ライフサイエンスコーパス: injure

1 aken with the populations that experimenters injure.

2 TBI by midline fluid percussion or were sham-injured.

3 ction occurs and whether the kidney has been injured.

4 pSMAD5-positive cells were found in the DMM-injured AC in MRL/MpJ mice than in normal mice.

5 uced in CCI-injured juvenile compared to CCI-injured adult immune cells.

6 primary cortical neurons and in vivo in the injured adult optic nerve.

7 l for resonant amplification was greatest in injured adult-sized lungs with higher regional quality f

8 ith loss of sensation due to degeneration of injured afferents and reduced incidence of post-injury h

9 d that spatial primitives/synergies of adult injured and neonatal injured rats differed insignificant

10 3-6 hours after trauma in the most severely injured and physiologically deranged patients was consis

11 stinct cardiomyocyte populations in healthy, injured, and regenerating mouse hearts.

12 istinct and are also among the most commonly injured, and therefore of important translational intere

13 Head-injured animals display features characteristic of mamma

14 s unchanged in CCI models compared with sham-injured animals.

15 Relative to injured APOE3 TR mice, injured APOE4 TR mice had more in

16 Relative to injured APOE3 TR mice, injured APOE4 TR mice had more inflammation, neurodegene

17 comeres, proliferating, and repopulating the injured area remain unclear.

18 ond-line coping response-such as licking the injured area to soothe suffering.

19 and epidermal keratinocytes directly into an injured area, replicating the layered skin structure.

20 sembly and cardiomyocyte protrusion into the injured area, respectively.

21 nd enhanced the mechanical properties of the injured area.

22 tion, proliferation, and protrusion into the injured area.

23 following injury, and some migrate into the injured area.

24 Injured arterial vessels were as follows: inferior glute

25 quantified by intravital microscopy of laser-injured arterioles.

26 Rats injured as adults were more similar in modularity to rat

27 nt, corneal NV occurred only through the non-injured aspect of the limbus.

28 ia of the peripheral nervous system, protect injured axons by virtue of a dramatic glycolytic upregul

29 Injured axons fail to regenerate in the adult CNS, which

30 The degeneration of injured axons involves a self-destruction pathway whose

31 effectiveness in augmenting regeneration of injured axons relevant to spinal cord injury.

32 e current assumption is that the decision of injured axons to degenerate is cell-autonomously regulat

33 ose yet unknown downstream effectors protect injured axons, dendrites, and synapses from degenerating

34 nt or knock-down larvae, the degeneration of injured axons, dendrites, and synapses from motoneurons

35 utonomously required for the degeneration of injured axons, dendrites, and synapses in Drosophila mel

36 ate sprouting and regeneration of spared and injured axons, to increase the strength of residual conn

37 itochondrial motility and energy deficits in injured axons.

38 injury, triggering selective degeneration of injured axons.

39 etabolic mechanism that controls the fate of injured axons.

40 alpha) triggers G3BP1 granule disassembly in injured axons.

41 involvement of PBG cells in regenerating the injured biliary epithelium and identified the signaling

42 ic agents to intentionally block diseased or injured blood vessels for therapeutic purposes.

43 Compared to severely injured blunt trauma patients without aortic injury, IT

44 ity-score matched control cohort of severely injured blunt trauma patients without aortic injury.

45 t, surgery, and their combination impact non-injured bones will improve treatment strategies for astr

46 ectional innate immune responses between the injured brain and lung, using a controlled cortical impa

47 ose of D-Sino attenuated inflammation in the injured brain areas by suppressing inflammatory cytokine

48 s become functionally integrated into stroke-injured brain circuitry is poorly understood.

49 lso indicate that restoring HN levels in the injured brain could represent a translational target for

50 Repair of the traumatically injured brain has been envisioned for decades, but regen

51 In addition to inflammation localised to the injured brain region, a growing body of evidence suggest

52 s) that elicit localised inflammation in the injured brain region.

53 precise role of astrocyte-derived E2 in the injured brain remains unclear.

54 ponses may amplify brain damage, but how the injured brain sends out signals to trigger systemic infl

55 ruitment of peripheral immune cells into the injured brain.

56 es old NSCs more resistant to regenerate the injured brain.

57 density compared with wild-type littermates injured by either protamine sulfate or nephrotoxic serum

58 months), the gluteus maximus muscle (GM) was injured by local injection of barium chloride solution (

59 n mediate a highly effective rescue of cells injured by oxidative stress and an improved cardiac outp

60 r ICsa can maximize the shelf-life of apples injured by P. expansum, validating a novel type of antim

61 biological contexts, including signals from injured cardiac cells undergoing oxidative stress, chara

62 s can affect "heart regeneration", replacing injured cardiac scar tissue with concomitant electrical

63 DA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formatio

64 the adhesion of Abeta-activated platelets to injured carotid arteries in mice.

65 atial and temporal changes of FCD content in injured cartilage using a novel finite element model tha

66 Release of molecular danger signals from injured cell mitochondria (mitochondria-derived damage-a

67 ly charged lipids in the inner leaflet in an injured cell.

68 nhibited axonal regeneration of mechanically injured cerebral cortex neurons from mice.

69 demyelination, and astrocytic gliosis in the injured cervical cord.

70 Injured children >=1 years old can receive up to 40 mL/k

71 Records of severely injured children age <18 years with rapid thromboelastog

72 Of 2,470 critically injured children, 103 (4.2%) met pediatric acute respira

73 respiratory distress syndrome among severely injured children.

74 the mechanical properties of the healthy and injured CNS myelin is challenging, and has largely relie

75 Elevating cAMP levels encourages injured CNS neurons to sprout and extend neurites.

76 tive gliosis, a pathological hallmark in the injured CNS of mammals.

77 regulate proliferation of stem cells in the injured CNS.SIGNIFICANCE STATEMENT The death of retinal

78 In this network analysis of 5,703 critically injured combat casualties, patterns of injury among fata

79 exposed to an alarm substance released from injured conspecific skin ("skin extract") [8, 9].

80 story of exposure to TBI was selected as non-injured controls (n = 32).

81 ransplantation of early-stage neurons to the injured cord may reconstruct the descending projections

82 of hematogenous innate immune cells into the injured cord.

83 spinal pathway, as chemogenetic silencing of injured corticospinal neurons transiently abrogated reco

84 sion of Kim1+ cells, indicating that acutely injured, dedifferentiated proximal tubule cells, rather

85 t neural stem cells drive regeneration of an injured DG has remained unclear.

86 mentary approach to clinical EVLP to recover injured donor lungs that could not otherwise be utilized

87 tion of the transcription factor CREB in the injured DRG after peripheral nerve injury.

88 cases the medial dorsal cutaneous nerve got injured during the fascial opening of the extensor compa

89 ficient microglia did not effectively engulf injured/dying neurons.

90 lved in the renewal of surface epithelium in injured EHBT.

91 Regeneration of denuded or injured endothelium is an important component of vascula

92 mune complexes along VWF strings released by injured endothelium that might propagate the risk of thr

93 DSB accumulation in injured epithelium led to impaired colonic healing and g

94 which diminishes their ability to repair the injured epithelium, shown by altered stem cell signaling

95 Zebrafish can faithfully regenerate injured fins through the formation of a blastema, a mass

96 urs after injury and that depriving recently injured flies of sleep slows the removal of both active

97 with low ML but high DD levels are severely injured, functionally coagulopathic and have poor clinic

98 Acutely injured genetically labeled clones coexpressed KIM1, VIM

99 ibrosis was more persistent in more severely injured Grp78 knockout (KO) mice.

100 However, injured H2-K1 cells eventually develop impaired self-ren

101 oss of MCs on the deafferented digits of the injured hand compared with the contralateral side.

102 ich monocytes are initially recruited to the injured heart and provide new insights into the heteroge

103 tain their production and recruitment to the injured heart are unclear.

104 to resurrect the infarcted heart results in injured heart enlargement and remodeling to maintain its

105 wound healing/remodeling in the ischemically injured heart, the reparative actions of CMCs may be att

106 basis for myofibroblast heterogeneity in the injured heart.

107 y standoff, representing a group of severely injured hearts as previously demonstrated.

108 in myocardial fibrosis and apoptosis in the injured hearts, highlighting a protective effect of boro

109 cardiac function in both adult and neonatal injured hearts.

110 evidence of a relative EEG slowing over the injured hemisphere.

111 antigen-expressing tumor cells, but may also injure hepatic sinusoids (sinusoidal obstruction syndrom

112 we demonstrate that mito-DAMPs released from injured hepatocyte mitochondria (with mtDNA as major act

113 cGAS) drives IRF3 activation in both alcohol-injured hepatocytes and the neighboring parenchyma via a

114 We find that injured host axons regenerate into 3D biomimetic scaffol

115 terozygous ((+)/-) knockout mice, as well as injured human and rodent kidneys.

116 itating axon regeneration in the diseased or injured human CNS, thus helping to reduce and/or recover

117 of the pathophysiological description of an injured human heart and hence put forward the zebrafish

118 stry for integrin alphavbeta8 in healthy and injured human liver demonstrated that human hepatocytes

119 Here we demonstrate that acutely injured human lungs declined for transplantation, includ

120 Scotopic b-waves were reduced in injured hWtEPOR mice compared with WT, and rod bipolar c

121 ound the central projections of peripherally injured Ia afferents, suggesting a possible causal relat

122 E) specimens obtained from combat casualties injured in Afghanistan.

123 ling and adhesion, were found reduced in CCI-injured juvenile compared to CCI-injured adult immune ce

124 of therapies to improve regeneration of the injured kidney and to prevent fibrosis requires a better

125 ates interstitial matrix accumulation in the injured kidney by promoting MMP13 production, which driv

126 owever, the effects of ATM inhibition on the injured kidney have not been explored.

127 veral profibrotic signaling molecules in the injured kidney, including Smad3, epidermal growth factor

128 acked the fate of monocytes recruited to the injured kidney.

129 e neutrophil and monocyte recruitment to the injured kidney.

130 p-regulated in renal epithelial cells of the injured kidney.

131 ifferentiate the sham and IRI even after the injured kidneys were recovered.

132 jured and destabilized medial meniscus (DMM)-injured knees from 8-wk-old C57BL/6J and MRL/MpJ mice.

133 The injured limb had greater vertical peak forces, with impr

134 been identified, the mechanisms by which the injured liver maintains vital functions prior to tissue

135 7 cells and enhanced IL-17 production in the injured liver.

136 lonal expansion of hepatocytes in normal and injured liver.

137 of sinusoid-associated cells in healthy and injured livers and reconstructed the single-lineage HSC

138 or cells [sprocs]) with diminished repair of injured LSECs and whether restoring signaling to recruit

139 ows that capillarization is due to repair of injured LSECs by BM endothelial progenitors that engraft

140 f signaling to recruit BM sprocs that repair injured LSECs renders steatotic liver more susceptible t

141 atory endocrine signals originating from the injured lung activate signaling pathways in the muscle t

142 Protective ventilation strategies for the injured lung currently revolve around the use of low Vt,

143 the TOLLIP gene in IPF lungs may predispose injured lung epithelial cells to apoptosis and to the de

144 emia diminished the ferroptotic damage in IR-injured lung tissue, consistent with the protective effe

145 erfusion of the relatively small fraction of injured lung.

146 Normal H2-K1(high) cells transplanted into injured lungs differentiate into alveolar cells and resc

147 osis, and prevented the decrease of MerTK in injured lungs from old mice.

148 idation data set (SAILS [Statins for Acutely Injured Lungs from Sepsis]; n = 745).

149 When introduced into dermis or bleomycin-injured lungs of mice, collectins MBL and SP-D were endo

150 rocytosis, and a decrease in MerTK levels in injured lungs.

151 restores the reproductive capability of the injured male rabbits.

152 Patients were severely injured (median injury severity score 33); 33% developed

153 on levels are higher in the glomeruli of NTS injured mice and passive Heymann membranous nephropathy

154 Chronically injured mice had greater mortality following S. pneumoni

155 profiles of the glomerulus from healthy and injured mice provides resources to identify novel diseas

156 Injured mice were randomized to receive vehicle or baica

157 which co-expressed Prox-1 in the DG of rmTBI-injured mice which coincided with enhanced cFos expressi

158 significant differences between healthy and injured mice with different brain diseases in vivo.

159 ocesses and has therapeutic effects in brain-injured mice without displaying overt side effects.

160 the pain state in the trigeminal ganglia of injured mice.

161 tive behavior outcomes at 1 DPI in the APOE4 injured mice.

162 nd b-waves were lower in the hWtEPOR than WT injured mice.

163 ng within both the cortex and hippocampus in injured mice.

164 riven KRT5(+)/KRT14(-) proliferation seen in injured mice; KRT14(+) cells were unaffected.

165 d intestinal epithelial cells and in acutely injured mucosa decreased the detrimental effects of PMNs

166 lymphatic structure, growth, and function in injured murine hearts.

167 l line-derived neurotrophic factor (GDNF) in injured muscle and increased expression of GDNF family r

168 e capacity and adaptability of the remaining injured muscle are unclear.

169 changes that result in lipid accumulation in injured muscle fibers.

170 either support the complete regeneration of injured muscle or facilitate pathologic fibrosis and mus

171 Changes in macrophage phenotype in injured muscle profoundly influence regeneration.

172 rtrophic processes that restore structure to injured muscle.

173 macrophages and slowed revascularization of injured muscle.

174 Zeb1-deficient injured muscles also display a delayed and poorer regene

175 ed to wild-type counterparts, Zeb1-deficient injured muscles exhibit enhanced damage that corresponds

176 the undamaged and regenerating myofibers of injured muscles.

177 ved macrophages (BMDMs) are recruited to the injured myocardium and are essential for cardiac repair

178 ls to the electrophysiological properties of injured myocardium is unknown.

179 Results: (68)Ga-FAPI-04 uptake in the injured myocardium peaked on day 6 after coronary ligati

180 ial presence of activated fibroblasts in the injured myocardium predicts the quality of cardiac remod

181 le, thus limiting the extent of irreversibly injured myocardium.

182 ytes may be a viable option for regenerating injured myocardium.

183 , CB(2)-positive lymphocytes infiltrated the injured nerve and possible CB(2)transfer from immune cel

184 Myeloid cells in the injured nerve, but not axotomized DRGs, strongly express

185 In the injured nerve, macrophages 'eat' apoptotic leukocytes, a

186 activity, should be considered to treat the injured nervous system.

187 y separable phases of dSarm signaling in the injured nervous system.

188 ling avenue toward functional restoration of injured nervous systems.

189 local subnetwork may be to compensate for an injured network, or it may be robust to mTBI and is exhi

190 apies have shown the potential to reactivate injured neural networks and promote re-emergence of cons

191 achieved via endocytosis of EFF-1 within the injured neuron.

192 By genetically marking injured neurons, we showed that the injury-induced trans

193 ge in regenerative medicine is the repair of injured neurons.

194 erestimated capability to repair a massively injured, nonfunctional DG.

195 ds were established in microfluidic devices, injured on-chip by exposure to lipotoxic agent (palmitat

196 In this study, we found that, in injured optic nerves, oligodendrocyte precursor cells (O

197 , compete for game species, and occasionally injure or kill people.

198 Overexpression of beta-Arr2 in injured or beta-Arr2-deficient SECs rescued eNOS functio

199 matory molecules to accelerate the repair of injured or diseased tissues.

200 sion of axon transport in all axons, whether injured or not, and decreased mechano- and chemosensory

201 Moreover, injured or trophically deprived Sarm1(-/-) and DR6(-/-),

202 tes tissue homeostasis in the neoplastic and injured pancreas.

203 ) hepatocytes shows that during recovery the injured parenchyma becomes repopulated and repaired by A

204 ce for behavioural improvement and growth of injured pathways in non-human primate spinal cord injury

205 reassigning 1 ICU for the yet to arrive next injured patient decreases ED dwell times, complications,

206 nce adverse consequences if they negligently injure patients.

207 , controlled trial, we assigned 240 severely injured patients (Injury Severity Score >15 [scores rang

208 Blood samples were drawn from critically injured patients (n = 27, ACITII-prospective observation

209 physiology could significantly shape how VML-injured patients and clinicians approach regenerative me

210 ecome profoundly dysfunctional in critically injured patients by an unknown mechanism, contributing t

211 smatch, reducing waiting times of critically injured patients by factors larger than two.

212 er PAMPer trial was performed on hypotensive injured patients from the scene.

213 treatment strategy for post-traumatic brain injured patients in minimally conscious state based on a

214 angement due to advanced shock in critically injured patients leads to the pulmonary sequestration of

215 ability of a hybrid environment for severely injured patients reduces time to intervention, total pro

216 However, injured patients that develop TIC can be difficult to id

217 that are increased in the plasma of severely injured patients that developed ARDS versus severely inj

218 patients that developed ARDS versus severely injured patients that did not, and assay if these increa

219 eted metabolomics profiling of 67 critically injured patients was completed to establish a metabolic

220 All severely injured patients who were transferred to the hybrid suit

221 hanism of platelet dysfunction in critically injured patients.

222 bolites accumulate in the plasma of severely injured patients.

223 systems have improved outcomes for severely injured patients.

224 P < .001), and increasing number of vessels injured per patient (adjusted odds ratio, 1.6 per one-ve

225 Intact, PG-depleted, and mechanically injured + PG-depleted cartilage samples (n = 33) were im

226 by regulating ESCRT III-mediated shedding of injured plasma membrane.

227 This direct effect of AngII on injured podocytes results in increased calcium transient

228 ivo and its in vitro-functional significance injured podocytes.

229 s interpretive review, we highlight that the injuring potential of the inflation pattern depends upon

230 Consistent with this, LukED and HlgAB injure primary human endothelial cells in a DARC-depende

231 dies on altered gene expression in the blast-injured rat cochlea may provide insights into new therap

232 he ventilatory pattern of the sham rat pups, injured rat pups had increased fR and predictability.

233 ives/synergies of adult injured and neonatal injured rats differed insignificantly, despite different

234 proves the endogenous ability of chronically injured rats to fight off pneumonia, a common cause of h

235 gions across subjects, we found the combined injured region at the group level occupied the entire WM

236 At the individual level, most detected injured regions (93.3%) were associated with decreased F

237 Using meta-analysis techniques to combine injured regions across subjects, we found the combined i

238 Consistently, in cisplatin-injured renal tubular cells in vitro, lithium enhanced a

239 Tgfb3 can stimulate pSmad3 expression in the injured retina, only Tgfb3 inhibits injury-dependent MG

240 Notch signaling on lin28a expression in post-injured retina.

241 P2RX7 inhibition in injured retinas also increased the expression of lin28a

242 Injured retinas in mammals do not regenerate and heal wi

243 In CoCl(2) -injured retinas, blockade of endogenous extracellular AT

244 lar logic behind the regenerative failure of injured RGC axons in adult mammals and suggested several

245 ort demonstrating in vivo neuroprotection of injured RGCs and optic nerve (ON) by AAV-mediated CRISPR

246 GF on RGCs is crucially involved to preserve injured RGCs such as in glaucomatous patients.

247 unction and molecular changes in spinal cord-injured (SCI) rats were investigated.

248 Single-cell RNA-sequencing of injured sciatic nerve identifies five macrophage subpopu

249 ction maturation, and functional recovery of injured sciatic nerves, and increased the ability of reg

250 sion and proliferation of macrophages around injured sensory neurons in dorsal root ganglia (DRG).

251 (injury severity score >= 15) and nonsevere injured septic patients had an odds ratio of 1.39 (95% C

252 lues of the dorsal and lateral tracts on the injured side closely tracked measurements of the behavio

253 iculospinal projections are destroyed on the injured side, resulting in impaired locomotion.

254 The lateral tract on the opposite (non-injured) side was minimally affected by the injury.

255 a glial scar and reducing cell death at the injured site.

256 ally to remove cellular membrane debris from injured sites, which is a prerequisite for tissue healin

257 fects associated with CTGF in MD and acutely injured skeletal muscle.

258 eils cell-specific ECM-remodeling effects in injured skeletal muscle.

259 ls promotes repair of acutely or chronically injured skeletal muscle.

260 polysaccharide (LPS)-treated or spared nerve injured (SNI) wild type (WT) and Ido1(-/-) mice underwen

261 lar interaction to direct axon growth in the injured spinal cord and the potential to use this strate

262 e neonatal and the adult (P > 90) normal and injured spinal cord of male and female mice.

263 Cell therapy for the injured spinal cord will rely on combined advances in hu

264 cal rationale for early decompression of the injured spinal cord, the influence of the timing of surg

265 tilage repair in mice and was switched on in injured synovium in prospective areas of cartilage forma

266 Our results explain why fibrosis occurs in injured tendons and present clinical challenges to enhan

267 6 + Abeta rats was not detrimental enough to injure the complete network.

268 drivers hold the potential to progressively injure the functional lung units of acute respiratory di

269 We injured the gluteus maximus muscle in mice aiming to inv

270 atment increased the work to fracture of the injured tibia.

271 f-injury based on the 2 models used, but the injured tissue dictates the systemic cytokine response.

272 genous bioelectric state by depolarizing the injured tissue during the first 3 h of regeneration alte

273 Brought into the injured tissue initially by migrated neutrophils, and th

274 ally inhibited ERK1/2 phosphorylation in the injured tissue, suggesting it may act through a combinat

275 TH17 cells and CX3CR1(+) monocytes into the injured tissue, which was accompanied by increased RIPK3

276 toration of vascular barrier function within injured tissue.

277 t role in the repair and regeneration of the injured tissue.

278 when it develops in the microvasculature of injured tissues and organs.

279 tive agents accelerating healing of infected injured tissues is crucial.

280 In this study, we show that fibroblasts in injured tissues undertake the clearance of collectins by

281 ly regulates neutrophil retention within the injured tissues with consequences for neutrophil clearan

282 y adult epithelium but upregulated in select injured tissues, including fibrotic lung.

283 complex molecular signatures and utility in injured tissues.

284 ished fibrosis and to regenerate chronically injured tissues.

285 AURKB deficiency during regeneration of the injured tissues: disrupted cell cycle progression, repre

286 12 months and compared them with a similarly injured trauma population.

287 tional expression of TRPM8 channels in these injured trigeminal primary sensory neurons.SIGNIFICANCE

288 The injured tubules acquired a proinflammatory and profibrot

289 Of CD133(+) cells, ~85% are within injured tubules and ~15% are interstitial.

290 collected during surgeries were cultured and injured under 3 conditions: (1) basal conditions, (2) ex

291 cohort study randomly selected 10,000 battle-injured United States military personnel.

292 f blood clots to wounds is necessary to seal injured vasculature and achieve hemostasis.

293 sed to evaluate association of the number of injured vessels, vessel grade, and vessel type (internal

294 d it can achieve rapid hemostasis in acutely injured vessels.

295 the perivascular space tracking a network of injured vessels.

296 Those who died were critically injured with a preponderance of traumatic brain injury a

297 n IFN-beta(-/-) TBI mice compared with their injured WT counterparts; improved neurological recovery

298 The possibility that pressure surges in injured xylem underlie these events has been evoked freq

299 lcidol enhanced the regenerative response of injured zebrafish hearts, whereas VDR blockade inhibited

300 or the successful repair and regeneration of injured zebrafish hearts.