ライフサイエンスコーパス: TEA

1 TEA acts as a fast blocker (resulting in decreased curre

2 TEA and PEA had similar serum sIgA.

3 TEA cluster 1 had the most subjects with a history of in

4 TEA cluster 2, the smallest cluster, had the most subjec

5 TEA cluster 3, the largest cluster, had normal lung func

6 TEA domain (TEAD) transcription factors are essential fo

7 TEA domain (TEAD) transcription factors serve important

8 TEA domain transcription factor-1 (TEAD-1) is essential

9 TEA inhibited total Kv current with an IC50 = 0.54 mm an

10 TEA transcription activates promoters associated with re

11 TEA(+) decreases the association rate of 21-amino-9alpha

12 TEA, guanidine, and tetramethylguanidine inhibition was

13 (TEA-thiolate(+) = -S(CH(2))(11)N(CH(2)CH(3))(3)(+); SC6F

14 is purpose a MtBE-H2O (1:1) system with 10mM TEA and HCl was applied leading to a phenolic fraction,

15 4 patients survived to hospital discharge (2 TEA alone, 3 TEA/LCSD combined, and 4 LCSD alone), 1 of

16 tional mechanistic details of the Pd(OAc)(2)/TEA-catalyzed aerobic alcohol oxidation system are discl

17 s to 15nS-V and becomes sensitive to Ca(2+), TEA, BK, and SK blockers.

18 ent is small (3nS-V), insensitive to Ca(2+), TEA, BK, and SK blockers.

19 und to be -0.11, -0.25, and -0.47 V vs E(1/2,TEA) (term is defined later in experimental), respective

20 21 TEA and 52 PEA children were recruited (28 PEA-OIT, 24 P

21 The highly cationic nanoparticle [Au(225)(TEA-thiolate(+))(22)(SC6Fc)(9)] adsorbs so strongly on P

22 rvived to hospital discharge (2 TEA alone, 3 TEA/LCSD combined, and 4 LCSD alone), 1 of the TEA alone

23 inhibitor, tetraethylammonium (TEA), and (4) TEA + l-NAME.

24 genic embryos show that a binding site for a TEA Domain (TEAD) transcription factor is essential for

25 (+) current in SCs was composed (> 70%) of a TEA (2 mm)-sensitive component that was mediated by the

26 there was a reduction in the prevalence of a TEA-sensitive 113 pS channel in neurones from TG2576 mic

27 First, by activating TEA-inhibitable K(+)(Ca) channels, endothelium-derived h

28 In addition, TEA-soy sizes had a BOD5/COD ratio of 0.44, much higher

29 T) infants evaluated at term equivalent age (TEA) and healthy full-term newborns using proton magneti

30 luded for cranial US at term-equivalent age (TEA).

31 hird trimester prior to term equivalent age (TEA).

32 The T early alpha (TEA) promoter in the murine Tcra locus generates noncodi

33 alpha-TEA stimulated both apoptosis and autophagy in murine ma

34 a-tocopheryl ether linked acetic acid (alpha-TEA) have been developed.

35 vative alpha-tocopheryloxyacetic acid (alpha-TEA) induces tumor cell apoptosis and may offer a simple

36 ltridecyl)chroman-6-yloxy acetic acid (alpha-TEA), induce human breast, prostate, colon, lung, cervic

37 ignaling programs are activated during alpha-TEA-induced tumor cell killing.

38 f caspase-dependent apoptosis enhanced alpha-TEA-induced autophagy.

39 We suggest that the ability of alpha-TEA to stimulate autophagy and enhance cross-priming of

40 the ether-linked acetic acid moiety of alpha-TEA were demonstrated by high-performance liquid chromat

41 VES or alpha-TEA treatment of cp70 cells with 5, 10, or 20 microg/ml

42 id chromatography analyses that showed alpha-TEA to remain intact, whereas VES was hydrolyzed to the

43 Here we report that alpha-TEA also triggers tumor cell autophagy and that it impro

44 Cell exposure to alpha-TEA generated double-membrane-bound vesicles indicative

45 cancer cell lines are exceptions, with alpha-TEA exhibiting greater proapoptotic effects.

46 ation with dendritic cells pulsed with alpha-TEA-generated autophagosomes reduced lung metastases and

47 to the same extent as tetra-ethyl ammonium (TEA) but did not affect the membrane potential.

48 methylhistamine (RAMH), tetraethyl ammonium (TEA), and 4-aminopyridine (4-AP) were applied in the sup

49 Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy of which

50 r to multimodal thoracic epidural analgesia (TEA) in patients undergoing open liver surgery.

51 was to compare thoracic epidural analgesia (TEA) to intravenous patient-controlled analgesia (IV-PCA

52 A preliminary techno-economic analysis (TEA) was conducted to elucidate primary cost drivers and

53 Our Tissue Enrichment Analysis (TEA) can be found within WormBase, and can be downloaded

54 crude reaction mixture with Bu(2)SnCl(2) and TEA at room temperature enabled facile isolation of mult

55 Furthermore, blockade of 4-AP- and TEA-sensitive K+ channels in the presence of TTX signifi

56 evated and prolonged the effects of BDNF and TEA on actin polymerization.

57 Addition of Cs(+) and TEA(+) to the growth medium confirmed the key role of th

58 ls insofar as it is insensitive to Cs(+) and TEA(+), but resembles voltage-independent channels of gl

59 IBTX and TEA/4-AP did not affect the basal [Ca(2+) ]i in isolated

60 ng of the coupling between permeant ions and TEA blockade.

61 lation of the TS evoked EPSPs and IPSPs, and TEA and 4-AP increased the average amplitude and decreas

62 (15 mM poly-L-SUCL, 25 mM each of NH4OAc and TEA (pH 8.0); 80% (v/v) methanol sheath liquid containin

63 Both L-NMMA and TEA attenuated bradykinin-mediated vasodilation in healt

64 l-NNA and TEA, as well as their combination, lowered CVC in young

65 enicillamine (SNAP) was inhibited by ODQ and TEA but was insensitive to PD98059.

66 =20:1) and blocked by internal paxilline and TEA.

67 sodium current (I(Na)) and 4AP-sensitive and TEA-resistant potassium current (I(K)).

68 th sine oculis-related homeobox 4 (Six4) and TEA domain family member 2 (Tead2) factors.

69 chloride (3 stocks), acetone (7 stocks), and TEA (3 stocks), respectively, and 0% for a validation se

70 transcription factor AP-2 gamma (Tfap2c) and TEA domain transcription factor 4 (Tead4) expression in

71 S-IPSCs persisted in the presence of TTX and TEA but not 4-AP.

72 inhibitor of the interaction between YAP and TEA domain transcription factor 4 [TEAD4]).

73 coactivator Yes-associated protein (YAP) and TEA domain family members (TEAD).

74 se Yes, the Yes-associated protein (YAP) and TEA domain TEAD2 transcription factor pathway are activa

75 d complexes [Fe(III) (L)(HL)], (1(D) ), and (TEA)[Fe(III) (L)(2) ], (1(E) ) exist in the low-spin S=1

76 s the value of thoracic epidural anesthesia (TEA) and left cardiac sympathetic denervation (LCSD) in

77 Whole-cell currents were inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating functiona

78 ning K(+) current with the addition of 4-AP, TEA-Cl, and glibenclamide; and 4) blocking I(Ca) with ca

79 ls, with Ca(2+)-sensitive K(+) and both 4-AP/TEA-sensitive and -insensitive currents; type 3 cells, w

80 nsensitive currents; type 3 cells, with 4-AP/TEA-sensitive and -insensitive K(+) and small Na(+) curr

81 sion for transcriptomic endotypes of asthma (TEA), gene signatures that discriminate phenotypes of di

82 AA (p < 0.025) and higher Cho (p < 0.001) at TEA when compared to healthy controls.

83 ectedly, S1P also enhances MRTF-A binding at TEA sites.

84 infants showed a larger ventricular size at TEA compared with term infants (P < .001).

85 owever, scarce reciprocal inhibition between TEA and Arg was found, while the biguanide metformin was

86 hare an evolutionarily conserved DNA-binding TEA domain, which binds to the MCAT cis-acting regulator

87 The K(+) channel blocker TEA could also reverse the inhibitory effect of Y-27632

88 For the Na pump, both TEA and TPA inhibited, but TMA did not.

89 which has been shown to interfere with both TEA binding and the interaction of K+ with an external b

90 under mild conditions (TMS-Cl/TEA or TMS-Br/TEA in refluxing CHCl(3)) that do not cause demetalation

91 t responses were not affected by apamin, but TEA evoked similar changes.

92 did not affect the rise in [Ca(2+) ]i , but TEA/4-AP strongly ( approximately 3-fold) enhanced [Ca(2

93 The I(A) amplitude was not affected by TEA at any concentration or membrane potential.

94 nd high conductance channels were blocked by TEA or 4-AP or 140 mM RbCl.

95 as insensitive to PD98059 but was blocked by TEA.

96 e-wide gene expression during development by TEA/ATTS family of transcription factors.

97 emical step is reductive quenching of Fl* by TEA because of the latter's greater concentration.

98 Occupancy by TEA completely prevented MTSET modification of a cystein

99 +) (and with extracellular Na(+) replaced by TEA), Fe(2)(+) carried detectable, whole-cell, inward cu

100 Hepatic accumulation of [(14)C]TEA in 14-day BDL rats was reduced to 29.6 +/- 10.9% of

101 e model substrate tetraethylammonium ([(14)C]TEA) was administered intravenously to BDL and control r

102 lled by using the tetraethylammonium cation (TEA(+)) and/or iodide anion (I(-)) as chemical inputs.

103 regulator (CFTR(inh)-172), or K(+) channels (TEA or XE991).

104 the BK calcium-dependent potassium channels (TEA (1 mM), paxilline (10 muM) and iberiotoxin (100 nM))

105 the ionic salt tetraethylammonium chloride (TEA(+)Cl(-)) or the zwitterion tricine(+/-).

106 Tetraethylammonium chloride (TEA) was used to inhibit K(+)(Ca) channel activation and

107 be deprotected under mild conditions (TMS-Cl/TEA or TMS-Br/TEA in refluxing CHCl(3)) that do not caus

108 ot influenced by l-NNA (all concentrations), TEA (4-400 mum) or their combination (400 mum) (P > 0.05

109 udied under similar experimental conditions (TEA(o) and K(i)).

110 cantly abrogated the concentration-dependent TEA inhibition.

111 oxygen species (ROS)-mediated, TAZ-dependent TEA domain transcription factor (TEAD) trans-activation.

112 ounded by the upstream INT1-2 and downstream TEA elements.

113 e), (2) tetraethylammonium (TEA), (3) EMLA + TEA (Combo), and (4) Ringer solution (Control).

114 hannels, and the mechanism by which external TEA slows C-type inactivation, have been considered well

115 nded on a residue required for extracellular TEA action, suggesting that the identified compound targ

116 ne in activation of its transcription factor TEA domain family member-binding domain (TEAD).

117 The basis for TEA inactivity in DN thymocytes is unclear, because Edel

118 ixture (2:1 ratio by volume up to 60 mL) for TEA and cisplatin-ethiodized oil emulsion (0.5 mg cispla

119 Pmp22 enhancers contain binding motifs for TEA domain (Tead) transcription factors of the Hippo sig

120 YAP in MKs and demonstrate a requirement for TEA domain (TEAD) transcriptional factors to comediate Y

121 eggin polyoxoanions of the general formula, (TEA)Hp Naq [H2 M12 (XO4 )O33 (TEA)]r H2 O where p, q, r=

122 NAME (P < 0.001 from control, P < 0.001 from TEA).

123 gnals but failed to alter membrane function (TEA uptake).

124 anism involving activation of PKA and highly TEA-sensitive K(+)-currents.

125 and several potassium channels (iberiotoxin, TEA, 4-amino-pyridine), but blockers of calcium channels

126 ia of Genes and Genomes was used to identify TEA clusters.

127 y deficit have recently been demonstrated in TEA: (i) accelerated long-term forgetting (ALF): the exc

128 Median overall survival in TEA and TACE was 24.3 months (95% confidence interval [C

129 cell invasiveness, associated with increased TEA domain-dependent transcription and CCN2/CTGF express

130 ive to conventional K(+) channel inhibitors (TEA, 4-AP and Ba(2+)) but completely inhibited by tetrac

131 Critical was the role of the intracellular TEA(+)-binding site.

132 Unlike the tetraethylammonium ion (TEA), neither JC638.2alpha nor C16 monostring TA279 prod

133 ies of the current (permeability to Na+, K+, TEA+, and Cs+; voltage insensitivity; and dependence on

134 ffects of inhibitors of BK (IBTX) and BK/Kv (TEA/4-AP) on [Ca(2+) ]i responses to a wide range of hyp

135 In contrast, at more distal locations, TEA transcription inhibits promoter activity through tra

136 cells was enhanced nearly twofold by 1.0 mM TEA, with a decrease in the paired pulse ratio (PPR), ef

137 In 10 mM TEA, potassium currents were reduced in all the bipolar

138 lular solution or during superfusion of 5 mm TEA, suggesting the presence of an additional BK-channel

139 hannel blocker; and (iv) 10 mm l-NNA + 50 mm TEA.

140 l-NAME), and nearly abolished with l-NAME + TEA (13 +/- 2%; P = 0.001 from sulfaphenazole + l-NAME),

141 ions of N(G)-monomethyl-l-arginine (L-NMMA), TEA, fluconazole, and their combination.

142 Lanthanides and Zn2+ (but not TEA+) suppressed the open probability without affecting

143 (+) channel blocker barium chloride (but not TEA, glybenclamide or tertiapin-Q) significantly occlude

144 eral formula, (TEA)Hp Naq [H2 M12 (XO4 )O33 (TEA)]r H2 O where p, q, r=[2,3,8] for 1 and [4,1,4] for

145 The ability of TEA transcription to coordinate the activity of multiple

146 ing FBF in all subjects, and the addition of TEA further reduced FBF after fluconazole, suggesting th

147 % of the plateau phase, as administration of TEA in combination with l-NAME abolished the majority of

148 /- 5.3 Hz), both sensitive to application of TEA (0.5 mm) and 4-aminopyridine (4-AP; 30 mum).

149 The neuroanatomical bases of TEA and its associated memory deficits are unknown.

150 opiate use further supported the benefit of TEA on patient experience.

151 These actions involve binding of TEA(+) to different, but weakly interacting, sites in th

152 annels also blocked by low concentrations of TEA.

153 nt study, we investigated both the effect of TEA(+) on [(3)H]ryanodine binding and the actions of thi

154 ntibody mimicked and occluded the effects of TEA and 4-AP in NTS and dorsal column nuclei neurones, b

155 However, ion-suppressing effects of TEA hamper mass spectrometry (MS) instrumentation sensit

156 e knock-out (DKO) mice, the large effects of TEA were absent, spike-evoked GABA release was larger, a

157 Evaluation of TEA clusters in children confirmed that TEA clusters 1 a

158 between the IC(50) values for inhibition of TEA transport by 14 different compounds and their calcul

159 Initiation of TEA and LCSD in patients with refractory VT was associat

160 After initiation of TEA, 6 patients had a large (> or =80%) decrease in VT b

161 A and MOR), less than the interconversion of TEA(+) in solution, a heteroatom-dependent (Al, B, Co, M

162 dine binding was observed in the presence of TEA(+), suggesting that the cation and alkaloid compete

163 t repolarization remained in the presence of TEA, MgTX, or both.

164 entical rates in the absence and presence of TEA.

165 Here, we have analyzed the significance of TEA transcription for Tcra locus regulation through the

166 an external binding site similar to that of TEA in the Kv2.1 outer pore, but with much higher affini

167 for YAP activation and the transcription of TEA domain (TEAD) family members.

168 tant displayed markedly reduced transport of TEA and cimetidine while retaining transport of 1-methyl

169 ent promoter that lies only 4 kb upstream of TEA promoter.

170 ails of the study illustrate that the use of TEA results in an active catalyst that has only one liga

171 or cysteine had a relatively minor effect on TEA potency.

172 ctivity through competing with the oncogenic TEA domain family of transcription factors (TEAD) for YA

173 ith ketorolac/diclofenac (IV-PCA, n = 66) or TEA (n = 77) within an enhanced recovery after surgery p

174 Addition of calpain inhibitors after BDNF or TEA treatment maintained RhoA levels elevated and prolon

175 de levels (P = 0.04) compared with the other TEA clusters.

176 inding of YAP to its transcriptional partner TEA domain family member 4 (TEAD4); TEAD4 binding requir

177 thienylethylammonium tin iodide perovskite (TEA(2)SnI(4)).

178 t not by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium), decynium-22, carnitine, PHA (p

179 The as-prepared TEA(2)SnI(4) also possessed superior photostability, sho

180 hoice of the N-protecting group (see scheme; TEA = triethylamine, TMS = trimethylsilyl).

181 VLM neurones indicate that a 4-AP sensitive, TEA insensitive current, with biophysical properties con

182 expressed in the heteromers includes shifted TEA sensitivity compared with KCNQ2 homomers.

183 Industrial weaving results showed TEA-soy protein had relative weaving efficiency 3% and 1

184 eater compared to TEA, EMLA and Combo sites (TEA, 630 +/- 512, P = 0.003; EMLA, 421 +/- 216, P < 0.00

185 e reactions of impurities unique to specific TEA and chloroform stocks, and thus indicative of their

186 seen for the uptake of the hOCT1 substrates TEA(+) and ASP(+).

187 In major HPB surgery, TEA provides a superior patient experience through impro

188 significant difference in overall survival, TEA demonstrated better complete tumor response, longer

189 Smads/YAP/TAZ/TEA domain transcription factor1 (TEAD1) complex formati

190 TEAD (TEA/ATTS domain) transcription factors are the most dist

191 complex with the transcription factor TEAD (TEA domain family member) directly induce LATS2 expressi

192 In addition to a highly conserved TEAD1 (TEA domain family member 1)-binding MCAT motif, nucleoti

193 h muscle development and uses its N-terminal TEA domain (TEAD) to bind M-CAT elements.

194 Tetraethylammonium (TEA) is frequently used to inhibit delayed rectifier K(+

195 ly to skin surface), (2) tetraethylammonium (TEA), (3) EMLA + TEA (Combo), and (4) Ringer solution (C

196 ovement of Ca2+, K+, and tetraethylammonium (TEA+) through the model RyR2 pore were simulated with ex

197 h 4-aminopyridine (4-AP)/tetraethylammonium (TEA)-sensitive and CdCl(2)-sensitive inward currents; ty

198 he external pore blocker tetraethylammonium (TEA) and depended on a residue required for extracellula

199 otassium channel blocker tetraethylammonium (TEA), and the selective adenosine triphosphate (ATP)-sen

200 ve K(+) channel blocker, tetraethylammonium (TEA), and a large-conductance Ca(2+)-activated K(+) (BK(

201 type for organic cations tetraethylammonium (TEA) was also transported by SlCAT2.

202 ssibility, extracellular tetraethylammonium (TEA) and tetramethylammonium application produces potent

203 rations of extracellular tetraethylammonium (TEA; IC(50) = 11.8 mM), but no specific antagonists were

204 on is composed of a fast tetraethylammonium (TEA)-sensitive component, determining the width and ampl

205 or some substrates (e.g. tetraethylammonium (TEA)), they have distinct selectivities for others (e.g.

206 ugh inhibition of highly tetraethylammonium (TEA)-sensitive ion channels that contribute to action po

207 a KCa channel inhibitor, tetraethylammonium (TEA), and (4) TEA + l-NAME.

208 Intracellular tetraethylammonium (TEA) inhibition was studied at the single-channel level

209 S inhibitor; (iii) 50 mm tetraethylammonium (TEA), a non-specific KCa channel blocker; and (iv) 10 mm

210 ted the effect of 1.0 mM tetraethylammonium (TEA; which blocks Kv3 channels) on inhibitory synaptic c

211 ced the effectiveness of tetraethylammonium (TEA(+)) as a blocker of K(+) translocation.

212 of the rapid transfer of tetraethylammonium (TEA(+)) at the 1,2-dichloroethane/water interface.

213 ride salts, specifically tetraethylammonium (TEA), tetrapropylammonium (TPA), tetrabutylammonium (TBA

214 ded, economical template tetraethylammonium (TEA(+) ) has been systematically examined by experimenta

215 ctrolytes containing the tetraethylammonium (TEA(+) ) inert cation is reported.

216 The location of the tetraethylammonium (TEA) binding site in the outer vestibule of K+ channels,

217 Using tetraethylammonium (TEA), a presynaptic potassium channel blocker, we show t

218 ntercation compared with tetraethylammonium (TEA(+)), due to the coordination of Li(+) to the carbona

219 slices with BDNF or with tetraethylammonium (TEA), which induces a chemical form of LTP, produces a r

220 [Cl(-)], [Na(+)], and [tetraethylammonium] ([TEA(+)]), but dependent on [H(+)].

221 ter pore, but with much higher affinity than TEA.

222 position equivalent to Shaker T449, and that TEA prevents a constriction that underlies inactivation

223 The prevailing model has been that TEA is coordinated by four amino acid side chains at the

224 We conclude that TEA modulates, in a concentration dependent manner, tau(

225 n of TEA clusters in children confirmed that TEA clusters 1 and 2 are associated with a history of in

226 Our results demonstrate that TEA(+) inhibits both K(+) translocation through RyR, and

227 onal experiments in Shaker demonstrated that TEA bound well to C-type inactivated channels, but did n

228 se results add weight to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy.

229 ch higher than 0.03 for PVA, indicating that TEA-soy sizes were easily biodegradable in activated slu

230 these findings rule out the possibility that TEA binding involves an intimate interaction with the fo

231 tudies over a wide voltage range reveal that TEA block has a complex voltage-dependence that also dep

232 These data suggest that TEA and LCSD may be effective additions to the managemen

233 Together, these data suggest that TEA is stabilized in a more external position in the out

234 function with TCRalpha promoters such as the TEA promoter to drive TCRalpha-chain gene assembly in th

235 profile in the circulation to determine the TEA cluster assignment in a cohort of children with asth

236 ring vertebrate neural tube development, the TEA domain transcription factor (TEAD) is the cognate DN

237 ocus, where cohesion-binding sites flank the TEA promoter and the Ealpha enhancer, and demarcate Tcra

238 e 0- to 48-hour pain scores was lower in the TEA group (78.6 vs 105.2 pain-hours, P = 0.032) with a 3

239 was no worse than the mean pain score in the TEA group by a margin of <1 point on an 11-point scale (

240 Pain scores were lower in the TEA group on PODs 0 and 1, but higher or equal on PODs 2

241 e was 1.7 in the IV-PCA group and 1.6 in the TEA group, establishing noninferiority.

242 to NO2 and subsequent NO2 collection in the TEA solution is >98% under a variety of controlled condi

243 A/LCSD combined, and 4 LCSD alone), 1 of the TEA alone patients underwent an urgent cardiac transplan

244 Thus, the inactivity of the TEA promoter in DN thymocytes is due primarily to intrin

245 a transcription terminator downstream of the TEA promoter.

246 vided that a sufficient concentration of the TEA reducing agent was present in solution.

247 ate constant and transfer coefficient of the TEA(+) transfer are compared with previously reported va

248 Reducing the TEA concentration from 40 mM to 1 mM significantly decre

249 Remarkably, the TEA promoter on this allele exhibits normal developmenta

250 fect in I(A) kinetics demonstrating that the TEA effects were not due to a reduction of extracellular

251 harmacological studies demonstrated that the TEA-sensitive component of I(K,slow), I(K,slow2,) is sel

252 vity of the Sd-Yki complex by binding to the TEA DNA-binding domain of Sd.

253 n of the ancillary dtb-bpy ligand, where the TEA radical cation serves as an effective hydrogen atom

254 locus (TCRalpha/delta(5DeltaT)) in which the TEA promoter lies in the same location as the Vdelta5 ge

255 clear translocation and interaction with the TEA domain (TEAD) transcription factor complex, which le

256 erleukin 6) through YAP association with the TEA domain-binding motif in the promoter region of infla

257 ethylammonium, and tetrapropylammonium, TMA, TEA, and TPA, respectively) did not inhibit PMCA.

258 sponse to L-NMMA was greater (P=0.04) and to TEA was lower (P=0.04) in healthy subjects compared with

259 growth by competing with YAP for binding to TEA-domain proteins (TEADs).

260 ax s) were significantly greater compared to TEA, EMLA and Combo sites (TEA, 630 +/- 512, P = 0.003;

261 IV-PCA was noninferior to TEA for the treatment of postoperative pain in patients

262 on strategy, 140 patients were randomized to TEA (N = 106) or intravenous patient-controlled analgesi

263 et initial Valpha-to-Jalpha recombination to TEA-proximal Jalpha segments and promote the ordered usa

264 sensitive to charybdotoxin and resistant to TEA.

265 e large conductance channel was sensitive to TEA, iberiotoxin, was activated in excised inside-out pa

266 enge, patients were classified as transient (TEA) or persistent (PEA) egg-allergic.

267 ssed by tetraethylammonium cation transport (TEA).

268 ent NO2 collection in a 20% triethanolamine (TEA) solution as nitrite and nitrate for delta(15)N anal

269 gradable sizing agents from triethanolamine (TEA) modified soy protein could substitute poly(vinyl al

270 ons of commercial stocks of triethanolamine (TEA), thionyl chloride, chloroform, and acetone.

271 the photosensitizer (PS) and triethylamine (TEA) as the sacrificial electron donor, these complexes

272 and compared with ammonia and triethylamine (TEA) for the separation of selected organic acids of gen

273 ansfer (PET) between 1(+) and triethylamine (TEA) undergo subsequent reactions to generate a previous

274 orate) under mild conditions (triethylamine (TEA) or molecular sieves) easily led to the correspondin

275 ith a mobile phase containing triethylamine (TEA) and hexafluoro-2-propanol (HFIP).

276 tion gas with base vapor from triethylamine (TEA), the charge reduction effect can be achieved and ut

277 in acetonitrile (with 0.25 M triethylamine (TEA)) thus identified as P(-) (singly reduced, nonproton

278 demonstrated the potential of triethylamine (TEA) for shifting the charge state pattern toward lower-

279 tion of a catalytic amount of triethylamine (TEA).

280 ster salts in the presence of triethylamine (TEA).

281 diethylmethylamine (DEMA) or triethylamine (TEA) through a T mixer coupled to a time-of-flight mass

282 flates with aryl amines using triethylamine (TEA) as base.

283 Eight patients underwent TEA, and 9 underwent LCSD (3 patients had both procedure

284 of 54.2+/-16.6 years; 13 men) who underwent TEA, LCSD, or both to control ventricular tachycardia (V

285 irect target genes of YAP/TAZ, regulated via TEA domain (TEAD) transcription factors.

286 ckel-Onsager theory of electrophoresis, when TEA(+)Cl(-) was added to the buffer.

287 NTB) and lateral superior olive (LSO); while TEA (1 mm) was employed to block Kv3-mediated outward po

288 re, the initial peak was just 17 +/- 2% with TEA + l-NAME (P < 0.001 from l-NAME).

289 zole (P = 0.02 from control), 71 +/- 3% with TEA (P = 0.01 from control), and further to 38 +/- 2% wi

290 Thus, these findings are consistent with TEA, guanidine, and tetramethylguanidine inhibiting from

291 Mechanistically, YAP cooperated with TEA domain transcriptional factor (TEAD) to activate the

292 Resting FBF decreased with TEA and L-NMMA in all subjects (P<0.001); however, the v

293 s persistently and significantly higher with TEA at 3 months (62 of 88 [70%] vs 39 of 76 [51%], P = .

294 r intralesional progression were longer with TEA than TACE (TTP, 34.6 months [95% CI: 28.2, 41] vs 26

295 ctive memory performance in 41 patients with TEA.

296 ter refrigerated storage, since samples with TEA and GRA extract showed the lowest values.

297 r TBARS values were obtained in samples with TEA and GRA extracts.

298 ediated vasodilation remained unchanged with TEA in healthy subjects but was significantly attenuated

299 ked reduction in the interaction of YAP with TEA domain (TEAD) transcription factors in the nuclei of

300 In hepatocytes and tumor cells, YAP/TEA domain transcription factor 4 (TEAD4)-dependent tran