ライフサイエンスコーパス: tissue injury

1 ively restricted in distribution to sites of tissue injury.

2 tures and results in decreased apoptosis and tissue injury.

3 vasculature, leading to neutrophil-dependent tissue injury.

4 ytokine that is commonly expressed following tissue injury.

5 implicated in many models of cell death and tissue injury.

6 in mouse models of MD and after acute muscle tissue injury.

7 neurons tend to activate together following tissue injury.

8 h are associated with NET-induced collateral tissue injury.

9 ar mechanisms underlying arsenicals-mediated tissue injury.

10 at eosinophils are required for IgE-mediated tissue injury.

11 ciated with exacerbated immune responses and tissue injury.

12 ecessary for proportional regeneration after tissue injury.

13 al role in shaping the pain experience after tissue injury.

14 stresses from pathogen infection and sterile tissue injury.

15 ntibodies (DSA) and other lesions of chronic tissue injury.

16 cells and remain dormant unless activated by tissue injury.

17 tive response that modulates the severity of tissue injury.

18 rwhelming infection, and developed extensive tissue injury.

19 for intestinal repair upon certain types of tissue injury.

20 optosis and IL-1beta release could aggravate tissue injury.

21 rdial environment that may prevent excessive tissue injury.

22 potential mechanism for porphyria-associated tissue injury.

23 of innate immune responses and contribute to tissue injury.

24 ructive neutrophils that contribute to renal tissue injury.

25 expressed and may be induced in response to tissue injury.

26 signal, driving inflammation and aggravating tissue injury.

27 cumulation of oxidative stress mediators and tissue injury.

28 ponent, is strongly elevated by wounding and tissue injury.

29 renal function better and had reduced renal tissue injury.

30 creased neural stem cell numbers in areas of tissue injury.

31 f intubation, suggestive of progressive soft tissue injury.

32 plasmic reticulum (ER) stress and subsequent tissue injury.

33 metabolic dysfunction, atherosclerosis, and tissue injury.

34 intravascular occlusion leading to ischemic tissue injury.

35 proinflammatory signaling pathway, regulates tissue injury.

36 , over developmental time, or in response to tissue injury.

37 es virus-induced activation of caspase 3 and tissue injury.

38 fect is independent of underlying disease or tissue injury.

39 ed inflammatory activation promotes fibrotic tissue injury.

40 s as rats that had been anesthetized without tissue injury.

41 ue fibrosis associated with inflammation and tissue injury.

42 tion may simultaneously prevent Hla-mediated tissue injury.

43 in preventing SEB-mediated inflammation and tissue injury.

44 omplement system is activated in response to tissue injury.

45 ntributing to both immunomodulation and host tissue injury.

46 ion in neutrophilic inflammation and reduced tissue injury.

47 in coordinating the outcomes of cellular and tissue injury.

48 diolipins), is activated in vivo after acute tissue injury.

49 ternal electrolytic currents responsible for tissue injury.

50 exaggerated cytokine responses, and greater tissue injury.

51 ion may underlie the development of cell and tissue injury.

52 ction of extracellular matrix in response to tissue injury.

53 failure of effective resolution may lead to tissue injury.

54 vention of oxidative stress and apoptosis in tissue injury.

55 e oxygen species (ROS), ensuing inflammatory tissue injury.

56 TCMR, suggesting similar pathophysiology of tissue injury.

57 siologic significance of phagocytosis during tissue injury.

58 ndent proinflammatory program in response to tissue injury.

59 nduced by infection, inflammation, or severe tissue injury.

60 ommitment can be overridden following severe tissue injury.

61 lf-renewal versus a pathological response to tissue injury.

62 FR and accelerates poststenotic kidney (STK) tissue injury.

63 o develop therapeutic strategies to minimize tissue injury.

64 ociated with hypersensitivity at the site of tissue injury.

65 s must avoid premature activation to prevent tissue injury.

66 , is a novel molecule that mitigates hypoxic tissue injury.

67 ctivate the NLRP3 inflammasome complex after tissue injury.

68 hil trafficking for successful resolution of tissue injury.

69 ine production, aggravating inflammation and tissue injury.

70 , but its dysregulation can cause autologous tissue injury.

71 sitivity reactions that frequently result in tissue injury.

72 tically-to exaggerated inflammation and host tissue injury.

73 p to decipher the inflammatory mechanisms of tissue injuries.

74 ic tool, we found that ATP release following tissue injury activates purinergic P2Y receptors, and mo

75 inst kidney injury by profoundly attenuating tissue injury, activation, and differentiation of myofib

76 Unexpectedly, the tumor-promoting effect of tissue injury also requires c-Met.

77 se to invading microbes, noxious stimuli, or tissue injury, an acute inflammatory response is mounted

78 d that IL33, an alarmin released early after tissue injury and a known regulator of type 2 immunity,

79 collectively beneficial in preventing local tissue injury and augmenting systemic antimicrobial immu

80 ing oncogenic mutation, but are activated by tissue injury and can serve to initiate colon cancer.

81 inflammation in the absence of infection) to tissue injury and cell death is required for normal woun

82 y localize complement inhibition to sites of tissue injury and complement activation, and in particul

83 mporally modulating these responses to limit tissue injury and control the resolution of inflammation

84 or TNF-alpha, all of which are implicated in tissue injury and elevated during tissue remodeling proc

85 ind adenosine triphosphate-mediated ischemic tissue injury and evaluate the role of extracellular ade

86 ystematically compared for quantification of tissue injury and functional impairment after MI using m

87 h permits accurate characterization of local tissue injury and holds the potential for sensitive and

88 njured patients and is driven by significant tissue injury and hypoperfusion.

89 nsight into mechanisms governing PMN-induced tissue injury and implicate PMN-MPs and MPO as important

90 expression is significantly increased after tissue injury and in many solid tumor types, including g

91 rotic tissue interferes with amelioration of tissue injury and induces abnormal tissue remodeling.

92 tive response that is mounted in response to tissue injury and infection.

93 en defined for many years as the response to tissue injury and infection.

94 sma immune surveillance system that controls tissue injury and infection.

95 innate immune system and rapidly respond to tissue injury and infection.

96 exes that restore homeostasis in response to tissue injury and infection.

97 ndent NKT cells, exhibited as much cutaneous tissue injury and inflammation as WT mice.

98 CD1d(-/-)) mice resist UVB-induced cutaneous tissue injury and inflammation compared with wild-type (

99 s preclinical disease models associated with tissue injury and inflammation.

100 for CD1d in promoting UVB-induced cutaneous tissue injury and inflammation.

101 4 T cells permit fungal infection and incite tissue injury and inflammation.

102 sing therapeutic target for various forms of tissue injury and inflammatory diseases.

103 an inflammatory response that can exacerbate tissue injury and lead to scarring.

104 , we show that IL-10 expression is driven by tissue injury and macrophage infiltration, while the p38

105 types are capable of detecting infection or tissue injury and mounting a coordinated molecular defen

106 otease that is actively secreted in areas of tissue injury and ongoing inflammation, where it partici

107 potent danger molecule that induces sterile tissue injury and organ dysfunction.

108 Extracellular histones are mediators of tissue injury and organ dysfunction; therefore they cons

109 rgets to limit crystal-induced cytotoxicity, tissue injury and organ failure.

110 skin keratinocytes, where it regulates skin tissue injury and pain after UVB overexposure, it is dis

111 UV overexposure leads to sunburn with tissue injury and pain.

112 Their activation restricts tissue injury and pathogen spread, but in some settings,

113 rix protein, is transiently expressed during tissue injury and plays a role in fibrogenesis and tumor

114 improve functional outcomes by both reducing tissue injury and promoting the development of reparativ

115 te of the macrophage depends on the stage of tissue injury and repair, reflecting a dynamic and diver

116 proteins mediate pleiotropic effects during tissue injury and repair.

117 lmonary myeloperoxidase activity, as well as tissue injury and sensitization of platelets to adenosin

118 totic cell death, especially in the areas of tissue injury and sterile inflammation.

119 sponse at the molecular level after an acute tissue injury and subsequent repair, and associate a spe

120 and IFNAR in restricting OROV infection and tissue injury and suggest that IFN signaling in nonmyelo

121 ow nitroxidative species are generated after tissue injury and the mechanisms by which they enhance n

122 al function ultimately mitigating myocardial tissue injury and the progression of vascular-proliferat

123 lecular alarm signal upon cellular stress or tissue injury and to exert biological functions as a pro

124 erventions to limit the extent of cumulative tissue injury and to promote repair in MS.

125 he immune processes normally associated with tissue injury and wound repair.

126 lammatory cell recruitment to local sites of tissue injury and/or infection is controlled by a pletho

127 n pain, inflammation, degenerative diseases, tissue injury, and cancer.

128 by limiting bacterial growth, inflammation, tissue injury, and coagulation.

129 nd severity of strategic and global cerebral tissue injury, and cognition in carotid artery disease (

130 romoting antibacterial responses, decreasing tissue injury, and enhancing pulmonary repair.

131 ng are hallmarks of the diabetic response to tissue injury, and excessive inflammasome activation has

132 or factor underlying differences in ischemic tissue injury, and generated a congenic strain set with

133 cytokines, is upregulated in the heart after tissue injury, and its sustained expression can contribu

134 t stages of inflammation and the response to tissue injury, and may be part of a peripheral gating me

135 delivery in an effort to reduce oxygen debt, tissue injury, and morbidity, is controversial.

136 attendant clinical sequelae of inflammation, tissue injury, and organ failure.

137 ely reflects the severity of PV replication, tissue injury, and PVN disease grades.

138 However, HA is degraded during tissue injury, and the functions of short-chain HA that

139 f five classes defined by different forms of tissue injury, and the mechanisms involved in pathogenes

140 status, their intrinsic susceptibilities to tissue injury, and their innate and varied resiliencies.

141 ases such as acute lung injury and ischaemic tissue injury are caused by the adhesion of a type of wh

142 The specific sites of tissue injury are strong determinants of clinical outcom

143 Physiochemical stress induces tissue injury as a result of the detection of abnormal m

144 healing and increased neovascularization on tissue injury as monitored by optical microangiography.

145 for the Mas receptor and may protect against tissue injury associated with renin-angiotensin system a

146 ether with both substance P and CGRP mediate tissue-injury associated pain.

147 ii) a plantar incisional wound as a model of tissue injury-based inflammation.

148 In response to tissue injury, both macrophages and mesenchymal stem cel

149 rombotic and/or inflammatory consequences of tissue injury by altering platelet and endothelial activ

150 MSCs can respond to tissue injury by anti- or proinflammatory activation.

151 n that CAMK2gamma protects against intestine tissue injury by increasing IEC survival and proliferati

152 The coagulation cascade is designed to sense tissue injury by physical separation of the membrane-anc

153 They can worsen tissue injury by producing reactive oxygen species and o

154 nation (I/R), damaged mitochondria propagate tissue injury by promoting cell death.

155 Reducing inflammation-mediated tissue injury by therapeutic inhibition might improve th

156 phil functions, which also play key roles in tissue injury, by providing details of neutrophil cytoto

157 Tissue injury can initiate bidirectional signaling betwe

158 Therefore, we hypothesized that lung-tissue injury can lead to lung-restricted immunity if it

159 Tissue injury can sensitize DRG neurons, causing heighte

160 ed by illness or tissue injury, however, and tissue injury can trigger AP activation in individuals w

161 However, reducing lethal tissue injury caused by intensive chemoradiotherapy duri

162 The degree of tissue injury caused by oxidative molecules, such as rea

163 develop excessive scar tissue as a result of tissue injury, chronic inflammation, or autoimmune disea

164 In response to tissue injury, circulating platelet-neutrophil aggregate

165 We conclude that tissue injury combined with loss of Tregs can lead to lu

166 n the benefits of young, and that peripheral tissue injury compounds the negative effects.

167 Ischemic tissue injury contributes to significant morbidity and m

168 une cell trafficking or function at sites of tissue injury contributes to the misdirection of sterile

169 Risk of arrhythmia and tissue injury decreased with increasing antenna distance

170 ad reduced viral titers and showed less lung tissue injury, despite 24- to 72-h-delayed treatment.

171 lammatory cell populations and dampening the tissue injury due to oxidative stress.

172 Rats that had undergone tissue injury during anesthesia had similar recollection

173 uced complement activation may contribute to tissue injury during chronic infection and acute intercu

174 duction of IL-1beta and IL-18, which mediate tissue injury during irinotecan-induced mucositis in mic

175 in regulating Hla-mediated inflammation and tissue injury during S. aureus SSSI.

176 ose a role for MDSCs in mitigating excessive tissue injury during TSS.

177 ances virus dissemination and contributes to tissue injury, exacerbating viral disease.

178 glycans (HSPGs) bind to and regulate various tissue injury factors through their heparan sulfate (HS)

179 for hemostasis and thrombosis and exacerbate tissue injury following ischemia and reperfusion.

180 Dense connective tissue injuries have limited repair, due to the paucity

181 mmation is typically triggered by illness or tissue injury, however, and tissue injury can trigger AP

182 mones can alter the inflammatory response to tissue injury; however, the precise mechanism by which e

183 In response to tissue injury, hyaluronan (HA) polymers are cleaved by h

184 tive response that modulated the severity of tissue injury, Id1 was conditionally depleted in the end

185 aspects of autoimmunity: passively acquired tissue injury in a developing fetus and clinical progres

186 ChR in protection against the progression of tissue injury in a model of severe, macrophage-mediated,

187 MET signaling promotes tumor formation after tissue injury in a mouse model of primary STS, and they

188 at CD4(+) T cell-derived IL-17F drives renal tissue injury in acute crescentic GN.

189 D47mAb blockade decreases IRI and subsequent tissue injury in DCD renal allografts in a large animal

190 th and a powerful driver of inflammation and tissue injury in disease.

191 dundant function in the development of renal tissue injury in experimental GN might be of great impor

192 acterial infections but also protection from tissue injury in hepatic ischemia/reperfusion injury.

193 at improving predictability of drug-induced tissue injury in humans include using stem cell technolo

194 monstrate that HMGB1 is pivotal for reducing tissue injury in IBD and other complex inflammatory diso

195 tion against pathogens, but may also promote tissue injury in inflammatory diseases.

196 licated oxidative damage as a major cause of tissue injury in MS.

197 Both APOL1 risk variants induced tissue injury in murine livers, the site of transgenic g

198 Severity of tissue injury in occlusive disease is dependent on the e

199 mplement activation is an important cause of tissue injury in patients with Ab-mediated rejection (AM

200 bution of stress perfusion abnormalities and tissue injury in patients with hypertrophic cardiomyopat

201 gic mechanisms leading to vaso-occlusion and tissue injury in SCD has now resulted in a burgeoning ef

202 IL-33, released during tissue injury in sepsis, activates type 2 innate lymphoi

203 sional phagocytes, exacerbating inflammatory tissue injury in sepsis.

204 (Fn-EDA+), which is produced in response to tissue injury in several disease states, has prothrombot

205 isease in which inflammatory lesions lead to tissue injury in the brain and/or spinal cord.

206 apeutic strategy for preventing irreversible tissue injury in the disease.

207 le in modulating local responses to ischemic tissue injury in the kidney and potentially other organs

208 d inflammation and contribute to LPS-induced tissue injury in the liver and kidney, two major organs

209 r levels of cytokine release and more severe tissue injury in the lung tissues of LKB1 KO mice than i

210 However, the extent of normal tissue injury in the lungs following high-LET radiation

211 an accelerate both systemic hypertension and tissue injury in the poststenotic kidney, restoring vess

212 Surprisingly, tissue injury in the spinal cord did not exhibit the sam

213 nstrating the contribution of neutrophils to tissue injury in this model.

214 ed acute inflammation can lead to collateral tissue injury in vital organs, such as the lung during t

215 the regulation of necroptosis and pathologic tissue injury, in directing IFN-beta production in macro

216 ion paraclinical tools capable of monitoring tissue injury.In no arena is this more amenable than AON

217 and other novel strategies to reduce normal tissue injury, increase tumor control, and expand the us

218 n the ability of MSCs to engraft at sites of tissue injury, increasing evidence suggests that MSCs ha

219 ve injury-induced heat hypersensitivity, and tissue injury-induced heat and mechanical hypersensitivi

220 ycarbonyl-1,4-dihydrocollidine, which causes tissue injury, inflammation, and fibrosis.

221 innate immune receptor Nlrp3 is involved in tissue injury, inflammation, and fibrosis; however, its

222 These are processes important in tissue injury, inflammation, and malignant growth.

223 lays a critical role in pain associated with tissue injury, inflammation, and nerve lesions.

224 Tissue injury initiates an inflammatory response through

225 c immune diseases, pathogenic infection, and tissue injury is a common medical condition.

226 Renal artery and peri-arterial soft tissue injury is greatest in the subacute phase, and lea

227 We herein document that this lack of tissue injury is largely due to the concurrent up-regula

228 use these self-Ags are normally sequestered, tissue injury is required to expose them to the immune s

229 in cell survival during cellular stress and tissue injury is unknown.

230 e the AM-induced response could itself cause tissue injury, it is unclear how AMs modulate the respon

231 Inflammation is triggered by tissue injury; it mediates wound healing and scar format

232 In response to tissue injury, macrophages become activated based on spe

233 Earlier detection of tissue injuries may enable initiation of timely interven

234 hese finding suggest that cellular damage or tissue injury may be an essential requisite for the deve

235 d suggest that the mechanisms and targets of tissue injury may differ among patient subgroups.

236 which regulate differentiation, and in vivo tissue injury models may induce lineage-independent endo

237 After tissue injury, monocytes and macrophages undergo marked

238 Cardiac tissue injury occurred with 17 ablations (50%).

239 otocol for detection of chemotherapy-induced tissue injuries of the brain, heart, and bone.

240 nfolded protein response hyperactivation and tissue injury of the exocrine pancreas.

241 Oxidative tissue injury often accompanies viral infection, yet the

242 environment or produced endogenously during tissue injury or drug metabolism.

243 a large variety of states in the absence of tissue injury or infection.

244 ein (CRP) concentrations rise in response to tissue injury or infection.

245 al nociceptive stimuli, which fail to induce tissue injury or inflammation, do not produce the same e

246 nd propagating danger signals resulting from tissue injury or inflammatory stimuli.

247 and, as a consequence, limit immune-mediated tissue injury or promote the establishment of persistent

248 cells (KC) play major roles in immunity and tissue injury or repair.

249 ion can be performed without causing cardiac tissue injury or significant arrhythmia.

250 e that the activation of HBCs observed after tissue injury or sustentacular cell ablation is caused b

251 categorized as stages II, III, and IV; deep tissue injury; or unstageable.

252 tion factor essential for protection against tissue injury, our data have revealed a novel mechanism

253 lder to define the nature and extent of soft tissue injuries prior to physical therapy.

254 Tissue injury prompts the release of a number of proalge

255 wever, after autoimmune attack has initiated tissue injury, PTPN22-R620W may foster inflammation thro

256 e system is considered to play a key role in tissue injury recognition and the subsequent development

257 Parameters of tissue injury, regeneration, and blood coagulation were

258 several key pathologic processes involved in tissue injury relating to lupus nephritis.

259 but the relevant T cell-derived mediators of tissue injury remain unknown.

260 okines, including IL-17F, in immune-mediated tissue injury remains to be fully elucidated.

261 ic input preceded postsynaptic firing, early tissue injury removed this temporal requirement and LTP

262 zed functions of macrophages at each step of tissue injury/repair.

263 flammatory response to UVB-induced cutaneous tissue injury, represents a clinical marker for non-mela

264 ladaptive wound healing responses to chronic tissue injury result in organ fibrosis.

265 Normal tissue injury resulting from cancer radiotherapy is ofte

266 The tissue injury resulting from initial dilation precipitat

267 Acute and chronic tissue injury results in the generation of a myriad of e

268 Wnt/beta-catenin pathway in tissue injury: roles in pathology and therapeutic opport

269 ntinel in the development and progression of tissue injury seen in chronic lung disease.

270 atory environment under both homeostatic and tissue injury states.

271 re we show that, in wild-type mice following tissue injury, stromal-derived factor-1 (Sdf1) is up-reg

272 Tissue injury, T-cell purinergic signaling, cytokines, a

273 owever, Er:YAG laser induced deeper gingival tissue injury than diode laser, as judged by bleeding at

274 uman colon is less susceptible to IR-induced tissue injury than small intestine.

275 s of male mice, and this was associated with tissue injury that caused diminished testosterone and in

276 topenia, hemolytic anemia, schistocytes, and tissue injury that characterize TTP.

277 The same signals of tissue injury that induce apoptosis in somatic cells act

278 virus (HBV) results in disparate degrees of tissue injury: the virus can either replicate without pa

279 al a novel mechanism for neutrophil-mediated tissue injury through oxidant-dependent, SHP-1-mediated

280 macrophages in mediating acute noninfectious tissue injury through regulation of neutrophil trafficki

281 notype that protects against extrapancreatic tissue injury to the lung, kidney and liver in experimen

282 tory molecules governing the transition from tissue injury to tissue repair, are largely unknown.

283 is involved in pathways leading, after lung tissue injury, to pulmonary fibrosis instead of normal h

284 Pathogenic infections and tissue injuries trigger the assembly of inflammasomes, c

285 Tissue injury triggers the activation and differentiatio

286 ctions but are also thought to contribute to tissue injury upon exposure to bacterial products, such

287 n a swine model (89% vs. 54%, P = 0.01), and tissue injury was minimal using a clinical treatment pro

288 surrounding the implants were harvested, and tissue injury was studied by using immunostaining.

289 +) blocks intercellular communication during tissue injury, we determined the X-ray crystal structure

290 released extracellularly by nerve and other tissue injury, we hypothesize that injection of ATP into

291 sion between these two populations following tissue injury, we provide evidence that NOTCH signaling

292 ivity, particularly at sites of ischemia and tissue injury where it is formed.

293 tected in the blood and migrated to areas of tissue injury where they adopted endothelial morphology

294 al mucosa may promote local inflammation and tissue injury, whereas their low phagocytic activity pre

295 hibit oxidative stress, PARP activation, and tissue injury, which are suppressed by pharmacological i

296 uscle progenitors is dramatically altered by tissue injury, which leads to faster kinetics of sarcoma

297 large-animal model a significant decrease in tissue injury with QTCC batteries compared with uncoated

298 H2O2 release and leukocyte recruitment after tissue injury, with none of the side effects associated

299 selectively reduce radiation-induced normal tissue injury without reducing tumoricidal effect, there

300 In peritoneal inflammation elicited by tissue injury, X-linked Cybb-null (X-CGD) mice exhibited