ライフサイエンスコーパス: CSF

1 CSF and plasma C4 levels were not significantly correlat

2 CSF Chit-1 and CHI3L1 are significantly increased in ALS

3 CSF glucose and protein levels were normal for 83/116 (7

4 CSF neurofilament light protein (NfL), plasma NfL, and C

5 CSF NfL appears to be a more sensitive measure than plas

6 CSF NfL elevations were more likely in individuals close

7 CSF parameters were not generally predictive of HHV-6 po

8 CSF tau concentrations at the time of the CM episode may

9 CSF-1 and IL-34 secretion from GF was evaluated in respo

10 CSF-1 and IL-34 were expressed and secreted constitutive

11 CSF-2 immunoreactivity was higher in abruption-complicat

12 FA-M/E was ordered on 1,025 CSF samples from 948 patients; 121 (11.8%) specimens wer

13 ion was examined with patient sera (n = 31), CSFs (n = 11), longitudinal serum samples (n = 15), and

14 Glymphatic influx of a CSF tracer was significantly enhanced at 30 d postsurger

15 HIV RNA was <=40 copies/mL in all CSF and plasma specimens.

16 e central nervous system (CNS) and analyzing CSF aids the diagnosis of CNS diseases, but our understa

17 I3L1 are significantly increased in ALS, and CSF Chit-1 and CHI3L1 levels correlate to the rate of di

18 n ChP organoids with a selective barrier and CSF-like fluid secretion in self-contained compartments.

19 the potential clinical utility of blood and CSF KLK8 as a biomarker for incipient AD.

20 2 mL; P < .001), and mean summated brain and CSF (33 mL; P < .001) at postflight day 1 with correspon

21 ynamics, and expansion of summated brain and CSF volumes.

22 iations between CT and baseline clinical and CSF parameters.

23 27.5%), normalizing vitreous echodensity and CSF in each case.

24 ilament light protein (NfL), plasma NfL, and CSF YKL-40 were elevated in this far-from-onset preHD co

25 (18)F-fluorodeoxyglucose PET and CSF p-tau changes occurred later in the fourth decade of

26 ggested that amyloid PET, (18)F-FDG PET, and CSF test combinations may add accuracy to clinical evalu

27 Amyloid PET, (18)F-FDG PET, and CSF test combinations may add accuracy to clinical evalu

28 Serum and CSF biomarkers of inflammation and blood-brain barrier (

29 mental changes in the ventricular system and CSF sources (including neural progenitors and choroid pl

30 ect staining (Gram and calcofluor white) and CSF cryptococcal antigen or by repeat ME panel testing.

31 ture media, as well as < 10 pM in artificial CSF.

32 We found no correlation between baseline CSF lactate levels and blood capillary lactate levels (p

33 higher among individuals with high baseline CSF lactate >5 mmol/L (35%; 38/109) as compared to indiv

34 We evaluated the association between CSF levels of 18 cytokines, previously found to be assoc

35 We also observed a high correlation between CSF C4 levels and age.

36 er CSF and/or plasma sTREM2 differed between CSF biomarker-defined Parkinson's disease participant su

37 increase in inflammatory biomarkers in both CSF and blood throughout the 48-hour study period.

38 al species previously detected in the brain, CSF or oral cavity of patients with AD.

39 ion of distance from the inner central canal CSF pool to the outer subpial surface.

40 anscriptomic and proteomic signatures of ChP-CSF organoids reveal a high degree of similarity to the

41 of PSST1 in cerebrospinal fluid-contacting (CSF-c) neurons of the hypothalamic paraventricular organ

42 Neuro-COVID CSF leukocytes featured an enriched interferon signature

43 The observed directional CSF flow can be explained by naturally occurring and/or

44 Ectopic CSF-cNs in the spinal cord of C57Bl/6N mice emerge durin

45 ly unimpaired participants (22 with elevated CSF amyloid-beta peptide 42 levels, 15 with elevated CSF

46 oid-beta peptide 42 levels, 15 with elevated CSF phosphorylated tau levels, mean age of 62.705 +/- 4.

47 enrolled in a study of cerebrospinal fluid (CSF) abnormalities in syphilis that was conducted at the

48 ed signaling factors in cerebrospinal fluid (CSF) and a key barrier between blood and brain.

49 agnostic performance of cerebrospinal fluid (CSF) and blood KLK8 for AD and mild cognitive impairment

50 l fluid (ISF) and human cerebrospinal fluid (CSF) and chronic sleep deprivation accelerates the sprea

51 Novel cerebrospinal fluid (CSF) and plasma biomarkers are among the earliest detect

52 Cerebrospinal fluid (CSF) and plasma from 35 patients with systemic lupus ery

53 lymerase genomes in the cerebrospinal fluid (CSF) and plasma in individuals with incomplete viral sup

54 HIV-1 evolution in the cerebrospinal fluid (CSF) and plasma may result in discordant drug resistance

55 f protein biomarkers in cerebrospinal fluid (CSF) and plasma using a highly sensitive proteomic immun

56 cterium tuberculosis in cerebrospinal fluid (CSF) are inadequate.

57 phenotypes in blood and cerebrospinal fluid (CSF) by flow cytometry in HIV-infected adults with crypt

58 we recently found that cerebrospinal fluid (CSF) concentration of the "social" neuropeptide arginine

59 The cerebrospinal fluid (CSF) contains an extracellular thread conserved in verte

60 enerative biomarkers in cerebrospinal fluid (CSF) differentiate patients with suspected normal pressu

61 e incidence of abnormal cerebrospinal fluid (CSF) flow dynamics in children with central nervous syst

62 urons were treated with cerebrospinal fluid (CSF) from patients with anti-NMDAR encephalitis or contr

63 ructure, and aqueductal cerebrospinal fluid (CSF) hydrodynamics relative to spaceflight and to establ

64 n, augmented aqueductal cerebrospinal fluid (CSF) hydrodynamics, and expansion of summated brain and

65 clinical presentation, cerebrospinal fluid (CSF) inflammation, and outcome from tuberculous meningit

66 Tau protein in cerebrospinal fluid (CSF) is a central and relevant biomarker of Alzheimer's

67 ship between plasma and cerebrospinal fluid (CSF) KP metabolites nor their association with inflammat

68 Cerebrospinal fluid (CSF) lactate levels can differentiate between bacterial

69 Cerebrospinal fluid (CSF) leakage is a risk factor for developing bacterial m

70 igated the potential of cerebrospinal fluid (CSF) lipocalin 2 (LCN2), a secreted glycoprotein that ha

71 d NFL concentrations in cerebrospinal fluid (CSF) or plasma in MCI Abeta+ and AD Abeta+.

72 different compared with cerebrospinal fluid (CSF) P-tau217, CSF P-tau181, and tau-PET (AUC range, 0.9

73 ricted to patients with cerebrospinal fluid (CSF) pleocytosis.

74 s (MS), but whether the cerebrospinal fluid (CSF) profile can help to identify patients at risk of di

75 Cerebrospinal fluid (CSF) protects the central nervous system (CNS) and analy

76 tion study (GWAS) of 59 cerebrospinal fluid (CSF) proteins with a connection to Alzheimer's disease (

77 ADNI) participants with cerebrospinal fluid (CSF) Ptau collected at baseline, diffusion tensor imagin

78 t work illuminating how cerebrospinal fluid (CSF) regulates brain function.

79 V/PeV RT-PCR testing of cerebrospinal fluid (CSF) samples in children impacted care of hospitalized n

80 Molecular testing of cerebrospinal fluid (CSF) using the BioFire FilmArray meningitis/encephalitis

81 ic data from plasma and cerebrospinal fluid (CSF) were analyzed with nonlinear mixed-effects modeling

82 protein alterations in cerebrospinal fluid (CSF), a proximal site to pathology.

83 In cerebrospinal fluid (CSF), we measured 3 macrophage and microglia-related pro

84 H), an expansion of the cerebrospinal fluid (CSF)-filled brain ventricles.

85 s increased presence in cerebrospinal fluid (CSF).

86 ctrometry in plasma and cerebrospinal fluid (CSF).

87 human blood plasma and cerebrospinal fluid (CSF).

88 plasma samples and 36 cerebral spinal fluid (CSF) samples taken from patients with subarachnoid or ve

89 tient biosamples, e.g. cerebrospinal fluids (CSF), and study their correlation with the disease manif

90 iple regression analysis and controlling for CSF biomarkers, we identified the effect of healthy agei

91 ive Mg isotopic analysis was carried out for CSF from hydrocephalus patients using only 5 muL of samp

92 Under the ATN framework, CSF analytes provide evidence of the presence or absence

93 o drain macromolecules and immune cells from CSF into cervical lymph nodes (CLNs).

94 phatics drain extravasated erythrocytes from CSF into CLNs after SAH, while suggesting that modulatin

95 h, logMAR VA, contrast sensitivity function (CSF [Freiburg acuity contrast test]), and quantitative B

96 and mesopic contrast sensitivity functions (CSF) are associated with incident motor vehicle crash in

97 cally responsible for T(h)17 (IL-17, IL-6, G-CSF) and T(h)1 differentiation and expression (IL-12, TN

98 rleukin-1RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.001).

99 tration of neutralizing antibodies against G-CSF only partially restored the myeloproliferation, sugg

100 Signaling by G-CSF, a regulator of neutrophil development, trafficking,

101 by granulocyte colony-stimulating factor (G-CSF) and administration of neutralizing antibodies again

102 hil numbers after IR, as well as following G-CSF-mediated bone marrow mobilization, which was indepen

103 rinking-resilient males showed the highest G-CSF, IL-13, and leptin levels.

104 The increased G-CSF was accompanied by an increased activation of the NF

105 We find that administration of G-CSF accelerates extinction and reduces cue-induced drug

106 Administration of G-CSF during extinction accelerated the rate of extinction

107 Blockade of G-CSF restored normal granulopoiesis in DeltaNC16A mice.

108 asis of evidence we studied the effects of G-CSF treatment on extinction and reinstatement of cocaine

109 ague Dawley rats were injected with PBS or G-CSF during (1) extinction or (2) abstinence from cocaine

110 okines that discriminated high responders (G-CSF, IFN-gamma, TNF-alpha) correlated with both egress o

111 to understand the involvement of glymphatic CSF-ISF exchange in tau pathology.

112 GM-CSF triggered TGFbeta1 expression by M2 TAMs by activati

113 ulations of both low-frequency (IL-10(+); GM-CSF(+)) and high-frequency (TNF(+)) cytokine-defined B c

114 L cells, but only in mice producing IL-3, GM-CSF, and SCF transgenically or in regular mice in which

115 inflammatory pain development in which a GM-CSF->CCL17 pathway appears critical, nerve growth factor

116 Although GM-CSF has been widely used in dendritic cell (DC) research

117 sment, serum CXCL10/IP-10 (P = 0.047) and GM-CSF (P = 0.050) were higher and nasopharyngeal RT-PCR cy

118 cytokines including IL6, IL17, MCP-1, and GM-CSF in the tumor-bearing host, and persisted as memory c

119 cyte colony-stimulating factors (GCSF and GM-CSF) enhance swarming and neutrophil ability to restrict

120 inflammation via production of IL-18 and GM-CSF.

121 us that coexpresses a PD-L1 inhibitor and GM-CSF.

122 ory cytokines: interleukin-17 (IL-17) and GM-CSF.

123 accompanied by high levels of circulating GM-CSF and TGFbeta1.

124 C cells lowered the levels of circulating GM-CSF, suppressed TAM recruitment, and decreased the level

125 We identified Csf2/GM-CSF as a primary complement-dependent inflammatory media

126 mmon beta (CSF2RB) chain family cytokines GM-CSF and IL-5.

127 ed toxicity, whereas perforin deficiency, GM-CSF deficiency, or modulation of the myeloid population

128 Taken together, we uncover T cell-derived GM-CSF as a key inducer of the chemokine CCL22 and thus, to

129 I/T/DIN/GM-CSF has significant antitumor activity in patients with

130 yte-macrophage colony-stimulating factor (GM-CSF) has many more functions than its original in vitro

131 yte-macrophage colony stimulating factor (GM-CSF) in nociceptor activation in male and female mice.

132 yte-macrophage colony-stimulating factor (GM-CSF) in vitro.

133 yte-macrophage colony-stimulating factor (GM-CSF) is a multipotent cytokine that prompts the prolifer

134 yte-macrophage colony-stimulating factor (GM-CSF) production by CD4(+) T cells.

135 yte-macrophage colony-stimulating factor (GM-CSF) signalling in astrocytes drives the expression of M

136 yte-macrophage colony-stimulating factor (GM-CSF), a myelopoietic growth factor and pro-inflammatory

137 ficant preclinical data have emerged from GM-CSF deletion/depletion approaches indicating that GM-CSF

138 e established the absence of a functional GM-CSF receptor in murine nociceptors, and suggest an indir

139 utoimmune disease, it remains unclear how GM-CSF is regulated at sites of tissue inflammation.

140 The authors identified GM-CSF secretion in a rare population of CD11c(+) CD4(+) T

141 In GM-CSF-deficient (Csf2(-/-)) mice, inflammation resolution

142 h apoptotic cells significantly increased GM-CSF production and T(H)2 cell differentiation.

143 Intriguingly, GM-CSF signaling amplifies inflammatory cytokine production

144 in macrophage lineage populations and is GM-CSF dependent, 2) for its action in arthritic pain and d

145 ning protein (CIS) is crucial in limiting GM-CSF signaling not only during inflammatory arthritis but

146 re, DCs from IL-9R(-/-) mice induced more GM-CSF production by T cells and exacerbated EAE upon adopt

147 tive discusses the pleiotropic biology of GM-CSF and the scientific merits behind these contrasting a

148 Key features of GM-CSF biology need to be defined better, such as the respo

149 Blockade or knockdown of GM-CSF can partially reduce immunosuppression of Ly6C(high)

150 creasing recognition of the importance of GM-CSF in autoimmune disease, it remains unclear how GM-CSF

151 Knockdown of GM-CSF in tumor cells also delays tumor progression with de

152 tion of NK cells, or specific ablation of GM-CSF production in NK cells, abrogated disease.

153 Furthermore, the neutralization of GM-CSF reduced cDC2s activation.

154 nstrate that monocytes in the presence of GM-CSF, TGF-beta1, and the Notch ligand DLL4 differentiate

155 y-state differentiation and maturation of GM-CSF-dependent DCs are insufficiently known.

156 of wild-type T cells or administration of GM-CSF.

157 These findings shed new light on GM-CSF biology in sterile tissue inflammation and identify

158 n which the cells were exposed to IL-3 or GM-CSF delivered using a cotransduction strategy.

159 plicated in asthma) but not IL-5, IL-9 or GM-CSF in response to IL-33.

160 creased the generation of those producing GM-CSF.

161 F, TGF-beta-treated) and proinflammatory (GM-CSF-treated) human monocyte-derived macrophages and micr

162 Clinical trials targeting GM-CSF or its receptor have shown encouraging efficacy and

163 t and reactivation into a pathogenic Th17/GM-CSF phenotype.

164 metry and ELISA experiments revealed that GM-CSF blockage in monocytes stimulated production of the c

165 nduced colonic pathology, indicating that GM-CSF constitutes a nonredundant inflammatory pathway in t

166 tion/depletion approaches indicating that GM-CSF is a potential target in many inflammatory/autoimmun

167 In addition, we observed that GM-CSF was not regulated by either interleukin 6 (IL-6) or

168 in tumor control in CRC and introduce the GM-CSF-IRF5 axis as a critical driver of the antitumor acti

169 cacy of miltefosine combined with topical GM-CSF (M+GM) versus miltefosine and placebo (M+P) versus s

170 Mycobacterium tuberculosis infection upon GM-CSF blockade.

171 infiltrate, and persistent arthritis, via GM-CSF production, as deletion of NK cells, or specific abl

172 The association of Miltefosine with GM-CSF do not improve therapeutic outcome.

173 tiative (n1 = 284; n2 = 553) with harmonized CSF assays of amyloid-beta and hyperphosphorylated tau (

174 hat the seeding-competent mHTT species in HD CSF are significantly elevated upon disease onset and wi

175 ntrations of eight MMPs in ventricular human CSF.

176 increase but plasma p-tau181 is increased if CSF Abeta has already changed prior to Abeta PET changes

177 In CSF of HTT gene expansion carriers, we found increased l

178 In CSF of VSP patients, NK cells (CD3-CD161 +) were increas

179 In CSF, worsening disease was associated with nominally sig

180 disease in symptomatic patients was 100% in CSF and 81.3% in plasma.

181 plaque and more neurofilament light chain in CSF.

182 r density and elevated NFL concentrations in CSF and plasma are associated in AD-vulnerable regions i

183 EVG concentrations in CSF and the CSF:plasma ratio remained stable (P = .203)

184 regions and increased NFL concentrations in CSF or plasma.

185 We analyzed circulating tumor DNA (ctDNA) in CSF to detect mutated genes.

186 nsity (R: 0.573; P < .01) and degradation in CSF (R: 0.611; P < .01).

187 The HAGH protein was not detected in CSF.

188 u protein and phospho-tau were determined in CSF.

189 ow a statistically significant difference in CSF C4 values between groups.

190 We calculated between-group differences in CSF concentrations of amyloid-beta1-42 peptide, tau prot

191 ificant differences in the ratios of DRMs in CSF and plasma were found in 3 individuals with HAND (3/

192 ort revealed that solute speed was faster in CSF compared to grey and white matter.

193 owed a statistically significant increase in CSF C4 levels between groups after adjusting for sex and

194 The diagnostic accuracy of KLK8 in CSF and blood was determined using receiver operating ch

195 kers of brain injury or neurodegeneration in CSF and blood.

196 and chemokine receptors were up-regulated in CSF memory B cells.

197 ction of T. pallidum DNA in blood or rRNA in CSF at the index episode were significantly lower in tho

198 moa(R) assay for quantification of tau368 in CSF was developed, while total tau (t-tau) was measured

199 The Gd-DOTA injection into CSF was performed on the bench after which the mice unde

200 um activation and cytoplasmic secretion into CSF.

201 Of the recurrent episodes, 27 had known CSF leakage (71%) of whom 20 (53%) had previous surgery

202 We pooled individual-level CSF data from 3 sequential cryptococcal meningitis clini

203 nd that mRNA expression of the CSF1R ligand, CSF-1, is increased in the brain of PD patients compared

204 eptor (CSF-1R), which has two known ligands: CSF-1 and interleukin-34 (IL-34).

205 Immunostaining localized CSF-2 primarily to decidual cell cytoplasm and cytotroph

206 In longitudinal CSF samples, available in 13 subjects, NPTX2 decreased a

207 ividuals with mid-range (22%; 25/112) or low CSF lactate (9%; 9/97; p=<.0001).

208 of age were less often female and had lower CSF opening pressure, fewer headaches, a higher chance o

209 The HP2 allele associated with lower CSF haemoglobin-haptoglobin complex levels.

210 servations of reduced cfmtDNA seen in lumbar CSF translated to the post-mortem ventricular CSF.

211 ventricular and parenchymal (glia-lymphatic) CSF pathways.

212 , interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.001).

213 d the effect of calcitriol on homeostatic (M-CSF, TGF-beta-treated) and proinflammatory (GM-CSF-treat

214 cells) are controlled by signals from the M-CSF receptor (CSF1R).

215 T(2B) and 5-HT(7) expression restricted to M-CSF-primed monocyte-derived macrophages (M-MO).

216 We also analysed matched CSF, post-mortem brain tissue, and iPSCs from the same p

217 stroke volume (14.6 muL; P = .045) and mean CSF peak-to-peak velocity magnitude (2.2 cm/sec; P = .01

218 We measured CSF concentrations of NPTX2 using an in-house ELISA, and

219 We measured CSF lactate in individuals with cryptococcal meningitis

220 ansformed colony-forming units (CFUs) per mL CSF were analyzed by general linear regression versus da

221 er's and Families' study, with baseline MRI, CSF biomarkers, APOE genotyping and neuropsychological e

222 In adults with ALS due to SOD1 mutations, CSF SOD1 concentrations decreased at the highest concent

223 Neonatal CSF AVP concentrations were significantly lower among AS

224 tural neuroimaging, functional neuroimaging, CSF and genetic testing.

225 Cerebrospinal fluid contacting neurons (CSF-cNs) represent a specific class of neurons located i

226 r accuracy than plasma P-tau181, plasma NfL, CSF P-tau181, CSF Abeta42:Abeta40 ratio, and MRI measure

227 All pathogens detected in nonpleocytic CSF samples were herpesviruses.

228 e, negative predictive value of nonpleocytic CSF samples, test yield and false-positivity rate, and t

229 425) and controls (defined as having normal CSF amyloid and tau and normal cognition, n = 127).

230 sanguinity of C57Bl/6J substrain with normal CSF-cN distribution and C57Bl/6N substrain with majority

231 er and lower than the Hb-binding capacity of CSF haptoglobin.

232 The cause of CSF leakage was identified in 49 of 65 episodes (75%), w

233 ipal component analyses revealed clusters of CSF inflammatory markers that were associated with high

234 Elevation of CSF-CCL2 was sufficient to drive ChP immune cell recruit

235 The expression of CSF-1 and IL-34 in gingival tissue and fibroblasts sugge

236 hangiogenesis, enhanced glymphatic influx of CSF, and reactive gliosis.

237 tion and C57Bl/6N substrain with majority of CSF-cNs in ectopic position.

238 pulsations only drive oscillatory motion of CSF in the PVS.

239 Here we investigate the performance of CSF p-tau217 as a biomarker of AD in comparison to p-tau

240 and Cyfip2 underlie the ectopic position of CSF-cNs in the spinal cord of C57Bl/6N mice.

241 during whole period devoted to production of CSF-cNs and reach their ventral destinations during firs

242 We identified a subset of CSF samples from individuals later diagnosed with ASD, m

243 tic (ROC) analyses and compared with that of CSF core biomarkers Abeta42, P-tau and T-tau.

244 se impairment could trigger translocation of CSF-cNs outside the central canal area, we took advantag

245 is of CNS diseases, but our understanding of CSF leukocytes remains superficial.

246 results show that the Reissner fiber acts on CSF-cNs and thereby contributes to establish body axis m

247 The analysis based on CSF tracer injection in combination with immunohistochem

248 iative (GENFI), all of whom had at least one CSF sample.

249 l RNA or specific IgM antibodies in serum or CSF.

250 Further, paired CSF and blood B cell subsets (RRMS; n = 7) were isolated

251 ied more frequently in plasma than in paired CSF (P = 0.0078).

252 e partial HIV-1 polymerase genomes in paired CSF and plasma samples from 12 HIV-1-positive participan

253 sCD14 was also elevated in patients' CSF and urine.

254 Our report shows that patients' CSF may be devoid of viral particles even when they test

255 ceptors in vitro after exposure to patients' CSF antibodies or SSM5, we used a functional assay based

256 ncubation of oligodendrocytes with patients' CSF or SSM5 but remained largely unaltered with the corr

257 RM, we did not find any difference in plasma/CSF or in cell-associated DNA/RNA viral load in anatomic

258 drivers of disease, including choroid plexus CSF hypersecretion, ependymal denudation, and damage and

259 nduction therapy and had serial quantitative CSF cultures.

260 is the colony stimulating factor-1 receptor (CSF-1R), which has two known ligands: CSF-1 and interleu

261 rom patients <=6 months old for whom routine CSF EV and PeV reverse transcription-PCR (RT-PCR) testin

262 ive cerebroventricular transfer of patient's CSF antibodies.

263 n plasma P-tau181, plasma NfL, CSF P-tau181, CSF Abeta42:Abeta40 ratio, and MRI measures (AUC range,

264 red with cerebrospinal fluid (CSF) P-tau217, CSF P-tau181, and tau-PET (AUC range, 0.90-0.99; P > .15

265 These findings indicate that CSF sTREM2 could serve as a surrogate immune biomarker o

266 Our data suggests that CSF-1 is involved in the survival and proliferation of t

267 The CSF Hb concentration after high-volume and low-volume aS

268 The CSF is produced by the choroid plexus (ChP), a protectiv

269 e observed inflammation in the brain and the CSF spaces in both posthaemorrhagic hydrocephalus (PHH)

270 EVG concentrations in CSF and the CSF:plasma ratio remained stable (P = .203) over time.

271 /plasma cells most clearly distinguished the CSF from blood compartments.

272 control fibroblasts and use to elucidate the CSF/brain and peripheral tissue expression of HTT in pre

273 lls to the CP, increased leukocytosis in the CSF and blood, but infiltration into the cortex remained

274 Thus, cancer cells appear to survive in the CSF by outcompeting macrophages for iron.

275 ments with the detection of the virus in the CSF has elicited an urgent need for investigating the po

276 Suspended in the CSF is an extracellular structure called the Reissner fi

277 and symptoms, and CHIKV-RNA was found in the CSF of 92.3% of these patients.

278 lence of IL-17-producing Th17.1 cells in the CSF of HTT gene expansion carriers, predominantly in pre

279 microglia/macrophage derived exosomes in the CSF of Parkinson's disease patients, we confirmed the pr

280 SARS-CoV-2 has been detected in the CSF of some patients.

281 at day 85 in the change from baseline in the CSF SOD1 concentration between the tofersen groups and t

282 tions in concentrations of biomarkers in the CSF were shown.

283 In the CSF, CDH6 levels were positively correlated with t-tau a

284 the availability of a chemical signal in the CSF.

285 etriaminepentaacetic acid injection into the CSF intraventricular space followed by nuclear medicine

286 Involvement of the CSF identified the group at greatest risk for early toxi

287 odeling and simulations demonstrate that the CSF flow is generated locally by caudally-polarized moti

288 We hypothesized that the CSF inflammatory response pattern after surgery would di

289 into fragments before being secreted to the CSF.

290 ancer cells, but not macrophages, within the CSF express the iron-binding protein lipocalin-2 (LCN2)

291 cingulate had previously been associated to CSF biomarkers in mild cognitive impairment and dementia

292 for the Reissner fiber-signaling pathway to CSF-cNs and rescue body axis morphogenesis.

293 pressure hydrocephalus (NPH) who respond to CSF drainage from patients who do not respond.

294 SF translated to the post-mortem ventricular CSF.

295 Parkinson's disease, we investigated whether CSF and/or plasma sTREM2 differed between CSF biomarker-

296 While CSF-1 has been extensively studied, the biology and func

297 cquired bacterial meningitis associated with CSF leakage from a prospective nationwide cohort study.

298 as not significantly different compared with CSF P-tau217 (AUC, 0.96; P = .22).

299 It correlated with CSF P-tau181 and predicted positive Tau positron emissio

300 -tau217 correlates better than p-tau181 with CSF and PET measures of neocortical amyloid-beta burden