ライフサイエンスコーパス: EAA

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

2 EAA treatment attenuated muscle atrophy and accelerated

3 EAA-antagonist resistant EPSCs were observed in the pres

4 EAA-induced mTORC1 signalling and protein synthesis incr

5 EAAs also attenuated atrophy in the nonoperated quadrice

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 acronutrients such as essential amino acids (EAA).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 All EAA antagonists inhibited the spontaneous discharge of M

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

64 the lowest contributions to the RDIs of all EAAs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 belong to clades capable of biosynthesizing EAA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 ated with removal and metabolism of the five EAA.

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

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

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

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

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

107 after a bolus ingestion of approximately 7 g EAAs.

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

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

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

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

112 -1,000 microm H2O2 enhanced swelling-induced EAA release by approximately 2.5-3-fold (EC50 approximat

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

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

115 of extracellular, rather than intramuscular EAAs.

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

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

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

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

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

121 3% greater (P < 0.05) after consumption of L-EAA (0.08 +/- 0.01%/h) than after consumption of EAA (0.

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

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

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

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

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

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

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

129 ed by simultaneous consideration of multiple EAA.

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

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

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

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

134 (0.08 +/- 0.01%/h) than after consumption of EAA (0.06 +/- 0.01%/h).

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

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

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

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

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

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

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

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

143 nhibit hypotonic swelling-induced release of EAA.

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

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

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

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

148 proteins after ingestion of a small dose of EAAs.

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

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

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

152 rdiovascular responses to microinjections of EAAs into the nTS.

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

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

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

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

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

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

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

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

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

162 ocked the VRAC currents and strongly reduced EAA release.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 2-fold with intake of leucine alone and with EAAs, respectively (P < 0.05).

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