ライフサイエンスコーパス: tissue injury

1 uption of blood supply and provokes ischemic tissue injury.

2 ry by minimizing endothelial dysfunction and tissue injury.

3 to ensure effective immunity while limiting tissue injury.

4 bited increased levels of markers reflecting tissue injury.

5 ively restricted in distribution to sites of tissue injury.

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

7 dicate microbes, but they also contribute to tissue injury.

8 siologic significance of phagocytosis during tissue injury.

9 ctivate the NLRP3 inflammasome complex after tissue injury.

10 , but its dysregulation can cause autologous tissue injury.

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

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

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

14 ue fibrosis associated with inflammation and tissue injury.

15 exaggerated cytokine responses, and greater tissue injury.

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

17 ction of extracellular matrix in response to tissue injury.

18 failure of effective resolution may lead to tissue injury.

19 vention of oxidative stress and apoptosis in tissue injury.

20 histones within the notochord bead following tissue injury.

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

22 TCMR, suggesting similar pathophysiology of tissue injury.

23 ndent proinflammatory program in response to tissue injury.

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

25 ommitment can be overridden following severe tissue injury.

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

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

28 o develop therapeutic strategies to minimize tissue injury.

29 ociated with hypersensitivity at the site of tissue injury.

30 e oxygen species (ROS) leading to myocardial tissue injury.

31 s must avoid premature activation to prevent tissue injury.

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

33 hil trafficking for successful resolution of tissue injury.

34 ine production, aggravating inflammation and tissue injury.

35 sitivity reactions that frequently result in tissue injury.

36 tically-to exaggerated inflammation and host tissue injury.

37 ed inflammatory responses that contribute to tissue injury.

38 tures and results in decreased apoptosis and tissue injury.

39 vasculature, leading to neutrophil-dependent tissue injury.

40 cell cycle (i.e., undergo paligenosis) after tissue injury.

41 ytokine that is commonly expressed following tissue injury.

42 i-related vascular calcification and chronic tissue injury.

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

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

45 neurons tend to activate together following tissue injury.

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

47 t for control of virus-induced morbidity and tissue injury.

48 ar mechanisms underlying arsenicals-mediated tissue injury.

49 ciated with exacerbated immune responses and tissue injury.

50 ecessary for proportional regeneration after tissue injury.

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

52 stresses from pathogen infection and sterile tissue injury.

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

54 cells and remain dormant unless activated by tissue injury.

55 tive response that modulates the severity of tissue injury.

56 o multiple stresses, including radiation and tissue injury.

57 is can result in irreversible nervous system tissue injury.

58 ysical link between ventilation strategy and tissue injury.

59 ic and electrical perturbations arising from tissue injury.

60 esulting in decreased inflammation following tissue injury.

61 s other oral analgesic agents for acute soft tissue injury.

62 y mediators dictates host defense as well as tissue injury.

63 y cytokines results in hyperinflammation and tissue injury.

64 ogens and clearance of cellular debris after tissue injury.

65 ular ATP activates inflammatory responses to tissue injury.

66 between ongoing damage and repair following tissue injury.

67 is vital for resolution of inflammation and tissue injury.

68 mechanisms that facilitate healthy repair of tissue injury.

69 terious and contribute to neuronal death and tissue injury.

70 ressed by multiple cell types in response to tissue injury.

71 p to decipher the inflammatory mechanisms of tissue injuries.

72 res, femoral distal cam, and associated soft-tissue injuries.

73 d is involved in acid-induced cell death and tissue injury(1-3).

74 After tissue injury, a dramatic shift in macrophage compositio

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

76 f TIPE results in excessive inflammation and tissue injury after allo-HCT, supporting that TIPE confe

77 s, impaired perfusion recovery and increased tissue injury after femoral artery ligation.

78 We find that tissue injury alone induces emergency hematopoiesis in m

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

80 tic factor-targeted therapies for a range of tissue injuries and disease.

81 Conclusion Soft-tissue injuries and osseous findings other than morpholo

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

83 eneficial than low CPE treatment in limiting tissue injury and accelerating post-stroke recovery.

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

85 njury (TBI) and may contribute to additional tissue injury and blood-brain barrier damage.

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

87 arget site with temperatures known to create tissue injury and cell death.

88 tion, IL-27 deficiency resulted in increased tissue injury and collagen deposition associated with hi

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

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

91 lammatory events may dictate the severity of tissue injury and coordinate the remodeling and repair e

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

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

94 4 hours at 4 degrees C), along with reducing tissue injury and fibrosis.

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

96 in kidney glomeruli is suspected to promote tissue injury and glomerulonephritis (GN).

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

98 the mechanism of sterile inflammation during tissue injury and identifying new immune targets for tre

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

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

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

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

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

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

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

106 4 T cells permit fungal infection and incite tissue injury and inflammation.

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

108 APP-103 reduces tissue injury and IRI-associated inflammatory responses

109 Endothelial dysfunction is a hallmark of tissue injury and is believed to initiate the developmen

110 There was evidence for oxidative stress, tissue injury and microscopic interstitial inflammation.

111 der of the exocrine pancreas associated with tissue injury and necrosis.

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

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

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

115 a profound inflammatory response leading to tissue injury and organ failure.

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

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

118 eposited in extravascular compartments after tissue injury and perform immune-stimulatory or inflamma

119 etic switches are often triggered by chronic tissue injury and play important roles in tissue repair.

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

121 tochondrial dynamics respond to cellular and tissue injury and promote tissue repair.

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

123 growth factor beta (TGF-beta) is induced on tissue injury and regulates tissue remodeling and wound

124 rs of immunity (S100A8, S100A9, galectin-3), tissue injury and repair (Serpine1/PAI-1) and growth fac

125 e stress, anti-inflammatory lipid mediators, tissue injury and repair, and growth factors with immuno

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

127 proteins mediate pleiotropic effects during tissue injury and repair.

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

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

130 he inflammatory response following cutaneous tissue injury and suggest that MLL1 regulates TLR4 expre

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

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

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

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

135 8)Ga-DOTA-ECL1i signal localized to sites of tissue injury and was independent of blood pool activity

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

137 mage and dysfunction, leading to cell death, tissue injury and, potentially, organ failure.

138 Parameters reflecting inflammation, tissue injury, and bacterial burden were measured.

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

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

141 OPN reduces inflammation, decreases tissue injury, and reduces bacterial loads during concur

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

143 A sequencing (scRNA-seq), mouse genetics and tissue injury approaches, we uncover cellular hierarchie

144 Thus, mechanisms involved in alcohol tissue injury are model-dependent at multiple levels and

145 nto the cytosol and its role in inflammatory tissue injury are not well understood.

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

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

148 does not fibrose (i.e. scar) in response to tissue injury as most other mammals, including humans, d

149 es genetic susceptibility to T-cell-mediated tissue injury as observed in a mouse model of intestinal

150 pendent necroptosis directs inflammation and tissue injury, as well as anti-viral host defense.

151 on of the intestinal mucosa is a hallmark of tissue injury associated with inflammatory bowel disease

152 mokine/cytokine production may contribute to tissue injury at the maternal/fetal interface.

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

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

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

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

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

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

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

160 Tissue injury can initiate bidirectional signaling betwe

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

162 Tissue injury can sensitize DRG neurons, causing heighte

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

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

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

166 Ischemic tissue injury contributes to significant morbidity and m

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

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

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

170 Neonatal tissue injury disrupts the balance between primary affer

171 Here, we show that, following severe tissue injury, Drosophila wing disc cells that survive e

172 Sterile tissue injury due to trauma also increases leukocyte dem

173 okines, chemokines, and receptors that cause tissue injury during rejection.

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

175 l pyruvate, has shown anti-inflammatory/anti-tissue injury effects in various animal models of diseas

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

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

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

179 ng host defense, pulmonary inflammation, and tissue injury following respiratory viral infections.

180 ARS-CoV-2] virus "receptor") that results in tissue injury from angiotensin II (Ang II)-mediated sign

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

182 sition in models of inflammatory disease and tissue injury have revealed points of commonality, as we

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

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

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

186 Despite enhanced tissue injury in C5aR2(-/-) IR mice, there were signific

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

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

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

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

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

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

193 The immune mechanisms that cause tissue injury in lupus nephritis have been challenging t

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

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

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

197 sional phagocytes, exacerbating inflammatory tissue injury in sepsis.

198 protein (CIRP) exaggerates inflammation and tissue injury in sepsis.

199 pathogen and is an important determinant of tissue injury in sepsis.

200 ld help in avoiding rejection and associated tissue injury in the allograft setting.

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

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

203 in severe organ damage, our understanding of tissue injury in the liver, adrenal glands, and lymphoid

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

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

206 ely contributed to complement activation and tissue injury in this strain.

207 etric analysis confirmed that the aggravated tissue injury in Tnfr1(-/-)/Mdr2(-/-) mice strongly corr

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

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

210 Whether autosis is involved in tissue injury induced under pathologically relevant cond

211 Tissue injury induces changes in cellular identity, but

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

213 Pain is a hallmark of tissue injury, inflammatory diseases, pathogen invasion

214 ction syndrome (MODS) following infection or tissue injury is associated with increased patient morbi

215 x (ECM)-producing myofibroblasts at sites of tissue injury is critical for normal tissue repair.

216 Hemostasis associated with tissue injury is followed by wound healing, a complex pr

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

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

219 matory responses, which can exacerbate local tissue injury, lead to chronic inflammation, or precipit

220 Fibrosis is often caused by chronic tissue injury leading to a persisting inflammatory respo

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

222 acute myocarditis, significant reductions in tissue injury markers occur during the first 12 months o

223 nce nor extent of the investigated CMR-based tissue injury markers were predictive of our pre-defined

224 Cardiac function, myocardial tissue injury, markers of inflammation, oxidative stress

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

226 ation of inflammatory gene expression during tissue injury may contribute to the control of damage an

227 ntify increased HDAC activity as a potential tissue-injury mechanism responsible for dysregulated epi

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

229 In terms of secondary tissue injury, moderate-to-severe cortical superficial s

230 After tissue injury, monocytes and macrophages undergo marked

231 ing agents as mechanism-driven ways to blunt tissue injury, morbidity, and mortality of COVID-19.

232 In a cutaneous tissue injury murine model, we found that TLR4 expressio

233 e, or multiple organ dysfunction; and direct tissue injury (n = 64, 21.9%) including brain and spinal

234 sts are poised to coordinate fibrogenesis in tissue injury, neoplasia, and aging.

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

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

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

238 ocyte demand; however, the effect of sterile tissue injury on hematopoiesis is not well described.

239 However, in the context of tissue injury or disease, large numbers of monocytes inf

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

241 evere viral infections often results in host tissue injury or even death.

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

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

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

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

246 Upon tissue injury or microbial invasion, a large number of n

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

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

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

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

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

252 Tissue injury prompts the release of a number of proalge

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

254 en) deposits are a near-universal feature of tissue injury, regardless of the nature of the inciting

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

256 mmatory pathways that affect the spectrum of tissue injury, remodeling, and repair.

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

258 circulation acts as a myokine to facilitate tissue injury-repair and regeneration.

259 kers for pro-inflammation, oxidative stress, tissue injury/repair, alarm anti-protease, anti-microbia

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

261 ted by NRF2 and those of the acute phase and tissue injury response pathways, in both patient groups.

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

263 Normal tissue injury resulting from cancer radiotherapy is ofte

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

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

266 -benign approach to mitigating blood loss in tissue-injury scenarios.

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

268 atory environment under both homeostatic and tissue injury states.

269 ting metastatic disseminations and excessive tissue injuries still remains a major concern.

270 In response to tissue injury, stromal cells secrete extracellular matri

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

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

273 testine seems less susceptible to IR-induced tissue injury than the male small intestine.

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

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

276 duce metaplastic differentiation at sites of tissue injury that culminates in transformed barriers co

277 lar starvation is typically a consequence of tissue injury that disrupts the local blood supply but c

278 in the classic neuroinflammatory sequelae of tissue injury that includes pain, immune cell infiltrati

279 iogenesis is a critical process in repair of tissue injury that is regulated by a delicate balance be

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

281 types are capable of detecting infection or tissue injury, thus mounting regulated immune response.

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

283 early intervention to prevent perioperative tissue injury to transplantable organs.

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

285 Tissue injury triggers the activation and differentiatio

286 Activated neutrophils can cause or worsen tissue injury, underscoring the need for calibration of

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

288 At baseline, severe tissue injury was evident with loss of luminal epithelia

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

290 tudies in human skin organoids as a model of tissue injury, we demonstrated that miR-135a-3p potently

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

292 l DNA, a danger signal that is released upon tissue injury, we examined the role of anesthetics on TL

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

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

295 are crucial for host defense but can lead to tissue injury when produced in excess.

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

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

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

299 igate the storm of inflammation and minimize tissue injury with high potential for adjunctive therapy

300 tion may act as a central mechanism coupling tissue injury with regeneration.