ライフサイエンスコーパス: CNS

1 CNS disorders, and in particular psychiatric illnesses,

2 CNS relapse occurred in only 4 patients.

3 h and implicated in secondary injury after a CNS insult.

4 On the basis of X-ray structures of a CNS-penetrating reactivator, monoxime RS194B, reversibly

5 We thus used a CNS-penetrant generic medication used in hypertension, i

6 were enriched for those involved in abnormal CNS synaptic transmission (PFDR = 0.02) and antigen proc

7 After trauma, regeneration of adult CNS axons is abortive, causing devastating neurologic de

8 larval CNS express para, while in the adult CNS para is broadly expressed.

9 d with a low dose of T. muris on d 105 after CNS prion infection coincided with enhanced astrocyte ac

10 n regeneration and functional recovery after CNS trauma.

11 ameliorates disease severity and alleviates CNS immunopathology and demyelination, associated with d

12 controlling MuPyV infection in the brain and CNS injury.IMPORTANCE A comprehensive understanding of J

13 tory role in oligodendrocyte development and CNS myelination.

14 onstrate convergence between nAb evasion and CNS neurovirulence in vivo by a frequent JCPyV-PML VP1 m

15 differentiated tissues such as the liver and CNS.

16 ted CNS relapse, or combined bone marrow and CNS relapse rates, or in toxicities observed for patient

17 lts in decreased oligodendrocyte numbers and CNS hypomyelination, although oligodendrocyte precursor

18 n-DCM, 462 patients), DCM (44 patients), and CNS (25 patients).

19 by promoting the expansion of peripheral and CNS-infiltrating IL-10(+) T cells.

20 ox10, a key transcription factor for PNS and CNS myelination and remyelination, to drag Sox10 out of

21 Anti-CNS antibody reactivity was evident in the sera of the M

22 uli are categorized in a decision-associated CNS region in Drosophila larvae, and then decoded by a g

23 Additionally, br-met-associated CNS-myeloid exhibited downregulation of Cx3cr1.

24 In contrast, accumulation of NF186 at CNS nodes does not undergo a switch; it is predominantly

25 In the brain, Tat can be taken up by CNS cells via receptor-mediated endocytosis.

26 , PD, schizophrenia, epilepsy, brain cancer, CNS infection (viral and fungal), multiple sclerosis, ce

27 Central nervous system-native myeloid cells (CNS-myeloids) and bone-marrow-derived myeloid cells (BMD

28 ad significantly fewer isolated and combined CNS relapses compared with patients who did not receive

29 Cerebral white matter pathology is a common CNS manifestation of Fabry disease, visualized as white

30 Swelling of the brain or spinal cord (CNS edema) affects millions of people every year.

31 Current CNS value is over $323 per milligram.

32 howed toxicity in mice, it also demonstrated CNS penetration in a PK study and significant reduction

33 identify and map both mature and developing CNS neurons that express choline acetyltransferase (ChAT

34 the development and regulation of different CNS macrophage populations.

35 hat had neuroprotective properties and drove CNS axon regeneration in vivo, in part via secretion of

36 using novel engineered carbon nanosheets (E-CNS) derived from sub-bituminous coal.

37 no CNS, (2) observed CNS, and (3) estimated CNS, all adjusted for age, sex, Charlson index, and stro

38 95% CI, 0.81-0.82]), moderate with estimated CNS (0.76 [0.75-0.76]), and lowest without CNS (0.69 [0.

39 At the end of the study, we evaluated CNS inflammation and parasite burden in the surviving mi

40 ns for developing effective biomaterials for CNS applications.

41 The standard of care for CNS prophylaxis for children with B-ALL and no overt CNS

42 the design of thermoresponsive hydrogels for CNS therapy are reviewed.

43 lts have important clinical implications for CNS drug delivery and clearance of CNS waste products, i

44 linear regressions, conducted separately for CNS and non-CNS survivors, identified associations betwe

45 r PET represents a novel diagnostic tool for CNS lymphoma with potential implications for theranostic

46 lacebo response rates in clinical trials for CNS indications, such as depression and schizophrenia, c

47 ial player in establishing a properly formed CNS through its role in the removal of genetically compr

48 A better understanding of the gut-CNS axis will shed new light on the mechanisms of diseas

49 RNA-seq demonstrated that even in a healthy CNS, astrocytes express TAM phagocytic receptors, which

50 esentative experimental systems to study HIV-CNS pathology.

51 gut elicits concomitant effects on the host CNS, which promote the homeostatic developmental balance

52 pulations of immune cells that influence how CNS-related immune responses develop.

53 oxia inducible factor 1alpha (HIF-1alpha) in CNS respiratory centres is necessary for ventilatory acc

54 The underlying alterations in CNS complement cascade proteins (C1q, C3), TLR4, and col

55 elevance, allowing for direct application in CNS focused imaging modalities.

56 ide an overview of the role of astrocytes in CNS inflammation, highlighting recent discoveries on ast

57 r results demonstrate that loss of Cx3cr1 in CNS-myeloid triggers a Cxcl10-mediated vicious cycle, cu

58 Although KV1.3 is not expressed in CNS tissue, intrathecal administration of a KV1.3 channe

59 ation, supporting their critical roles in in CNS pathogenesis.

60 In summary, we prove a role for microglia in CNS-GVHD, identify the TAK1/TNF/MHC-II axis as a mediato

61 However, HRP3-II overexpression in CNS co-cultures did not alter myelination.

62 d glial progenitors and mature cells play in CNS angiogenesis and neurovascular barrier maturation ha

63 physiological factors occurred, primarily in CNS and visceral sensitivity measures, providing new ins

64 eplication and/or latent HIV reactivation in CNS reservoirs, thereby reducing HIV-associated neuroinf

65 l complement proteins and their receptors in CNS dysfunction, recent data suggest that they exert neu

66 V who abuse opioids had higher reservoirs in CNS than the lymphoid system.

67 t actin nucleation, plays a critical role in CNS myelination, and its absence leads to several myelin

68 est that they exert neuroprotective roles in CNS homeostasis through continued refinement of synaptic

69 ost immunity.IMPORTANCE The current trend in CNS disease biology is to attempt to understand the neur

70 N transcript, a construct previously used in CNS injury models.

71 ene fusion-positive solid tumours, including CNS activity due to its ability to penetrate the blood-b

72 ce of isolated bone marrow relapse, isolated CNS relapse, or combined bone marrow and CNS relapse rat

73 /- 1% of neurons in the embryonic and larval CNS express para, while in the adult CNS para is broadly

74 es in the mouse CNS at ~25% of blood levels (CNS blood content is only ~1%-6%) and delivers neurotens

75 s.IMPORTANCE IFN-alpha/beta induction limits CNS viral spread by establishing an antiviral state, but

76 is as manifest by an increase in CD45(-/low) CNS cells expressing A2B5, an early marker in oligodendr

77 er diagnosis, including leukaemia, lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft-tissue sa

78 minantly targeted to both forming and mature CNS nodes via its cytoplasmic domain and requires intact

79 Using the eye as a model CNS tissue, here we show that ectopic expression of Oct4

80 mechanisms by which oligodendroglia modulate CNS angiogenesis remain elusive.

81 l filopodial retraction and in turn modulate CNS gas exchange.

82 romatin landscapes of acutely isolated mouse CNS ECs.

83 It accumulates in the mouse CNS at ~25% of blood levels (CNS blood content is only ~

84 Mouse polyomavirus (MuPyV) CNS infection causes encephalopathology and may provide

85 loss of neural APA in elav/fne double mutant CNS, the first genetic background to largely abrogate th

86 powerful therapeutics for neurodegenerative CNS diseases.

87 stress transcriptomics identified neurotoxic CNS innate immune populations and may enable discovery o

88 Cox-proportional hazards models with (1) no CNS, (2) observed CNS, and (3) estimated CNS, all adjust

89 ssions, conducted separately for CNS and non-CNS survivors, identified associations between PA consis

90 hazards models with (1) no CNS, (2) observed CNS, and (3) estimated CNS, all adjusted for age, sex, C

91 dict mortality was highest when the observed CNS was included (C statistic, 0.82 [95% CI, 0.81-0.82])

92 toimmune disease characterized by attacks of CNS inflammation that are often severe and predominantly

93 tions for CNS drug delivery and clearance of CNS waste products, including Abeta, and for understandi

94 rrelations occurred between a combination of CNS and visceral sensitivity parameters, and GSRS-IBS to

95 n of in situ nasal gel for brain delivery of CNS acting moieties.

96 has a pivotal role in the early diagnosis of CNS complications that potentially are severely debilita

97 CNS) and analyzing CSF aids the diagnosis of CNS diseases, but our understanding of CSF leukocytes re

98 t is made possible by two unique features of CNS vasculature absent in the peripheral organs.

99 MFSD7c is required for the normal growth of CNS blood vessels and that ablation of this gene results

100 atified by previous platinum use, history of CNS metastases, and oestrogen and progesterone receptor

101 In this review, we focus on the impact of CNS-resident cells of the innate immune system for the d

102 of BDNF on metabolism that is independent of CNS activity.

103 We show that the nature and intensity of CNS FBRs are determined by definable properties that sig

104 eted toward understanding the involvement of CNS white matter.

105 ain fatty acids in vitro and in vivo Loss of CNS FAO results in robust accumulation of long-chain acy

106 fy the TAK1/TNF/MHC-II axis as a mediator of CNS-GVHD, and provide a TAK1 inhibitor-based approach ag

107 B(regs) is associated with normalization of CNS immune milieu and concurrent activation of oligodend

108 bnormal MoCA scores (<26) were predictive of CNS disease; low scores (<22) were associated with poor

109 ovide layered diagrammatic representation of CNS divisions, according to their arrangement in corresp

110 ntemporary adjuvant therapies on the risk of CNS metastasis development.

111 Survivors of CNS tumors (9.5%; 95% CI, 5.2% to 13.8%) and bone tumors

112 f the incidence, risk factors, and timing of CNS metastasis is needed to inform surveillance strategi

113 Treatments of CNS with 1 M of H(2)SO(4), HNO(3,) and NaOH solutions we

114 Microglia, a type of CNS immune cell, have been shown to contribute to ethano

115 that could advance current understanding of CNS pathophysiological alterations associated with SARS-

116 rapeutic molecules, medical interventions on CNS disorders are mostly limited to treat symptoms rathe

117 thelin-1 (ET-1) along with Abeta toxicity on CNS pathogenesis; driven by the anatomical and functiona

118 anomedicines displaying either ubiquitous or CNS-specific epitopes triggered the formation and expans

119 pheral neuropathies, neuromyelitis and other CNS disorders.

120 hylaxis for children with B-ALL and no overt CNS involvement remains IT MTX.

121 scribe the TIME of >6000 primarily pediatric CNS tumors using a deconvolution approach (methylCIBERSO

122 ent evidence-also participates in postinjury CNS recovery, chronic neurodegenerative conditions, and

123 onal profiling of oxidative stress-producing CNS innate immune cells identified a core oxidative stre

124 rbonate, and higher current density promotes CNS growth while suppressing CNT growth.

125 hanistic understanding of HIFalpha-regulated CNS myelination from the previous Wnt-dependent view to

126 elopment of new immunotherapies that reverse CNS damage and restore lost neurological function across

127 l genetic deletion of PTEN results in robust CNS axon regrowth, while PTEN repression with short hair

128 logy of carbon, termed Carbon Nano-Scaffold (CNS) with wide a range of high surface area graphene pot

129 actory disease, and seven (3%) had secondary CNS involvement.

130 hocytes are therefore critical for selective CNS entry of autoantibodies, microglial activation, and

131 ur motifs of conserved nucleotide sequences (CNSs) were also determined, which are essential for the

132 sing soil, coco-peat with nutrient solution (CNS) and water (soaked (8 h), germinated (36 h) and harv

133 We localize specific CNS abdominal neurons where de-repressed Hth compromises

134 ds: Adults and Pediatrics, Brain/Brain Stem, CNS, Computer Aided Diagnosis (CAD), Computer Applicatio

135 Early recognition of such CNS complications may improve functional outcome and sur

136 From 2012-2015, 203 patients with suspected CNS infections were included, of whom 56 (27%) were diag

137 tic infection of the central nervous system (CNS) (odds ratio [OR], 3.7; P < .001), imperfect adheren

138 the nilotinib group, central nervous system (CNS) amyloid burden was significantly reduced in the fro

139 ne system within the central nervous system (CNS) and altered the paradigm for successful immunothera

140 d (CSF) protects the central nervous system (CNS) and analyzing CSF aids the diagnosis of CNS disease

141 CAG expansion in ~50 central nervous system (CNS) and peripheral postmortem tissues from seven adult-

142 -1 reservoirs in the central nervous system (CNS) are challenging to address due to low penetration o

143 mples from the human central nervous system (CNS) are currently available in brain banks.

144 e synthetized in the central nervous system (CNS) as well as enterochromaffin cells of the gastrointe

145 The central nervous system (CNS) barriers are crucial interfaces between the CNS and

146 Central nervous system (CNS) blood vessels contain a functional blood-brain barr

147 air has key roles in central nervous system (CNS) development, mediating axonal, and neuronal navigat

148 sease progression in central nervous system (CNS) diseases such as amyotrophic lateral sclerosis (ALS

149 P) type of GBS or in central nervous system (CNS) diseases.

150 their involvement in central nervous system (CNS) disorders, and in particular in Alzheimer's disease

151 t assemble the human central nervous system (CNS) during development and maintain its function throug

152 Loss of central nervous system (CNS) FAO did not result in gross neuroanatomical changes

153 ation throughout the central nervous system (CNS) following many neurotropic virus infections.

154 Inflammation in the central nervous system (CNS) has been linked to demyelination and remyelination.

155 The adult human central nervous system (CNS) has very limited regenerative capability, and injur

156 asome contributes to central nervous system (CNS) homeostasis specifically through its regulation of

157 Disease involved the central nervous system (CNS) in 71 subjects (49%).

158 myeloid cells in the central nervous system (CNS) in the pathogenesis of multiple sclerosis (MS) and

159 mTOR inhibitors for central nervous system (CNS) indications.

160 ding viral causes of central nervous system (CNS) infection among hospitalized neonates and young inf

161 Central nervous system (CNS) infections cause substantial morbidity and mortalit

162 iptomic landscape of central nervous system (CNS) innate immune cells contributing to oxidative stres

163 ocyte entry into the central nervous system (CNS) is essential for immune surveillance but is also th

164 Over time, the central nervous system (CNS) loses function and regenerative capacity(5-7).

165 other non-microglial central nervous system (CNS) macrophage subtypes include border-associated menin

166 adiotherapy (RT) for central nervous system (CNS) malignancies are often long-lasting without any cli

167 t cancers, including central nervous system (CNS) malignancies.

168 idate of interest in central nervous system (CNS) myelination and remyelination, and we sought to inv

169 Central nervous system (CNS) neurodegeneration is defined by a complex series of

170 ng PSST mRNAs in the central nervous system (CNS) of Scyliorhinus canicula using in situ hybridizatio

171 PyV infection in non-central nervous system (CNS) organs, but their relative contributions to MuPyV c

172 s implemented in the central nervous system (CNS) remains poorly understood.

173 immune cells of the central nervous system (CNS) survey their surroundings with their cytoplasmic pr

174 ediment for targeted central nervous system (CNS) therapeutics, especially with carboxylic acid-conta

175 t how they enter the central nervous system (CNS) through the blood-brain barrier (BBB) remains poorl

176 information from the central nervous system (CNS) to peripheral targets.

177 ics in children with central nervous system (CNS) tumors before intraventricular therapy has not been

178 ansmitter within the central nervous system (CNS) with fast, transsynaptic, and modulatory extrasynap

179 tissue damage in the central nervous system (CNS), and none directly promote repair.

180 se cells play in the central nervous system (CNS), and this work has been greatly facilitated by micr

181 ant cell type in the central nervous system (CNS), performing complex functions in health and disease

182 nt in the cephalopod central nervous system (CNS), Scaros, Croll, and Baratte only recently described

183 mmune disease of the central nervous system (CNS), with characteristic inflammatory lesions and demye

184 myeloid cells in the central nervous system (CNS).

185 ersistently inflamed central nervous system (CNS).

186 h other cells in the central nervous system (CNS).

187 ating disease of the central nervous system (CNS).

188 o, especially in the central nervous system (CNS).

189 by microglia in the central nervous system (CNS).

190 he physiology of the central nervous system (CNS).

191 ure elsewhere in the central nervous system (CNS).

192 biquitously tile the central nervous system (CNS).

193 r cell debris in the central nervous system (CNS).

194 t macrophages of the central nervous system (CNS).

195 regeneration in the central nervous system (CNS).

196 ic plasticity in the central nervous system (CNS).

197 d pathologies of the Central Nervous System (CNS); however, their coordinating mechanisms are unclear

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

199 Our group has demonstrated that CNS myelin-specific CD8 T cells unexpectedly harbor immu

200 The CNS synthesis splits CO(2) by electrolysis in molten car

201 nications between gut microorganisms and the CNS continues to uncover critical and previously unappre

202 tory, digestive, and urinary systems and the CNS.

203 barriers are crucial interfaces between the CNS and the periphery.

204 ion, and attenuated inflammation in both the CNS and PNS.

205 he early embryonic precursors colonizing the CNS, but originate primarily from late embryonic precurs

206 ice demonstrated that STAT6 KO in either the CNS or periphery exacerbated ICH outcomes.

207 cells administered ICV also traffic from the CNS into the periphery; following clearance of ATRT xeno

208 ncement of GlcNAc exposure on T cells in the CNS ameliorated clinical EAE symptoms.

209 ceptors (I(2)-IR), widely distributed in the CNS and altered in patients that suffer from neurodegene

210 molecular mechanisms that drive FBRs in the CNS and have important implications for developing effec

211 by FAM222A is predominantly expressed in the CNS and is increased in brains of patients with AD and i

212 cells throughout the body, including in the CNS and the immune system.

213 h contributed to regeneration failure in the CNS by favorably producing triglyceride (TG) storage lip

214 in the PLP1 gene, which is expressed in the CNS by oligodendrocytes.

215 s from 12 HIV-1-positive participants in the CNS HIV Antiretroviral Therapy Effects Research (CHARTER

216 lk between astrocytes and other cells in the CNS in the context of neuroinflammation and neurodegener

217 genetic induction of lipid cacostasis in the CNS of normal mice was associated with ALS-like lipid pa

218 ding to have the greatest instability in the CNS, and liver in the periphery.

219 In the CNS, early-life stress (1) decreased 2-arachidonoyl glyc

220 study demyelination and remyelination in the CNS, in the context of MS.

221 various IL-10 producing immune cells in the CNS, including most prominently Ly49D(+) NK cells and ne

222 as important sources of microbial DNA in the CNS, opening novel opportunities for therapeutic interve

223 In distinction to LNs, in the CNS, the size of latent SIV reservoirs was higher in the

224 n current models of enhancer function in the CNS, we review how enhancers regulate gene expression ac

225 alphaSN is an abundant protein in the CNS, which potentially could overwhelm clearance of cyto

226 termine the activity of PD-1 blockade in the CNS.

227 parasite DNA, cysts, or inflammation in the CNS.

228 rsistent, low-level viral replication in the CNS.

229 are dynamic immunosurveillance cells in the CNS.

230 ng in the oligodendroglial lineage or in the CNS.

231 y associated with CD8 T cell activity in the CNS.

232 naptic transmission at high frequency in the CNS.

233 pe-specific effects of mTOR signaling in the CNS.

234 ts, 4-AP can prevent neuroaxonal loss in the CNS.

235 rophages are important HIV reservoirs in the CNS.

236 e blood-brain barrier (BBB), and infects the CNS in the early stages of infection.

237 es, neutrophils, and B cells infiltrated the CNS.

238 axon regeneration of adult neurons into the CNS after injury.

239 dvancement of systemic inflammation into the CNS and facilitate to understand the interplay between t

240 ncharged forms capable of diffusing into the CNS and multiple zwitterionic forms optimal for reactiva

241 nding against invasion of pathogens into the CNS remain unclear.

242 atment, direct cell transplantation into the CNS to restore myelin has been tested in animal models o

243 nt drug nuclear receptor modulators into the CNS while masking them as functional receptor ligands in

244 tivation, and antibody infiltration into the CNS, and have their olfactory function partially restore

245 ood-brain barrier to deliver a gene into the CNS.

246 to investigate mitochondrial function of the CNS in vivo.

247 ephalomyelitis virus (TMEV) infection of the CNS is cleared in C57BL/6 mice by a CD8 T cell response

248 a from this largely unexplored region of the CNS may help explain the limited success of previous bra

249 this Perspective, we discuss the rise of the CNS regenerative drugs, the main biological techniques u

250 ly concerned with immune surveillance of the CNS, and-according to recent evidence-also participates

251 Microglia, resident immune cells of the CNS, are thought to defend against infections.

252 ia are the main immune effector cells of the CNS.

253 st prevalent congenital malformations of the CNS.

254 S) is a chronic demyelinating disease of the CNS.

255 s is a chronic, demyelinating disease of the CNS.

256 le target for demyelinating disorders of the CNS.SIGNIFICANCE STATEMENT Replacement of oligodendrogli

257 Microglia are parenchymal macrophages of the CNS; as professional phagocytes they are important for m

258 strocytes having an excitatory action on the CNS sympathetic control circuits.SIGNIFICANCE STATEMENT

259 ood cerebrospinal fluid barrier, protect the CNS from external agents.

260 arachnoid mater, and dura mater-surround the CNS, encompassing the cerebrospinal fluid produced by th

261 However, the meninges surrounding the CNS host diverse populations of immune cells that influe

262 l shows pathological deficits throughout the CNS including accumulation of lysosomal storage material

263 l detachment and degeneration throughout the CNS, including in the optic nerve, corpus callosum, and

264 HDC-positive cell populations throughout the CNS, including the optic gland and the peduncle, optic,

265 hanism of synaptic modulation throughout the CNS.

266 s that hinder mass and drug transport to the CNS are described, highlighting the distinct features of

267 e MBP-specific CD8+ T cells recruited to the CNS during CD4+ T cell-initiated EAE engaged in determin

268 gnate TR1 cells and their recruitment to the CNS-draining lymph nodes, sparing their liver-draining c

269 s and migration of inflammatory cells to the CNS.

270 disease and the fungal dissemination to the CNS.

271 neuronal output, which propagates toward the CNS, thus shaping the pain sensation.

272 ecular signatures of immune cells within the CNS at defined times following infection with a neuroada

273 Within the CNS synaptic transmission set, we identify individual si

274 Within the CNS, JCPyV predominately targets two cell types, oligode

275 athologic inflammatory conditions within the CNS, such as multiple sclerosis and its animal model, ex

276 her potentiates viral replication within the CNS, which can lead to HIV-associated neuropathology.

277 ted protein trafficking mechanism within the CNS.

278 hronic and persistent replication within the CNS.

279 sponsible for cellular phenotypes within the CNS.

280 oad range of tumours that develop within the CNS.

281 contributes in neuroinflammation within the CNS.

282 r patterning and tissue mechanics within the CNS.

283 ory transcriptional modules, contributing to CNS pathology in EAE and, potentially, multiple sclerosi

284 performed by applying RECIST 1.1 criteria to CNS target lesions by investigator assessment.

285 nistered macrophages deliver therapeutics to CNS, including glial cell line-derived neurotrophic fact

286 The results showed that H(2)SO(4)-treated CNS exhibited the highest adsorption capacity.

287 ption process of Pb(II) on H(2)SO(4)-treated CNS.

288 a promising non-invasive method for treating CNS tumours.

289 ble caring for offspring, but the underlying CNS changes are poorly understood.

290 ted ART during acute HIV infection underwent CNS assessments across four ATI remission trials.

291 plore astrocytes within the adult vertebrate CNS in vivo.

292 We found that a patient with VZV CNS vasculopathy had antibody that neutralized interfero

293 nya infection was more often associated with CNS disease (26 [47%] of 55 patients with chikungunya in

294 enges in assessing response in children with CNS tumours.

295 enges in assessing response in children with CNS tumours.

296 cluded, of whom 56 (27%) were diagnosed with CNS infections and 16 were diagnosed with bacterial meni

297 estigation of immunotherapy in patients with CNS disease from NSCLC is warranted.

298 ology and clinical outcomes of patients with CNS infections from a prospective surveillance study tha

299 d CNS (0.76 [0.75-0.76]), and lowest without CNS (0.69 [0.69-0.70].

300 is still expressed along the adult zebrafish CNS neuraxis in most locations seen in larvae.