ライフサイエンスコーパス: death

1 hat together contribute to organ failure and death.

2 coccal alpha-toxin-induced keratinocyte cell death.

3 d (or could have led) to major disability or death.

4 systemic and led to multiorganic failure and death.

5 uiescent HSPCs, resulting in their apoptotic death.

6 reatest risk of sudden and nonsudden cardiac death.

7 a behaved differently in the context of cell death.

8 d by progressive retinal ganglion cell (RGC) death.

9 ved for the two measures with late all-cause death.

10 l abnormalities, and prevention of premature death.

11 to donate each year at the time of imminent death.

12 he frequency and/or timing of either form of death.

13 togonial death and reduces overall germ cell death.

14 alertness, causing premature disability and death.

15 atrophy might occur at least 10 years before death.

16 ation of RIPK1 was sufficient to induce cell death.

17 associated with increased organ failure and death.

18 tic alternatives, leading to amputations and death.

19 ion panel determined ILD hospitalization and death.

20 lays p death, while eat-2 mutation reduces P death.

21 cellular calcium (Ca(2+)) over time and cell death.

22 an result in loss of mating opportunities or death.

23 Michael Polanyi, as well as the 40th of his death.

24 ranscription factor EB and, eventually, cell death.

25 s amount of heating alone did not cause cell death.

26 reased in the surviving spouse after patient death.

27 A hybrid structures, leading to motor neuron death.

28 progenitor cells (OPCs) it induces cellular death.

29 NMDA), which is excito-toxic and induces RGC death.

30 lture medium were sufficient to promote cell death.

31 murium infection, eventually leading to cell death.

32 MEKK4 dramatically reduces cystine-deprived death.

33 ng in activity-dependent, non-apoptotic cell death.

34 table increase in donation after circulatory death.

35 e from diagnosis to death, and the causes of death.

36 ferative burst that is followed by apoptotic death.

37 patients with very severe AS at high risk of death.

38 eptibility to cardiac arrhythmias and sudden death.

39 mic instability and ultimately leads to cell death.

40 rom changes in soil chemistry following tree death.

41 s, but mass fluctuations continue until cell death.

42 ER stress pathways that promote acinar cell death.

43 rred in 32%, and 5% had treatment-associated deaths.

44 There were nine treatment-related deaths.

45 ions (MIs; nonfatal and fatal) and acute CHD deaths.

46 and are responsible for most cancer-related deaths.

47 form efforts to reduce disparities in sepsis deaths.

48 cer (n = 134) were significantly reduced (40 deaths [0.025% per year] v 94 deaths [0.038% per year];

49 ly reduced (40 deaths [0.025% per year] v 94 deaths [0.038% per year]; HR, 0.65; 95% CI, 0.45 to 0.94

50 sted hazard ratio for disease progression or death, 0.65; P<0.001).

51 o immune checkpoint blockade with programmed death 1 (PD-1) targeted agents, novel immunotherapies an

52 s, and relatively few PD-1+ (programmed cell death 1-positive) T cells, an immunophenotypic pattern a

53 , which typically results in disease or cell death [1].

54 antibody that inhibits PD-L1 and programmed death-1 (PD-1) and PD-L1 and B7-1 interactions, reinvigo

55 h ligand-1 (PD-L1) interacts with programmed death-1 (PD-1) and the immunostimulatory molecule CD80 a

56 The anti-Programmed cells Death-1 was stopped and a topical corticosteroid treatme

57 3; 95% CI, 0.63-1.39; P = .74) or noncardiac death (15 [1.4%] for the bivalirudin group vs 11 [1.0%]

58 ardial infarction, stroke, or cardiovascular death); 2) a MedDiet intervention [supplemented with ext

59 es were noted in the rates of 1-year cardiac death (44 [4.0%] for the bivalirudin group vs 48 [4.3%]

60 for 1 y and prevent approximately 18,600 CVD deaths (95% CI: 17,600, 19,500), gaining approximately 2

61 iated with an increased rate of ILD-specific death (adjusted hazard ratio, 2.3; 95% confidence interv

62 factors to measure to predict progression to death after coronary heart disease is established.

63 The effect of pirfenidone on death after hospitalization is uncertain.

64 ciated with a 27% reduction in the hazard of death after LVAD (adjusted hazard ratio, 0.73; 95% confi

65 During the same period, deaths after breast cancer (n = 134) were significantly

66 ality improvement program had a reduction in deaths after inpatient surgery over the first 3 years of

67 with a reduction in the odds of in-hospital death among patients aged 18-49 years (adjusted odds rat

68 n, accompanied by excessive necroptotic cell death and a reduced number of secretory epithelial cells

69 Long-term trends in excess risk of death and cardiovascular outcomes have not been extensiv

70 estimated for the association between early death and demographic, clinical, and socioeconomic facto

71 n, neutrophil accumulation, endothelial cell death and desquamation, and mural thrombosis.

72 ronamine (T1AM), on cell proliferation, cell death and DNA damage was studied in two ovarian cancer c

73 ere associated with higher risks for patient death and graft loss, although SRL + MPA was associated

74 All-cause death and incident chronic kidney disease were secondary

75 action motifs (RHIM) play a key role in cell death and inflammatory signalling(1-3).

76 lth of soldiers is adversely affected by the death and injury of other unit members, but whether risk

77 ower incidence of the composite of all-cause death and MI (hazard ratio [HR]: 0.65; 95% confidence in

78 urs was also associated with a lower risk of death and myocardial infarction (odds ratio, 0.76; 95% c

79 EG1 and VdEG3 acted as PAMPs to trigger cell death and PAMP-triggered immunity (PTI) independent of t

80 ation, compromise synchronous spermatogonial death and reduces overall germ cell death.

81 -gamma-induced remyelinating oligodendrocyte death and remyelination failure in the cuprizone model (

82 Based on risk of death and return on investment, high-risk groups of the

83 x uncontrolled studies reported low rates of death and serious adverse events (0% to 1.25%) in nontra

84 or suppression of a caspase-independent cell death and the long-term survival of FA-treated cells.

85 investigated the mechanisms of splenic cell death and their relationship to control of parasitemia a

86 Eliminating PEPD causes cell death and tumor regression due to p53 activation.

87 tudies to estimate changes in the numbers of deaths and in life years and life expectancy at birth, a

88 coronary heart disease death, cardiovascular death, and all-cause mortality by 28% (P=0.020), 25% (P=

89 differentiation of stem cell, cell survival/death, and cellular metabolism under both physiological

90 ed exaggerated inflammasome activation, cell death, and IL-18 secretion, suggesting that restoring mi

91 protecting tumour cells from MYC-driven cell death, and indeed, MYC selects for this pathway in part

92 to prevent B cell activation, increase cell death, and induce tolerance in vivo.

93 tment-related adverse events associated with death, and one patient died from treatment-related adver

94 eline and (2) the incidence of death, sudden death, and other cardiac adverse events.

95 Myocardial infarction, cardiovascular death, and repeat revascularization cumulative incidence

96 einopathy, the median time from diagnosis to death, and the causes of death.

97 2) cases of infant invasive GBS disease, (3) deaths, and (4) disabilities.

98 health that causes hundreds of thousands of deaths annually.

99 lls or to selectively induce programmed cell death (apoptosis) or uncontrolled cell death (necrosis).

100 role in the early stages of programmed cell death (apoptosis).

101 rtality after AKI is high, but the causes of death are not well described.

102 At death, as many as 10(10) colony-forming units were found

103 ted "effector" genes that contribute to cell death, as well as genes that affect the sensitivity of B

104 Cardiovascular death at 30 days occurred in 221 of 9155 patients (2.4%)

105 mbined with ART resulted in reduced rates of death at both 24 weeks and 48 weeks without compromising

106 gained, pound372 207 (268 162-1 903 385) per death averted, and pound628 874 (434 902-4 740 724) per

107 r of unnecessary treatments generated per TB death averted, if standard Xpert were switched to Xpert

108 tments generated, the projected number of TB deaths averted, and the projected number of unnecessary

109 , those with a SPRM-predicted risk of sudden death below the median had no reduction in mortality wit

110 le to induce efficient apoptotic cancer cell death both in vitro and in vivo through tumor-specific (

111 ed reactive oxygen species and necrotic cell death, both of which were mitigated by ATF6 overexpressi

112 eading cause of mortality in HFpEF is sudden death, but little is known about the underlying mechanis

113 educed the hazard of disease progression and death by 79%.

114 NMDAR in non-neuronal cells results in cell death by excitotoxicity, hindering the development of ce

115 uation of organ support after declaration of death by neurologic criteria (outside of organ donation;

116 We analysed deaths by governorate and over time.

117 d case-cohort design to estimate the risk of deaths by suicide and attempted suicide in individuals d

118 One death (by suicide) occurred in the MVC-TDF group but was

119 phase and the risk of coronary heart disease death, cardiovascular death, and all-cause mortality by

120 a composite global rank score (hierarchy of death, cardiovascular hospitalizations, and percent chan

121 In fully adjusted models, only death-censored graft loss remained significant (HR, 1.38

122 dian follow-up of 19 months, there was 100% (death-censored) renal allograft survival with estimated

123 inically meaningful reduction in the risk of death compared with bortezomib.

124 ignificantly higher risk of disease-specific death compared with ultralow-risk patients by Cox analys

125 diagnoses, health services utilization, and death data.

126 inter-organelle communication, and cell life/death decisions.

127 out half, and the estimated number of excess deaths declined by about a third.

128 ggering constitutive caspase-8-mediated cell death dependent on FADD but independent of Ser(533) phos

129 cellular apoptotic pathways, increases cell death, diminishes autophagy, and reduces cancer formatio

130 ndeed, SseK1 caused the GlcNAcylation of the death domain-containing proteins FADD and TRADD, whereas

131 -lung transplant and the composite rates for death, double-lung transplant, or restenosis at 36 month

132 ing invasive pneumococcal disease (IPD), but deaths due to IPD still occur.

133 Transient activation of apoptotic cell death during early age correlated well with the differen

134 with 3%, 14%, 19%, and 28% increased risk of death during TB treatment [first quintile, referent; sec

135 igh-dose vaccine in preventing postinfluenza deaths during 2012-2013 and 2013-2014, when influenza vi

136 f diarrhea, 109000 diarrheal DALYs, and 1560 deaths each year.

137 ading cause of vaccine-preventable childhood death, even though highly effective pneumococcal conjuga

138 to CQ, resulting in increased apoptotic cell death following treatment.

139 determined the age- and sex-adjusted risk of death for each type of synucleinopathy, the median time

140 Median time of death for patients with FMF was 61 months (range, 16-81)

141 ], 0.47 to 0.82), as well as a lower risk of death from any cause (hazard ratio, 0.70; 95% CI, 0.50 t

142 osis was not associated with reduced risk of death from any cause or from cancer for patients whose t

143 defined as the time from randomisation until death from any cause), analysed in the intention-to-trea

144 Antifibrinolytics reduce death from bleeding in trauma and post-partum haemorrhag

145 ction worsens and is largely attributable to death from cardiovascular disease, although cancer incid

146 ; 95% CI: 0.99 to 1.32), but higher risks of death from coronary heart disease (HR: 1.45; 95% CI: 1.2

147 e after CRC diagnosis with decreased risk of death from CRC and overall mortality.

148 mes included ICU admission rate, in-hospital death, functional status, and quality of life (12-Item S

149 g function and is the third leading cause of death globally.

150 of XLP-2 and VEO-IBD XIAP mutations on cell death have been inconsistent.

151 of brain damage, nursing home admission, or death (hazard ratio, 0.67; 95% CI, 0.53 to 0.84).

152 nts, RBC transfusion was not associated with death (hazard ratio, 1.07; 95% CI, 0.88-1.30; p = 0.52).

153 confidence interval, 1.11-1.60; P=0.002) and death (hazard ratio, 2.10; 95% confidence interval, 1.60

154 and AF treatment, as well as 2-year risk of death, hospitalization, thromboembolic events, heart fai

155 severe ALI (HR, 0.26 [95% CI, .13-.55]), and death (HR, 0.19 [95% CI, .16-.23]) compared with nonuser

156 s resulted in a 25% reduction in the risk of death (HRR = 0.73, 95% CI:0.58 to 0.91) and accounted fo

157 lity risk was found for concordant causes of death (i.e., siblings dying from the same causes) but no

158 Pyroptosis is a form of cell death important in defenses against pathogens that can a

159 odegenerative phenotype leading to premature death in 36% of the population.

160 r ETI and containment of stress-induced cell death in Arabidopsis.

161 The importance of cell death in brain development has long been appreciated, bu

162 nding of mechanisms and consequences of cell death in complex organisms is the inability to induce an

163 ongestion, and extensive midzonal hepatocyte death in control mice, which were strongly minimized in

164 ogue HNG protects from stressor-induced cell death in fibroblasts, cardiomyoblasts, neuronal cells, a

165 used by OGD/ischemia contributes to neuronal death in hippocampal neurons via diverse effects on NADP

166 This review will focus on the role of cell death in maintenance of T-cell homeostasis and outline n

167 r virus (CDV) cause high mortality rates and death in many carnivores.

168 rvention aimed at the prevention of neuronal death in neurodegenerative diseases.

169 utrophil depletion abrogated protection from death in Nlrp3(-/-) mice in response to CLP.

170 ardial infarction, stroke, or cardiovascular death in patients with established atherosclerotic cardi

171 LK to activate downstream signaling and cell death in RGCs, including in a mouse model of optic nerve

172 nockdown of GP130 or IL-2Rgamma induced cell death in selected JAK inhibitor-sensitive cells.

173 One death in the everolimus group (acute kidney injury assoc

174 n of cerebral blood flow (CBF) leads to cell death in the infarct core, but tissue surrounding the co

175 cardiovascular disease, the leading cause of death in the United States.

176 Cancer is one of leading causes of death in the world and occurs in more than two hundred t

177 cytokine-mediated beta-cell dysfunction and death in type 1 diabetes mellitus, although the mechanis

178 3 exposures, and estimated total respiratory deaths in 2010 that were attributable to long-term annua

179 ultimately comprising a quarter of civilian deaths in 2016.

180 ection (ALRI) resulting in 55 000 to 199 000 deaths in children younger than 5 years in 2005.

181 Deaths in HIV-positive people have decreased since the i

182 y injury associated with diarrhoea), and two deaths in the combination group (diarrhoea and urinary s

183 Of note, 1 in 3 of the deaths in this cohort occurred in women without obstruct

184 ty to the mTORC1 signaling pathway and cause death, indicating that persistent signaling supports sen

185 d physiological changes associated with cell death induced by algicidal bacteria.

186 Two toxic deaths (infections) were recorded, both in patients who

187 kilometer and use of NSAIDs at baseline and death information at follow-up.

188 NTERPRETATION: For most sudden natural adult deaths investigated by HM Coroners, PMCTA could be used

189 The primary cause of death is cardiovascular disease at about 14 years.

190 viduals of known period of burial and age at death is described.

191 e were followed until their first CHF event, death, last follow-up date, or December 31, 2011.

192 Programmed death ligand-1 (PD-L1) interacts with programmed death-1

193 Atezolizumab is a humanised antiprogrammed death-ligand 1 (PD-L1) monoclonal antibody that inhibits

194 uggest that components of the classical cell death machinery also have important non-cell-death (non-

195 suggests the mechanisms and kinetics of cell death may be influenced by nano-scale metal oxide materi

196 not undergoing surgery, competing causes of death may diminish the benefit, and there is no evidence

197 0%) from Northern Sweden were included (7121 deaths; mean follow-up: 13.7 y).

198 The combined endpoint was cardiovascular death, MI, or stroke at 1 year.

199 ore (disability range, 0 [no symptoms] to 6 [death]; minimum clinically important difference, 1 point

200 A sex-stratified illness-death model was applied to estimate the adjusted hazard

201 (MACE) assessed as the composite of cardiac death, myocardial infarction, and target vessel revascul

202 as a composite of adjudicated cardiovascular death, myocardial infarction, or ischemic stroke.

203 The primary end point was death, myocardial infarction, or unstable angina hospita

204 kin, undergoing an alternative route of cell death, namely cornification rather than apoptosis.

205 cell death (apoptosis) or uncontrolled cell death (necrosis).

206 death machinery also have important non-cell-death (non-apoptotic) functions in flies, nematodes, and

207 cular events (MACE, a composite of all-cause death, nonfatal myocardial infarction [MI], heart failur

208 Three deaths occurred (2 hydroxyurea, 1 placebo, and none from

209 No deaths occurred in this trial.

210 Six patient deaths occurred, all deemed related to underlying medica

211 ctions, 156 HF events, and 38 cardiovascular deaths occurred.

212 mean follow-up period of 12.4 y, 3259 (31%) deaths occurred.

213 val, 1.6-9.7) and a family history of sudden death (odds ratio, 3.2; 95% confidence interval, 1.1-9.4

214 ars of smoking ( Ptrend = .008), with HR for death of 1.49 (95% CI, 1.05 to 2.10) for > 60 pack-years

215 To counter premature death of a virus-infected cell, poxviruses use a range o

216 he endosymbiont from the host results in the death of both.

217 -7 breast carcinoma cells, which caused cell death of cancer cells followed by phagocytosis of cell d

218 suggest that A1 astrocytes contribute to the death of neurons and oligodendrocytes in neurodegenerati

219 n analysis explored risk factors for interim death or cardiac transplantation.

220 month mortality (safety outcome) and 3-month death or dependency (modified Rankin Scale (mRs) >/=3;ef

221 to 24 hours after birth reduces the risk of death or disability at 18 months among infants with hypo

222 ignificant change in the combined outcome of death or discharge to hospice (-1.3%/y [95% CI, -3.2% to

223 Rates for death or double-lung transplant and the composite rates

224 No treatment-related death or graft-versus-host disease had been reported; 15

225 ndently associated with an increased risk of death or heart transplantation (all Ps<0.001).

226 Patients were followed up until death or were censored on December 31, 2013.

227 0.003), possibly due to competing causes of death over this dose interval.These results confirm and

228 as used to examine trends in rates of sudden death over time.

229 While ATP depletion led to cell death, over-acetylated tubulin led to inhibition of moti

230 the first incident myocardial infarction or death owing to coronary heart disease, and stroke, defin

231 oke, defined as the first nonfatal stroke or death owing to stroke.

232 t cells, HS triggered an iron-dependent cell death pathway that was characterized by depletion of GSH

233 tic activation of the caspase dependent cell death pathway.

234 t activate the apoptotic or necroptotic cell death pathway.

235 eals the effect of antiviral programmed cell death pathways on inflammation, shows that caspase-8 act

236 erstanding the implications of distinct cell death pathways will help in the development of therapeut

237 nce between predicted (hospital mean of 6.18 deaths per 1000 admissions based on preimplementation tr

238 ctual mortality rates (hospital mean of 6.48 deaths per 1000 admissions; P=0.57).

239 reatment could prevent approximately 107 500 deaths per year.

240 uch as what initiates or terminates the cell death period.

241 ed this system to characterize NOD2 and cell death phenotypes driven by XIAP.

242 tive CVD (coronary heart disease and stroke) deaths prevented or postponed and life-years gained (LYG

243 From 2005 to 2014, rates of death prior to discharge and serious morbidities decreas

244 ls expressing a low level of programmed cell death protein 1 and a high level of OX40 were associated

245 cancer was the highest of any cancer and the death rate was second to that of lung cancer.

246 In plants, regulated cell death (RCD) plays critical roles during development and

247 ponse to induction of extrinsic apoptosis by death receptors or intrinsic apoptosis by chemotherapeut

248 The dataset also may be incomplete in TBI death recording or contain misclassification of mortalit

249 l record billing codes, procedure codes, and death records.

250 ng age (20-59 years) using linked census and death records.

251 arized using risk ratios (RRs) for number of deaths/recurrences and hazard ratios (HRs), with 95% con

252 Prescribed Drug Register, and the Causes of Death Register.

253 l Health Insurance Claims Data, the National Death Registry, and the bundled-payment enrollment file.

254 vince-wide health databases and the National Death Registry.

255 5 in blocking apoptotic and necroptotic cell death responses.

256 In general, causes of death responsible for more YLLs overall also contributed

257 iaz and colleagues (2017) proposes that this death results from cell competition arising from differe

258 We ascertained outcomes (death, return to care, hospital admission, other hospita

259 This increased risk of death rises exponentially as kidney function worsens and

260 rosis-associated mutant, E478G, induced cell death selectively in 661W cells.

261 sts that RARgamma initiates the formation of death signaling complexes by mediating RIP1 dissociation

262 per kinase (DLK) has been implicated in cell death signaling secondary to axonal damage in retinal ga

263 Exclusion criteria were missing key data, death sooner than 24 h after the index date, therapy wit

264 ing 30-day mortality, in-hospital and 30-day death/stroke, procedural success, intensive care unit an

265 l signatures unique to various modes of cell death, such as cells undergoing apoptosis versus necrosi

266 lvement at baseline and (2) the incidence of death, sudden death, and other cardiac adverse events.

267 s, these HD neurons were more susceptible to death than WT neurons and formed Htt aggregates under th

268 ted from cells undergoing nonprogrammed cell death that signal tissue and cell damage.

269 ough day 5; and a two-component composite of death through day 30 or use of a mechanical cardiac assi

270 nd points were a four-component composite of death through day 30, renal-replacement therapy through

271 dent bulk autophagy prevents premature plant death, thus extending the lifespan of virus reservoirs a

272 he contribution of non-respiratory causes of death to global influenza-associated mortality should be

273 eutic strategies tailored to manipulate cell death to limit T-cell survival (eg, autoimmunity and tra

274 e banks is the effect of the increased donor death-to-operation time which inevitably occurs during t

275 of 3.9+/-2.4 years, the primary end point of death, transplant, or admission for heart failure was re

276 gene I (RIG-I) initiates ZBP1-mediated cell death via the RIG-I-MAVS-IFN-beta signaling axis.

277 an time from palliative care consultation to death was 10 hours (interquartile range, 3.36-66 hours).

278 TEM cell death was prevented with neutralizing anti-IL-2 Ab or ST

279 ients might be willing to donate at imminent death, we estimate that between 76 and 396 people in the

280 The strongest predictors of in-hospital death were cardiogenic shock (odds ratio, 6.01; 95% conf

281 In multivariate analysis, risk factors for death were presence of blood in stool and severe dehydra

282 n, ABC-transporter gene expression, and cell death were used to select a suitable glyphosate concentr

283 odels on the risk of a disease milestone and death were used.

284 Among the competitive athletes, two deaths were attributed to hypertrophic cardiomyopathy an

285 Four (< 1%) on-study deaths were attributed to therapy.

286 ents died from adverse events; five of these deaths were judged to be related to treatment (two in th

287 During a mean follow-up of 9.2 years, 552 deaths were observed, of which 207 were of cardiovascula

288 me was a composite of long-term CV events or death, which was assessed via national health care datab

289 For example, glp-1 mutation only delays p death, while eat-2 mutation reduces P death.

290 increased susceptibility and apoptotic cell death with oxidative stress.

291 sal health with patient outcomes and patient death with spousal outcomes were examined using Cox and

292 Death within 1 year after initial therapy for AML.

293 Time to readmission or death within 12 months adjusted for the number of previo

294 tation and the combined end point of RVAD or death within 14 days of LVAD were assessed with stepwise

295 tatin initiators had a lower risk of ALI and death within 18 months compared with statin nonusers.

296 <7 days of life, lethal chromosomal anomaly, death within 48 hours, inability to determine AKI status

297 e of repeat ED visit, hospital admission, or death within 7 days of discharge.

298 th severe extracranial injuries (AIS >/= 3), death within 72 hours, or hospital stay <48 hours were e

299 a major cause of cirrhosis and liver-related deaths worldwide.

300 Outcome Measures: HIV transmissions and deaths, years of life, and budgetary outlays (2015 U.S.