ライフサイエンスコーパス: be corrected by

1 mass, suggesting that early myotomal defects are corrected by a Dmrt2-independent mechanism.

2 tiple aberrant phenotypes of mutant L77R can be corrected by a second naturally occurring S envelope

3 CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. virus infection.

4 ulations at -80% to +50%, where results have been corrected by a low modeling bias of 28%.

5 the pathogenic effect of a germline mutation is corrected by a second somatic event.

6 These abnormalities were corrected by a course of broad-spectrum oral antibi

7 F508del-CFTR mistrafficking may be corrected by acting directly on mutant CFTR itself or

8 s for the low cloning efficiency which could be corrected by adding yet to be identified, sperm-deriv

9 to persist and kill this host, a defect that was corrected by adding inorganic iron to the inocula.

10 n wild-type macrophages, and this defect can be corrected by addition of exogenous apoE protein.

11 itivity to thrombin, but these defects could be corrected by addition of subthreshold amounts of aden

12 This was corrected by addition of purified Asp protein.

13 nhanced activation-induced cell death, which was corrected by addition of the PI3Kdelta inhibitor IC8

14 in the ASM knockout (ASMKO) mouse brain can be corrected by adeno-associated virus serotype 2 (AAV2)

15 n the neomycin phosphotransferase (neo) gene were corrected by adeno-associated virus (AAV)-mediated

16 indicated that HFD-induced oxidative stress was corrected by adiponectin.

17 cal forests, and we show that this error can be corrected by adjusting the maximum carboxylation rate

18 Hypoglycemia after gastric bypass can be corrected by administration of a GLP-1 receptor antag

19 demand within the retina is impaired and may be corrected by alpha-lipoic acid (LPA), a drug that inh

20 High cardiomyocyte stiffness was corrected by alpha-B crystallin probably through rel

21 mino-acid activation and tRNA esterification are corrected by aminoacyl-tRNA synthetase-catalyzed edi

22 ty of a pgsA null allele of Escherichia coli was corrected by an N-terminal truncated derivative of t

23 r in nonisolated animals, a deficit that can be corrected by anxiolytic drug treatment.

24 as into all comparisons in a way that cannot be corrected by any refinement in laboratory analysis.

25 ects of tau as found in FTDP-17 patients can be corrected by application of antisense oligonucleotide

26 It is now shown that this deficiency may be corrected by applying an ultra-thin monolayer of a mo

27 shown to change significantly when the gaps are corrected by approximate inclusion of many-electron

28 onal condition; it is intractable and cannot be corrected by argument or evidence.

29 n osteochondroprogenitors or osteoblasts can be corrected by asfotase-alpha enzyme therapy aimed at r

30 creased immunoglobulin diversity, and cannot be corrected by booster immunization.

31 of cyclin A with Cdk1, but this defect could be corrected by both inhibitory and noninhibitory analog

32 -induced changes in urinary NO(x) and PGE(2) were corrected by both COX inhibitors.

33 Thus, HIGM1 can be corrected by CD40L trans-splicing, leading to functio

34 nt suppression of hepatic glucose production are corrected by chronic relaxin.

35 exhibit a "slugger" phenotype, which cannot be corrected by co-development with wild-type cells.

36 of apparent 'gain-of-function' mutations can be corrected by co-transfection of wild-type EPM2A cDNA,

37 ApoE-induced hyperlipidemia was corrected by co-infection with a recombinant adenovi

38 in a 9 +/- 2 mmHg decrease in PET,CO2, which was corrected by CO2 supplementation of the inspired air

39 n homeostasis of CD4(+) iNKT cells and Tregs were corrected by coablation of P2X(7).

40 test indicated a failure to absorb Cbl that was corrected by coadministration of IF.

41 Hypertriglyceridemia was corrected by coinfection of mice with recombinant ad

42 These defects can be corrected by combined deletion of E2f1.

43 When this bias is corrected (by comparing, for example, the conservatio

44 within the repeat that abolish exon skipping are corrected by compensatory mutations in the pre-mRNA.

45 These defects could be corrected by complementation of ompA.

46 er of experimental biases, many of these can be corrected by computational analysis.

47 ardinal features of CD8(+) T cell exhaustion were corrected by conditionally deleting Blimp-1.

48 values for experimentally detected proteins are corrected by considering their mRNA levels and (2) p

49 n caused by maternal alcohol consumption may be corrected by controlling the activity of these second

50 Each abnormality was corrected by corresponding morphology-directed repai

51 he negative ciliogenesis regulator CP110 and was corrected by CP110 depletion.

52 , and iPSC line in which the V247fs mutation was corrected by CRISPR/Cas9-based genome editing (V247f

53 ng, contraction and apoptosis; abnormalities were corrected by CRISPR-based editing of the FBN1 mutat

54 tion at position +1489 of the TAP-1 gene and was corrected by cycloheximide, which inhibits RNA degra

55 alpha-deficient erythroid colonies could not be corrected by cytokines, such as vascular endothelial

56 The urine concentration defect could not be corrected by [deamino-Cys1,D-Arg8]-vasopressin (DDAVP

57 sjunction occurs at a high frequency and can be corrected by delaying the onset of anaphase.

58 The defects in Mdm2+/- Mdm4+/- mice are corrected by deletion of a single p53 allele.

59 neal keratocytes derived from a GCD2 patient was corrected by delivering a CRISPR plasmid expressing

60 Subsequently, the sickle mutation was corrected by delivering CRISPR/Cas9 with adenovirus

61 ional abnormalities of dystrophic muscle can be corrected by delivery of full-length dystrophin to ad

62 Small looped mispairs are corrected by DNA mismatch repair (MMR).

63 Single base mispairs and small loops are corrected by DNA mismatch repair, but little is know

64 Small looped mispairs are corrected by DNA mismatch repair.

65 errors that arise during DNA replication can be corrected by DNA polymerase proofreading or by post-r

66 have demonstrated that CFTR dysfunction can be corrected by drug-like molecules.

67 rylation defect in LIG4-defective cells that was corrected by ectopic expression of catalytically dea

68 The defect in Cby assimilation was corrected by ectopic expression of pduX or by supple

69 e defect in IFN-alpha-driven Th1 development was corrected by ectopic expression of T-bet within prim

70 rine model of MPS VII have not been shown to be corrected by either bone marrow transplantation or ge

71 omonucleotide runs and that these errors can be corrected by either mismatch repair (MMR) or proofrea

72 nts) and those with thiamine auxotrophy that was corrected by either L-tyrosine or thiazole (ThiH* mu

73 week 48 fitness deficit persisted when G36D was corrected by either site-directed mutagenesis or wee

74 Disease liability is corrected by eliminating this B-cell specificity, pro

75 ed cell-cell adhesion in VHL-null RCC4 cells were corrected by enforced expression of VHL, a dominant

76 gressively less reliable over time, and must be corrected by environmental sensory inputs when availa

77 ect of hypocotyl elongation in fk-J79 cannot be corrected by exogenous BRs.

78 CcsBA with mutations in these TMD histidines is corrected by exogenous imidazole, a result analogous

79 Gene annotation of the identified proteins was corrected by experimental data, and an interesting c

80 BP2-dependent microRNA maturation, which can be corrected by exposure to the fluoroquinolone enoxacin

81 The c-di-AMP levels in both mutants could be corrected by expressing the respective gene.

82 compared with wild-type cells, a defect that is corrected by expressing a tagged copy of TbRFT1 in th

83 These defects are corrected by expression of an engineered ER-mitochon

84 These defects are corrected by expression of human BRIP1 lacking the B

85 These phenotypes are corrected by expression of one of two enzymes: NADH

86 ucleotide-sensing TLRs in 3d dendritic cells are corrected by expression of wild-type UNC93B1.

87 n of human wild-type COQ4 cDNA but failed to be corrected by expression of COQ4 cDNAs with any of the

88 ction of the 50S subunit; both defects could be corrected by expression of E. coli L27 from an extrac

89 These defects can be corrected by expression of human GM-CSF and IL-4 in h

90 mutant cells reveal a bias towards LTGC that is corrected by expression of wild-type but not cancer-p

91 This defect is corrected by expression of wild-type XRCC2 and also b

92 , strongly impaired in strains lacking COQ4, was corrected by expression of human wild-type COQ4 cDNA

93 ect in ICRF-193-induced mitotic delay, which was corrected by expression of wild-type BRCA1.

94 ovo variant calls in disease candidate genes were corrected by FamSeq as mendelian variants, and the

95 The apoptosis defect could be corrected by FAS overexpression in vitro.

96 rowth found in Znt7-deficient mice could not be corrected by feeding the mutant mice with a diet cont

97 The anemia of sublytic homozygotes can be corrected by feeding with a high-iron diet or by pare

98 defect in the neurulation-stage embryo that is corrected by folic acid.

99 ther the MLIV phenotype in fibroblasts could be corrected by fusing normal cells to MLIV cells and fu

100 that this disorder in humans can potentially be corrected by gene therapy.

101 To assess whether VWF deficiency can be corrected by gene transfer, a plasmid expressing the

102 The enzyme defect can be corrected by gene transfer.

103 n the setting of partial ADA deficiency that is corrected by gene therapy.

104 These phenotypic alterations were corrected by gene complementation.

105 O) CTLs, which was cell autonomous and could be corrected by GrB deficiency.

106 iomeningitis virus-specific CTL, which could be corrected by GrB deficiency.

107 These defects are corrected by hepatic overexpression of full-length P

108 ulated MGU, but only exercise-stimulated MGU was corrected by HK II overexpression.

109 larger or more complex mutations that cannot be corrected by homologous recombination.

110 cessive dystrophic epidermolysis bullosa can be corrected by homology-directed DNA repair.

111 , the atrophy induced by visceral adipocytes was corrected by IGF-II/insulin growth factor binding pr

112 Diabetes was corrected by IK transplantation in all pancreatectom

113 alpha-) induced apoptotic killing, which can be corrected by IL-6.

114 trate that an abnormal tumor epigenotype can be corrected by in vitro reprogramming, and suggest that

115 ractant stromal-derived factor 1alpha, which was corrected by in vitro DIZE treatment.

116 Higher F(passive) in HFPEF was corrected by in vitro PKG administration.

117 repared from Igf1-/- brains, and the deficit is corrected by inclusion of Igf1 in the incubation medi

118 The resulting imbalance in gene dosage is corrected by increased expression from the single X c

119 gates, and increased P. aeruginosa adherence were corrected by incubating CF respiratory epithelial c

120 ht into how everyday damage to the ENS might be corrected by indwelling stem cells and prospects for

121 thrombus formation in the mPF4(-/-) animals was corrected by infusing hPF4 over a narrow concentrati

122 VWF-A1 display a bleeding phenotype that can be corrected by infusion of human platelets.

123 o cGMP when tested ex vivo, a phenotype that was corrected by infusion of gp91ds-tat into the mice.

124 This abnormality was corrected by infusion of purified HCII but not ovalb

125 r necrosis factor (TNF)-alpha production and was corrected by injecting recombinant TNF-alpha or an a

126 cell development were identified that could be corrected by injection of rIL-7 in vivo.

127 reduced expression of runx1; this phenotype was corrected by injection of human RAD21 mRNA, but not

128 ased apoptosis in Fancd2-deficient zebrafish were corrected by injection of human FANCD2 or zebrafish

129 ing that the conformational change could not be corrected by intermolecular interactions with the wil

130 f dysfunctional endothelial NO synthase that was corrected by intracellular tetrahydrobiopterin suppl

131 iours displayed by the eIF4E-transgenic mice are corrected by intracerebroventricular infusions of th

132 the glia-targeted mice, blood pressure could be corrected by intracerebroventricular injection of the

133 This overestimation was corrected by introducing a multiplication factor of

134 This defect was corrected by introducing copies of the wild-type reg

135 ite outgrowth capacity in FAD mutant neurons was corrected by introducing PLD1 into these cells.

136 ght mice, where Rag1 or Artemis deficiencies were corrected by introducing the missing gene with gamm

137 Each of the above-mentioned defects was corrected by introduction of the second-site compens

138 educed serum-stimulated proliferation, which was corrected by ionomycin or reconstitution of Bid, par

139 from insufficient iron uptake, since it can be corrected by iron supplementation.

140 lomeruli, of diabetic rats and this increase was corrected by ISO, whereas ABA had a weaker effect.

141 irculating neutrophils from patients with CF are corrected by ivacaftor, thus illustrating additional

142 21Cip1 and senesced prematurely; this defect was corrected by knocking down CDK inhibitor levels with

143 mpared among studies because mistakes cannot be corrected by laboratory analysis.

144 riant NKT (iNKT) cell numbers that could not be corrected by later intervention with vitamin D or 1,2

145 Importantly, these alterations were corrected by lentiviral expression of wild-type PIN

146 g rats with Intralipid or corticosterone and were corrected by leptin replacement.

147 bnormalities of alveolar macrophage function were corrected by local expression of GM-CSF in the lung

148 t hematopoietic stem cell dysfunction, which is corrected by loss of Bak and Bax.

149 has no effect when the hypercholesterolemia is corrected by macrophage apoE expression.

150 , indicating that the recombination gradient was corrected by matching the DIS.

151 This sensitivity is corrected by methionine and seems to result from dest

152 and rare mismatches that escape proofreading are corrected by mismatch repair (MMR).

153 ow relaxation caused by alpha-Tm mutants can be corrected by modifying calcium handling with Parv.

154 We then show that this bias can be corrected by modifying the downward momentum flux to

155 size estimate due to the missing fibers can be corrected by multiplication with the square root of t

156 e SMA hyporeactivity of PVL-20G and RAL rats was corrected by N(G)()-monomethyl-L-arginine, and nitri

157 This pathological phenotype was corrected by nebivolol but not metoprolol in a dose-

158 Refractoriness to epinephrine could be corrected by nitric oxide pathway inhibitors such as

159 asoconstriction in young adults with VVS can be corrected by nitric oxide synthase inhibition, demons

160 e conclude that lack of randomization cannot be corrected by normalization or by analytical methods.

161 We here show how this problem can be corrected by obtaining maximum-likelihood estimates o

162 Fortunately, this discrepancy can be corrected by one of two simple computational approach

163 sults suggest that processing of HIV Gag can be corrected by one or more genes present on human chrom

164 incidence of preterm birth, a condition that was corrected by oral administration of the selective CO

165 d liver function tests in CFTR-knockout kits were corrected by oral administration of ursodeoxycholic

166 These phenotypes were corrected by over-expressing GFP-tagged RP2.

167 ional defects in PPARalpha(-/-) hearts could be corrected by overexpressing the insulin-independent g

168 the late flowering phenotype of such mutants is corrected by overexpressing CO.

169 crophages from P. carinii-infected hosts can be corrected by overexpression of GATA-2, a plasmid cont

170 mice experience hepatic hypertrophy that can be corrected by pasireotide.

171 sful, while ET in a patient with a minor AHP was corrected by performing a bimedial recession.

172 False-positive contacts were corrected by performing the same analysis on proces

173 whether defects in hepatic fat oxidation can be corrected by peroxisome proliferator-activated recept

174 and lowers satiety ratio, and these effects are corrected by pharmacological administration of OEA.

175 hese effects were blunted when hyperglycemia was corrected by phlorizin treatment of diabetic rats or

176 Thus, total FV deficiency can be corrected by plasma administration, which partially r

177 hours of Fas agonist treatment, which could be corrected by pretreatment with IGFBP-1.

178 oxorubicin-mediated apoptosis, deficits that were corrected by programmed expression of the enzyme.

179 ent across samples for the same gene, it can be corrected by proper experimental design and analysis.

180 olyl but not asparaginyl hydroxylation which was corrected by provision of exogenous 2-oxoglutarate (

181 These defects were corrected by provision of a young-ECM but not old-E

182 lting in functional brain failure, which can be corrected by raising plasma glucose concentrations.

183 These effects were corrected by rapamycin treatmentin vivo Importantly

184 in ARG-deficient cells and that this defect is corrected by reconstituting ARG expression.

185 impaired ability to present antigen in vivo, were corrected by reconstituting these animals with norm

186 The polydactyly of Dkk1(d/d) mice was corrected by reduced expression of Lrp5 or Lrp6.

187 This excess can be corrected by reducing signaling by Gp1 mGluRs, and nu

188 rmation due to erroneous ligand usage, which was corrected by reducing Fgf9 gene dosage.

189 Growth defects of an sse1Delta mutant were corrected by reducing PKA signaling through overexp

190 s of excess FA availability on the liver can be corrected by reduction of dietary intake of sugars an

191 tion of PC2 increases cAMP levels, which can be corrected by reexpression of wild-type PC2 but not by

192 Drift, even though very small in this study, is corrected by referencing versus an internal standard.

193 alibration is not performed can be large and are corrected by regression calibration.

194 Data were corrected by regression analysis to eliminate effec

195 he impaired invasion of TgDCX-null parasites are corrected by reintroduction of a TgDCX coding sequen

196 This accumulation is corrected by reintroduction of wild-type FANCJ.

197 These abnormalities are corrected by removing the excess cholesterol from th

198 First, incidence rates were corrected by removing age-, sex-, and calendar year

199 esults indicate that NKT cell deficiency can be corrected by repeated alpha-GalCer treatment and that

200 The misfolding phenotype is corrected by replacing the HLA-B27 B pocket with one

201 ioral flexibility and that birth defects can be corrected by replenishing crucial growth factors.

202 aused by VEGF/SphK inactivity in these cells are corrected by replenishment of VEGF.

203 The defects are corrected by restoration of the missing BLOC-1 subun

204 nt amplitude and facilitated recovery, which was corrected by restoration of SMN1 in SMA MNs.

205 sing a narrow beam of ataxic Kcnc3-null mice were corrected by restoration of Kv3.3 channels specific

206 These defects are corrected by restoring Sply expression or by introdu

207 high bone mass of lipodystrophic mice could be corrected by restoring serum leptin level, suggesting

208 ry synaptic transmission in PMDS neurons can be corrected by restoring SHANK3 expression or by treati

209 This abnormality was corrected by restoring ADAMTS13 activity in cTTP ser

210 the development of red pulp macrophages that is corrected by retroviral Spi-C expression in bone marr

211 bject to 'treatment bias', some of which can be corrected by risk adjustment.

212 e first time, that OSS uncouples eNOS, which was corrected by RNAi of NOXO1.

213 tional error, which was usually minor, could be corrected by rotating the images as needed.

214 ed by broad-spectrum antibiotic therapy, can be corrected by selectively stimulating mucosal epitheli

215 suboptimal hemodynamic response, which could be corrected by sequential pacing.

216 OD/SCID mice and that this homing defect can be corrected by sequential treatment with chromatin-modi

217 These defects can be corrected by silencing the mitochondrial calcium unip

218 Both conditions were corrected by silencing the gene.

219 hemorrhage-induced reductions in muscle pO2 were corrected by SNO-Hb-repleted RBCs, but not by contr

220 ytes by TG2-/- peritoneal macrophages, which was corrected by soluble extracellular TG2.

221 e trafficking of some HERG LQT mutations may be corrected by specific pharmacological strategies.

222 The hypertension in the 10% hypomorphs is corrected by spironolactone or amiloride at doses tha

223 This defect in differentiation can be corrected by stimulating cells with the PPARgamma ago

224 s Paul Modrich showed how replication errors are corrected by strand-directed mismatch repair in Esch

225 ividual's phase shift to exogenous melatonin was corrected by subtracting their phase shift to placeb

226 with increased superoxide in the db/db mice, was corrected by superoxide scavenging.

227 with HAE-N (4 in each subcategory) and could be corrected by supplemental C1 inhibitor in 4 of them.

228 Importantly, all of these effects could be corrected by supplementation with IGF-1.

229 Clinically, this can be corrected by supplementation with recombinant Epo.

230 This defect was corrected by supplementation of exogenous neuraminid

231 P2 or Lyn knock-out on platelet response can be corrected by supplementing cyclic GMP.

232 The defect in epithelial invasion was corrected by supplying spb1 in trans.

233 pathogenic gain-of-function cascade that can be corrected by suppressing expression of the repeat tra

234 mutant outer membrane protein, OmpF315, can be corrected by suppressor mutations that lower lipopoly

235 n [+/-SE], 24.4+/-0.86), after which lesions were corrected by surgery or angioplasty if needed.

236 Impaired CTL responses to NS5 were corrected by syngeneic transfer of control DCs.

237 rulation defects in alpha(-) beta(-) strains were corrected by synthesis of chromosome-saturating lev

238 The M cell deficit in RANKL null mice was corrected by systemic administration of exogenous RA

239 onstrated that this underestimation of D can be corrected by taking diffusion during photobleaching i

240 meation in alpha-SNAP-deficient cells cannot be corrected by tethering multiple Stim1 domains to Orai

241 he 186 and 220 loops and the flip of Gly-219 are corrected by the active site inhibitor H-D-Phe-Pro-A

242 s and 95-kD/68-kD B-Raf ratios, changes that are corrected by the administration of OPC-31260 or OPC-

243 ction, metabolism, and antioxidative defense are corrected by the dose of ARI (sorbinil, 65 mg/kg/d i

244 psilateral misprojections in adcy8 morphants are corrected by the expression of an nrp1a rescue const

245 These defects are corrected by the introduction of a genomic copy of t

246 of mispairs are generated, but most of these are corrected by the mismatch-repair system.

247 hat ambiguous mistakes in bimanual movements are corrected by the non-dominant hand, and responsibili

248 r fold-changes <250-fold by QRTPCR and could be corrected by the calibration function F(c) = F(a(cDNA

249 simplifications of the TOPS diagrams and can be corrected by the development of more precise secondar

250 thology in dystrophin-deficient mdx mice can be corrected by the elevated production of nitric oxide

251 erizing drug, TBZ; both of these defects can be corrected by the high-copy suppressors.

252 ty on semisolid agar plates; this defect can be corrected by the introduction of ppk gene in trans.

253 intrinsic to the hemopoietic system and can be corrected by the re-expression of a wild-type FANCC g

254 These pathfinding errors can be corrected by the reexpression of DCC within OR111-7 t

255 SCs) derived from HD patient fibroblasts can be corrected by the replacement of the expanded CAG repe

256 This attenuation could be corrected by the single E627K amino acid change, furt

257 by gene conversion, the freshly mutated copy being corrected by the presence of the many other wild-t

258 table to a nonfermentable carbon source that is corrected by the expression of Bcl-x(L).

259 This deficiency is corrected by the expression of wild-type (wt) protein

260 This is corrected by the reintroduction of wild-type VHL, imp

261 However, this mislocalization was corrected by the addition of copper to cells via a p

262 d under anoxic photoheterotrophic conditions was corrected by the addition of DMB or B(12) to the cul

263 had a marked increase in blood glucose that was corrected by the addition of HK II overexpression.

264 Poor T cell responses to allostimulation were corrected by the activation and expansion process.

265 LTP) and enhancement of long-term depression were corrected by the AMPK inhibitor compound C (CC).

266 h excess protein levels and elevated mitosis were corrected by the in vivo administration of L-DOPA (

267 lity control procedures were applied; errors were corrected by the registry concerned.

268 Both of these biases were corrected by the updated model.

269 Many errors arising during replication are corrected by these exonuclease activities.

270 roliferation in Stat5b-/- splenocytes cannot be corrected by this treatment.

271 play low bone mass, and that this osteopenia is corrected by Tnf deletion.

272 functional and the structural abnormalities were corrected by topical cholesterol.

273 th HCT116 cells, in which the MMR deficiency was corrected by transfection with a vector containing t

274 7R4) showed a heat-sensitive phenotype that was corrected by transformation with serine palmitoyltra

275 icient, osteopetrotic Csf1(op)/Csf1(op) mice were corrected by transgenic expression of the precursor

276 SUR1 trafficking mutants, the defects could be corrected by treating cells with sulfonylureas or dia

277 This trafficking defect, however, could be corrected by treating cells with the oral hypoglycemi

278 trophy phenotype, and that the phenotype can be corrected by treatment of juvenile animals.

279 ect, the systemic hypertension in mice could be corrected by treatment with an exogenous NO source.

280 mia, and pancytopenia of DHFR deficiency can be corrected by treatment with folinic acid.

281 Both defects can be corrected by treatment with LCAT.

282 ere hereditary obesity and diabetes that can be corrected by treatment with the hormone.

283 n, HDMEC migration, and tube formation could be corrected by treatment with the PGT inhibitor T26A, c

284 The adhesive defect was corrected by treatment of TSP2-null fibroblasts with

285 tilatory responses to chronic hypoxia, which were corrected by treatment with a HIF-2alpha inhibitor.

286 ical features of scurvy; these abnormalities were corrected by treatment with vitamin C.

287 mical and cognitive defects in these mutants are corrected by treatments that modulate metabotropic g

288 These dangerous lesions are corrected by two primary pathways of double strand b

289 tions introduced by LTP and aniracetam could be corrected by uniform stretching of the responses, sug

290 principal cellular defect in FXS, which may be corrected by using mGluR antagonists.

291 e in acute lung injury, an effect that could be corrected by using PI3K inhibitors that are safe to u

292 ack of correlation produces bias that cannot be corrected by using reference materials alone.

293 integrin, whereby nonspecific rupture events were corrected by using a new mathematical approach.

294 Rates of illness were corrected by validating interview and family histor

295 /ank aortic smooth muscle cells and explants were corrected by Vanin-1 knockout.

296 anticoagulant protein C pathway in PAEC may be corrected by viral transduction of these cells.

297 The bias can be corrected by weighting techniques, which take into ac

298 These defects could be corrected by wild-type BTG3 but not by a mutant impai

299 marily because of extrinsic defects that can be corrected by WT leukocytes.

300 ot perform NER in the bulk of the genome and are corrected by XPC protein, which forms a complex with