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 rient status vary with inflammation, and can be corrected by a regression-based approach [Biomarkers

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

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

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

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

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

8 effects of staining on the tissue phase maps were corrected by a mathematical normalization.

9 Postoperatively, esotropia and head turn were corrected by a mean of 31.3 PD and 18.2 degrees, re

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

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

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

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

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

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

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

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

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

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

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

21 patients with complete DiGeorge syndrome can be corrected by allogeneic thymus transplantation.

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

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

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

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

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

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

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

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

30 We show that the gametogenesis defects can be corrected by ASF1A and ASF1B transgenes, and that ASF

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

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

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

34 was impaired in gigaxonin-null zebrafish and was corrected by both pharmacological activation of the

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

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

37 This abnormal rheology cannot be corrected by changing pH or calcium levels in the bat

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

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

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

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

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

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

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

45 Hypertriglyceridemia was corrected by coinfection of mice with recombinant ad

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

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

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

49 ) binding, but most aberrant binding effects were corrected by compensatory mutations.

50 These defects could be corrected by complementation of ompA.

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

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

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

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

55 Each abnormality was corrected by corresponding morphology-directed repai

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

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

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

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

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

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

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

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

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

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

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

67 21% because of distal pressure drift; these were corrected by disengagement of the guiding catheter

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

69 Small looped mispairs are corrected by DNA mismatch repair.

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

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

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

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

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

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

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

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

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

79 ovascular leakage in CD31-deficient mice can be corrected by enhancing the glycolytic flux via pharma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 These phenotypic alterations were corrected by gene complementation.

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

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

106 These adverse effects are corrected by heating the immersion objective or avoi

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 germline induces double-stranded breaks that are corrected by homology-directed repair, which copies

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

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

113 Diabetes was corrected by IK transplantation in all pancreatectom

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

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

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

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

118 Here, the thermal transport equation is corrected by including heat absorption due to phase t

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

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

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

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

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

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

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

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

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

128 This has now been corrected by inserting an additional reference at p

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

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

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

132 This overestimation was corrected by introducing a multiplication factor of

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

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

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

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

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

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

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

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

141 21Cip1 and senesced prematurely; this defect was corrected by knocking down CDK inhibitor levels with

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

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

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

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

146 ere, the dispersion of refractive components is corrected by leveraging the inherent dispersion of me

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 form of consecutive esotropia and exotropia were corrected by means of 26.1PD and 65.6PD while recur

152 ecurrent exotropia and recurrent hypertropia were corrected by means of 34.3PD and 11PD respectively

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

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

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

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

157 ore fusion, differences persisting at fusion are corrected by modulating fusing front width within ea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 tion rate, indicating that Pole-P301R errors are corrected by Poldelta proofreading and MMR.

180 rors in the alignment of peaks, which cannot be corrected by post hoc application of batch effect cor

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

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

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

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

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

186 These effects were corrected by rapamycin treatmentin vivo Importantly

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

188 ed cortical maps in adult Fmr1 knockout mice was corrected by rectifying the chloride imbalance durin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 We found that a vast majority of errors can be corrected by sampling more clones per tumor, and by i

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

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

220 Both were corrected by specific procedures.

221 asticity in the Ts65Dn mouse model of DS can be corrected by specifically targeting nonlinear dendrit

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

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

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

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

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

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

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

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

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

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

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

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

246 subset of model states whose dynamics should be corrected by the ANN by examining the correlation bet

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

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

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

250 ced defect in proline utilization, which can be corrected by the heterologous expression of human MCU

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

252 d-generation sequencing (TGS) long reads can be corrected by the high-quality second-generation seque

253 ulating OT in cerebrospinal fluid, which can be corrected by the oral administration of nicotinamide

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

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

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

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

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

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

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

261 Subsequently, the minor deviation is corrected by the formation of coherent twin boundarie

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

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

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

265 This perturbed trajectory was corrected by the NKCC1 antagonist bumetanide and acc

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

267 Both were corrected by the addition of exogenous Xkid (Xenopu

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

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

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

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

272 yond which long reads are too error-prone to be corrected by these methods.

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

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

275 tient's skin fibroblasts, and this phenotype was corrected by transfection with the wild-type but not

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

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

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

279 abnormalities and impaired cell growth that are corrected by treatment with myriocin, a sphingolipid

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

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

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

283 Both defects can be corrected by treatment with LCAT.

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

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 myocardial injury, cardiomyocyte loss cannot be corrected by using currently available clinical treat

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 show that this potential structural bias can be corrected by using the appropriate non-isotropic kern

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

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

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

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