ライフサイエンスコーパス: EAA

1 EAA is associated with worse neurocognitive function and

2 EAA measures biological aging through DNA methylation pa

3 EAA measures deserve further study as potential tools fo

4 EAA samples had a lower percentage of CD-3-expressing ce

5 EAA treatment attenuated muscle atrophy and accelerated

6 EAA values were calculated as residuals from the linear

7 EAA was assessed via GrimAge, PhenoAge, and DunedinPACE

8 EAA was associated with genetic variation in APOL2, sugg

9 EAA was estimated using 4 established "clocks": Horvath

10 EAA-antagonist resistant EPSCs were observed in the pres

11 EAA-induced mTORC1 signalling and protein synthesis incr

12 EAAs also attenuated atrophy in the nonoperated quadrice

13 EAAs detected by OCTA in diabetic eyes are significantly

14 d the equation MPS = (2.68 x [EAA])/(1.51 + [EAA]) (P < 0.01).

15 eline rates even though plasma essential AA (EAA) concentrations remained elevated (+130% at 120 min,

16 A custom algorithm detected extrafoveal AA (EAA) excluding the central 1-mm circle in projection-res

17 Children (n = 135) with accelerated EAA had higher PHV (beta 0.018, p = 0.0008) although the

18 V showed higher epigenetic age acceleration (EAA) according to all EAA estimators (mean 2.5 years, 95

19 l outcomes were epigenetic age acceleration (EAA) clocks.

20 t exposures and epigenetic age acceleration (EAA) produced more precise effect estimates when using p

21 consumption on epigenetic age acceleration (EAA) using clinical biomarkers, including liver function

22 Changes in epigenetic age acceleration (EAA) were investigated as the primary outcome in materna

23 uma experience, epigenetic age acceleration (EAA), and shortened DNA methylation-based telomere lengt

24 referred to as epigenetic age acceleration (EAA), which may reflect accelerated biological aging.

25 ein anabolic effect of essential amino acid (EAA) + sucrose intake in older subjects by improving nut

26 which interferes with excitatory amino acid (EAA) action.

27 The essential amino acid (EAA) density of a food also emerged as a novel concept a

28 2) on spontaneous and excitatory amino acid (EAA) induced nucleus tractus solitarius (NTS) neuronal a

29 rptive state and after essential amino acid (EAA) ingestion on three occasions: before (PRE), after b

30 three infusions of an excitatory amino acid (EAA) mixture applied at the same interval were more effe

31 Hcy is metabolized to excitatory amino acid (EAA) neurotransmitters, such as homocysteic acid (HCA) a

32 ability of these same excitatory amino acid (EAA) receptor antagonists to modulate morphine dependenc

33 y be blocked by using excitatory amino acid (EAA) receptor antagonists.

34 cids were prepared as excitatory amino acid (EAA) receptor antagonists.

35 enate, a non-specific excitatory amino acid (EAA) receptor subtype antagonist, on the regional accumu

36 oth NMDA and non-NMDA excitatory amino acid (EAA) receptor subtypes are involved in the integration o

37 The NMDA receptor, an excitatory amino acid (EAA) receptor, appears to be involved in the development

38 teraction of GABA and excitatory amino acid (EAA) receptors in the basolateral amygdala (BLA) in regu

39 The activation of excitatory amino acid (EAA) receptors within the central nervous system is asso

40 lective antagonism of excitatory amino acid (EAA) receptors within the ventral respiratory group (VRG

41 Ca(2+) accumulation, excitatory amino acid (EAA) release and neuronal death.

42 presumed nonvesicular excitatory amino acid (EAA) release have not been established.

43 Excessive excitatory amino acid (EAA) release in cerebral ischemia is a major mechanism r

44 The effects of essential amino acid (EAA) supplementation during moderate steady state (ie, e

45 to assess changes in excitatory amino acid (EAA) transmission in the nucleus accumbens produced by r

46 Excitatory amino acid (EAA) transmission in the rostral portion of the ventrola

47 Dietary removal of an essential amino acid (EAA) triggers the integrated stress response (ISR) in li

48 otor system, sends an excitatory amino acid (EAA)-containing projection to the ventral pallidum (VP),

49 e the potentiation of excitatory amino acid (EAA)-mediated transmission at the level of dopaminergic

50 d the hypothesis that excitatory amino acid (EAA)-mediated transmission plays a role in generating th

51 by deficiencies in any essential amino acid (EAA); EAA deficiency leads to rapid expression of genes

52 are the most abundant essential amino acids (EAA) (mg/g protein).

53 The essential amino acids (EAA) and total amino acids (TAA) slightly decreased, rat

54 na, stimulation with excitatory amino acids (EAA) can generate nitric oxide (NO) and increase levels

55 AF contained all the essential amino acids (EAA) except lysine and threonine, as required by pre-sch

56 eases the release of excitatory amino acids (EAA) from brain tissue of animals with bacterial meningi

57 lytes, including the excitatory amino acids (EAA) glutamate and aspartate, via a ubiquitously express

58 ux in the presence of essential amino acids (EAA) is the rate-limiting step that activates mTOR.

59 s the presence of all essential amino acids (EAA), especially histidine, tryptophan, and valine, alth

60 gh concentrations of excitatory amino acids (EAA), such as glutamate, results in neuronal death.

61 as a function of five essential amino acids (EAA).

62 acronutrients such as essential amino acids (EAA).

63 and higher content of essential amino acids (EAAs) (488.6-402.9 mg/g of protein respectively).

64 ed by the release of excitatory amino acids (EAAs) and peptides attributable to an injury-induced bar

65 ce P (SP) as well as excitatory amino acids (EAAs) appear to be released in response to stimulation o

66 utyric acid (GABA) and excitant amino acids (EAAs) are essential for coding many auditory tasks in th

67 Essential amino acids (EAAs) are key factors in determining dietary protein qua

68 tary protein provides essential amino acids (EAAs) for the synthesis of new proteins plus an array of

69 anism for removal of excitatory amino acids (EAAs) from the extracellular space of the central nervou

70 nions, including the excitatory amino acids (EAAs) glutamate and aspartate.

71 Essential amino acids (EAAs) have been shown to attenuate muscle loss during pe

72 examined the role of excitatory amino acids (EAAs) in activation of noradrenergic locus coeruleus (LC

73 examined the role of excitatory amino acids (EAAs) in the activation of midbrain dopaminergic (DA) ne

74 , 50 microM NMDA) of excitatory amino acids (EAAs) into the AP elicited an initial pressor and tachyc

75 , microinjections of excitatory amino acids (EAAs) into the nucleus tractus solitarii (nTS), in a reg

76 cting availability of essential amino acids (EAAs) limits aminoacylation of tRNAs by their cognate EA

77 Extracellular excitatory amino acids (EAAs) were detected from the same microdialysis samples.

78 on to the LC include excitatory amino acids (EAAs), corticotropin-releasing factor (CRF), and endogen

79 g 20-30 % protein and essential amino acids (EAAs), present a promising source of sustainable plant-b

80 causes a release of excitatory amino acids (EAAs), which in turn activate non-NMDA receptors.

81 lus ingestion of 15 g essential amino acids (EAAs).

82 ence of the remaining essential amino acids (EAAs).

83 at least 5 different essential amino acids (EAAs).

84 cological profiles of the swelling-activated EAA release pathway and Cl- currents.

85 d the MDR-1 blocker verapamil did not affect EAA release or VRAC currents.

86 mean (+/-SEM) net phenylalanine uptake after EAA ingestion was significantly less in the elderly (9.9

87 All EAA antagonists inhibited the spontaneous discharge of M

88 oward an association of higher levels of all EAA measures at baseline with serious clinical events.

89 etic age acceleration (EAA) according to all EAA estimators (mean 2.5 years, 95% CI 1.89-3.22 for Hor

90 lated to adult, body weight of 70 kg) of all EAAs was observed in freshwater micro-algal products, es

91 the lowest contributions to the RDIs of all EAAs.

92 Although EAA was associated with higher BMI (beta 0.16, p = 0.004

93 ncreasing the concentration of leucine in an EAA supplement consumed during steady state exercise eli

94 of BAT SNA and BAT thermogenesis through an EAA-mediated activation of second-order, arterial chemor

95 red for n+-Si/SAND/In2O3/Au devices using an EAA/In3+ molar ratio = 10.

96 red for n+-Si/SAND/In2O3/Au devices using an EAA/In3+ molar ratio = 10.

97 not mediate the association between ACEs and EAA.

98 Both the DAI and EAA were effective at identifying aging phenotypes, and

99 Associations between dietary factors and EAA were tested, adjusting for sex, energy intake, and b

100 We postulated that excess Hcy and EAA neurotransmitters may partly mediate methotrexate (M

101 ate and lactate in the first step medium and EAA and Glu in the second step medium were competent to

102 ve effects of l-NAME with respect to .OH and EAA levels as well as MRI lesion volume.

103 d with various stress-related phenotypes and EAA.

104 ion approximately 280% more than placebo and EAA-Leu after exercise.

105 F showed better protein efficiency ratio and EAA/TAA (total) %, indicating the presence of good quali

106 other sex steroids were not significant, and EAA was not associated with sex steroid levels in girls.

107 ggest that 17betaE2 inhibits spontaneous and EAA-induced NTS neuronal activity through 17betaE2 activ

108 Thus, the decrease in GABA and EAAs identified in the IC by previous studies may be att

109 le, if any, of the kainate receptor, another EAA receptor, remains unknown.

110 ctroactive surface area to geometrical area (EAA/GA approximately 134%), as evident from the Fe(CN)6(

111 South Florida (Everglades Agricultural Area, EAA) were computed from 2005 to 2012.

112 ctional status in extensive alopecia areata (EAA) scalp skin.

113 s hallmarks of experimental allergic asthma (EAA).

114 At baseline, EAAs for SVC, ICP, and DCP were all significantly correl

115 12.03, p = 0.0014), but associations between EAA and other sex steroids were not significant, and EAA

116 Associations between EAA and outcomes were evaluated by multivariate Cox mode

117 and VAT did not mediate associations between EAA and PHV, while SAT explained 8.4% of the association

118 y, a synergistic effect was observed between EAA and mating stimulation, because a subthreshold EAA i

119 belong to clades capable of biosynthesizing EAA.

120 , 0.31-0.94) years of greater skin and blood EAA, and 0.45 (95% CI, 0.07-0.83) years of greater intri

121 proteins are acutely regulated by the blood [EAA] over their normal diurnal range, but become saturat

122 atio of EAA RDA to the calculated whole-body EAA composition was derived.

123 ely inhibits VRACs, potently suppressed both EAA release and VRAC currents.

124 A correlation between the pattern of both EAAs and NEAAs in body proteins, and their usage, was as

125 Central GCN2 activation by EAA deprivation is also linked to an acute aversive feed

126 tolerance is more sensitive to modulation by EAA receptor antagonists than is the development of morp

127 xamined: ZD-7288, a blocker of HCN channels; EAA-090, an NMDA antagonist; and WAY-132983, a muscarini

128 Child EAA at 7, 9, and 14 years of age was estimated using DNA

129 its aminoacylation of tRNAs by their cognate EAAs and activates the nutrient-sensing kinase, general

130 d blood essential amino acid concentration ([EAA], mM) was hyperbolic and fitted the equation MPS = (

131 with the enchytraeid Enchytraeus crypticus, EAA derived almost exclusively from gut bacteria when th

132 DCP EAA was significantly associated with worse visual acuit

133 s significantly associated with baseline DCP EAA (odds ratio = 3.39, P = .002).

134 Our data demonstrate EAA in AUD and suggest that disease severity further acc

135 ored the effects of H2O2 on volume-dependent EAA release in cultured astrocytes, measured as the rele

136 suggest that (i) astrocytic volume-dependent EAA release is largely mediated by the VRAC, and (ii) th

137 Insulin signaling increased during EAA+sucrose ingestion in both groups (P < 0.05).

138 iciencies in any essential amino acid (EAA); EAA deficiency leads to rapid expression of genes regula

139 bre diets, whereas most of the enchytraeids' EAA derived from dietary sources when fed on lower fibre

140 Our data suggest that endogenous EAA receptor-mediated neurotransmission throughout the V

141 renal-axis acting in concert with endogenous EAAs from mossy fiber input.

142 asic discharge evoked by stimuli that engage EAA afferents to the LC, including sciatic nerve stimula

143 cursor solutions consisting of ethanolamine (EAA) and InCl3 in methoxyethanol.

144 cursor solutions consisting of ethanolamine (EAA) and InCl3 in methoxyethanol.

145 ne (NMA) and 9-ethanolaminomethylanthracene (EAA).

146 icant source for the increased extracellular EAAs seen in such conditions.

147 Alcalase-assisted extraction (EAA) was the most effective in the recovery of polypheno

148 in synthesis was responsive to only the five EAA used in its determination, with sensitivity to any s

149 ated with removal and metabolism of the five EAA.

150 Almost all gut taxa are candidates for EAA supplementation because almost all belong to clades

151 n whether VRAC serves as a major pathway for EAA release from swollen cells.

152 r explore potential mechanisms and sites for EAA release, we studied the release of preloaded [3H]-D-

153 CNMa and a greater compensatory appetite for EAAs.

154 scalp biopsies, suggesting that T-cells from EAA scalp have undergone activation.

155 Isonitrogenous (10 g EAA) drinks with different leucine contents [leucine-enr

156 after a bolus ingestion of approximately 7 g EAAs.

157 , median age 69 y), higher preoperative Grim EAA was associated with reduced OS (hazard ratio (HR 1.1

158 epression was associated with higher GrimAge EAA (beta, 0.06 [95% CI, 0.02 to 0.10] years; P = .01) i

159 th-EAA p=0.0008; Hannum-EAA p=0.059; GrimAge-EAA p=0.0021; and PhenoAge-EAA p<0.0001).

160 years of follow-up, PhenoAge-EAA and GrimAge-EAA showed no differences, whereas Horvath-EAA slightly

161 Hannum-EAA; 2.8 years, 1.97-3.68 for GrimAge-EAA; and 7.3 years, 6.40-8.13 for PhenoAge-EAA), with al

162 for Hannum-EAA (Horvath-EAA p=0.0008; Hannum-EAA p=0.059; GrimAge-EAA p=0.0021; and PhenoAge-EAA p<0.

163 statistically significant except for Hannum-EAA (Horvath-EAA p=0.0008; Hannum-EAA p=0.059; GrimAge-E

164 Horvath-EAA; 1.4 years, 0.74-1.99 for Hannum-EAA; 2.8 years, 1.97-3.68 for GrimAge-EAA; and 7.3 years

165 rs treated with CNS-directed therapy, higher EAA, measured by PCGrimAge, or DunedinPACE is associated

166 Boys with higher EAA had lower total testosterone (beta - 12.03, p = 0.00

167 (95% CI, 0.17-1.15) years of greater Horvath EAA, 0.62 (95% CI, 0.31-0.94) years of greater skin and

168 y significant except for Hannum-EAA (Horvath-EAA p=0.0008; Hannum-EAA p=0.059; GrimAge-EAA p=0.0021;

169 mean 2.5 years, 95% CI 1.89-3.22 for Horvath-EAA; 1.4 years, 0.74-1.99 for Hannum-EAA; 2.8 years, 1.9

170 e-EAA showed no differences, whereas Horvath-EAA slightly decreased (median difference, -0.53 years;

171 acuity (r = -0.24, P = .02), but SVC and ICP EAA were not.

172 monstrated that IFN-gamma-producing cells in EAA scalp were not greater in number than in normal spec

173 Expression of CD-69 was found only in EAA scalp biopsies, suggesting that T-cells from EAA sca

174 setting and suggest that T-cell responses in EAA scalp are tightly, albeit aberrantly, regulated via

175 at repeated cocaine administration increases EAA transmission in the nucleus accumbens only in rats t

176 -1,000 microm H2O2 enhanced swelling-induced EAA release by approximately 2.5-3-fold (EC50 approximat

177 Using international EAA RDA values, an average ratio of EAA RDA to the calcu

178 rapidly, the concentration of intramuscular EAAs was below basal levels.

179 f MPS and the concentration of intramuscular EAAs; indeed, when MPS was increasing most rapidly, the

180 of extracellular, rather than intramuscular EAAs.

181 5% CI, 0.07-0.83) years of greater intrinsic EAA compared with children whose mothers did not work du

182 SNs and PSNs is not attenuated by ionotropic EAA antagonists, suggesting that another receptor or tra

183 ventilated rats to determine the ionotropic EAA receptor subtypes involved in baroreceptor afferent

184 ses of ligand gated ion channel (ionotropic) EAA receptors.

185 A substantial fraction of ischemic EAA release occurs via volume-regulated anion channels (

186 Its EAA composition is like the children and adults' referen

187 erent leucine contents [leucine-enriched (l)-EAA, 3.5 g leucine; EAA, 1.87 g leucine] were consumed d

188 3% greater (P < 0.05) after consumption of L-EAA (0.08 +/- 0.01%/h) than after consumption of EAA (0.

189 as greater (P < 0.05) after consumption of L-EAA than after consumption of EAA.

190 ied EAAs with leucine, EAAs without leucine (EAA-Leu), leucine alone, or flavored water (placebo; con

191 nd were randomly supplied EAAs with leucine, EAAs without leucine (EAA-Leu), leucine alone, or flavor

192 mine out of cells and transport of L-leucine/EAA into cells.

193 ts [leucine-enriched (l)-EAA, 3.5 g leucine; EAA, 1.87 g leucine] were consumed during exercise.

194 Tryptophan is the most limiting EAA.

195 s process as a function of a single limiting EAA may not be adequate and might be better represented

196 Inhibition of the mTOR pathway by limiting EAAs, or by specific inhibitors, induces the Treg-specif

197 ed by simultaneous consideration of multiple EAA.

198 nts vaccinated with IFA, CpG, and the native/EAA or analog/ELA Melan-A(MART-1)(26-35) peptide, bindin

199 Injection of the nonselective EAA receptor antagonist kynurenic acid into the BLA prev

200 The genome-wide meta-analysis of EAA in AUD revealed a significant single nucleotide poly

201 Microinfusion of antagonists of EAA receptors (3 mm kynurenic acid, 100 microm AP-5, or

202 Calculations of EAA in adults using DNA methylation have been found to a

203 The H2O2-induced component of EAA release was attenuated by the Ca2+ chelator 1,2-bis(

204 (0.08 +/- 0.01%/h) than after consumption of EAA (0.06 +/- 0.01%/h).

205 protein synthesis during the consumption of EAA+sucrose was significantly higher after the exercise

206 nsumption of L-EAA than after consumption of EAA.

207 The excitatory effects of EAA were significantly inhibited in the presence of 17be

208 ercise appears to increase the efficiency of EAA use for muscle anabolism and to lower the meal thres

209 to the VP, and to determine the influence of EAA receptor subtypes, in vivo intracellular recordings,

210 The magnitude of EAA release correlated with the levels of the .OH adduct

211 wind-up, perhaps via positive modulation of EAA activity.

212 (EPSP) or current (EPSC) in the presence of EAA receptor antagonists (40-100 microM D-APV+20 microM

213 national EAA RDA values, an average ratio of EAA RDA to the calculated whole-body EAA composition was

214 ino acids (TAA) slightly decreased, ratio of EAA to TAA increased, while the calculated protein effic

215 nhibit hypotonic swelling-induced release of EAA.

216 These results support the role of EAA receptor subtypes in the phospholipases-catalyzed fo

217 Additionally, studies of EAA in low-income countries with diverse populations are

218 e VP contains both NMDA and AMPA subtypes of EAA receptors.

219 ce of extensive symbiotic supplementation of EAA by microbial gut symbionts and demonstrates that sym

220 dium DAI group experienced 1.8 more years of EAA (beta = 1.77; 95% CI, 0.84-2.69; P < .001), independ

221 high DAI group experienced 3.7 more years of EAA (beta = 3.66; 95% CI, 2.47-4.85; P < .001), whereas

222 mine whether ingestion of a smaller bolus of EAAs is associated with diminished accretion of muscle p

223 proteins after ingestion of a small dose of EAAs.

224 A reinvestigation of the effects of EAAs into the nTS in unanesthetized animals became neces

225 nts were randomized to ingest either 20 g of EAAs (n = 16) or placebo (n = 12) twice daily between me

226 ponse was enhanced by 60-75% after intake of EAAs compared with that of leucine alone (P < 0.05).

227 rdiovascular responses to microinjections of EAAs into the nTS.

228 A higher proportion of EAAs in relation to total protein content was observed i

229 y, we measured swelling-activated release of EAAs as D-[3H]aspartate efflux, and VRAC-mediated Cl- cu

230 in source to attain the daily requirement of EAAs to accomplish various health outcomes because these

231 s, using microinjections of the solutions of EAAs in artificial cerebrospinal (aCSF) fluid, confirmed

232 (CaCC), niflumic acid, had little effect on EAA release and only partially inhibited swelling-activa

233 ed genome-wide association studies (GWAS) on EAA, including pathway analyses.

234 although this response is enhanced by other EAAs and does not appear to be caused by alterations in

235 obiome that did not produce leucine or other EAAs showed higher expression of CNMa and a greater comp

236 n this way may potently promote pathological EAA release and brain damage in ischemia.

237 p=0.059; GrimAge-EAA p=0.0021; and PhenoAge-EAA p<0.0001).

238 e-EAA; and 7.3 years, 6.40-8.13 for PhenoAge-EAA), with all differences being statistically significa

239 After 4 years of follow-up, PhenoAge-EAA and GrimAge-EAA showed no differences, whereas Horva

240 ed, which echoed the slowly declining plasma EAA profile.

241 so potentially function as mediators, pooled EAA measures for 2 clocks remained statistically signifi

242 NAEs and 96 aging-related events).A positive EAA by Horvath's clock was associated with a 50% higher

243 Additionally, positive EAA according to GrimAge V1-V2 was linked to a four-fold

244 Secondary analyses showed more pronounced EAA in individuals with more severe AUD-associated pheno

245 ctrum anion channel blockers strongly reduce EAA release in cerebral ischaemia and other pathological

246 e was consistently associated with a reduced EAA adjusted for sociodemographic covariates, smoking st

247 after bedrest, only older adults had reduced EAA-induced protein synthesis rates and increased MAFBX

248 ocked the VRAC currents and strongly reduced EAA release.

249 no effect on VRAC currents and up-regulated EAA release.

250 ding T69E/A, S70E/A, S87E/A, T69E/S70A/S87A (EAA), T69A/S70E/S87A (AEA), T69A/S70A/S87E (AAE), T69E/S

251 gly up-regulates astrocytic volume-sensitive EAA release via a CaMKII-dependent mechanism and in this

252 etermination, with sensitivity to any single EAA falling to zero as supply of the EAA exceeded protei

253 not exhibit a preference for any of the six EAA nectar profiles; however, four of the EAA profiles s

254 es taken from 12 patients with long-standing EAA (average disease duration 14 years, 95% hair loss) a

255 d mating stimulation, because a subthreshold EAA infusion combined with subthreshold numbers of intro

256 acted protein (DCPI-D(8)) exhibited superior EAAs (40.36 %) leading hydrophilic amino acids (60.16 %)

257 se on 4 occasions and were randomly supplied EAAs with leucine, EAAs without leucine (EAA-Leu), leuci

258 Surprisingly, EAA scalp T-cells produced less IL-2 and CD-8 T-cells pr

259 s significantly associated with baseline SVC EAA (odds ratio = 8.73, P = .04).

260 r to function as partners both for symbiotic EAA supplementation and for digestion of insoluble plant

261 onts also function as partners for symbiotic EAA supplementation is important because the question of

262 We conclude that EAA receptors in the medulla are critical for generation

263 These results confirm that EAA receptors in the right NA are capable of modulating

264 This research evaluated the hypothesis that EAA receptors in bovine dental pulp activate a populatio

265 The EAA group performed better at 2 and 6 weeks after surger

266 The EAA-antagonist resistant EPSC appears to be due in part

267 The EAA-antagonist resistant EPSC current-voltage relation w

268 in RUTF has the potential to restore all the EAA, but it is possible that enrichment with amino acids

269 ate the regulation of iCGRP secretion by the EAA receptor agonists AMPA, kainate, NMDA, and L-glutama

270 we characterize two of these, designated the EAA-like and the loop1 motifs.

271 ery for placebo versus -6.2 +/- 2.2% for the EAA group (F = 14.14, P = 0.001).

272 surgery compared with -3.4 +/- 3.1% for the EAA group (F = 5.16, P = 0.036) and a -18.4 +/- 2.3% cha

273 he annual surface outflow P loading from the EAA averaged 157.2 mtons originating from Lake Okeechobe

274 ocated at the NBD-TMD interface, namely, the EAA loops from the TMDs, and the Q-loop and the ENI moti

275 hich was abolished by microinjections of the EAA antagonist kynurenic acid (109 nl, 100 mM) or the no

276 ective area represented less than 23% of the EAA area (172 farms).

277 single EAA falling to zero as supply of the EAA exceeded protein synthetic needs.

278 yanobacteria contain unusual variants of the EAA loop sequence that defines membrane-intrinsic protei

279 orters is actually a modified version of the EAA motif, which was originally believed to be present o

280 ix EAA nectar profiles; however, four of the EAA profiles stimulated feeding.

281 t related to differences at the level of the EAA receptor/effector mediating bursting, it is argued t

282 ly reduced swelling-activated release of the EAA tracer D-[(3)H]aspartate.

283 we tested the contribution of LRRC8A to the EAA release in brain glia.

284 bited when astrocytes were preexposed to the EAA transport inhibitor threo-hydroxy beta-aspartic acid

285 tic peatlands derived more than 80% of their EAA from bacteria.

286 nse to antigen when any 1, or more, of these EAAs are limiting, which is associated with a reduced ma

287 This EAA-antagonist resistant EPSC was observed in about 70%

288 and CFTR gene products do not contribute to EAA permeability.

289 underlying genetic variation contributing to EAA in AUD, we performed genome-wide association studies

290 rganization/United Nations University RDA to EAA content ranged between 1.35 (phenylalanine + tyrosin

291 the kappa-OR agonist were not restricted to EAA afferents, as U50488 also attenuated tonic LC activa

292 cluding the brain, and is highly specific to EAA deficiency.

293 When these two EAA receptor antagonists were combined, their ability to

294 is mediated by both NMDA- and non-NMDA-type EAA channels.

295 nipulations can also influence unpotentiated EAA-mediated transmission elsewhere in the brain, the po

296 randomized crossover study examined whether EAA supplementation with 2 different concentrations of l

297 sent study was undertaken to determine which EAA receptor subtypes are involved in baroreceptor affer

298 nor allele A of rs916264 was associated with EAA and with increased mRNA expression in hippocampus (p

299 2-fold with intake of leucine alone and with EAAs, respectively (P < 0.05).

300 bolic and fitted the equation MPS = (2.68 x [EAA])/(1.51 + [EAA]) (P < 0.01).