ライフサイエンスコーパス: failure of @3 to

1 a threshold probability range of fast-track failure of 5% to 20% is used to determine who should be

2 ted (155) was primarily due to amplification failures of 1 to 3 targets.

3 etastases (CLM) have different biology after failure of oxaliplatin (FOLFOX) compared to 5-fluorourac

4 mild to moderate C. difficile infection and failure of a 6- to 8-week taper with vancomycin or at le

5 The market failure of antibiotics is due to a combination of scient

6 Failure of these mechanisms leads to a diverse spectrum

7 Failure of grassland soils to accumulate SOC was attribu

8 The failure of ppk1 spores to accumulate polyP results in a

9 Intravital imaging revealed a failure of the mutant neutrophils to accumulate at and s

10 The failure of the motor system to accurately predict less p

11 re of non-adherent behaviour may explain the failure of purely educational interventions to achieve s

12 of maturation was, in turn, promoted by the failure of M1 phagosomes to acidify.

13 Failure of the ECV to acidify would prevent both upregul

14 igen-presenting cell-T-cell axis rather than failure of neutrophils to act as effector cells and that

15 )beta(1) integrin expression, resulting in a failure of integrin to activate PP2A phosphatase, which

16 The failure of pancreatic beta cells to adapt to an increasi

17 oid leukemia (AML) is thought to reflect the failure of current therapies to adequately target leukem

18 The present review will explain why the failure of glucocorticoids to adequately manage patients

19 unction the result of a maladaptive UPR or a failure of the UPR to adequately adapt?

20 er of undesirable side effects and resultant failure of the patients to adhere to treatment.

21 ral lifestyles in the Levant by suggesting a failure of foraging societies to adjust.

22 processes are closely associated, the recent failure of antialbuminuric therapies to affect CV outcom

23 n in cardiomyocytes by 70% and resulted in a failure of desmin to align with Z disks and disrupted ce

24 The failure of transdermal nicotine to alter reward-related

25 arasitism; (iii) this behavior resulted in a failure of active copies to amplify which systematically

26 The perception exists that failure of antibiotic treatment due to antibiotic resist

27 mandible, and cleft palate resulting from a failure of palatal shelves to appropriately elevate and

28 e of CARM1 methyltransferase activity led to failure of cells to arrest in the G1 phase of the cell c

29 The innate immune deficits included the failure of bacterial foci to attract macrophages and NK

30 a reduction in the basal level of INa and a failure of PKA stimulation to augment the current that m

31 The failure of cell proliferation to be properly regulated i

32 d assessed how this would be affected by the failure of the interventions to be developed or scaled u

33 ifficulty may partially explain the frequent failure of AIV to become pandemic.

34 in a SERCA-dependent manner, leading to the failure of plasmatocytes to become activated and migrate

35 ely provide a biological explanation for the failure of these tumors to become invasive.

36 d 165 were demonstrated to contribute to the failure of maRAVV VP40 to bud from human cells, and resi

37 Analysis of times to infection indicates a failure of models to capture infrequent long-range conta

38 e due to high placebo response rates and the failure of standard statistical approaches to capture he

39 h the WT littermates at day 21, suggesting a failure of transition from acute to chronic inflammation

40 pathogenic missense mutations is a resulting failure of PC1 to traffic to cilia regardless of GPS cle

41 g HPS may be caused by capillary leakage and failure of lymphatic vessels to clear fluids.

42 s have also substantially contributed to the failure of translation of cardioprotection to clinical p

43 s independent of S1P-mediated chemotaxis and failure of FTY720 to close lymphatic stromal channels an

44 Failure of the optic fissure to close gives rise to an o

45 aling is very slow and is characterized by a failure of the wound epidermis to close across amputated

46 ngs might, at least partially, be due to the failure of glucocorticoid replacement therapy to closely

47 otype characterized by a decrease in valves, failure of Prox1(high) cells to cluster, and rounding of

48 low population density-may then result in a failure of the species to colonize, even if the habitat

49 ) is a cardiomyopathy caused by intrauterine failure of the myocardium to compact.

50 Failure of myelin to compensate for larger axonal diamet

51 onse to genetically induced obesity due to a failure of the beta-cells to compensate for peripheral i

52 g REG-1, which was confirmed by quantitative failure of an RPK1 mutation to complement the high and l

53 play parathyroid and thymus hypoplasia and a failure of these organ primordia to completely separate

54 cells whose function may reflect success or failure of the host to contain infection.

55 experiments demonstrated an almost complete failure of Hhex-null HSCs to contribute to lymphoid line

56 transplantation, there was a nearly complete failure of Mtg16(-/-) cells to contribute to thymocyte d

57 s and high parasite density, suggesting that failure of antibody to control parasitaemia may contribu

58 lack of NK activation may contribute to the failure of innate immune responses to control HIV at the

59 Motivated by the failure of LMMs to control type I errors in a GWAS of as

60 The failure of peri-TP mATG to control antidonor memory resp

61 target, as well as its possible role in the failure of, or resistance to, conventional anti-VEGF the

62 epithelial integrity and consequently in the failure of the alveoli to correctly respond to injury an

63 k of a known correlate of protection and the failure of a neutralizing antibody to correlate with pro

64 However, the failure of BMI to correlate with preschool asthma sugges

65 Failure of vaccination to curtail spread of this disease

66 Failure of subordinates to decrease their sniffing frequ

67 The failure of novel drug candidates to delay progression to

68 ecreased Akt phosphorylation, resulting from failure of the exocyst to deliver basolateral proteins t

69 Failure of OFOQ to detect HIV-1 infection was frequent a

70 ts resulting in STR in neutropenic patients, failure of passive surveillance to detect STR, and lack

71 h may be the main reason responsible for the failure of PBR to detect the occurrence of EBLF north of

72 Knockdown of AGBL2 results in a failure of the cell to detyrosinate the C-terminal EEY r

73 BIM that promotes deletion of the B cell and failure of mice to develop Abs to the Ag upon subsequent

74 t to test the extent to which the success or failure of S. hermonthica parasites to develop on a part

75 or selectivity of agonists, and the inherent failure of antibodies to differentiate between the large

76 Ultimately, inhibition of Wnt1 resulted in failure of oval cells to differentiate into hepatocytes

77 sulted in mitochondrial oxidative damage and failure of SODA/DeltasodA promastigotes to differentiate

78 reactivation which is likely linked with the failure of the monocytes to differentiate to a DC phenot

79 LA inhibits CXCR4 expression, resulting in a failure of monocytes to directionally migrate toward CXC

80 This model also replicated surprising failures of bees to discriminate certain seemingly highl

81 e temperature is indicated by the widespread failure of replicated chromosomes to disjoin.

82 pharmacologic efficacy is reconciled by the failure of bromodomain inhibition to displace endogenous

83 oproteins I and E, which may account for the failure of sensitive antibody tests to distinguish HSV-1

84 characterized in its most severe form by the failure of the forebrain to divide.

85 ization of base excision repair enzymes, the failure of cells to downregulate Mule after DNA damage r

86 e solutes in hemodialysis patients reflect a failure of passive diffusion methods to duplicate the ef

87 of circulating neutrophils, suggesting that failure of macrophages to efficiently clear apoptotic ne

88 Current theories attribute aging to a failure of selection, due to either pleiotropic constrai

89 t to transmission dynamics could explain the failure of bat culls to eliminate rabies and suggests th

90 investigate one possible explanation for the failure of CTLs to eliminate tumors, specifically, the c

91 tions in tumors, where it contributes to the failure of immune cells to eliminate cancer cells.

92 echanisms of HCV persistence or the frequent failure of interferon (IFN) to eliminate it.

93 served in GRTH-null mice (azoospermic due to failure of spermatids to elongate).

94 cantly, defects in root formation, including failure of the root to elongate, were observed by postna

95 3PHD-H3K4me3 binding was demonstrated by the failure of ING3PHD mutant proteins to enhance ING3-media

96 d mutations in the raw gene that result in a failure of the SGPs to ensheath the GCs, leading to defe

97 an established growth phase (anagen) caused failure of hair follicles to enter a normal catagen regr

98 sential for this nuclear localization, and a failure of TCA cycle enzymes to enter the nucleus correl

99 mediated knockdown of KHARON mRNA results in failure of the calcium channel to enter the flagellar me

100 cell quiescence supposedly contribute to the failure of imatinib mesylate (IM) to eradicate chronic m

101 persists for the life of the host due to the failure of the immune response to eradicate the bacteriu

102 Failure of the immune system to eradicate viruses result

103 eventually recur; this is attributed to the failure of TKI treatment to eradicate leukemia-initiatin

104 -Fos homozygous mice lack osteoclasts with a failure of the teeth to erupt and with an arrest of root

105 Furthermore, we show that failure of transcription complexes to escape the pause r

106 renchyma in FTY720-treated animals, due to a failure of the cells to establish adhesion on the sinus,

107 repro8 causes male-limited infertility, with failure of spermatocytes to exit meiotic prophase via th

108 The failure of TACE to exit the endoplasmic reticulum in the

109 ed by turnover of Aep3p, as evidenced by the failure of aep3 mutants to express a recoded ARG8(m) whe

110 Our data indicate that the failure of Dd2 to express the sialic acid-independent in

111 The failure of mESCs to express IFNalpha/beta was further de

112 y we show that the underlying mechanism is a failure of spinal motor neurons to extend axons to their

113 Conformational diseases result from the failure of a specific protein to fold into its correct f

114 sence of an accessible end; in addition, the failure of aberrant RNAs to fold into compact structures

115 In conclusion, our findings suggest that the failure of a repressive complex to form or stabilize in

116 We set out to investigate if the failure of cultured mesenchyme cells to form bioengineer

117 n result in decreased cell proliferation and failure of dorsal anterior cartilages to form.

118 e ear is abnormal projection outgrowth and a failure of fusion to form the semicircular canal pillars

119 nt evidence that the primary cause of DRS is failure of the abducens nerve to fully innervate the lat

120 that disrupted endocytic trafficking led to failure of F to function with M for VLP assembly.

121 1a in cerebellar cultured neurons leads to a failure of lysosomes to fuse with endosomes and autophag

122 VDR) deficiency (knockout [KO]) results in a failure of mice to generate an airway hyperreactivity (A

123 nhibited by SSB, possibly accounting for the failure of RecA to generate products in the presence of

124 Seed dormancy is defined as a temporary failure of a viable seed to germinate in conditions that

125 Thermoinhibition, or failure of seeds to germinate at warm temperatures, is c

126 The size reduction results from a failure of muscle fibers to grow during early postnatal

127 The failure of excess RppH to hasten rpsT P1 and yfcZ degrad

128 hout the co-depletion of topo IIbeta, is the failure of chromosomes to hypercompact when delayed in M

129 Failure of SRY expression due to hypermethylation was fu

130 lation outside the ICU for acute respiratory failure of heterogeneous causes and to identify the pred

131 lic volume in both groups, consistent with a failure of CI to improve a 25% decrease in interstitial

132 Due to the failure of current therapeutics to improve outcomes in p

133 he uncoupling is interesting in light of the failure of experimental Abeta therapies to improve mild

134 parg-BKO mice, an effect associated with the failure of rosiglitazone to improve liver insulin recept

135 as a central target in glioma and traces the failure of existing drugs to incomplete/nondurable inhib

136 t of the cardiac cell cycle in M-phase and a failure of cardiomyocyte progenitors to incorporate into

137 This therapeutic effect is associated with a failure of CD8 T cells to increase tissue homing recepto

138 result from impaired insulin secretion due a failure of insulin content to increase with age.

139 nitoring committee recommendation due to the failure of linsitinib to increase either progression-fre

140 diversity dependence comes largely from the failure of species richness to increase with clade age i

141 ignificant progress has been hindered by the failure of C. trachomatis to induce clinically relevant

142 The mechanisms underlying the failure of C5aR1(-/-) BMDCs to induce experimental aller

143 ology, which has usually been interpreted as failure of p53 to induce senescence.

144 ments was the sole independent predictor for failure of PVS to induce ejaculation.

145 We report a case of failure of clindamycin therapy due to inducible clindamy

146 egulation of activity in the DMN, and that a failure of this regulation leads to inefficient cognitiv

147 We propose that failure of plzA mutant cells to infect mice was due to a

148 therapy studies have shown that a persistent failure of activated lymphocytes to infiltrate tumors re

149 The loss of efficacy correlated with failure of the knockout CTLs to infiltrate into tumors u

150 educed ketone body oxidation correlates with failure of ketone bodies to inhibit fatty acid oxidation

151 lopment of resistance has been attributed to failure of the antibody to inhibit phosphoinositide 3-ki

152 inical models, focusing on the successes and failures of this research to instruct and translate clin

153 n heavy-chain locus (Igh), consistent with a failure of AID to interact with the endonuclease APE1.

154 The mechanism involved failure of APC to interact with the cytoplasmic domain o

155 nd EAAT4 from the Golgi is disrupted through failure of the L253P mutation to interact with Arp1.

156 ant of S. cerevisiae Fob1 were caused by the failure of the proteins to interact with two members of

157 of SNX1 expression via RNAi resulted in the failure of D(5)R to internalize and bind GTP, blunting o

158 Failure of cancer surgery to intraoperatively detect and

159 of TWIST1, SNAI2, and ZEB2 induction, and a failure of cells to invade and metastasize.

160 y, we reported that this pattern indicates a failure of the seizure to invade the area, because of a

161 A in archived specimens may have been due to failure of the extraction method to isolate DNA from fix

162 A failure of cytotoxic T cells to limit or contract inflam

163 a suggest that these defects result from the failure of activated RhoA to localize at intercellular i

164 Failure of mutant polycystins to localize to cilia aboli

165 K and ERK activation was responsible for the failure of monocyte-to-macrophage differentiation, in tu

166 hoproliferative syndrome (ALPS) represents a failure of apoptotic mechanisms to maintain lymphocyte h

167 ot defect arises during germination and is a failure of bps1 mutants to maintain their shoot apical m

168 We propose that failure of c-MYC to maintain these tumors is the result

169 The failure of cells to maintain mitotic arrest, due to lack

170 Synapse loss can be caused by the failure of live neurons to maintain functional axons and

171 ion results, in part, from a cell-autonomous failure of MuSC to maintain the damage-repair cycle init

172 tn mutant mice, which is consistent with the failure of OHC stereocilia to maintain stable interactio

173 oss of chic function in the soma resulted in failure of somatic cyst cells to maintain germ cell encl

174 untoward long-term side effects and ultimate failure of the agent to maintain strength.

175 negative staff attitudes and behaviour, and failure of services to make reasonable adjustments.

176 way appears to play an important role in the failure of immune reactivity to malignant plasma cells i

177 The failure of ltn1 cells to manage mHtt was traced to anoth

178 The failure of a code to match its owner at a later time poi

179 In summary, failure of podocytes to match glomerular tuft growth in

180 n discrimination observed in microbes is the failure of genetically distinct colonies to merge freely

181 HSCR is caused by the developmental failure of ENS progenitors to migrate into the gastroint

182 , leading to widespread infection due to the failure of leukocytes to migrate into infected tissue si

183 sufficient paraxial mesoderm, rather than a failure of mesoderm precursors to migrate away from the

184 RNA polymerase II recruitment and results in failure of the locus to migrate to the nuclear interior,

185 association and causation may result from a failure of oral vitamin D to mimic the effect of dermall

186 of the demographic costs associated with the failure of a species to modify its phenology in response

187 The failure of drugs to modify pain end points in clinical t

188 teractions are responsible, in part, for the failure of association studies to more fully explain com

189 This failure of HuRDelta/Delta mice to mount a T cell-depende

190 The failure of TRB3(-/-) islets to mount an optimal JNK acti

191 he newborn intestine inhibits TLR4, and that failure of NOD2 signaling leads to NEC through increased

192 Failure of the ECV to neutralize would result in a vacuo

193 The failure of these phases to occur in a timely, progressiv

194 ced filament elongation, ovule abortion, and failure of flowers to open.

195 P1 knockout females is impaired because of a failure of sperm to penetrate the cumulus.

196 in the system decreases primarily due to the failure of parasite species to persist.

197 This accounts for the failure of signaling-based biomarkers to predict clinica

198 industrialized countries may result from the failure of current vaccines to prevent nasopharyngeal co

199 /3 deficiency caused by disruption of PCSK1, failure of enteroendocrine cells to produce functional h

200 aternally inherited TE families, caused by a failure of the maternal strain to produce the piRNAs nec

201 One practical consequence is the failure of most quantification assays to properly detect

202 that defects in dorsal closure can result in failure of the amnioserosa to properly degenerate, which

203 6) identifies a form of ASD resulting from a failure of the brain to properly import amino acids.

204 ed to defects in CNS regeneration, including failure of the cephalic ganglia to properly pattern and

205 Failure of T cells to protect against cancer is thought

206 The failure of traditional mixed superacids to protonate wea

207 e ETA assumption for valid inference and the failure of conditional regression to provide marginal es

208 The failure of fava bean consumption to provoke natriuresis

209 Bundle failure occurred by failure of cross-links leading to pull-out of microtubul

210 Failure of this transition leads to pulmonary hypertensi

211 e extinction of apes in the late Miocene and failure of Old World monkeys to radiate into multiple sp

212 Despite the recent failure of therapies designed to raise HDL-cholesterol i

213 rast, no-go decisions are best captured by a failure of the execution process to reach the decision t

214 is a pathology of pregnancy that results in failure of the fetus to reach its genetically determined

215 The failure of knockdown approaches to recapitulate the chan

216 lege of Cardiology; 4) major reasons for the failure of physician-scientists to receive funding from

217 toimmune and allergic phenomena because of a failure of the immune system to receive proper microbial

218 Failure of the chaperone system to recognize or fold the

219 esponse to FVIII-PS could be due either to a failure of the immune system to recognize the antigen (i

220 show that the splicing defect is due to the failure of U2AF(65) to recognize the pseudouridylated po

221 Some critics have claimed that failures of IARC Working Groups to recognize study weakn

222 Failure of Il1rl2(-/-) mice to recover from DSS-induced

223 These data suggest that the failure of pineal function to recover is not attributabl

224 f decreased p65 promoter recruitment or of a failure of bound p65 to recruit p-RNAP II.

225 before the onset of angiogenesis resulted in failure of invading endothelial cells to recruit pericyt

226 Failure of NKp65 to recruit Syk is not due to an alterat

227 was confirmed by in situ hybridization and a failure of disease to recur after CD3 T cell depletion.

228 The disproportionate failure of regenerating tubules to redifferentiate in ra

229 h persistent activation of NPY neurons and a failure of leptin to reduce the firing rate or hyperpola

230 The failure of niacin to reduce cardiovascular events in two

231 d severity of IgA nephropathy, may reflect a failure of rituximab to reduce levels of specific antibo

232 oal-directed therapy was associated with the failure of this intervention to reduce postoperative mor

233 comes from excellent clinical outcomes, the failure of treatment intensification to reduce residual

234 in activated, but not quiescent, SCs causes failure of the cells to reestablish quiescence and allow

235 ller CNVs in individuals with autism and the failure of most large hotspots to refine to single genes

236 The failure of axons to regenerate was strongly correlated w

237 Failure of fibrotic liver to regenerate after resection

238 al cord and other types of CNS injury is the failure of injured axons to regenerate and to re-build t

239 injury to CNS fiber tracts is accompanied by failure of severed axons to regenerate and results in li

240 The failure of the CNS neurons to regenerate axons after inj

241 The failure of sRNAs to regulate target mRNAs in these mutan

242 euristic model suggests that for some women, failure of the GABAA receptor to regulate overall GABA-e

243 ronal signals in the dACC, but also a common failure of dACC lesions to reliably abolish conflict-dri

244 Failure of SAs to remodel is causally associated with pr

245 We postulate that the failure of tissue macrophages to remove senescent erythr

246 This dysfunction appeared rooted in a failure of Sun2-null cells to reorganize their microtubu

247 The mechanisms underpinning the failure of inflammation to resolve in diseased musculosk

248 Prolonged ileus-the failure of postoperative ileus to resolve within a few d

249 hronic inflammatory diseases may represent a failure of the inflammatory twitch to resolve toward bas

250 ever, it is becoming increasingly clear that failure of some patients to respond to checkpoint inhibi

251 l sodium channel (ENaC) is attributed to the failure of mutated CFTR to restrict ENaC-mediated Na(+)

252 The failure of TI plasmablasts to secrete IgM was not a cons

253 overexpressing neurons could be linked to a failure of plasticity-inducing protocols to selectively

254 Failure of Deltaami1 mutant cells to separate also led t

255 The disappointing recent failure of fluoroquinolone-containing regimens to shorte

256 gnition has largely focused on successes and failures of animals to solve certain cognitive tasks, bu

257 hermal sensitivity in predicting the success/failure of symbionts to spread into novel species follow

258 AH, we demonstrated reduced FA oxidation via failure of palmitoylcarnitine to stimulate oxygen consum

259 The failure of S193A livers to stop regeneration correlates

260 esolution of lung fibrosis is blocked by the failure of adenosine levels to subside.

261 Failure of the DvH to successfully transition contribute

262 niacin and places them in the context of the failure of AIM-HIGH to support the HDL-C-increasing hypo

263 sent from NT3/TrkA endosomes, explaining the failure of NT3 to support retrograde TrkA transport and

264 The failure of CREMalpha to suppress Syk expression in SLE T

265 ose homeostasis is driven by a near complete failure of insulin to suppress hepatic glucose productio

266 However, failure of Lats1/2 knockdown to suppress LKB1-mediated Y

267 rikingly, the biological consequences of the failure of MC1R variants to suppress PI3K/AKT signaling

268 A and putamen to levodopa, which heralds the failure of neural networks to suppress involuntary dyski

269 ed astroglia into scar borders, and caused a failure of astroglia to surround inflammatory cells, res

270 This failure of HAS1 to synthesize hyaluronan was compensated

271 lastic syndrome (MDS) has been attributed to failure of current chemotherapeutic regimens to target l

272 tation of the GLR genes GLR1 and GLR2 causes failure of sperm cells to target the female reproductive

273 ab5 binding and PLA1 activation and caused a failure of VipD mutant proteins to target to Rab5-enrich

274 akage from intermediate-depth strata through failures of annulus cement, three to target production g

275 are 35-40% of normal, ICL damage results in failure of XPF to localize to telomeres, markedly increa

276 Disrupting both domains led to a complete failure of Pcdh15a to localize to the hair bundle.

277 reduction in proliferation, suggesting that failure of progenitor proliferation contributes to the h

278 damage, and restore tissue homeostasis, and failure of this response contributes to the pathology of

279 Despite the failure of virus spread to the tumor, infection resulted

280 of elucidating the mechanisms underlying the failure of effective immunity to this emerging infectiou

281 crucial for maintaining tissue homeostasis, failure of which can lead to tissue degeneration or hype

282 The adjusted HR of failure of the microstent relative to trabeculectomy was

283 rs, questions have been raised regarding the failure of some preclinical work to translate to clinica

284 onsible for low levels of IFN-beta caused by failure of MOLF STING to translocate from the endoplasmi

285 e Rap1 GTP loading in CLL cells results from failure of Rap1-containing endosomes to translocate to t

286 The failure of clinical trials to treat sepsis demonstrates

287 pattern of abnormality may contribute to the failure of medication to treat symptoms in these individ

288 lationship between programmed parameters and failure of modern ICDs to treat VF.

289 bcallosal cingulate has been associated with failure of response to treatment in MDD, and it is a pot

290 d extent of sperm-egg fusion is not due to a failure of Tpst2-null sperm to trigger establishment of

291 gl2-deficient mice show valve aplasia due to failure of endothelial cells to undergo rearrangements a

292 sition of basement membrane, and a resultant failure of hearts to undergo cell movements associated w

293 s due to a reduction in beta-cell mass and a failure of pancreatic islets to undergo compensatory hyp

294 erved, resulting from impaired apoptosis and failure of the anterior mesenchyme to undergo SOX9-depen

295 Failure of trabecular myocytes to undergo appropriate ce

296 This delay is characterized by the failure of neonatal lungs to upregulate proinflammatory

297 Our data also may shed light on the failure of strategies to use MMP inhibitors in cancer tr

298 acial grimacing when attempting to smile and failure of the urinary bladder to void completely despit

299 sence of a functional oral periderm and that failure of this process contributes to VWS.

300 t immunization schedules, exacerbated by the failure of vaccines to work in the first months of life.