ライフサイエンスコーパス: PNS

1 PNS (5 Hz), which was tested at the threshold (T) intens

2 PNS axons have a better regenerative capacity, mediated

3 PNS axons have a high intrinsic regenerative ability, wh

4 PNS can reflect an individual's regulatory capacity of f

5 PNS has become one of the main constraints on the use of

6 PNS is an effective treatment in the short term for bowe

7 PNS myelin glycoproteins contain highly abundant sulfate

8 2 mm bipolar electrode spacing resulted in a PNS threshold increase of 5.5+/-2.2 V (P=0.003) and 2.8+

9 ealistic coil geometries to directly address PNS in the design process.

10 ticide use and PNS function by administering PNS tests to 701 male pesticide applicators in the Agric

11 n is as abundant as the triplet in the adult PNS and exists in a relatively fixed stoichiometry with

12 is a subunit of neurofilaments in the adult PNS.

13 a frontal compensatory processes, may affect PNS regulation, thereby compromising older adults' capac

14 n levels and ErbB2 receptor expression after PNS injury were disrupted in the absence of alphaBC.

15 NS), as SCs enable axons to regenerate after PNS injury.

16 reactivity inhibits axon regeneration after PNS injury in an animal model.

17 llerian degeneration and remyelination after PNS injury.

18 e was significantly lower in group 1 for all PNS-O stages (P < 0.001).

19 ssociated neurodegeneration links to altered PNS regulation during mental effort in older adults, and

20 neurodegeneration is associated with altered PNS regulation and that compensatory processes linked to

21 glial response to injury between the CNS and PNS and highlights features of the PNS glial response th

22 nserved mechanism that promotes both CNS and PNS developmental myelination.

23 has been demonstrated previously in CNS and PNS injury models of neuropathic pain.

24 -specific factors modulate AS during CNS and PNS myelination.

25 rotein kinases (MAPKs), in promoting CNS and PNS myelination.

26 and likely local translation in both CNS and PNS neurons suggests an active role in the regenerative

27 ryogenesis, Lov is expressed in many CNS and PNS neurons.

28 cial emotions within and between the CNS and PNS remains unknown.

29 ntral and peripheral nervous system (CNS and PNS) domains along the same axon.

30 ntral and peripheral nervous system (CNS and PNS), respectively, resulting in severe dysregulation of

31 ote healing and regeneration in both CNS and PNS, via transplantation of glial progenitors or the imp

32 lin and axonal integrity in both the CNS and PNS.

33 elopmental myelination in the intact CNS and PNS.

34 urium) was also found in the copepod CNS and PNS.

35 Preoperative PNS-O and PNS-P showed no significant difference between groups (P

36 ited thicker PNS and CNS myelin sheaths, and PNS myelin abnormalities, such as tomacula and myelin in

37 apidly induces phosphorylation of Smad3, and PNS nearly completely prevents this effect.

38 at APC loss delays radial axonal sorting and PNS myelination.

39 a crucial role in radial axonal sorting and PNS myelination.

40 ed associations between OP pesticide use and PNS function by administering PNS tests to 701 male pest

41 Our findings suggest the ascidian PNS can serve as an in vivo model to study the underlyin

42 186 expression is reduced by >99% and 94% at PNS and CNS nodes, respectively.

43 These results show that Nav at PNS nodes are still maintained in a nodal complex when n

44 Gliomedin and NrCAM at PNS and brevican at CNS nodes are largely lost with neur

45 aimed to elucidate the relationship between PNS function and AD-associated neurodegeneration by test

46 Neurite outgrowth in both PNS and CNS neuronal cultures consistently stalls at 1-2

47 pathway, which controls myelination in both PNS and CNS.

48 was higher if the presentation was a classic PNS, if it was different from stiff-person syndrome or c

49 ed with this autoimmunity or develop classic PNS.

50 tion program and reveal that similar to CNS, PNS axon-glial metabolic interactions are most likely me

51 nd through inhibitory scar tissue at the CNS-PNS transitional zone before entering into a pro-regener

52 Despite its role as a major constraint, PNS considerations are only indirectly incorporated in t

53 These results reveal that stem cell-derived PNS neurons are able to form functional connections with

54 marize and discuss how studies of Drosophila PNS and NMJ development have provided guidance in experi

55 dilatation and increased constriction during PNS.

56 deletion had no obvious effect on embryonic PNS.

57 PNS), yet few studies have directly examined PNS infection.

58 eductase mRNA levels in both male and female PNS offspring in the NTS, and in the PVN in males.

59 ogesterone concentrations in male and female PNS rats, respectively.

60 r, our data indicate that Akt is crucial for PNS myelination driving axonal wrapping by unmyelinated

61 the size of the linear region as a proxy for PNS thresholds or by conducting human experiments after

62 These findings support a potential role for PNS hypoxic damage in the motor impairment that results

63 dependent outgrowth and traction forces from PNS (dorsal root ganglion (DRG)) and CNS (hippocampal) n

64 and show that loss of alphaII spectrin from PNS axons causes preferential degeneration of large-diam

65 Functional PNS regeneration requires injured axons to return to the

66 n cells with activated ERK1/2 hypermyelinate PNS axons, suggesting that ERK1/2 signaling is a conserv

67 The presence of PNS was verified (ie, PNS threshold <2 V at 0.5 ms in unipolar configuration).

68 nsity grid derived from Scheimpflug imaging (PNS-P [%]).

69 ticides is associated with signs of impaired PNS function among pesticide applicators.

70 In PNS axons, axotomy activates Neu3 sialidase, increasing

71 In PNS females, adenovirus-mediated gene transfer was used

72 normalized HPA axis responses to IL-1beta in PNS males.

73 in and metalloproteinase proteins (ADAMs) in PNS myelination, but there is no evidence if they also p

74 escued axon regeneration in CNS axons and in PNS axons after Neu3 sialidase blockade.

75 GlcNAc-6-O-sulfation) is highly conserved in PNS myelin between these species.

76 Contrary, in PNS glia, but not in neurons, proteolytic processing pro

77 lysis of axonal capsid transport dynamics in PNS neurons.

78 0 protein, the most abundant glycoprotein in PNS myelin and mutations in which at the glycosylation s

79 died the role of integrins in axon growth in PNS axons; in the present study, we investigate whether

80 shment of a quiescent or latent infection in PNS neurons is a hallmark of most alpha herpesviruses.

81 framework for revealing pathways involved in PNS axon regrowth after injury, we applied a comprehensi

82 gate whether integrin mechanisms involved in PNS regeneration may be altered or lacking from mature C

83 ts close relationship with neurofilaments in PNS diseases associated with neurofilament accumulation.

84 (500 ng/kg, i.v.) in PNS females, but not in PNS males.

85 essential step in regeneration occurring in PNS (sensory) but not CNS (retinal) axons in adult rat.

86 Nevertheless, there is a 38% reduction in PNS conduction velocity.

87 The MAPK/ERK pathway has a critical role in PNS development.

88 sterone metabolism or increased secretion in PNS rats was indicated by greater plasma testosterone an

89 gene SUZ12 functions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by coopera

90 H responses to IL-1beta (500 ng/kg, i.v.) in PNS females, but not in PNS males.

91 R-124 in epidermal midline cells, whereas in PNS midline cells miR-124 silences Notch, Neuralized and

92 There are several important differences in PNSs when occurring in association with HL and NHL compa

93 unclear if such activity occurs in infected PNS ganglia in living animals and if it correlates with

94 During saline infusion PNS significantly (P < 0.05) increased bladder capacity

95 FP-3'-beta-actin mRNA accumulates in injured PNS axons before activation of the transgene promoter pe

96 ient to convert epidermal midline cells into PNS neurons, consistent with a role in modulating Notch

97 d knowledge about their differentiation into PNS derivatives.

98 ly conjugated ligands that selectively label PNS, which could allow visualization of peripheral nerve

99 is model, we were able to reproduce measured PNS thresholds of two leg/arm solenoid coils with good a

100 tudy demonstrates that GlcNAc6ST-1 modulates PNS myelination and myelinated axonal survival through t

101 nd, onconeural antibodies are absent in most PNSs associated with lymphomas with the exceptions of Tr

102 ns were identified in both porcine and mouse PNS myelin, demonstrating that the 6-O-sulfation of N-ac

103 -specific effects of human apoE on the mouse PNS.

104 bricated based on 2D phosphorene nanosheets (PNSs).

105 When compared with the 106 non-PNS cases, those with PNS were older (median age, 60 yea

106 erminus, mediate signals required for normal PNS and CNS physiology.

107 A, was previously implicated in CNS, but not PNS myelination.

108 Notably, PNS injury triggers a coordinated regenerative gene expr

109 cycle, we find that, during entry, axons of PNS neurons support robust, bidirectional capsid motilit

110 In axons of PNS neurons, cytoplasmic dynein provides force for retro

111 x, which in turn resulted in a high level of PNS activity at rest, as well as strong PNS activity wit

112 ation, and an electrocardiography measure of PNS (high frequency heart rate variability; HF-HRV).

113 ations between pesticide use and measures of PNS function were estimated with linear and logistic reg

114 The presence of PNS was verified (ie, PNS threshold <2 V at 0.5 ms in un

115 is molecule is a novel negative regulator of PNS myelination.

116 on of Krox20 (Egr2), the master regulator of PNS myelination.

117 Yet, the relationship of PNS function to cognitive decline and abnormal frontal f

118 Studies of PNS integrin traffic have identified molecules that can

119 predominant (group 2)] had a 3-week trial of PNS.

120 Furthermore, the type and frequency of PNSs are different between HL and NHL; whereas LE and PC

121 These hemocyte responses depend on PNS activity, as shown by agonist treatment and transien

122 the effects of bipolar electrode spacing on PNS and LV pacing thresholds.

123 As predicted from the in vivo organization, PNS-like axon bundles elaborated by apical cocultures we

124 mato/ polymyositis in both HL and NHL, other PNSs are uncommon and have only been reported as isolate

125 Our PNS model consists of an accurate body model for electro

126 During bipolar pacing, PNS threshold increased as bipolar electrode spacing was

127 e tissue environment between the peripheral (PNS) and central (CNS) nervous systems, we compare subst

128 system (NS), spreading into the peripheral (PNS) and more rarely the central (CNS) nervous systems.

129 o fulfilled criteria of definite or possible PNS without concomitant onconeural antibodies were inclu

130 Preoperative PNS-O and PNS-P showed no significant difference between

131 With increasing preoperative PNS-P, effective phacoemulsification time increased in b

132 Mean preoperative PNS staging was assessed using an automatic ordinal scal

133 -derived neurotrophic factor (GDNF) promotes PNS development and kidney morphogenesis via a receptor

134 cocultures allowing an analysis of putative PNS/CNS axon length ratios.

135 l-section electron microscopy to reconstruct PNS neurons and their hitherto unknown synaptic networks

136 f these mRNAs in CNS axons from regenerating PNS axons may relate to differences in the growth capaci

137 e roles played by PNG homologs in regulating PNS development of the invertebrate chordate Ciona intes

138 assessed using an automatic ordinal scaling (PNS-O, grades 0-5) and a manually defined density grid d

139 bers of myelinating Schwann cells and severe PNS hypomyelination.

140 1) dysmyelination is less severe in the shk PNS than in the CNS, but TBs, which are present in both

141 article Imaging (MPI) to humans is similarly PNS constrained.

142 Similarly, PNS threshold increased by 6.5+/-3.7 V with 1 mm and by

143 for the first time, a framework to simulate PNS thresholds for realistic coil geometries to directly

144 First, some PNSs such as sensory neuronopathy or Lambert-Eaton myast

145 Nucleus staging (Pentacam nucleus staging; PNS) was evaluated using Pentacam HR (Oculus); endotheli

146 Pudendal nerve stimulation (PNS) aims to maximize afferent or efferent stimulation f

147 eactivity to perivascular nerve stimulation (PNS) and adrenoreceptor (AR) activation during blood flo

148 ansmission), perivascular nerve stimulation (PNS) evoked dilatation in Young but not Old MAs while di

149 Phrenic nerve stimulation (PNS) is a common complication of cardiac resynchronizati

150 m contraction via phrenic nerve stimulation (PNS) substantially reduces MV-induced proteolytic activi

151 nough to cause Peripheral Nerve Stimulation (PNS).

152 essors, such that adult prenatally stressed (PNS) offspring display exaggerated HPA axis responses to

153 l of PNS activity at rest, as well as strong PNS activity withdrawal in response to the mental effort

154 hese methods can be broadly applied to study PNS disorders and lay the groundwork for future therapeu

155 endently (0.1-50 mg kg(-1), i.v.) suppressed PNS inhibition of bladder overactivity at low intensity

156 Paraneoplastic neurological syndromes (PNSs) rarely associate with Hodgkin lymphoma (HL) and no

157 h the peripheral and central nervous system (PNS and CNS, respectively).

158 lecule regulating peripheral nervous system (PNS) and central nervous system (CNS) myelination.

159 t at nodes in the peripheral nervous system (PNS) and central nervous system (CNS).

160 tween the injured peripheral nervous system (PNS) and CNS is the pro- and antiregenerative responses

161 ent of Drosophila peripheral nervous system (PNS) and neuromuscular junction (NMJ) have been identifi

162 of neurons in the peripheral nervous system (PNS) and retina.

163 aintenance of the peripheral nervous system (PNS) are essential for an organism to survive and reprod

164 tress in diabetic peripheral nervous system (PNS) argue for a major role of the ER stress pathways in

165 d the role of the peripheral nervous system (PNS) as a microenvironment in hematopoiesis.

166 vely expressed by peripheral nervous system (PNS) axons and Schwann cells.

167 in the mammalian peripheral nervous system (PNS) can regenerate axons after injury, in part, by enha

168 Injury to the peripheral nervous system (PNS) causes a dramatic shift in SC molecular phenotype a

169 nges and of their peripheral nervous system (PNS) connective tissue counterpart: fibroblasts, having

170 ells; SCs) of the peripheral nervous system (PNS) could be purified and expanded in number in tissue

171 both the CNS and peripheral nervous system (PNS) during development.

172 tes the epidermal-peripheral nervous system (PNS) fate choice in tail midline cells.

173 ated with adverse peripheral nervous system (PNS) function.

174 ivery of cargo to peripheral nervous system (PNS) has broad clinical and preclinical applications.

175 xic damage to the peripheral nervous system (PNS) has not been addressed.

176 ose levels in the peripheral nervous system (PNS) have been implicated in the pathogenesis of diabeti

177 system (CNS) and peripheral nervous system (PNS) in PD.

178 tem (CNS) but not peripheral nervous system (PNS) injury.

179 POINTS: The parasympathetic nervous system (PNS) is critical for adaptation to environment demands.

180 BSTRACT: The parasympathetic nervous system (PNS) is critical for adaptation to environment demands.

181 ive events in the peripheral nervous system (PNS) is still to be established, and the mechanisms thro

182 yelination of the peripheral nervous system (PNS) is unknown.

183 ting with pain or peripheral nervous system (PNS) manifestations, 39% were LGI1-IgG seropositive (7%

184 ry neurons of the peripheral nervous system (PNS) must signal to the motor circuits of the central ne

185 s are involved in peripheral nervous system (PNS) myelination.

186 nfected, cultured peripheral nervous system (PNS) neurons exhibited aberrant electrical activity afte

187 e-long latency in peripheral nervous system (PNS) neurons of their native hosts.

188 axons of cultured peripheral nervous system (PNS) neurons.

189 s that infect the peripheral nervous system (PNS) of infected hosts as an integral part of their life

190 ic neurons of the peripheral nervous system (PNS) play a critical role in regulating the immune syste

191 yet axons in the peripheral nervous system (PNS) regrow, albeit to a limited extent, after injury.

192 that make up the peripheral nervous system (PNS) relies on the activity of transcription factors enc

193 ether ScNs of the peripheral nervous system (PNS) synapse with CN neurons of the central nervous syst

194 central (CNS) and peripheral nervous system (PNS) that nourish neurons and maintain homeostasis.

195 ic control of the peripheral nervous system (PNS) would enable novel studies of motor control, somato

196 n clusters of the peripheral nervous system (PNS), and blood cells (hemocytes) require the PNS for th

197 wann cells in the peripheral nervous system (PNS), and enteric glial cells.

198 In the peripheral nervous system (PNS), developmental axon pruning relies on receptor-medi

199 e detected in the peripheral nervous system (PNS), especially in lip and foot regions of the anterior

200 ating glia of the peripheral nervous system (PNS), originate from multipotent neural crest cells that

201 S but also in its peripheral nervous system (PNS), which, as in other "myelin mutants", is not as sev

202 try zone show the peripheral nervous system (PNS)-CNS transition of regrown axons.

203 Apparent peripheral nervous system (PNS)-like and central nervous system (CNS)-like axonal p

204 ily affecting the peripheral nervous system (PNS).

205 ter injury in the peripheral nervous system (PNS).

206 ctor (NGF) in the peripheral nervous system (PNS).

207 wann cells in the peripheral nervous system (PNS).

208 in the Drosophila peripheral nervous system (PNS).

209 pathology in the peripheral nervous system (PNS).

210 milar role in the peripheral nervous system (PNS).

211 entral (CNS) and peripheral nervous systems (PNS) arise from the neural plate.

212 both the CNS and peripheral nervous systems (PNS), yet few studies have directly examined PNS infecti

213 s showing much less growth after injury than PNS neurons.

214 r quantities of translational machinery than PNS axons, leading to the conclusion that the capacity f

215 the applied fields are powerful enough that PNS limits their application in fast imaging sequences l

216 yelin sheath length, as well as reports that PNS axonal neuregulin-1 type III regulates the initiatio

217 The PNS sensor exhibits an ultrahigh sensitivity to NO2 in d

218 ests not only in the entire CNS but also the PNS, likely affecting both afferent and efferent neural

219 at nodes of Ranvier in both the CNS and the PNS.

220 the sodium channel, are less affected at the PNS node than in the CNS.

221 In contrast, the PNS is severely hypomyelinated and lacks large diameter

222 hypothesis that the disease ascends from the PNS to the CNS as proposed by Braak's hypothesis.

223 .1B locus is differentially expressed in the PNS and CNS, and generates multiple splice isoforms in t

224 time taste receptor-expressing cells in the PNS and CNS.

225 uency firing, and at nodes of Ranvier in the PNS and some nodes in the CNS.

226 s failed to rescue nodal organization in the PNS and the CNS.

227 myelination of axons by Schwann cells in the PNS are essential for normal nerve function.

228 Dorsal root (DR) axons regenerate in the PNS but turn around or stop at the dorsal root entry zon

229 nificant effect on axonal myelination in the PNS either.

230 PA receptor (AMPAR)-mediated currents in the PNS glia of vertebrates and provide new insights into th

231 ation has been demonstrated, its role in the PNS has not been established and remains uncertain.

232 eir polarity, and that radial sorting in the PNS is a key polarization event that requires Pals1.

233 ng pathways that regulate myelination in the PNS remain poorly understood.

234 ms regulating Schwann cell plasticity in the PNS remain to be elucidated.

235 gesting 4.1B may function differently in the PNS versus CNS.

236 These anatomical changes in the PNS were associated with mechanical allodynia, even in t

237 t Caspr localization was not affected in the PNS, even after 1 year; and 4.1R was neither expressed,

238 cific antibodies to demonstrate that, in the PNS, four other neuronal sodium channel isoforms were al

239 In the PNS, Rem2 was abundant in a subpopulation of neurons in

240 ample, even before myelination begins in the PNS, Schwann cells must radially sort axons to form 1:1

241 nd generates multiple splice isoforms in the PNS, suggesting 4.1B may function differently in the PNS

242 In the PNS, the extracellular matrix (ECM) incorporates a basal

243 es can establish quiescent infections in the PNS, with rare but often fatal CNS pathology.

244 se MCT1, MCT2, and MCT4 are expressed in the PNS.

245 t MCT expression and lactate function in the PNS.

246 augmentation of the growth potential in the PNS.

247 gulated by single growth factors like in the PNS.

248 nn cells are the main glial cell type in the PNS.

249 l myelination and axonal degeneration in the PNS.

250 axonal regeneration and remyelination in the PNS.

251 ct control of functional nerve repair in the PNS.

252 lying axonal wrapping and myelination in the PNS.

253 regulation of myelin sheath thickness in the PNS.

254 to 1 or 2 mm may significantly increase the PNS threshold without compromising LV pacing thresholds.

255 ping epidermal sensory neurons (ESNs) of the PNS and act downstream of Notch signaling, which negativ

256 gand, is expressed by sensory neurons of the PNS and regulates the proliferation and adhesion of hemo

257 Remarkably, the nerves of the PNS are capable of regenerating after trauma.

258 An examination of the PNS expression indicates that lov functions in the late

259 e CNS and PNS and highlights features of the PNS glial response that, with continued study, might rev

260 rosophila parallels the emerging role of the PNS in hematopoiesis and immune functions in vertebrates

261 s that Akt controls several key steps of the PNS myelination.

262 a comprehensive, system-wide analysis of the PNS of a rodent model of DN.

263 , in the developmental isoform switch of the PNS, myelination does not play a signaling role as that

264 During early development of the PNS, Pals1-deficient mice had impaired radial sorting of

265 for the systematic genetic dissection of the PNS-hematopoietic axis in the future.

266 jority of neurons and all of the glia of the PNS.

267 al cord, but not in the sciatic nerve of the PNS.

268 ann cells (SCs) are myelinating cells of the PNS.

269 onstrate that larval hemocytes depend on the PNS as an attractive and trophic microenvironment.

270 nct compartmental effects of diabetes on the PNS that could underlie the distal-proximal distribution

271 ts that the dependence of sensitivity on the PNS thickness is dictated by the band gap for thinner sh

272 al and technical advances in research on the PNS.

273 ggest that therapies designed to protect the PNS may provide clinical benefit.

274 NS), and blood cells (hemocytes) require the PNS for their survival and recruitment to these microenv

275 Emerging approaches to target the PNS such as bioelectronics could be useful in improving

276 The connectome reveals that the PNS input arises from scattered groups of these epiderma

277 to survive and reproduce, and damage to the PNS by disease or injury is often debilitating.

278 esting the tumor itself does not trigger the PNS.

279 solid tumors in patients with lymphoma, the PNSs often develops at advanced stages of the disease.

280 Infection with virulent PRV caused these PNS neurons to fire synchronously and cyclically in high

281 These "PNS-only" mutations (Y151C, V181M, R183C and L239I) form

282 oximately 10(15) cm(-2) for the 4.8-nm-thick PNS when exposed to 20 p.p.b. NO2 at 300 K.

283 aximum response is observed for 4.8-nm-thick PNS, with a sensitivity up to 190% at 20 parts per billi

284 hosphodiesterase promoter, exhibited thicker PNS and CNS myelin sheaths, and PNS myelin abnormalities

285 This PNS-hematopoietic connection in Drosophila parallels the

286 Thus, PNS and CNS abnormalities may involve different aspects

287 ration of 5alpha-reduced steroids acutely to PNS rats overrides programming of hyperactive HPA axis r

288 ry vector for transport of various cargos to PNS in preclinical and clinical settings.

289 s involving multiple pathways was central to PNS regenerative capacity.

290 the source(s) and targeting of components to PNS nodes of Ranvier.

291 sensory nerves) enhanced MA constriction to PNS (P 0.05) by approximately 20% in Young but not Old m

292 derstanding how SC metabolism contributes to PNS function and in developing new strategies for treati

293 tively) were given subacutely (over 24 h) to PNS rats to seek reversal of the "programmed" hyper-resp

294 al regulator of the Schwann cell response to PNS injury in vivo.

295 ictor of central nervous system (CNS) versus PNS involvement (>50 years; odds ratio = 15, p < 0.001).

296 nsgenic mouse Oct6(DeltaSCE/betageo) , whose PNS myelination is delayed in the first postnatal week b

297 MA networks, vasoconstriction increased with PNS frequency (1-16 Hz) but was approximately 20% less i

298 An early intervention with PNS and/or pharmaceutical inhibition of Smad3 may preven

299 pared with the 106 non-PNS cases, those with PNS were older (median age, 60 years vs 48 years; P = .0

300 that E(2) plays in the developing zebrafish PNS, particularly at the neuromuscular level.