ライフサイエンスコーパス: death

1 edictors of intensive care unit admission or death.

2 m asymptomatic cases to severe pneumonia and death.

3 10%) and heart failure event/cardiovascular death.

4 velopment, from early instar larvae to adult death.

5 tly triggered AMPK-dependent autophagic cell death.

6 e susceptible to both IgA- and IVIG-mediated death.

7 on of the plasma membrane and bacterial cell death.

8 common but important cause of sudden cardiac death.

9 a)-induced signalling and prevention of cell death.

10 ure, cardiovascular morbidity, and premature death.

11 s the second leading cause of cancer-related death.

12 h into immunologically silent apoptotic cell death.

13 l year 4 with a continued 3-fold increase in death.

14 348 and Asp-387 during the execution of cell death.

15 ousing symbiotic bacteria, during their cell death.

16 nly 1 patient experiencing progression and 1 death.

17 than one decompensating event; and grade 6 = death.

18 posite that equates ventilation on day 28 to death.

19 doses that are not related to increased cell death.

20 ion are characterized by excessive osteocyte death.

21 year, and it is the fourth leading cause of death.

22 melanoma cell proliferation and reduces cell death.

23 and malignant disease, as well as all-cause death.

24 a number needed to treat of 36 to prevent 1 death.

25 een certain antihypertensive medications and death.

26 KO brain exhibited hypoxia and neuronal cell death.

27 f various health conditions, disability, and death.

28 factors associated with rehospitalization or death.

29 , and 0.80 (95% CI, 0.72-0.88) for all-cause death.

30 compromised motor performance, and premature death.

31 ily involvement in neurodevelopment and cell death.

32 rogression to heart failure, disability, and death.

33 ine factors associated with COVID-19-related death.

34 er will probably become the leading cause of death.

35 pressure, eventually resulting in macrophage death.

36 , immunity, proteostasis and programmed cell death.

37 ot meristematic cells from heat-induced cell death.

38 eased risk of recurrence and cancer-specific death.

39 croptosis, a regulated form of necrotic cell death.

40 therapy in preventing symptomatic stroke or death.

41 treatment failure, unacceptable toxicity, or death.

42 Suicide is a leading cause of death.

43 ght to cause rod and cone photoreceptor cell death.

44 These alterations rapidly induced bacterial death.

45 d sex, driven by early and noncardiovascular death.

46 surface may determine antibody-mediated cell death.

47 25% ICU admissions, 23% intubations, and 13% deaths.

48 ibuted to underlying disease and no neonatal deaths.

49 (61.4-66.1), averting 4.8 million (4.1-4.8) deaths.

50 rgan damage, ultimately leading to premature deaths.

51 uals and is responsible for 12,000 to 56,000 deaths.

52 ) is one of the most common causes of cancer deaths.

53 ore, co-blockade of TIM3 and programmed cell death 1 (PD1) can result in tumour regression in preclin

54 d 1 (PDL1) with its receptor programmed cell death 1 (PD1) inhibits T cell responses, and blockade of

55 The interaction of programmed cell death 1 ligand 1 (PDL1) with its receptor programmed cel

56 severe adverse events [1.22 (1.11-1.34)] and death [1.17 (1.04-1.32)].

57 Excluding 2 postoperative deaths, 1- and 5-year overall survival (OS) and recurren

58 ers using immunotherapy with programmed cell death-1 (PD-1) checkpoint blockade.

59 ted in part by expression of programmed cell death-1 (PD-1) encoded by the Pdcd1 gene.

60 ith glutaminase, dual TORC1/2, or programmed death-1 inhibitors.

61 ns with COVID-19 and SUD had worse outcomes (death: 13.0%, hospitalization: 50.7%) than Caucasians (d

62 t for this analysis was the composite of (1) death; (2) rehospitalization for heart failure symptoms

63 tion: 41.0%) than general COVID-19 patients (death: 6.6%, hospitalization: 30.1%) and African America

64 0%, hospitalization: 50.7%) than Caucasians (death: 8.6%, hospitalization: 35.2%).

65 s with SUD had significantly worse outcomes (death: 9.6%, hospitalization: 41.0%) than general COVID-

66 h significantly increased risk for all-cause death (adjusted hazard ratio for moderate and severe deg

67 FTR, or a postoperative death after a complication, is currently a nationally en

68 ncer, and the second cause of cancer-related deaths (after lung cancer) among women.

69 8; P = 0.001) and donor with anoxic cause of death (aHR, 0.51; P = 0.007) were associated with lower

70 ys), the combined endpoint of cardiovascular death, all-cause stroke, myocardial infarction, or rehos

71 for intubated subjects excluding neurologic deaths also demonstrated good discrimination (all area u

72 y to substantially reduce severe illness and death among children worldwide.

73 ot chronic lung disease, was associated with death among hospitalized patients warrants further inves

74 nvolution by exacerbating inflammation, cell death and adipocytes repopulation.

75 ssion, increased hospital length of stay and death and are not predicted by ICU or ward physicians.

76 activation of NLR SUMM2 for initiating cell death and autoimmunity.

77 agnostic brain CT are associated with 1-year death and dependence after intracerebral hemorrhage, ind

78 iated with higher relative risks of neonatal death and greater absolute rate differences in neonatal

79 ome contributes to cholestasis-mediated cell death and inflammation through mechanisms involving acti

80 es to dissect the roles of caspase-8 in cell death and inflammation.

81 tep in signal transduction that impacts cell death and inflammatory signaling downstream of various i

82 PI(3)P-deficient P. falciparum precedes cell death and is reversible after withdrawal of the stress c

83 As a leading cause of death and morbidity, heart failure (HF) is responsible f

84 loride injury, associated with increased HSC death and reduced migration.

85 be attributed to axon degeneration/neuronal death and sustained neuroinflammation.

86 T), who provided serial blood samples before death and their bodies for rapid autopsy.

87 organoids is associated with increased cell death and transcriptional dysregulation indicative of an

88 There were 42 (4.0%) deaths and 188 MACE in 174 (16.6%) patients.

89 cases, 138.5 thousand (95% UI: 128.7-142.5) deaths and 3.3 million (95% UI: 3.1-3.4) DALYs globally.

90 ng the leading causes of vaccine-preventable deaths and morbidity globally.

91 ifetime (i.e., followed from 2015 through to death), and result in a health-related net monetary bene

92 -related AEs in 16% and 31% (no drug-related deaths), and treatment-emergent nephrotoxicity in 10% an

93 0.54 (95% CI, 0.39-0.76) for cardiovascular death, and 0.80 (95% CI, 0.72-0.88) for all-cause death.

94 ad an altered state of activation, increased death, and higher production of IL27.

95 gression of motor neuron axons, motor neuron death, and muscle degradation and atrophy can also be re

96 he composite outcome of blood transfusion or death, and number of blood transfusions from randomisati

97 We examined the mean age at HCV-associated death, and rates and proportions by sex, race/ethnicity,

98 characterized by synaptic loss, motor neuron death, and reduced neuronal activity in spinal sensory-m

99 tely results in programmed execution of cell death, and the nature of this cell death is determined b

100 iated and inflammatory cytokine-induced CEnC death, and to elucidate the mechanism by which this cyto

101 ht (aOR, 1.91; 95% CI, 1.33-2.76), and fetal death (aOR, 2.23; 95% CI, 1.14-4.37).

102 ture that results in right heart failure and death, are usually assessed with invasive procedures suc

103 LPS can cause death as a result of septic shock, and its lipid A core

104 evaluated by immunoblotting, ELISA, and cell death assays, respectively.

105 The SMR for COVID-19 death associated with HIV was 2.39 (95%CI 1.96-2.86); po

106 an iron-dependent form of nonapoptotic cell death associated with oxidized polyunsaturated phospholi

107 in sub-Saharan Africa (SSA) where cases and deaths associated with COVID-19 are rising(1).

108 ture.IMPORTANCE Whether clinical illness and deaths associated with elephant endotheliotropic herpesv

109 tion factor 4GI (eIF4GI) and of its homolog, death-associated protein 5 (DAP5), are elevated.

110 for calculation) of excess COVID-19-related deaths, assuming relative impact (as relative risks [RRs

111 e as a proxy, whereby breast cancer cases or deaths at age 50 years or older were regarded as postmen

112 There was one maternal death attributed to underlying disease and no neonatal d

113 The decreases in deaths attributed to mortality change from 1990 to 2017

114 ng to 3.9 million (95% CI 2.5-5.6) premature deaths averted annually.

115 se in younger HCV viremic donors after brain death being identified.

116 difference in 8-year risk for breast cancer death between continuing and stopping screening was -1.0

117 eration with no difference in apoptotic cell death between control and Ddr1(-/-) animals.

118 ity, by showing that any amplification under death-Birth updating is necessarily bounded and transien

119 ulation ageing was associated with increased death burden.

120 artilage, with no evidence of augmented cell death by activation of caspase 3.

121 ng, we examined the risks of CRC and related death by baseline colonoscopy adenoma findings.

122 Anti-apoptotic members suppress cell death by deploying a surface groove to capture the criti

123 ere was no significant difference in rate of death by suicide between soccer players and controls.

124 atients, and there was one treatment-related death caused by grade 4 dyspnoea (in cohort C).

125 The primary endpoint was 1-year tumor-death censored graft and patient survival.

126 nt follow-up was 6.3 years, during which 287 death-censored graft failures and 424 deaths occurred.

127 xams, telephone interviews, and hospital and death certificate codes.

128 generate the AFRAID (Analysis of Frailty and Death) clock, which accurately predicts life expectancy

129 imilarly, female patients had higher odds of death compared to males (OR = 1.26, 95% CI 1.21-1.30).

130 opausal breast cancer for both new cases and deaths compared with higher income countries.

131 RR of death comparing patients with recent systemic anticancer

132 ed models showed good performance to predict death (concordance index: 0.77-0.78).

133 As SARS-CoV-2 infections and death counts continue to rise, it remains unclear why so

134 at the state-level, using publicly available death data within a Bayesian hierarchical semi-mechanist

135 The risk of death decreased by 17% per 1,000-MBq increase in the tot

136 iopsy-proven acute rejection, graft loss, or death), delayed graft function, patient and graft surviv

137 n-activated protein kinase (MAPK) activating death domain protein, regulates various cellular functio

138 independent factors associated with risk of death during CHIKV infection.

139 olism, contributing to stationary phase cell death during exposure to weak acid stress.

140 ls is a promising approach for reducing cell death during gastrointestinal passage and controlling th

141 unknown mortalin substrate and cell survival/death effector.

142 detection of chromatin condensation and cell death, enabling studies of viral plaque formation with s

143 p of 3.7 +/- 2.9 years, there were 208 CV or death events.

144 ican trypanosomiasis is causing thousands of deaths every year in the rural areas of Africa.

145 eishmaniasis is responsible for up to 30,000 deaths every year.

146 The number of excess deaths, excess deaths per 100,000 people and relative in

147 s of colorectal cancer (CRC) and CRC-related death following adenoma removal are uncertain.

148 Sepsis is the most common cause of death for patients in intensive care worldwide due to a

149 Models excluding neurologic deaths, for intubated subjects, and for intubated subjec

150 Tuberculosis (TB) is the leading cause of death from a single infectious agent, requiring at least

151 We assessed risk factors for death from COVID-19 among black inpatients at an urban c

152 ion rate (eGFR), end-stage renal disease, or death from renal causes), the individual components of t

153 The rate of deaths from cardiovascular causes per 100 patient-years

154 re limited data on how such anomalies affect deaths from injuries.

155 RSV was also associated with 25.0-37.5% of deaths from medical causes (n = 8).

156 erse events: 6 relapses, 1 treatment-related death (from septicemia) during remission, and 1 secondar

157 osis (TB) is the leading infectious cause of death globally, and drug-resistant TB strains pose a ser

158 heart disease remains the foremost cause of death globally, with survivors at risk for subsequent he

159 rs unique to necroptotic proteins, this cell death has been found to occur in virtually all tissues a

160 nce (HR 1.58, CI 1.21-2.06) and CRC-specific death (HR 1.59, CI 1.19-2.12).

161 829-1.638; p = 0.377) and short-term risk of death (HR, 1.134; 95% CI, 0.894-1.438; p = 0.301) as non

162 Caspases regulate cell death, immune responses, and homeostasis.

163 these kinases results in paralysis and worm death in a mammalian host.

164 Heart failure (HF), the leading cause of death in developed countries, occurs in the setting of r

165 vasculature, causing cancer cell hypoxia and death in distant avascular regions.

166 aling pathways and promotes accelerated cell death in HSV-infected cells.

167 ckdown caused stress-gene overactivation and death in human EndoC-betaH1 cells.

168 ant huntingtin (mHTT) leads to neuronal cell death in Huntington's disease (HD) are not fully underst

169 te reveals that CHIKV-ECSA strains can cause death in individuals from both risk and non-risk groups,

170 PN diet led to vigorous seizures and a quick death in KO mice.

171 t failure hospitalization and cardiovascular death in patients with heart failure and reduced ejectio

172 rdiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neop

173 ce hospitalization for HF and cardiovascular death in patients with type 2 diabetes mellitus.

174 s in the G(2)/M phase (89%); 2) induces cell death in PC3 cells even after the removal of the compoun

175 The major cause of death in prostate cancer patients can be attributed to m

176 lysis indicated an increase in necrotic cell death in the lungs of superinfected mice compared to mic

177 One patient died by sudden death in the placebo group.

178 The lead agent protects neurons from death in vivo.

179 s the second leading cause of cancer-related death in women and is a complex disease with high intrat

180 scular disease (CVD) is the leading cause of death in women, who have a notable increase in the risk

181 of ALRI hospital admissions, and 4% of ALRI deaths in children under 5 years.

182 dence of deaths with respiratory/circulatory deaths in the first year after an RSV episode.

183 4,232 confirmed or probable COVID-19-related deaths in the US.

184 Cell death, inflammation, and tuft cell markers were downregu

185 unction convert inflammatory pyroptotic cell death into immunologically silent apoptotic cell death.

186 n of cell death, and the nature of this cell death is determined by the specific caspases involved.

187 Thus, cell death is often closely associated with the induction of

188 nsideration, this reduction in the number of deaths is projected to produce a gain of 318 million lif

189 As a cell undergoes apoptotic cell death, it experiences changes in morphology and ion conc

190 vation of porcine donation after circulatory death kidneys.

191 Programmed death ligand 1 (PD-L1) and PD-L2 are ligands for PD-1; t

192 as surface expression of CD86 and programmed death ligand 1 (PD-L1).

193 Tumor programmed death-ligand 1 expression and MSI-H/MMR-D status were no

194 ptosis is an independent, "stand-alone" cell death mechanism that fully compensates for the absence o

195 tial pitfalls, of the approach using a birth-death model with both synthetic and experimental data, a

196 Therefore birth-death models are central to macroevolutionary as well as

197 scular events (a composite of cardiovascular death, myocardial infarction or other acute coronary syn

198 in the ipilimumab group) of 302 anticipated deaths observed (about 73% of the originally planned 88%

199 Death occurred in 7 patients (4%) who received SNF472 an

200 , and 214% higher if an outbreak with sudden deaths occurred in the same month.

201 Treatment-related deaths occurred in two (<1%) patients in the atezolizuma

202 ch 287 death-censored graft failures and 424 deaths occurred.

203 ons; ROS production; and ultimately cellular death of beta-endorphin neurons.

204 Metastasis is the primary cause of death of cancer patients.

205 Apoptotic cell death of the treated HeLa and BE(2)-C cells was demonstr

206 ease inhibitor SerpinB9 (Sb9) results in the death of tumor cells in a granzyme B (GrB)-dependent man

207 dystrophy (DMD) causes severe disability and death of young men because of progressive muscle degener

208 Fungal diseases are responsible for the deaths of over 1.5 million people worldwide annually.

209 rimary safety end points were device related death or adverse events, and major bleeding within 72 ho

210 powered to assess effects on cardiovascular death or all-cause death or to characterise effects in c

211 The primary outcome was death or colectomy within 90 days after the index test.

212 rtality in those with a final disposition of death or discharge were less than 40%.

213 d chlorpromazine at 12.5 mg every 4 h, until death or discharge.

214 f metabolic stress predominate and beta cell death or dysfunction occurs.

215 8%) pancreas grafts were lost due to patient death or graft failure after >25 years.

216 -OS was associated with a 14% lower risk for death or HF hospitalization (hazard ratio: 0.86; 95% con

217 aseline to 1 month and the composite rate of death or HF hospitalization between 1 month and 2 years

218 nge that was associated with reduced risk of death or HFH between 30 days and 2 years (adjusted hazar

219 py on the primary endpoint of cardiovascular death or hospital admission for heart failure was 0.38 (

220 tion of laboratory reports returned prior to death or hospital discharge.

221 2; P = 0.004) and with a higher incidence of death or initiation of dialysis (hazard ratio, 1.48; 95%

222 The primary outcome was a composite of death or neurodevelopmental impairment (cognitive delay,

223 t NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by modulat

224 The primary outcome was time to death or symptomatic stroke confirmed by imaging, assess

225 effects on cardiovascular death or all-cause death or to characterise effects in clinically important

226 at greatest risk for early toxicity-related death or treatment failure.

227 Avoiding 1.75 million deaths or 20.5 trillion person years of life lost would

228 No deaths or cases of inflammatory bowel disease were repor

229 BEC for intermediate-risk PE, there were no deaths or device-related adverse events and a significan

230 rom baseline, CKD-related hospitalization or death, or ESKD.

231 ificantly affecting cell proliferation, cell death, or UPR induction in murine myeloblast 32D and hum

232 cedure related to infection; (2) PJI-related death; or (3) use of long-term suppressive antibiotics.

233 there were 858 incident CVD events and 1209 deaths over a median of 13.0 y.

234 ascular disease was the most common cause of death, particularly in months 0-3 post-transplant (1.18

235 Necroptosis is a cell death pathway involved in inflammation and disease.

236 ing screening was -1.0 (95% CI, -2.3 to 0.1) death per 1000 women (hazard ratio, 0.78 [CI, 0.63 to 0.

237 (38%) participants died, corresponding to 22 deaths per 1,000 person-years.

238 The number of excess deaths, excess deaths per 100,000 people and relative increase in death

239 One death possibly related to treatment (myocardial infarcti

240 A total of 39 CHIKV-deaths presented with neurological signs and symptoms, a

241 on of the bacterial chromosome, causing cell death prior to completion of phage replication.

242 This programmed cell death process is mediated by several signalling pathways

243 rise to physical observables during the cell death process.

244 ents newly treated with anti-programmed cell death protein 1 (PD-1) agents (nivolumab or pembrolizuma

245 Programmed cell death protein 1 (PD-1) has become one of the most invest

246 Some very low death rate countries such as Eastern Asia, Central Europ

247 imately 16%-46% of the decreased CVD-related death rate from 1999 to 2014 may be attributable to decr

248 c resistance crisis will result in an annual death rate of 10 million people by the year 2050.

249 Death rates ranged from a low of 1.60 (95% CI, 1.07-2.29

250 ist removal rate for "too sick" and waitlist death ratios, so waitlist management practice at individ

251 nvironmental stresses undergo regulated cell death (RCD) when homeostatic programs fail to maintain v

252 released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predicted ligan

253 and businesses lost, and more than 1 million deaths recorded to date.

254 s for hospital admissions, malignancies, and death regarding liver, cardiovascular, and malignant dis

255 1990 to 2017 were more than the increases in deaths related to population ageing for the whole world,

256 vation option for donation after circulatory death renal grafts compared with conventional hypothermi

257 00-520,000) cumulative TB incident cases and deaths, respectively, would occur between 2020 and 2035

258 tion of the early coordinated non-lytic cell death response, ultimately supports the inflammatory bre

259 There was one death resulting from a treatment-related adverse event i

260 lity (RR, 0.98 [95% CI, 0.87-1.11]), cardiac death (RR, 0.89 [95% CI, 0.71-1.12]; P=0.33), or MI (RR,

261 Additionally, the suicide death sample was found to have increased genetic risk fo

262 While suicide attempt and suicide death share a substantial proportion of their hereditary

263 rain slices we found that D(1)R-induced cell death signaling and neuronal degeneration, are mitigated

264 king the cytokine-mediated inflammatory cell death signaling pathway identified here may benefit pati

265 osis owing to concomitant activation of cell death signalling pathways; these cells are poised to apo

266 The selective pressure imposed by extrinsic death signals and stressors adds to the challenge of iso

267 ewer expected kidney donors per 100 eligible deaths than non-Gulf States.

268 Ferroptosis is a regulated form of cell death that occurs when phospholipids with polyunsaturate

269 for the competing risk of noncardiovascular death, the magnitude and direction of the factors associ

270 ncreatic, and lung cell lines triggered cell death through PTCH proapoptotic signaling.

271 enetic lesions drives the activation of cell death to eliminate cells with defective genome.

272 the largest cross-sectional cohort of CHIKV-deaths to date reveals that CHIKV-ECSA strains can cause

273 on; discharges, transfers, readmissions, and deaths (trajectories) for 6 months following discharge f

274 rtance in proliferation, apoptosis, and cell death ultimately renders them hot targets in cancer ther

275 r intermediate 5-year risk of sudden cardiac death underwent cardiac magnetic resonance imaging.

276 ed protein response (UPR) signaling and cell death upon ER stress induction.

277 hils can undergo a nonapoptotic type of cell death using components of the necroptotic pathway, inclu

278 Importantly, the rate of death was inversely proportional to age, such that frail

279 One malaria-associated inpatient death was observed during the study period.

280 ant difference in the risk of cardiovascular death was observed for patients with and without postope

281 One treatment-related death was reported (intracranial hematoma).

282 One death was reported among the 196 patients before randomi

283 One of these deaths was due to gastric adenocarcinoma, which was asse

284 ome signaling, cytokine production, and cell death were evaluated by immunoblotting, ELISA, and cell

285 f the factors associated with cardiovascular death were minimally changed.

286 The rates of hospitalization or death were similar in the two groups.

287 inpatient cases had ICU stays and 2% died; 3 deaths were associated with C. difficile and 1 with noro

288 Two deaths were related to brainstem anesthesia.

289 ted odds ratios (95% CI; p-value) for infant deaths were significantly increased for NO2, PM10, and S

290 per 100,000 people and relative increase in deaths were similar between men and women in most countr

291 pneumonia were independently associated with death, whereas the gastrointestinal phenotype was associ

292 pidemic has increased the number of overdose deaths with a concomitant increase in younger HCV viremi

293 e demonstrate good 3 week model forecasts of deaths with low error and good coverage of our credible

294 design to evaluate the relative incidence of deaths with respiratory/circulatory deaths in the first

295 ciated with future risk of CVA, MI, CHF, and death, with higher degrees of retinopathy appearing to c

296 Stroke is the second leading cause of death worldwide and a leading cause of disability.

297 , stroke remains the second leading cause of death worldwide and the number one cause for acquired lo

298 emphysema that represents a leading cause of death worldwide.

299 e leading causes of permanent disability and death worldwide.

300 em that has already caused more than 662,000 deaths worldwide.