ライフサイエンスコーパス: cellular injury

1 ate dehydrogenase (LDH) release (an index of cellular injury).

2 gated radiation-induced oxidative stress and cellular injury.

3 ly, provide a survival signal that minimizes cellular injury.

4 a dominant negative mutant of Atg5 increased cellular injury.

5 chnologies use very different means to cause cellular injury.

6 therapeutic approaches for the treatment of cellular injury.

7 uction is an important mediator of oxidative cellular injury.

8 ays a prominent role in various of models of cellular injury.

9 uction is an important mediator of oxidative cellular injury.

10 inflammatory effects in models of tissue and cellular injury.

11 erexpression of iNOS resulted in NO-mediated cellular injury.

12 O) confers cytoprotection against tissue and cellular injury.

13 rkedly attenuated NO formation and prevented cellular injury.

14 contribute to heat shock protection against cellular injury.

15 ronal function; however, high levels lead to cellular injury.

16 notype in this kindred and may cause type II cellular injury.

17 that compromise redox homeostasis and induce cellular injury.

18 show histologic evidence of rejection and/or cellular injury.

19 nation-induced cardiac myocyte apoptosis and cellular injury.

20 induce oxidant production and, consequently, cellular injury.

21 de (100 micromol/L), but not P-1075, blunted cellular injury.

22 acrophages are the prototype of this form of cellular injury.

23 blood and hemoglobin (Hb) play in mediating cellular injury.

24 containing compounds can provide measures of cellular injury.

25 oted by inflammatory processes and oxidative cellular injury.

26 d cells which can be readily activated after cellular injury.

27 neuronal survival may depend on the type of cellular injury.

28 ration, an effect that was highly related to cellular injury.

29 ell precursor infiltration into the areas of cellular injury.

30 pression would protect against or potentiate cellular injury.

31 e (PARS) contribute to peroxynitrite-induced cellular injury.

32 n contact with endothelial cells, it induces cellular injury.

33 -, which results in amino acid nitration and cellular injury.

34 ally and synergistically in various forms of cellular injury.

35 oach to disorders involving .O2-/NO-mediated cellular injury.

36 , suggesting release of FGF-2 with sublethal cellular injury.

37 cycle, play a central role in ONOO--mediated cellular injury.

38 sed oxidative stress, DNA damage and chronic cellular injury.

39 -free DNA (cfDNA) is a noninvasive marker of cellular injury.

40 proteins and other macromolecules to promote cellular injury.

41 supplementation prevented ethanol-associated cellular injury.

42 chronic inflammatory processes that mediate cellular injury.

43 which CTSB regulates protease activation and cellular injury.

44 n mitochondrial function may lead to further cellular injury.

45 ectly inhibits mitochondrial function during cellular injury.

46 holangiocyte lipoapoptosis as a mechanism of cellular injury.

47 e development of the nervous system or after cellular injury.

48 th severe sepsis was examined for markers of cellular injury.

49 limit ALI by attenuating neutrophil-induced cellular injury.

50 of V(1A) receptor (V(1A)R) activation during cellular injury.

51 d accumulation of ubiquitinated proteins and cellular injury.

52 f proinflammatory cytokines that cause acute cellular injury.

53 ificant hepatic steatosis, inflammation, and cellular injury.

54 nificantly increased vascular disruption and cellular injury.

55 nd hematopoietic TRIF contributed to distant cellular injury.

56 ath for cells to "defend" [Ca(2+)](i) during cellular injury.

57 ctional organelles that are major sources of cellular injury.

58 g the ER processing capacity and alleviating cellular injury.

59 troke core and penumbra and often exacerbate cellular injury.

60 effects of low pHe on zymogen activation and cellular injury.

61 partially CFTR dependent, but was not due to cellular injury.

62 sis in SSc-associated ILD (SSc-ILD) involves cellular injury, activation/differentiation of mesenchym

63 rum restored autophagic activity and reduced cellular injury after hypoxia/reoxygenation (H/R) in pri

64 , aberrant Ca2+ homeostasis in the course of cellular injuries and certain diseases of the CNS appear

65 These cellular injuries and sepsis severity can be mitigated b

66 oplasmic RNA as an important early marker of cellular injury and a sensitive indicator of various mod

67 rved in a variety of cells in the process of cellular injury and apoptosis, these studies suggest tha

68 Oxidative injury underlies the cellular injury and cell death in a variety of disease s

69 biochemical pathways that lead to secondary cellular injury and contribute to cell death.

70 Cellular injury and death are ubiquitous features of dis

71 Hypoxia/reoxygenation causes cellular injury and death associated with a number of pa

72 kinetically favored reaction contributing to cellular injury and death at sites of tissue inflammatio

73 results in localization of MSCs to areas of cellular injury and death in the liver.

74 ptake of Hcy-S-Hg-S-Hcy and the induction of cellular injury and death was demonstrated in the hOAT1-

75 Hypoxia/reoxygenation (H/R) causes cellular injury and death.

76 nvironmental and clinical insults results in cellular injury and death.

77 A protected against oxidative stress-induced cellular injury and death.

78 evere oxidant stress and contributes to lung cellular injury and death.

79 ize sheep Abs bound to podocytes can lead to cellular injury and development of FSGS.

80 growth factor that they require, leading to cellular injury and disruption of the filtration apparat

81 her dissection of APOL1-mediated pathways to cellular injury and dysfunction in kidney (and other) ce

82 ole for Ca2+-permeable AMPARs in excitotoxic cellular injury and epileptogenesis.

83 These data suggest that CR reduces cellular injury and improves heat tolerance of old anima

84 osine concentration is increased at sites of cellular injury and inflammation, and adenosine is known

85 istinct transcriptional changes that favored cellular injury and inflammation, and impaired hepatocyt

86 l virulence by enabling the fungus to induce cellular injury and maintain a deep-seated infection.

87 nvironmental stress is critical to alleviate cellular injury and maintain cellular homeostasis.

88 nucleoside that is generated in response to cellular injury and orchestrates the balance between tis

89 tion through its neutralization may minimize cellular injury and organ dysfunction.

90 the key transcriptomic markers of important cellular injury and regeneration processes across this h

91 ronic liver diseases with repeated cycles of cellular injury and regeneration.

92 plementary mechanism, the microbe can induce cellular injury and release self antigens, which generat

93 ichment of genes in pathways consistent with cellular injury and repair due to environmental stress a

94 The pathophysiology of cellular injury and repair has been extensively studied

95 ively studied, RB function in the context of cellular injury and repair has remained largely unexplor

96 ve-reparative alterations: ongoing cycles of cellular injury and repair manifested with EC swelling/l

97 responses involved both in the mechanisms of cellular injury and repair via activation of MAPK pathwa

98 inhibitor, GKT, decreased radiation-induced cellular injury and restored SMPDL3b basal levels of exp

99 immunohistochemical staining for markers of cellular injury and stress, including connexin-43 and ki

100 vement of peroxynitrite in cytokine-mediated cellular injury and suggest the therapeutic potential of

101 sults suggest a novel molecular link between cellular injury and the inflammatory response.

102 uctions in metabolism, (b) the prevention of cellular injury, and (c) the maintenance of functional i

103 C and steroid receptor activation, ischemic cellular injury, and apoptosis.

104 y noninfectious causes, including trauma and cellular injury, and can have off-target effects in whic

105 We targeted inflammation, cellular injury, and gut leakiness in a randomized clini

106 ion of the plasma membrane often accompanies cellular injury, and in muscle, plasma membrane resealin

107 hogens use to evade immune mechanisms, cause cellular injury, and induce disease.

108 Liver biopsy assessment of steatosis, cellular injury, and lobular inflammation did not detect

109 al focal ischemia models of preconditioning, cellular injury, and neuroprotection.

110 ductions in markers of immune activation and cellular injury, and preservation of organ function.

111 n imbalance that overwhelms the UPR, induces cellular injury, and provokes acinar metaplasia.

112 esults in free radical formation, leading to cellular injury, and that blue filters can reduce this r

113 n the role of extranuclear TDP-43 in causing cellular injury, and the discovery of a new sIBM autoant

114 ways prior to the occurrence of irreversible cellular injury, and to successfully intervene using inn

115 occal enrichment, lymphocytic activation and cellular injury, and were replicated in an independent c

116 g rupture enable detection of the mechanical cellular injury as crackling sounds.

117 denosine triphosphate (ATP), are released by cellular injury, bind to purinergic receptors expressed

118 inflammatory injury and in chemical-induced cellular injury, both of which are mediated in part thro

119 tent and severity of inflammation-associated cellular injury by controlling the switch between the pr

120 The protection against cellular injury by PARS-/- phenotype or INH2BP waned whe

121 Hypoxia/reoxygenation induces cellular injury by promoting oxidative stress.

122 ranscriptional responses, preventing further cellular injury by removing biochemical damage and renew

123 es cytoprotection against ischemic and toxic cellular injury by signaling through the PI3K-AKT and MA

124 df15 mRNA expression, indicating that direct cellular injury can induce Gdf15 expression in the absen

125 Similarly, cellular injury can release endogenous 'damage'-associat

126 +) macrophages that were induced at sites of cellular injury close to the hepatic scar in mouse model

127 ism in NASH, determining the pathogenesis of cellular injury, defining predisposing genetic abnormali

128 Moreover, cellular injury demonstrated by aspartate aminotransfera

129 Cellular injury disrupts these intercellular contacts, c

130 ase A(2) (PLA(2)) enzymes may play a role in cellular injury due to ATP depletion.

131 provide radiobiological mechanisms of acute cellular injury during SBRT for VT, which may have an an

132 tivation has been shown to contribute to the cellular injury during various forms of oxidant stress i

133 These studies therefore describe a model of cellular injury effected by specific Ab to ribosomal "P"

134 An antioxidant diminished cellular injury, fibrosis and DNA damage, but not lobula

135 tudies that have used the apoptotic model of cellular injury have suggested that enhanced ceramide ge

136 nt mice during recovery exhibited persistent cellular injury, impaired alveolar and endothelial cell

137 function, has been implicated as a cause of cellular injury in a number of central nervous system pa

138 1, we found that deltaPKC inhibition reduced cellular injury in a rat hippocampal slice model of cere

139 tative stem cells is the predominant form of cellular injury in acute experimental GVHD.

140 igh steady-state levels of RRVs may underlie cellular injury in APOL1 nephropathy, and that intervent

141 RAGE and HMGB1 may be important mediators of cellular injury in fetuses delivered in the setting of i

142 ls of non-heme reactive iron correlated with cellular injury in hyperoxia whereas lower levels of hem

143 wever, the role for miR-15b as a mediator of cellular injury in organs such as the lung has yet to be

144 within the endoplasmic reticulum (ER) causes cellular injury in patients with the classical form alph

145 Cellular injury in post-diarrheal hemolytic-uremic syndr

146 (eIF2) is an important mechanism mitigating cellular injury in response to diverse environmental str

147 ibosyl polymerase pathway contributes to the cellular injury in shock and endothelial injury.

148 IL-6 was necessary and sufficient to mediate cellular injury in spinal cord organotypic tissue cultur

149 no evidence for redox imbalance or oxidative cellular injury in the absence of metabolic stress.

150 t may ameliorate contractile dysfunction and cellular injury in the face of an ischemic insult.

151 transcription 3 (STAT3) signaling and caused cellular injury in the human renal tubular cell line.

152 generation, stress protein accumulation, and cellular injury in the liver.

153 ulation does not cause insulin resistance or cellular injury in the liver.

154 urther investigate the mechanism of ischemic cellular injury in this animal, we tested the hypothesis

155 For defining further the pattern of cellular injury in this model, serial kidney sections of

156 ymeric F-actin and is an important aspect of cellular injury in tissue ischemia.

157 ted autophagy is associated with progressive cellular injury in various liver pathologies.

158 ion of PARS protects against oxidant-induced cellular injury in vitro and exhibits anti-inflammatory

159 ne and cytoskeletal properties, resulting in cellular injury in vitro.

160 e or complement-depleted mice showed reduced cellular injury in vivo compared with those in wild type

161 calpain activity are common early events in cellular injury, including that of hepatocytes.

162 Mutant KRAS and cellular injuries induce KLF4 expression, and ectopic ex

163 robably is a compensatory response to combat cellular injury induced by LPS.

164 to test the protective effects of insulin on cellular injury induced by the pancreatitis-inducing age

165 Cellular injury induces an adaptive response whether the

166 lular ATP and ADP levels are associated with cellular injury, inflammation, and thrombosis.

167 ascular pathologies, neurochemical deficits, cellular injury, inflammation, oxidative stress, mitocho

168 n of liver metabolism, oxidative stress, and cellular injury/inflammation.

169 Rather, LeTx may cause direct cellular injury insensitive to vasopressors.

170 One mechanism of resulting cellular injury involves endothelial internalization of

171 se of such mitochondrial 'enemies within' by cellular injury is a key link between trauma, inflammati

172 articles may lead to different outcomes when cellular injury is assessed, leading to differences in s

173 common view holds that nitric oxide-induced cellular injury is caused by oxidative stress.

174 Hypoxic cellular injury is influenced by the mTORC1 pathway, but

175 echanistic studies revealed that HDM-induced cellular injury is NADPH oxidase (NOX)-dependent, and ap

176 Cellular injury is not initiated through localized defor

177 mouse hearts to ischemia/reperfusion, where cellular injury is thought to result in part from Ca acc

178 ysosomal degradative pathway of autophagy in cellular injury is unclear, because findings in nonhepat

179 injury, and although hypothermia can reduce cellular injury, its capacity to influence the villous m

180 is unknown, but it has been associated with cellular injury, lipid transport, apoptosis, and it may

181 Cellular injury markers lactate dehydrogenase and aspart

182 peroxidation, in addition to causing direct cellular injury, may further contribute to cisplatin-ind

183 ot been examined in other cell types or in a cellular injury model.

184 ough necrosis ensues at the sites of massive cellular injury, most cells in the body die through a mo

185 These findings provide possible evidence for cellular injury (NAA loss reflecting neuroaxonal cell da

186 atives was evaluated in an in vitro model of cellular injury on cortical neurons.

187 ry autocoid that is generated as a result of cellular injury or stress, interacts with specific G pro

188 and nucleic acids-released or exposed during cellular injury or stress, which shape immune responses

189 roduction appears to be a response to either cellular injury or to specific cytotoxic exoproducts pro

190 at act in concert to either prevent or limit cellular injury or transformation.

191 duction that could be initiated by microbes, cellular injury, or neurogenic or inflammatory signals;

192 Histological features of steatosis, cellular injury, parenchymal inflammation, Mallory bodie

193 Hypoxia and other stress signals cause cellular injury partly through the action of p53.

194 The p53/p21 pathway of reaction to cellular injury, potentially leading to apoptosis, may p

195 vivo by using a left ventricular balloon and cellular injury quantified by assay of troponin I releas

196 1) may be useful therapeutically to minimize cellular injury, reduce viral replication, and attenuate

197 ms and cell signaling events responsible for cellular injury remain to be elucidated.

198 ium overload that leads to mitochondrial and cellular injury requires dynamic control of mitochondria

199 nt of the 39 bases from -74 to the TATA box (cellular injury response element, CIRE) upstream of the

200 ncogene-induced phenotypic conversion of the cellular injury response of mouse and human cells was me

201 tes in H(2)O(2)-mediated gene regulation and cellular injury response through PDCD4 and the activator

202 ces rapid and dynamic changes to O-GlcNAc is cellular injury, resulting from environmental stress (fo

203 Extensive cellular injury results in the release of nuclear protei

204 lysophosphatidylcholine, a lipid product of cellular injury, signaling via the G protein-coupled rec

205 In addition, autologous MSCs suffered less cellular injury than allogeneic MSCs after contacting se

206 ns, appears to be a viable strategy to limit cellular injury that is the substrate of neurodegenerati

207 introduce specific local and global modes of cellular injury that likely contribute to spine, filopod

208 a highly effective approach to decrease the cellular injury that occurs following reperfusion of isc

209 ular patterns (DAMPs), which are products of cellular injury that stimulate the innate immune system

210 necrotic cells may be a signal of tissue or cellular injury that, when sensed by DCs, induces and/or

211 view of the important role of superoxide in cellular injury, there has been a great need for methods

212 asion of BMEC was accompanied by evidence of cellular injury; this cytotoxicity was correlated to bet

213 is established through experimentally-based cellular injury thresholds for white matter regions.

214 reshold that captures changes from different cellular injuries to provide a more comprehensive evalua

215 ported yearly, but predictive correlation of cellular injury to impact tissue strain is still lacking

216 data along a time course spanning from acute cellular injury to organ failure.

217 Cell walls from both organisms produced cellular injury to similar degrees in pure astrocyte cul

218 with oligomers producing elevated levels of cellular injury toward undifferentiated PC12 cells (PC12

219 sm underlying the initiation of cell and sub-cellular injuries ultimately responsible for the diffuse

220 KRN5500 induced cellular injury via caspase-dependent apoptosis involvin

221 ized hemolysin extracts of GBS cultures, and cellular injury was assessed by lactate dehydrogenase (L

222 Cellular injury was assessed by solubilization of NaK AT

223 he anti-CD38 antibodies in inducing pericyte cellular injury was evaluated using the same cytotoxicit

224 onfers stress tolerance to multiple forms of cellular injury, we explored the role(s) of O-GlcNAc in

225 improved kidney function and reduced kidney cellular injury when administered to male C57BL/6 mice i

226 hinery downstream of Beclin1, did not affect cellular injury, whereas expression of a dominant negati

227 y data revealed the presence of multifaceted cellular injuries which highlight the need for multimoda

228 IV-2-infected animals contained a pattern of cellular injury, which was characterized by (1) nuclear

229 protective against kainate- or AMPA-induced cellular injury, while beta-NAAG was partially neuroprot

230 macrophage functions, they directly inflict cellular injury within the arterial wall.

231 limiting oxidative stress, inflammation, and cellular injury within the CNS and other tissues.