ライフサイエンスコーパス: control value

1 d to control white matter (mean 38 +/- 4% of control value).

2 1beta (approximately 3.5-fold increase over control value).

3 -related manner (maximal reduction, 98% from control values).

4 ecreased in the diabetic rats (94 +/- 18% of control values).

5 d increased at 24 hr of reperfusion (191% of control values).

6 eversed by lowering corticosterone below the control value.

7 ange that included aPTT values 1.5 times the control value.

8 , n=13, P<0.001) compared with the untreated control value.

9 activity reconstitution to about 50% of the control value.

10 reduction in protein synthesis to 45% of the control value.

11 ptotic PMNs 280 +/- 62% above the no protein control value.

12 pS K+ channel, defined by NPo, to 26% of the control value.

13 the lung colony count reduced to 33% of its control value.

14 tration-dependent manner, down to 70% of the control value.

15 levated >100-fold compared with the Cys-less control value.

16 ope from mutant Tm had approximately 36% the control value.

17 % in uninjured A/J fibres, restoring them to control values.

18 res, pCa(50) and n(H) were increased towards control values.

19 ils to 60%, 20%, and 18% of their respective control values.

20 ietin levels were 2 to 10 times greater than control values.

21 r 52 days restored quinine-stimulated FLI to control values.

22 lume fraction remained unchanged relative to control values.

23 ons and converted into z-scores based on the control values.

24 ccurred and all other parameters remained at control values.

25 to similar levels, approximately 5-fold over control values.

26 els of dimethylglycine were much higher than control values.

27 n with 0.1 mM ATP, which was 245 +/- 15 % of control values.

28 arance was 1.5-fold reduced as compared with control values.

29 ow resistance and systemic BP, compared with control values.

30 s, phosphorylation of Akt was 123 +/- 21% of control values.

31 endent inhibition of transcription to 50% of control values.

32 though decreasing, were still elevated above control values.

33 ation were also significantly different from control values.

34 CE +/- FC elevations, rising as much as 10x control values.

35 enhanced hippocampal ACh output relative to control values.

36 of mdx mice were 17 % and 22 % greater than control values.

37 sed over the first 5 mm, and then paralleled control values.

38 density in vagotomized NGNs were similar to control values.

39 tion scores not significantly different from control values.

40 e, 38% and 158% with pGz, relative to paired control values.

41 d 2 hours after induction of LTP relative to control values.

42 g which time plantaris mass also returned to control values.

43 icrovesicle formation indistinguishable from control values.

44 tuber yield was decreased by 90% compared to control values.

45 enerating elements had reached only 7-39% of control values.

46 rombinase activity up to 6-fold greater than control values.

47 n in [Ca2+](i) ranging from 60% to 150% over control values.

48 n radiopharmaceutical (4000-5000-fold) above control values.

49 longated progressively over 6 mo to approach control values.

50 4 mmHg) and HR (61+/-11 bpm) with respect to control values.

51 f the radiolabeled substrate to over 200% of control values.

52 d increase at 15 h, then rapidly declined to control values.

53 series, lower RLC phosphorylation to 60% of control values.

54 5-HT concentrations ranged from 3 to 45% of control values.

55 raised by 5 and 10 mmHg, respectively, above control values.

56 -8% of control and continued to remain below control values.

57 The K1 of AIB was increased 25 times control values.

58 %, and for 5-HT were to 73%, 44%, and 19% of control values.

59 control, whereas trkC mRNA levels fell below control values.

60 up-regulation ranged from 40% to 250% above control values.

61 ference was not statistically different from control values.

62 n levels and functional activity returned to control values.

63 improvement during remission but not to the control values.

64 24 hr postinjury, respectively, compared to control values.

65 Parkinson's disease patients was 37% of the control values.

66 duced to 2.6% +/- 2.1% and 38.4% +/- 1.3% of control values.

67 zymographic activity increased by >100% from control values.

68 e chronic ethanol consumption, compared with control values.

69 reased and firing rates returned to close to control values.

70 urst of ROS production to 200-400-fold above control values.

71 and docked vesicles were nearly restored to control values.

72 ollowing TAC, leptin reduced the APD towards control values.

73 re compared with age- and disc size-adjusted control values.

74 tralaterally projecting axons was four times control values.

75 cular volume were reduced when compared with control values.

76 rom the EC, was decreased by 42% relative to control values.

77 cular myocytes in co-culture were similar to control values.

78 g enzyme activity, and AT1 remained close to control values.

79 5.6 [4.3-6.9] ng/mL) was similar to referent control values.

80 t-synaptic folding were approximately 50% of control values.

81 calcium followed by a slower decline toward control values.

82 ptic potentials and currents were similar to control values.

83 e task, their acquisition rate lagged behind control values.

84 ng both NET B(max) and HED HU to 8% of their control values.

85 s after AT the EPSC decay times recovered to control values.

86 rmance over a 30-min delay to 27% of vehicle controls values.

87 sulin concentrations returned to euglycaemic control values (0.30 +/- 0.01 ng ml(-1)) in R fetuses (0

88 0+/-0.5% (mean+/-S.E.M.) above pre-injection control values 165 min after drug administration.

89 cell radioactivity) were raised relative to control values (2.0% +/- 0.2%, n = 10, P = .008).

90 reased in patients (1.86 +/- 0.05) to 86% of control values (2.14 +/- 0.08) (P = 0.01).

91 vels in hypoxia-exposed fish had returned to control values 24 h after the DO in the tanks was restor

92 exposures, with activity levels returning to control values 24 h later.

93 Using the median control value (29.22) as a cutoff, 63% of the cases were

94 re increased significantly about 4-fold over control values (29 +/- IU/L) by enteral ethanol (113 +/-

95 min decreased the mean NP(o) reversibly from control value 3.20 to 0.40.

96 ible, with enzyme levels returning to 90% of control values 48 h after removal of drug.

97 Plasma glucose levels exceeded nondiabetic control values (7.7+/-0.2 mmol/l) in both diabetic group

98 enzyme activity had recovered only to 15% of control values, a recovery dependent on regeneration of

99 for dipeptidyl peptidase was higher than the control value after 4 days of T4 administration.

100 LV stroke volume was reduced from the control value after rapid pacing, was unchanged with eit

101 Transcript levels returned to control values after 1 h of incubation at 37 degrees C,

102 2-fold, respectively), then decreased toward control values after 10 d.

103 quency adaptation that partially returned to control values after 10 min of angioII exposure.

104 r of DNA synthesis, was increased to 448% of control values after 2 days of camostat feeding, rapamyc

105 doubled after 6 h of hypoxia but returned to control values after 3 d.

106 tein levels were observed, which declined to control values after 5-6 days of hormone exposure.

107 t was decreased significantly to 62 +/-7% of control values after a 48-h washout.

108 nt (80 mg/kg i.p. x 4 days) but decreased to control values after a 48-h washout.

109 MS than in control subjects and increased to control values after bosentan administration.

110 -induced CHF values), and returned to within control values after combined blockade.

111 Each fell to control values after ECT.

112 itis in the submandibular gland, returned to control values after HU-308 treatment.

113 was also increased more than threefold above control values after naphthalene treatment.

114 These kinetic constants regained control values after reconstitution of the thin filament

115 were significantly increased and returned to control values after recovery.

116 hough retinal energy metabolites returned to control values after the recovery period, retinal GSH re

117 e also effective in lowering cGMP levels (to control values) after applied stress, also consistent wi

118 recovery took place, in many cases almost to control values, after 168 h.

119 reases reconstitution activity to 40% of the control value and reduces functional binding of the muta

120 ot increase caspase activity above untreated control values and a pancaspase inhibitor did not protec

121 ejection fraction (EF) by only 1%+/-4% from control values and correlated linearly (r> or = 0.96) wi

122 kin-7 (P = 0.007) were increased compared to control values and remained elevated for 1 month, simila

123 When work was decreased, [NADH]m overshot control values and then slowly returned.

124 us knockout mice was reduced to 58 +/- 3% of control values and there was a 21 +/- 2% reduction in Ca

125 of DETA-NONOate treatment, which returned to control values and which was followed by another wave of

126 of 1207 +/- 173 (36-fold over the wild-type control value) and 821+/-38 fmol/mg protein (69-fold), r

127 gyrus peaked at 4 hr of reperfusion (140% of control values) and declined thereafter, changes in area

128 ulation of CV taste buds ( approximately 75% control values) and may relate to peripheral and/or cent

129 severity of withdrawal (after subtraction of control values), and by design these differences were in

130 s with actin alone had approximately 40% the control value, and the slope from mutant Tm had approxim

131 or (eIF)4E with 4E-BP1 was reduced to 50% of control values, and eIF4G*eIF4E complex assembly was inc

132 nd myocyte length both increased by 15% from control values, and LV fractional shortening fell by 20%

133 Me-Phe4,Gly5-ol]enkephalin responses back to control values, and were confirmed in SH-SY5Y cells endo

134 stants) or qualitative (relative change from control values) approaches.

135 Therapeutic ranges of 1.5 to 2.5 times the control value are subtherapeutic for most modern aPTT re

136 c acid was found to increase by over 50% its control value as early as 3-h post ischaemia, parallelin

137 sion group significantly increased above the control values as early as 4 d after the lesion and rema

138 r population to approximately 35% and 15% of control values, as determined by morphologic analysis, v

139 approximately 40% at pH 4 and pH 9 over the control value at pH 6.5.

140 bumin was increased to approximately 160% of control values at 1 and 10 min after treatment.

141 oxamer 188 (P188) restored cell viability to control values at 24 h postinjury.

142 estored total and amiloride-sensitive AFC to control values at 48 h pi.

143 po, with a significant decline to well below control values at 7 and 14 dpo.

144 E(GABA) recovered to control values at longer latencies post-STEP (2-8 weeks)

145 FAP was increased to 125%, 134%, and 149% of control values at MA doses of 20, 30, or 40 mg/kg, respe

146 nretinal TI(a) and TI(v) were increased over control values at P19, but only TI(v) decreased by P22.

147 antly reduced 100- to 1,000-fold compared to control values at various times postinfection.

148 oad was higher in the AD group compared with control values, but further statistically significant di

149 lin G levels and avidity were slightly below control values, but levels maintained were higher than t

150 eased irreversibly to more than 15 times the control value by 10 min.

151 s restored to 75-80% of the wild-type apoA-I control value by double deletion mutants apoA-I[delta(1-

152 (the calcium loading rate is restored to the control value by reconstitution with FKBP12); and 4) RyR

153 All parameters were back to control values by 12 months.

154 l cortex, increasing signal 5.2+/-1.8% above control values by 174 min; its effects were, however, mo

155 eurons then progressively increased to reach control values by 20 weeks.

156 -solar-simulated radiation, but recovered to control values by 24 h.

157 of H3-(methyl)arginine 17, H3meR17, exceeded control values by 30%, and this was associated with the

158 GFR in postpartum women was elevated above control values by 41%; 149+/-10 versus 106+/-3 ml/min pe

159 escence in the stimulated fibres returned to control values by 5 min after contractions.

160 f agonist treatment, and slowly recovered to control values by 6 days of treatment.

161 20% at day 3 after MI (P < 0.05) and fell to control values by day 5.

162 ections and with protein levels returning to control values by day 7 post-treatment.

163 A treatment and were partially normalized to control values by desipramine pretreatment.

164 ve oxygen species, which both shifted toward control values by expressing a recombinant, wild-type AP

165 in heterozygous controls and was restored to control values by infusion of PRL, suggesting a function

166 sewhere in the left hemisphere deviated from control values by only 8%.

167 nd strengths, but these could be restored to control values by re-surfacing of the dentin with a bur.

168 d rose to a maximum after 1 d, exceeding the control values by sevenfold.

169 < 0.05) and 48 +/- 10% (n = 6, P < 0.05) of control values by the phosphatidylinositol 3-kinase (PI3

170 tients with heart failure were compared with control values by using two-tailed t tests, and transit

171 8.7 microm); returning to normal (similar to control values) by day 7 with DOP and day 35 with LAS an

172 nd TNNT2p.K217del samples were normalized to control values confirming the pathogenic effects of the

173 Control values consisted of previously published data fr

174 drawal of NH(4)(+) restored E(m) to close to control values despite a persistent change in V(c).

175 overall patterns of movement returned toward control values driven by reciprocal compensatory changes

176 s at rest, but were significantly lower than control values during exercise and recovery (P < 0.029 a

177 seline values and by 8 weeks had returned to control values, except the DG-SMm which showed only a 10

178 ect any increase in BDNF concentration above control values following chronic depolarization with 40

179 AI returned to control values following reinfusion.

180 ich flow was reduced to approximately 50% of control values for 60 minutes (n=6) in swine.

181 y was highly effective in the maintenance of control values for absolute force for both EDL and soleu

182 and correlated linearly (r> or = 0.96) with control values for all simulated arrhythmias.

183 fferent UVA intensities, but returned toward control values for healthy volunteers.

184 the new method gave values within 4 to 8% of control values for protein (without bound phenols) as de

185 o was asked to submit 10 consecutive quality control values for several key organism-drug combination

186 ts after the clamp but remained identical to control values for TZD-treated rats.

187 pendent task performance relative to vehicle control values (group young OVX+Veh) but nonetheless led

188 of transplant recipients did not differ from control values; however, MEP was blunted by 30% relative

189 results due to elimination of an average or control value in comparison with classical routine appro

190 consumption decreased to 47% +/- 18% of the control value in the detached retina during normoxia; hy

191 s demonstrated a six-fold increase above the control value in the intestinal tissue in rats on day 1

192 xtent of neuronal loss was lower than 15% of control values in 1-methyl-4-phenyl-1,2,3,6-tetrahydropy

193 /molecular (SLM) declining to 60% and 68% of control values in 1-month and 2-month post-SE, respectiv

194 d mice decreased exponentially to 10%-20% of control values in about 30 min.

195 ns were significantly increased from healthy control values in acute pancreatitis patients at present

196 hours post-ischemia, CRH levels returned to control values in all regions except the dentate gyrus (

197 though DNA synthesis was decreased to 16% of control values in anti-CD3-stimulated Hut-78, the produc

198 content following depolarisation returned to control values in approximately 12 min via Na(+)-Ca(2+)

199 nly group (P<0.05) but decreased to referent control values in both CHAM groups in the MI region (P<0

200 part be associated with different threshold control values in different kits.

201 Control values in drug-naive slices were: T(on)=193+/-8

202 tem, Cav1.2 mRNA was reduced to 11 +/- 1% of control values in homozygous floxed mice and the mice di

203 ining restored GABA(A) gamma2 levels towards control values in motoneuronal pools of both muscles.

204 the cell layer to levels that were 35-69% of control values in old chondrocytes and had no effect on

205 This incidence dropped to close to control values in the long term despite a 2-6% rate of s

206 ties were reduced by 55 to 57% compared with control values in the mutation-bearing AD cases in the m

207 ock by zinc, with current reduced to 0.58 of control values in the presence of 100 microM zinc.

208 e uptake was reduced to 60, s 37, and 30% of control values in the sciatic nerve, L5 dorsal root gang

209 V E responses to hypoxia were unchanged from control values in young animals, whereas V E respones in

210 of ENFs increased significantly relative to control values, in later stages (16-24 d after implantat

211 rols, but they increased slightly, away from control values, in placebo-treated patients.

212 The increase is approximately 5-fold above control values, is comparable to the induction elicited

213 of nmol/mg protein and shown as percents of control values (mean +/- SE).

214 m SRL-treated NHPs compared with grafts from controls, values (mean+/-SEM) were IA, 2.9+/-0.9 versus

215 Compared with control values (n = 10), there was a significant (P < 0.

216 of kindling, but only when compared to sham control values (needle insertion only) in the same anima

217 (54 +/- 11%; t test, p < 0.05) than the mean control value of 1,847.

218 al lung phosphatidylcholine synthesis from a control value of 12.7 +/- 1.2 to 5.5 +/- 0.3 nmol phosph

219 atidylcholine pool size was reduced from the control value of 2.65 +/- 0.05 to 1.61 +/- 0.08 micromol

220 transit time was likewise unchanged from the control value of 26 +/- 2 s, indirectly suggesting that

221 creased fibrinogen degradation rate from the control value of 4.3 +/- 1.0 mg/kg/h to 11.8 +/- 1.4 mg/

222 ntricular dP/dt max of 19.6 +/- 2.9 % from a control value of 6136 +/- 228 mmHg s-1.

223 decrease in lung dynamic compliance from the control value of 66 +/- 6 to 55 +/- 6 mL/cm H2O for burn

224 e in the fractional mobility of CD2 from the control value of 68 +/- 1% to 45 +/- 2% (mean +/- SEM).

225 The mean change was 8.3 +/- 2.9 % from a control value of 6850 +/- 450 mmHg s-1.

226 g: the time to 50% emptying increased from a control value of 69 +/- 9 to 87 +/- 11 min (mean +/- SEM

227 dulin binding and enzyme activation from the control values of 182 +/- 2 and 422 +/- 22 nm to 116 +/-

228 and GFR were not significantly altered from control values of 3.76 +/- 0.2 ml/min.g and 0.69 +/- 0.0

229 ated in 97% of patients compared with normal control values of 4.1+/-1.65 microgram/mL.

230 formulations differed significantly from the control values of the chemotactic index (all P > 0.25).

231 ectrically couple 2 isolated myocytes with a controlled value of coupling conductance (Gc).

232 strates a method for producing CNT FETs with controlled values of the turnoff gate voltage, and more

233 reversible, returning towards and exceeding control values on cellular recovery, which potentially i

234 ere all significantly elevated compared with control values, only plasma IL-6 levels significantly de

235 during locomotion generally converged toward control values over time, but significant differences pe

236 etamide (DMA), reduced the motility over the control value (P<0.5), whereas 10% dimethylformamide (DM

237 - to 6-fold increase in uptake compared with control values (P < 0.001).

238 nexin V uptake by 3- to 6-fold compared with control values (P < 0.002).

239 of JDM patients were 35-40% below the normal control values (P < 0.003).

240 ed intracellular adenosine to 125 +/- 18% of control values (p < 0.01), consistent with the possibili

241 an, FE(NO), C(W), and urine NOx increased to control values (p < 0.05).

242 d by septic serum and averaged 61% +/- 6% of control values (p <.05).

243 diac Cx43 protein levels decreased to 59% of control values (P<0.01), but conduction velocity was not

244 TIMP-3 (74+/-23%) was reduced compared with control values (P<0.05) and TIMP-2 was elevated (128+/-3

245 shortening velocity was reduced by 35% from control values (P<0.05) in both MI groups.

246 1 to 3 were reduced in non-MFS compared with control values (P<0.05).

247 364+/-21 versus 141+/-5 g/cm(2)) from normal control values (P:<0.05).

248 When compared with control values, patients demonstrated significantly grea

249 Compared with control values, plasma cGMP concentrations were increase

250 ercapnia in all dogs to an average of 19% of control values (range 0-38%; n = 6), whereas CB chemoref

251 rcapnia in all dogs to an average of 223% of control values (range 204-235%; n = 4).

252 The decrease from control values ranged from 10% to 40%, depending on surf

253 ein, of almost fourfold (densitometric value/control value ratios of 3.79 +/- 1.16 versus 1.00 +/- 0.

254 Compared with control values, relative glucose metabolic rate in the v

255 ke of [125I]AHIgG of 4.4, 3.0, and 2.1 times control values, respectively at 8 h after the infusion o

256 162) and L-selectin (CD62L) (to 33 and 5% of control values, respectively), at a time when the levels

257 mum nodal weight decreases, 86% and 88% from control values, respectively).

258 +/- 0.2, 83.7 +/- 3.0 and 88.9 +/- 3.7 % of control values, respectively).

259 levels (at 30 and 90 days, 132% and 168% of control values, respectively).

260 ion were 100.6 +/- 0.1 and 90.5 +/- 1.5 % of control values, respectively).The reduced myofilament Ca

261 transport, was approximately 90 and 40% over control values, respectively, in fast-twitch white and r

262 GE(2) was 5.7-fold and 6.3-fold greater than control values, respectively, whereas TNF-alpha (10 ng/m

263 to 39 and 7% of the corresponding untreated control values, respectively.

264 functional levels of 8% and less than 1% of control values, respectively.

265 e 147.1 +/- 13.2 and 174.8 +/- 23.2 % of the control values, respectively.

266 1alpha and Gi3alpha were about 20 and 40% of control values, respectively.

267 were enhanced to 274+/-76% and 217+/-69% of control values, respectively.

268 e examined across patients and compared with control values, right amygdala atrophy was always accomp

269 al contractility was reduced to 14 +/- 1% of control values shortly before death.

270 ccluded nares decreased cell death levels to control values, suggesting an inverse relationship betwe

271 cerebral artery velocities were 18-26% below control values throughout late infancy and early childho

272 gotomized NGNs was shifted -9 mV relative to control values (V(1/2), -74 +/- 2 vs. -65 +/- 2 mV, P <

273 in eIF4E associated with eIF4G to 10% of the control value was also noted.

274 In addition, an 123% increase over control values was detected in the copper sulfate group

275 Third, a decisive increase over control values was observed in both MHC class I Ag-restr

276 on of EETs, 14,15-DHET, and 20-HETE from the control values was observed in coronary venous plasma.

277 The magnitude of decrease in HR from control values was similar in both groups.

278 amino acid concentration of medium to 75% of control values was sufficient to induce the growth of en

279 The rate of return of pH and ADP to control values was the same in wild-type and mutant mice

280 - 5.0%) peak tensions (normalized to initial control values) were significantly reduced (P < 0.05) wi

281 (triple Shc mutant) but was reversed back to control values when either wild-type Shc or the family m

282 nsiently at 2 hours compared with stationary control values, whereas at high shear stress (25 dyn/cm2

283 hese areas were reduced to less than half of control values, whereas average volume elsewhere in the

284 il reduced SS Ca2+ spark frequency to 38% of control values, whereas Ca2+ spark activity from nj-SR w

285 ansport of both proteins to less than 10% of control values, whereas disruption of microtubules by tr

286 Ring3 expression increased 5-fold over control values, whereas expression of the other transcri

287 vessel diameter and cell length returned to control values, which indicated that during acute vasoco

288 ne concentration by approximately 30% of the control value while GSH and cysteine concentrations incr

289 l CO2 flux was approximately 1000-fold above control values with 0.5 mg/ml carbonic anhydrase.

290 - 0.45%, 293% +/- 1.3%, and 220% +/- 0.5% of control values with 10, 20, 40, and 80 ng/mL EGF, respec

291 d, but receptor function recovered to 83% of control values with a half-time of about 10.5 min.

292 BP was restored to control values with pertussis toxin Gi-signaling inhibit

293 after acute ischemic stroke when compared to control values, with peak elevations at 48 h after strok

294 ect on EB-albumin extravasation decreases to control values within 1.5 h in normal brain; however, th

295 the down-regulation of CYP2B1 mRNA to 20% of control values within 12 h of treatment, and this was no

296 Npy mRNA, which fell to approximately 20% of control values within 3 days after treatment with Dox.

297 Such altered dilation returned to control values within 4 h in I+R animals and within 12 h

298 ke of HDL [3H]cholesteryl ether by 50-60% of control values without altering the extent of cell assoc

299 values between 34% and 45% and restoring the control values without stress induction in the G1 phase

300 ivers of diabetic mice was normalized to the control value, yet O-GlcNAcylation and the association o