ライフサイエンスコーパス: acid treatment

1 d GSI-treated cells and responded to okadaic acid treatment.

2 own improved outcomes in patients given anti-acid treatment.

3 ame deacetylated and hyperactive after oleic acid treatment.

4 Mn(2+) or Mg(2+)/ethylene glycol tetraacetic acid treatment.

5 long the megakaryocyte lineage upon valproic acid treatment.

6 ction of neural differentiation via retinoic acid treatment.

7 valproic acid and suberoylanilide hydroxamic acid treatment.

8 nd provides neuroprotection following kainic acid treatment.

9 prepared using perfusion fixation and tannic acid treatment.

10 at are released from them by trichloroacetic acid treatment.

11 orylated downstream of p38 after arachidonic acid treatment.

12 fractions, which are generated by the nitric acid treatment.

13 icit, salinity, low temperature, or abscisic acid treatment.

14 evels also increase in response to salicylic acid treatment.

15 eceptor signaling as enriched after palmitic acid treatment.

16 as differentiation deficiency upon retinoic acid treatment.

17 high-fat diet feeding and in vitro palmitic acid treatment.

18 ight benefit from initiating acetylsalicylic acid treatment.

19 ty, decreased significantly after zoledronic acid treatment.

20 ty of keratin filament collapse upon okadaic acid treatment.

21 EN promoter, which was increased by palmitic acid treatment.

22 essary for SOS induction following nalidixic acid treatment.

23 affect cyclin D3 stability, despite retinoic acid treatment.

24 histology seen in association with ascorbic acid treatment.

25 which rearranged to the desired structure on acid treatment.

26 oxin forms were generated by trichloroacetic acid treatment.

27 gene traps were also responsive to retinoic acid treatment.

28 ansform into neuron-like cells upon retinoic acid treatment.

29 ic disulfide and was readily removed by mild acid treatment.

30 ut not 4 hours or 96 hours, following kainic acid treatment.

31 ce in a latent form that can be activated by acid treatment.

32 minotransferase (ALT) values during valproic acid treatment.

33 se HPLC and is easily removed using standard acid treatment.

34 id metal can be recovered from dispersion by acid treatment.

35 MAPK activity was not decreased by retinoic acid treatment.

36 and following, 192 wk of all-trans retinoic acid treatment.

37 he core spiroketal moiety of tautomycin upon acid treatment.

38 ssion was repressed in response to salicylic acid treatment.

39 iggered DLD can undergo rapid cleavage under acid treatment.

40 age can be ameliorated by all-trans retinoic acid treatment.

41 hosphorylation of T288 is induced by okadaic acid treatment.

42 in the rat hippocampus after systemic kainic acid treatment.

43 min after 10 microM alpha-naphthaleneacetic acid treatment.

44 ic and osmotic stresses, as well as abscisic acid treatment.

45 d of neuronal differentiation after retinoic acid treatment.

46 ipped peptides from SLA molecules by a brief acid treatment.

47 partially recovered 8 weeks after removal of acid treatment.

48 P-1-mediated transcription following okadaic acid treatment.

49 A) activity, which was suppressed by okadaic acid treatment.

50 erexpression of sentrin, but not by retinoic acid treatment.

51 rradiation, DNA damaging agents, or retinoic acid treatment.

52 moter of STAT1 directly responds to retinoic acid treatment.

53 side chains by mild trifluoromethanesulfonic acid treatment.

54 sequential exposure to light irradiation and acid treatment.

55 m penetrating into the porous support during acid treatment.

56 r and the removal of the linker fragments by acid treatment.

57 ratory chain recovered following obeticholic acid treatment.

58 tly increased in choroids following retinoic acid treatment.

59 ng pathogen infection, drought, and abscisic acid treatment.

60 shock/resuscitation was restored by valproic acid treatment.

61 am ABRE elements were responsive to abscisic acid treatment.

62 dative carbon-hydrogen bond cleavage, and an acid treatment.

63 anced cellular differentiation upon retinoic acid treatment.

64 amounts of FMN were found in milk following acid treatment.

65 activation of bHLH05 and mimicking jasmonic acid treatment.

66 ype mice after 2,4,6-trinitrobenzenesulfonic acid treatment.

67 mperature, heat, abscisic acid and salicylic acid treatments.

68 ponded to gibberellic acid, but not abscisic acid, treatment.

69 .11 to -0.01) than did those not taking anti-acid treatment (-0.12 L, -0.17 to -0.08; difference 0.07

70 through hydrazinolysis/high pH (4.0) nitrous acid treatment/[3H]NaBH4 reduction.

71 first endotoxin challenge), acetylsalicylic acid treatment (80 mg acetylsalicylic acid daily for the

72 After lysophosphatidic acid treatment, 85% of the mature supporting cells that

73 Furthermore, okadaic acid treatment abrogated the lyso-PC induced promoter au

74 ing for extended periods or high-temperature acid treatment (acetolysis), suggesting fossilization po

75 Where palmitic acid treatment activated Chop(+/+) and Chop(-/-) macroph

76 t, in NT2-N cells after 13 weeks of retinoic acid treatment, all GABA(A) receptor subtype mRNAs were

77 Generally, regardless of water or acetic acid treatment, all the zein preparations had similar FT

78 an be selectively unmasked by a reduction or acid treatment, allowing the installation of N-acetyl an

79 ol, with neutral ethylene diamine tetracetic acid treatment alone after scaling and root planing.

80 Polyinosinic-polycytidylic acid treatment also ameliorated liver fibrosis induced b

81 Retinoic acid treatment also results in a shift of muscle identit

82 Twelve-week acid treatment also significantly increased NOX5, mPGES1

83 Uric acid treatment also was found to diminish clinical signs

84 cl-1 protein stability was increased by bile acid treatment, an effect duplicated by proteasome inhib

85 lial cells in response to excessive palmitic acid treatment, an obesity-like condition.

86 as single-walled carbon nanotubes (SWNTs) by acid treatment and annealing.

87 3, which was further accentuated by retinoic acid treatment and by the presence of risk alleles at th

88 by up to threefold in response to salicylic acid treatment and challenges with mannitol.

89 l of the GPI anchors by aqueous hydrofluoric acid treatment and cleavage at aspartate-proline bonds b

90 to investigate the association between anti-acid treatment and disease progression in IPF.

91 The inhibition effect of naphthylphthalamic acid treatment and exogenous IAA application depends on

92 alkyl or aryl group at C-5, followed by mild acid treatment and exposure to 1,8-diazabicyclo[5.4.0]un

93 ed in Li-O(2) cells between 2 and 4 V, using acid treatment and Fenton's reagent, and combined with d

94 hat is normally seen upon all-trans-retinoic acid treatment and is characterized by the up-regulation

95 on of trophic factors is induced by retinoic acid treatment and is inhibited by a retinoid receptor a

96 Okadaic acid treatment and PP2A knockdown promoted MST1/2 phosph

97 NT were lightly functionalized by the nitric acid treatment and that the degree of functionalization

98 denocarcinoma (OE33) cells were subjected to acid treatment and used in transfection experiments.

99 yposensitive responses to auxin and abscisic acid treatments and enhanced far-red light/phyA-mediated

100 chemical methods, such as alkali treatment, acid treatment, and solventogenesis.

101 cells and later assigned into control, folic acid-treatment, and folic acid-treatment with granulocyt

102 e observation that genes induced by retinoic acid treatment are likely to be developmentally regulate

103 regulating the long-term events after kainic acid treatment are not clear.

104 Controlled clinical trials of anti-acid treatments are now needed.

105 racteristics were similar in both zoledronic acid treatment arms.

106 5) was entirely phosphorylated after okadaic acid treatment, as confirmed biochemically by CDK2 kinas

107 ility to predict crossmatch results than the acid treatment assay.

108 ercentage of predicted, patients taking anti-acid treatment at baseline had a smaller decrease in FVC

109 ty to salinity, osmotic stress, and abscisic acid treatment at the seedling stage, and a reduction in

110 tate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the and

111 stic regression model found that obeticholic acid treatment, baseline NAS > 5, baseline triglyceride

112 on of MAPK nuclear entry induced by retinoic acid treatment because the cytoskeletal disrupting agent

113 Novobiocin and nalidixic acid treatment both resulted in rapid loss of RarA foci.

114 ndoderm-like cells was inducible by retinoic acid treatment but not by conditions of sterol depletion

115 script accumulation was induced by salicylic acid treatment but was not observed during lesion format

116 f OsGR3 was greatly increased with salicylic acid treatment but was not significantly affected by met

117 ionic stress (NaCl), and exogenous abscisic acid treatment, but failed to accumulate in response to

118 ithramycin affects cellular response to bile acid treatment by altering the expression of multiple bi

119 o the decreased toxicity of the chronic bile acid treatment by increasing the hydrophilicity of the b

120 cells are also unable to respond to retinoic acid treatment by producing nestin-positive neural stem

121 ly deficient in SOS induction upon nalidixic acid treatment by using a dinD::lacZ reporter construct.

122 e reduced retinoic acid levels, and retinoic acid treatment can elicit growth-inhibitory signals in p

123 pG2, retinoic acid, clofibric acid, and bile acid treatment can only modestly increase hepatitis B vi

124 as heat-moisture treatment (HMT) and citric acid treatment (CAT).

125 Bile acid treatment caused necrosis predominantly in stellate

126 Ethanol-polyunsaturated fatty acid treatment caused the following: i) hepatosteatosis,

127 D-amino acid treatment caused the release of amyloid fibers that

128 reas Staphylococcus aureus (Sa) lipoteichoic acid treatment confirmed that many late-response genes c

129 Anti-acid treatment could be beneficial in patients with IPF,

130 Abscisic acid treatment decreased the expression of several genes

131 Acetylsalicylic acid treatment did not attenuate the development of athe

132 The acid treatment did not favor the recolonization of bacte

133 nd SHP expression levels resulting from bile acid treatment did not greatly modulate HBV RNA and DNA

134 n protein gene-small interfering ribonucleic acid treatment effects were of limited duration, restric

135 Dichloroacetic acid treatment elevated acetyl-CoA levels, restored mTOR

136 Destruction of this site by acid treatment eliminated mAb 8E6 binding but had no eff

137 n, the gene most highly induced by nicotinic acid treatment encodes a putative major facilitator supe

138 lled carbon nanotubes (MWNTs) that underwent acid treatment followed by annealing at increasing tempe

139 tionalized with oxygen groups using standard acid treatments followed by selective reduction via anne

140 ethodology developed involves two sequential acid treatments followed by stepwise ethanol precipitati

141 ible quinone groups using a high temperature acid treatment, followed by anodic polarization.

142 nd early embryonic differentiation, retinoic acid treatment for 4 days resulted in suppression of cel

143 dle in the development of successful nucleic acid treatments for hemophilia.

144 factors in the long-term events after kainic acid treatment, gel mobility-shift and Western blot anal

145 vation: UV, singlet oxygen, and hypochlorous acid treatments generally render the genome nonreplicabl

146 Similarly, in isolated aorta, oleic acid treatment generates LD in EC ex vivo.

147 nflammatory phenotype in the acetylsalicylic acid treatment group was accompanied by a decrease in ur

148 d that NT2-N cells after 5 weeks of retinoic acid treatment had moderate peak currents, GABA EC(50,)

149 While fatty acid treatment had no detectable effect upon stress-indu

150 Wounding and abscisic acid treatment had similar effects.

151 In patients with CAD, long-term ascorbic acid treatment has a sustained beneficial effect on EDNO

152 nts in ASD symptoms with leucovorin (folinic acid) treatment have been reported in some children with

153 in different tissues, stresses and abscisic acid treatment highlighted temporal and spatial diversif

154 Within 2 h of retinoic acid treatment, Hoxa1 is rapidly recruited to target sit

155 tudies demonstrated that short-term ascorbic acid treatment improves endothelial function.

156 promoter methylation increased after pulsed acid treatment in a time-dependent manner.

157 te widespread neurotoxicity following kainic acid treatment in C57BL/6J mice, and reveal increased se

158 early as 15 min following all-trans-retinoic acid treatment in LA-N-5 cells.

159 garding the safety and efficacy of bempedoic acid treatment in long-term studies involving patients w

160 Furthermore, we show that retinoic acid treatment in mature heart valves is sufficient to p

161 Lipoic acid treatment in mice on HFD prevented several HFD-indu

162 overexpressing Barrett's cells or induced by acid treatment in SEG1 EA cells was significantly decrea

163 nhanced sensitivity to linoleic or linolenic acid treatments in combination with HL, consistent with

164 In addition, acid treatment increased intracellular Ca(2+) and phosph

165 Acid treatment increased intracellular Ca2+, and a block

166 In skeletal muscle cells, oleic acid treatment increased intracellular levels of cyclic

167 Inhibition of either GRP78 or linoleic acid treatment increased MCP-1 serum levels, decreased C

168 In SEG1 cells, acid treatment increased mRNA expression of NOX5-S, but

169 Jasmonic acid treatment increased mRNA levels and the capacity fo

170 Notably, valproic acid treatment increased pancreatic endoderm formation,

171 Both storage and ascorbic acid treatment increased potential bioaccessibility of p

172 Moreover, valproic acid treatment increases histone H4 acetylation levels a

173 ration, NaCl, methyl jasmonate, and abscisic acid treatments indicating its possible role in plant st

174 increased over time, and insensitive to mild acid treatment, indicating that it was retained within c

175 express EGFP under normal conditions, kainic acid treatment induced intense expression of EGFP in inj

176 tabilizing factor and that taxol and okadaic acid treatment induces apoptosis in HL-60 cells through

177 We found that retinoic acid treatment inhibited the phosphorylation of Elk-1, a

178 In the latter, palmitic acid treatment inhibits glucose-induced insulin gene tra

179 ed membrane cannot retain DPA during heat or acid treatments innocuous for dormant spores, resulting

180 The facile acid treatment is capable of weakening the bonding of zi

181 to a mild heat stress prior to omega-6 fatty acid treatment led to an adaptive or hormetic response,

182 Lysophosphatidic acid treatment led to phosphorylation of radixin precedi

183 ze (Cohen's d=0.91), indicating that folinic acid treatment may be more efficacious in children with

184 r events, this study indicates that ascorbic acid treatment may benefit patients with CAD.

185 Omega-3 fatty acid treatment may have beneficial effects in regulating

186 In conclusion, ascorbic acid treatments may improve consumer quality of stored s

187 ong-term (192 wk) topical all-trans retinoic acid treatment (n = 5).

188 s to a similar phenotype to that of retinoic acid treatment, namely bud formation in the absence of a

189 Retinoic acid treatment of A(-) mice at the peak of the infection

190 All trans-retinoic acid treatment of A404 cells induced a strong increase i

191 uence of cascade events are mediated through acid treatment of an Ugi adduct that affords 1,5-benzodi

192 In contrast, induced alpha-chitin from acid treatment of beta-chitin had few polymorphic modifi

193 Lysophosphatidic acid treatment of cells induced KSR-1 translocation to t

194 gments by GyrA antiserum following nalidixic acid treatment of cells.

195 Acid treatment of densely substituted 2-silyl-1,2-dihydr

196 family member Foxa1 is activated by retinoic acid treatment of embryonic stem cells, binds its DNA co

197 ecipitation assay demonstrated that retinoic acid treatment of H441 cells greatly stimulated both RAR

198 Furthermore, we show that myristic acid treatment of hepatocytes increases both VTV budding

199 Taxol or okadaic acid treatment of HL-60 cells results in proteolysis of

200 Retinoic acid treatment of HL60 promyelocytic leukemia cells for

201 Acid treatment of HLA-A*0201+ target cells resulted in t

202 Resveratrol and valproic acid treatment of one of the CSC lines resulted in a sig

203 Ursodeoxycholic acid treatment of OVA-sensitized mice prior to OVA aeros

204 mall chemical chaperone tauroursodeoxycholic acid treatment of Pak2-CKO mice substantiated that Pak2

205 omewhat consistent with reports on the folic acid treatment of patients with pernicious anemia, but s

206 , removal of the surface-displayed mannan by acid treatment of periodate-borohydride cells exposes gl

207 Okadaic acid treatment of primary rat hepatocytes decreased both

208 tionale for a combined TLR3 agonist/retinoic acid treatment of prostate and breast cancer.

209 Acid treatment of purpurinimide 23 produced the correspo

210 Polyinosinic-polycytidylic acid treatment of RAG(-/-) mice transplanted with B6 but

211 Arachidonic acid treatment of RIES cell lysates and ionophore stimul

212 However, the salicylic acid treatment of systemically infected tissues did not

213 antigen flow beads assay were retested after acid treatment of the beads.

214 tional groups are readily overcome upon mild acid treatment of the enzyme, which releases free heme f

215 s achieved in yields of 80-90% by subsequent acid treatment of the hydrochars, addition of base to ac

216 -87% based on starting manures by subsequent acid treatment of the hydrochars, addition of base to ac

217 phenotype was partially rescued by retinoic acid treatment of the pregnant females.

218 Mild acid treatment of the resulting DNA generates polynucleo

219 Acid treatment of the sample prior to mass spectrometric

220 hyperphosphorylation, in response to okadaic acid treatment of the transfected cells, were observed.

221 inal kinase was not activated by arachidonic acid treatment of these cells.

222 Cycloheximide reversal or phosphonoacetic acid treatment of wild-type virus-infected cells as well

223 ere that auxin (10 &mgr;M naphthalene acetic acid) treatment of strips does not result in plasma memb

224 in concentrations were also determined after acid-treatment of milk and were 4-5 times higher than fo

225 e (2 g PO) and long-term (500 mg/d) ascorbic acid treatment on EDNO-dependent flow-mediated dilation

226 The effect of acetyl salicylic acid treatment on mortality of patients with systemic in

227 uration of MDSC by either all-trans-retinoic acid treatment or active immunoreceptor tyrosine-based a

228 is of fin phenotypes obtained after retinoic acid treatment or altering the hedgehog signaling levels

229 tochondrial lipid composition by lithocholic acid treatment or by ablation of the lipid transport pro

230 Upon differentiation of ESCs by retinoic acid treatment or LIF deprivation, PDCD2 levels declined

231 Reversing the order of light irradiation and acid treatment or only using individual stimulation does

232 In contrast, abscisic acid treatment or osmotic stress of P. patens does not a

233 replication was blocked by either nalidixic acid treatment or thymine starvation, the transcription

234 e promoters that are responsive to salicylic acid treatment or tobacco mosaic virus infection.

235 coatings, blasting by various substances, by acid treatments, or by combinations of the treatments.

236 WNT signaling combined with FGF and retinoic acid treatments over the course of 18 days generates cel

237 th filamentous structure abolished by formic acid treatment (PHF(FA)) and fetal human tau protein.

238 xide derived from TATP via UV irradiation or acid treatment produced ECL emissions upon cathodic pote

239 Abscisic acid treatment promoted JAZ12 degradation, and KEG knock

240 n protein gene-small interfering ribonucleic acid treatment promoted T cell differentiation towards p

241 arboxylic acid and 2,4-dichlorophenoxyacetic acid treatments promoted root hair formation in both wil

242 optimized DELFIA procedure incorporating an acid treatment protocol is introduced for use with Eu(II

243 orphyrin with DIBAL-H/NaBH(4) and subsequent acid treatment provided the corresponding free-base 10(3

244 Oleic acid treatment rapidly increased the interaction between

245 obese mice, activation of FXR by obeticholic acid treatment reduced miR-802 levels and improved insul

246 higher molecular mass for r-p53 from okadaic acid treatment relative to control, suggesting a higher

247 s damaged by the sputtering process, and the acid treatment removes the damaged layer of carbon.

248 duced to die by low potassium or homocysteic acid treatment, respectively.

249 highly active during heat shock, as okadaic acid treatment restores phosphorylation of both factors

250 In contrast, acetylsalicylic acid treatment resulted in enhanced plasma levels of tum

251 Neonatal acetic acid treatment resulted in higher sensitivity to CRD in

252 follicle cycle with depilation and retinoic acid treatment resulted in nearly 50% transfection effic

253 oth wild-type and Prkdc(-/-) neurons, kainic acid treatment resulted in rapid induction of DNA damage

254 Pamoic acid treatment results in a preferential increment of no

255 Retinoic acid treatment results in reduced wnt signaling, which l

256 Tannic acid treatment revealed a thin strand, 150-200 nm long a

257 stable than Plin5-Atgl complexes, and oleic acid treatment selectively promoted the interaction of P

258 em mass spectrometry revealed that upon bile acid treatment, SHP was phosphorylated at Ser26, within

259 tissue RNA-Seq analysis showed that carnosic acid treatment significantly altered expression of genes

260 on regulatory factor-9 and IRG1 and itaconic acid treatment significantly decreased endothelial angio

261 Acid treatment significantly decreased IkappaBalpha and

262 Pulsed acid treatment significantly increased H(2)O(2) producti

263 Pulsed acid treatment significantly increased mPGES1 mRNA and p

264 imaging showed that long-term dichloroacetic acid treatment significantly reduced the hypertrophy obs

265 pollen-specific APA switching and salicylic acid treatment-specific APA clearly demonstrated such dy

266 Gibberellic acid treatment stimulates the rate of tension wood forma

267 Now, a simple yet robust acid-treatment strategy is used to judiciously create an

268 expressed in <10% of microglia after kainic acid treatment, suggesting that microglia are not a majo

269 r than 10-fold in the medium after nalidixic acid treatment, suggesting these were released specifica

270 ceptible to DSS and trinitrobenzene sulfonic acid treatment than wild-type FVB/6 mice, as demonstrate

271 enes regulated by salt, osmotic and abscisic acid treatments than with genes regulated by cold acclim

272 ociated with chromatin remodeling after bile acid treatment that was blunted by inhibition of the end

273 It was found that, after the acid treatment, the first covalently bonded PEI layer an

274 After acid treatment, the total amount of MelQx (unmetabolized

275 yer was not removed but was denatured by the acid treatment; the mineral was trapped in this gelatino

276 Thus, we conclude that retinoic acid treatment to induce F9 cell differentiation uncoupl

277 IgG, and after ethylene diamine tetraacetic acid treatment to obviate complement interference.

278 ds were subjected to singlet oxygenation and acid treatment to provide artemisinin analogues.

279 vel of morphine tolerance induced by okadaic acid treatment to the same level of tolerance observed i

280 verexpression or NFKB/RELA inducer, valproic acid, treatment to result in reduced KIT expression and

281 and transcript following all-trans-retinoic acid treatment was accompanied by changes in localizatio

282 Zoledronic acid treatment was associated with a significantly reduc

283 ike fibres response to the approximately 3 s acid treatment was not affected by a vanilloid receptor

284 The acid treatment was resultant in removing proteins and la

285 n additional 213 genes specific to nicotinic acid treatment were altered.

286 hanges in 564 individuals beginning valproic acid treatment were examined.

287 deficit, sodium chloride (NaCl), or abscisic acid treatments were shown to exhibit a significant incr

288 Finally, tauroursodeoxycholic acid treatments were used to demonstrate that the protei

289 leukocytes after polyinosinic-polycytidylic acid treatment, whereas a moderate increase of IFNs was

290 biquitinated, and this was enhanced by oleic acid treatment, which also reduced total CD36 protein in

291 lings exposed to drought as well as abscisic acid treatment, which implies coordinated changes in the

292 Upon retinoic acid treatment, which induces disease remission in APL,

293 I layers) were prepared in ethanol following acid treatment, which partially removed the associated o

294 m of gliadin insolubility was solved by mild acid treatment, which renders an acid-hydrolysed gliadin

295 he TATA box in cells prior to 9-cis retinoic acid treatment, which was abolished following promoter a

296 ompetence was observed following longer term acid treatment, which was even more marked than that of

297 A regimen of lithocholic acid treatment, which was tolerated by wild-type and PXR

298 cells as effectors, we demonstrated that the acid-treatment, which stripped SLA molecules of bound pe

299 glial cultures by combining 3-nitropropionic acid treatment with concurrent glucose deprivation.

300 nto control, folic acid-treatment, and folic acid-treatment with granulocyte-colony stimulating facto