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 and 2 had a slight increase in IC50 (3- to 5-fold change).

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

5 WRKY70 were also found upregulated with high fold change.

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

7 in both studies with concordant direction of fold change.

8 mmune responses were those with the greatest fold change.

9 ) by column(s) such as p-value, q-value, and fold change.

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

11 ssification of signals based on the observed fold changes.

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

13 onsiderably less power for detecting smaller fold changes.

14 .30; P < .001), whereas FHA antibodies fell (fold-change, 0.56; 95% CI, .48-.65; P < .001).

15 lar for cluster-2 versus cluster-1 (relative fold-change, 0.99; 95% CI, .86-1.14; P = .91), but great

16 lysis, 14 microRNAs were associated with PR (Fold Change: 0.91-1.27, p-value: 0.004-0.05).

17 pants than male participants (geometric mean fold-change 1.33, 95% CI 1.06-1.68; p=0.014), and longer

18 P) being the most strongly upregulated (log2 fold-change 1.87, P = 0.0001) and its expression was ass

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

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

21 ater in cluster-3 versus cluster-1 (relative fold-change, 1.45; 95% CI, 1.01-2.09; P = .045).

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

23 ad decreased abundance of lipoxygenase (mean fold-change -13.1), an enzyme responsible for product sp

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

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

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

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

28 in (mean fold-change -3.7) and legumin (mean fold-change -2.5) and concomitant increase in their low

29 99 genes (DEGs; false discovery rate P<0.05, fold change |2|, controlling for confounds) previously a

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

31 2 fold change -3.19, P=.05), and Dorea (log2 fold change -3.00, P=.05) were underrepresented among su

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

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

34 or storage globulin proteins phaseolin (mean fold-change -3.7) and legumin (mean fold-change -2.5) an

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

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

37 miRNA in periodontitis (Read count - 227630; fold change - 5.82).

38 in their low molecular weight isoforms (mean fold-change 6.4 and 8.3, respectively).

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

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

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

42 -320, miR-222 and miR-15a showed the highest fold change among the overexpressed miRNAs.

43 -100, miR-101 and miR-497 showed the highest fold change among the underexpressed miRNAs.

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

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

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

49 oteins were identified on the basis of their fold change and statistical significance between groups.

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

51 all cases, tuning leads to trade-offs in the fold-change and the ability to distinguish cellular stat

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

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

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

55 d per cell, number of marker genes and their fold change, and number of single cells successfully pro

56 boptimal temperatures their induction range, fold change, and response to decreasing temperatures are

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

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

59 Expression fold changes are similarly affected.

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

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

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

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

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

65 ides for each method, with highly correlated fold-changes between workflows.

66 olite analysis, showing that the accuracy of fold-change calculations can be significantly improved.

67 nge compression), implying that conventional fold-change calculations directly using MS signal intens

68 was highly influenced by the ACC (up to 631-fold change), chlorogenic acid was similarly influenced

69 80% of phosphosites exhibiting large (>/=1.5-fold) changes compared to control can be modulated by or

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

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

72 r real metabolic concentration ratios (i.e., fold-change compression), implying that conventional fol

73 tional 97 significant metabolic features had fold changes corrected by more than 0.1.

74 genes (DEGs; false discovery rate <0.05; log-fold change cutoff = 0) from 36,007 expressed Populus ge

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

76 t that similar mechanisms of cell memory and fold change detection may be important in diverse signal

77 to compute relative signals, that is perform fold change detection.

78 or binding to kappaB motifs, could reproduce fold-change detection across the experimentally measured

79 Fold-change detection buffers against stochastic variati

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

81 of TNF-NF-kappaB signaling, which implements fold-change detection from competition for binding to ka

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

83 It is unknown whether fold-change detection is maintained at NF-kappaB target

84 evels of TNF-inducible transcription exhibit fold-change detection of NF-kappaB, which may buffer aga

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

86 aneously varied across promoters to maintain fold-change detection while also matching other trends i

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

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

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

90 ut while maintaining robustness of NF-kappaB fold-change detection.

91 Fold change differences in gene expression were recorded

92 irwise comparisons within the input files by fold change direction (sign).

93 t of a ligand-binding domain (aptamer) whose folding changes drive changes in gene expression.

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

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

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

97 The fold change expression of Acan and Runx2 induced by Adv-

98 ferentially expressed genes (DEGs), 249 with fold change (FC) >2.

99 rentially expressed genes (DEGs) with log(2) fold change (FC) >|1| and 106 highly DEGs (log(2) FC >|2

100 rison with the non-cancerous tissues (median fold change (FC) = 0.3143; P = 0.0003).

101 5p were up-regulated in individuals with FL (fold change (FC) = 1.55, p = 1.36 * 10(-14) and FC = 1.2

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

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

104 lse discovery rate [FDR] <= 0.1 and absolute fold change [FC] expression >= 1.15).

105 f 428 differentially expressed genes (DEGs) (fold-change, FC >= 1.5; adjusted P <= 0.1) were identifi

106 thelial transcriptome, a total of 672 genes (fold-change, FC >= 1.5; adjusted-p <= 0.05) showed signi

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

108 ities are usually directly used to calculate fold changes for quantitative comparison.

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

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

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

112 % presented with increasing glucagon levels (fold change glucagon120/0 >/=1).

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

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

115 ringent conditions (raw P-value < 0.05, log2 fold change > 0.5), we defined a 73-gene set characteris

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

117 tized only (false discovery rate <= 0.05 and fold change > 1.5).

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

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

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

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

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

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

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

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

126 d genes (false discovery rate of 0.1 and log fold change >0.75)], with many differentially expressed

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

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

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

130 l expressed genes identified by a cut-off of fold change >2 and adjusted P value < 0.05.

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

132 y expressed genes (DEG) (p < 0.05, FDR <0.1, fold change >2) between the BRSV challenged and control

133 is lesions versus in controls, respectively (fold change >= 2; false discovery rate [FDR] < 0.05).

134 xpressed genes between the three conditions (fold change >=0.5 in either direction; p < 0.05).

135 iabetes compared to those who did not (log(2)fold change >=1.25 and false discovery rate <=5%).

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

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

138 gnificantly up-regulated in SBNET (P < 0.05; fold-change >2) based on multiple normalization strategi

139 662 DEGs in nonlesional AD, vs healthy skin (fold-change >=2, FDR <0.05), with 100% sample recovery.

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

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

142 24 hrs and 48 hrs using a pFDR < 0.01 and a [fold change] > 2 threshold.

143 HM groups, respectively (adjusted p < 0.05; |fold change|> 2.0).

144 ssion analyses were performed using DESeq2 (|fold change|>1.5 and false discovery rate < 0.3), in pat

145 undances of pantothenate (P = 0.02) based on fold change (high/low RFI).

146 4a, the blue-red colour scale for fold change in ageing/disease regulation included a blue

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

148 1 treatment resulted in significantly higher fold change in ASCs among patients with HBsAg <100 IU/ml

149 the larger QRSarea/LVEDV ratio in women (25-fold change in beta from 0.12 to 0.09).

150 For a 10-fold change in body size (i.e., from 20 to 200 mm), the

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

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

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

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

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

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

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

158 red with their young adult counterparts when fold change in expression levels of GzmB, CD107a, IFN-ga

159 An approximate 8-fold change in expression of the cardiac contractile reg

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

161 Fold change in HI and antibody binding to HA1 trends hig

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

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

164 Median log-fold change in Ki-67 was greater with palbociclib plus l

165 es correlates with similar strength with the fold change in nuclear NF-kappaB.

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

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

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

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

170 direct ligand contacts, we observed a >1000-fold change in sialic acid binding affinity.

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

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

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

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

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

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

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

178 aria episodes and showed significantly lower fold changes in CD4+PD1+ and CD4+PD1+LAG3+ compared to t

179 chemoprevention had no observable effect on fold changes in CD8 T cells expressing PD1 or CD160.

180 s that are reversible and responsible for 30-fold changes in conductivity of the metal-organic framew

181 hase grown crystals and exhibit reversible 8-fold changes in conductivity upon illumination at modest

182 3 proteins with statistically significant >2 fold changes in dystrophic serum abundance.

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

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

185 mpared with younger individuals, with larger fold changes in males than in females.

186 degree of unsaturation exhibited the highest fold changes in mixed fields compared to photons alone.

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

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

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

190 Isoform-specific differences include 18-fold changes in the maximum power output per myosin-1C m

191 ed and had highly consistent gene expression fold changes in the two cohorts.

192 ximum power output per myosin-1C motor and 4-fold changes in the velocity and the resistive force at

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

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

195 ular function activation state (Z-score) and fold-change in AKT phosphorylation were calculated.Resul

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

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

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

199 s identified a nearly perfect correlation of fold-change in expression for those differentially expre

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

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

202 as the difference between the groups in mean fold-change in urinary Kidney Injury Molecule-1 (KIM-1).

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

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

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

206 gnificant metabolic features were found with fold changes larger than 1.5, and an additional 97 signi

207 effect size, often in terms of a logarithmic fold change (LFC).

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

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

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

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

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

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

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

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

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

217 in CAD subjects compared to Non-CAD (NAD(+) fold change: non-CAD 1.00 +/- 0.17 vs. CAD 0.32 +/- 0.12

218 1.00 +/- 0.17 vs. CAD 0.32 +/- 0.12* and ATP fold change: non-CAD 1.00 +/- 0.294 vs. CAD 0.01 +/- 0.0

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

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

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

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

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

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

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

226 ong the four cocoa genotypes analysed with a fold change of >=2.

227 vaccine only (absolute difference of log(10)-fold change of 0.64 [95% CI 0.39 to 0.89]; p=0.0002) and

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

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

230 5 mg BLP) achieved plateau responses with a fold change of 1.5 after first vaccination that remained

231 n marker genes are expected to be only up to fold change of 2, choice of the single cell algorithm is

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

233 to achieve plateau responses with a maximum fold change of 2.4, whereas high-dose recipients (350 mu

234 e 1 protein following hypoxia-reoxygenation; fold change of 3.17 (P <= 0.05) and 6.97 (P <= 0.05) res

235 ound that when marker genes are expressed at fold change of 4 or more, either Seurat or SIMLR algorit

236 operating characteristic of 0.84 and optimal fold change of 4.9.

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

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

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

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

241 Using criteria of a fold change of greater than 2 and a false discovery rate

242 idobacterium spp. significantly decreased by fold change of individual operational taxonomic units in

243 n treatment difference in the geometric mean-fold change of normalised KIM-1 was 1.08 (95% CI 0.87-1.

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

245 rnal PTSD were in opposite directions, while fold changes of shared DEGs associated with both materna

246 Similarly, fold changes of shared DEGs associated with maternal PTS

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

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

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

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

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

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

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

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

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

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

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

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

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

260 cantly differentially expressed genes (>=2.0-fold change, p-value < 0.05, FDR <0.05).

261 The table includes log-transformed fold change, P-value and q-value for each small molecule

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

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

264 ichment analysis of ranked DEGs (score = log fold change/p value) in the endocervix and ectocervix re

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

266 e at 9 and 18 months (at 18 months, ratio of fold-change patisiran/placebo 0.45, P<0.001).

267 sed on these formulas predicts precisely the fold change r* of mRNA numbers from [Formula: see text]

268 d to non-cancer epithelium (p < 0.05, log(2) fold change range: -0.423 to -0.987), while no significa

269 7-5p, miR-25-3p, miR-92a-3p, and miR-29b-3p; fold change range: 0.64-83, p = 0.0002-0.01) and increas

270 3p, miR-126-3p, miR-146a-5p, and miR-27b-3p; fold change range: 1.41-3.60, p = 0.001-0.006).

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

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

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

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

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

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

277 o use of fresh cells (95% probability of < 2-fold change), supporting continued use of frozen storage

278 Median log-fold change (suppression) of cleaved poly (ADP-ribose) p

279 is usually quantified as a continuous score-fold-change, test-statistic, P-value-comparing biologica

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

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

282 Ciprofloxacin exposure shows an almost 2-fold change throughout the treatment of pediatric ALL.

283 Ciprofloxacin exposure shows an almost two-fold change throughout the treatment of pediatric ALL.

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

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

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

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

288 or the top 15 up-regulated fragments, linear fold change varied from 2,053- to 622-fold.

289 p 15 down-regulated fragments in CLL, linear fold change varied from 314- to 52-fold.

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 ernal age at Holocaust exposure shared DEGs, fold changes were in the opposite direction.

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

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

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