ライフサイエンスコーパス: demise

1 nuclear translocation and subsequent glioma demise.

2 ogical communities, from initiation to their demise.

3 K1 is free to unveil its program of cellular demise.

4 hat SC metabolic deficits may lead to axonal demise.

5 cells to ensure silent, noninflammatory cell demise.

6 fying kidney injury and accelerating nephron demise.

7 oals work selflessly, resulting in their own demise.

8 T cells to cause inflammation and beta cell demise.

9 lantic, from exponential growth to its rapid demise.

10 tion in causing the passenger pigeon's rapid demise.

11 y a critical role in poly(I:C)-induced fetal demise.

12 estriction, fetal liver hypocellularity, and demise.

13 n that lead to energy depletion and cellular demise.

14 e, how T cells use autophagy to hasten their demise.

15 of the contributing factors in motor neuron demise.

16 nce of events leading to dopaminergic neuron demise.

17 nc-finger protein LIN-29 to promote cellular demise.

18 nst degenerative disorders that lead to cell demise.

19 athway is not involved in photoreceptor cell demise.

20 develops but the embryo itself suffers early demise.

21 initiator caspase-8, and ultimately cellular demise.

22 and fetal growth retardation and subsequent demise.

23 pair of DNA breaks or after replication fork demise.

24 ng to increased myocardial mass and neonatal demise.

25 i) in glioma cells that was followed by cell demise.

26 reases [Ca(2+)](i) and initiates glioma cell demise.

27 owing then leads to graft ischemia and organ demise.

28 l effects, including tissue damage and fetal demise.

29 r multiple occurrences of intrauterine fetal demise.

30 h other factors, contributed to its eventual demise.

31 ts sequelae are the most common mechanism of demise.

32 ccounts of the human Y chromosome's imminent demise.

33 aortic valvuloplasty carries a risk of fetal demise.

34 s of epithelial cell polarity, and embryonic demise.

35 ociated proteins, and generalized epithelial demise.

36 ith subsequent cardiac failure and embryonic demise.

37 ly detectable archaeological record of their demise.

38 input rather than a symptom of the neuron's demise.

39 decreased cardiomyocyte proliferation before demise.

40 c reticulum injury contributes to motoneuron demise.

41 ophila melanogaster, also contributes to its demise.

42 signaling for other purposes without risk of demise.

43 death remains the most common cause of fetal demise.

44 pro-survival responses, leading to cellular demise.

45 in these mice may contribute to their rapid demise.

46 tions about mitochondrial routes to cellular demise.

47 sis is an established pathway for islet cell demise.

48 eeks; 15 (25.4%) resulted in first-trimester demise.

49 organelles that lead ultimately to a cell's demise.

50 ey are a determinant of infectivity and host demise.

51 mal ribosomal DNA circles, which cause yeast demise.

52 rologic symptoms, which usually led to rapid demise.

53 nenolone or progesterone did not cause fetal demise.

54 duced c-Jun activation and dopaminergic cell demise.

55 al cardiac gene program and eventual cardiac demise.

56 inflammation-induced preterm birth and fetal demise.

57 had episodes of acute rejection before graft demise.

58 al arthrogryposis, and early fetal/postnatal demise.

59 disputes with Guarita leading to the Paredao demise.

60 ovascular system, often with early postnatal demise.

61 term decline, or thriving until their sudden demise.

62 chromosomal aberrations, and tumor clonogen demise.

63 n, which can result in microcephaly or fetal demise.

64 deficiency or actually drives the germ-cell demise.

65 ions tested to date failed to halt beta cell demise.

66 cy can cause congenital abnormities or fetal demise.

67 lternatively, pathogen subversion caused its demise.

68 devastating congenital abnormities or fetal demise.

69 d fetal tissues, and protected against fetal demise.

70 rotection against placental damage and fetal demise.

71 ng as a factor contributing to Neanderthals' demise.

72 r characterized by rapid and uniform patient demise.

73 at together contribute to photoreceptor cell demise.

74 f these tumor cells and leads to their rapid demise.

75 wed by irreversible caspase-independent cell demise.

76 cies toxicity) drive cellular dysfunction or demise.

77 e stress and light-independent photoreceptor demise.

78 follow-up (5%), 15 terminations (6%), and 41 demises (17%).

79 icular hemorrhage (1.4%), intrauterine fetal demise (2.8%), and neonatal death (1.4%).

80 robability of technical success [94%], fetal demise [4%], and biventricular circulation [66%]), the m

81 spontaneous abortions, 18 intrauterine fetal demise, 672 pregnancy terminations and 87 were lost to f

82 become adversely activated and mediate fetal demise, a common complication of early pregnancy.

83 on of the bladder, hydronephrosis, and rapid demise after parturition.

84 The male-induced demise also occurred in other species of nematodes, sugg

85 Synaptic demise and accumulation of dysfunctional proteins are th

86 ppropriately monitor patients for neurologic demise and effect early transfer to a center capable of,

87 d the functions and consequences of cellular demise and elucidated several of the key cell death path

88 biochemical properties of alpha-syn protein, demise and function of nigral dopaminergic neurons, and

89 I molecules, leading ultimately to beta-cell demise and insulin insufficiency.

90 mitation hinders the quantification of bloom demise and its regulation by biological processes [5, 6]

91 from multiple clades successively drove the demise and replacement of mackerel sharks due to a failu

92 iple carnivore clades successively drove the demise and replacement of the two extinct canid subfamil

93 lead molecule, which prevents DAergic neuron demise and striatal DAergic denervation in vivo against

94 ty, effectively delays coordinated host-cell demise and supports its intracellular propagation.

95 at may be exploited to both block CD4 T cell demise and the chronic inflammatory response generated d

96 Intrauterine fetal demise and/or preterm birth were observed in 54% of preg

97 ns, contributions of beta-cells to their own demise, and epigenetic predispositions affecting both im

98 lectively lead to placental abruption, fetal demise, and female sterility, thereby placing BMPR2 at a

99 ll death is a defined pathway for islet cell demise, and mitochondrial dysfunction contributes to isl

100 phenotype secretome, followed by RPE and PRC demise, and that ELVs 32 and 34 blunt these events and e

101 he mice showed no evidence of fetal/neonatal demise, and there was no evidence of proliferation in th

102 treatment modalities designed to promote its demise are all ultimately ineffective, leading to diseas

103 Preterm birth and fetal demise are likely the direct result of toxin-induced dam

104 therefore, that the reasons for its ultimate demise are to be sought in Holocene not Pleistocene even

105 and mechanisms that cause age-related tissue demise are unclear.

106 gle mutant mice, likely as a result of rapid demise at a young age from other causes.

107 than protecting cells, HSF-1 promotes their demise by activating components of the ubiquitin proteas

108 The further reduction of photoreceptor cell demise by co-treatment with calpastatin and salubrinal s

109 HK97 contributes to its own demise by expressing the product of an open reading fram

110 nt cell death checkpoint that restricts cell demise by inactivating RIPK1.

111 ization in B-CLLs support resistance to cell demise by inhibiting an early player of apoptotic signal

112 estigated the impact of human hunting on its demise by integrating genetic data, GPS-based ocean curr

113 ce suggests that a cell can initiate its own demise by necrosis in a manner that initiates both infla

114 3 levels increase, it contributes to its own demise by up-regulating the transcription of S100B as pa

115 inant of cell death in this scenario because demise can be avoided under conditions favoring accumula

116 sicles (EVs) released during cell stress, or demise, can contain a barcode of the cell origin, includ

117 s with unexplained fetal arrhythmia or fetal demise combined with a documented CaM mutation.

118 ic-ischemic (H-I) injuries at term and their demise contributes to neurological disorders.

119 The male-induced demise could occur without mating and required only expo

120 for all populations, with the timing of the demise dependent on the amount of skew.

121 To achieve swift cell demise during apoptosis, caspases cleave essential prote

122 utophagy, which arbitrates cell survival and demise during stress conditions, requires further assess

123 Following their near-demise during the end-Permian extinction, crinoids under

124 ion and cannot induce antigen-specific fetal demise even when artificially activated.

125 ctant management is favored if risk of fetal demise exceeded 12% or probability of biventricular circ

126 the family with recurrent intrauterine fetal demise exhibited the CALM3-E141K mutant allele in 25% of

127 To understand the consequences of their demise for community assembly, we tracked community stru

128 stem models is likely to slow predictions of demise for coral reef ecosystems.

129 ising the question of the importance of such demise for cortical wiring.

130 The likelihood of demise from acute kidney injury requiring dialysis in pa

131 Their longevity and sudden demise has been explained however, by the trapping of an

132 e intracellular mechanisms that govern their demise have begun to be elucidated.

133 in utero, and OPCs that emerge before their demise have migration and proliferation defects and rapi

134 orest environment followed by their eventual demise have remained enigmatic.

135 The 'impending demise' hypothesis thus rests on understanding the degre

136 successful in 84% of 143 fetuses with fetal demise in 8%.

137 xcitation of motor neurons can prevent their demise in a mouse model of inherited ALS by a mechanism

138 Mitral regurgitation was present before demise in all affected recipients evaluated with color D

139 s are a major cause of coccolithophore bloom demise in both temperate and sub-temperate oceanic regio

140 he ultimate targets to prevent the capillary demise in diabetic retinopathy.

141 new therapeutic approach to avert cognitive demise in DM.

142 weaning age leading to litter starvation and demise in early to mid-lactation.

143 s that may contribute to RGC dysfunction and demise in glaucoma.

144 ad been shown to prevent fetal infection and demise in mice.

145 l expansion in some situations and apoptotic demise in others.

146 of mitochondrial potential precedes cellular demise in several programmed cell destruction pathways,

147 n-challenged IL5tg mice, which undergo rapid demise in the absence of exogenous cytokine support.

148 ects of drugs that prevent retinal capillary demise in the diabetic rat.

149 e-2 might be the cause of excessive neuronal demise in the striatum of Abeta + ET1 rats.

150 r mechanisms underlying pancreatic beta-cell demise in type 1 diabetes.

151 vented preterm delivery and alleviated fetal demise in utero elicited after cPAF administered by i.p.

152 vented preterm delivery and alleviated fetal demise in utero elicited by i.p. LPS administration in l

153 own that necroptosis contributes to cellular demise in various pathophysiological conditions, includi

154 pregnancy is a leading cause of human fetal demise; in particular, trauma to the brain may lead to d

155 Potential factors contributing to their demise include climatic change, human impact, or some co

156 esulted in placental insufficiency and fetal demise, infections at midstage (E9) resulted in reduced

157 Current hypotheses for this early demise involve relatively minor biotic events, but are a

158 esults identify an immune mechanism of fetal demise involving IL-10 deficiency, NK cells, and inflamm

159 own, there is increasing evidence that their demise is a result of a combination of genetic and envir

160 Our data indicate that early demise is due to mechanisms other than myelin loss and s

161 t abnormal autophagy activation and neuronal demise is due to severe, neuron-specific, nicotinamide a

162 While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibili

163 The St. Paul mammoth demise is now one of the best-dated prehistoric extincti

164 The mechanistic basis of age-related thymic demise is unclear, but prior evidence suggests that calo

165 chain reaction of beta cell dysfunction and demise leading to onset and progression of diabetes.

166 ations that are responsible for the neuron's demise may soon help in developing effective preventativ

167 antibodies; intrauterine fetal anemia and/or demise occurred in a subset of KEL-positive pups born to

168 nological constraints for both the onset and demise of a Cryogenian glaciation from the same continen

169 nse to novel odors and eventually led to the demise of adult-born GCs.

170 e cation channel, mediates Ca2+ overload and demise of anoxic neurons.

171 The demise of antibacterial drug discovery brings the spectr

172 romoting T regulatory cell expansion and the demise of antitumor CD8(+) effector T cells, thus contri

173 r this pattern is a consequence of the rapid demise of asexual lineages, an unusual degree of mutatio

174 sis of retinal ganglion cells, and prevented demise of axons in the optic nerve.

175 cefixime or ceftriaxone heralds the possible demise of beta-lactam antibiotics as effective treatment

176 The cause of demise of both Tc and superfluid density ns on the overd

177 epletion during HIV-1 infection involves the demise of bystander CD4 T cells due to abortive infectio

178 lution of shallow marine carbonates, and the demise of carbonate shell-bearing organisms suggest glob

179 In addition, the demise of carnivore seems to be a consequence of the hum

180 of the death effector pathway to insure the demise of cells committed to apoptosis.

181 chemical pathways that lead to the organized demise of cells.

182 ocean stripped of (most) life but rather the demise of certain eukaryotic organisms, leading to a dec

183 ole of climate change in the development and demise of Classic Maya civilization (300 to 1000 C.E.) r

184 olar Dynamics Observatory (SDO) observed the demise of comet C/2011 N3 (SOHO) within the low solar co

185 Although many studies have associated the demise of complex societies with deteriorating climate,

186 ollowing the last glacial maximum (LGM), the demise of continental ice sheets induced crustal rebound

187 early molecular pathways associated with the demise of DA neurons, including those of inflammatory ex

188 disease were still capable of inhibiting the demise of dopaminergic neurons and concomitant loss of n

189 Some have speculated that the demise of early modern humans at that time was due in pa

190 terrestrial environments contributed to the demise of early Supe settlements.

191 was traditionally taken as evidence for the demise of ferruginous oceans, but recent geochemical stu

192 optic nerve head was followed by progressive demise of ganglion cells and their axons, the hallmarks

193 d, and induced apoptosis, with a progressive demise of ganglion cells in the retina and their axons c

194 cells, progressive demyelination, and early demise of GLD patients.

195 Growth of Group I is accompanied by demise of Group II on irradiation with visible light (la

196 Varroa mites may cause the serious demise of honey bees by suppressing bee immunity and by

197 eared, and this has been argued to cause the demise of HTS with overdoping.

198 amatic loss of cTECs, accompanied by a rapid demise of immature thymocytes.

199 ysical processes, and that lead to the rapid demise of large-scale algal blooms in the oceans.

200 ntact rates and potentially accelerating the demise of large-scale phytoplankton blooms.

201 pLHBM-Dimer transgene prevented the neonatal demise of LpL knockout mice; however, these mice were hy

202 vector-only controls and resulted in a rapid demise of mice bearing those tumors.

203 gy of Parkinson's disease is the progressive demise of midbrain dopamine neurons and their axonal pro

204 The imminent demise of montane species is a recurrent theme in the cl

205 gest that the Protoaurignacian triggered the demise of Neandertals in this area.

206 l of modern humans in western Europe and the demise of Neandertals.

207 humans, who could only enter Europe when the demise of Neanderthals had already started.

208 ers, which could therefore contribute to the demise of neurons subjected to oxidative damage.

209 ly leads to dysfunction and, ultimately, the demise of neurons through a series of multiple events.

210 activity, promotes autophagy and causes the demise of neurons.

211 active oxygen species (ROS) and leads to the demise of neurons.

212 time points, a potential explanation for the demise of Nmt1-/- embryos.

213 leogene mass extinction, 66 Ma, included the demise of non-avian dinosaurs.

214 etaceous mass extinction, which includes the demise of nonavian dinosaurs.

215 of neurons are thought to contribute to the demise of normal behavior in the disease state.

216 a poor visual outcome are likely also due to demise of optic nerve axons.

217 The final demise of photoreceptors occurs via apoptosis involving

218 macular degeneration is characterised by the demise of photoreceptors, which precedes the loss of und

219 l degeneration lose sight due to the gradual demise of photoreceptors.

220 me pathological amyloid proteins lead to the demise of post-mitotic tissue.

221 Striking changes include the demise of previously dominant staghorn coral Acropora ce

222 ion and calpain activation contribute to the demise of protein turnover by the ubiquitin/proteasome p

223 ut recBC conditions, indicating preferential demise of replication bubbles.

224 ed to be primarily responsible for the early demise of Salmonella-infected TLR4-deficient mice.

225 ult life, the mutant protein only causes the demise of selective neuronal subtypes.

226 ying the fetal alloantigen leads to enhanced demise of semiallogeneic fetuses within a litter.

227 decades have witnessed the introduction and demise of several different antithrombotic medications f

228 es' for studying the origin, maintenance and demise of species.

229 ecular machineries that cause the programmed demise of specific cells, but have also allowed us to ge

230 Pronouncements regarding the demise of such encounters are premature.

231 ptosis, but the precise role of RIPKs in the demise of T cells lacking FADD or casp8 activity is unkn

232 surviving member of the Elasmotheriinae, the demise of the 'Siberian unicorn' marked the extinction o

233 Parkin deficiency leads to the premature demise of the catecholaminergic neurons of the ventral m

234 want grazing to cease, presumably leading to demise of the cattle.

235 The demise of the cell resembles many forms of necrosis, ins

236 and cathepsin D independently and led to the demise of the cell.

237 this induction is sufficient to promote the demise of the cell.

238 omal DNA circles (ERCs), which can cause the demise of the cell.

239 the activation of caspases and the ultimate demise of the cell.

240 ts of cationic Au-NPs resulting in the rapid demise of the cells.

241 on of many North American megafauna, and the demise of the Clovis archeological culture.

242 n infection that will ultimately lead to the demise of the host.

243 There is no evidence that the demise of the Match has had any effect on wages.

244 ly was designed to solve re-emerged with the demise of the Match.

245 The demise of the Neanderthals and the nature of the possibl

246 d strategies used by males to accelerate the demise of the opposite sex (hermaphrodites).

247 ciated with age that ultimately leads to the demise of the organism.

248 whether humans or climatic change caused the demise of the Pleistocene megafauna.

249 The demise of the snake community after amphibian loss demon

250 The rise and demise of these branches (clades) are ultimately determi

251 thway in chondrocytes, thereby promoting the demise of these cells.

252 ochemical pathways involved in the selective demise of these neurons are still unclear.

253 at the nematode feeding site, promoting the demise of this biotrophic interface.

254 yed an important role in the development and demise of this complex civilization.

255 lant activity and thrombin generation in the demise of thrombomodulin-null embryos, and suggests that

256 ells in the bone marrow in addition to local demise of thymic cells.

257 he equator are caught in the gap between the demise of traditional cultural institutions and the rise

258 y to be a contributing factor leading to the demise of trophoblasts.

259 echnological innovations, market demands, or demise of various human cultures for last 4000 years.

260 arlier extinction history, especially by the demise of volatile taxa in the end-Cretaceous mass extin

261 y for congenital anomalies can prevent fetal demise or alter the course of organ development, resulti

262 me was perinatal mortality, defined as fetal demise or death before neonatal discharge.

263 iomyopathy/endocardial fibroelastosis suffer demise or need for transplant.

264 with the exceptions of an intrauterine fetal demise owing to acrania and a molar pregnancy.

265 ventricular outcome (P<0.0001), intrauterine demise (P=0.036), and early termination (P<0.0001) were

266 posure and adverse pregnancy outcomes (fetal demise, prematurity, low birth weight and congenital ano

267 posure and adverse pregnancy outcomes (fetal demise, prematurity, low birth weight, congenital anomal

268 er, germ line Ott1 deletion results in fetal demise prior to embryonic day 10.5, indicating additiona

269 clearly resulted from human overhunting, its demise raises questions about the Pleistocene overkill m

270 gnancy followed by a normal heart rate had a demise rate of 7.6% (nine of 118), which is similar to t

271 The cell demise relied on the presence of caspase-3/7 but not cas

272 logical mechanisms responsible for embryonic demise remain elusive.

273 e and the events leading up to their violent demise remain intensely debated.

274 the likelihood of subsequent first-trimester demise remains elevated (approximately 25%) even if the

275 station (E14.5) and the cause of their early demise remains unclear.

276 is generally perceived as a passive cellular demise resulted from unmanageable physical damages.

277 rs, is probably relevant in speeding up cell demise, since RNA interference-mediated Mcl-1 silencing

278 ertical transmission of ZIKV can cause fetus demise, stillbirth, or severe congenital abnormalities a

279 y use distinct mechanisms to cause beta-cell demise that possibly involve activation of third-party c

280 nic day 6.5 (E6.5) or E7.5 resulted in fetal demise that was associated with ZIKV infection of the pl

281 nction in neurons, leading to their eventual demise through apoptosis.

282 growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood.

283 roapoptotic receptor agonists cause cellular demise through the activation of the extrinsic and intri

284 with competitors or hasten post-reproductive demise, thus decreasing competition for resources, they

285 tal pressures or attribute the Neanderthals' demise to competition with modern humans, who occupied t

286 tastrophic consequences associated with fork demise, translesion synthesis (TLS) polymerases such as

287 ate over the course of bloom development and demise using a diverse suite of molecular tools and in s

288 Postnatal demise was associated with cardiac enlargement and defec

289 Presentation associated with fetal demise was more common in the second trimester (55.3%),

290 This rate of demise was significantly higher than that of 7.2% (28 of

291 The rates of first-trimester demise were 60.6% for pregnancies with slow heart rates

292 pontaneous abortion, preterm birth and fetal demise were assessed for a temporal and etiological rela

293 actions, autophagy may contribute to neuron demise when dysregulated.

294 ovel mutations in ABCA12 gene after neonatal demise, which helped in providing prenatal diagnosis in

295 disruption of the plasma membrane to a cell demise with a nearly intact plasma membrane.

296 iate patient selection and low risk of fetal demise with FAV are critical factors for obtaining a sur

297 ture peripheral responses and their ultimate demise, with particular emphasis on mouse NK cells and v

298 d for appropriate case selection, led to its demise within 30 years.

299 on molecular or genetic regulations of cell demise without a proper characterization of the phenotyp

300 iminated, preventable excess recurrent fetal demise would be 17%, 25%, and 33%, respectively.