ライフサイエンスコーパス: MAM

1 MAM administration leads to a hyperdopaminergic state co

2 MAM is a peptide mapping method utilizing mass spectrome

3 MAM is a promising approach that provides some distinct

4 MAM protein was extracted efficiently by a surfactant-ai

5 MAM rats also demonstrated dose-dependent improvement in

6 MAM regulates a number of key cellular functions, includ

7 MAM-treated male rats were exposed to acute and repeated

8 MAM-treated rats exhibited a heightened level of anxiety

9 li were randomly assigned to provide to 1264 MAM children aged 6-35 mo one of 4 dietary supplements c

10 cks on an acidic surface of the neuropilin-2 MAM domain to polysialylate O-glycans on the adjacent li

11 ns (with the highest rates in sarcoma [47%], MAM [37%], and NET [32%]), grade 2 in 706 lesions (with

12 Because RS data are usually collected in a MAM assay, no additional work is required from the analy

13 Our results suggest that CMT2AMFN2 is a MAM-related disorder but is not a respiratory chain-defi

14 Thus, mTORC2 is at the core of a MAM signaling hub that controls growth and metabolism.

15 human erythroid cell line (BEL-A2) abolishes MAM expression.

16 that received methyl azoxymethanol acetate (MAM) gestationally exhibited higher levels of anxiety pe

17 the mitotoxin methyl azoxymethanol acetate (MAM), we examined the convergent projections from the ve

18 the mitotoxin methyl azoxymethanol acetate (MAM).

19 thylating agent methylazoxymethanol acetate (MAM) at gestational day 17 exhibit as adults behavioral

20 biomarkers in a methylazoxymethanol acetate (MAM) rat model of schizophrenia and saline-treated contr

21 The methylazoxymethanol acetate (MAM) rodent model proposes that psychosis develops as a

22 examined in the methylazoxymethanol acetate (MAM) rodent model to observe its effects on a hyperdopam

23 ministration of methylazoxymethanol acetate (MAM) to induce a developmental disruption, which in turn

24 ed the prenatal methylazoxymethanol acetate (MAM, E17) exposure model to determine the alterations of

25 ophrenia in the methylozoxymethanol acetate (MAM) rodent model of the disease.

26 ats, we used the methylzoxymethanol acetate (MAM) model to determine whether POM may indirectly norma

27 results demonstrate that the E. coli adhesin MAM(HS) facilitates retention of a gut commensal by atta

28 In addition, adolescent MAM-treated animals displayed a blunted HPA axis cortico

29 f BLA neurons in both peripubertal and adult MAM rats.

30 Accompanied with this change, adult MAM rats exhibited a significant decrease in spine densi

31 eightened anxiety was also observed in adult MAM animals, as well as higher firing rates of BLA neuro

32 induced increase in BLA theta power in adult MAM rats, supporting a persistent normalization by this

33 revents the hyperdopaminergic state in adult MAM rats.

34 the power of BLA theta oscillations of adult MAM rats showed a larger increase in response to conditi

35 ations in MFN2 in CMT2A patient cells affect MAM function, which might provide insight into pathogene

36 FLT1 inhibition does not affect MAM recruitment to metastatic lesions but regulates a se

37 hildren who sustained recovery for 1 y after MAM treatment.

38 pleomorphic "megamitochondria" with altered MAMs in brown adipocytes lacking the Sel1L-Hrd1 protein

39 between them, organic molecular amphiphiles (MAMs) and inorganic nanoparticle (NP) amphiphiles (NPAMs

40 this paper we describe the application of an MAM based method for site specific quantification of N-l

41 In this study, an MAM method for examination of residue-specific glycan pr

42 WH-210, and PB-22, their 5-fluoro analogues (MAM-2201, EAM-2201, and 5F-PB-22, respectively), and the

43 This shows that signal-anchored MAM proteins can make use of hydrophobic interactions in

44 eatic cancer [17%], sarcoma [SAR] [13%], and MAM [8%]), and grade 3 in only 15 lesions.

45 ues in SAR (3.5 +/- 1.8; range, 0.8-2.7) and MAM (3.6 +/- 2.2; range, 0.9-11.6).

46 2 controls StAR processing and activity, and MAM is thus a central location for initiating mitochondr

47 ) and that ER-mitochondrial connectivity and MAM function are upregulated in AD We now show that C99,

48 , deoxycholate negatively regulates IcsA and MAM in S. sonnei resulting in reduction in attachment an

49 tation/on-pellet digestion (SOD) method, and MAM proteome was quantified by an ion-current-based MS1

50 d by specific interactions between mucin and MAM(HS) in a sulfation-dependent manner.

51 udy reported correlation between obesity and MAM formation in mouse liver cells, and obesity-related

52 ated SAM with weight-based RUTF rations, and MAM with ready-to-use supplementary food (RUSF).

53 Combined treatment for SAM and MAM is non-inferior to standard care.

54 e bacterial taxa underrepresented in SAM and MAM microbiota were characterized in gnotobiotic mice an

55 partial (MUAC, edema) definitions of SAM and MAM.

56 formin improved both insulin sensitivity and MAM integrity.

57 was growth factor-stimulated, and mTORC2 at MAM interacted with the IP3 receptor (IP3R)-Grp75-voltag

58 ed the housekeeping activity of IRE1alpha at MAMs from its canonical role in the unfolded protein res

59 of inositol-1,4,5-trisphosphate receptors at MAMs by operating as a scaffold.

60 educe the hyperdopaminergic activity in both MAM rats and in wild type rats following restraint stres

61 ver and an altered lipid composition of both MAM and mitochondrial membranes.

62 hensive proteome profiling of isolated brain MAM from long-term type 2 diabetic mice vs. non-diabetic

63 tumors (NET; n = 77, 15.3%), mammary cancer (MAM; n = 68, 13.5%), hepatocellular carcinoma (HCC; n =

64 phology, and surface pattern by coassembling MAMs of block copolymers (BCPs) and NPAMs comprising ino

65 engineered bacterium expressing a commensal MAM on its surface in preventing pathogen attachment and

66 mTORC2 controlled MAM integrity and mitochondrial function via Akt mediate

67 ta) and IL-6 by human myeloma marrow-derived MAMs.

68 (Neu5Ac) could be monitored by the developed MAM approach with data readout highly comparable to QC m

69 mTORC2 deficiency disrupted MAM, causing mitochondrial defects including increases i

70 To dissect MAM activation/cytokine pathways, we analyzed Toll-like

71 TLR4 may cooperate with MHC class II during MAM-induced responses.

72 Our data establish MAM as a new blood group system and demonstrate an inter

73 Interestingly, only a subset of F2 and F3 MAM rats exhibited increases in dopamine neuron populati

74 In female MAM rats, POM significantly reduced DA neuron population

75 Case fatality rates were 1.1% (12/1,098) for MAM and 1.2% (6/513) for SAM.

76 were 1.43 (95% CI 0.53-3.87, p = 0.480) for MAM and 2.56 (95% CI 0.99-6.70, p = 0.052) for SAM.

77 these questions into four major aspects for MAM implementation in a cGMP environment for both new an

78 o and in Mali, respectively; K estimates for MAM were 4.7 in Burkina Faso and 5.1 in Mali.

79 o estimate mortality hazard ratios (HRs) for MAM and SAM.

80 o were enrolled on discharge from an SFP for MAM.

81 lities, might be an alternative strategy for MAM treatment in rural food-secure areas, provided that

82 for NET, HCC, and CCC and lowest values for MAM, CRC, and SAR.

83 re provide evidence that offspring born from MAM-treated rats possess a susceptibility to develop asp

84 re, cultured erythroid progenitor cells from MAM-negative individuals show markedly increased prolife

85 e proportion of children that recovered from MAM was significantly higher in the group that received

86 soy/whey RUSF in facilitating recovery from MAM.

87 r overexpression of the mitochondrial fusion/MAM-tethering protein MFN2 nor inhibition/ablation of th

88 getics and calcium homeostasis; however, how MAM is affected under diabetic condition remains elusive

89 However, MAM localization of Bax results in its increased ubiquit

90 from the gut commensal Escherichia coli HS (MAM(HS)), which contains an array of seven mammalian cel

91 The clinically important MAM blood group antigen is present on haematopoietic cel

92 ention could be an alternative for improving MAM management.

93 The alterations in MAM function described here could also provide insight i

94 insight into the significant alterations in MAM proteome associated with activation of the UPR in di

95 Anxiety-like behaviors in MAM rats were not ameliorated by prepubertal exposure to

96 haloperidol-induced depolarization block in MAM rats, which may underlie the acute psychotic state o

97 PFC-evoked responses in control rats, but in MAM-treated rats there was a significant inhibition at s

98 o HLA-DR leads to a conformational change in MAM structure allowing its interaction with TLR2 and TLR

99 In contrast, in MAM-treated rats BLA stimulation increased vHipp-evoked

100 ition of ER with mitochondria, a decrease in MAM function, and an increase in mitochondrial fragmenta

101 These results highlight defects in MAM as a cellular mechanism contributing to CMT2A pathol

102 alization in endosomes, can also be found in MAM, where it is normally processed rapidly by gamma-sec

103 oncentration of unprocessed C99 increases in MAM regions, resulting in elevated sphingolipid turnover

104 of spontaneously active dopamine neurons in MAM rats but not in controls.

105 acellular electrophysiological recordings in MAM- and saline-treated rats to evaluate the effect of c

106 he hyperdopaminergic activity selectively in MAM rats.

107 loss abrogated the "inflammatory switch" in MAM within nascent myeloma lesions and licensed macropha

108 d the direct involvement of TLR2 and TLR4 in MAM binding and presentation to T cells.

109 .0; range, 0.2-6.3) and the lowest values in MAM (1.7 +/- 0.8; range, 0.2-4.1), CRC (1.8 +/- 0.9; ran

110 the distribution of functional receptors in MAMs vs. the rest of ER/mitochondrial membranes, a param

111 ow that CSF1-mediated autocrine signaling in MAMs is downstream of FLT1 and can restore the tumor-pro

112 or TLR4 with HLA-DR significantly increases MAM binding and the subsequent T cell activation compare

113 e tumor-promoting activity of FLT1-inhibited MAMs.

114 d that different criteria for admission into MAM treatment programmes select children with difference

115 lish that Bax recruitment to the MAM and its MAM-associated degradation (MAMAD) are a newly described

116 We found that juvenile MAM-treated rats emitted significantly more calls, spent

117 Moreover, we found GRP75, a key MAM tethering protein, was drastically reduced by long-t

118 onstrate inactivating mutations in ten known MAM-negative individuals.

119 an myeloma-associated monocytes/macrophages (MAM), but not myeloma plasma cells, constitute the predo

120 lation of metastasis-associated macrophages (MAMs) recruited to the lung that promote tumor cell seed

121 t, versikine Myeloma-associated macrophages (MAMs), rather than tumor cells, chiefly produced V1-VCAN

122 rophages, metastasis-associated macrophages (MAMs), which originate from inflammatory monocytes (IMs)

123 d prevalence of moderate acute malnutrition (MAM) and SAM, as well as mortality and recovery at each

124 Children with moderate acute malnutrition (MAM) are treated based on low weight-for-length z-score

125 Children with moderate acute malnutrition (MAM) are treated with lipid-based nutrient supplement (L

126 ition (SAM) and moderate acute malnutrition (MAM) from AM incidence and prevalence using representati

127 ho recover from moderate acute malnutrition (MAM) have high rates of relapse in the year after nutrit

128 f children with moderate acute malnutrition (MAM) is based on food supplementation in outpatient prog

129 Management of moderate acute malnutrition (MAM) is, currently, focused on food supplementation appr

130 nt of childhood moderate acute malnutrition (MAM) remains unsettled.

131 tion (SAM) from moderate acute malnutrition (MAM) with different products and programs.

132 d treatment, to moderate acute malnutrition (MAM) with persistent microbiota immaturity.

133 Moderate acute malnutrition (MAM), defined as weight-for-length z score between -3 an

134 in treatment of moderate acute malnutrition (MAM).

135 parsed using maximal almost-unique matches (MAMs).

136 Rare variants in MDGAs (MAM domain-containing glycosylphosphatidylinositol ancho

137 und in the mitochondria-associated membrane (MAM) fraction, no RAS components could be detected in pu

138 ochondria/mitochondrial-associated membrane (MAM) in the absence of lipid droplet biosynthesis, but a

139 Mitochondria-associated membrane (MAM) signaling from the sarcoplasmic reticulum (SR) and

140 hed on the mitochondria-associated membrane (MAM), the site of ER-mitochondria Ca(2+) flux.

141 th the mitochondrion-associated ER membrane (MAM) and mitochondrial proteins.

142 The mitochondria-associated ER membrane (MAM) plays a critical role in cellular energetics and ca

143 termed mitochondria-associated ER membrane (MAM).

144 a-associated endoplasmic reticulum membrane (MAM) prior to its translocation to the mitochondrial mat

145 known as mitochondrion-associated membranes (MAM), and to mitochondria.

146 calize at mitochondria-associated membranes (MAM), where mitochondria are closely apposed with the en

147 known as mitochondria-associated membranes (MAM).

148 called mitochondria-associated ER membranes (MAM).

149 ing at mitochondria-associated ER membranes (MAM).

150 ciated endoplasmic reticulum (ER) membranes (MAM) and that ER-mitochondrial connectivity and MAM func

151 ciated endoplasmic reticulum (ER) membranes (MAM), a structurally and functionally distinct subdomain

152 Mitochondria-associated membranes (MAMs) are central microdomains that fine-tune bioenerget

153 to the ER mitochondria-associated membranes (MAMs), is involved in posttranslational modification and

154 efined as mitochondria-associated membranes (MAMs), which were recently implicated in the regulation

155 known as mitochondria-associated membranes (MAMs).

156 to as mitochondria-associated ER membranes (MAMs), and they play an important role in, for example,

157 called Mitochondria-Associated ER Membranes (MAMs), is known to play an important role in the occurre

158 called mitochondria-associated ER membranes (MAMs), where their membranes are in close apposition.

159 ned as mitochondria-associated ER membranes (MAMs), which are essential for calcium, lipid and metabo

160 own as mitochondria-associated ER membranes (MAMs).

161 ciated endoplasmic reticulum (ER) membranes (MAMs) are functional domains between both organelles inv

162 odels of breast cancer pulmonary metastasis, MAMs uniquely express FLT1.

163 g 4-vinylpiridine (VIPY) and methacrylamide (MAM) as functional monomers, ethylene glycol dimethacryl

164 pose is known as the multi-attribute method (MAM).

165 ry-based quantitative multiattribute method (MAM) for biotherapeutics is its high variability between

166 demonstrated using a multiattribute method (MAM), which can quantify multiple post-translational mod

167 (E17) to the neurotoxin methylazoxymethanol (MAM).

168 efficacy on maleimide-activated microplates (MAM) and gold electrodes.

169 Targeting to mitochondria/MAM and/or the stability of Rdh10 require both the N-ter

170 type 1, which also localizes to mitochondria/MAM before lipid droplet synthesis, and associates with

171 rmacological inhibition of the mitochondrial MAM protein, cyclophilin D (CypD), altered insulin signa

172 Mycoplasma arthritidis-derived mitogen (MAM) is a member of the superantigen family that structu

173 ptors for the multivalent adhesion molecule (MAM) from the gut commensal Escherichia coli HS (MAM(HS)

174 27 which is a multivalent adhesion molecule (MAM) required for invasion of epithelial cells and macro

175 y shown that multivalent adhesion molecules (MAMs) are abundant in both pathogenic and commensal bact

176 sins, termed Multivalent Adhesion Molecules (MAMs) that are essential for initial binding of bacteria

177 The cell-surface molecules, MAM domain-containing glycosylphosphatidylinositol ancho

178 Recently, multi-attribute monitoring (MAM), i.e., the quantification of multiple post-translat

179 ects of ER-mitochondrial connectivity and of MAM function were indeed altered, and correlated with di

180 ese results strongly suggest that binding of MAM to HLA-DR leads to a conformational change in MAM st

181 measures were all higher in visual cortex of MAM rats (posterior hyperactivity), which might parallel

182 The orbitofrontal cortex of MAM rats showed lower resting-state functional magnetic

183 Disruption of MAM integrity by genetic or pharmacological inhibition o

184 We found uniform distribution of MAM in neurons.

185 a mathematical model to study the effects of MAM Ca2+ dynamics on global Ca2+ activities.

186 Regional effects of MAM on the expression of parvalbumin-positive cells (PV)

187 nd (F2) and third (F3) filial generations of MAM-treated rats displays a schizophrenia-like phenotype

188 ltered insulin signaling, the implication of MAM dysfunctions in insulin resistance is unknown.

189 The incidence of MAM by weight-for-length z score (WLZ) and/or mid-upper

190 for insulin signaling and that induction of MAM prevented palmitate-induced alterations of insulin s

191 tral role in coordinating the interaction of MAM proteins with the outer mitochondrial membrane trans

192 ebT, the latter of which is an orthologue of MAM-7 that was previously reported to be an outer membra

193 Perturbation of MAM function has previously been suggested in Alzheimer'

194 A total of 1,313 non-redundant proteins of MAM were identified, among which 144 proteins were found

195 Collectively, our data reveal a new role of MAM integrity in hepatic insulin action and resistance,

196 Whereas supplement-based treatment of MAM was found to be more effective than the provision of

197 portance of milk protein in the treatment of MAM, because the use of a novel whey RUSF resulted in hi

198 ined recovery in children after treatment of MAM.

199 g and after supplementation for treatment of MAM.

200 f 4 dietary supplements for the treatment of MAM.

201 dy composition (BC), to improve treatment of MAM.

202 her dietary supplements for the treatment of MAM; CSB++ yielded intermediate results.

203 pontaneously active DA neurons in the VTA of MAM rats to control levels without affecting DA firing i

204 cer IRE1alpha as a structural determinant of MAMs that controls mitochondrial calcium uptake.

205 hange in INS-1E cells, whereas disruption of MAMs altered glucose-stimulated insulin secretion (GSIS)

206 ng metastasis foci, as well as the number of MAMs accumulated in tumor-challenged lung in mice.

207 obesity leads to a marked reorganization of MAMs resulting in mitochondrial calcium overload, compro

208 The role of MAMs in beta-cells is still largely unknown, and their i

209 The role of MAMs is critical for intracellular Ca2+ dynamics as they

210 ne quantitatively the physiological roles of MAMs, as well as mitochondrial quality control and ATP p

211 Their grafting on MAM greatly increased the sensitivity of the ELOSA test

212 The enhancing effect of TLR2 or TLR4 on MAM-induced T cell proliferation was not due to TLR liga

213 ER; mitochondria-associated ER membranes or 'MAM').

214 Two novel mono(amidine) organocatalysts (MAM) were discovered to provide high levels of enantiose

215 ed ER-mitochondrial apposition and perturbed MAM function lie at the heart of AD pathogenesis.

216 e meprin A5 antigen-mu tyrosine phosphatase (MAM) domain and the O-glycan-containing linker region of

217 Thus, in the prenatal MAM-exposure SZ model, NMDAR expression and function is

218 Mechanistically, Ccr1 deficiency prevents MAM retention in the lung by reducing MAM-cancer cell in

219 ematopoietic cells of all humans except rare MAM-negative individuals.

220 ion of the CCL2 receptor CCR2, the recruited MAMs secrete another chemokine ligand CCL3.

221 events MAM retention in the lung by reducing MAM-cancer cell interactions.

222 Up-regulated MAM-associated proteins were found in the AD brain and a

223 e effectiveness of a simplified, unified SAM/MAM protocol for children aged 6-59 months.

224 The ER-mitochondrial contact site (MAM) is essential for fission of mitochondria prior to e

225 n Nox4 at the ER-mitochondria contact sites (MAMs) is a pro-survival mechanism that inhibits calcium

226 The S. sonnei MAM mediates intimate attachment to host cells, which is

227 In behavioral studies, MAM (vs. SHAM) rats displayed abnormal orbitofrontal cor

228 Thus, targeting MAM-based adherence is a promising strategy for displaci

229 e comparative data obtained demonstrate that MAM by LC-MS peptide mapping can, in principle, adequate

230 not clear; however, we now demonstrate that MAM induces differential DNA methylation, which may be h

231 Our results demonstrate that MAM quantification of individual glycan species from bot

232 We demonstrated that MAM integrity is required for insulin signaling and that

233 Interestingly, we also found that MAM complexed with soluble HLA-DR is capable of binding

234 We found that MAM-exposed animals have significantly altered NMDAR pro

235 We have found that MAM-localized functions are increased significantly in c

236 Our results showed that MAM fails to bind to TLR2- and TLR4-transfected cells.

237 The MAM method, by virtue of the increased sensitivity and s

238 The MAM region of the ER is a lipid raft-like domain closely

239 The MAM(HS) adhesin interacted with a range of host receptor

240 FUNDC1 accumulates at the MAM by associating with the ER membrane protein calnexin

241 C1/IP3R1 and Grp75/IP3R1 interactions at the MAM interface.

242 Nox4 mediates redox signaling at the MAM of stressed cells to augment Akt-dependent phosphory

243 through spatially confined signaling at the MAM to regulate ER to mitochondria calcium flux and trig

244 mitochondria are physically connected at the MAM.

245 could also be simultaneously detected by the MAM method.

246 the pathogenesis of Alzheimer's disease: the MAM hypothesis.

247 attenuated reversal learning deficits in the MAM but not acute PCP model.

248 onstrate abnormal stress responsivity in the MAM model of schizophrenia and suggest that these animal

249 t mesolimbic dopamine neuron function in the MAM model of schizophrenia.

250 nd neuroendocrine responses to stress in the MAM model of schizophrenia.

251 cient to prevent DA hyperresponsivity in the MAM model, measured by electrophysiological recordings a

252 tem function and associated behaviors in the MAM model.

253 s not due to TLR ligand contamination in the MAM preparation.

254 ed with PCP to resemble that observed in the MAM rat.

255 terations in dopamine neuron function in the MAM rodent model.

256 In the MAM, StAR interacts with mitochondrial proteins Tom22 an

257 r these data uncover TMX2 as a sensor in the MAM-regulated redox signaling pathway and identify it as

258 tion via Akt mediated phosphorylation of the MAM associated proteins IP3R, Hexokinase 2, and phosphof

259 ission and mitophagy at the interface of the MAM by working in concert with DRP1 and calnexin under h

260 ecific acidic residues on the surface of the MAM domain are critical for neuropilin-2 polysialylation

261 t in part, by regulating the turnover of the MAM protein, sigma receptor 1 (SigmaR1).

262 Our work demonstrates that the MAM method is a suitable approach for providing quantita

263 ombined with functional validation, that the MAM-E17 rat model reproduces hippocampal deficits releva

264 esults establish that Bax recruitment to the MAM and its MAM-associated degradation (MAMAD) are a new

265 te that wild-type alpha-syn localizes to the MAM and modulates mitochondrial morphology, and that the

266 we establish that vMIA retargets Bax to the MAM as well as to the OMM from immediate early through l

267 Similar to the MAM rats, DA neuron population activity was increased in

268 DRP1 is thereby recruited to the MAM, and mitochondrial fission then occurs.

269 in motif and palmitoylation to target to the MAM.

270 Using the MAM (methylazoxymethanol acetate) rat model of schizophr

271 nce did not affect StAR association with the MAM and thus its mitochondrial targeting.

272 in the vHipp, which are consistent with the MAM model of schizophrenia.

273 hese studies are broadly consistent with the MAM model, caution is required when comparing data acros

274 evant signaling pathways associated with the MAM proteome changes in diabetes, most significantly the

275 and undergoes physical interaction with the MAM-associated and ER folding chaperone calnexin and ER

276 mTORC2 localization to MAM was growth factor-stimulated, and mTORC2 at MAM inte

277 o-use supplementary food (RUSF), in treating MAM through first-line rural health services.

278 hosphate is completely released from Gd-TREN-MAM below pH 2.

279 In water at neutral pH, Gd-TREN-MAM binds phosphate with high affinity (Ka = 1.3 x 10(4)

280 even under strong acidic conditions, Gd-TREN-MAM can be used at least 10 times in a pH-based recyclin

281 Gd-TREN-MAM is highly selective for phosphate over other anions

282 onyl))tris(4-ox o-4H-pyran-3-olate) (Gd-TREN-MAM).

283 r sorting protein-2 and sigma1 receptor, two MAM-associated proteins, were shown to be essential for

284 We propose that upregulated MAM function at the ER-mitochondrial interface, and incr

285 The upregulated MAM binding and activity in HLA-DR/TLR-transfected cells

286 The mechanisms by which MAM produces this phenotype are not clear; however, we n

287 While Bax association with MAM lipid rafts was detected in HCMV-infected cells, ass

288 a-syn result in its reduced association with MAM, coincident with a lower degree of apposition of ER

289 There were 36 deaths: 12 among children with MAM and six among children with SAM.

290 l recruited 6- to 23-month-old children with MAM in Burkina Faso.

291 ine the treatment effect among children with MAM included by MUAC and aged >/=6 mo with lengths <67 c

292 Based on this study, children with MAM mainly gain fat-free tissue when rehabilitated.

293 utritional supplementation for children with MAM.

294 mong 6-23 months old Burkinabe children with MAM.

295 velopment among 6-23-month-old children with MAM.

296 opment, and immune function in children with MAM.

297 oncentrate in the treatment of children with MAM. kg(-1) . d(-1) for up to 12 wk.

298 iation of Bax and apoptosome components with MAM lipid rafts.

299 mpairments were qualitatively distinct, with MAM increasing perseverative responding, whereas the PCP

300 not enter the mitochondria or interact with MAM-associated proteins, and therefore steroidogenesis w