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

3 uction is an important mediator of oxidative cellular injury.

4 inflammatory effects in models of tissue and cellular injury.

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

6 O) confers cytoprotection against tissue and cellular injury.

7 rkedly attenuated NO formation and prevented cellular injury.

8 contribute to heat shock protection against cellular injury.

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

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

11 that compromise redox homeostasis and induce cellular injury.

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

13 n mitochondrial function may lead to further cellular injury.

14 nation-induced cardiac myocyte apoptosis and cellular injury.

15 induce oxidant production and, consequently, cellular injury.

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

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

18 ectly inhibits mitochondrial function during cellular injury.

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

20 containing compounds can provide measures of cellular injury.

21 oted by inflammatory processes and oxidative cellular injury.

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

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

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

25 ell precursor infiltration into the areas of cellular injury.

26 pression would protect against or potentiate cellular injury.

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

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

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

30 ally and synergistically in various forms of cellular injury.

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

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

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

34 holangiocyte lipoapoptosis as a mechanism of cellular injury.

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

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

37 limit ALI by attenuating neutrophil-induced cellular injury.

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

39 d accumulation of ubiquitinated proteins and cellular injury.

40 f proinflammatory cytokines that cause acute cellular injury.

41 ificant hepatic steatosis, inflammation, and cellular injury.

42 nificantly increased vascular disruption and cellular injury.

43 nd hematopoietic TRIF contributed to distant cellular injury.

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

45 g the ER processing capacity and alleviating cellular injury.

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

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

48 which CTSB regulates protease activation and cellular injury.

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

50 a dominant negative mutant of Atg5 increased cellular injury.

51 chnologies use very different means to cause cellular injury.

52 therapeutic approaches for the treatment of cellular injury.

53 uction is an important mediator of oxidative cellular injury.

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

55 These cellular injuries and sepsis severity can be mitigated b

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

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

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

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

60 Cellular injury and death are ubiquitous features of dis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 Moreover, cellular injury demonstrated by aspartate aminotransfera

110 Cellular injury disrupts these intercellular contacts, c

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

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

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

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

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

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

117 1, we found that deltaPKC inhibition reduced cellular injury in a rat hippocampal slice model of cere

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

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

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

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

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

123 Cellular injury in post-diarrheal hemolytic-uremic syndr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 Cellular injury induces an adaptive response whether the

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

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

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

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

145 One mechanism of resulting cellular injury involves endothelial internalization of

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

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

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

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

150 Cellular injury is not initiated through localized defor

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

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

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

154 Cellular injury markers lactate dehydrogenase and aspart

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 KRN5500 induced cellular injury via caspase-dependent apoptosis involvin

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

187 Cellular injury was assessed by solubilization of NaK AT

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

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

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

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

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

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

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