ライフサイエンスコーパス: MMN

1 MMN area is useful to diagnose attention deficits and MH

2 MMN generation was well explained (>90% variance) by dip

3 MMN is a sensitive index of the neural systems engaged i

4 MMN is thought to represent a comparison of the features

5 MMN occurrence reflects the individual JND for temporal

6 MMN results showed effects of language experience and at

7 MMN source analysis indicated dipoles in both auditory c

8 MMN supplementation was associated with a small increase

9 MMN to FM tones and functional connectivity together acc

10 MMN was also observable for both the 15 ms and 185 ms ri

11 MMN was assessed in N=28 SZ patients immediately before

12 MMN was present in all NH listeners and CI users when th

13 aims of this work were to assess whether (1) MMN is altered in cirrhotic patients with MHE, compared

14 Among primiparous women (IFA = 131; MMN = 110; LNS = 128), the LNS group had greater mean bi

15 e rate ratio [IRR] 1.03, 95% CI: 0.92, 1.16; MMN-0 versus MMN-12: 1.05, 95% CI: 0.93, 1.18).

16 with MHE, compared to those without MHE, (2) MMN changes in parallel with performance in attention te

17 and/or MHE in a longitudinal study, and (3) MMN predicts performance in attention tests and/or in th

18 his analysis included 1057 women (IFA = 349, MMN = 354, LNS = 354).

19 ally analyse the knowledge accumulated about MMN over the past 30 years, culminating in a state-of-th

20 Additionally, MMN was examined in three related conditions: bipolar di

21 The relationship between AER, MMN to FM tones, and rsfMRI was assessed in the subset w

22 ive function, which are reflected in altered MMN.

23 alone at age 12 mo than in the IFA (49%) and MMN (49%) groups.

24 IFA (79.1 +/- 2.9 cm and -0.87 +/- 0.99) and MMN (79.1 +/- 2.9 cm and -0.91 +/- 1.01) groups (P = 0.0

25 ic accuracy (reported for ALS vs non-ALS and MMN vs non-MMN).

26 phy in the differential diagnosis of ALS and MMN.

27 s (auditory steady-state response [ASSR] and MMN) suggest improvement in information processing.

28 ume overall and in the SCN, SON, VM, DM, and MMN.

29 in women who started consuming FA, IFA, and MMN before the 12th week of gestation (4.6%, 4.2%, and 3

30 nces of SPB for women consuming FA, IFA, and MMN were 5.7%, 5.6% and 5.1%, respectively.

31 st and sequentially all cortical layers, and MMN is elicited independent of the frequency tuning of A

32 rences were found when comparing the LNS and MMN groups among primiparous women, and no group differe

33 fically with psychoacoustic measurements and MMN recordings.

34 An oddball design was used and both N1 and MMN components were examined.

35 ed to test the effects of neurochemistry and MMN amplitude on DST performance.

36 detected between the functional outcomes and MMN amplitudes at frontal and frontocentral sites.

37 rst time the effects of memantine on PPI and MMN in CPD subjects.

38 nderstanding the basis for deficient PPI and MMN in psychotic disorders, as reduced NMDA activity is

39 es a potential link between neuronal SSA and MMN.

40 l was used to assess the effects of iron and MMNs and the interaction between these factors.

41 tcentral gyrus in the absence of an auditory MMN.

42 This study examined auditory MMN in otherwise healthy chronic cannabis users compared

43 Behavioral and ERP data including auditory MMN and P300 were collected during each test day.

44 The amplitude of auditory MMN was unchanged by tDCS.

45 findings, showing generators of the auditory MMN along the superior temporal gyrus with no evidence o

46 C would reduce ketamine effects on behavior, MMN, and P300 in healthy humans.

47 Associations between MMN, cannabis use measures, and symptoms were examined.

48 In conclusion, MMN activity appears to be a promising candidate as an e

49 In contrast, MMN amplitude correlated significantly and independently

50 (MMN-0 = 20 [1 death]; MMN-6 = 21 [1 death]; MMN-12 = 20 [0 death]).

51 imilar between groups (MMN-0 = 20 [1 death]; MMN-6 = 21 [1 death]; MMN-12 = 20 [0 death]).

52 d by the duration + frequency double deviant MMN, are compromised before psychosis onset and can enha

53 The duration + frequency double deviant MMN, but not the single deviant MMNs, significantly pred

54 In addition, NAC reduced frequency-deviant MMN amplitude and increased target and novelty P3 amplit

55 The decrements in frequency-deviant MMN amplitude produced by ketamine and NAC were not addi

56 ons for the frequency- and intensity-deviant MMNs and P300.

57 uble deviant MMN, but not the single deviant MMNs, significantly predicted the time to psychosis onse

58 The sensitivity to diagnose MMN (vs ALS and healthy control participants) was seven

59 ular ultrasound and MRI to aid in diagnosing MMN and in further elucidation of its pathophysiological

60 recordings pointed to statistically distinct MMN topographies across senses, implying differential un

61 In the meta-analysis, duration MMN achieved the highest effect size measures.

62 g-term users also exhibited reduced duration MMN relative to control subjects and short-term users an

63 PCP significantly reduced rodent duration MMN (p<0.001) and theta-band (p<0.01) response.

64 ction and support utility of rodent duration MMN as a translational biomarker for investigation of me

65 Overall, we demonstrate that rodent duration MMN shows neuro-oscillatory signature similar to human M

66 At baseline, rodent duration MMN was associated with increased theta (theta)-frequenc

67 y enhanced PPI in CPD subjects, and enhanced MMN across subject groups.

68 nd under some conditions, memantine enhances MMN; these findings present a challenge to understanding

69 4%, 35%), and 5% (2%, 9%) in the Fe, MMN, Fe+MMN, and placebo groups, respectively.Daily iron supplem

70 cronutrients; MMN group), iron plus MMNs (Fe+MMN group), or placebo capsules.

71 , 30% (24%, 35%), and 5% (2%, 9%) in the Fe, MMN, Fe+MMN, and placebo groups, respectively.Daily iron

72 y control subjects completed a multi-feature MMN paradigm, which included duration, frequency, and in

73 re not significantly different in the FeFol, MMN, and PE + MNN groups but were all higher than in the

74 f language experience and attentional focus: MMN amplitudes were smaller for American compared to Jap

75 leted an electroencephalographic session for MMN, magnetic resonance spectroscopy for glutamate and G

76 res 24 wk after recruitment (effect size for MMN groups combined: 0.084 SD/24 wk, 95% CI: 0.005, 0.16

77 Frequency MMN was similarly attenuated in short- and long-term use

78 binding to MNs was detected using sera from MMN patients with and without detectable anti-GM1 IgM an

79 Sensory gating, MMN, and P300 have been demonstrated to be impaired in s

80 Children of mothers given MMN had a mean score of 0.11 SD (95% CI 0.01-0.20, p=0.0

81 , GABA, the ratio of glutamine to glutamate, MMN amplitude, and DST.

82 to receive 12 wk of iron (60 mg; Fe group), MMNs (14 other micronutrients; MMN group), iron plus MMN

83 th 0.09 presentations per wk for all groups (MMN-0 versus MMN-6: adjusted incidence rate ratio [IRR]

84 supplementation were similar between groups (MMN-0 = 20 [1 death]; MMN-6 = 21 [1 death]; MMN-12 = 20

85 ans and rhesus macaques and found homologous MMN and P3a ERPs during an auditory oddball paradigm.

86 However, MMN and P3a reductions were unrelated in both UHR and FE

87 bin in nonpregnant Cambodian women; however, MMNs did not confer additional significant benefit.

88 However, unlike the human MMN, larger deviant responses were characterized by the

89 ble novelty correlates aligning to the human MMN.

90 e novelty in a manner analogous to the human MMN.

91 neuro-oscillatory signature similar to human MMN, along with sensitivity to the NMDAR antagonist and

92 and 49.9 +/- 2.1 cm (P = 0.104) in the IFA, MMN, and LNS groups, respectively.

93 .5), 7.8% (4.3-11.4), and 7.3% (4.0-10.7) in MMN, PE, and PE + MMN groups (all, p < 0.001), respectiv

94 pathogenicity of anti-GM1 IgM antibodies in MMN patients and link their presence to the clinical cha

95 ge effect size (P=0.0004, d=1.0) deficits in MMN generation across deviant types.

96 The role of glutamate and GABA in MMN and verbal working memory deficits in schizophrenia

97 In contrast, nerves in MMN were characterized by fascicular swellings (reader 1

98 Recently, our group showed a reduction in MMN to changes in the duration and intensity of backgrou

99 dicted, patients showed robust reductions in MMN across FM stimulus type (p = 0.005), particularly to

100 e groups no longer differed significantly in MMN amplitude during deviant pitch tones, and the degree

101 ion signs were more prominent in ALS than in MMN.

102 Larger MMN amplitudes recorded both before and after the traini

103 arned English after age 10, exhibited larger MMN and P3a responses than early bilinguals, across all

104 had fewer years of L2 experience had larger MMN, P3a, and LN responses than those who learned it ear

105 on, hyperarticulated stimuli elicited larger MMNs for both language groups, suggesting vowel space ex

106 y deviants, along with At the network level, MMN deficits engaged canonical somatomotor, ventral atte

107 dings reinforce recent human studies linking MMN deficits to theta-band neuro-oscillatory dysfunction

108 group comparison: LNS compared with non-LNS (MMN + IFA).

109 The subjects with BD had significantly lower MMN amplitudes at the frontal and frontocentral electrod

110 INTERPRETATION: Maternal MMN had long-term benefits for child cognitive developme

111 ized to daily LNS or multiple micronutrient (MMN) capsules during pregnancy through 6 mo postpartum o

112 ; standard of care), multiple micronutrient (MMN), protein-energy (PE), or PE + MMN daily from enrolm

113 Multiple micronutrients (MMN) are commonly prescribed in pediatric primary health

114 upplementation with multiple micronutrients (MMN) has been hindered by little evidence of the effects

115 upplementation with multiple micronutrients (MMN) or iron + folic acid (IFA), versus folic acid (FA)

116 upplementation with multiple micronutrients (MMN) or iron and folic acid (IFA) in Indonesia.

117 ron with or without multiple micronutrients (MMNs) on hemoglobin concentration in nonpregnant Cambodi

118 capsule containing multiple micronutrients (MMNs), or one 20-g sachet of SQ-LNS (LNS, containing 118

119 g; Fe group), MMNs (14 other micronutrients; MMN group), iron plus MMNs (Fe+MMN group), or placebo ca

120 n analysis and structural equation modeling, MMN and diagnostic group were significant independent pr

121 howed age-appropriate mismatch negativities (MMNs) to sounds, but older children (12-16 years; n = 23

122 functional outcomes and mismatch negativity (MMN) activity in participants with mood disorders.

123 otential studies as the mismatch negativity (MMN) and has been observed in several sensory modalities

124 Auditory mismatch negativity (MMN) and P300 event-related potentials (ERPs) are reduce

125 s is on sensory gating, mismatch negativity (MMN) and P300, thereby discussing which parameters allow

126 elated brain potentials mismatch negativity (MMN) and P300.

127 For example, the mismatch negativity (MMN) and P3a event-related potentials (ERPs), neurophysi

128 stimulation, as well as mismatch negativity (MMN) and P3a event-related potentials.

129 EEG measures of EAIP, mismatch negativity (MMN) and P3a, are sensitive to the neural systems engage

130 ated potential known as mismatch negativity (MMN) and provides a potential link between neuronal SSA

131 Mismatch negativity (MMN) and visual P1 are established event-related potenti

132 nses, as indexed by the mismatch negativity (MMN) component of the auditory event-related potential (

133 Here, we examined the mismatch negativity (MMN) component of the event-related potential elicited a

134 The mismatch negativity (MMN) component of the human event-related potential prov

135 response resembled the mismatch negativity (MMN) evoked by surprising or unlikely events in traditio

136 generation of auditory mismatch negativity (MMN) generation are among the most widely replicated neu

137 prepulse inhibition and mismatch negativity (MMN) in SZ patients and healthy subjects (HS).

138 Mismatch negativity (MMN) indexes pre-attentive information processing dysfun

139 Auditory mismatch negativity (MMN) is a biomarker for schizophrenia thought to reflect

140 The mismatch negativity (MMN) is a brain event-related potential marker of change

141 The mismatch negativity (MMN) is a preattentive component of the auditory event-r

142 Mismatch negativity (MMN) is an auditory event-related potential that reflect

143 The mismatch negativity (MMN) is an event related potential evoked by violations

144 Mismatch negativity (MMN) is an extensively validated biomarker of cognitive

145 The observation that mismatch negativity (MMN) is consistently impaired in schizophrenia has gener

146 The auditory mismatch negativity (MMN) is significantly reduced in schizophrenia.

147 The mismatch negativity (MMN) is thought to index the activation of specialized n

148 electroencephalographic mismatch negativity (MMN) response.

149 ion ability [indexed by mismatch negativity (MMN) responses].

150 , with the multisensory mismatch negativity (MMN) significantly different from the sum of the unisens

151 ts (NCSs) who underwent mismatch negativity (MMN) testing via their participation in the Consortium o

152 Mismatch negativity (MMN) to FM tones was assessed in 43 patients/36 controls

153 Mismatch negativity (MMN) was used to index discrimination of the temporally-

154 e two systems using the mismatch negativity (MMN), a well studied EEG effect evoked by acoustic devia

155 ed to determine whether mismatch negativity (MMN), an event-related potential index of auditory senso

156 The significance of the mismatch negativity (MMN), an event-related potential measured in humans whic

157 Mismatch negativity (MMN), an evoked potential calculated by subtracting the

158 between groups for the mismatch negativity (MMN), but the late discriminative negativity (LDN) was r

159 ed PTSD showed enhanced mismatch negativity (MMN), increased theta power (5-7 Hz), and stronger suppr

160 itory change detection, mismatch negativity (MMN), is one of the most consistent findings in schizoph

161 f neurodynamics, namely mismatch negativity (MMN), P300, and contingent negative variation (CNV), as

162 EG/ERP study, using the mismatch negativity (MMN), P3a, and late negativity (LN), we examined differe

163 ic brain potential, the mismatch negativity (MMN), when listeners did not attend to the auditory stim

164 ere presented to derive mismatch negativity (MMN), which reflects the ability to automatically detect

165 ogram (EEG) paradigm of mismatch negativity (MMN).

166 n (PPI) of startle) and mismatch negativity (MMN).

167 esponses--including the mismatch negativity (MMN).

168 rical recordings of the mismatch negativity (MMN).

169 uditory discrimination (mismatch negativity; MMN) responses to phoneme and tone changes in sequences

170 associated with multifocal motor neuropathy (MMN) including disease pathophysiology, diagnostic crite

171 rosis (ALS) and multifocal motor neuropathy (MMN) relies on clinical examination and electrophysiolog

172 m patients with multifocal motor neuropathy (MMN) using human induced pluripotent stem cell (iPSC)-de

173 (reported for ALS vs non-ALS and MMN vs non-MMN).

174 ial nucleus (VM), medial mammillary nucleus (MMN), and lateral hypothalamic area (LHA).

175 hical Cox regression examined the ability of MMN to predict time to psychosis onset in CHR patients.

176 udy expands upon an earlier meta-analysis of MMN impairment in schizophrenia by examining impairment

177 of 21 tests showed a positive coefficient of MMN versus IFA (p=0.0431) with effect sizes from 0.00-0.

178 for the MMN, which models the disruption of MMN observed in schizophrenia, may occur at a mechanisti

179 the mechanisms behind the lack of effect of MMN supplementation on morbidity measures and limited ef

180 The effectiveness of MMN in improving morbidity or growth in sick children pr

181 We assessed the effects of MMN and associations of biomedical (ie, maternal and chi

182 indered by little evidence of the effects of MMN on fetal loss and infant death.

183 Examination of MMN and P3a malleability in patients after their first d

184 , that accounts for the critical features of MMN.

185 ficits of large effect size in generation of MMN (d>1.26) and P300 (d=1.08) relative to comparison su

186 to determine whether initial malleability of MMN and P3a to 1-h of auditory-based TCT predicts improv

187 for a better understanding of the nature of MMN impairment in schizophrenia, as well as its potentia

188 es remain unresolved regarding the nature of MMN impairment.

189 The pattern of MMN alterations in cannabis users differed from that typ

190 s and caution with systematic prescribing of MMN.

191 rt glutamatergic and GABAergic regulation of MMN and verbal working memory function in schizophrenia.

192 seline after the initial 1-h dose of TCT) of MMN and P3a predicted improvements in verbal learning as

193 These findings encourage future trials of MMN as a biomarker for individual assignment, prediction

194 dent in older CPD patients, whereas those on MMN were most evident in younger subjects.

195 Study participants with ALS or MMN underwent MR neurography of the lumbosacral plexus,

196 ndomly assigned to receive daily FA, IFA, or MMN from the period before 20 weeks' gestation to delive

197 Starting use of FA, IFA, or MMN supplements before the 12th week of gestation produc

198 0.12), antenatal supplementation with MMN or MMN + PE resulted in 42.4% (95% CI 20.1-64.6; p < 0.001)

199 4), and 7.3% (4.0-10.7) in MMN, PE, and PE + MMN groups (all, p < 0.001), respectively, than in the F

200 d 15.4% (9.6-21.2; p < 0.001) in PE and PE + MMN groups, compared with the FeFol group (74.9 IU/mL, 6

201 nutrient (MMN), protein-energy (PE), or PE + MMN daily from enrolment (mean [SD] 13.7 [3.3] weeks' ge

202 .4% (0.19-6.5; p = 0.038) higher in the PE + MMN group than in the FeFol group (3.47 IU/mL, 3.29-3.66

203 We performed MMN analysis as well as attention and coordination tests

204 other micronutrients; MMN group), iron plus MMNs (Fe+MMN group), or placebo capsules.

205 Significant pretraining vs posttraining MMN amplitude reduction was also observed (p<0.02).

206 stic startle magnitude and habituation, PPI, MMN, autonomic indices, and subjective self-rating scale

207 The resulting scheme generates realistic MMN waveforms, explains the qualitative effects of devia

208 Reduced MMN amplitude was linked to poor verbal working memory i

209 Patients also exhibited reduced MMN to all deviant types.

210 In this report, we examine whether reduced MMN, as well as P3a, another index of auditory deviance

211 in 5 years of illness onset, whereas reduced MMNs to changes in sound frequency were only seen in pat

212 Consistent with prior reports, MMN-related thalamocortical activity was strongly inhibi

213 generation of a higher-order brain response (MMN) versus sensory responses.

214 evaluate physiological properties of rodent MMN, along with sensitivity to NMDAR agonist and antagon

215 ple, hierarchically related PEs in a "roving MMN" paradigm.

216 rly to those with schizophrenia, should show MMN alterations related with attention deficits.

217 had shown significant MMNs at Time 1 showed MMNs that were reduced and, for nonspeech, absent at Tim

218 stage of processing, we observed significant MMN effects for both head-independent and head-centered

219 Children who had shown significant MMNs at Time 1 showed MMNs that were reduced and, for no

220 Notably, a similar MMN reduction can be achieved with NMDA receptor (NMDAR)

221 Simultaneously, MMN was obtained to unattended pitch, duration, and inte

222 Smaller MMN amplitude was significantly associated with lower GA

223 d that Greek speakers in general had smaller MMNs compared to English speakers, confirming previous s

224 al gyrus with no evidence of a somatosensory MMN in this region, whereas a robust somatosensory MMN w

225 increase in peak amplitude of somatosensory MMN after anodal tDCS (F(1,9) = 8.98, P < 0.02, mean dif

226 reduction in peak amplitude of somatosensory MMN after cathodal tDCS (F(1,9) = 7.15, P < 0.03, mean d

227 se bidirectional modulation of somatosensory MMN and the dependence of somatosensory MMN on the cereb

228 sory MMN and the dependence of somatosensory MMN on the cerebellum.

229 se to explore the mechanism of somatosensory MMN, and specifically its dependence on the cerebellum.

230 this region, whereas a robust somatosensory MMN was recorded from postcentral gyrus in the absence o

231 In the longitudinal study, MMN area improved in parallel with performance in attent

232 For this study, MMN data to frequency, intensity and duration-deviants w

233 In summary, MMN studies have produced the most convincing results un

234 inly in matrix regions of auditory thalamus, MMN generators are most prominent in layer 1 of cortex a

235 It is generally accepted that MMN represents a chronic progressive immune-mediated mot

236 y chi2 test), supporting the contention that MMN serves as an intermediate biomarker linking glutamat

237 We found that MMN impairment 1) likely reflects a vulnerability to dis

238 ng characteristic curve analyses showed that MMN area predicts attention deficits in the number conne

239 Logistic regression analyses showed that MMN area predicts performance in attention tests and in

240 These results suggest that MMN, as well as P3a, to duration deviants are reduced in

241 The MMN amplitude was significantly reduced to frequency but

242 The MMN deficits are independently related to premorbid func

243 The MMN is then modelled as the superposition of the electri

244 The MMN to duration versus other deviants was differentially

245 The MMN was compared between users and control subjects as w

246 The MMN wave area was reduced in patients with MHE, but not

247 issociating SSA from sensory novelty and the MMN.

248 auditory novelty detection as indexed by the MMN is dissociable from SSA at the level of activity enc

249 Early first-level processing indexed by the MMN was sensitive to stimulus predictability: here, atte

250 duration discriminations, represented by the MMN, were generated in the same cortical regions regardl

251 antagonists, which are known to disrupt the MMN, suppressed the magnitude of multiunit responses in

252 rther, the NMDA sensitivity reported for the MMN, which models the disruption of MMN observed in schi

253 However, the MMN may also reflect the violation of a prediction based

254 ented that validates our key hypothesis: the MMN results from active cortical prediction rather than

255 normal subjects, including reductions in the MMN and the P3a.

256 with 13.7% in the IFA group and 12.9% in the MMN group (P = 0.12).

257 Children of anaemic mothers in the MMN group scored 0.18 SD (0.06-0.31, p=0.0047) higher in

258 ighest in the LNS group, intermediate in the MMN group, and lowest in the IFA group, but except for m

259 sed risk of low birthweight for those in the MMN group, with a 33% (RR 0.67, 0.51-0.89, p=0.0062) dec

260 Moreover, the MMN amplitudes evoked from the left forebrain and midbra

261 work advances a formal understanding of the MMN and--more generally--illustrates the potential for d

262 The source activity of the MMN from the left anterior cingulate cortex, inferior fr

263 We investigate possible homologs of the MMN in macaque primary auditory cortex (A1) using a freq

264 ous studies demonstrating sensitivity of the MMN to language background.

265 to sound omission, and a sensitivity of the MMN to NMDA receptor antagonists.

266 Peak amplitudes and source activity of the MMN were compared across groups.

267 sensory novelty, a defining property of the MMN, however, has not been resolved.

268 nt for the major empirical properties of the MMN.

269 of deviant probability and magnitude on the MMN - in terms of latency and amplitude--and makes quant

270 Source solution further revealed the MMN involved the neural activations from the visual cort

271 nd standing with assistance earlier than the MMN group (B = 0.51; 95% CI: 0.12, 0.89; P = 0.029).

272 The results showed that the MMN amplitude for the first call note was significantly

273 This has been taken to suggest that the MMN is a correlate of true change or "deviance" detectio

274 Results showed that the MMN reflects sensitivity only to the formant structure o

275 he neurobiological mechanisms underlying the MMN is still lacking, and its computational foundations

276 requency analysis revealed that, whereas the MMN reflected enhanced intertrial coherence in the theta

277 hich shares several characteristics with the MMN.

278 matrix (nonlemniscal) thalamic afferents to MMN generation.

279 from the ratio of glutamine to glutamate to MMN to verbal working memory (P = .38 [root-mean-square

280 ldhood development, and policy change toward MMN.

281 Irrespective of deviant type, MMN was significantly reduced in ESZ and CHR patients re

282 his study investigates mechanisms underlying MMN impairments in schizophrenia using event-related pot

283 tly different from the sum of the unisensory MMNs.

284 A, the relative risks of SPB for those using MMN and IFA were 0.99 (95% confidence interval: 0.85, 1.

285 [IRR] 1.03, 95% CI: 0.92, 1.16; MMN-0 versus MMN-12: 1.05, 95% CI: 0.93, 1.18).

286 ntations per wk for all groups (MMN-0 versus MMN-6: adjusted incidence rate ratio [IRR] 1.03, 95% CI:

287 In agreement with visual MMN studies, single-unit IT responses were greater for t

288 nsensus, the sensitivity to diagnose ALS (vs MMN and healthy control participants) was 19 of 22 (86%

289 We also examined whether MMN predicted subsequent conversion to psychosis in CHR

290 rlying pathophysiology, specifically whether MMN represents an axonal or demyelinating neuropathy and

291 While MMN has been extensively used in human electrophysiologi

292 Community-wide MMN supplementation has shown limited and heterogeneous

293 ients, similar to our reported findings with MMN.

294 ver, the association of glutamate level with MMN has not been directly examined in patients with schi

295 62.3 years +/- 9.0), eight participants with MMN (seven men and one woman; mean age, 57.6 years +/- 1

296 rural Gambia, maternal supplementation with MMN combined with PE during pregnancy enhanced antibody

297 , 0.09-0.12), antenatal supplementation with MMN or MMN + PE resulted in 42.4% (95% CI 20.1-64.6; p <

298 mentation with unfortified SQ-LNS for 12 wk (MMN-0) to be consumed in daily portions.

299 th micronutrient-fortified SQ-LNS for 12 wk (MMN-12), (2) supplementation with micronutrient-fortifie

300 wk followed by unfortified SQ-LNS for 6 wk (MMN-6), or (3) supplementation with unfortified SQ-LNS f