ライフサイエンスコーパス: demise

1 deficiency or actually drives the germ-cell demise.

2 estriction, fetal liver hypocellularity, and demise.

3 n that lead to energy depletion and cellular demise.

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

5 of the contributing factors in motor neuron demise.

6 nce of events leading to dopaminergic neuron demise.

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

8 nst degenerative disorders that lead to cell demise.

9 athway is not involved in photoreceptor cell demise.

10 develops but the embryo itself suffers early demise.

11 initiator caspase-8, and ultimately cellular demise.

12 and fetal growth retardation and subsequent demise.

13 pair of DNA breaks or after replication fork demise.

14 ng to increased myocardial mass and neonatal demise.

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

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

17 owing then leads to graft ischemia and organ demise.

18 h other factors, contributed to its eventual demise.

19 ts sequelae are the most common mechanism of demise.

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

21 aortic valvuloplasty carries a risk of fetal demise.

22 s of epithelial cell polarity, and embryonic demise.

23 ociated proteins, and generalized epithelial demise.

24 ith subsequent cardiac failure and embryonic demise.

25 ly detectable archaeological record of their demise.

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

27 decreased cardiomyocyte proliferation before demise.

28 c reticulum injury contributes to motoneuron demise.

29 ophila melanogaster, also contributes to its demise.

30 signaling for other purposes without risk of demise.

31 rotection against placental damage and fetal demise.

32 death remains the most common cause of fetal demise.

33 pro-survival responses, leading to cellular demise.

34 in these mice may contribute to their rapid demise.

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

36 tions about mitochondrial routes to cellular demise.

37 sis is an established pathway for islet cell demise.

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

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

40 mal ribosomal DNA circles, which cause yeast demise.

41 rologic symptoms, which usually led to rapid demise.

42 r characterized by rapid and uniform patient demise.

43 nenolone or progesterone did not cause fetal demise.

44 duced c-Jun activation and dopaminergic cell demise.

45 al cardiac gene program and eventual cardiac demise.

46 inflammation-induced preterm birth and fetal demise.

47 had episodes of acute rejection before graft demise.

48 yglutamine proteins results in eventual cell demise.

49 ore vigorous inflammatory response and rapid demise.

50 causal mutations with eventual photoreceptor demise.

51 ing the pathway from death receptors to cell demise.

52 ce neuronal cell survival or ensure cellular demise.

53 at together contribute to photoreceptor cell demise.

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

55 wed by irreversible caspase-independent cell demise.

56 cy can cause congenital abnormities or fetal demise.

57 cies toxicity) drive cellular dysfunction or demise.

58 e stress and light-independent photoreceptor demise.

59 nuclear translocation and subsequent glioma demise.

60 ogical communities, from initiation to their demise.

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

62 lternatively, pathogen subversion caused its demise.

63 devastating congenital abnormities or fetal demise.

64 hat SC metabolic deficits may lead to axonal demise.

65 cells to ensure silent, noninflammatory cell demise.

66 fying kidney injury and accelerating nephron demise.

67 oals work selflessly, resulting in their own demise.

68 T cells to cause inflammation and beta cell demise.

69 lantic, from exponential growth to its rapid demise.

70 d fetal tissues, and protected against fetal demise.

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

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

73 n't they cause disease and lead to our rapid demise?

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

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

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

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

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

79 Synaptic demise and accumulation of dysfunctional proteins are th

80 oxyecdysone (20E) and involves mitochondrial demise and cell shrinkage.

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

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

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

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

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

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

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

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

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

90 resented with perinatal disease and neonatal demise, and the less severe, nonperinatal group, in whic

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

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

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

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

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

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

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

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

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

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

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

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

103 lung preservation contributes to early graft demise by recruiting leukocytes, activating complement,

104 3 levels increase, it contributes to its own demise by up-regulating the transcription of S100B as pa

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

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

107 were more commonly associated with neonatal demise (chi(2) = 11.54, P = 0.003).

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

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

110 In contrast to the lymphoid demise, cux/CDP(Delta HD/Delta HD) mice demonstrated mye

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

112 tion, and variable frequency of intrauterine demise determined by parental FX genotype.

113 the operating room, or led to the patient's demise due to continued attempts to complete all surgica

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

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

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

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

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

119 odegeneration begins in infancy and leads to demise generally by 4-6 years of age.

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

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

122 ly brief career and his unanticipated sudden demise have lessened the fame of Dr. Lyons to which he i

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

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

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

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

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

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

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

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

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

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

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

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

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

136 f a woman who experienced intrauterine fetal demise in the second trimester of pregnancy.

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

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

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

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

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

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

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

144 rly embryonic demise or with relatively late demise involving a well-formed fetus.

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

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

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

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

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

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

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

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

153 h the normal function of the cell and in its demise makes these channels prime targets for future res

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

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

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

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

158 ination intermediates similarly leads to the demise of affected cells.

159 ver, the late age at disease onset and rapid demise of affected individuals markedly hamper collectio

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

161 The demise of antibacterial drug discovery brings the spectr

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

163 diagnostic procedures is contributing to the demise of applied plant pathology.

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

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

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

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

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

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

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

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

172 isrupts this process and uncouples apoptotic demise of chondrocytes and cartilage degradation, result

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

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

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

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

177 uclein aggregation, which contributes to the demise of dopamine neurons.

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

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

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

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

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

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

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

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

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

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

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

189 Any talk of the demise of in vitro cultivation as a useful mechanism for

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

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

192 pression of hLpL(HBM) prevented the neonatal demise of LpL knockout mice.

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

194 s led to the rapid activation and subsequent demise of Mac1(high) resident peritoneal macrophages.

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

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

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

198 dent apoptotic pathway may contribute to the demise of motor neurons in ALS and that targeting key mo

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

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

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

202 ajor characteristic lesions that lead to the demise of neurons in Alzheimer's disease.

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

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

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

206 antimicrobial properties, mitigates both the demise of nigrostriatal dopaminergic neurons and the for

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

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

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

210 er, we provide documentation that before the demise of Pennsylvanian age coal-swamp forests, a highly

211 ycemia is a possible mechanism for the early demise of pericytes in diabetic retinopathy.

212 The final demise of photoreceptors occurs via apoptosis involving

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

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

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

216 l communication have led some to predict the demise of printed journals.

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

218 ctors that contribute to the survival versus demise of Ras-transformed cells is essential to our unde

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

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

221 disorders that range pathologically from the demise of select groups of nuclei to pervasive degenerat

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

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

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

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

226 ative disease characterized by the selective demise of specific neuronal populations leading to impai

227 With the demise of subsidized trade, the absence of aid from the

228 Pronouncements regarding the demise of such encounters are premature.

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

230 onal soma are also major contributors to the demise of the axonal appendage.

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

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

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

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

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

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

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

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

239 The early demise of the dynamo could have arisen through a change

240 d Hawaiian oceanic basalts indicate that the demise of the georeactor is approaching.

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

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

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

244 r, new data suggest that rumors of the rapid demise of the mossy cells might have been greatly exagge

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

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

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

248 he multifocal inflammatory lesions and early demise of the TGF-beta1 null mice.

249 overy after BM suppression, resulting in the demise of the treated mice.

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 n attempt to document better the decline and demise of two Alaskan Pleistocene equids, I selected a l

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 s are associated with either early embryonic demise or with relatively late demise involving a well-f

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

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

267 Thus, the commitment to mitochondrial demise precedes the commitment to execution events.

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 However, the mechanism signaling their demise remains poorly understood.

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

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

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

279 the testa manufactures components before its demise that can maximize testa strength, whereas the end

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

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

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

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 ty, one cannot say precisely when georeactor demise will occur, whether in the next century, in a mil

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

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.