ライフサイエンスコーパス: NAA

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

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

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

4 aded to nicotinic acid adenine dinucleotide (NAAD).

5 These mice have no detectable NAA.

6 effect of 8-week risperidone monotherapy on NAA.

7 rade dysplasia was not associated with AA or NAA.

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

9 oma number had the greatest association with NAA.

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

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

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

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

14 l concentrations (50-100 nM) was degraded to NAAD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Both NAA and tCr correlated with Global Assessment of Functio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Although the NAA dicarboxylate transporter NaDC3 is primarily thought

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 Ethanol reduced cortical GABA and NAA levels in humans.

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

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

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

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

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

206 ffect of ibuprofen on hippocampal volume and NAA loss.

207 NAA may be an important risk modifier for methylation in

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

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

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

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

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

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

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

215 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 NAA-RFs are photonic crystal structures produced by sinu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 which a clinician has specifically requested NAA testing.

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

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

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

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

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

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

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

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

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

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

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

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

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

291 NAA was the metabolite characterized by the greatest reg

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

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

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

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

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

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

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

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

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