ライフサイエンスコーパス: NAA

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

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

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

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

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

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

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

8 es more genes were induced than repressed by NAA.

9 These mice have no detectable NAA.

10 effect of 8-week risperidone monotherapy on NAA.

11 rade dysplasia was not associated with AA or NAA.

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

13 oma number had the greatest association with NAA.

14 apacity to transport alphaKG, succinate, and NAA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 Both NAA and tCr correlated with Global Assessment of Functio

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

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

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

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

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

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

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

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

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

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

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

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

55 ring of nicotinic acid adenine dinucleotide (NaAD) and cleaves the phosphoanhydride bond to release A

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 Although the NAA dicarboxylate transporter NaDC3 is primarily thought

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

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

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

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

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

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

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

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

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

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

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

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

169 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).

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

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

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

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

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

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

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

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

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

179 roup of nicotinic acid adenine dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treate

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

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

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

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

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

185 formed from NR and discover that the rise in NAAD is a highly sensitive biomarker of effective NAD(+)

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

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

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

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

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

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

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

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

194 ffect of ibuprofen on hippocampal volume and NAA loss.

195 NAA mapping of the brain may provide early surveillance

196 NAA may be an important risk modifier for methylation in

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

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

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

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

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

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

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

204 e ion-neutral reaction between HF and Na(2)A(NaA)(n)(+), gas-phase reagent ions produced by nano-ESI

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

206 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 action with the donor NA group deriving from NAAD, produced by newly described endolysosomal activiti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 NAA-RFs are photonic crystal structures produced by sinu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 verting nicotinic acid adenine dinucleotide (NaAD) to NAD(+) Some members of the NadE family use l-gl

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

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

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

284 eviously unidentified metabolic pathway from NaAD using unprecedented carboxylase and sulfur transfer

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

286 NAA was strongly and negatively correlated with FCVRS ac

287 NAA was the metabolite characterized by the greatest reg

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

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

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

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

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

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

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

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

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

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

298 rt that nicotinic acid adenine dinucleotide (NAAD), which was not thought to be en route for the conv

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

300 nanochannels could be created by assembling NaA zeolite crystals into a continuous, defect-free sepa