ライフサイエンスコーパス: premature

1 of age in children whose birth was extremely premature.

2 o end reliance on acceptability judgments is premature.

3 oter downstream of the CTCF insulator led to premature activation of the ectopic promoter.

4 IIH subunits XPB, XPD, and p8 lead to severe premature ageing and cancer propensity in the genetic di

5 observed with age in littermates, suggesting premature ageing of dopamine synapses in GKI mice.

6 ng hearts would show impaired function and a premature ageing phenotype.

7 (Casp2(-/-)) mice develop normally but show premature ageing-related traits and when challenged by c

8 ological alterations that invariably lead to premature aging and death.

9 rdiovascular system during physiological and premature aging and discusses the mechanisms underlying

10 he HSC and MPP phenotypes are reminiscent of premature aging and stressed hematopoiesis, and indeed p

11 epletion of Foxp1 in bone marrow MSCs led to premature aging characteristics, including increased bon

12 are a hallmark of premature aging.HGPS is a premature aging disease caused by mutations in the nucle

13 s and from patients with progeria, a genetic premature aging disease.

14 HDV infection, the largest to date, revealed premature aging of immune cells and impaired T-cell func

15 affect Leydig cell function, likely causing premature aging of the testes and impaired liver metabol

16 Based on observations in the premature aging syndrome Hutchinson-Gilford progeria, we

17 HSCs and progenitor cells, and in preventing premature aging.

18 me biogenesis and activity are a hallmark of premature aging.HGPS is a premature aging disease caused

19 Small-airways instability resulting in premature airway closure has been recognized as a risk f

20 eumonia is a well-recognized lung disease of premature and malnourished babies.

21 otypes per se do not shape social reality is premature and overly reductionist.

22 ion of the termitophile-related features and premature and presumptive phylogenetic placement of Cret

23 rlying basis of thalassemia pathology is the premature apoptotic destruction of erythroblasts causing

24 about the resilience of these ecosystems is premature because the impact of past climate events may

25 Furthermore, loss of GAS2L3 results in premature binucleation of cardiomyocytes accompanied by

26 hies, myopic surface ablation could induce a premature biomechanical elastic response rather than a p

27 humans that cBF integrity is impaired after premature birth and links neonatal complications with lo

28 ge in the motor impairment that results from premature birth and suggest that therapies designed to p

29 l of UPI and oxygen-fluctuations and removed premature birth as a confounding factor.

30 We report for the first time that premature birth is associated with altered cerebellar me

31 l the end of pregnancy, we hypothesized that premature birth would disrupt interneuron production and

32 Children with urinary tract anomalies, premature birth, or major comorbidities were excluded fr

33 ing cause of neurological deficits following premature birth.

34 e, inherited retinal dystrophy that leads to premature blindness.

35 d mesenchymal stem-like cells (nMSCs) showed premature bone differentiation, a phenotype paralleled b

36 ffected by skeletal ciliopathies suffer from premature bone growth arrest, mirroring skeletal feature

37 e-dependent cardiovascular disease involving premature calcification of the aortic valve, a phenotype

38 autosomal dominant disorder associated with premature cardiovascular disease (CVD).

39 f glycolysis rescued the mutant phenotype of premature cartilage maturation, thereby indicating that

40 Nrf2 preactivation reduced premature catagen and hair growth inhibition induced by

41 e sufficient statistical power for examining premature, cause-specific mortality in patients recently

42 airs mitotic spindle orientation, leading to premature cell cycle exit and Purkinje cell (PC) progeni

43 3 inflammasome activation exist, which cause premature cell death and disease progression.

44 such as lipopolysaccharides), which leads to premature cell death, callose deposition, or phloem prot

45 ythroblasts causing oxidative stress and the premature cell death.

46 ability of liquid electrolytes also leads to premature cell failure as a result of parasitic reaction

47 nt receptor is tempered by the activation of premature cellular senescence in an NF1-deficient backgr

48 on of Ezh2 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and

49 ere viable and had an increased frequency of premature centriole separation, accompanied by reduced d

50 ve important implications for the control of premature cervical ripening and prevention of preterm bi

51 e differentiation, a phenotype paralleled by premature clavicle ossification in Eif4a3 haploinsuffici

52 te stabilization suppresses inappropriate or premature cleavage, enhancing processing fidelity.

53 opening, hinders its expansion and leads to premature closure in most instances.

54 ufficiency, increased diastolic tension, and premature contractions; ranolazine treatment counteracte

55 diabetes, or dyslipidemia; family history of premature coronary artery disease; never smoking; sympto

56 nevitability of death (patients), preventing premature death (clinicians), and ensuring safety (regul

57 ing from progressive infantile paralysis and premature death (type I) to limited motor neuron loss an

58 ockade of embryogenesis, adult sterility and premature death 18-24 months post-treatment.

59 ic heart disease (RHD) is a leading cause of premature death and disability in low-income countries;

60 Type 2 diabetes leads to premature death and reduced quality of life for 8% of Am

61 et syndrome, including spontaneous seizures, premature death and seizures triggered by hyperthermia.

62 of cause-specific outcomes examined, risk of premature death during the first year after discharge wa

63 a and neurodegenerative phenotype leading to premature death in 36% of the population.

64 e hypothyroidism leads to growth defects and premature death in mice, we assayed for changes in thyro

65 nal calcification, renal tubular injury, and premature death in multiple animal models.

66 To counter premature death of a virus-infected cell, poxviruses use

67 leading to a severe skin barrier defect and premature death of newborn animals.

68 eads to cardiac conduction abnormalities and premature death owing to arrhythmia.

69 ubertal nadir androgen condition resulted in premature death, maintenance of androgen levels extended

70 odelling, decline of cardiac performance and premature death, thereby limiting the use of betaAR agon

71 late-onset lymphoid cancer development, and premature death.

72 l lung disease, ulcerative skin lesions, and premature death.

73 behavioral abnormalities, and prevention of premature death.

74 ss to fibrosis and cirrhosis contributing to premature death.

75 nd adults and that, if untreated, results in premature death.

76 with no indications of cardiac pathology or premature death.

77 pread central nervous system dysfunction and premature death.

78 heart failure, reduced quality of life, and premature death.

79 ical degeneration that causes disability and premature death.

80 lead to a considerable change in the risk of premature death.

81 sible for averting 180,000 (117,000-389,000) premature deaths between 1990 and 2012.

82 Of an estimated 1.10 million premature deaths caused by PM2.5 pollution throughout Ch

83 desh contributes to the largest reduction of premature deaths from ambient air pollution, preventing

84 d with about 38,000 PM2.5- and ozone-related premature deaths globally in 2015, including about 10 pe

85 tely 174,000 global PM2.5- and ozone-related premature deaths in 2040.

86 uding about 10 per cent of all ozone-related premature deaths in the 28 European Union member states.

87 (PM2.5) amount to approximately 22.5 million premature deaths prevented between 2000 and 2100.

88 We find that, of the 3.45 million premature deaths related to PM2.5 pollution in 2007 worl

89 olid fuels is associated with over 4 million premature deaths worldwide every year including half a m

90 As a result, p53cKO mice presented premature defects in mTEC-dependent regulatory T-cell di

91 ined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebr

92 of siRNAs and the protection of siRNAs from premature degradation before reaching the target cells.

93 t this segment either stabilizes Pxr against premature degradation during vegetative growth or positi

94 EZH2 premature degradation in proliferating myoblasts is prev

95 tions by ALLINIs or mutations in IN leads to premature degradation of both the viral RNA genome and I

96 The complex prevents the premature degradation of cyclin B1.

97 r (CFTR) anion channel causes misfolding and premature degradation.

98 o the plasma membrane by shielding them from premature degradation.

99 al timer that preserves naivete and prevents premature deleterious developmental decisions.

100 ral complications, including miscarriage and premature delivery.

101 ba1, and loss of this interaction results in premature delocalization of Rga1 from the immediately pr

102 al model of Cdc42 polarization predicts that premature delocalization of Rga1 leads to more frequent

103 Premature depletion of the PF reserve leads to subfertil

104 me Dicer from nephron progenitors results in premature depletion of the progenitors and increased exp

105 as well as the current passed in response to premature depolarizations that normally helps protect ag

106 ore aggressive disease phenotype, leading to premature development of complications, with adverse eff

107 al attentional network and may contribute to premature diagnostic closure, an important cause of diag

108 assist the advance of approaches to prevent premature diagnostic closure.

109 n proliferation gene expression and suppress premature differentiation driven by GRHL3.

110 In contrast, premature differentiation in ST8SIA4-negative cultures e

111 These mutants display premature differentiation of keratin 5-positive (Krt5(+)

112 edies the high mitotic index and rescues the premature differentiation of Mcph1-deficient neuroprogen

113 Ectopic expression of Cdh1 leads to premature differentiation of neuroprogenitors, mimicking

114 NV)-NS2A, leads to reduced proliferation and premature differentiation of radial glial cells and aber

115 arises from neither increased GSC death nor premature differentiation.

116 ustain tissue self-renewal while suppressing premature differentiation.

117 ects on sleep and daytime alertness, causing premature disability and death.

118 This defect causes the premature disassembly of individual Z-rings, leading to

119 (confirmed viral load >/=50 copies per mL or premature discontinuations, with last viral load >/=50 c

120 t impaired social bonds increase the risk of premature disease and death.

121 We found that single kinesins undergo premature dissociation, but not preferential pausing, at

122 MRN complex to damaged DNA, leading to both premature DNA damage checkpoint termination and inhibiti

123 boptimal properties of NP platforms, such as premature drug leakage during preparation, storage, or b

124 New nanocarriers able to minimize the premature drug release in blood circulation while releas

125 SLs and ENTSLs did not impact size or caused premature drug release in physiological buffer.

126 ith acute coronary syndrome (ACS) to promote premature EC aging and thrombogenicity.

127 we find that overproduction of DDK leads to premature Eco1 degradation.

128 of chronic inflammatory diseases by driving premature endothelial senescence.

129 ted from the nucleus for the cell to prevent premature entry to mitosis, and retaining Cyclin B1-Cdk1

130 Treatment with TRbeta agonists stimulated premature erythroblast differentiation in vivo and allev

131 n adaptive lymphoid cells EZH2 prevented the premature expression of Cdkn2a and the consequent stabil

132 nt seen in humans exposed to the stress of a premature extrauterine environment is modulated by genet

133 rane into mother and bud compartments caused premature formation of deposits in the daughter cells.

134 revalent human birth defect characterized by premature fusion of calvarial bones.

135 to 8% of wild-type sporulating cells trigger premature germination during differentiation in a GerA-d

136 tion of GerA during sporulation resulting in premature germination.

137 re developmentally equivalent to the extreme premature human infant can be physiologically supported

138 Loss of Gfi1 resulted in premature induction of effector genes and the transcript

139 uster signaling' here) was needed to prevent premature induction of interferon-gamma (IFN-gamma) expr

140 f strains across body sites implies that the premature infant microbiome can exhibit very low microbi

141 nical observation of reduced ROP severity in premature infants after caffeine treatment for apnea sug

142 GF levels on the developing organ systems of premature infants are unknown, and there are limited lon

143 Participants included 7483 premature infants at risk for ROP with a known ROP outco

144 the potential for delivering timely care to premature infants at risk for serious ROP.

145 tively collected high quality (1)H-MRS in 59 premature infants born </=32 weeks and 61 healthy full t

146 the skin, mouth, and gut of two hospitalized premature infants during the first month of life.

147 Premature infants often require oxygen supplementation a

148 results indicating that endothelial cells of premature infants who later develop BPD or die have impa

149 Participants in the e-ROP Study were premature infants with a birth weight less than 1251 g a

150 om May 1, 2011, to October 31, 2013, in 1257 premature infants with birth weights less than 1251 g in

151 Between May 2015 and September 2016, 61 premature infants with type 1 ROP in 1 or both eyes were

152 Cronobacter sakazakii and typically affects premature infants.

153 ption in production of interneurons in human premature infants.

154 impacts the health and future development of premature infants.

155 ight partially restore neurogenesis in human premature infants.SIGNIFICANCE STATEMENT Prematurity res

156 ER and ERL1 also prevented premature initiation of the fiber differentiation proces

157 ciated with higher snow densities and led to premature interruption due to critical hypoxia (SpO2 </=

158 eatitis is a complex disorder involving both premature intracellular protease activation and inflamma

159 Responses ranging from premature leaf senescence and partial canopy dieback to

160 showed early expression of zygotic genes and premature lengthening of cell cycles.

161 studies reported that progesterone prevented premature LH surges during ovarian hyperstimulation in w

162 Amyloid deposition is associated with premature loss of normal Abeta42 day/night patterns in o

163 nks also prevent flattening of capsomers and premature maturation.

164 We determined that this premature mitotic exit is due to defects in spindle asse

165 anaphase" signals are diluted, resulting in premature mitotic exit.

166 han control ExECs, indicating suppression of premature mobilization that has been noted in the contex

167 AMCase-deficient mice exhibit premature morbidity and mortality, concomitant with accu

168 We estimated 21,000 premature mortalities per year from EGU emissions, drive

169 We estimate 10,000 premature mortalities per year from RC emissions, driven

170 ately 670 cardiovascular and 300 respiratory premature mortalities within North America could be attr

171 study, we aimed to estimate health impacts (premature mortalities) attributable to PM2.5 and O3 from

172 ong-term exposure to PM2.5 and PM2.5-related premature mortality (PM2.5-mortality) and its response t

173 ions of social isolation and loneliness with premature mortality are well known, but the risk factors

174 re we combine four global models to estimate premature mortality caused by fine particulate matter (P

175 By contrast, premature mortality decreased substantially across all a

176 ilepsy have greatly increased probability of premature mortality due to sudden unexpected death in ep

177 Historical trends in PM2.5-related premature mortality during 1990-2010 across the northern

178 a global target of reducing tobacco use and premature mortality from non-communicable diseases by a

179 This appears to be a key contributor to the premature mortality gap.

180 To investigate premature mortality in a nationwide cohort of patients r

181 ing cessation, have contributed to declining premature mortality in Hispanic individuals, black indiv

182 Between 1999 and 2014, premature mortality increased in white individuals and i

183 Reduction of premature mortality is a UN Sustainable Development Goal

184 hat the effect of NO2 from road traffic upon premature mortality was ten-fold greater than that of PM

185 sed with psoriasis have an increased risk of premature mortality, but the underlying reasons for this

186 n Indians and Alaska Natives had the highest premature mortality, followed by black individuals.

187 including diabetes-associated morbidity and premature mortality.

188 tional decline and comorbidities, leading to premature mortality.

189 may lead to substantial comorbid disease and premature mortality.

190 uscle function in conditions of weakness and premature muscle fatigue.

191 diseases and can lead to muscle weakness and premature muscle fatigue.

192 ma (lineage 'Mnola') in the oral cavity of a premature neonate.

193 ation and identified ID1, a HLH inhibitor of premature neurogenesis, as a target.

194 f active embryonic RGCs by stimulating their premature neuronal differentiation while preventing quie

195 progenitor cell proliferation, induction of premature neuronal differentiation, and interruption of

196 tainable Development Goal (SDG) 3.4-reducing premature non-communicable disease mortality by a third

197 revealed active Cdk1 to be mandatory for the premature onset of chromosome condensation during G2 and

198 refore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cy

199 Premature ovarian insufficiency (POI) is a frequent long

200 fied aged wines, and has also been linked to premature oxidative aging (premox).

201 KAr isoform that does not bind cAMP triggers premature parasite egress from infected cells followed b

202 hat NBR1-independent bulk autophagy prevents premature plant death, thus extending the lifespan of vi

203 hey usually suffer from low ductility due to premature plastic instability by source-limited crystal

204 akaryopoiesis with an enhanced proportion of premature platelets.

205 yclin B, and meiotic defects consistent with premature PNG activation.

206 er, delays SG assembly and facilitates their premature post-stress disassembly.

207 Moreover, premature postnatal deletion of Pofut1 in skeletal myofi

208 reveal that ER and ERL1 redundantly prevent premature progression of sequential events in secondary

209 ted in abrogation of the mitotic checkpoint, premature progression through mitosis, marked aneuploidy

210 However, an accidental or premature release of a gene drive construct to the natur

211 ed rats and controls did not differ in their premature responding and glycine and serine levels in vm

212 etween levels of these neurotransmitters and premature responding normally evident in alcohol-naive s

213 receptor antagonist, reduced cocaine-evoked premature responses in 5-CSRTT when administered systemi

214 Specifically, DAMGO increased premature responses, regressive errors, and random error

215 Preterm premature rupture of membrane (pPROM) is associated with

216 , in some pregnancies complicated by preterm premature rupture of membranes (pPROM), membranes heal s

217 abor) or vaginal (labor) deliveries, preterm premature rupture of membranes, and spontaneous preterm

218 as an emerging cause of chorioamnionitis and premature rupture of membranes, which are associated wit

219 Preterm premature rupture of the membranes had the highest numbe

220 entry by keeping p21 levels low, preventing premature S-phase exit upon DNA damage.

221 with the dissolved PhIP but clearly induced premature senescence activities that may be caused by a

222 hibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse embryonic fibroblasts and

223 cogenic Ras causes proliferation followed by premature senescence in primary cells, an initial barrie

224 evels of senescence marker genes, leading to premature senescence of KO siliques, whereas RCS and sen

225 at lung cancer cells escape oncogene-induced premature senescence through down-regulation of caveolin

226 or Xbp1 splicing promotes growth arrest and premature senescence through hyperactivation of the IRE1

227 n by IRE1alpha is essential for HRas-induced premature senescence.

228 ase activity and upregulated p16, indicating premature senescence.

229 cells and found that such treatment induced premature senescence.

230 The mitotic checkpoint system prevents premature separation of sister chromatids in mitosis and

231 back to disrupted cell-cycle kinetics and a premature shift to asymmetric cell divisions impairing p

232 We demonstrate that premature silencing of LINE-1 elements decreases chromat

233 ription regulation through its prevention of premature sister-chromatid separation and the formation

234 nation of compromised bipolar attachment and premature spindle assembly checkpoint silencing in the m

235 This premature stabilization requires the conserved microtubu

236 ations of spermidine(3+) did not produce the premature stalling observed in experiments.

237 eotide substitution (c.565G>T) introducing a premature stop codon (p.Glu189*).

238 nucleotide (C64T) at codon 22, leading to a premature stop codon (R22X) in the albino robust capuchi

239 One mutation resulted in a premature stop codon and absent protein, while the secon

240 (SNP) mutation in the GL4 gene resulted in a premature stop codon and led to small seeds and loss of

241 AT gene showed a mutation that resulted in a premature stop codon and protein truncation leading to c

242 single amino acid substitution (G299V) or a premature stop codon causing strong virulence attenuatio

243 metabotropic receptor 3 (GRM3) gene gained a premature stop codon in BMD cells, and silencing GRM3 in

244 Furthermore, the premature stop codon introduced by the CHADL frameshift

245 Whole-exome sequencing revealed a homozygous premature stop codon mutation in the gene encoding MYSM1

246 first exon that was predicted to result in a premature stop codon.

247 Drug-induced readthrough over premature stop codons (PTCs) is a potentially attractive

248 d mRNA decay (NMD) of transcripts containing premature stop codons and related to the ATM and ATR kin

249 rafish abcd1 mutant allele lines introducing premature stop codons in exon 1, as well as obtained an

250 arger proportion of the repertoire exhibited premature stop codons in some elderly subjects, indicati

251 in rat showed the translational footprint of premature stop codons in Ttn, TTNtv-position-independent

252 CD8(+) T cell recognition were not observed, premature stop codons were observed in 7% and 56% of tax

253 Two mutations were predicted to introduce premature stop codons, and one was predicted to result i

254 that acquired sequence variations that cause premature STOP codons, loss of STOP codons and single nu

255 Adverse events caused the premature study discontinuation of 12 individuals (4.4%)

256 rate and volume that eliminate the danger of premature swelling rupturing the sutured area.

257 ings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expressi

258 6% of patients with RDEB harbor at least one premature termination codon (PTC) mutation in COL7A1, an

259 ndividuals with a mutation that introduces a premature termination codon (PTC) that prevents synthesi

260 and demonstrate that its inclusion creates a premature termination codon (PTC), that leads to a 65kDa

261 the levels of both endogenous and exogenous Premature Termination Codon (PTC)-containing mRNA isofor

262 due to loss-of-function mutations creating a premature termination codon and the degradation of the m

263 ed OsPCS2b transcript that bears the unusual premature termination codon besides the canonically spli

264 bnormalities, but a child homozygous for the premature termination codon displayed symptoms consisten

265 , and results in a frameshift and subsequent premature termination codon in each.

266 tically isolated family was found to carry a premature termination codon in Leiomodin1 (LMOD1), a gen

267 ygous protein-altering variants, including a premature termination codon, in CRKL.

268 novel motif, resulting in a frameshift and a premature termination codon.

269 In-frame premature termination codons (PTCs) account for approxim

270 mRNAs containing premature termination codons (PTCs) are rapidly degraded

271 hway that recognizes and degrades mRNAs with premature termination codons (PTCs).

272 found to be highly conserved and introduced premature termination codons into coding regions.

273 ated decay (NMD) eliminates transcripts with premature termination codons.

274 Our results show that ribosome premature termination may lead to non-intuitive ribosome

275 ults in antisense transcription termination, premature termination of a proportion of sense transcrip

276 f this site in one STS (AtTPS19) resulted in premature termination of carbocation intermediates and a

277 a 7bp deletion in CERKL cDNA that caused the premature termination of CERKL.

278 or the large, multidomain DEBS1, substantial premature termination of protein translation was observe

279 A mutation in tsv causes premature termination of the gene product.

280 the aptamer domain of the riboswitch induces premature termination of the mRNA synthesis of ligand-as

281 caused at least in part by nonadherence and premature termination of treatment.

282 ll present T cell epitopes downstream of the premature termination site that may render the subject t

283 12 mg/L (nucleotide insertions or deletions, premature termination, tandem repeat, nonstop, and misse

284 tional RNA cleavage mechanism acts to induce premature termination.

285 We argue that this conclusion is premature: The experience-agency framework may capture p

286 R activity and junctional tension to inhibit premature TJ complex formation in lower layers while pro

287 We conclude that it is premature to explain belief in gods as 'intuitive', and

288 with a floxed polyadenylation signal causing premature transcriptional termination of the Lepr gene w

289 There were no premature treatment discontinuations.

290 exterior envelope glycoprotein and CD4; (ii) premature triggering of conformational changes in the en

291 somes to continue with translation through a premature UAG stop codon located in a beta-galactosidase

292 observed (0 indicates no ectopy; 1, isolated premature ventricular beats; 2, bigeminy; 3, couplets; a

293 Ventricular tachycardia and premature ventricular complexes (PVCs) most frequently o

294 Variability in premature ventricular contraction (PVC) coupling interva

295 ts referred for left ventricle outflow tract premature ventricular contraction ablation, an aortic va

296 Premature ventricular contraction rate increased with ex

297 e patients with left ventricle outflow tract premature ventricular contraction were included.

298 In contrast, VT or premature ventricular contractions in the setting of a s

299 Premature ventricular contractions originating in the le

300 Premature ventricular contractions were common in ARVC p