ライフサイエンスコーパス: NSE

1 NSE > 33 ng/ml has a high false-positive rate in patient

2 NSE > 33 ng/ml levels measured 1-3 days after cardiac ar

3 NSE and tau are better associated with NCD and less infl

4 NSE and tau protein at the 6-hour time point were both s

5 NSE can pinpoint the nanoscale dynamics changes in a hig

6 NSE directly probes coherent (i.e., pair correlated) sca

7 NSE levels were assessed in blood samples obtained 24, 4

8 NSE levels were deregulated in leukemias and were influe

9 NSE was a robust predictor of neurological outcome in a

10 NSE, S100beta, or BIS alone predicted neurological outco

11 NSE-apoE mice and similar models may facilitate the prec

12 NSE-Rb db/db mice were infected with T. cruzi to determi

13 d NO-mediated compensatory responses in 2K1C NSE-AT(1a) peripheral arteries during this later phase,

14 are always slender and elongate, the PGP 9.5/NSE population comprise two morphological types--one sle

15 lar in overall shape to the pyriform PGP 9.5/NSE population, gustducin never colocalizes with PGP 9.5

16 r 36 degrees C does not significantly affect NSE levels.

17 get temperature did not significantly affect NSE values.

18 The neuronal expression of an NSE-Fig4(Cys486Ser) transgene in vivo prevented the neon

19 2 hours after CPR (FPR 10; 95% CI, 6-16) and NSE levels were not.

20 Double-label studies show that PGP 9.5 and NSE always colocalize.

21 cted C-33 LNCaP cells, ERK was activated and NSE level was elevated, and cells obtained the NE-like p

22 cted C-33 LNCaP cells, ERK was activated and NSE was elevated.

23 presence of PD98059, the ERK activation and NSE elevation were abolished, following a dose-response

24 mice compared with those in infected FVB and NSE-Rb db/db mice.

25 the resulting inflammation in Hand2(+/-) and NSE-noggin mice was compared with that of wild-type litt

26 ntin, and negative for A2B5, CNPase, NF, and NSE.

27 s approach is the multiplexing of ProGRP and NSE with the additional ability to perform fingerprintin

28 ighest concentrations in week 1 of S100B and NSE were associated with poor outcome, as were highest c

29 te small-angle neutron scattering (SANS) and NSE scattering properties.

30 uron-specific enolase promoter-driven apoE3 (NSE-apoE3) or apoE4 (NSE-apoE4) transgenic mice.

31 promoter-driven apoE3 (NSE-apoE3) or apoE4 (NSE-apoE4) transgenic mice.

32 N-LEPR-B and neuron-specific enolase-LEPR B (NSE-LEPR-B).

33 Emerging CSF biomarkers NSE, VLP-1, HFABP, and YKL-40 were moderately associated

34 blot analysis was performed on bitransgenic NSE-tTA, TetOp-DeltaFosB, and single-transgenic NSE-tTA

35 e hypothesize that increased levels of blood NSE may characterize LHON carriers as a biomarker of ong

36 s of db/db mice that are hemizygous for both NSE-LEPR-B and SYN-LEPR-B transgenes (Nse+Syn db/db).

37 tals the enzyme forms the asymmetric complex NSE x Mg2 x SO4/NSE x Mg x Cl, where "/" separates the d

38 with NSE-apoE3 mice and wild-type controls, NSE-apoE4 mice showed impairments in learning a water ma

39 flexes, and motor scores 72 hours after CPR; NSE levels at admission, 12 hours after reaching target

40 th Alzheimer's disease, whereas those of CSF NSE, VLP-1, HFABP, and YKL-40 were moderate (average rat

41 -preferring mice that overexpress DeltaFosB (NSE-tTA x TetOp-DeltaFosB) exhibit less avoidance of the

42 molecule diffusion to the simulation-derived NSE and potential problems in their estimation are exami

43 r was demonstrated successful in determining NSE in clinical serum samples.

44 a marker for the overall nerve distribution, NSE antibodies revealed abundant smooth and varicose ner

45 etic or biochemical tumor marker (MYCN, DNA, NSE, or ferritin), or by both unamplified MYCN and aneup

46 ron scattering (SANS) and neutron spin echo (NSE) spectroscopy were used to measure the tertiary stru

47 30.4 %) carriers with significantly elevated NSE levels (mean = 75.8 +/- 42.3 mug/L), 9/14 (64.3%) we

48 levation (STE) and non-ST-segment elevation (NSE) groups and by the presence or absence of abnormal R

49 f 2.8 kb of the rat neuron-specific enolase (NSE) 5' flanking region fused to a cDNA encoding the ful

50 Serum levels of neuron-specific enolase (NSE) and neuron-enriched S100 beta (S100beta) were measu

51 Neuron-specific enolase (NSE) is a biomarker for neuronal stress.

52 Neuron-specific enolase (NSE) is a widely-used biomarker for prognostication of n

53 eptide (ProGRP) and neuron specific enolase (NSE) is presented, which involves coextraction by immuno

54 Serum neuron specific enolase (NSE) measurements, brain imaging findings, somatosensory

55 ining for MCP-1 and neuron specific enolase (NSE) or glial fibrillary acidic protein (GFAP) showed th

56 Human neuron-specific enolase (NSE) or isozyme gamma has been expressed with a C-termin

57 that antibodies to neuron-specific enolase (NSE) preferentially label a subpopulation of photorecept

58 s incorporating the neuron specific enolase (NSE) promoter and either a rat GAP-43 cDNA or the corres

59 c, incorporated the neuron-specific enolase (NSE) promoter and the internal ribosome entry site (IRES

60 nder control of the neuron-specific enolase (NSE) promoter develops a FOP-like phenotype.

61 rol of 1.8-kilobase neuron-specific enolase (NSE) promoter for this purpose.

62 nic mice using the neuron- specific enolase (NSE) promoter or a modified glial fibrillary acidic prot

63 the control of the neuron-specific enolase (NSE) promoter show both markedly increased bone formatio

64 n, we have used the neuron-specific enolase (NSE) promoter to express human apoE3 or apoE4 at similar

65 nder control of the neuron-specific enolase (NSE) promoter.

66 nder control of the neuron specific enolase (NSE) promoter.

67 chemical sensor for neuron specific enolase (NSE) was developed by electrochemical polymerizing ionic

68 ogranin A (CgA) and neuron-specific enolase (NSE) were assessed monthly if elevated at baseline.

69 increased level of neuron-specific enolase (NSE), a classical marker of neuronal cells.

70 ed for detection of neuron-specific enolase (NSE), a traumatic brain injury (TBI) protein biomarker,

71 neuromarkers S100B, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP), in add

72 ologic examination, neuron-specific enolase (NSE), and median nerve somatosensory-evoked potentials (

73 S-100b, neuron specific enolase (NSE), and tau protein were assayed as MBIs preoperativel

74 these cells contain neuron-specific enolase (NSE), tyrosine hydroxylase (TH) and 5-hydroxytryptamine

75 rabbit antisera to neuron-specific enolase (NSE), tyrosine hydroxylase (TH), neuropeptide Y (NPY), v

76 Serotonin, neuron-specific enolase (NSE), ubiquitin carboxyl terminal hydrolase (PGP 9.5), a

77 r apoE4 in neurons [neuron-specific enolase (NSE)-apoE] or astrocytes [glial fibrillary acidic protei

78 o-localization with neuron-specific enolase (NSE)-IR, but is especially prominent in cell bodies of a

79 ofilament (NF), and neuron specific enolase (NSE).

80 ne ionic liquid and neuron specific enolase (NSE).

81 accuracy than serum neuron-specific enolase (NSE; the area under the receiver operating characteristi

82 earing a transgene (neuron-specific enolase [NSE]-Rb) expressing the B isoform of LEPR, the isoform c

83 sion in children with nonsyndromic epilepsy (NSE) over the course of >/=10 years from initial diagnos

84 osal biopsies of normal squamous epithelium (NSE), BE and EAC obtained from a patient who progressed

85 this setting of shared physiologic erasure, NSEs harbor a malignancy-associated hypermethylation cor

86 phosphatase (TRAP) and nonspecific esterase (NSE) activity, which are selective markers for the osteo

87 exploration of a Natural Sources Exclusion (NSE) provision within the TMDL.

88 key nonsense-mediated RNA decay switch exon (NSE) in ATM is repressed by U2AF, PUF60 and hnRNPA1.

89 Surprisingly, most of the cells expressing NSE::LacZ outside the olfactory bulb were astrocytes.

90 apoE4 and, to a significantly lesser extent, NSE-apoE3 mice; however, no fragments were detected in G

91 cteristic curve was 0.91 for tau vs 0.86 for NSE at 72 hours, p = 0.00024).

92 Furthermore, NSE levels were nearly three times greater in asymptomat

93 pM (=700 pg/mL), for total ProGRP and gamma-NSE, respectively.

94 munometric assays for total ProGRP and gamma-NSE, were seen in the analyses of patient serum samples.

95 At 48 and 72 h, NSE predicted neurological outcome with areas under the

96 Of 613 cohort members, 347 had NSEs, of whom 294 (85%) were followed >/=10 years (maxim

97 High NSE cutoff values with false positive rates </=5% and ti

98 y exacerbation of renovascular hypertension, NSE-AT(1a) and nontransgenic (NT) mice underwent 2-kidne

99 To test this hypothesis, NSE-tTA x TetOp-DeltaFosB mice with normal or overexpres

100 In NSE-apoE mice, the pattern of apoE fragmentation resembl

101 dia accompanied this early increase in BP in NSE-AT(1a) mice, as did a substantial cardiovascular reg

102 rtan caused significant falls in basal BP in NSE-AT1a mice but had no effect in nontransgenic control

103 ceptors to the maintenance of baseline BP in NSE-AT1a mice, particularly effective baroreflex bufferi

104 -old NSE-apoE4 mice but barely detectable in NSE-apoE3 mice.

105 LEPR-B transgene expression in NSE-Rb db3J/db3J mice partially corrected the increased

106 -apoE4 mice and, to a much lesser extent, in NSE-apoE3 mice but not in GFAP-apoE3 or GFAP-apoE4 mice.

107 ignificantly increased apoE fragmentation in NSE-apoE4 but not NSE-apoE3 mice.

108 The decrease in cerebellar growth in NSE(Cre/+)/CII(F/F) mice is due to reduced proliferation

109 nd2(+/-) mice and significantly increased in NSE-noggin animals.

110 stabilized at significantly lower levels in NSE-AT(1a) mice despite marked elevations in Ang II leve

111 mplexes assessed were significantly lower in NSE-apoE4 neurons compared with NSE-apoE3 neurons.

112 so accumulated in an age-dependent manner in NSE-apoE4 mice and, to a much lesser extent, in NSE-apoE

113 monal profile was only partially restored in NSE-HPrP/mPrP(0/0) mice and was similar to that of mPrP(

114 The NREM and SWA deficit was restored in NSE-HPrP/mPrP(0/0) mice but not in GFAP-HPrP/mPrP(0/0).

115 unctional overexpression of the transgene in NSE-AT1a mice.

116 The control vector, pTR-UF4, incorporated NSE promoter-driven GFP expression only.

117 d db/db mice compared with those in infected NSE-Rb db/db and FVB wild-type mice.

118 SSPE patients and our work with MV-infected NSE-CD46(+) mice, which express the measles receptor CD4

119 the full complement of short LEPR isoforms (NSE-Rb db/db mice) were similar to those of NSE-Rb db3J/

120 vioral analyses, we demonstrate that NRG1-IV/NSE-tTA mice exhibit abnormal behaviors relevant to schi

121 developed a transgenic mouse model (NRG1-IV/NSE-tTA) in which human NRG1-IV is selectively overexpre

122 Median NSE values were 18 ng/ml versus 35 ng/ml, 15 ng/ml versu

123 eceptor was constructed and transgenic mice (NSE-AT1a) were generated.

124 In genetically modified db/db mice, (NSE-Rb db/db mice), central leptin signaling is reconsti

125 petition of adjacent pseudoexons to modulate NSE levels.

126 and multinucleated cells and TRAP-negative, NSE-positive mononuclear precursors were identified.

127 ic and central expression of PrP in neurons (NSE-HPrP/mPrP(0/0)) or in glia cells (GFAP-HPrP/mPrP(0/0

128 rs reflecting neurodegeneration (T-tau, NFL, NSE, VLP-1, and HFABP), APP metabolism (Abeta42, Abeta40

129 clinically as seminoma (SE) and nonseminoma (NSE), the latter including the pluripotent embryonal car

130 ansgenic mice that have greater than normal (NSE-noggin mice, which overexpress noggin under the cont

131 ased apoE fragmentation in NSE-apoE4 but not NSE-apoE3 mice.

132 mononuclear/giant cells, and the occasional NSE-positive precursor, expressed an intense signal for

133 3% (4/28), 16.0% (8/50) and 12.2% (12/98) of NSE, BE, low-grade dysplasia, HGD and EAC tissues, respe

134 The appearance of NSE immunoreactivity in the different classes of retinal

135 in an age-dependent manner, in the brains of NSE-apoE4 and, to a significantly lesser extent, NSE-apo

136 nt production of beta-s-APP in the brains of NSE-APP mice and enzyme-linked immunosorbent assay analy

137 expression was reduced in the cerebellum of NSE(Cre/+)/CII(F/F) mice, thereby leading to decreased A

138 Colocalization of NSE with SV2 indicated that cone cells began to make syn

139 hey also demonstrate that the combination of NSE with MD is potentially useful for determining the fo

140 the NE-like morphology and the elevation of NSE in C-33 LNCaP cells.

141 Axonal extensions of NSE-labeled cone cells were shown to interact with those

142 Levels of NSE and S100beta were higher in patients with poor outco

143 suggests that the decreased fat phenotype of NSE-DeltaFosB mice is independent of the changes in the

144 This study investigated the role of NSE as a prognostic marker of outcome after out-of-hospi

145 well as the alpha- and the gamma-subunit of NSE isoenzymes.

146 d by ELISA specific for the gamma subunit of NSE.

147 (NSE-Rb db/db mice) were similar to those of NSE-Rb db3J/db3J mice, suggesting that the short LEPR is

148 The body weights of NSE-Rb transgenic mice that possessed the full complemen

149 e hippocampus were prominent in 21-month-old NSE-apoE4 mice but barely detectable in NSE-apoE3 mice.

150 gustducin never colocalizes with PGP 9.5 or NSE.

151 Patients with an early CgA or NSE response had a longer PFS compared with patients wit

152 erapeutic hypothermia, use of motor score or NSE, as recommended in current guidelines, could possibl

153 er between and individually quantify ProGRP, NSE, and their isoform and isoenzyme variants, respectiv

154 rol of the neuron-specific enolase promoter (NSE-PDGF-A) resulted in a striking hyperplasia of retina

155 control of neuron-specific enolase promoter (NSE::LacZ) from the SVZ of adult mice into the striatum

156 f angiotensin II (Ang II) type 1a receptors (NSE-AT(1a)) to unmask the role of the brain renin-angiot

157 After removing NSE templates, a molecularly imprinted sensor was succes

158 nd an increasing profile over time in S100B, NSE, and GFAP.

159 High, serial NSE values are strong predictors of poor outcome after O

160 Serum NSE concentrations in carriers (27.17 +/- 39.82 mug/L) w

161 Serum NSE levels are higher in LHON carriers compared with aff

162 Serum NSE levels were determined by ELISA specific for the gam

163 le carriers had significantly elevated serum NSE levels.

164 It may be significantly better than serum NSE, which is recommended in guidelines and currently us

165 Op-DeltaFosB founder lines but not in single NSE-tTA transgenic controls.

166 forms the asymmetric complex NSE x Mg2 x SO4/NSE x Mg x Cl, where "/" separates the dimer subunits.

167 P-TFII knockout mice using a tissue-specific NSE-Cre recombinase.

168 Using neutron spin-echo spectroscopy (NSE), normal mode analysis, and a statistical-mechanical

169 Using neutron spin echo spectroscopy (NSE), we show salt-concentration-dependent excitation of

170 plication of neutron spin-echo spectroscopy (NSE).

171 We show that NSE spectroscopy can determine the domain mobility tenso

172 Results show that NSE-AT(1a) mice developed hypertension much more rapidly

173 The NSE activation was haplotype-specific and was most promo

174 The NSE results provide insights into the nature of protein

175 The NSE-immunoreactive photoreceptors were identified as con

176 The NSE-Rb transgene was expressed in the brain, with low le

177 Because the NSE promoter drives expression primarily in neurons, thi

178 similar to that previously reported for the NSE-LEPR-B transgene.

179 most promoted by cytosine at rs609621 in the NSE 3' splice-site (3'ss), which is predominant in high

180 k of mortality/MI (hazard ratio 0.93) in the NSE group at 180 days.

181 ratio 0.79 in the STE group and 0.81 in the NSE group) and with risk of mortality/MI (hazard ratio 0

182 In the NSE group, 8152 of 19 304 (42%) had abnormal RF.

183 spite this partial rescue, later in life the NSE-Fig4(Cys486Ser) transgenic mice display significant

184 LFS was successfully employed to measure the NSE level in clinical blood plasma samples taken from de

185 confirm that a significant component of the NSE arises from internal dynamics.

186 The late onset phenotype of the NSE-Fig4(Cys486Ser) transgenic mice demonstrates that th

187 dates as the mediators of the effects of the NSE-Rb transgene on energy homeostasis, ingestive behavi

188 te the internal motion's contribution to the NSE signal, with the largest being classic hinge bending

189 id cyclases in that it does not contain the "NSE/DTE" motif on helix H that specifically chelates Mg(

190 ith the surfactant in the trans form through NSE measurements of the Q-dependent effective diffusion

191 wed high selectivity and sensitivity towards NSE, produced a linear response in the concentration ran

192 -tTA, TetOp-DeltaFosB, and single-transgenic NSE-tTA control mice to determine the pattern of DeltaFo

193 king blood vessel endothelial cells, whereas NSE-IR apparently marks the layer of smooth muscle cells

194 ignificantly elevated S-100b levels, whereas NSE and tau were not significantly influenced.

195 F-IR is more prominent in the nucleus, while NSE-IR is more prominent in the cytoplasm and neurites.

196 Compared with NSE-apoE3 mice and wild-type controls, NSE-apoE4 mice sh

197 tly lower in NSE-apoE4 neurons compared with NSE-apoE3 neurons.

198 13 bird exclusion structure, consistent with NSE.

199 occurs in over one-half of young people with NSE and generally persists.