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 may be an important risk modifier for methylation in

3 NAA was the metabolite characterized by the greatest reg

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

5 NAA-RFs are photonic crystal structures produced by sinu

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

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

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

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

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

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

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

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

14 However, after day 28, NAA/Cho significantly increased in relation to a signifi

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

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

17 In patients, rostral ACC NAA and Cr concentrations were significantly lower than

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

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

20 zed the concentrations of N-acetylaspartate (NAA) and choline (Cho) in each ROI to the concentration

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

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

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

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

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

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

27 Absolute N-acetylaspartate (NAA) levels from the DLPFC were significantly elevated i

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

29 f the neuronal metabolite N-acetylaspartate (NAA) was measured in the human normal-appearing corpus c

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

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

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

33 examine concentrations of N-acetylaspartate (NAA), a marker of neuronal integrity and function, and c

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

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

36 e (Glu), glutamine (Gln), N-acetylaspartate (NAA), and choline (Cho) levels in the right and left pos

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

38 e (ATP, ATP-catabolites), N-acetylaspartate (NAA), antioxidant defenses (ascorbic acid, glutathione),

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

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

41 ns of neurometabolite for N-acetylaspartate (NAA), choline, creatine, and lactate were measured.

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

43 te rostral and caudal ACC N-acetylaspartate (NAA), creatine (Cr), and choline (Cho) concentrations.

44 th p < 0.05); for lactate/N-acetylaspartate (NAA), only xenon-augmented hypothermia reduced the slope

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

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

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

48 egnancies, a reduction in N-acetylaspartate (NAA)/choline ratio and detection of lactate methyl are e

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

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

51 maps (choline, creatine, N-acetylaspartate [NAA], and/or citrate), and statistical analysis involvin

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

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

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

55 ic acid (BTOA) and 1-naphthaleneacetic acid (NAA), into the active site indicates that NAA and BTOA a

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

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

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

59 uberculosis (TB) nucleic acid amplification (NAA) tests and the clear benefits of immediate diagnosis

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

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

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

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

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

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

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

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

68 Ethanol reduced cortical GABA and NAA levels in humans.

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

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

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

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

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

74 at baseline than in control individuals, and NAA levels were significantly correlated with pain-sympt

75 c NAA, we investigated the effect of NAA and NAA-producing B cells in disease development in the auto

76 These results indicate that NAA and NAA-producing B cells play an important role in protecti

77 ffect of ibuprofen on hippocampal volume and NAA loss.

78 te and N-acetylaspartyl glutamate (summed as NAA) fell steadily during the infusion by 8 +/- 3% (p =

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

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

81 ain metabolite levels of N-acetyl aspartate (NAA), choline (tCHO), creatine (CR), myoinositol (MI), a

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

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

84 l metabolites, including N-acetyl-aspartate (NAA), an amino acid exclusively synthesized in the mitoc

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

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

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

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

89 phocreatine [PCr] to Pi, N-acetyl aspartate [NAA] to creatine [Cr], and lactate to Cr) and diffusion-

90 rked decrease in the cerebral levels of ATP, NAA, ascorbic acid, glutathione and NAD(+) and a signifi

91 Natural autoantibodies (NAA) and their associated B cells constitute a substanti

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

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

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

95 Z and HC were apparent, correlations between NAA/Cr and Glx/Cr in healthy subjects in the hippocampus

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

97 Both NAA and tCr correlated with Global Assessment of Functio

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

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

100 Levels of both NAA and NAAG are reported to be decreased in ALS.

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

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

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

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

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

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

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

108 these normalized metabolites (i.e., NAA/Cho, NAA/norCre, and Cho/norCre) by averaging all patients an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 These mice have no detectable NAA.

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

137 nefits of immediate diagnosis of TB disease, NAA tests frequently are not used in the diagnosis of pu

138 The elevated DLPFC NAA levels and the lack of decreasing trends in NAA with

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

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

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

142 atios of these normalized metabolites (i.e., NAA/Cho, NAA/norCre, and Cho/norCre) by averaging all pa

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

144 ther involving the measurement of endogenous NAA and NAAG levels using HPLC.

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

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

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

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

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

150 of Public Health Laboratory would allow for NAA test identification of approximately 54 (74%) of 72

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

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

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

154 Right MTL showed no rearing effects for NAA, but right NAA was positively related to body mass,

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

156 e a strategy for identifying individuals for NAA testing on the basis of nonclinical risk criteria th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 rior cingulate cortex (ACC) and hippocampus; NAA/Cr and glutamate + glutamine (Glx)/Cr ratios were ob

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

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

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

179 The gradual decline in NAA levels suggests inhibition of neural or metabolic ac

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

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

182 had a lack of an age-associated decrease in NAA levels, a trend seen in the control subjects.

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

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

185 sed in relation to a significant increase in NAA/norCre and a decrease in Cho/norCre; interestingly,

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

187 No significant differences were observed in NAA-to-Cr or lactate-to-Cr ratio.

188 levels and the lack of decreasing trends in NAA with age in the 22q11DS group relative to control su

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

190 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

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

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

193 ted to reported pain, left posterior insular NAA and Cho levels were significantly higher at baseline

194 extracellular NAAG is rapidly converted into NAA and glutamate by the catalytic enzyme glutamate carb

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

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

197 rporation from corresponding substrates into NAA and NAAG, and the other involving the measurement of

198 Lactate/NAA showed a strong positive correlation with TUNEL; nuc

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

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

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

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

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

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

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

208 by early pain (before scan 1), whereas lower NAA/choline was predicted by pain exposure throughout th

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

210 p=0.028) and reduced subcortical gray matter NAA/choline (beta=-0.0006, p=0.004).

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

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

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

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

222 We demonstrate that use of nonclinical NAA test selection criteria is an effective strategy for

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

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

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

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

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

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

229 By detecting reduced diffusion of NAA parallel to axons in white matter, DTS may thus be c

230 rototypic NAA, we investigated the effect of NAA and NAA-producing B cells in disease development in

231 a reason for the increased effectiveness of NAA and BTOA as auxins in planta and provides a tool for

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

233 We found that the expression of NAA in MRL-lpr mice prevented proteinuria and reduced ki

234 ized that a disruption in the homeostasis of NAA and glutamate in SZ is present.

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

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

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

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

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

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

241 in the literature concerning the recovery of NAA after riluzole treatment.

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

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

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

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

246 effect of 8-week risperidone monotherapy on NAA.

247 etween caudal and rostral measurements, only NAA in patients was different from that in control subje

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

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

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

251 rade dysplasia was not associated with AA or NAA.

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

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

254 nsgenic (sd-tg) mice expressing a prototypic NAA, we investigated the effect of NAA and NAA-producing

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

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

257 culated N-acetylaspartate to choline ratios (NAA/choline), lactate to choline ratios, average diffusi

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

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

260 more cell membrane per unit volume, reduced NAA in ACC appears to be coupled with increases in overa

261 which a clinician has specifically requested NAA testing.

262 B cases over a 1-year period while requiring NAA testing for only 933 (17%) of 5,469 individuals subm

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

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

265 showed no rearing effects for NAA, but right NAA was positively related to body mass, irrespective of

266 icant differences between caudal and rostral NAA concentration are found in ACC of patients with schi

267 lic health laboratories primarily perform TB NAA tests only on a targeted subset of specimens, usuall

268 o targeted testing, some laboratories use TB NAA tests universally for all respiratory specimens, tho

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

270 We found that NAA parallel diffusivity is lower in MS (p = 0.030) and

271 In the hippocampus we found that NAA/Cr and Glx/Cr ratios were significantly correlated i

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

273 These results indicate that NAA and NAA-producing B cells play an important role in

274 ating characteristic analysis indicated that NAA/Cho in tumor shows a high prediction to 6-month over

275 d (NAA), into the active site indicates that NAA and BTOA are likely to be poor substrates for this e

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

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

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

279 Although the NAA dicarboxylate transporter NaDC3 is primarily thought

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

281 by an inability to identify the gene for the NAA biosynthetic enzyme aspartate N-acetyltransferase (A

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

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

284 on from lupus nephritis and suggest that the NAA B cells may have an immune regulatory function via t

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

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

287 The metabolite ratios of choline to NAA and choline plus creatine to citrate did not show si

288 Relative to pretreatment values, NAA/Cho in ET was unchanged through day 28.

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

290 It remains controversial whether NAA contribute to or protect from autoimmune diseases.

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