ライフサイエンスコーパス: fold change

1 iable effect on allergen PC15 (2-fold to 500-fold change).

2 ally abundant between phases (P < 0.05, >/=2-fold change).

3 eached a plateau between 75 and 480 min (>50-fold change).

4 ty (e.g. the equivalent to a gene expression fold-change).

5 mmune responses were those with the greatest fold change.

6 WRKY70 were also found upregulated with high fold change.

7 of percentages, network analysis, and taxon fold change.

8 wever, this increase did not reflect a >/= 2-fold change.

9 in both studies with concordant direction of fold change.

10 ime points, with 95% confidence intervals on fold-change.

11 occupancy changes at FLC did not reflect RNA fold changes.

12 onsiderably less power for detecting smaller fold changes.

13 either high-expressed and/or exhibited high fold changes.

14 only 5 RNAs, with FDRs of <0.001-fold and >2-fold changes.

15 ssification of signals based on the observed fold changes.

16 .30; P < .001), whereas FHA antibodies fell (fold-change, 0.56; 95% CI, .48-.65; P < .001).

17 change -1.65, P=.02), and Clostridium (log2 fold change -1.47, P=.002) were underrepresented among s

18 log2 fold change -2.22, P=.009), Dorea (log2 fold change -1.65, P=.02), and Clostridium (log2 fold ch

19 d use cut-offs as low as log10(ratio) = 0.1 (fold-change = 1.26), generating larger gene lists that v

20 ls was observed in HIV-associated anal SCCs (fold change, 12.69; P < .001).

21 00 M(-1)), five pi-pi contacts produced a 17-fold change (126 000 M(-1) right arrow over left arrow 7

22 strains compared with nonadjuvanted vaccine (fold change 16.8 vs 4.3 for H3N2 and 7.0 vs 1.6 for B).

23 ed in pregnant women versus controls (median fold-change 2.60 vs 1.49 [interquartile range, 0.94-7.53

24 The genera Haemophilus (log2 fold change -2.15, P=.003), Dialister (log2 fold change

25 fold change -2.15, P=.003), Dialister (log2 fold change -2.22, P=.009), Dorea (log2 fold change -1.6

26 old change -3.41, P=.03), Oscillospira (log2 fold change -2.80, P=.03), Lactococcus (log2 fold change

27 99 genes (DEGs; false discovery rate P<0.05, fold change |2|, controlling for confounds) previously a

28 y PT antibodies increased post-immunization (fold-change, 2.64; 95% confidence interval [CI], 2.12-3.

29 was very highly expressed in HH-HCC (median fold change 2291, p = 0.0072) and was detected by immuno

30 2 fold change -3.19, P=.05), and Dorea (log2 fold change -3.00, P=.05) were underrepresented among su

31 fold change -2.80, P=.03), Lactococcus (log2 fold change -3.19, P=.05), and Dorea (log2 fold change -

32 The genera Citrobacter (log2 fold change -3.41, P=.03), Oscillospira (log2 fold chang

33 alNAc was significantly increased in pooled (fold change = 3.33, p < 0.001) and individual (p = 0.009

34 significantly (P = 2 x 10(-7)) reduced (mean fold change, 3.5 [SEM, 0.7]) in splenic aspirates from p

35 eased in inflammatory lesional morphea skin (fold change = 30.6, P = 0.006), and preliminary transcri

36 Using a cut-off of >1.5-fold change, 48 microRNA were Rapamycin-induced, while 4

37 the top 966 genes altered (>log2 = 1.8, 3.5-fold change), 670 genes were downregulated and 296 genes

38 reservoir did not change significantly (1.16-fold change; 95% confidence interval [CI], .70- to 1.92-

39 ession models showed that rates of biomarker fold change accelerated from 6-8 years before death with

40 er, we describe and characterize log allelic fold change (aFC), the magnitude of expression change as

41 -320, miR-222 and miR-15a showed the highest fold change among the overexpressed miRNAs.

42 -100, miR-101 and miR-497 showed the highest fold change among the underexpressed miRNAs.

43 ular statistic pair induces a lower bound on fold-change among the set of discoveries.

44 class correlation coefficient, and performed fold change analysis, which was further extended to inve

45 For three target proteins, protein fold change and absolute copy per cell values measured b

46 selected from the microarray data based upon fold change and biological relevance, and 8 of these tra

47 when the following criteria were applied: >2-fold change and false discovery rate <0.05.

48 2 differentially expressed regions with >|2| fold change and p </= 0.05.

49 XCR4, ITGB2, and EGF) were selected based on fold change and P value and further validated using an i

50 re altered, using nominal thresholds of >1.4-fold change and P<0.001.

51 nt analysis (GSEA), a score that can combine fold change and P-value together is needed for better ge

52 cance score pi-value by combining expression fold change and statistical significance (P-value), and

53 gnificant bias in the expression levels, the fold change and the correlations between expression leve

54 ered between the ADG groups based on t-test, fold changes and partial least square discriminant analy

55 ads to more accurate estimates of expression fold-changes and tests of differential expression compar

56 ation, Y: +10 +/- 4 fold change; O: +4 +/- 2 fold change) and anabolic hormone milieu (testosterone,

57 ed upon P value, area under the curve (AUC), fold change, and biological plausibility.

58 ificance (adjusted p = 0.0032), the greatest fold change, and was markedly elevated in colon and jeju

59 sed power with large sample size, large log2 fold-change, and low dispersion.

60 eversible chaperone binding, chromatin fiber folding changes, and previously undescribed modification

61 to urine volume, specific gravity and median fold change are compared for their capacity to recover l

62 also improved the ability to detect reliably fold changes as small as 1.33-fold for the same 20 MCF-d

63 tal size required to reliably detect a given fold change at a given template concentration.

64 c-di-GMP binding by the riboswitch induces folding changes at atypical splice site junctions to mod

65 The fold-change behavior of individual genes tended to be co

66 The 13 lipids with a high fold change between smokers with and without COPD showed

67 ween two techniques for both read counts and fold changes between given conditions.

68 ontains the expression information including fold changes between normal and tumor samples for mRNAs

69 sponse is strong and robust, with 5- to >300-fold changes between the 'on' and 'off' states.

70 l distances are calculated from pathway mRNA fold changes between two cells.

71 st estimating protein fold-changes from mRNA fold-changes between different cell-types, and highlight

72 The coefficient of variation of fold-changes between pairs of samples was less than 40%.

73 croarray to assess the TTA method showed low fold-change bias (less than twofold difference and Pears

74 80% of phosphosites exhibiting large (>/=1.5-fold) changes compared to control can be modulated by or

75 ulated from DEBtox parameters indicated a 27 fold change comparing exposure from 48 to 720 hours (sum

76 Analytic approaches confined to fold-change comparisons of gene expression patterns betw

77 gest that based on the chosen statistical or fold change cut-off; microarray analysis can provide ess

78 on-lesional) was found using statistical and fold-change cut-offs.

79 By using both fold change cutoffs and a weighted gene coexpression net

80 Fold-change detection buffers against stochastic variati

81 The experimental realization of fold-change detection circuit highlights the programmabi

82 eter tuning, this synthetic circuit exhibits fold-change detection for four successive rounds of two-

83 teins play a prominent role in systems where fold-change detection has been proposed.

84 connections to system equivalence and to the fold-change detection property.

85 ll as sensitivity to input changes including fold-change detection, a response that depends only on f

86 mical systems that show exact adaptation and fold-change detection.

87 memory of the preligand state necessary for fold-change detection.

88 generalizations to the Weber-Fechner law and fold-change detection.

89 s well as the parameter regimes required for fold-change detection.

90 n live reporter cells, we found evidence for fold-change detection.

91 Notably, these studies reveal modest (~1.5-3-fold change) effects on M. tuberculosis replication.

92 Although fold change estimates determined by using RNA-seq showed

93 erase chain reaction (RT-qPCR) platforms for fold change estimates than for raw abundance estimates,

94 5p were up-regulated in individuals with FL (fold change (FC) = 1.55, p = 1.36 * 10(-14) and FC = 1.2

95 Arbitrary fold change (FC) cut-offs of >2 and significance p-value

96 near models were used to assess the per gene fold change (FC) for stimulated versus unstimulated samp

97 Using a fold change (FC) of 2.0 as a threshold value, the gene e

98 Fold changes (FC) to a wild-type control HIV-1 strain ra

99 egulations of antimicrobial peptides (S100A8/fold change [FCH], 13.04; S100A9/FCH, 11.28; CCL20/FCH,

100 gnificant relationship (r(2) = 0.78) between fold-changes for RNA-Seq and qPCR.

101 he platform comes preloaded with logarithmic fold changes from 44 data sets on Mvarphi stimulation.

102 Measured phosphopeptide fold-changes from alpha-casein spiked into wild-type zeb

103 e results caution against estimating protein fold-changes from mRNA fold-changes between different ce

104 Differential gene expression (fold-change), gene ontology (GO; biological process) and

105 % presented with increasing glucagon levels (fold change glucagon120/0 >/=1).

106 s showed suppression of glucagon at 120 min (fold change glucagon120/0 <1) during OGTT, whereas 21-34

107 In the longitudinal study, an increase of fold change glucagon120/0 was associated with an improve

108 entially expressed between these two groups (Fold change > 1.2).

109 Using stringent criteria (Fold change > 1.5; FDR < 0.05), three genes were found t

110 total of 111 probesets (91 annotated genes, fold change > 2.0 and false discovery rate < 0.25) were

111 rongly upregulated in sebaceous hyperplasia (fold change > 4, 54.1-fold).

112 was detected for more than 3,500 genes (log2 fold change >/= 1, false discovery rate </= 0.01), many

113 relaxed cutoffs for differential expression (fold change >/=1.2; nominal P value <0.01), we identifie

114 oci and 247 hypermethylated loci were found (fold change >/=1.3; P < 0.005; cases vs. controls).

115 R-induced transcriptomic responses (absolute fold change >/=1.5 and P</=0.05) were comparable in IWAT

116 ons between groups were made with a combined fold change >/=2 and Student's t-test p-value < 0.05 to

117 kines with significant different expression (fold change >/=2 or </=-2, and q-value <5%) between expo

118 osure (916 and 356 genes, respectively, with fold change >/=2, p<0.05, unpaired t-test).

119 ts of miR-133a defined in unstressed hearts (fold change >/=25%, false discovery rate <0.02), only 4

120 Genes were identified (corrected p < 0.05, fold change >/=|1.2|), and functional analysis was perfo

121 is versus idiopathic dilated cardiomyopathy (fold change >1.2; false discovery rate <5%) from which a

122 ntly altered the abundance of 76 proteins (a fold change >1.4, or <0.6, p-value <0.05) and several of

123 Overall, 4,901 genes with a fold change >1.5 and a false discovery rate <5% were det

124 wenty-seven differentially expressed miRNAs (fold change >1.5; P value <0.01) were identified, includ

125 es were differentially expressed in HDM APT (fold change >2 and false discovery rate < 0.05), with in

126 according to the ANOVA models, and a log(2)-fold change >2.5 were considered to be differentially ex

127 At P < 0.01 and log(2)-fold change >2.5, there were significant changes in gene

128 e identified (false discovery rate </= 0.05, fold change >|1.5|) and used to develop a prediction mod

129 fferentially expressed compared with adults (fold-change >/= 50%, false discovery rate = 0.02) and th

130 erential gene expression (thresholds P<0.05; fold-change >1.5) and pathway activation (Ingenuity) wer

131 cross diseases for statistical significance (fold change>/=1.5 and false discovery rate</=0.05), to i

132 up-regulated in alcohol dependent subjects (fold change>/=1.5, false discovery rate (FDR)</=0.3; p<0

133 ied as common in both cohorts (p-value 0.05, fold change>2) with 24 miRNAs downregulated.

134 fy differentially expressed genes (criteria: fold change, >/= 2.0; false discovery rate </= 0.05) in

135 24 hrs and 48 hrs using a pFDR < 0.01 and a [fold change] > 2 threshold.

136 Across serotypes, fold change in antibody concentrations were higher for t

137 We report an 18-fold change in apparent Ca(2+) binding affinity upon ill

138 e discovery rate, 1040 genes exhibited >1.15-fold change in both conditions; 297 were upregulated and

139 Proteins with a >1.5-fold change in cases compared with controls with a P<0.0

140 three pi-pi contacts with light caused an 8-fold change in chloride affinity (40 300 M(-1) right arr

141 ecules using dRT-LAMP chemistry detected a 2-fold change in concentration of HIV-1 RNA despite a 6 de

142 ferential expression defined as at least a 2-fold change in either direction and a P-value </=0.05.

143 A 10-fold change in electrolyte concentration shifts the Fc(+

144 /muL (95% CI: 0.070, 0.301x10(3)/muL) per 10-fold change in endotoxin; p=0.004) in the NHANES.

145 ine deaminase, we obtained a approximately 3-fold change in enzyme activity by the photocontrolled mo

146 nd known long non-coding RNAs were ranked by fold change in expression between tumours that subsequen

147 Genes with the greatest fold change in expression displayed the largest positive

148 We identified SNPs associated with fold change in expression level rather than raw expressi

149 We determined the orientation by a three-fold change in fluorescence intensity.

150 lforhodamine B (monosodium salt) exhibited a fold change in fluorescence of 2.85.

151 valuated using in vitro assays measuring the fold change in IC(50) caused by resistance mutations.

152 The standard measure, fold change in IC(50), does not correlate well with chan

153 /Km ratios) and l (l-THA; approximately 5000-fold change in kcat/Km ratios) alternative substrates.

154 rred l-serine-O-sulfate ( approximately 1200-fold change in kcat/Km ratios) and l (l-THA; approximate

155 nal approach that correlates gene expression fold change in lesional skin with the Psoriasis Area and

156 F-induced transcription correlates best with fold change in nuclear NF-kappaB, not absolute nuclear N

157 ive Fe in the medium were similar over a 250-fold change in nutrient Fe levels.

158 nse patterns change substantially over a 100-fold change in odor concentration, apparently degrading

159 Results were expressed as the fold change in outcome over deciles of baseline risk of

160 minary longitudinal analysis showed that the fold change in PR3 RNA levels in WG PBMCs corresponded t

161 ve isotope abundance of each peptide and the fold change in protein abundance during growth.

162 kinase inhibition was unchanged despite a 10-fold change in receptor concentration.

163 nd taurocholate were also detected with high fold change in rejection.

164 n-based MRI contrast agent that provides a 9-fold change in relaxivity via switching between the Mn(3

165 is indicated an overall 5,000-fold and 1,100-fold change in selectivity, respectively, for the Glu- a

166 mode against glucose and a subsequent 1,600-fold change in specificity of the ancestral protein.

167 duced for face identity were tolerant to a 2-fold change in stimulus size, suggesting that they refle

168 of single-site binding typically spans an 81-fold change in target concentration, an effect that limi

169 changes, which caused a approximately 70,000-fold change in the ancestral protein's specificity.

170 A nearly 10-fold change in the branching ratio between C2/C3 crackin

171 n protein spots with the highest significant fold change in the cooked samples were involved in carbo

172 n the dark, with tunable kinetics and a >150-fold change in the dissociation constant (Kd).

173 to monovalent, which resulted in a near 1000-fold change in the equilibrium association constant, by

174 el of nuclear Smad3 varied across cells, the fold change in the level of nuclear Smad3 was a more pre

175 riene E4 was the metabolite with the highest fold change in the rejection group compared to nonreject

176 In undoped films we demonstrate more than 10-fold change in the thermal free-carrier concentration pr

177 ABT-737 treatment, this agent induces a two-fold change in the transcription of nearly 430 genes.

178 onal work capacity is demonstrated over a 10-fold change in yarn cross-sectional area, which is impor

179 for multiple hypotheses, LMP1 TES2 caused >2-fold changes in 1,916 mRNAs; 1,479 RNAs were upregulated

180 , diDO-IPTL quantification discriminates 1.5-fold changes in abundance of over 1000 proteins with 88%

181 3 proteins with statistically significant >2 fold changes in dystrophic serum abundance.

182 3, TNFSF11, and TNFRSF11B and genes with >10-fold changes in either direction such as CHRM3, IL12B an

183 Among them, 26 genes show more than two-fold changes in expression level in an OmpR knock-out st

184 There were significant >/= 2-fold changes in expression of >4000 genes during treatme

185 e to viral infections, with relatively small fold changes in IFN-beta expression resulting in the act

186 e detection, a response that depends only on fold changes in input, and not on absolute changes.

187 t the FN nanofibers underwent 3.3-fold and 9-fold changes in length and width, respectively, and that

188 Fold changes in mRNA up to 10,000-fold for CYP1A1 in viv

189 a dominant role in determining most dynamic fold changes in protein levels.

190 to signal transduction in cells, respond to fold changes in signal relative to background.

191 ys revealed that 53 genes had greater than 3-fold changes in the expression in Sp1-silenced NHKs as c

192 r response to cadmium showed globally larger fold changes in TO1 when compared to TO2; iii) the inter

193 ectrometry (LC-MS), and we find that up to 5-fold changes in tRNA abundance can be quantified from su

194 pposing strategies to achieve differential 2-fold changes in X-linked gene expression.

195 e substitution, and that there is a small (3-fold) change in the photokinetics of the forward reactio

196 Moderate ( approximately 2-fold) changes in the ratio of DNA template to nuclear ex

197 veloped a mathematical model to quantify the fold-change in concentration of any molecule included in

198 val [CI] = 2.61-7.00; P < .001) and LN (2.32 fold-change in DNA; 95% CI = 1.22-4.41; P = .01).

199 integrated HIV DNA compared with blood (4.26 fold-change in DNA; 95% confidence interval [CI] = 2.61-

200 ng both the absolute level of expression and fold-change in expression using the fluorescent protein

201 = .045) and CD38+HLA-DR+ CD8+ T cells (1.40 fold-change in integrated HIV DNA per 1-unit increase in

202 grated HIV DNA with PD-1+ CD4+ T-cells (1.44 fold-change in integrated HIV DNA per 10-unit increase i

203 model, we find that one key parameter - the fold-change in protein concentration necessary for lumin

204 antitatively reproducible, including minimal fold-changes in IL13, TNFSF11, and TNFRSF11B and genes w

205 adding and removing phosphate group(s) is 3-fold: changes in the local/global geometry, alterations

206 nd 1246 were the most upregulated miRs (>1.5-fold change) in a NanoString profiling miR panel.

207 s revealed changes (p-value </= 0.05, >/=1.5-fold change) in lipid, purine, and sterol metabolism in

208 antly up-regulated or down-regulated (>/=1.5-fold change) in OA PBLs, at a false discovery rate of 5%

209 s P-value) and biological relevance (such as fold change) into consideration.

210 The 3-fold change is consistent with DNA release from an order

211 than 2-fold (FDR corrected p-value </=0.032, fold change (log2) >/= 1) in response to gemfibrozil exp

212 than 2-fold (FDR corrected p-value </=0.032, fold change (log2) >/= 1) in response to gemfibrozil exp

213 ngly downregulated in PP versus normal skin (fold change < 0.25, 44.4-fold) and strongly upregulated

214 n and overall the effect sizes were minimal (fold change <1.1).

215 d out by their significance level (p-value), fold change, mass-to-charge ratio, retention time, and i

216 for unparalleled precision enabling smaller fold change measurements.

217 icantly increased proinflammatory cytokines (fold-change messenger RNA: interleukin-1beta = 7.6, mono

218 ctor-alpha = 2.2) and proteolysis effectors (fold-change messenger RNA: muscle RING-finger protein 1

219 ere selected by combined analysis of maximum fold changes (MFCs) in concentrations and P-values resul

220 adjacent breast tissues, including 74 with a fold change more than two of which 17 were never reporte

221 levels in the littermate controls (0.2-0.44-fold change, n = 4 in 2 separate experiments).

222 c gravity (2.3-fold), postacquisition median fold change normalization (1.8-fold increase), postacqui

223 for raw abundance estimates, suggesting that fold change normalization against a control is an import

224 A:DNA ratio and c-MYC induction: Y: +4 +/- 2 fold change; O: +1.9 +/- 1 fold change), translational e

225 ficiency (S6K1 phosphorylation, Y: +10 +/- 4 fold change; O: +4 +/- 2 fold change) and anabolic hormo

226 al inhibition studies to achieve significant fold changes observed by acetylation proteomics methods.

227 significantly differed (P < .05) with a log2 fold change of >/= 1.0 between patient groups were inter

228 nscription of 2692 genes (p value of <0.001, fold change of >/=2) after 7 days of exposure, whereas C

229 n increase for 14 miRNAs with a minimum log2 fold change of +/- 0.5.

230 predictor of overall survival (HR for a two-fold change of 1.23, 95% CI 1.13-1.34; p<0.0001) and non

231 lapse mortality (cause-specific HR for a two-fold change of 1.24, 1.12-1.38; p<0.0001).

232 tathione-s-transferase GSTe2 with respective fold change of 11.2, 6.3, 5.5 and 2.8.

233 threshold of pFDR < 0.05, 3 RNAs exceeded a fold change of 2.

234 pecies at 9415.45 Da demonstrates an average fold change of 4.7 (p-value 0.017) and was identified as

235 s. 74.9 days, respectively; 6.7-fold vs. 3.7-fold change of cytokines, respectively), suggesting the

236 symptomatic patients, the mean (SD; 95% CI) fold change of expression of proinflammatory mediators i

237 In contrast, the mean (SD; 96% CI) fold change of expression of TGF-beta1 messenger RNA (mR

238 A fold change of greater than 1.5 and a false discovery ra

239 studies are powered well for detecting large fold changes of ChIP enrichment over the control sample,

240 om mouse, corresponding to expected relative fold changes of one for mouse proteins and from 0.25 to

241 The relative fold changes of the RT-qPCR validation were in line with

242 step resulting in significant distortions in fold changes of the transcripts.

243 gest that miRNA and mRNA pairs with opposite fold changes of their expression and with inverted corre

244 n skin accounted for 54% of the variation in fold changes of urinary PAH metabolites (p < 0.002).

245 ted virus-specific plasmablast responses and fold-change of T-cell responses, respectively.

246 Because miR 19b showed the highest fold-change of the cluster members, activated HSCs were

247 tivity levels indicated the up-regulation (6-fold change) of TcP5CDH during the infective stages of t

248 For individual genes, regulations (fold changes) of histone modifications and transcript le

249 Using a cutoff of 2-fold change or more, a total of 250 ROS-sensitive genes

250 ients with Alzheimer's disease and controls (fold change) or the ratio between biomarker concentratio

251 ed proteins showed either a strikingly large fold-change, or were completely suppressed or newly indu

252 r expressed in PET false-negative cases (5.3-fold change, P < .001) which provides a mechanistic expl

253 ween children with PA and NA children (45.59-fold change, P < .001), followed by IL5 and then IL13.

254 tween children with PA and NA children (23.3-fold change, P < .01) and children with PS (18.5-fold ch

255 ilumab treatment signature of 821 probes (>2-fold change, P < .05) significantly modulated in the 300

256 change, P < .01) and children with PS (18.5-fold change, P < .05).

257 of the differential proteome data sets (>/=2-fold change, P < 0.05), showed that several proteins inv

258 th controls (1.73 +/- 0.93 vs 0.75 +/- 0.66; fold change, P < 0.05).

259 with a mass-to-charge ratio, retention time, fold change, p-value, and relative intensity.

260 lorie intake increased among ES (1.5 +/- 0.2 fold-change, P = 0.02) but not controls (1.1 +/- 0.1 fol

261 nge, P = 0.02) but not controls (1.1 +/- 0.1 fold-change, P = 0.30).

262 23 decreasing in abundance (greater than 1.5-fold change; P < 0.005).

263 ificantly differentially expressed spots (>2-fold change; P < 0.05) between the subtypes of JIA.

264 e unloading gene expression profiles (>/=1.5-fold change; P < 0.05).

265 CD4-CD8- T cells (mean +/- SEM 1.35 +/- 0.12-fold change; P = 0.008), stimulated FoxP3 expression in

266 ptor variants, with highly precise relative (fold-change) quantification of tRNAs.

267 T and sWAT at the two and four weeks and the fold-change ranged from 0.19 to 0.77.

268 and wnt9a) correlated more strongly with the fold change, rather than the level, of nuclear Smad3.

269 d Poly(I:C), respectively, with at least a 1-fold change relative to unexposed thrombocytes.

270 Responding to fold change requires that the system senses signal on a

271 xpression (1.6- to 7.2-fold and 8.3- to 33.9-fold changes, respectively), and the force characteristi

272 response than ADC, with 2.8-fold versus 1.3-fold changes, respectively, by day 5 of drug treatment.

273 The precision of the fold-change response was observed throughout the signali

274 ver a large dynamic range in both expression fold change (spanning nearly four orders of magnitude) a

275 entially expressed proteins (at least +/-1.5-fold change; Student's t test, P < 0.05) were identified

276 ng protein-substrate linker density up to 50-fold changed tethering, but did not affect osteogenesis,

277 e intramolecular ET rate constants almost 10-fold: changes that are correlated with increased flexibi

278 odological variation, we generated and used 'fold change', that is, ratio of mean amyloid uptake (glo

279 The loss of the Bet v 1-fold changes the protein's interaction with the human im

280 Using a fetal/postnatal log2-fold change threshold of 0.5, genes associated with synd

281 d formal statistical techniques to translate fold changes to profiles of microRNA targets which were

282 tion: Y: +4 +/- 2 fold change; O: +1.9 +/- 1 fold change), translational efficiency (S6K1 phosphoryla

283 tissues demonstrated that the consistency of fold-change trends in a single short amplicon between sn

284 target RNAs showed a concordance of 100% of fold-change trends in at least two short amplicons, whic

285 For each condition, low fold-changes typified the altered transcriptome.

286 ted and 35 down-regulated genes (p<0.01, 1.5 fold change [up and down]).

287 were significantly upregulated, with median fold change values of 2.9, 31.7, 4.6, and 6.8, respectiv

288 We found that genes with <2-fold change values were quantitatively reproducible betw

289 respectively, for deriving the isoform-level fold change values.

290 Fold change was determined using the DeltaDeltaCt method

291 This fold change was even larger for the subset of deletions

292 The median annual fold change was higher in NCs than in ECs and negatively

293 entified and 740 proteins that presented a 4-fold change were considered a CRC proteomic signature.

294 ersus-control differential expression, their fold changes were </= 1.33, and an independent cohort yi

295 Proteins with the largest median fold changes were SAA (serum amyloid protein A), NPS-PLA

296 ntially expressed lncRNAs with more than 2.0-fold change when compared the expression profiles of P1

297 measured by quantitative PCR, and the median fold change, when compared with the median of healthy co

298 gle promoters and their resulting expression fold change will be altered with changes in affinity.

299 A 2-fold change with a corrected P < 0.05 was considered dif

300 in vitro (false discovery rate, </=0.001; 2-fold change) with 557 showing decreased and 329 showing