ライフサイエンスコーパス: acid treatment

1 at are released from them by trichloroacetic acid treatment.

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

3 orylated downstream of p38 after arachidonic acid treatment.

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

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

6 evels also increase in response to salicylic acid treatment.

7 as differentiation deficiency upon retinoic acid treatment.

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

9 ty, decreased significantly after zoledronic acid treatment.

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

11 ratory chain recovered following obeticholic acid treatment.

12 essary for SOS induction following nalidixic acid treatment.

13 affect cyclin D3 stability, despite retinoic acid treatment.

14 histology seen in association with ascorbic acid treatment.

15 which rearranged to the desired structure on acid treatment.

16 oxin forms were generated by trichloroacetic acid treatment.

17 gene traps were also responsive to retinoic acid treatment.

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

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

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

21 tly increased in choroids following retinoic acid treatment.

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

23 minotransferase (ALT) values during valproic acid treatment.

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

25 MAPK activity was not decreased by retinoic acid treatment.

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

27 he core spiroketal moiety of tautomycin upon acid treatment.

28 ssion was repressed in response to salicylic acid treatment.

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

30 hosphorylation of T288 is induced by okadaic acid treatment.

31 in the rat hippocampus after systemic kainic acid treatment.

32 min after 10 microM alpha-naphthaleneacetic acid treatment.

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

34 d of neuronal differentiation after retinoic acid treatment.

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

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

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

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

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

40 moter of STAT1 directly responds to retinoic acid treatment.

41 side chains by mild trifluoromethanesulfonic acid treatment.

42 b appeared in the plasma membrane even after acid treatment.

43 nal plasticity during development and kainic acid treatment.

44 partially inhibited by nordihydroguaiaretic acid treatment.

45 ls were induced to differentiate by retinoic acid treatment.

46 nes are induced to differentiate by retinoic acid treatment.

47 ssion of both genes was induced by salicylic acid treatment.

48 shock/resuscitation was restored by valproic acid treatment.

49 m penetrating into the porous support during acid treatment.

50 am ABRE elements were responsive to abscisic acid treatment.

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

52 anced cellular differentiation upon retinoic acid treatment.

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

54 activation of bHLH05 and mimicking jasmonic acid treatment.

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

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

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

58 ame deacetylated and hyperactive after oleic acid treatment.

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

60 long the megakaryocyte lineage upon valproic acid treatment.

61 ction of neural differentiation via retinoic acid treatment.

62 valproic acid and suberoylanilide hydroxamic acid treatment.

63 nd provides neuroprotection following kainic acid treatment.

64 prepared using perfusion fixation and tannic acid treatment.

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

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

67 .11 to -0.01) than did those not taking anti-acid treatment (-0.12 L, -0.17 to -0.08; difference 0.07

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

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

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

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

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

73 Oleic acid treatment activated mitogen-activated protein (MAP)

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

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

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

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

78 Retinoic acid treatment also promotes the association of the GTP-

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

80 Uric acid treatment also was found to diminish clinical signs

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

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

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

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

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

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

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

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

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

90 that are responsive to dietary fat and fatty acid treatment and may serve as surrogate endpoints in f

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

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

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

94 bass and neuraminidase treatment, labile to acid treatment, and was inhibited by high MW dextran sul

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

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

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

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

99 racteristics were similar in both zoledronic acid treatment arms.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Bile acid treatment caused necrosis predominantly in stellate

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

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

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

120 ing resulting from either beta A4 or okadaic acid treatment, Congo red specifically attenuated only b

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

122 Abscisic acid treatment decreased the expression of several genes

123 Acetylsalicylic acid treatment did not attenuate the development of athe

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

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

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

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

128 Okadaic acid treatment enhanced the binding of p53 to a consensu

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

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

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

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

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

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

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

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

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

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

139 Wounding and abscisic acid treatment had similar effects.

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

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

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

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

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

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

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

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

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

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

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

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

152 Acid treatment increased intracellular Ca2+, and a block

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

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

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

156 Jasmonic acid treatment increased mRNA levels and the capacity fo

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

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

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

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

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

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

163 its ability to support HDMEC binding, while acid treatment inhibited G361 binding by 50%.

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

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

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

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

168 Lysophosphatidic acid treatment led to phosphorylation of radixin precedi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 Retinoic acid treatment of HL60 promyelocytic leukemia cells for

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

188 Retinoic acid treatment of irradiated PML/RARalpha mice enhanced

189 Retinoic acid treatment of NB4 and NTERA-2 cells, and hexamethyle

190 However, following all trans retinoic acid treatment of NB4 cells a significant relocalisation

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

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

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

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

195 Okadaic acid treatment of primary rat hepatocytes decreased both

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

197 Acid treatment of purpurinimide 23 produced the correspo

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

199 Arachidonic acid treatment of RIES cell lysates and ionophore stimul

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

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

202 Acid treatment of the cells, which disrupts internalizat

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

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

205 -87% based on starting manures by subsequent acid treatment of the hydrochars, addition of base to ac

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

207 Mild acid treatment of the resulting DNA generates polynucleo

208 Acid treatment of the sample prior to mass spectrometric

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

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

211 Acid treatment of TSP-1 almost completely abrogated its

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

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

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

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

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

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

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

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

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

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

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

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

224 mental loss of the tympanic ring by retinoic acid treatment, or duplication of the ring in Hoxa-2 nul

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

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

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

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

229 Abscisic acid treatment promoted JAZ12 degradation, and KEG knock

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

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

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

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

234 Oleic acid treatment rapidly increased the interaction between

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

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

237 standard on thin-layer plate, sensitivity to acid treatment, resistance to alkaline hydrolysis, and a

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

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

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

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

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

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

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

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

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

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

248 Acid treatment significantly decreased IkappaBalpha and

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

250 Pulsed acid treatment significantly increased mPGES1 mRNA and p

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

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

253 Gibberellic acid treatment stimulates the rate of tension wood forma

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

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

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

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

258 MeIQx and PhIP were measured in urine after acid treatment that quantitatively hydrolyzes the Phase

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

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

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

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

263 As a result of polyunsaturated fatty acid treatment, there is a marked elevation of lipid hyd

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

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

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

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

268 al amount of PhIP in the 12-24 h urine after acid treatment was 0.9 +/- 0.4% (mean +/- SD) of the dos

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

270 Zoledronic acid treatment was associated with a significantly reduc

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

272 The acid treatment was resultant in removing proteins and la

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

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

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

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

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

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

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

280 Oleic acid treatment, which protects apoB from rapid intracell

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

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

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

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

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

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

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