairment scale in children with spinal AVF.

13 heathment of approximately 30% of myelinated spinal axons at injury epicenter 3 months after SCI, dem

14 The assessment of global spinal balance together with lower extremity alignment s

15 ogic sequences for the detection of probable spinal bone metastases, thereby providing an opportunity

16 f the internal ventricular system and in the spinal canal during respiratory cycles.

17 rons within different sites of the vestibulo-spinal circuitry of behaving macaque monkeys during temp

18 We developed a computational model of spinal circuits consisting of four rhythm generators cou

19 control, we show that malformation of these spinal circuits leads to hyperexcitability of the monosy

20 o how the dopaminergic system interacts with spinal circuits to promote pain plasticity.

21 to CPG function, with the exception of a few spinal circuits where the functional significance of mot

22 descending systems play in the maturation of spinal circuits.

23 gulation of opioid genes: broken symmetry in spinal circuits.

24 m that ensures the bilateral symmetry of the spinal column.

25 T and KO mouse visceral yolk sac, brain, and spinal column.

26 ssed in the axonal growth cones of embryonic spinal commissural neurons, motoneurons, dorsal root gan

27 receptor, promotes recovery after traumatic spinal contusion injury in mice, a benefit achieved in p

28 Here, using cultured spinal cord (SC) neurons grown using a compartmented pla

29 of axons growing into a lesion epicenter in spinal cord after a concomitant dorsal column transectio

30 ying and tracking inflammatory damage in the spinal cord after TAR in a mouse model.

31 hen activating muscles, motor neurons in the spinal cord also activate Renshaw cells, which provide r

32 l ganglionic eminence (MGE) into adult mouse spinal cord ameliorates mechanical and thermal hypersens

33 as an example of non-monotonic coding in the spinal cord and better explains observations in human ps

34 ch as estradiol, that are synthesized in the spinal cord and brainstem and act locally to influence p

35 cine corelease is particularly common in the spinal cord and brainstem, but its presence in the midbr

36 found that AAVrh10 transduces neurons in the spinal cord and dorsal root ganglia of immunodeficient m

37 uleus (LC) projects throughout the brain and spinal cord and is the major source of central noradrena

38 rowth of embryos by contributing both to the spinal cord and mesoderm.

39 ish mutants in which OPCs migrate out of the spinal cord and myelinate peripheral motor axons, we ass

40 ich there is widespread demyelination of the spinal cord and optic nerves, we also show that thinly r

41 t neural stem cells, derived from the murine spinal cord and organized as neurospheres, can be trigge

42 hysiological effector systems, including the spinal cord and other peripheral organs.

43 n of BzATP resulted in ROS production in the spinal cord and oxidative DNA damage in dorsal horn neur

44 Bar(CRH) neurons project to the lumbosacral spinal cord and ramify extensively in two regions: the d

45 igrate extensively in the demyelinated mouse spinal cord and remyelinate axons.

46 including fever, viremia, and viral loads in spinal cord and testes-and increased mortality.

47 (HD)-within the various compartments of the spinal cord and their potential impact on the local vasc

48 s) that fuel embryo elongation by generating spinal cord and trunk mesoderm tissue.

49 This foreshortened spinal cord appears to be related to anisotropic growth

50 c stiffness of the injured rat neocortex and spinal cord at 1.5 and three weeks post-injury using ato

51 Quantitative measurements of spinal cord atrophy are important in fully characterizin

52 The blood-spinal cord barrier (BSCB) plays significance roles in r

53 lls into symptomatic G93A mice towards blood-spinal cord barrier (BSCB) repair.

54 al impact on the local vasculature and blood-spinal cord barrier (BSCB).

55 ymphocytes from the blood into the brain and spinal cord by blocking the adhesion molecule alpha4-int

56 +ChABC treatment of the chronically contused spinal cord can provide a permissive substrate for the r

57 t is hardwired; but it is now clear that the spinal cord changes continually as new behaviors are acq

58 g genetic approaches in the mouse to map the spinal cord circuits that transmit and gate the cutaneou

59 Neurobiotin retrograde transport from the spinal cord combined with immunofluorescence revealed sp

60 d events (SREs) such as pathologic fracture, spinal cord compression, or the necessity for radiation

61 native codon-derived DPRs in chick embryonic spinal cord confirmed in vitro data, revealing that each

62 hanisms for epigenetic regulation within the spinal cord constitute the starting point for handedness

63 We report that, after spinal cord contusion injury in adult female mice, the b

64 frequency (p = 0.04) correlate with T4 to T9 spinal cord cross-sectional area in HAM/TSP.

65 Spinal cord cross-sectional area was measured in individ

66 load (p = 0.01) was associated with thinner spinal cord cross-sectional area.

67 opositivity, (2) myelitis attack and (3) MRI spinal cord demonstrating ring-enhancement.

68 tant in fully characterizing these and other spinal cord diseases.

69 (pC/EBPbeta) and its upstream pathway in the spinal cord dorsal horn (SCDH).

70 that many neurons in laminae I and V of the spinal cord dorsal horn and caudal spinal trigeminal nuc

71 cinergic inhibitory neurotransmission in the spinal cord dorsal horn gates nociceptive signaling, is

72 athways that were changed in astrocytes from spinal cord during chronic EAE involved decreases in exp

73 e hypothesis that inducing plasticity in the spinal cord during chronic stroke could improve recovery

74 earch team has demonstrated that lumbosacral spinal cord epidural stimulation (scES) and activity-bas

75 gative, acylated SOD1 fibrils to organotypic spinal cord failed to produce the SOD1 inclusion patholo

76 d RGS10 protein levels are suppressed in the spinal cord in a nerve injury-induced neuropathic pain m

77 hage-specific mRNA directly from the injured spinal cord in mice and performed RNA sequencing to inve

78 defects in axon projection of DRG toward the spinal cord in vivo Furthermore, live-cell imaging of en

79 s within the ependymal layer of the original spinal cord include populations of neural stem/progenito

80 udy participant was a 53-year-old man with a spinal cord injury (cervical level 4, American Spinal In

81 ied in 384 patients with clinically complete spinal cord injury (SCI) and consequent anejaculation.

82 Spasms after spinal cord injury (SCI) are debilitating involuntary mu

83 Spinal cord injury (SCI) induces a centralized fibrotic

84 ays significance roles in recovery following spinal cord injury (SCI), and diabetes mellitus (DM) imp

85 Spasticity, a common complication after spinal cord injury (SCI), is frequently accompanied by c

86 Following spinal cord injury (SCI), newly formed endothelial cells

87 Following spinal cord injury (SCI), the innate immune response of

88 Also, in rat T9-T10 hemisection spinal cord injury (SCI), we demonstrated that the tailo

89 y associated with persistent pain induced by spinal cord injury (SCI).

90 examine their therapeutic potential to treat spinal cord injury (SCI).

91 cytes that protect tissue and function after spinal cord injury (SCI).

92 he recovery of hand motor function following spinal cord injury (SCI).

93 hand dexterity increased in individuals with spinal cord injury after the I-wave protocol.

94 an reveal early inflammation associated with spinal cord injury after thoracic aortic ischemia-reperf

95 receptor, promotes recovery after traumatic spinal cord injury in mice, a benefit achieved in part b

96 of rehabilitation strategies in humans with spinal cord injury is to strengthen transmission in spar

97 veral neurological disorders such as stroke, spinal cord injury, multiple sclerosis, amyotrophic late

98 s system to restore motor function following spinal cord injury, the role of cortical targets remain

99 ipate in neuronal development, angiogenesis, spinal cord injury, viral invasion, and immune response.

100 migration and reversed astroglial fate after spinal cord injury.

101 sticity that improves breathing in models of spinal cord injury.

102 ecruitment of spinal motor neurons following spinal cord injury.

103 least one to three LTMR classes, as well as spinal cord interneurons and corticospinal neurons.

104 Two distinct MRI patterns of spinal cord involvement were described according to T2-w

105 that develops following injuries to brain or spinal cord is a major obstacle for tissue repair in cen

106 ABSTRACT: The dorsal horn (DH) of the spinal cord is an important site for modality-specific p

107 enesis of brain disease, but its role in the spinal cord is unclear.

108 (whole brain and gray matter), and cervical spinal cord lesions (T2LV) and atrophy.

109 ticospinal tract axons in the contralesional spinal cord makes a significant contribution to sensorim

110 onstrate that endogenous RGS10 is present in spinal cord microglia, and RGS10 protein levels are supp

111 urological examination, a baseline brain and spinal cord MRI scan obtained less than 3 months from cl

112 eolytic targets of calpain in Xenopus laevis spinal cord neurons both in vivo and in vitro Inhibition

113 FT most closely resembles that of the adult spinal cord niche.

114 her (64)Cu-rituximab uptake in the brain and spinal cord of huCD20tg EAE, and B220 immunostaining ver

115 n, particularly of minor U12 introns, in the spinal cord of mice 30 d after SMA induction, which was

116 activity regulate locomotor networks in the spinal cord of neonatal mice.

117 In the spinal cord of patients with ALS, but not Con, AD or CJD

118 cal changes also occur at every level of the spinal cord of PPT1-deficient (Ppt1(-/-) ) mice before t

119 Lumbar spinal cord PET signal was significantly higher in EAE m

120 Dopaminergic modulation of spinal cord plasticity has long been recognized, but cir

121 man reflex is associated with reduced dorsal spinal cord potassium chloride cotransporter expression

122 Using a novel ex vivo spinal cord preparation, here we identify the functional

123 We propose that spinal cord regeneration in geckos represents a truncati

124 e deep dorsal horn is a poorly characterized spinal cord region implicated in processing low-threshol

125 subunits to AMPAR-mediated signaling in the spinal cord remains unclear.

126 subunits to AMPAR-mediated signaling in the spinal cord remains unclear.

127 stiffness properties that are well suited to spinal cord repair by supporting cell growth mechano-bio

128 Spinal cord ring-enhancement accompanies one-third of NM

129 The spinal cord showed architectural distortion, severe neur

130 We utilized ex vivo spinal cord slice cultures (SCSC) to demonstrate that an

131 king of Slack channels also occurs in intact spinal cord slices and that it is carried out by adaptor

132 INs using targeted patch-clamp recording in spinal cord slices from adult transgenic mice that expre

133 In spinal cord slices, clonidine reduced the frequency of c

134 ed current in mouse dorsal horn neurons from spinal cord slices.

135 ed from large lamina I neurons in horizontal spinal cord slices.

136 on the mechanisms of axonal guidance in the spinal cord that provide for a discussion of the current

137 the transcriptome of both the cerebellum and spinal cord that was consistent with glial activation an

138 Previous work measures spinal cord thinning in chronic progressive myelopathies

139 Spinal cord tissue from heterozygous (ARQ/VRQ or ARH/ARQ

140 iated viral vectors, serotype-9 (scAAV-9) in spinal cord tissues after intraspinal injection of mouse

141 he central canal of the brain ventricles and spinal cord to circulate the cerebral spinal fluid (CSF)

142 hundred fifty thousand axons emerge from the spinal cord to innervate the human upper limb, of which

143 By selectively ablating microglia in the spinal cord using a saporin-conjugated antibody to Mac1,

144 Targeting the spinal cord via intrathecal administration of an adeno-a

145 aluated for motor impairment, mortality, and spinal cord viral load.

146 most completely absent in both the brain and spinal cord when intracranial and intrathecal injections

147 that lacked CCR7 were retained in brain and spinal cord while wild type DC migrated to cervical lymp

148 Na](+) adducts was observed in samples from spinal cord with demyelination, while the intensity of t

149 direct and trans-synaptic infection from the spinal cord with rabies viruses that carry glycoproteins

150 form to the circumvolutions of the brain and spinal cord without damaging neural tissues or triggerin

151 Circuits in the sensorimotor system (e.g., spinal cord) are thought to be assembled sequentially [1

152 logical analysis of the dorsal root ganglia, spinal cord, and cerebellum.

153 ulted in essentially no PPT1 activity in the spinal cord, and vice versa.

154 tomic regions when comparing astrocytes from spinal cord, cerebellum, cerebral cortex, and hippocampu

155 n and brainstem regions and project onto the spinal cord, have long been recognised as key links in t

156 In the developing dorsal spinal cord, multiple BMPs are required to specify senso

157 In sum, when a new behavior changes the spinal cord, sensory feedback to the brain guides furthe

158 In the spinal cord, the expression of other proteins identifies

159 This new variant is undetectable in brain or spinal cord, the only and most abundant known sources of

160 mutant SOD1 protein in the disease-affected spinal cord, where concomitant increases in copper and S

161 ing between prefrontal areas, brainstem, and spinal cord, which might represent a flexible mechanism

162 The second derived feature is the very short spinal cord, which terminates midway along the thoracic

163 despite implantation into the injured rodent spinal cord, yet they support delayed functional recover

164 orsal horn and RVM neurons to uncover an RVM-spinal cord-primary afferent circuit controlling pain th

165 several hundred micrometers of the zebrafish spinal cord.

166 by mechanosensory feedback in the vertebrate spinal cord.

167 , and importantly, also in the injured human spinal cord.

168 t architectures within these lineages in the spinal cord.

169 h as autonomic regions of the brain stem and spinal cord.

170 s (NSPCs) that contribute to the regenerated spinal cord.

171 prion-like propagation of oligomeric SOD1 in spinal cord.

172 ociceptors have distinct morphologies in the spinal cord.

173 gral part of neural circuits for itch in the spinal cord.

174 Fos immunoreactivity pattern in the cervical spinal cord.

175 that governs axonal wiring of the zebrafish spinal cord.

176 thin band of tissue at the caudal end of the spinal cord.

177 erotonin innervation of motor neurons in the spinal cord.

178 time window for development of the brain and spinal cord.

179 ained excitation of neurons in slices of rat spinal cord.

180 ophage activation in the white matter of the spinal cord.

181 ement and/or acute blood products within the spinal cord.

182 remove netrin from different regions of the spinal cord.

183 cross five lumbosacral segments in the human spinal cord.

184 neurons project mostly to the hindbrain and spinal cord.

185 ectable in skeletal muscle, heart, brain and spinal cord.

186 of myelinating Schwann cells in the injured spinal cord; invasion of peripheral myelinating (P0+) Sc

187 Spinal cords from EAE-challenged Plg(-) mice demonstrate

188 ted, matured, and integrated into the rodent spinal cords over a time frame that aligned with the nor

189 (CCS) is S-acylated in both human and mouse spinal cords, and in vitro in HEK293 cells.

190 A-binding protein TDP-43 in their brains and spinal cords, and rare mutations in the gene encoding TD

191 in those sections from mechanically injured spinal cords.

192 nistered by stereotaxic injection into mouse spinal cords.

193 D in diabetic rats was rapidly normalized by spinal delivery of duloxetine acting via 5-hydroxytrypta

194 iratory tract diseases, liver cirrhosis, and spinal disc herniation); causes of mortality (all-cause,

195 multielectrode array was used to record C4/5 spinal discharge before [baseline (BL)], during, and 15

196 Second neoplasms, spinal disorders, and pulmonary disease were major contr

197 Neither spinal dorsal ascending tract transection nor H-reflex c

198 Transcriptional changes in superficial spinal dorsal horn neurons (SSDHN) are essential in the

199 in lamina I and II neurons within the rodent spinal dorsal horn, a principal site of action for opiat

200 ous biased agonism at mGluR1) and changes in spinal dynorphin/KOR signaling represent a novel mechani

201 strus), concomitant with the ebb and flow of spinal dynorphin/KOR signaling, functions as a switch, p

202 A spinal ejaculation generator (SEG) has been identified i

203 Regulation of spinal EM2 antinociception by both the nature of the end

204 itch, preventing or promoting, respectively, spinal EM2 antinociception.

205 om motor cortex were robustly augmented with spinal epidural stimulation delivered at an intensity be

206 es and spinal cord to circulate the cerebral spinal fluid (CSF).

207 of retraction: the article "Role of Cerebral Spinal Fluid in Space Flight Induced Ocular Changes and

208 3.4pg/ml, IQR = 25.2-65.3) or both brain and spinal gadolinium-enhancing lesions (62.5pg/ml, IQR = 42

209 loride cotransporter expression and impaired spinal gamma-aminobutyric acid type A receptor function,

210 cotherapies capable of increasing inhibitory spinal glycinergic neurotransmission hold in providing n

211 tis, angiography was uniformly negative, and spinal imaging frequently demonstrated longitudinally ex

212 he translational potential of this marker of spinal inhibitory dysfunction in human painful diabetic

213 acid type A receptor function, indicative of spinal inhibitory dysfunction.

214 inal cord injury (cervical level 4, American Spinal Injury Association Impairment Scale category A).

215 children with cerebral AVF and the American Spinal Injury Association impairment scale in children w

216 in foreign-body infections (arthroplasty or spinal instrumentation).

217 rather than following the expected embryonic spinal intermediates.

218 The impact of AIH on cervical spinal interneuron (C-IN) discharge and connectivity is

219 We find that assemblies of excitatory spinal interneurons are recruited by sensory input into

220 genetics to directly target major classes of spinal interneurons as well as motor neurons during spas

221 Here we identified a subset of spinal interneurons, labeled by gastrin-releasing peptid

222 tic actuators selectively in LC neurons with spinal (LC(:SC)) or prefrontal cortex (LC(:PFC)) project

223 t signaling could improve rehabilitation and spinal learning.SIGNIFICANCE STATEMENT Published data sh

224 ing speed and if this is accomplished at the spinal level.

225 d to impaired transmission at a cortical and spinal level.

226 region-specific CSNs terminate in different spinal levels and locations, therefore preferentially co

227 It may act by shielding brainstem and spinal locomotor centers from abnormal cortical input af

228 t LTM training maximizes the contribution of spinal locomotor circuits as well as remnant supraspinal

229 culospinal neurons that in turn activate the spinal locomotor networks.

230 for larval exposures included cardiac edema, spinal malformation, and craniofacial deformities and th

231 -quality evidence), massage, acupuncture, or spinal manipulation (low-quality evidence).

232 nt therapy, cognitive behavioral therapy, or spinal manipulation (low-quality evidence).

233 tions between corticospinal tract fibres and spinal motoneurones undergo activity-dependent reorganiz

234 in vivo paired recordings between identified spinal motoneurons and skeletal muscle cells in larval z

235 In larval zebrafish, spinal motoneurons are recruited in a topographic gradie

236 rojects to cortical neurons, and projects to spinal motoneurons controlling hand muscles.

237 tinuous communication between the cortex and spinal motoneurons, but the neurophysiological basis of

238 neuromuscular junction (NMJ) dysfunction and spinal motor neuron (MN) loss.

239 t-latency pathways linking motor cortex with spinal motor neurons are selectively activated during on

240 Reticulospinal neurons project to spinal motor neurons controlling hand muscles and extens

241 nd have a crucial role in the recruitment of spinal motor neurons following spinal cord injury.

242 from the cellular model with laser-captured spinal motor neurons from C9ORF72-ALS cases, we also dem

243 n the serum of patients with MS to brain and spinal MRI.

244 Spinal muscular atrophy (SMA) is a common and often fata

245 Spinal muscular atrophy (SMA) is a hereditary neurodegen

246 Spinal muscular atrophy (SMA) is a neurodegenerative dis

247 Spinal Muscular Atrophy (SMA) is a neuromuscular disorde

248 Spinal muscular atrophy (SMA) is a progressive neurodege

249 Spinal muscular atrophy (SMA) is an autosomal-recessive

250 Spinal muscular atrophy (SMA) is caused by deficiency of

251 Spinal Muscular Atrophy (SMA) is caused by diminished Su

252 eutic approach to SMA.SIGNIFICANCE STATEMENT Spinal muscular atrophy (SMA) is caused by the loss of m

253 genital myotonic dystrophy type 1 (CDM1) and spinal muscular atrophy (SMA) patients.

254 Here we show that, in a mouse model of spinal muscular atrophy (SMA), a reduction in propriocep

255 Spinal muscular atrophy (SMA), an autosomal recessive ne

256 Spinal muscular atrophy (SMA), the leading genetic cause

257 Homozygous SMN1 loss causes spinal muscular atrophy (SMA), the most common lethal ge

258 Spinal muscular atrophy is an untreatable potentially fa

259 lformations in cortical development (MCD) or spinal muscular atrophy with lower extremity predominanc

260 ype-2, distal hereditary motor neuropathies, spinal muscular atrophy with parkinsonism and the later

261 entified in patients with a dominant form of spinal muscular atrophy, but how these mutations cause d

262 hereditary causes are recognised, including spinal muscular atrophy, distal hereditary motor neuropa

263 efects may be one strategy in treating human spinal muscular atrophy.

264 ty and neuropathic pain behaviors in the rat spinal nerve ligation (SNL) model.

265 ts in DRG neurons is downregulated following spinal nerve ligation (SNL).

266 avid lesions not only were found in impinged spinal nerves but also were associated with nonspinal ca

267 e injured DRGs (defined as DRGs with injured spinal nerves) of living SNL rats.

268 cial plexiform neurofibromas and symptomatic spinal neurofibromas were more prevalent in these indivi

269 1)H NMR spectroscopy of media from astrocyte-spinal neuron co-cultures and astrocyte-only cultures.

270 To examine metabolic changes in astrocyte-spinal neuron co-cultures, we carried out metabolomic an

271 Both excitatory (E) and inhibitory (I) spinal neurons are necessary for motor behavior, but the

272 mmation in mice by ablating a group of adult spinal neurons defined by developmental co-expression of

273 and glutamate-containing varicosities appose spinal neurons that express MOR along with mGluRs and mE

274 In cultured dorsal spinal neurons, blockade of Kv3.4 by blood depressing su

275 dium pump-mediated afterhyperpolarization in spinal neurons, mediated by spike-dependent increases in

276 due to C9orf72 expansion was being driven by spinal onset males (HR 1.56 (95% CI 1.25 to 1.96).

277 However, the impact of ADS on spinal pain processing has not been explored, nor whethe

278 KEY POINTS: Spinal parvalbumin-expressing interneurons have been ide

279 children presenting at least one cerebral or spinal pial arteriovenous fistula (AVF), and to describe

280 ns [acute intermittent hypoxia (AIH)] evokes spinal plasticity.

281 rd combined with immunofluorescence revealed spinal-projecting Galphat-S-ir reticular neurons in the

282 SOD1(G93A) ) we previously demonstrated that spinal respiratory motor plasticity elicited by acute in

283 nic long-term facilitation (pLTF), a form of spinal respiratory motor plasticity that improves breath

284 Twenty-four patients (55%) with a spinal schwannoma had a constitutional mutation, while o

285 Prototype fully automated spinal segmentation and fracture detection software were

286 que model to investigate the role of defined spinal segments in the control of ejaculation.

287 VS) to elicit ejaculation when the concerned spinal segments were injured was studied in 384 patients

288 this time, reorganization and refinement of spinal sensorimotor circuits occurs as supraspinal proje

289 xcitability of motoneurons and to changes in spinal sensory processing.

290 ivity in small-diameter dorsal root ganglia, spinal slices, and in a mouse model of pain induced by N

291 these paradigms has been the integration of spinal stereotactic radiosurgery (SSRS), allowing delive

292 ally dependent on the timing and position of spinal stimulation.

293 entally manipulating ADS strongly influences spinal summation consistent with sex differences in beha

294 ng the later-developing collateral cardinal, spinal, superficial lateral and superficial intersegment

295 ited lack of informed consent) who underwent spinal surgery and filed a malpractice claim were studie

296 literature investigating informed consent in spinal surgery malpractice.

297 ablation of Panx1 in microglia abolished the spinal synaptic facilitation and ameliorated the sequela

298 ight support and locomotion without explicit spinal transmission of motor commands through the lesion

299 V of the spinal cord dorsal horn and caudal spinal trigeminal nucleus and in the nucleus of the soli

300 receives orofacial nociceptor afferents, the spinal trigeminal nucleus.