ライフサイエンスコーパス: damage

1 strong fields, they suffer from irreversible damage.

2 o protect other proteins from stress-induced damage.

3 s (DSB) are the most deleterious type of DNA damage.

4 tegies for >25 types of DNA modification and damage.

5 condary vascular damage due to ganglion cell damage.

6 rological injury, including stroke and nerve damage.

7 at the expense of incurring substantial DNA damage.

8 migration of microglia to sites of neuronal damage.

9 itor the persistence and progression of lung damage.

10 in the next mitosis generates extensive DNA damage.

11 tients with proteinuria, indicating podocyte damage.

12 death that relies on iron-mediated oxidative damage.

13 leaves or those exposed to volatile cues of damage.

14 sDNA and repair genomic loci affected by DNA damage.

15 9 (Covid-19) is associated with diffuse lung damage.

16 S- and JNK-mediated Mmp2 upregulation and BM damage.

17 ation and reflect ongoing pathophysiological damage.

18 tively localized in the nucleus prior to DNA damage.

19 ssive inflammatory responses and endothelial damage.

20 of PV stenosis, artery, nerve, or esophageal damage.

21 borating the influence of rainfall on forest damage.

22 unction, and increases the risk of end-organ damage.

23 ubicin (DXR)-induced small intestine mucosal damage.

24 enuated neutrophil-mediated endothelial cell damage.

25 two key elements involved in ischemic brain damage.

26 integrity for easy collection of lead after damage.

27 amage followed by progressive secondary axon damage.

28 hen released in excess, inflict irreversible damage.

29 ion arrest, allowing replication despite DNA damage.

30 tant hub for processing various types of DNA damage.

31 peutics intended to mitigate cardiomyopathic damage.

32 ity is further increased to 60-fold by dsDNA damage.

33 the main targets of HOCl, from HOCl-mediated damage.

34 a and modulated across the boundary of light damage.

35 ants by immune cells results in acute tissue damage.

36 bolism or other perturbations that cause DNA damage.

37 under pathological conditions to cause cell damage.

38 d that muscle deprived of SMN was profoundly damaged.

39 boats are two approaches to reduce pollution damages.

40 nse protein regulated in development and DNA damage 1 (REDD1) is necessary for the development of oxi

41 In contrast, vmPFC/mOFC damage abolished neither scaling nor asymptote of the dr

42 location pairs, which fundamentally suppress damage accumulation and preserve the structural stabilit

43 ed WNT signaling and was associated with DNA damage accumulation.

44 d in the loss of 59 lives and $25 billion in damages across the southeastern U.S.

45 ary defensive functions and excessive tissue damage actions.

46 nstrated a notably similar pattern of axonal damage adjacent to the gray-white interface.

47 f neutrophil extracellular traps in helminth damage after primary infections.

48 y, and in anticancer therapies involving DNA damage agents.

49 Upon exposure of human cells to DNA-damaging agents, NUCKS1 controls the resolution of RAD54

50 uses either sensitivity or resistance to DNA-damaging agents.

51 fects of ionizing radiation, among other DNA damaging agents.

52 for cross-sectional associations between VF damage and activity fragmentation.

53 response and PKR and markedly increased DNA damage and apoptosis caused by dysregulation of TDP-43 l

54 revented, leading to the accumulation of DNA damage and cell death.

55 fy a surprising role for Cds1 in driving DNA damage and disrupted chromosomal segregation under certa

56 t drug-induced oxidative stress-mediated DNA damage and execution with potential therapeutic implicat

57 tream pathological effects, including tissue damage and fetal demise.

58 iple factors, including cellular stress, DNA damage and immune surveillance.

59 a displaced single-stranded DNA) create DNA damage and lead to genomic instability.

60 DNA damage and metabolic disorders are intimately linked wit

61 est study that comprehensively assessed tree damage and mortality from lightning strikes, we estimate

62 ramide accumulation in podocytes to cellular damage and nephrotic syndrome.

63 S phase entry causes replication stress, DNA damage and oncogenesis, highlighting the need for strict

64 scular) endothelial cells in response to DNA damage and oxidant stress regulated in part by a BMPR2 d

65 itination on lysine 13/15 (K13/K15) upon DNA damage and promotes the accrual of downstream repair fac

66 ecting cells from replication-associated DNA damage and promoting cellular recovery.

67 ends from inappropriately activating the DNA damage and repair responses.

68 hway previously shown to associate with lung damage and severity of influenza virus infection.

69 ischemic injury and migrate to the areas of damage and stimulate revascularization largely by paracr

70 rity becomes compromised during cytoskeletal damage and stress by reducing For3 levels.

71 In addition, endothelial damage and thromboinflammation, dysregulation of immune

72 tential to protect the retina from oxidative damage and to prevent or slow down diabetic retinopathy.

73 patterns of ancestral admixture and putative-damaging and novel variation, both within and between po

74 red for the treatment of uncontrolled tissue-damaging and thrombotic responses in COVID-19.

75 carcinogenesis by causing inflammation, DNA damage, and activation of beta-catenin signaling.

76 (CCl(4)) to induce mutations, chronic liver damage, and carcinogenesis.

77 IECs increases markers of inflammation, DNA damage, and cell proliferation and increases colorectal

78 in levels, increased reactive oxygen species damage, and elevated GDF15 and FGF21 levels, indicating

79 loss leads to double-strand break (DSB) DNA damage, and the apoptotic response is exacerbated by con

80 kes red cells highly vulnerable to oxidative damage, and therefore susceptible to hemolysis.

81 esults show that perceptual deficits from AN damage are smaller than generally expected, and potentia

82 tion between brain regions lying outside the damaged area contributes to spatial deficits in a way th

83 The measurement of UV-induced DNA damage as a dosimeter of exposure and predictor of skin

84 nd marked advance of liver fibrosis (chronic damage), as well as necrosis of hepatocytes in zone 3 of

85 distinguish acute (protective) and chronic (damaging) associated changes with diabetes.

86 perspective and could possibly be decoded as damage-associated molecular patterns.

87 dentified a distinct AT2-lineage population, damage-associated transient progenitors (DATPs), that ar

88 s against oxidative (78%) and cellular (90%) damage at a 3 ug/L concentration (corresponding to 0.03

89 Specific radiation damage at RT was observed at disulfide bonds but not at

90 mical parameters reflecting decreased tissue damage at systemic level and improved renal function in

91 of blood flow not being restored and tissue damage being observed in histology.

92 brain pathologies are associated with liver damage, but a direct link has long remained elusive.

93 tes are unable to respond immediately to DNA damage, but instead mount a G2/M DDR that evolves slowly

94 r response to microbial infection and tissue damage, but its aberrant activation can lead to autoinfl

95 FLD, Escherichia coli LPS may increase liver damage by inducing macrophage and platelet activation th

96 Cellular DNA can be damaged by spontaneous hydrolysis, reactive oxygen speci

97 strikes, we estimate that lightning directly damages c.

98 s of compounds that not only targets the DNA damage cancer response machinery but also simultaneously

99 uisite, FXR seems to influence the degree of damage caused by atorvastatin depending on its interacti

100 the DNA synthesis defects and suppresses DNA damage caused by INO80 depletion.

101 m cells to generate new cells that replenish damaged cells.

102 n of the Trp53 tumor suppressor or Chek2 DNA damage checkpoint kinase rescued Smc5 cKO neurodevelopme

103 duced foci (TIFs), indicating defects in DNA damage checkpoint signaling.

104 on of the conserved helicase PIF1 and/or DNA damage checkpoint-mediator RAD9.

105 s in a clonal population to cisplatin, a DNA-damaging chemotherapeutic agent.

106 the accrual of downstream repair factors at damaged chromatin.

107 of CHD at least as high as that observed for damaging coding DNVs.

108 ter progression of glaucomatous visual field damage compared to matched glaucoma patients (n = 26) wi

109 gly, infected chub exhibited lower oxidative damage compared to uninfected fish, irrespective of thei

110 ations of markers of inflammation and tissue damage compared with healthy controls, and metabolic cha

111 These results indicate significant tissue damage consistent with the development of hemorrhagic fe

112 onent of the glomerular physiology and their damage contributes to the progression of chronic kidney

113 H. pylori-induced replication stress and DNA damage depend on the presence of co-transcriptional RNA/

114 ppropriate control measures for an extremely damaging disease in terms of animal health, productivity

115 Lipopolysaccharide (LPS)-mediated intestinal damage, driven by STAT1-induced inflammation, was also p

116 rt that L1 activity triggers FOA through DNA damage-driven apoptosis and the complement system of imm

117 Myocardial damage due to acute ST-segment elevation myocardial infa

118 ready experiencing some of the most dramatic damage due to anthropogenic climate change, and the situ

119 lar insult in addition to secondary vascular damage due to ganglion cell damage.

120 irculation with a feed-forward loop of organ damage, due to vasoconstriction, leukocyte adherence, an

121 ng this region at greater risk of mechanical damage during brain tissue deformation from traumatic br

122 lecular patterns (DAMPs) released from cells damaged during ischemia-reperfusion injury (IRI), in hea

123 (RT), creating free radicals and local tumor damage, effectively boosting the local RT dose at the tu

124 issues, leading to severe symptoms and organ damage (eg, cytopenias, liver dysfunction, portal hypert

125 Endomembrane damage elicits homeostatic responses including ESCRT-dep

126 5-AzadC-induced DNA damage enhanced P-TEFb occupancy via a mechanism that in

127 es SYK and NADPH oxidase to cause phagosomal damage even when spliced into a heterologous receptor an

128 ng variations strongly determine the type of damage evolution, i.e., the creep or fatigue, during the

129 l acuity, patients with glaucomatous macular damage exhibit diminished facial recognition, which is p

130 DAI causes immediate, sporadic axon damage followed by progressive secondary axon damage.

131 Neurologic damage following cardiac arrest remains a major burden f

132 smoking-related lung cancer risk and tissue damage from other inhaled toxins.

133 owing I/R injury secondary to the collateral damage from sustained myocardial inflammation within the

134 t removes RNA polymerase (RNAP)-stalling DNA damage from the transcribed strand (TS) of active genes.

135 In response to damage, Gal9 displaces USP9X from complexes with TAK1 an

136 Damaging GATA6 variants cause cardiac outflow tract defe

137 hat pathogens that reduce yields by directly damaging harvestable plant tissues have received much le

138 arlier stages before irreversible structural damage has occurred.

139 F480 macrophages and increased clearance of damaged hepatocytes.

140 or thrusts within the orogen has resulted in damaging historical seismicity, whereas south of the Mai

141 It is widely known that cigarette smoke damages host defenses and increases susceptibility to ba

142 ust to variations in the extent of ON tissue damage, image quality, and species of mammal.

143 ion of atorvastatin during MI limits cardiac damage, improves cardiac function, and mitigates remodel

144 d plays an important role in cerebrovascular damage in AD, we investigated the role of the Abeta-fibr

145 of estrogen have been shown to stimulate DNA damage in breast epithelial cells through mechanisms med

146 f estrogen receptor alpha, and increased DNA damage in cells.

147 ction and reduction of PMN-associated tissue damage in chronic inflammatory diseases.

148 to prevent cytotoxic T-cell-mediated tissue damage in complex immune disorders exhibiting upregulati

149 Cells confront DNA damage in every cell cycle.

150 tween real-life benzene exposure and genetic damage in future risk assessment.

151 he addition of ADP-ribose moieties after DNA damage in human cells.

152 the chronic inflammation elicited by muscle damage in humans.

153 knowledge might help in detecting local DNA damage in live cells, as well as in aiding our biophysic

154 Fatigue damage in metals manifests itself as irreversible disloc

155 issue, we inflicted substantial DG-specific damage in mice of either sex either by diphtheria toxin-

156 reveal that excessive placental DNA damage in murine models for Cornelia de Lange syndrome r

157 d chromatin accessibility, ameliorated light damage in our mouse model, supporting a causal link betw

158 us forms of replication perturbation and DNA damage in S phase, suggesting it acts as a post-replicat

159 ve stress and the induction of oxidative DNA damage in spermatozoa.

160 ndent gene expression without any mechanical damage in the brain.

161 The importance of tissue damage in the pathophysiology of GVHD rationalizes the d

162 ther illuminates the concentration of severe damage in the town of Compton, where accounts suggest ve

163 In vivo, rtPDT induces cellular damage in tumors, shown by strong expression of cleaved

164 penetrating property attributes to synaptic damage in vivo, we have generated adeno-associated virus

165 ssibly through the accumulation of oxidative damage, in particular in the mitochondrial genome.

166 ity by responding to a large spectrum of DNA damage, including double strand breaks (DSBs) that inter

167 Results show that starch damage increased significantly as the screen aperture si

168 The presence of DNA damage increases the frequency of pausing.

169 We observed cell wall damage induced by bedaquiline and moxifloxacin through s

170 DNA damage induced by chemotherapy drugs, such as topoisomer

171 ow temperature and ambient CO(2) exacerbated damage induced by nanoplastics, while elevated CO(2) and

172 Neonatal tissue damage induces long-term deficits in inhibitory synaptic

173 n requires the Gadd45 (Growth arrest and DNA-damage-inducible) gene family, very little is known abou

174 O depletion decreases sensitivity to the DNA damage-inducing chemotherapy agent doxorubicin.

175 autoinflammatory diseases by limiting tissue damage/inflammation.

176 uctural change characterises global neuronal damage, investigating microstructural alterations provid

177 The response to DNA damage is critical for cellular homeostasis, tumor suppr

178 es suggests that extrapulmonary invasion and damage is likely, which indeed has already been demonstr

179 A major cause of damage is local inflammatory responses, which may spread

180 Nevertheless, DNA damage is sufficient to induce activation of canonical p

181 Fragile site damage is thought to arise from the aberrant repair of s

182 Fusarium-damaged kernels and deoxynivalenol analyses supported th

183 chanisms of direct virus-induced neural-cell damage leading to demyelination and axonal loss, which a

184 ikely to choose undamaged leaves compared to damaged leaves or those exposed to volatile cues of dama

185 Laser-mediated tissue damage let us test the functional significance of these

186 ctive in DNA synthesis and had increased DNA damage levels, suggesting a role for zinc in maintaining

187 onal slide scanner for quantification of DNA damage levels.

188 ymbiont may protect itself and its host from damaging light radiation.

189 chanisms including the oxidative stress, DNA damage, lysosomal dysfunction, inflammatory cascade, apo

190 iquitination of TAK1 thus activating AMPK on damaged lysosomes.

191 NAION and POAG with similar RNFL and macular damage, macular OCT-A shows less involvement of superfic

192 immunofluorescence distribution of oxidative damage markers, and of SOD2 (superoxide dismutase 2), PG

193 ating the fellow eye's level of visual field damage (MD) or rate significantly improved these models.

194 physicochemical properties and of oxidative damage mechanisms for multiple strains in a species.

195 y myeloid cell recruitment and expression of damage mediators.

196 ce, compensatory strategies for this type of damage might exist.

197 in ligase Parkin promotes the degradation of damaged mitochondria via mitophagy and mutations in Park

198 2 (sTREM2), as well as a marker of neuronal damage, neurofilament light chain (NfL), using enzyme-li

199 ic byproducts that stimulate immune-mediated damage of hepatocytes and the biliary tree.

200 However, it did not lead to oxidative damage of the enriched batches or affect the moisture an

201 to exacerbation of postischemic inflammatory damage of the myocardium and corresponding decline in ca

202 a region that may initiate the formation of damaging oligomeric species.

203 also mitigated the adverse impact of housing damage on functional status, suggesting a buffering mech

204 es of the stem cell response to increases in damaged or aggregated proteins remain unclear.

205 Temporally harmonized elimination of damaged or unnecessary organelles and cells is a prerequ

206 of homes with no history of dampness, water damage, or visible mold ("no mold").

207 .g. lipopolysaccharides (LPS), cytokines and damage- or pathogen-associated molecular patterns (DAMPs

208 Within neurons, it helps to remove damaged organelles and misfolded or aggregated proteins

209 maintaining cellular homeostasis by clearing damaged organelles, pathogens, and unwanted protein aggr

210 nt membrane repair and autophagic removal of damaged organelles.

211 stablished that EBOV results in severe organ damage, our understanding of tissue injury in the liver,

212 Progressive end-organ damage, partly related to a systemic vasculopathy, is in

213 Blue light-induced RPE cellular damage preceded the photoreceptors loss.

214 growth, changes associated with endothelial damage (preeclampsia, eclampsia, and HELLP syndrome), an

215 otect stressed cancer cell by degradation of damaged proteins and organelles.

216 nt of a suite of materials characterization, damage quantification, and therapeutic techniques that e

217 itochondrial function trigger release of DNA damaging reactive oxygen species.

218 diverse biological processes, including DNA damage repair (Fanconi anemia), telomere maintenance (dy

219 ounds that interfere with transcription, DNA damage repair and the cell cycle.

220 and Bloom Syndrome (BS) are disorders of DNA damage repair caused by biallelic disruption of the WRN

221 ncer xenograft models that carry certain DNA damage repair deficiencies.

222 g neurodevelopment, but it also mediates DNA damage repair essential to proliferating neural progenit

223 ion of an analog-sensitive CDK12 reduces DNA damage repair gene expression, but selective inhibition

224 iotherapy and chemotherapy by inhibiting DNA damage repair is proposed as a therapeutic strategy to i

225 e (drug extrusion, drug degradation, and DNA damage repair) and using rate constants of these reactio

226 M1, BAP1 and SETD2), DNA methylation and DNA damage repair, all of which have been associated with cl

227 chromosome inactivation, imprinting, and DNA damage repair, and mutations in SMCHD1 can cause faciosc

228 ect 3D genome structure integrity during DNA damage repair.

229 equired for efficient HR-mediated chromosome damage repair.

230 ly that NTMT1 regulates cell mitosis and DNA damage repair.

231 The ubiquitin system regulates the DNA damage response (DDR) by modifying histone H2A at Lys15

232 essing the expression of BRCA1 and other DNA damage response (DDR) genes.

233 les in base excision repair and ATR-Chk1 DNA damage response (DDR) pathways, it remains unknown how t

234 nd joining (NHEJ) repair pathway and the DNA damage response (DDR).

235 Here, we investigate the impact of DNA damage response and repair on 3D genome folding using Hi

236 G-quadruplex DNA along with the related DNA damage response at the telomere.

237 study, we report that inhibitors of the DNA damage response kinase ATR can significantly potentiate

238 instead activate an attenuated telomeric DNA damage response that lacks accompanying telomere fusions

239 SMC5/6 depletion triggers a CHEK2-p53 DNA damage response, as concomitant deletion of the Trp53 tu

240 HELLS has been implicated in the DNA damage response, but its mechanistic function in repair

241 ein in the Fanconi anemia pathway of the DNA damage response.

242 suppressor and a master regulator of the DNA damage response.

243 is, the role of regulated development of DNA damage responses 1 (REDD1), a negative regulator of mTOR

244 or kinases responsible for orchestrating DNA damage responses.

245 intenance of genomic stability relies on DNA damage sensor kinases that detect DNA lesions and phosph

246 stic trauma disrupts cochlear blood flow and damages sensory hair cells.

247 mproved cardiac function, reduced myocardial damage, shock, lung injury and improved survival indepen

248 mechanically-induced irreversible structural damage should be largely prevented.

249 necrotic tissue that requires sensing of the damage signal ATP.

250 sDNA, including DNA replication, repair, and damage signaling.

251 espite increasing RIF1 "end-blocking" at DNA damage sites.

252 r how co-morbidities related to an aging and damaged soma can hinder achievement of ACM benefit.

253 lpXP, which selectively removes and degrades damaged subunits.

254 symptoms, some patients present other severe damage such as cardiovascular, renal and liver injury or

255 re complex symptoms associated with parietal damage, such as constructional ataxia.

256 tes in zone 3 of the Rappaport acinus (acute damage), supporting the hypothesis of ACLF.

257 e a slow-cycling state following stress (DNA damage, targeted therapy, and aging).

258 BRCA1-deficient cells and altered repair of damaged telomeres, can be explained from this viewpoint.

259 rely affected by multiple sclerosis-specific damage than short-range connections.

260 ting the modulation of transcription and DNA damage that may be mediated by the action of HDAC and PP

261 rm impurities into an easily removable form, damage the DNA of microorganisms and their spore forms,

262 However, iron overload can damage the organism through a variety of mechanisms, inc

263 s often not feasible or desirable, as it can damage the polymer's integrity, leading to loss of funct

264 rom 3D CT images by medical experts to avoid damaging the mandibular nerve inside the canal.

265 glycaemia may increase influenza severity by damaging the pulmonary epithelial-endothelial barrier an

266 rse the analyte-surface interaction, without damaging the SERS substrate, allowing for efficient sens

267 ited to DNA lesions within seconds after DNA damage through a mechanism dependent on its DNA binding

268 immune complexes-stimulated acute pulmonary damage through reducing vascular permeability changes an

269 lation of co-transcriptional R-loops and DNA damage to avert genomic instability and neurodegeneratio

270 sage distilled from the discussions was that damage to epithelial surfaces lies at the origin of the

271 Chemotherapy and irradiation cause DNA damage to hematopoietic stem cells (HSCs), leading to HS

272 It causes massive damage to livestock worldwide.

273 ution are limited by the potential for laser damage to living tissues.

274 cancer and can occur as a consequence of DNA damage to the epithelium by UVR or chemical carcinogens.

275 in rats, morphing electronics caused minimal damage to the rat nerve, which grows 2.4-fold in diamete

276 ual exploration.SIGNIFICANCE STATEMENT Focal damage to the right cerebral hemisphere may result in a

277 o a spiral shape to prevent photoirradiation damage to their photosynthetic surfaces.

278 r, a dysregulated macrophage response can be damaging to the host, as is seen in the macrophage activ

279 define a role for PrimPol in HR-mediated DNA damage tolerance.

280 ological processes, about the fabrication of damage-tolerant composite materials.

281 nces DNA end-labeling, and protects from DNA damage, ultimately blocking the proneoplastic effects of

282 higher bacterial load and exacerbated organ damage, ultimately leading to premature deaths.

283 ng in vivo but may cause irreversible tissue damage under dysregulated or acute exposure conditions.

284 loroplast thylakoids (Thys) are specifically damaged upon (1)O(2) generation and associate with plast

285 Radiation damage usually leads to detrimental effects such as embr

286 -confidence risk genes, each containing 2 DN damaging variants in unrelated probands: CHD8 and SCUBE1

287 Long-term damage was found in the ablated core (mean fractional an

288 g FL exposure is not triggered by the lower "damaging" wavelengths of light (UVB and UVA from 300-400

289 Using data from patients with focal brain damage, we demonstrate that there is a strong psychometr

290 itochondrial H(2)O(2) emission and oxidative damage were greater in Taz(KD) than in wild-type (WT) he

291 autoubiquitination and degradation upon DNA damage, whereas S429A substitution protects MDM2 from au

292 phosphorylated by ATM at Ser-1003 after DNA damage, which enhances the catalytic activity of USP52.

293 As a result, ROS-mediated protein damage, which is substantial during the aging of short-l

294 nother mechanism wherein 5-AzadC induced DNA damage, which then resulted in enhanced occupancy of NF-

295 Here, we relate patterns of brain damage with deficits to the content and structure of spo

296 d candidate blood biomarkers of neurological damage with possible clinical utility, many of which who

297 n this study of glaucoma patients with early damage with the 24-2 test, there was little evidence tha

298 We aimed to quantify glycocalyx damage within human liver grafts after organ preservatio

299 To determine the severity of damage within these connections, (i) fractional anisotro

300 myeloperoxidase inhibition suppressed kidney damage without augmenting adaptive immune responses, sug