ライフサイエンスコーパス: PNS

1 PNS axons have a high intrinsic regenerative ability, wh

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

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

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

5 PNS is clinically underdiagnosed despite its impact on p

6 PNS myelin glycoproteins contain highly abundant sulfate

7 PNS results from a complex molecular interplay between t

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

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

10 CK2alpha's appearance in axons after PNS nerve injury correlates with disassembly of axonal G

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

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

13 llerian degeneration and remyelination after PNS injury.

14 therapeutic targets for remyelination after PNS-CNS injury.

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

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

17 Several microglial activation-associated and PNS macrophage-enriched genes were also expressed in spi

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

19 ith disruption to myelin in both the CNS and PNS caused by a mutation in a previously uncharacterized

20 Both the CNS and PNS displayed inflammation, while the PNS was also chara

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

22 regulation of actin dynamics during CNS and PNS myelination.SIGNIFICANCE STATEMENT Myelin is critica

23 i increased the abundance of several CNS and PNS neuron subtypes regenerated or maintained through ho

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

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

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

27 ntral and peripheral nervous system (CNS and PNS, respectively) are composed of distinct neuronal and

28 tral and peripheral nervous systems (CNS and PNS, respectively).

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

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

31 to ensure proper ensheathment of the CNS and PNS.

32 attenuated inflammation in both the CNS and PNS.

33 underlying Obesity-associated neuropathy and PNS dysfunction.

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

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

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

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

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

39 dverse effects (nirAEs) that can manifest as PNSs.

40 186 expression is reduced by >99% and 94% at PNS and CNS nodes, respectively.

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

42 ward increased triglyceride synthesis blocks PNS neuron regeneration, whereas shifting it toward memb

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

44 t implications for our understanding of both PNS and CNS myelination and myelin repair.

45 Prion RT-QuIC was positive in all CJD PNS samples, whereas western blotting detected PrP(Sc) i

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

47 ed with this autoimmunity or develop classic PNS.

48 l location for which they are designed (CNS, PNS, or special senses).

49 central and peripheral nervous system (CNS, PNS) demyelination.

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

51 mall number of select cells traverse the CNS-PNS boundary and connect these two major subdivisions of

52 ng the development and plasticity of the CNS-PNS interface.

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

54 tion and axon guidance at the vertebrate CNS-PNS border.

55 he otic vesicle and other neurons in the CNS/PNS.

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

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

58 dilatation and increased constriction during PNS.

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

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

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

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

63 nds to Sox10, a key transcription factor for PNS and CNS myelination and remyelination, to drag Sox10

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

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

66 rios in which nirAEs fulfil the criteria for PNSs and examine their frequency and clinical presentati

67 ed/accumulates via its ectodomain to forming PNS (hemi)nodes by diffusion trapping, whereas it is lat

68 wth, although depletion of Csnk2a1 mRNA from PNS axons decreases regeneration and increases G3BP1 gra

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

70 Functional PNS regeneration requires injured axons to return to the

71 In PNS axons, axotomy activates Neu3 sialidase, increasing

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

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

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

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

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

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

78 s into the node and highlight differences in PNS and CNS node assembly.

79 lysis of axonal capsid transport dynamics in PNS neurons.

80 crophages as well as selectively enriched in PNS macrophages.

81 0 protein, the most abundant glycoprotein in PNS myelin and mutations in which at the glycosylation s

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

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

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

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

86 ased Schwann cell numbers and myelination in PNS neuron-glia co-cultures.

87 (500 ng/kg, i.v.) in PNS females, but not in PNS males.

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

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

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

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

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

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

94 treatment algorithms has renewed interest in PNSs.

95 tivation of Sox10 target genes and increases PNS and CNS remyelination efficiency.

96 d knowledge about their differentiation into PNS derivatives.

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

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

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

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

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

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

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

104 trate that SC NMDA-R is essential for normal PNS development and for preventing development of pain s

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

106 and highlight differences in the assembly of PNS and CNS nodes.SIGNIFICANCE STATEMENT Nodes of Ranvie

107 the correct spatial and temporal assembly of PNS nodes of Ranvier.

108 The role of (18)F-FDG PET in assessment of PNS in head and neck cancer remains to be explored, in c

109 Assessment of PNS on (18)F-FDG PET requires knowledge of relevant neur

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

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

112 f CaP precipitation, permitting detection of PNS by NMR and determination of their formation rates, e

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

114 identifies subtypes and cell-type markers of PNS cells and a partially conserved autoimmunity module

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

116 Using a male Sprague Dawley rat model of PNS-CNS injury, we show that oral treatment with a novel

117 ulation of NF186, a key adhesion molecule of PNS and CNS nodes.

118 The significantly lower prevalence of PNS involvement in typical sCJDMM(V)1 suggests that the

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

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

121 Studies of PNS integrin traffic have identified molecules that can

122 MM(V)1, had symptoms or signs suggestive of PNS involvement occurring at onset in 18 cases (17 VV2-M

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

124 dations for the prevention and management of PNSs that can occur during ICI therapy.

125 kpoint inhibition, we provide an overview of PNSs, including the main syndromes, types of neuronal au

126 , the use of ICIs might increase the risk of PNSs, in particular, in patients with the types of cance

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

128 romising for future translational studies on PNS and CNS remyelination.

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

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

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

132 white matter fiber tracts of the peripheral (PNS) and central (CNS) nervous systems during myelinatio

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

134 g-induced conversion (RT-QuIC) in postmortem PNS samples from 14 subjects.

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

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

137 nervous system and that OECs are primarily "PNS glia."

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

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

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

141 ced PNS withdrawal during stress and reduced PNS activation during recovery; however, these associati

142 PM2.5 was generally associated with reduced PNS withdrawal during stress and reduced PNS activation

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

144 ion factor 1A1 (eEF1A1) negatively regulates PNS and CNS remyelination.

145 Remarkably, PNS macrophages constitutively expressed genes previousl

146 Some evidence suggests that resident PNS-MPs along with MPs of hematogenous origin may be inv

147 c characterization of the nondiseased rodent PNS.

148 dominant negative symptoms of schizophrenia (PNS), and minimal positive/depressive/extrapyramidal sym

149 ssion considers the evolution of the sensory PNS in the phylum Chordata.

150 bers of myelinating Schwann cells and severe PNS hypomyelination.

151 ze the role of nerve environment for shaping PNS macrophage identity.

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

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

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

155 f oversaturated calcium phosphate solutions, PNS with a hydrodynamic radius of R(h) ~ 1 nm is formed

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

157 derlying formation of prenucleation species (PNS) that precede solid-liquid phase separation.

158 Perineural spread (PNS) refers to tumor growth along large nerves, a macros

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

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

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

162 nough to cause Peripheral Nerve Stimulation (PNS).

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

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

165 Paraneoplastic neurological syndromes (PNSs) comprise a group of disorders that can affect any

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

167 ing in cells of the peripheral nerve system (PNS).

168 we measured parasympathetic nervous system (PNS) activity using continuous electrocardiogram monitor

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

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

171 cell types in the peripheral nervous system (PNS) and pinpoint specific genes that are major contribu

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

173 ivity in both the peripheral nervous system (PNS) and the central nervous system (CNS).

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

175 ages (MPs) of the peripheral nervous system (PNS) are the main cellular agent controlling this proces

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

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

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

179 pid metabolism in peripheral nervous system (PNS) contributes to the pathogenesis of neuropathy remai

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

181 range of CNS and peripheral nervous system (PNS) disease.

182 kinson's disease, peripheral nervous system (PNS) disorders such as chemotherapy-induced, diabetic, a

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

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

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

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

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

188 cribe the sensory peripheral nervous system (PNS) in the tail of a cephalochordate, Asymmetron lucaya

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

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

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

192 generation in the peripheral nervous system (PNS) is the slow rate of regrowth.

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

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

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

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

197 es using cultured peripheral nervous system (PNS) neurons have demonstrated that KIF1A, a kinesin-3 m

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

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

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

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

202 ther cells in the peripheral nervous system (PNS) remains limited.

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

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

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

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

207 inly in the adult peripheral nervous system (PNS), but also in adult neurons of the central nervous s

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

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

210 ple axons; in the peripheral nervous system (PNS), Schwann cells (SCs) myelinate a single axon.

211 evelopment of the peripheral nervous system (PNS), Schwann-cell-secreted gliomedin induces the cluste

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

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

214 These peripheral nervous system (PNS)-experienced microglia can travel to distal CNS area

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

216 including in the peripheral nervous system (PNS).

217 d function of the peripheral nervous system (PNS).

218 ons affecting the peripheral nervous system (PNS).

219 ily affecting the peripheral nervous system (PNS).

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

221 tions in the host peripheral nervous system (PNS).

222 acrophages of the peripheral nervous system (PNS).

223 expressed in the peripheral nervous system (PNS): Na(V) 1.7, Na(V) 1.8 and Na(V) 1.9.

224 peripheral and the central nervous systems (PNS and CNS).

225 the peripheral and central nervous systems (PNS and CNS, respectively) is a prerequisite for functio

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

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

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

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

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

231 We further show that PNS macrophages rely on IL-34 for maintenance and arise

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

233 le in the study of pathologies affecting the PNS.

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

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

236 diseases and conditions that compromise the PNS.

237 , suggesting that this layer constitutes the PNS-CNS immunological barrier.

238 glia limitans (the glial layer defining the PNS-CNS border) is considered unique as it consists of i

239 ion from latency, infection spreads from the PNS back via axons to the peripheral mucosal tissues, a

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

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

242 wever, iron absorption and management in the PNS are poorly understood.

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

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

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

246 In the PNS of Caspr-null mice, diffusion trapping mediated by t

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

248 ed a severe and progressive pathology in the PNS, characterized by dysmyelination and swelling of the

249 d in the severe degeneration of axons in the PNS, inducing a full-blown neuropathy.

250 In the PNS, myelination occurs postnatally when Schwann cells (

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

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

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

254 l myelination and axonal degeneration in the PNS.

255 axonal regeneration and remyelination in the PNS.

256 ct control of functional nerve repair in the PNS.

257 lying axonal wrapping and myelination in the PNS.

258 regulation of myelin sheath thickness in the PNS.

259 ated gene expression and immune cells in the PNS.

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

261 t MCT expression and lactate function in the PNS.

262 ffect of Na(V) 1.6 channel activation in the PNS.

263 therapies for demyelinating diseases in the PNS.

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

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

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

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

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

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

270 hanges in the immune cell populations of the PNS.

271 equence, for an effective myelination of the PNS.

272 nsequence, for the normal myelination of the PNS.SIGNIFICANCE STATEMENT To determine the function of

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

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

275 al and technical advances in research on the PNS.

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

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

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

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

280 ment in typical sCJDMM(V)1 suggests that the PNS tropism of sCJD prions is strain dependent.

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

282 NS and PNS displayed inflammation, while the PNS was also characterized by fibrosis, massive infiltra

283 d remyelination, which is one reason why the PNS is significantly better at recovery compared with th

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

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

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

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

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

289 Thus, PNS and CNS abnormalities may involve different aspects

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

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

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

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

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

295 2.5 exposure across pregnancy in relation to PNS withdrawal and activation, indexed by changes in res

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

297 ika infection was more often associated with PNS disease (26 [63%] of 41 patients with Zika infection

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

299 In patients with PNS, (18)F-FDG PET shows both abnormality along the cour

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