ライフサイエンスコーパス: failure to

1 bitor without a washout period after primary failure to a first TNF inhibitor.

2 Failure to account for fluctuation-dependent coexistence

3 Pershing et al concluded that failure to account for temperature in the assessment and

4 Failure to account for this source of calories in critic

5 Failure to accumulate was partly the result of chronic s

6 ear probabilities of chronic persistent DME (failure to achieve a central subfield thickness <250 mum

7 an 12 months since last dose of rituximab or failure to achieve at least a minor response.

8 ry prevention ICD implantation were low, and failure to achieve GDMT was associated with significantl

9 with an onset during infancy that results in failure to achieve motor milestones and in death or the

10 ged exposure to immunosuppressive therapies, failure to achieve tolerance, and inadequate clinical re

11 Failure to acknowledge the limitations of clinical trial

12 ponse to muscle loading resulting in chronic failure to adapt and remodel.

13 satisfied modeling assumptions and, notably, failure to address batch-specific truncation of low abun

14 Failure to address inpatient penicillin allergies result

15 The agency's failure to adequately account for the risks of perchlora

16 e maintenance of memory representations, not failures to adequately encode stimuli.

17 The higher the rates of failure to adhere to the protocol and dropout from the s

18 easons for failed GlideScope intubation were failure to advance the tube into the larynx or trachea (

19 Failure to aggressively use mOPV to respond to circulati

20 Hemispatial Neglect (HN) is a failure to allocate attention to a region of space oppos

21 Failure to amplify the mitochondrial cytb gene of Nycter

22 ital-level rates of secondary complications (failure to arrest complications) vary widely, are associ

23 Failure to assemble adequate perisomatic inhibition is t

24 Hereby, failure to assemble higher molecular weight complexes of

25 Failure to assemble such complexes provoked photodynamic

26 of drugs that may cause or exacerbate heart failure to assist healthcare providers in improving the

27 Failure to attain uterine receptivity will impede blasto

28 , particularly at 40 degrees C, suggesting a failure to autoregulate at high-input states.

29 size that raphe dysfunction contributes to a failure to autoresuscitate from multiple hypoxic events,

30 ility attributed to their hydrophobicity and failure to be inserted into viral membranes.

31 ors by undergoing structural plasticity, and failure to be resilient and preserve normal structure an

32 Failure to branch is restricted to regions where YAP act

33 ted with outcomes of remission and treatment failure to CBT and antidepressant medication and survive

34 Failure to clear amyloid-beta (Abeta) from the brain is

35 tent PFOS treatment in mice finally led to a failure to clear the pathogen completely.

36 ted in significantly more severe disease and failure to clear the virus.

37 Hsp104 deficiency curing is a result of failure to cleave the Sup35p amyloid filaments to make n

38 The primary outcome of reducing the failure to collect >/=2 x 10(6) CD34(+)/kg recipient wei

39 The rate of failure to collect a sample and the mean time for perfor

40 voices in ASD individuals could be due to a failure to combine acoustic features, even though such f

41 Failure to complete genome replication and defective che

42 a sativa) seeds exhibit thermoinhibition, or failure to complete germination when imbibed at warm tem

43 common reasons for removal are anestrus and failure to conceive.

44 on of the variant histone H2aV, we find that failure to concentrate FLASH and/or U7 snRNP in the HLB

45 sporidium and Escherichia coli, we show that failure to consider biphasic pathogen dynamics can lead

46 es of fear' in natural systems may stem from failure to consider dynamic temporal changes in predatio

47 Failure to consider the geomorphic context of stream net

48 w insight into the mechanisms underlying the failure to control autoimmunity in T1D and might lead to

49 reduced somatic hypermutation coupled with a failure to control chronic viral infection.

50 Instead, failure to control HCV replication was likely caused by

51 In chronic hepatitis B (CHB), failure to control hepatitis B virus (HBV) is associated

52 neoformans is a consequence of the combined failure to control pulmonary fungal replication and immu

53 The failure to control TB stems from an incomplete understan

54 nd increased mortality, which indicates that failure to convert macrophages from the F4/80(int)CD206(

55 Failure to coordinate the cell cycle in early cleavage a

56 rom aberrant morphogenetic cell movements to failure to correctly orient structures, such as hairs an

57 rs700635[C] is also associated with failures to correctly splice out CASP8 intron 8 in breas

58 nd consequently degraded by SCF(FBW)(7alpha) Failure to degrade SOX9 promotes migration, metastasis,

59 health-care delivery, and concern about its failures to deliver social benefit, has driven a search

60 e in tolerized macrophages is accompanied by failure to deposit active histone marks at promoters of

61 lass of substrates for this pathway, and the failure to destroy misfolded proteins is associated with

62 Failure to detect clinical deterioration in the hospital

63 Based on failure to detect FP markers in exudate samples, we conc

64 l limitations-the most significant being the failure to detect low levels of infection.

65 Failure to detect the predicted T-shaped intermediate tr

66 s critical for avoiding predation [4,5], and failure to detect these calls [6,7] as a result of anthr

67 sults strongly suggest there is frequently a failure to detect trophozoites in routine examination, r

68 tor assessment of a patient's risk for heart failure to determine eligibility.

69 ofacial abnormality in humans and represents failure to develop 1 or more permanent teeth.

70 al progenitors results in hydronephrosis and failure to develop a patent pelvic-ureteric junction.

71 Although our failure to develop an efficient barcode joining scheme p

72 ens as one possible mechanism leading to the failure to develop or loss of oral tolerance.

73 ients with acetaminophen-induced acute liver failure to develop sepsis, which may culminate in multip

74 Failure to diagnose B12 deficiency can have dire consequ

75 Failure to diagnose late-onset type 1 diabetes can have

76 Failure to diagnose primary hyperparathyroidism and refe

77 Failure to diagnose transient ischaemic attack is a wast

78 Confusion arises from failure to distinguish between a genetically transmitted

79 one neuropeptide (oxytocin), combined with a failure to distinguish between different social domains,

80 shortcomings in the authors' case, such as a failure to distinguish proximate and ultimate explanatio

81 d the production of longer 3'-UTR mRNAs, and failure to do so leads to aberrant splicing and producti

82 f CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.

83 Failure to downregulate Wnt signaling can result in embr

84 associated opportunistic infections due to a failure to effectively engage in care, highlighting the

85 Failure to effectively resolve MG activation can be prob

86 eased propensity of beta events predicts the failure to effectively transmit information through spec

87 ening complication directly related to renal failure to either an early or a delayed strategy of rena

88 he development of curative treatments as the failure to eliminate therapy-persistent leukemic stem ce

89 p in some individuals, which may be due to a failure to eliminate viral RNA and Ag and/or persistent

90 n via massive vesicle release and subsequent failure to endocytose lost vesicles.

91 MC, thus highlighting distinct reasons for a failure to engage in the desired behavior.

92 showed: accumulation of FAS-mutated B cells; failure to enrich single V, D, J genes and single V-D, D

93 We investigate the failure to ensure COs in juvenile male mice.

94 These government actions, and the failure to ensure humane prison conditions, constitute v

95 cells, genetic ablation of SOX2 results in a failure to establish acini but not ducts.

96 polarity is established, however there is a failure to establish action potential firing.

97 rest, differentiation of leukaemic cells and failure to establish leukaemia in immunodeficient mice.

98 Thus, failure to establish long-term protective Ab titers agai

99 Failure to establish the FGF-dependent glia structure di

100 Failure to evidence this neural profile after the age of

101 uses of and potential solutions for apparent failures to exert the mental effort required of us.

102 tibility to subsequent asthma stemmed from a failure to expand functional neuropilin-1(+) regulatory

103 adverse effects of surgery (52 [30.4%]) and failure to explain alternative treatment options (17 [9.

104 ost common informed consent allegations were failure to explain risks and adverse effects of surgery

105 of a variant Hox gene repertoire and by the failure to express a key enzyme involved in retinoic aci

106 accumulated bystander mutations indicating a failure to express their products at the cell surface in

107 could suggest a genetic association, but the failure to find consistent evidence of this phenotype in

108 Low activity could result from either failure to form a functional Cas9-gRNA complex or inabil

109 ulated phagosomal maturation, resulting in a failure to form an activation-induced Rab7(+) endosomal/

110 We propose that failure to form discrete chromosome territories is the c

111 sordered assembly of Sep4 and the subsequent failure to form infection cushions, suggesting that prop

112 requires the import receptors Tom70/71, and failure to form these structures exacerbates preexisting

113 down GATA3 in primate embryos resulted in a failure to form trophectoderm.

114 Failure to fully implement this program results in struc

115 ructure, potentially explaining a subsequent failure to function as a transcriptional activator of Il

116 g problem of over-fitting and the subsequent failure to generalise.

117 of Hsp104 function in yeast cells leads to a failure to generate new propagons, the molecular entitie

118 51 or Brh2 caused accelerated senescence and failure to generate survivors on semi-solid medium.

119 vars are susceptible to thermoinhibition, or failure to germinate at temperatures above approximately

120 ype 1-infected patients with prior virologic failure to HCV DAA-containing therapy.

121 PE as PPE, which could potentially result in failure to identify a life-threatening disorder causing

122 ministered TRPA1 agonists justifies previous failure to identify a precise link between AIs and AIMSS

123 rences about population processes, where the failure to identify both short- and long-term ecological

124 The failure to identify mutation carriers among probands rep

125 atients with paracetamol-induced acute liver failure to identify those needing emergency liver transp

126 Failure to improve clinical outcome occurred even though

127 Failure to improve engagement in HIV care in the United

128 Failure to improve the 6MWT distance by at least 20% was

129 Failure to improve with appropriate first-line antibioti

130 lethality in mice, which was associated with failure to inactivate mTORC1 during fasting.

131 ta Ser(389) to Ala mutant mice, we show that failure to inactivate nuclear GSK3beta by Ser(389) phosp

132 Redefining induction failure to include morphologic induction failure and/or

133 Our results show that failure to incorporate human dimensions into ecosystem m

134 The failure to increase insulin sensitivity after training c

135 idation after training and contribute to the failure to increase insulin sensitivity.

136 they are valuable for identifying points of failure to increase network resilience in, for example,

137 Despite the widespread failure to increase ploidy prior to entering meiosis, th

138 nadequate beta-cell expansion accompanied by failure to induce PRLR-dependent target genes regulating

139 ads to primary cilia defects and a resultant failure to inhibit growth factor signaling.

140 l of this work is to bridge microscopic cell failure to macroscopic manifestations of aging.

141 visceral adiposity, lower exercise capacity, failure to maintain core body temperature during cold st

142 Self-care is vital for patients with heart failure to maintain health and quality of life, and it i

143 ncided with liver dysfunction reflected by a failure to maintain hydrogen sulfide production or apoli

144 months after stopping TKI was predictive of failure to maintain MMR later on.

145 Failure to maintain NFkappaB signals after the peak of t

146 howed impaired production of ribosomes and a failure to maintain proliferative capacity after stimula

147 Factor A increased the risk of failure to maintain step-down treatment most significant

148 We hypothesized that failure to maintain the same PGC surface before and afte

149 tivity, and poor recovery was predicted by a failure to maintain ventral anterior cingulate cortex ac

150 f normal cell geometry can be explained by a failure to maintain wall stiffness specifically at geome

151 shortfall in health-care professionals; and failure to match inpatient and acute care facilities to

152 -mediated control of viral replication and a failure to mature local antigen-presenting cells (APCs).

153 plete adjustment for confounding factors and failure to measure lifetime use or the pattern of alcoho

154 Failure to meet a threshold improvement in the oxygenati

155 We propose that failure to meet excessive metabolic challenges coupled w

156 Trial ineligibility was mostly due to failure to meet inclusion criteria (87% of screening ass

157 d relatively inflexible both in terms of the failure to modulate the magnitude of lose-shift strategy

158 whereas 24 (10%) developed progressive heart failure to New York Heart Association functional classes

159 Interpreting a failure to observe priming may not be as simple as Brani

160 ts effectiveness is frequently undermined by failure to obtain follow-up colonoscopy after positive t

161 Failure to obtain informed consent and associated medica

162 To investigate the failure to obtain informed consent as an allegation in m

163 age-related learning deficits emerge from a failure to optimize learning according to the three fact

164 MENT Infertility affects 15%-20% of couples; failure to ovulate is a common cause.

165 nts have differing GABA dependencies and the failure to parse WM into components would lead to missin

166 lar signature consistent with exhaustion and failure to participate in antimicrobial defense.

167 Specifically, the failure to perceive T2 was foreshadowed by a T1-induced

168 s might have evidence regarding refusal; and failure to permit overrules could weaken trust in the do

169 ontributes to human diseases ranging from BM failure to premature aging syndromes and cancer.

170 of donor cells near the lesion epicenter and failure to produce functional improvement in an all-fema

171 bility to acidify media during growth due to failure to produce oxalic acid.

172 .70 vs 2.77 instances per hour, P = .03) and failure to progress (mean, 1.20 vs 0.13 instances per ho

173 eficiency in FLS leads to S-phase arrest and failure to progress through the cell cycle.

174 were influenced by residual confounding and failure to propagate uncertainty (i.e., account for the

175 cal dynein inhibition in zebrafish result in failure to properly distribute mbp mRNA in oligodendrocy

176 UVB-induced DNA damage, including through a failure to properly suppress DNA synthesis on UVB-damage

177 ed with D2/3 antagonist radiotracers, is the failure to provide information about D2/3 receptors conf

178 receptive fields were expanded, suggesting a failure to prune divergent retinal inputs.

179 We examined rates of claim reversal (failure to purchase approved prescription), delayed init

180 mptoms, lymphadenopathies, and/or multiorgan failure to rapidly document the diagnosis and provide ti

181 s and irregular fluctuations that indicate a failure to reach a steady state.

182 Fluctuations in progeny production and failure to reach population equilibrium at the genomic l

183 omly assigned 2157 patients with acute heart failure to receive a continuous intravenous infusion of

184 erformed to identify factors associated with failure to receive annual testing during antipsychotic t

185 EGFR-TKI use, EGFR-TKI resistance mutation, failure to receive EGFR-TKI after WBRT/SRS, or insuffici

186 ndomly assigned patients with advanced heart failure to receive either the new centrifugal continuous

187 ng (reported as adjusted OR [95% CI]), lower failure to receive testing was associated with older age

188 ins commonly cause adverse effects reflect a failure to recognise the limitations of other sources of

189 Failure to recognize pelvic compensation can lead to und

190 problems, financial/employment problems, and failure to recognize the family were also statistically

191 " Multiple definitions of the same term, and failure to recognize their underlying assumptions, have

192 Failures to recognize or adequately process these genomi

193 cyte/monocyte progenitor cell apoptosis, and failure to reconstitute peripheral myeloid populations.

194 The reasons for this failure to recover are not established although the exte

195 rolyte leakage were directly associated with failure to recover from drought upon rewatering in Brass

196 e triple mutant T-bet is associated with its failure to recruit chromatin remodeling complexes to the

197 Failure to recruit p300 during either phase leads to abo

198 dopaminergic state following withdrawal, the failure to reduce immobility in the modified FST indicat

199 ering interventions, possibly accounting for failure to reduce outcomes in patients with hypertension

200 Failure to reduce the dose in patients with severe kidne

201 rate their hearts following injury, and this failure to regenerate myocardium is a leading cause of h

202 on of cell proliferation and migration, with failure to regulate these processes resulting in disease

203 The loss of YTHDF2 results in the failure to regulate transcript dosage of a cohort of gen

204 of DNA methylation defects results from the failure to reinforce rather than reset this modification

205 Failure to remove a retrievable inferior vena cava (IVC)

206 again, inaccuracies in DNA transactions and failures to remove mutagenic lesions cause heritable gen

207 Mild deficiency usually results from failure to render food B12 bioavailable or from dietary

208 Failure to repair DNA damage efficiently can lead to can

209 Failure to repair the sarcolemma leads to muscle cell de

210 Failure to replace Bacille Calmette-Guerin vaccines with

211 Wang et al report a failure to reproduce our biochemical observation that th

212 contentious debate about the extent to which failures to reproduce certain results might also reflect

213 neage specification can induce LTTM and that failure to rerepress chromatin is one epigenetic mechani

214 Failure to rescue (death after postoperative complicatio

215 Failure to rescue (FTR) has been proposed as an underlyi

216 complications (OR 1.67; 95% CI 1.34, 2.08), failure to rescue (OR 2.72; 95% CI 1.25, 5.94), and read

217 admissions, but lower risk-adjusted rates of failure to rescue and 30-day mortality than did nonteach

218 admissions, but lower risk-adjusted rates of failure to rescue and 30-day mortality than did nonteach

219 serious complications with similar rates of failure to rescue and overall 30-day mortality.

220 These findings suggest that failure to rescue deteriorating patients is more common

221 Complications associated with failure to rescue included acute renal failure, septic s

222 (esophagectomy) of the observed variation in failure to rescue rates across hospitals.

223 ange: OR 1.09-1.62) significantly influenced failure to rescue rates for all procedures.

224 n of overall postoperative complications and failure to rescue rates on the observed increased mortal

225 ication rates ranged from 25.0% to 72.2% and failure to rescue rates ranged from 0.0% to 25.0%.

226 Failure to rescue rates varied up to 11-fold between ver

227 gistic regression modeling, we evaluated how failure to rescue rates were influenced by specific hosp

228 al characteristics are associated with lower failure to rescue rates, these macrosystem factors expla

229 stics on the between-hospital variability in failure to rescue rates.

230 Failure to rescue was the number of deaths in patients w

231 ame procedure type at the same hospital; and failure to rescue, defined as in-hospital death after th

232 Failures to rescue rates were higher in patients 80 year

233 andardized clinical pathway could impact the failure-to-rescue rate after cytoreductive surgery (CRS)

234 ed management facilitated a reduction in the failure-to-rescue rate and improved the quality of care.

235 The failure-to-rescue rate is a useful metric for evaluating

236 The failure-to-rescue rate was 4.4% for the entire period, b

237 Mortality (-0.5; 95% CI, -0.9 to -0.1) and failure-to-rescue rates (-4.5; 95% CI, -7.4 to -1.6) als

238 or associations with major complications and failure-to-rescue.

239 renal complications were associated with the failure-to-rescue.

240 in response to oxidative stress may indicate failure to reseal, predisposing membranes to rupture.

241 tic cells, have been implicated as causes of failure to resolve gut inflammation in inflammatory bowe

242 Failure to resolve inflammation after infection precipit

243 untreated, TB mortality is associated with a failure to resolve pulmonary immunopathology.

244 In wild-type mice, failure to resolve tubular injury after unilateral ische

245 This failure to resorb established calcifications may contrib

246 The problem with IST is failure to respond and the development of late clonal di

247 LV pacing were difficult CS anatomy (n =12), failure to respond to conventional CRT (n = 10), and a h

248 Failure to restart replication forks stalled at genomic

249 enhanced dorsal aorta vessel elasticity and failure to restrict aortic diameter.

250 ased production of modulatory molecules, and failure to restrict parasite replication.

251 s after hospitalization and risk factors for failure to return to home, readmission, and death should

252 Failure to scale up has severe personal and social conse

253 Depletion of ARHGAP18 resulted in a failure to secrete endothelin-1 and a reduction in neutr

254 Failure to secrete sufficient quantities of insulin is a

255 vention on the Regulation of Whaling and the failure to successfully regulate whaling that led to the

256 Molecularly, the failure to suppress gene expression corresponded with de

257 associated with primary virological failure (failure to suppress HIV-1 within 9 months) in patients w

258 s transient protection was probably due to a failure to sustain elevated SIRT1 activity and downstrea

259 of repair cells and regeneration tracks, and failure to sustain expression of repair cell markers, in

260 Importantly, failure to target Mrc1 for degradation during recovery i

261 Here we apply a new model of elastic-brittle failure to test the alternative view that successive epi

262 their damage tolerance and insensitivity of failure to the presence of flaws even when made entirely

263 fies the outcomes of remission and treatment failure to these interventions.

264 Elevated sweat chloride levels, failure to thrive (FTT), and lung disease are characteri

265 Classical symptoms of CS patients include failure to thrive and a severe neuropathology characteri

266 ions and gastrointestinal disorders, such as failure to thrive and delayed gastric emptying, together

267 usually presents in the newborn period with failure to thrive and metabolic crisis leading to coma o

268 pmental delay, progressive microcephaly, and failure to thrive).

269 d Mut(ko/ki) mice survive post-weaning, show failure to thrive, and show increased methylmalonic acid

270 sy including infantile spasms, irritability, failure to thrive, and stereotypic hand movements.

271 r, neutrophilic dermatitis/panniculitis, and failure to thrive, but without obvious primary immunodef

272 A2 who exhibited global developmental delay, failure to thrive, dilated cardiomyopathy and epilepsy,

273 idge-Ropers syndrome (BRS), characterized by failure to thrive, global developmental delay, feeding p

274 r that presents during infancy, resulting in failure to thrive, hepatomegaly, and hepatic failure, an

275 use an early onset multisystem disorder with failure to thrive, immunodeficiency and neurological sym

276 on of patients with PYCR2 mutations included failure to thrive, microcephaly, craniofacial dysmorphis

277 ma, hypotrichosis, severe nail dystrophy and failure to thrive, two heterozygous mutations in ABCA12

278 l heart disease, skeletal abnormalities, and failure to thrive.

279 spectrum disorder, developmental regression, failure-to-thrive, exercise intolerance/fatigue) was ass

280 n auxotrophy of the pyc::tn strain is due to failure to transcriptionally induce late stage biotin bi

281 her AHR constitutive nuclear localization or failure to translocate to nucleus, underlying an alloste

282 hesized that calpainopathy may result from a failure to transmit loading-induced Ca(2+)-mediated sign

283 This failure to undergo Ag-induced aerobic glycolysis is caus

284 Failure to undergo MET during development leads to the i

285 The failure to undergo remyelination is a critical impedimen

286 e S187A mutant died in the first week due to failure to undergo the peroxisome proliferator-activated

287 Failure to up-regulate genes in C3KO muscles is due, in

288 show reduced NHEJ efficiency, with a drastic failure to up-regulate RAD51 expression and manifestly f

289 Underlying the chromosomal instability is a failure to up-regulate the meiotic recombination 11 (Mre

290 patients with complete peripheral vestibular failure to update their angular travelled distance durin

291 d environment was shown to contribute to the failure to upregulate CD25.

292 sis genes prominently in RP-mediated DBA and failure to upregulate components of the translational ap

293 ation of hypoxia inducible factor 1alpha and failure to upregulate pfkfb3 We also show that Francisel

294 In a multivariate analysis, failure to use an oral vancomycin taper preceding FMT wa

295 Underuse-the failure to use effective and affordable medical interven

296 Thus, failure to use lactate is detrimental and is possibly re

297 is required for mitotic progression because failure to vesiculate the Golgi activates the canonical

298 left ventricular mechanical assist device or failure to wean from it at 96 hours after study drug ini

299 ommon in MV patients and is a major cause of failure to wean patients from ventilator support.

300 n complication was sepsis (42%), followed by failure to wean ventilator (31%), and organ space surgic