ライフサイエンスコーパス: APV

1 APV blocked the facilitatory effect of preexposure.

2 APV blocked these effects, suggesting that the loss of a

3 APV did not significantly influence this dilatory respon

4 APV infused into RSC also impaired retrieval of recent m

5 APV infusion into the BLA was reported to block the expr

6 APV infusions into dorsal CA1 attenuated detection of a

7 APV or DRV binds with HIV-1 protease via both hydrophobi

8 APV reduced background activity in the normal eye more t

9 APV RNA and antibodies were also detected in two differe

10 APV RNA was detected in samples examined from geese, spa

11 APV SP concentrations were consistently lower than BP co

12 %APV was defined as the sum of plaque volume divided by t

13 APV, CNQX, and bicuculline were included to block fast s

14 fter TBI, we unmasked a persistent, abnormal APV-sensitive hyperexcitability that was bilateral and l

15 ere blocked by 4-aminophosphonovaleric acid (APV) and CNQX whereas the outward current only was block

16 he presence of D-aminophosphonovaleric acid (APV)- and ifenprodil-sensitive NMDA receptors, and found

17 Dl-2-amino-5-phosphonopentanoic acid (APV) blocked NMDA's effects on delta subunit expression.

18 nist D(-)-2-amino-5-phosphonopentanoic acid (APV) or the CaM kinase II inhibitor KN-62.

19 sts D-(-)-2-amino-5-phosphonopentanoic acid (APV) plus 6,7-dinitroquinoxaline-2,3-dione (DNQX) or APV

20 f 50 microM 2-amino-5-phosphonovaleric acid (APV) and 20 microM 6-cyano-7-nitroquinoxaline-2,3-dione

21 tagonists D-2-amino-5-phosphonovaleric acid (APV) and 7-Cl-kynurenic acid, as well as allosteric modu

22 tagonist DL-2-amino-5-phosphonovaleric acid (APV) completely blocked fear conditioning to a tone stim

23 ntagonist D,L-amino-5-phosphonovaleric acid (APV) did not lead to major alterations of PPD.

24 tenuated by 2-amino-5-phosphonovaleric acid (APV) infusions, whereas lateral perforant path plasticit

25 onists, D,L-2-amino-5-phosphonovaleric acid (APV) or 6,7-dinitroquinoxaline-2,3-dione (DNQX), enhance

26 d 50 microM 2-amino-5-phosphonovaleric acid (APV)) were dramatically reduced during the DSI period.

27 LA with d,l-2-amino-5-phosphonovaleric acid (APV), a competitive NMDA receptor antagonist.

28 antagonist 2-amino-5-phosphonovaleric acid (APV), but were eliminated by both the non-NMDA glutamate

29 bited by DL-2-amino-5-phosphonovaleric acid (APV).

30 agonists DL-2-amino-5-phosphonovaleric acid (APV; 50 mM) or DL-2-amino-5-phosphonopentanoic acid (AP5

31 gonists, D-2-amino-5-phosphono-valeric acid (APV) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX).

32 Rats were preexposed to a chamber after APV administration.

33 g that diagnostic tests and vaccines against APV C are likely to exhibit broad cross-reactivity.

34 of LTP by puffing DL-aminophosphonovalerate (APV), an N-methyl-D-aspartate (NMDA) receptor blocker in

35 ine (ZDV), lamivudine (3TC), and amprenavir (APV), given alone and in combination with the 2 nucleosi

36 ns of atazanavir, lopinavir, and amprenavir (APV).

37 The protease inhibitor amprenavir (APV) generates a signature set of HIV type 1 (HIV-1) pro

38 Although chemically similar to amprenavir (APV), the potency of TMC114 is substantially greater.

39 itution is often associated with amprenavir (APV) and darunavir (DRV) resistance, while the I50L subs

40 ive calcium channels, NMDA receptors, and an APV-resistant influx consistent with calcium-permeable A

41 n in group 4, where a mixture of cocaine and APV was used.

42 ed a comparable dose-dependent dilation, and APV elicited a significantly smaller dose-dependent cons

43 nly marginally attenuated by dizocilpine and APV.

44 egree (J45) and 0-dregree meridians (J0) and APV most often presented higher coefficient values for K

45 to blockade of the NMDA receptor by Mg2+ and APV, we confirmed that chronic treatment with NT-3 did n

46 ents equivalent to those of tetrodotoxin and APV, whereas addition of BDNF and NGF each increased sta

47 plexed with wt HIV-1 protease and TMC114 and APV complexed with an MDR (L63P, V82T, and I84V) proteas

48 nthalpy for ATV binding to I50V variants and APV binding to I50L variants, leading to hypersusceptibi

49 iameter (MLD), minimal lumen area (MLA) and %APV.

50 les quantification of luminal narrowing and %APV.

51 A low concentration of the NMDA antagonist APV (5 microM) mimicked the inhibition of ethanol of per

52 e density was blocked by the NMDA antagonist APV, but not by the AMPA/KA antagonist DNQX.

53 ifferential training in the NMDAR antagonist APV (DL-2-amino-5-phosphonovalerate) blocked not only th

54 ty can be reproduced by the NMDAR antagonist APV and by Ca(2+)-activated slow conductance K(+) (SK) c

55 ccur in the presence of the NMDAR antagonist APV, but the decay of the responses was still prolonged.

56 cked by the NMDA receptor (NMDAR) antagonist APV, apparently acting at NMDARs on primary afferents.

57 rons shows that the NMDA receptor antagonist APV (100 microM) blocked the early development of the te

58 ons of Vehicle, the NMDA receptor antagonist APV (2.5 microg/side), or the cAMP inhibitor Rp-cAMPS (1

59 as abolished by the NMDA receptor antagonist APV and partially reduced by cycloheximide.

60 LTP was blocked by NMDA receptor antagonist APV in the hippocampus of homing pigeon, but was APV-res

61 ng infusions of the NMDA receptor antagonist APV into the DH or VH blocked the learning-induced enhan

62 DNQX as well as the NMDA receptor antagonist APV more potently attenuated cholinergic signals evoked

63 Before P9, the NMDA receptor antagonist APV or the non-NMDA receptor antagonist CNQX blocked the

64 not blocked by the NMDA receptor antagonist APV, anti-p75(NTR) function-blocking antiserum, or previ

65 was blocked by the NMDA receptor antagonist APV, intracellular BAPTA, the CaM kinase inhibitors KN-6

66 were blocked by the NMDA receptor antagonist APV.

67 ocking the NMDA receptor with the antagonist APV significantly improved the temporal processing abili

68 ppressed by a non-specific NMDAR antagonist (APV) or AMPA receptor antagonist (CNQX).

69 an N-methyl-D-aspartate receptor antagonist (APV).

70 However, the NMDA receptor antagonist, APV, elicited a dose-dependent constriction.

71 l injection of the NMDA receptor antagonists APV or MK801 transiently induced GFP-synaptobrevin clust

72 Additional experiments showed that intra-BLA APV infusions substantially interfere with the expressio

73 he absence or presence of the NMDAR blocker, APV, hereby unmasking the NMDAR component in this proces

74 Both APV and TMC114 fit predominantly within the substrate en

75 diated synaptic transmission is strong, both APV and CNQX decrease dendritic arbor branch length, con

76 continued to block the prolonged bursts, but APV merely shortened their duration.

77 both the 5alpha-reductase inhibitors and by APV.

78 y finasteride and dutasteride, as well as by APV.

79 ding current transients that were blocked by APV and ifenprodil.

80 When sacral NMDA receptors were blocked by APV, the sacral CPGs were suppressed, VF neurons with no

81 ased ORN activity, which could be blocked by APV.

82 Similar cytotoxity was caused by APV or ACB in group 3.

83 Paroxysmal discharges were curtailed by APV and were similar to responses recorded from the dent

84 mics of HIV-1 protease and the inhibition by APV and DRV, providing useful information to the design

85 s were completely blocked by DNQX but not by APV.

86 This LTP inhibition was overcome by APV and NVP-AAM077 but not ifenprodil, suggesting that z

87 d potential after bicuculline was reduced by APV (20 microM).

88 lation observed with E2 alone was reduced by APV and Rp-cAMPS, suggesting that estrogenic enhancement

89 rents are elevated by NMDA and suppressed by APV in these neurons.

90 nalysis of the avian pneumovirus subgroup C (APV C) matrix (M2) gene of cell culture-adapted isolates

91 ous synaptic blockers (picrotoxin, CGP55845, APV, DNQX, E4CPG, and MSPG), we demonstrated that this d

92 CNQX, APV, bicuculline, CGP35348 (GABAB receptor antagonist),

93 cine-10-carboxylic acid methyl ester], CNQX, APV, and TTX, and was inhibited in the presence of an ex

94 dy used glutamate receptor antagonists (CNQX/APV) or low calcium to block synaptic transmission, allo

95 intensity was raised in the presence of CNQX/APV, a second alkalinization arose, presumably due to di

96 In group 4, a combination of cocaine +APV was added at a concentration 1 mg+25 microl/ml of cu

97 The bath solution contained APV, CNQX and bicuculline to block ionotropic glutamate

98 Regardless of the testing context, APV infusion into BLA completely blocked the expression

99 significant dose-dependent decreases in CSA, APV, and CBF.

100 influence serotonin-induced changes in CSA, APV, or CBF.

101 ist D-(-)-2-amino-5-phosphonovaleric acid (D-APV) as well as the broad-spectrum glutamate receptor an

102 st D(-)-2-amino-5-phosphonopentanoic acid (D-APV) into the basolateral amygdala before a memory react

103 e of D(-)-2-amino-5-phosphonovaleric acid (D-APV), an NMDA-site antagonist.

104 st, D-(-)-2-amino-5-phosphonovaleric acid (D-APV).

105 agonist D-2-amino-5-phosphonovaleric acid (D-APV).

106 ence of D-2-amino-5-phosphonovaleric acid (D-APV, 50 microM), 6-cyano-7-nitro-quinoxaline-2,3-dione (

107 e receptor antagonists (NBQX, 5 microm and D-APV, 10 microm), electrical stimulation of the ipsilater

108 6365, but not the NMDA receptor antagonist d-APV, prevented BDNF-induced GluA1 surface expression as

109 nsitivity to the glutamate-site antagonist d-APV.

110 he non-subunit-selective NMDAR antagonist, D-APV, in organotypic hippocampal slice cultures.

111 ng the application of an NMDAR antagonist, D-APV, onto the cortical surface.

112 Importantly, the NMDAR antagonists, D-APV and R-CPP, attenuated AD currents carried by Panx1,

113 of EAA receptor antagonists (40-100 microM D-APV+20 microM CNQX, or 5 mM kynurenic acid) plus the GAB

114 either 25 microM bicuculline or 25 microM D-APV.

115 by Panx1, and the combined application of D-APV and (10)panx (a Panx1 blocker) inhibited AD currents

116 In contrast, infusion of d-APV immediately after the memory reactivation session ha

117 at the reconsolidation-impairing effect of D-APV is correlated with downstream reductions in expressi

118 mited either by moderate concentrations of D-APV or by voltage clamping cells at negative membrane po

119 s could not be prevented by application of d-APV, the glutamate-site NMDAR antagonist, and were still

120 itic spines are reduced in the presence of D-APV.

121 Chronic NVP-AAM077 or D-APV treatment had little effect on these measures.

122 In contrast, the D-APV treatment of DAKO brains did not augment NR2A labeli

123 ochemistry revealed that, as expected, the D-APV treatment of wild-type (WT) mouse cortex increased t

124 HVc" EP-SPs were relatively insensitive to D-APV but almost completely abolished by CNQX.

125 ly recorded CF responses were reduced when D-APV was bath applied.

126 al blockade of NMDA receptor channels with D-APV or chelation of intracellular calcium ions with EGTA

127 nist, 5,7-dichlorokynurenate (DCK) or with D-APV, respectively, did not result in agonist-induced ope

128 ography (TEE) are currently used to diagnose APVs, but did not provide complete information in our pa

129 gnetic resonance imaging correctly diagnosed APVs and ASDs in all patients (100%) who underwent surge

130 findings, suggesting that passive diffusion (APV), slowed elimination (ZDV), and either active accumu

131 bath application of an NMDAR antagonist (dl-APV), indicating that these NMDARs are functional.

132 after blocking NMDA receptors (50 microM DL-APV), non-NMDA receptors (20 microM CNQX), or blocking b

133 zymatic activity, even in the presence of dl-APV.

134 with tetrodotoxin nor NMDA receptors with dl-APV altered the effects of morphine.

135 PET RMBF and Doppler APV were linearly correlated (r = .60; P < .001), as wer

136 Either APV or naloxone infusions into dorsal CA3 disrupted both

137 Dorsal dentate gyrus infusions of either APV or naloxone attenuated detection of a spatial change

138 virus (APV) infections and were analyzed for APV genome and infectious particles.

139 the quadruple mutant and gain in binding for APV, demonstrating the powerful combination of virology,

140 the chemical moieties at the P1 position for APV/DRV and the P2 position for ATV.

141 rating characteristic curve was highest for %APV (0.85) compared with diameter stenosis (0.68), area

142 Sera from APV-infected turkeys consistently contained antibodies t

143 es C) containing 100 microM caged glutamate, APV (2-amino-5-phosphonovaleric acid), and high divalent

144 (2.5 vs. 3.8 mm(2), p = 0.01), and greater %APV (48.9% vs. 39.3%, p < 0.0001).

145 sera from turkey flocks suspected of having APV infection, 133 (72.3%) were positive by M protein EL

146 t the substitutions at residue 50 affect how APV, DRV, and ATV bind the protease with altered van der

147 To explain how APV, DRV, and ATV susceptibility are influenced by mutat

148 asal average peak velocity (bAPV), hyperemic APV (hAPV), diastolic/systolic velocity ratio (DSVR), an

149 P<.001) as well as ET-1-induced decreases in APV (P=.05) and CBF (P=.012).

150 il, and other drugs previously implicated in APV among 30 patients with vasculitis and the highest ti

151 o net change in CSA but induced increases in APV and CBF, the extent of which did not change signific

152 Training in APV blocked this differential synaptic enhancement.

153 induced small decreases in CSA but increased APV and CBF.

154 EC stimulation (HFS; 100 Hz, 1 sec) induced APV-sensitive short-term potentiation (2.5-fold) that ge

155 Infectious APV was recovered from sentinel duck samples.

156 blockade of NMDA receptors (NMDARs) with D,L-APV, but only in BDNF-treated neurons, suggesting that C

157 heres treated with an inactive enantiomer, L-APV.

158 to freezing in predicting group membership (APV vs. ACSF) and both to be better predictors than the

159 r antagonists (20 microM CNQX and 100 microM APV), confirming that glutamate is the neurotransmitter

160 EPES-aCSF (without HCO(3)(-)) plus 50 microM APV and 10 microM DNQX.

161 but were blocked by 25 microM CNQX/50 microM APV.

162 eter stenosis, area stenosis, MLD, and MLA, %APV by coronary CTA improves identification, discriminat

163 Passage of the triple-mutant APV-resistant HIV-1 strain in MT4 cells, in the presence

164 ked by inhibitors of NMDA receptors (NMDARs; APV) or CaM-kinase kinase (STO-609), the upstream activa

165 Interestingly, at p60, in the absence of APV, no or very little LTD was found in KO that was comp

166 The combination application of APV and cadmium enhanced the epileptiform activity.

167 at was completely restored by application of APV.

168 uggest that a sizable proportion of cases of APV with high titers of anti-MPO antibodies are drug-ass

169 several other drugs may cause some cases of APV, and the majority of these cases have been associate

170 Ps were suppressed by a low concentration of APV indicating they were regulated by NMDA receptors.

171 routine indirect ELISA for the detection of APV/US antibodies in turkey sera.

172 immunosorbent assay (ELISA) for diagnosis of APV infection, a newly emergent disease of turkeys in Un

173 The antiretroviral effect of APV monotherapy was related to APV concentrations.

174 When the effect of APV on background activity was measured, there was diffe

175 In normal animals, the effect of APV on the contrast-response curve was similar in the tw

176 GTS-21 (5 microM) increased the frequency of APV- and NBQX-sensitive currents, while 5-HI+4OH-GTS-21

177 Surprisingly, infusion of APV only into RSC, but not ACC or DH, abolished retrieva

178 ts were obtained with intra-BLA infusions of APV before contextual fear conditioning in rats that had

179 by inhibiting NMDARs in RSC via infusions of APV before tests for context fear in mice.

180 d set of experiments, intra-BLA infusions of APV markedly impaired the normal expression of postshock

181 tly impaired by intra-amygdalar infusions of APV.

182 Injection of APV (20 mM, 2 microliters, I.C.V.; n = 6), an antagonist

183 tetanus, slices tetanized in the presence of APV, and control slices receiving test stimulation only.

184 t of PTP could be induced in the presence of APV, indicating that it is not mediated by NMDA receptor

185 As expected, in the presence of APV, we found more LTD in the mouse KO than in WT.

186 ognize the approximately 47-kDa N protein of APV/US by Western immunoblot analysis.

187 btained from birds showing clinical signs of APV infection.

188 ical and histologic findings were typical of APV.

189 pid and comprehensive anatomic definition of APVs and ASDs in patients with adult congenital heart di

190 For the diagnosis of APVs, the MRI and catheterization results agreed in 74%

191 Addition of %APV to other measures showed significant reclassificatio

192 potential was blocked by nitrendipine and/or APV and facilitated by bicuculline, showing that the cha

193 s 6,7-dinitroquinoxaline-2,3-dione (DNQX) or APV alone but not DNQX alone.

194 When infectious HRSV or APV was used as helper virus, replication could occur on

195 ultured in NMDA antagonists (microM MK801 or APV) revealed that antagonist exposure blocked the migra

196 ntaining NMDA receptor antagonists (MK801 or APV) were positioned in the dentate gyrus during the sti

197 ercome the effects of either tetrodotoxin or APV.

198 ainst calcium-binding proteins, parvalbumin (APV) or calbindin (ACB) was added at a concentration 25

199 tagonist D(-)-2-amino-5-phosphonopentanoate (APV; 100 microM).

200 MDA antagonists 2-amino-5-phosphonovalerate (APV) and N-acetyl-aspartyl-glutamate, than the excitator

201 eceptor blocker 2-amino-5-phosphonovalerate (APV) caused a slight reduction of the visual response, w

202 ncentrations of 2-amino-5-phosphonovalerate (APV) did not block either LTP or LTD despite producing >

203 nfused with D,L-2-amino-5-phosphonovalerate (APV) into the BLA or central nucleus of the amygdala (CE

204 A) antagonist D-2-amino-5-phosphonovalerate (APV) was then applied, and the effect on the contrast-re

205 observed that D-2-amino-5-phosphonovalerate (APV), a competitive NMDAR antagonist, blocked the effect

206 r antagonist DL-2-amino-5-phosphonovalerate (APV).

207 tor antagonist, 2-amino-5-phosphonovalerate (APV).

208 Infusion of 2-amino-5-phosphonovalerate (APV; 100 microM), an inhibitor of N-methyl-D-aspartate (

209 or antagonist D,L-2-amino-5-phosphovalerate (APV) on the facilitatory effect of context preexposure.

210 turkey farms experiencing avian pneumovirus (APV) infections and were analyzed for APV genome and inf

211 The avian pneumovirus (APV) outbreak in the United States is concentrated in th

212 The matrix (M) protein of avian pneumovirus (APV) was evaluated for its antigenicity and reliability

213 yncytial virus (HRSV) and avian pneumovirus (APV) was studied using minigenomes containing a reporter

214 (United States-specific) avian pneumovirus (APV/US) was expressed in Escherichia coli, and antibodie

215 recombinant M protein or denatured purified APV proteins by Western analysis.

216 Nineteen men receiving APV monotherapy and 12 men receiving triple therapy dona

217 selective antagonists of the NMDA receptor (APV) both prevent induction of TH expression in OE-OB co

218 The recombinant APV/US N protein was used in a sandwich-capture enzyme-l

219 eas only 18 (52.9%) were positive by routine APV ELISA 28 days after infection.

220 e by M protein ELISA but positive by routine APV ELISA, were not reactive with either recombinant M p

221 eas only 99 (53.8%) were positive by routine APV ELISA.

222 had given false-positive results by routine APV ELISA.

223 cherichia coli was compared with the routine APV ELISA that utilizes inactivated virus as antigen.

224 (F), and second matrix (M2) genes of 15 U.S. APV strains isolated between 1996 and 1999 revealed betw

225 that wild birds may be involved in spreading APV infection.

226 blocking both ionotropic receptor subtypes (APV and CNQX).

227 Twenty consecutive patients with suspected APVs were studied by MRA after inconclusive assessment b

228 the wt enzyme (K(d) = 4.5 x 10(-12) M) than APV (K(d) = 3.9 x 10(-10) M).

229 The APV effect did not depend on the exact cannula positions

230 The APV M gene isolated from the wild birds had over 96% pre

231 plasmids, a minigenome containing either the APV leader or trailer was recognized and substantial lev

232 is reduced by a factor of 13.3, whereas the APV binding constant is reduced only by a factor of 5.1.

233 nd specific test for detecting antibodies to APV.

234 With regard to APV, the sensitivity of inhibitory LTP was an order of m

235 ral effect of APV monotherapy was related to APV concentrations.

236 nt to SQV and, unexpectedly, resensitized to APV.

237 3 rapidly acquired significant resistance to APV, an integrase inhibitor raltegravir, and a GRL-09510

238 activation of mTOR-S6K is also resistant to APV and inhibited by Ca(2+) channel blockers and higher

239 Although TTX, APV, and CNQX treatment had no effect, blockade of GABA(

240 e 10th day cultures were immunostained using APV and ACB antibodies.

241 plasmic antibody (ANCA)-positive vasculitis (APV) are largely unknown.

242 Posterior corneal astigmatic power vector (APV) >0.23 diopter (D) yielded a test for overt Kc with

243 Posterior corneal vectors APV and Blur constitute objective supplemental parameter

244 ts with suspected anomalous pulmonary veins (APVs) and atrial septal defects (ASDs) using fast cine m

245 enotic Doppler average peak flow velocities (APV; cm/s) and coronary flow velocity reserve (CFR) were

246 asound, average coronary peak flow velocity (APV) by intravascular Doppler velocimetry, and coronary

247 ormance of percent aggregate plaque volume (%APV), which represents cumulative plaque volume as a fun

248 in the hippocampus of homing pigeon, but was APV-resistant in the hippocampus of non-homing pigeon.

249 wever, the facilitation was not blocked when APV, an NMDA receptor antagonist, was applied together w

250 t (V82T/I84V)) as well as their binding with APV and DRV inhibitors.

251 tion, which reduced the area of contact with APV and SQV; (ii) the compensating I84L mutation, which

252 Our earlier experiments with APV used a nondifferential training protocol, in which d

253 over 96% predicted amino acid identity with APV/Minnesota 2A, which was isolated earlier from domest

254 Hyperpolarization of L7 or incubation with APV interfered with both enhancement of facilitation wit

255 onal fear was exhibited by rats infused with APV into the CEA but not the BLA.

256 s, animals received intra-BLA infusions with APV (2.5 microg/side) or artificial CSF.

257 ion, which improved hydrophobic packing with APV; and (iii) the G-to-V mutation at residue 48, which

258 counted for 12% of the 250 new patients with APV and anti-MPO who were tested during the study period

259 ity with tetrodotoxin or NMDA receptors with APV dramatically reduced the proportion of GABAergic neu