ライフサイエンスコーパス: NAA

1 NAA and NAAG as well as aspartoacylase (ASPA), the enzym

2 NAA mapping of the brain may provide early surveillance

3 NAA may be an important risk modifier for methylation in

4 NAA tests may be used in combination with culture due to

5 NAA was strongly and negatively correlated with FCVRS ac

6 NAA was the metabolite characterized by the greatest reg

7 NAA, Cr, Cho, NAA/Cr, NAA/Cho, and Cho/Cr values were ev

8 NAA-RFs are photonic crystal structures produced by sinu

9 NAA/Cho and Cho/Cr ratios correlated with the scaled gro

10 NAA/Cr in the high-dose davunetide group (N=8) suggested

11 NAA/Cr was unchanged for combined high- and low-dose dav

12 The delta (15)NAA approach reveals variation in TP within and among sp

13 ent from delta (15)Nbulk data, and delta (15)NAA data suggest that two insectivorous species (Lasiuru

14 her terrestrial organisms and that delta (15)NAA provides a reliable approach for addressing question

15 sotopes of individual amino acids (delta (15)NAA) and bulk-tissue carbon (delta (13)Cbulk) and nitrog

16 ive was to assess the precision of delta (15)NAA-based estimates of TP relative to other approaches.

17 We now report that ablating NAA synthesis by constitutive genetic disruption of Nat8

18 clude both abnormal myelination and abnormal NAA diffusion within axons.

19 Whether accumulating NAA, absence of NAA-derived acetate, or absence of any u

20 nchyma showed decreases in N-acetylasparate (NAA) and tissue water T2, and increases in choline-conta

21 s to have lower levels of N-acetylaspartate (NAA) and glycerophosphocholine plus phosphocholine (GPC

22 ray brain matter based on N-acetylaspartate (NAA) and on membrane-derived complex lipids.

23 natural 13C abundance of N-acetylaspartate (NAA) and the appearance of 13C-labeled glutamate, glutam

24 be done because thalamic N-acetylaspartate (NAA) concentration alone accurately predicted an adverse

25 It is unclear whether N-acetylaspartate (NAA) depletions documented in schizophrenia patients mig

26 atalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.

27 N-Acetylaspartate (NAA) is one of the most abundant amino acid derivatives

28 N-acetylaspartate (NAA) is synthesized by aspartate N-acetyltransferase (ge

29 Baseline N-acetylaspartate (NAA) level, myo-inositol (mI) in normal-appearing white

30 elevated choline (Cho)-to-N-acetylaspartate (NAA) ratio (hereafter, Cho/NAA ratio) and whether their

31 diffusion coefficient of N-acetylaspartate (NAA) was significantly elevated, suggesting intra-axonal

32 n, glutamate, serine, and N-acetylaspartate (NAA) were reduced after LPS, whereas glutamine was incre

33 (Cr), choline (Cho), and N-acetylaspartate (NAA) were segmented into 81 regions with Automated Anato

34 yo-inositol and decreased N-acetylaspartate (NAA)).

35 at white matter levels of N-acetylaspartate (NAA), a chemical involved in the metabolic pathway for m

36 Studies indicate that N-acetylaspartate (NAA), a marker of neuronal integrity, and choline, a mar

37 N-acetylaspartate (NAA), an indicator of neuronal mitochondrial function, n

38 nd lower brain glutamate, N-acetylaspartate (NAA), and creatine concentrations in MSUD patients, whic

39 nal integrity measured by N-acetylaspartate (NAA), brain volume, and clinical outcomes in a large, pr

40 abolite concentrations of N-acetylaspartate (NAA), choline (Cho) and creatine (Cr).

41 Concentrations of N-acetylaspartate (NAA), choline (Cho), creatine (Cr), myo-inositol (mI), a

42 30) and smokers (n = 35), N-acetylaspartate (NAA), choline-containing compounds, creatine-containing

43 decrease in the levels of N-acetylaspartate (NAA), myo-inositol (mI), scyllo-inositol (sI), glycine,

44 opy to measure prefrontal N-acetylaspartate (NAA), which is mainly localized in neurons, and total cr

45 (ASPA), which hydrolyzes N-acetylaspartate (NAA).

46 dicarboxylates as well as N-acetylaspartate (NAA).

47 with thalamic volumes and N-acetylaspartate (NAA)/choline (Cho), and fractional anisotropy of white-m

48 gle voxel (basal ganglia) N-acetylaspartate (NAA)/Choline, NAA/Creatine and myo-inositol/Creatine rat

49 ation between hippocampal N-acetylaspartate (NAA)/Cr and Glx/Cr in patients with schizophrenia were f

50 DTS to study metabolite (N-acetylaspartate, NAA) diffusion within axons in patients with BDP (n=21)

51 , galactose, and an N-acetylated amino acid (NAA), showed a high sensitivity (86.9% [75.8-94.2]) and

52 ts; brain volume and N-acetyl aspartic acid (NAA) decreased steadily, but no published quantitative M

53 se where the auxin 1-naphthaleneacetic acid (NAA) was applied to pre-veraison grape berries.

54 brane-permeable auxin 1-naphthylacetic acid (NAA).

55 vanced adenoma (AA) and nonadvanced adenoma (NAA).

56 When plotted against NAA-TBPro, DC-TBPro had the highest correlation [coeffic

57 stimation of the following metabolites: Ala, NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, NAAG,

58 -GA-PEI)-modified nanoporous anodic alumina (NAA) interferometers with reflectometric interference sp

59 fS) combined with nanoporous anodic alumina (NAA) platforms when detecting different analytes under d

60 urpose first, the nanoporous anodic alumina (NAA) was fabricated.

61 this purpose, the nanoporous anodic alumina (NAA) was first fabricated.

62 Recently, nucleic acid amplification (NAA) tests have shown promise for the diagnosis of TBM,

63 as compared with nucleic acid amplification (NAA)-based assays for determining the etiology of vagini

64 etermination by neutron activation analysis (NAA) and inductively coupled plasma mass spectrometry (I

65 Neutron activation analysis (NAA) was used for validation purposes.

66 ated the effect of Native American ancestry (NAA) and diet on biomarkers for lung cancer risk.

67 ignificant reductions of NAA (P < 0.001) and NAA/Cr + Pcr (P < 0.001), and significant improvement in

68 Urine organic acids (especially alphaKG and NAA) and SLC13A3 mutations should be screened in patient

69 t that the lack of increase in brain Asp and NAA is possibly because of its active utilization by the

70 Although brain Asp and NAA levels did not change by betaOHB administration, a 4

71 e synthesis of cytosolic aspartate (Asp) and NAA, which is impeded by aralar deficiency, presumably t

72 The combination of Cho/Cr and NAA/Cho ratios measured in the posterior periventricular

73 ynaptic immunoreactivity and both NAA/Cr and NAA/mI in the posterior cingulate gyrus.

74 burden was associated with lower NAA/Cr and NAA/mI.

75 sample, higher NAA and Glu in the DLPFC and NAA concentrations in multiple lobar gray matter and whi

76 o a substantial increase in Asp (3-fold) and NAA (4-fold) levels.

77 opy at 3T to longitudinally estimate Glu and NAA concentrations from large areas of normal-appearing

78 We also considered GMV and NAA/Cr differences between patients with CFS and 26 sex-

79 previous reports, we tested whether GMV and NAA/Cr in the dorsolateral prefrontal cortex are associa

80 ptoms was the main predictor of both GMV and NAA/Cr in the left dorsolateral prefrontal cortex of pat

81 re pain was associated with reduced GMVs and NAA/Cr, over and above the effects of fatigue, depressiv

82 apacity to transport alphaKG, succinate, and NAA.

83 ffect of ibuprofen on hippocampal volume and NAA loss.

84 As NAA and Glu are commonly regarded to reflect neuronal he

85 ssue-specific (ako) Nat8l-ko mice as well as NAA-supplemented mice on various diets.

86 tate-glutamate (NAAG) to N-acetyl aspartate (NAA) and glutamate.

87 els of the neuron marker N-acetyl aspartate (NAA), along with higher levels of glutamate (Glu) and Gl

88 MRS metabolite ratios of N-acetyl aspartate (NAA)/creatine (Cr), NAA/myoinositol (mI), and mI/Cr meas

89 MRS was used to measure N-Acetyl-aspartate (NAA) and myo-inositol (mI).

90 bolite concentration for N-acetyl-aspartate (NAA), choline (Cho) and creatine (Cr).

91 ociated with increased N-acetyl-l-aspartate (NAA) in the anterior cingulate and insular cortices, and

92 brain concentration of N-acetyl-L-aspartate (NAA) is a characteristic feature of Canavan disease, a v

93 Genetic suppression of N-acetyl-l-aspartate (NAA) synthesis, previously shown to block brain vacuolat

94 endroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevates brain NAA

95 at prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in central nervous

96 Baseline NAA/Cr correlated with the composite MCCB score (R=0.52,

97 The association between NAA and risk for methylation was assessed using generali

98 detected no significant correlations between NAA alterations and PANSS-P (P = 0.679) or PANSS-G (P =

99 Both NAA and NAAG elicited the expression of a novel immunore

100 Both NAA and tCr correlated with Global Assessment of Functio

101 n reduced synaptic immunoreactivity and both NAA/Cr and NAA/mI in the posterior cingulate gyrus.

102 wer tissue water content and a role for both NAA and Cho, as osmolytes is proposed.

103 acetate and l-aspartic acid, elevates brain NAA and causes "spongiform" vacuolation of superficial b

104 In the brain, NAA delivers the acetate moiety for synthesis of acetyl-

105 In the brain, NAA is considered an important energy metabolite for lip

106 ation coupled with off-line determination by NAA enabled the determination of more extracted As speci

107 an 98% when compared to values determined by NAA.

108 es more genes were induced than repressed by NAA.

109 (FFD) after weaning but could be rescued by NAA supplementation.

110 T infants had significantly lower cerebellar NAA (p < 0.025) and higher Cho (p < 0.001) at TEA when c

111 ants and were noted to have lower cerebellar NAA, Cho and Cr concentrations compared with those witho

112 NAA, Cr, Cho, NAA/Cr, NAA/Cho, and Cho/Cr values were evaluated visual

113 n the OSA and the control group for NAA/Cho, NAA/Cr and Cho/Cr ratios for both hippocampal regions.

114 ing characteristics (ROC) curve for NAA/Cho, NAA/Cr and Cho/Cr ratios.

115 Cho/NAA ratio in ADC-rCBV ROIs was compared with that in con

116 ratio of choline to N-acetyl-aspartate (Cho/NAA) may provide additional information on tumor extent

117 and nonenhancing regions showed elevated Cho/NAA ratios, which were significantly higher than those i

118 -acetylaspartate (NAA) ratio (hereafter, Cho/NAA ratio) and whether their volumes correlated with pro

119 onclusion:(18)F-FET uptake and increased Cho/NAA ratio are not always congruent and may represent dif

120 lumes for (18)F-FET uptake and increased Cho/NAA were 19 +/- 20 cm(3) (mean +/- SD) and 22 +/- 24 cm(

121 mass in (18)F-FET PET and MRS imaging of Cho/NAA, determined by simultaneously acquired, 3-dimensiona

122 al ganglia) N-acetylaspartate (NAA)/Choline, NAA/Creatine and myo-inositol/Creatine ratios were measu

123 d elevations in central nervous system (CNS) NAA and progressively worsening leukodystrophy.

124 The diagnostic accuracy of the combined NAA-based test construct was approximately 20 to 25% hig

125 onstrates that the proposed system combining NAA-RFs with RfS has outstanding capabilities to develop

126 Finally, the results of a commercial NAA test (GenProbe Aptima Trichomonas vaginalis assay; A

127 We compared NAA-TBPro with DC-TBPro and 2 protein estimates from the

128 reatine (Cr) and N-acetylaspartyl compounds (NAA) and standardised neuropsychological test scores.

129 Conclusion NAA/Cr levels decreased in the motor cortex in patients

130 A/Cr + Pcr (P = 0.500) compared to controls; NAA levels were negatively correlated with PANSS total s

131 Conversely, NAA-treated wild-type mice showed reduced adipocyte resp

132 When lesion volume was added as a covariate, NAA also showed a significant correlation with executive

133 In patients with CSM, NAA normalized to Cr (NAA/Cr) levels were significantly lower 6 months after s

134 s of N-acetyl aspartate (NAA)/creatine (Cr), NAA/myoinositol (mI), and mI/Cr measured in the posterio

135 NAA, Cr, Cho, NAA/Cr, NAA/Cho, and Cho/Cr values were evaluated visually and b

136 GPC/Cr and decreased left thalamic tNAA/Cr, NAA/Cr were detected.

137 T2 lesions; and N-acetylaspartate/creatine (NAA/Cr) levels in WM.

138 cts of davunetide on change in NAA/creatine (NAA/Cr) and choline/creatine (choline/Cr) over 12 weeks

139 Results In patients with CSM, NAA normalized to Cr (NAA/Cr) levels were significantly

140 ingulate and insular cortices, and decreased NAA in posterior cingulate and parietal cortices.

141 tion of increased Cho/Cr ratio and decreased NAA/Cho ratio predicted impaired motor outcome at a corr

142 Intact white matter integrity with decreased NAA/Cr levels suggests that mitochondrial metabolic dysf

143 projections and synaptic pruning (decreasing NAA, Ch, Cr, Glx) in posterior regions, support age-rela

144 These mice have no detectable NAA.

145 PANSS-G (P = 0.668) symptom changes; nor did NAA/Cr + Pcr changes with alterations in PANSS-P (P = 0.

146 Smokers showed lower DLPFC NAA, Cr, mI and Glu concentrations and lower lenticular

147 rated greater age-related decreases of DLPFC NAA and anterior cingulate cortex and DLPFC Glu levels.

148 d suggests the existence of the NAT8L-driven NAA metabolism as a novel pathway to provide cytosolic a

149 n response to auxin, cytoplasmic auxin (i.e. NAA) stimulated a lesser response.

150 To this end, NAA-RFs are filled with different solutions of d-glucose

151 Structurally engineered NAA-RFs are combined with reflection spectroscopy (RfS)

152 ed nanoporous anodic alumina photonic films (NAA-PFs) and reflectometric interference spectroscopy (R

153 of nanoporous anodic alumina rugate filters (NAA-RFs) for real-time and label-free biosensing applica

154 ng nanoporous anodic alumina rugate filters (NAA-RFs) modified with human serum albumin (HSA) and ref

155 First, NAA platforms are structurally engineered in order for o

156 reased concentrations of cerebrospinal fluid NAA and dicarboxylates (including alphaKG) were observed

157 y associated with reduced concentrations for NAA, Cho, and Cr.

158 er operating characteristics (ROC) curve for NAA/Cho, NAA/Cr and Cho/Cr ratios.

159 nur7/nur7)) mice that are also deficient for NAA synthase Nat8L (Nat8L(-/-)/Aspa(nur7/nur7)).

160 es between the OSA and the control group for NAA/Cho, NAA/Cr and Cho/Cr ratios for both hippocampal r

161 toacylase (ASPA), the enzyme responsible for NAA degradation, are significantly reduced in glioma tum

162 re, we demonstrate that acetate derived from NAA is not essential for myelin lipid synthesis and that

163 re the intensity of the reflected light from NAA to the CCD decreased.

164 TCP measurements from NAA are corroborated by indirect measurements based on l

165 (DeltaOT(eff)) of PEI-GA-PEI-functionalized NAA interferometers are monitored in real-time by RIfS,

166 Glu/NAA ratio was tested as a predictor of brain volume loss

167 ocampi, and significantly higher Glu and Glu/NAA in the right hippocampus.

168 ith higher levels of glutamate (Glu) and Glu/NAA.

169 ease the rate of NAA decline, and higher Glu/NAA[NAWM] ratio increases the rate of decline of brain v

170 Each 10% increase in Glu/NAA[NAWM] was associated with a loss of 0.33% brain volu

171 oad was positively correlated with right Glu/NAA in PTSD patients.

172 e examined together in relation to right Glu/NAA, only re-experiencing symptoms remained a significan

173 vely correlated with right Glu and right Glu/NAA.

174 -aspartate plus N-acetyl-aspartyl-glutamate (NAA) to creatine (Cr) and choline compounds (Cho) to Cr

175 AA concentrations at 3 to 4 years of age; GM NAA concentrations remained reduced at 9 to 10 years of

176 Most notably, a dynamic reversal of GM NAA reductions was observed in the children with ASD.

177 een the ASD and DD groups in the rates of GM NAA, Cho, and Cr changes between 3 and 10 years of age.

178 By contrast, persistent GM NAA reductions in the children with DD suggest a differe

179 ngs in the stuttering sample included higher NAA:Cr and Cho:Cr ratios (regression coefficient, 197.4-

180 Across the sample, higher NAA and Glu in the DLPFC and NAA concentrations in multi

181 Administration of the IgM NAA to MRL-lpr mice also delayed the onset of nephritis.

182 Further work to improve NAA tests would benefit from the availability of standar

183 plore the effects of davunetide on change in NAA/creatine (NAA/Cr) and choline/creatine (choline/Cr)

184 udinal decline in NAA[GM] (-0.06mM change in NAA[GM] /yr for each unit increase in Glu; p = 0.004).

185 ctive of accelerated longitudinal decline in NAA[GM] (-0.06mM change in NAA[GM] /yr for each unit inc

186 n myo-inositol occurs before the decrease in NAA in hippocampus but not cortex; the hippocampus shows

187 gs support the hypothesis that a decrease in NAA/Cr is associated with loss of synapses and early pTa

188 ents presented no significant differences in NAA (P = 0.084) or NAA/Cr + Pcr (P = 0.500) compared to

189 tide appeared to produce modest increases in NAA/Cr and choline/Cr in DLPFC in people with schizophre

190 yr in NAA[NAWM] (p < 0.001) and 0.15mM/yr in NAA[GM] (p = 0.056).

191 WM] was predictive of a loss of 0.28mM/yr in NAA[NAWM] (p < 0.001) and 0.15mM/yr in NAA[GM] (p = 0.05

192 ter maturation (increasing FA and increasing NAA, Ch, Cr concentrations accompanying advancing age) i

193 s, and parietal white matter with increasing NAA and glutamate and decreasing myoinositol and choline

194 We now demonstrate that inhibiting NAA synthesis by intracisternal administration of a lock

195 tions of glutamate, glutamine, myo-inositol, NAA, creatine and choline.

196 y on mGluR3 and by reducing degradation into NAA and glutamate resulting in reduced cell death in mod

197 ase II (GCP II) rapidly hydrolyzes NAAG into NAA and glutamate.

198 d an AUC of 0.74 (0.66-0.80), and of lactate-NAA (>0.22) had an AUC of 0.94 (0.89-0.97).

199 erence fringe pattern about the mid-latitude NAA transmitter is due to a 3 km reduction in the effect

200 nly one intact Nat8L allele accumulated less NAA, developed a less severe pathology, phenotypic impro

201 In adult life, NAA deficiency promotes a beneficial metabolic phenotype

202 Here we investigated longitudinal NAA changes in drug-naive first-episode patients (FEP) w

203 P = 0.032) in Hispanics with high versus low NAA.

204 was associated with elevated mI/Cr and lower NAA/mI ratios, but not with NAA/Cr.

205 mpal cortices and amygdala, as well as lower NAA:Cr and Cho:Cr ratios (regression coefficient, 119.8-

206 years of age, the ASD group exhibited lower NAA, Cho, and Cr concentrations than did the TD group in

207 Even the BD + IR/GI subjects had lower NAA than the euglycemic participants (t(4)(3) = 2.13, p

208 PTSD patients exhibited significantly lower NAA in right and left hippocampi, and significantly high

209 Higher pTau burden was associated with lower NAA/Cr and NAA/mI.

210 In the periventricular white matter, NAA/Cho ratio in OSA patients was significantly lower th

211 est-based findings included lower group mean NAA:Cr ratio in stuttering than nonstuttering participan

212 Both the mean NAA/Cr and Cho/Cr ratio values were significantly higher

213 rats demonstrate the following metabolites: NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, NAAG,

214 on brain volume, prompting the use of the mI:NAA ratio in normal-appearing white matter as a predicto

215 The mI:NAA ratio in normal-appearing white matter has consisten

216 Furthermore, the mI:NAA ratio predicted clinical disability (Multiple Sclero

217 i.e., sensing principle) of gelatin-modified NAA-PFs (i.e., sensing element) during enzymatic digesti

218 n offset) on the sensitivity of HSA-modified NAA-RFs toward indomethacin, a model drug.

219 verify that the combination of HSA-modified NAA-RFs with RIfS can be used as a portable, low-cost, a

220 treatment induces an acute reduction of MPFC NAA during the early phase of schizophrenia, which may b

221 gether with the marked increment in neuronal NAA synthesis supports the role of NAA as a lipid precur

222 brain and the likely involvement of neuronal NAA in postnatal myelination in these mice.

223 ruption of Nat8l, which encodes the neuronal NAA-synthetic enzyme N-acetyltransferase-8-like.

224 u concentrations and lower lenticular nuclei NAA level; smokers also demonstrated greater age-related

225 MRS metabolite peak-area ratios (n=160) of NAA-creatine (<1.29) had an AUC of 0.79 (0.72-0.85), of

226 e (<1.29) had an AUC of 0.79 (0.72-0.85), of NAA-choline had an AUC of 0.74 (0.66-0.80), and of lacta

227 Whether accumulating NAA, absence of NAA-derived acetate, or absence of any unknown functions

228 demonstrated that the diagnostic accuracy of NAA tests is currently insufficient for them to replace

229 lysis to evaluate the diagnostic accuracy of NAA tests with cerebrospinal fluid (CSF) samples against

230 es expressed NaDC3 and, thus, are capable of NAA up-take.

231 TR and the apparent diffusion coefficient of NAA correlated with more adverse outcomes in the patient

232 The apparent diffusion coefficient of NAA did not differ from healthy controls, suggesting no

233 s suggest that lowering the concentration of NAA in the brains of children with Canavan disease would

234 correlations of cerebellar concentrations of NAA, Cho and Cr (Spearman correlations of 0.59, 0.64 and

235 This study sought to examine the effects of NAA and NAAG on primary tumor-derived glioma stem-like c

236 Therefore, inhibition of NAA synthase is a promising therapeutic option for CD.

237 wever, indicates that complete inhibition of NAA synthase may bear unforeseeable risks for the patien

238 To test this, we measured levels of NAA across white matter and gray matter in the brain usi

239 The levels of NAA and tCr were lowest among BD + T2DM, intermediate in

240 for myelin lipid synthesis and that loss of NAA-derived acetate does not cause the myelin phenotype

241 ed sensitivity, specificity, PLR, and NLR of NAA tests against CRS were 68% (95% CI, 41 to 87%), 98%

242 s models, Glu was examined as a predictor of NAA decline, annualized percentage brain volume change,

243 gher Glu concentrations increase the rate of NAA decline, and higher Glu/NAA[NAWM] ratio increases th

244 ients demonstrated significant reductions of NAA (P < 0.001) and NAA/Cr + Pcr (P < 0.001), and signif

245 neuronal NAA synthesis supports the role of NAA as a lipid precursor during postnatal myelination.

246 ically, our data point to a possible role of NAA as modulator of pancreatic insulin secretion and sug

247 We identified an important role of NAA availability in the brain during adolescence, as 75%

248 However, the role of NAA in peripheral tissues remained elusive.

249 cteristic peak in the reflection spectrum of NAA-RFs (Deltalambdapeak).

250 GSC malignancy and suggests that the use of NAA or NAAG is not an appropriate therapeutic approach t

251 ting from deficiency of the oligodendroglial NAA-cleaving enzyme aspartoacylase.

252 Groups also were compared on NAA, choline-containing compounds, Cr, and mI concentrat

253 tochrome c by immobilized trypsin enzymes on NAA-NH(2) into the heme-peptide fragment.

254 effect of 8-week risperidone monotherapy on NAA.

255 Then, the most optimal NAA platforms combined with PLS and RIfS are quantitativ

256 Subsequently, optimized NAA-RFs are used as sensing platforms to determine the b

257 ignificant differences in NAA (P = 0.084) or NAA/Cr + Pcr (P = 0.500) compared to controls; NAA level

258 rade dysplasia was not associated with AA or NAA.

259 In the brains of CD patients, NAA accumulates to high millimolar concentrations.

260 Finally in antipsychotic-naive patients, NAA was reduced in right frontal gyri (19 voxels, CCLAV

261 Finally, the performance of the PEI-GA-PEI-NAA sensor for real-life applications is demonstrated us

262 y and chemical selectivity of the PEI-GA-PEI-NAA sensor to Cu(2+) ions is verified by screening six d

263 However, as this study demonstrates, PLS-NAA platforms are more sensitive than RIfS-NAA ones.

264 en PE/Cr and baseline SaO2; and left putamen NAA/Cr and SaO2 nadir (all p < 0.05).

265 nd N-acetylaspartylglutamate/creatine ratio (NAA/Cr) in a group of 89 women with CFS.

266 RS with the assessment of metabolite ratios (NAA/Cr, Cho/Cr, mI/Cr), as well as DTI with evaluation o

267 creased Cho/Cr ratio (P < .03) and a reduced NAA/Cho ratio (P < .01) compared to those without impair

268 ls and examined the relationship of regional NAA levels and cardiovascular risk factors as indexed by

269 S-NAA platforms are more sensitive than RIfS-NAA ones.

270 re negatively correlated with left and right NAA, and positively correlated with right Glu and right

271 alized with 3-aminopropyl trimethoxy silane (NAA-NH(2)).

272 of pancreatic insulin secretion and suggest NAA as a critical energy metabolite for adipocyte and wh

273 pain was associated with decreased thalamic NAA/Cho and microstructural alterations in thalamocortic

274 Our data clearly support the hypothesis that NAA accumulation is the major factor in the development

275 The NAA/Cho ratio across six regions was significantly lower

276 The NAA/Cho ratio value was statistically lower in the acute

277 The NAA/Cr ratio was significantly lower (P </= .01) in eigh

278 Although the NAA dicarboxylate transporter NaDC3 is primarily thought

279 istically significant difference between the NAA and Cho levels in the acute kernicterus patients and

280 Furthermore, the NAA B cells produced large amounts of IL-10 upon TLR sti

281 low frequency radiowave observations of the NAA 24.0 kHz transmitter, Cutler, Maine, made from Halle

282 , and negative likelihood ratio (NLR) of the NAA tests against culture were 82% (95% confidence inter

283 After that, the pore walls of the NAA were modified with (3-aminopropyl) trimethoxysilane

284 were then attached to the pore walls of the NAA-NH(2) by using glutaraldehyde (GA) as the cross-link

285 y, the trypsin enzyme was immobilized on the NAA pore walls.

286 Then, the NAA pore walls were functionalized with 3-aminopropyl tr

287 ing and T2 at MR imaging correlated with the NAA/Cho ratio (P < .05 for both) but not with the Cho/Cr

288 oncentrations including Glx (Glu+Gln), tNAA (NAA+NAAG), mI all had coefficient of variations between

289 ified with (3-aminopropyl) trimethoxysilane (NAA-NH(2)).

290 correlated with clinical stage of HCC, were NAA, dimethylglycine, 1-methylnicotinamide, methionine,

291 e in the amygdala, cortex and striatum while NAA decreased only in the hippocampus and cortex at 17-2

292 Total Cr was associated with NAA (beta = .52, t(5)(6) = 5.57, p = .000001).

293 tal infection was negatively associated with NAA and Cr (p < 005), while cerebral cortical brain inju

294 oma number had the greatest association with NAA.

295 and BIA unit was developed and compared with NAA as proof of principle.

296 mI/Cr and lower NAA/mI ratios, but not with NAA/Cr.

297 iagnosed with AA and 954 (32%) patients with NAA.

298 Treatment with NAA or NAAG significantly increased GSC growth and suppr

299 WM NAA/Cr tended to increase with laquinimod and decrease w

300 The DD group exhibited reduced GM and WM NAA concentrations at 3 to 4 years of age; GM NAA concen