ライフサイエンスコーパス: cell injury

1 factors in APOL1 renal risk variant-mediated cell injury.

2 ene expression, and it is a key mechanism of cell injury.

3 th the magnitude of complement-induced lytic cell injury.

4 trations (500 mum) that were associated with cell injury.

5 M) abrogated TLCS-induced Ca(2+) signals and cell injury.

6 y study epithelial closure in the absence of cell injury.

7 lar mechanism(s) underlying toxicant-induced cell injury.

8 uption of neural processes and biomarkers of cell injury.

9 tion, vascular inflammation, and endothelial cell injury.

10 hibitor did not protect against APAP-induced cell injury.

11 rane attack complex (MAC) as the effector of cell injury.

12 the presence of proinflammatory signals and cell injury.

13 eates vulnerability in both compartments for cell injury.

14 of the OGD and simulated reperfusion-induced cell injury.

15 on zymogen activation, amylase secretion, or cell injury.

16 a-acinar cell zymogen activation, and acinar cell injury.

17 hogens, as well as danger signals related to cell injury.

18 for Src inhibitors as an approach to reduce cell injury.

19 sting did not alter the severity of regional cell injury.

20 ikely to have implications in other types of cell injury.

21 id accumulation, foam cells, and endothelial cell injury.

22 had evidence for alveolar epithelial type 1 cell injury.

23 h are characterized by prominent endothelial cell injury.

24 ment of chronic inflammation and endothelial cell injury.

25 Ngb expression and exacerbated H2O2-induced cell injury.

26 ment of chronic inflammation and endothelial cell injury.

27 viral gene expression cascade and limit host cell injury.

28 the form of cytoplasmic increases, leads to cell injury.

29 mice after streptozotocin (STZ)-induced beta-cell injury.

30 s that female sex steroids protect from beta-cell injury.

31 and STAT3 in hyperoxic lung and endothelial cell injury.

32 und to confer protection against endothelial cell injury.

33 -ethylhexyl)phthalate (MEHP)-induced Sertoli cell injury.

34 d lipid peroxidation and hepatic endothelial cell injury.

35 in NSAID-induced gastric mucosal and gastric cell injury.

36 otecting macrophages from adriamycin-induced cell injury.

37 nerated oxidant stress, synergize to promote cell injury.

38 rate can be accompanied by progressive beta-cell injury.

39 locker amiloride attenuated acidosis-induced cell injury.

40 ding to chronic inflammation and endothelial cell injury.

41 accumulates within hepatocytes causing liver cell injury.

42 sanoid species that promote inflammation and cell injury.

43 ased from hemoproteins during hemorrhage and cell injury.

44 y a role in the response to pancreatic islet cell injury.

45 use rather than a consequence of parenchymal cell injury.

46 st complement-mediated glomerular epithelial cell injury.

47 under conditions of inflammatory stress and cell injury.

48 Sertoli cells could rescue the PFOS-induced cell injury.

49 biting GAPDH phosphorylation should decrease cell injury.

50 stimulation, pathogen infection, or sterile cell injury.

51 oxidative- and nutrient-deprivation-induced cell injury.

52 ng vascular remodeling following endothelial cell injury.

53 lular processes that underlie virus-mediated cell injury.

54 tected cells from proteotoxic stress-induced cell injury.

55 e increased which is an indication of neuron cell injury.

56 prevented activation of NF-kappaB and acinar cell injury.

57 he zebrafish and mammalian responses to hair cell injury.

58 axis protected against the oxidant-mediated cell injury.

59 ntrols were analyzed in an in vitro model of cell injury.

60 rodent models of neurodegeneration or nerve cell injury.

61 (HMGB1, histones) confirmed coagulopathy and cell injury.

62 ion only at concentrations that cause acinar cell injury.

63 about the direct role of TGFbeta in tubular cell injury.

64 ent that has been implicated in a variety of cell injuries.

65 sed by germ cells after MEHP-induced Sertoli cell injury acts upon Sertoli cell TNFR1 and activates N

66 nd in which steatogenesis, inflammation, and cell injury aggravate ER stress seems to be at play.

67 gations defining the mechanism of epithelial cell injury, alternative macrophage activation and effer

68 numbers is due to losses in cell viability, cell injury and a subsequent inability to be detected by

69 IPF is characterized by alveolar epithelial cell injury and activation with interstitial inflammatio

70 blation with liposomal doxorubicin increases cell injury and apoptosis in the zone of increased coagu

71 ains fixed, and stained to assess regions of cell injury and axonal dysfunction.

72 (sRAGE) levels, a marker of type I alveolar cell injury and BOS.

73 ion of human GST A4-4 (hGSTA4-4) to vascular cell injury and consequent transplant arteriosclerosis i

74 Hyperoxia causes cell injury and death associated with reactive oxygen sp

75 Hepatocyte growth factor also prevented cell injury and death by increasing the expression of th

76 The degree of cell injury and death does not account for severity of s

77 hat activation of PKC-delta promotes tubular cell injury and death during albuminuria, broadening our

78 rstitial inflammation, fibrosis, and tubular cell injury and death, but the mechanisms underlying the

79 overexpression stimulated, independently of cell injury and death, release of numerous chemokines an

80 n disease (PD) and the molecular pathways of cell injury and death, we remain without therapies that

81 to XIAP, forming SNO-XIAP, and thus promotes cell injury and death.

82 ism, but excessive oxygen (hyperoxia) causes cell injury and death.

83 tion of calcium signaling that occurs during cell injury and disease, promotes cell death.

84 ation of polymorphisms related to epithelial cell injury and dysfunction and abnormal wound healing,

85 ute to atherogenesis by inducing endothelial-cell injury and dysfunction.

86 use and effect relationship between modes of cell injury and ER stress remains elusive.

87 zing radiation (IR) as a model of adult stem cell injury and identified a regeneration defect in agin

88 s overexpressing COX-2, high glucose induced cell injury and increased both expression of the pro(ren

89 This can lead to cell injury and inflammation resulting in nonalcoholic s

90 m transgenic mice display early-onset acinar cell injury and inflammatory cell infiltration.

91 Epithelial cell injury and inflammatory responses were increased in

92 zation causes the least amount of myocardial cell injury and is associated with superior long-term ou

93 hese data suggest that miRNAs linked to beta-cell injury and islet inflammation might be useful bioma

94 ciated molecular patterns are released after cell injury and killing.

95 hich is specifically used to confirm thermal cell injury and lack of viability.

96 local flow disturbance, reducing endothelial cell injury and local thrombosis (P<0.05).

97 Folate is postulated to protect against cell injury and long-term risk of cancer.

98 for modulating downstream bioeffects such as cell injury and mechanotransduction in ultrasound therap

99 s point to Ndfip1 as a sensor protein during cell injury and Ndfip1 up-regulation as a cue for BRAT1

100 These activated zymogens then cause acinar cell injury and necrosis, a characteristic of pancreatit

101 HMGB1 is passively released during cell injury and necrosis, or actively secreted during im

102 No difference in markers of cell injury and organ dysfunction was observed between r

103 gulation activation is not a prerequisite of cell injury and organ dysfunction.

104 ic renal allografts, which show both tubular cell injury and proliferation, display down-regulation o

105 Finally, in a model of lung secretory cell injury and regeneration, we show that loss of Foxp1

106 the effects of hypercapnic acidosis on lung cell injury and repair by confocal microscopy in a model

107 ures of VOD, with an emphasis on endothelial cell injury and risk factors.

108 d to induce disease directly by causing beta cell injury and subsequent release of autoantigens and i

109 e role against hypoxia/reoxygenation-induced cell injury and suggest the therapeutic potential of MSR

110 cantly but incompletely reducing endothelial cell injury and T cell infiltration into the graft one o

111 ontin (OPN) is a cytokine up-regulated after cell injury and tissue repair.

112 has been shown to occur in some contexts of cell injury and to be essential for loss of cell viabili

113 r pathways, upstream (eg, protecting against cell injury) and downstream (eg, regulating CCN2 activit

114 nstrated significant endothelial and Kupffer cell injury, and a progressive lesion developed 24 to 48

115 uced pathological calcium transients, acinar cell injury, and activation of c-Jun N-terminal kinase,

116 located to mitochondria early during tubular cell injury, and both siRNA knockdown of Drp1 and expres

117 ome and autophagosome formation, exacerbated cell injury, and decreased cell viability in cultured NR

118 on of insulin-producing cells, islet or beta-cell injury, and genetic models of impaired beta-cell fu

119 ocytes and neutrophils, vascular endothelial cell injury, and intense vasculocentric infiltrates with

120 ation between the characteristics of ICW and cell injury, and potential strategies to mitigate cavita

121 rombotic glomerular lesions with endothelial cell injury, and renal dysfunction.

122 le in which ER stress promotes inflammation, cell injury, and steatosis and in which steatogenesis, i

123 eleased by neurocytotoxic Abs or other brain cell injury, and the resulting immune complexes stimulat

124 bile-induced NF-kappaB activation and acinar cell injury are mediated by calcineurin, and a mechanism

125 membrane dynamics and how they contribute to cell injury are unclear.

126 also attenuated inflammation and endothelial cell injury as demonstrated by reduced plasma levels of

127 y peptide prevented bile acid-induced acinar cell injury as measured by lactate dehydrogenase leakage

128 or 2 hours resulted in significantly reduced cell injury, as shown by lactate dehydrogenase-release a

129 Tubule cell injury, as shown by loss of villi, tubule dilation,

130 terfering RNA, pharmacological analysis, and cell injury assays, we show that activation of TRPM7 cha

131 Interestingly, PFOS-induced Sertoli cell injury associated with a down-regulation of the gap

132 albuminuria (indicative of renal endothelial cell injury) associated with hypoxemia.

133 shear adaptation (P = 0.03) and evidence of cell injury at sites of nonuniform shear profiles that a

134 se and SLO is associated with augmented host cell injury beyond that produced by SLO alone, but the m

135 pectrin breakdown products, SBDPs) and glial cell injury biomarker, glial fibrillary acidic protein (

136 helpful in preventing chronic ER stress and cell injury by alleviating protein misfolding in the ER.

137 ished that lipid peroxidation contributes to cell injury by altering the basic physical properties an

138 This may represent a novel mechanism of host cell injury by bacteria.

139 effects of AMPK and that TGF-beta1 promoted cell injury by blocking AMPK-mediated tuberin phosphoryl

140 means to ameliorate oxidative stress-induced cell injury by either inhibiting Ser(36) phosphorylation

141 rier (BTB), PFOS was found to induce Sertoli cell injury by perturbing actin cytoskeleton through cha

142 was found to block the PFOS-induced Sertoli cell injury by rescuing the PFOS-induced F-actin dis-org

143 brain slices were used for quantification of cell injury by spectrophotometric measurement of formaza

144 contributes to the progression of myocardial cell injury, cardiac fibrosis, and left ventricular (LV)

145 city is an important, unrecognized factor in cell injury caused by FA.

146 The neuronal cell injury caused by I/R is associated with the activat

147 LI in wild-type mice and reduced endothelial cell injury caused by mitochondrial extract-primed human

148 ory failure is a serious consequence of lung cell injury caused by treatment with high inhaled oxygen

149 Renal tubular cell injury causes dysregulation of SR-B1, ABCA-1, and L

150 Reactive oxygen species (ROS)-mediated cell injury contributes to the pathophysiology of cardio

151 hat were subjected to stretch injury using a cell injury controller device.

152 The degree of bacterial cell injury could be quantified using chemometric method

153 -limiting enzyme in polyamine catabolism) in cell injury, cultured kidney (HEK 293) cells conditional

154 ular with immune signaling and regulation of cell injury, death, growth, and proliferation.

155 Hydrogen peroxide-induced oxidative cell injury downregulates TMIGD1 expression and targets

156 abetes (CFRD) is thought to result from beta-cell injury due in part to pancreas exocrine damage and

157 lays an important role in tubular epithelial cell injury during acute kidney injury (AKI).

158 rostructural properties influence epithelial cell injury during airway reopening.

159 The factors limiting bystander cell injury during an Ag-specific immune response in viv

160 nd render them more or less vulnerable to NK cell injury during autoimmune vasculitis, such as granul

161 how fiber structure and mechanics influences cell injury during cyclic airway reopening as occurs dur

162 quired for movement of dysferlin to sites of cell injury during repair patch formation.

163 Hippocampal neural stem-cell injury during whole-brain radiotherapy (WBRT) may p

164 (miRNAs) might be useful biomarkers of beta-cell injury/dysfunction that would allow more accurate s

165 rome is characterized by alveolar epithelial cell injury, edema formation, and intraalveolar contact

166 rat salivary Pa-4 epithelial cells to resist cell injury elicited by 1% O(2)- or hypoxia-mimetic desf

167 developments include the role of epithelial cell injury, endoplasmic reticulum stress and Wnt signal

168 (CS)-induced pulmonary and renal endothelial cell injury explains the association between albuminuria

169 conjunction with endothelial and epithelial cell injury, followed by fibrogenesis.

170 inflammation, and endothelial and epithelial cell injury, followed by repair that can be adaptive and

171 orylation of GAPDH correlates with increased cell injury following oxidative stress, suggesting that

172 olution of alveolar edema in ARDS, including cell injury from unfavorable ventilator strategies or pa

173 transplantation in the animals in which beta-cell injury had been induced.

174 Mesangial cell injury has a major role in many CKDs.

175 and predisposition to altered metabolism and cell injury have contributed to our current understandin

176 otein (HSP) expression and response to renal cell injury, HSP72 and HSP25 were differentially inhibit

177 lografts and then correlated with epithelial cell injury, immune cell accumulation, and collagen depo

178 r results suggest that pulmonary endothelial cell injury in a genetically susceptible mouse strain tr

179 duced albuminuria and glomerular endothelial cell injury in a PAR2-dependent manner.

180 system disorders, prevents apoptotic SH-SY5Y cell injury in an oxidative stress model of oxygen-gluco

181 pathobiology of AT deficiency, mechanisms of cell injury in diseases associated with aggregation-pron

182 DSA) causes complement-dependent endothelial cell injury in kidney transplants, as assessed by expres

183 ress preconditioning attenuates H2O2-induced cell injury in LLC-PK1 cells by preventing an increase i

184 icularly calcium ions, in neuronal and glial cell injury in multiple sclerosis, as well as in non-inf

185 Hypoglycemia was not associated with cell injury in P7 rats.

186 nt effectors are known to contribute to host cell injury in several inflammatory diseases.

187 after injury) to assess oxidative stress and cell injury in the hippocampus or 4 months after injury

188 red blood cells, which can cause endothelial cell injury in the kidney that may lead to thrombus form

189 ights the vascular occlusion and endothelial cell injury in the medulla that contribute to sickle cel

190 ominent antioxidant effect and resistance to cell injury in these cells.

191 rtant for the genesis of hepatic parenchymal cell injury in this model.

192 ramylasemia, edema, inflammation, and acinar cell injury in TLCS-induced, but not caerulein-induced,

193 e results revealed that propofol exacerbates cell injury in vascular smooth muscle cells with increas

194 gonize toxin activity, preventing human lung cell injury in vitro and protecting experimental animals

195 differ in their ability to cause endothelial cell injury in vitro, nor did antibiotic-mediated eradic

196 od cell (RBC) injury in vivo and endothelial cell injury in vitro.

197 O(2) derived from urate oxidation to prevent cell injury in vitro; during therapy, disulfide-linked p

198 that can directly measure the extent of beta-cell injury in vivo in patients receiving islet grafts a

199 ecognize self-antigens under conditions (eg, cell injury) in which the self-tissue might elaborate im

200 d showed less hepatocellular and endothelial cell injury, in agreement with better-preserved liver hi

201 nduced renal fibrosis and tubular epithelial cell injury independent of TGF-beta1 activity.

202 creased protein-S-glutathionylation prior to cell injury, indicating that thiol oxidation is involved

203 insulin directly protects pancreatic acinar cell injury induced by bona fide pancreatitis-inducing a

204 re secondary to extensive tubular epithelial cell injury induced by the lytic replication of BKV.

205 Diabetes-induced kidney cell injury involves an increase in matrix protein expre

206 Pulmonary endothelial cell injury is central to the pathophysiology of acute l

207 Endothelial cell injury is crucial in the development of human ather

208 closure of epithelial gaps in the absence of cell injury is governed by the collective migration of c

209 In the transplant setting, endothelial cell injury is induced by multiple factors, including br

210 nance of the bronchial airway epithelium, CE cell injury is resolved through a mechanism involving re

211 of age, but, unlike in skeletal muscle, the cell injury is sublethal and causes only mild cardiomyop

212 athophysiologic context in which endothelial cell injury is the triggering event that initiates and d

213 mental glaucoma models if selective ganglion cell injury is to be sought.

214 sensitive and specific marker of myocardial cell injury, is useful in diagnosing and assessing progn

215 The results showed that severe endothelial cell injury leading to hemorrhage in the brain and other

216 angial cell proliferation, whereas mesangial cell injury leads to foot process fusion and proteinuria

217 ed mice have pulmonary and renal endothelial cell injury linked to increased endothelial cell AGEs an

218 of one of 34 or one of 25 in normal or oval cell injury livers, respectively.

219 cell nuclear pleomorphism and focal tubular cell injury, lysis, and karyorrhexis were observed as ea

220 d-dimer and cell injury markers (HMGB1, histones) confirmed coagulop

221 dentify clusterin as a pivotal factor in the cell injury mechanism of nephropathic cystinosis and pro

222 s an important role in restraining bystander cell injury mediated either by defined TCR transgenic T

223 MiRNAs including miR-375 (linked to beta-cell injury), miR-21 (associated with islet inflammation

224 Using hypoxia-reoxygenation (H/R) as a cell injury model, we evaluated cell survival and caspas

225 Sox9(+) cells were traced in multiple oval cell injury models using both histology and fluorescence

226 to the hepatocyte pool, even in classic oval cell injury models.

227 hepatocyte-driven regeneration in mouse oval cell injury models.

228 tis by promoting pancreatic edema and acinar cell injury/necrosis and that this phenomenon is depende

229 ion also reduces pancreatic edema and acinar cell injury/necrosis in two dissimilar experimental mode

230 ic microangiopathies is vascular endothelial cell injury of various origins, resulting in microangiop

231 in the absence of histologically significant cell injury, often manifesting clinically as seizures.

232 lenging to study the impact of dopamine (DA) cell injury on corticostriatal activity in vivo due to l

233 els have been used as biomarkers to evaluate cell injury or activation in patients with pathological

234 ssion, we have investigated the effect of DA cell injury or DA receptor antagonism on immediate-early

235 ption of this dynamic equilibrium may herald cell injury or death and may contribute to developmental

236 astrocyte immunoreactivity-indicating either cell injury or death-and functionally disrupted the BBB

237 compromise of cell structure and ultimately cell injury or death.

238 of P. aeruginosa and suggested no permanent cell injury or direct killing of bacteria.

239 GI2 on hypoxia/reoxygenation-induced tubular cells injury or I/R kidneys by measuring oxidative stres

240 nable development of interventions to reduce cell injury, our research has focused on understanding m

241 that act as sensors of microbial presence or cell injury, Paneth cells as the main epithelial cell ty

242 ding should facilitate the identification of cell injury pathways and corresponding therapeutic targe

243 ical for resistance to intestinal epithelial cell injury, potentially mediated by APOA1.

244 Alveolar type II epithelial (ATII) cell injury precedes development of pulmonary fibrosis.

245 tion of CypD and that peroxynitrite-mediated cell injury predominates in the absence of CypD.

246 to this neuropathy, we examined a marker of cell injury/regeneration (activating transcription facto

247 at feeding and increased sensitivity to beta cell injury relative to wild-type (WT) controls.

248 acute neutrophilic inflammatory response to cell injury requires the signaling protein myeloid diffe

249 ge to the peripheral nerves triggers Schwann cell injury response in the distal nerves in an event te

250 e injury signal that triggers distal Schwann cell injury response.

251 e whereas (99m)Tc-duramycin, a new marker of cell injury, senses cell death via apoptosis or necrosis

252 receptors by endogenous PGE(2) released in a cell-injury setting is neuroprotective.

253 cellular defenses on neurotoxicant-elicited cell injury, SH-SY5Y cells were pretreated with D3T for

254 l requirements for specific versus bystander cell injury suggest that there are opportunities for inh

255 rovide a mechanism to account for the severe cell injury that follows hypoxia and reoxygenation when

256 rhosis develops after a long period of liver-cell injury that leads to the deposition of collagen, le

257 taneously conditions endothelial and Kupffer cell injury that may ultimately lead to the failure of t

258 ent cascade is an ancient means of detecting cell injury that precedes the evolution of adaptive immu

259 iculate actin is a marker for sepsis-induced cell injury, that plasma gelsolin has a crucial protecti

260 the stressful conditions (e.g., infection or cell injury), the exact roles of these molecules in the

261 The translocation of HMGB1, a marker of cell injury, the downregulation of proteins that functio

262 athogenesis including the role of structural cell injury, the pathogenic role of macrophages and lymp

263 as not associated with increased hippocampal cell injury, the trauma-induced reductions in CBF and po

264 inoleic acid metabolites are released during cell injury, these findings suggest a mechanism for inte

265 o fibrosis after proximal tubular epithelial cell injury, this mechanism may have widespread relevanc

266 Bile acid exposure causes pancreatic acinar cell injury through a sustained rise in cytosolic Ca(2+)

267 es bile acid-induced pancreatitis and acinar cell injury through aberrant intracellular Ca(2+) signal

268 PFOS was found to induce Sertoli cell injury through disruptive effects on actin microfil

269 compensatory changes in response to Purkinje cell injury, thus illustrating an important feature of P

270 tects kidney epithelial cells from oxidative cell injury to promote cell survival.

271 aling pathway appears to amplify cytotoxic T cell injury to the epidermal basal cell compartment.

272 addition to parent lipids, might exacerbate cell injury under oxidative stress conditions.

273 autophagy and its pathological role in renal cell injury using in vitro and in vivo models of ischemi

274 PFOS induces Sertoli cell injury using testicular cells isolated from rodent

275 pathologic angiogenesis in relation to glial cell injury, VEGF protein, and mRNA levels of key mediat

276 a greater reduction in metabolic crisis and cell injury volumes compared to a cerebral perfusion pre

277 Cell injury was assessed by lactate dehydrogenase leakag

278 ytes were exposed to type I collagen (COL1); cell injury was assessed by morphologic and biochemical

279 Moreover, bystander cell injury was not entirely nonspecific but rather requ

280 dUTP nick-end labeling staining, widespread cell injury was observed in SFTPC-/- and SFTPC+/+ mice 1

281 oxetine to improve hyperglycemic endothelial cell injury was unique among serotonin reuptake blockers

282 del of naphthalene-induced airway epithelial cell injury, we showed that necrosis activates the ASC i

283 lation, foam cell generation and endothelial cell injury were all increased by hyperlipidemia, wherea

284 urements of optic nerve and retinal ganglion cell injury were assessed by magnetic resonance imaging

285 TLCS-induced Ca(2+) release and cell injury were reduced by 30 and 95%, respectively, in

286 Rejecting grafts with extensive endothelial cell injury were refractory to immunotherapy.

287 ty acid binding protein, a marker of tubular cell injury, were dramatically reduced by PP but not NPP

288 olar lavage RTI40 levels, a marker of type I cell injury, were similar with or without recruitment ma

289 llular activation of digestive zymogens, and cell injury when these responses are induced by exposure

290 ng molecule that is generated in response to cell injury where it orchestrates tissue protection and

291 PFOS induces human Sertoli cell injury which can be rescued by overexpressing p-FAK

292 hic transition, host cell adherence, or host cell injury, which are all established virulence attribu

293 yperamylasemia, pancreatic edema, and acinar cell injury, which closely mimic pancreatitis in humans.

294 associated with vasculopathy and endothelial cell injury, which could potentially increase the risk o

295 The acute response to vascular cell injury, which underpins vasculo-occlusive pathologi

296 lular Zn(2+) accumulation and Zn(2+)-induced cell injury, while silencing TRPM7 by small interfering

297 (AP) suggest a strong association of acinar cell injury with cathepsin B-dependent intracellular act

298 d to correlate strongly with the severity of cell injury, with CICW in the range of 33 mum/s to 93 mu

299 In contrast, cell injury, with marked vulnerability in the dentate gy

300 uently leads to a self-amplifying cascade of cell injury within the lung from which the lung cannot r