ライフサイエンスコーパス: insult

1 manifest itself 1-2 weeks after the initial insult.

2 control mice conspicuous protection against insult.

3 pathway rapidly activated during pancreatic insult.

4 reased afterward, becoming normal on 30 d of insult.

5 dividuals survive despite the strong genetic insult.

6 Trib3 strongly protected neurons from Abeta insult.

7 ticularly when the cells are under radiation insult.

8 and other epithelia that act as barriers to insult.

9 response in brain stem cells upon oncogenic insult.

10 crease in this process from day 14 after the insult.

11 proper cognitive function against exogenous insult.

12 s in DNA methylation induced by a subsequent insult.

13 oves contraction force after severe ischemic insult.

14 n (i.e., scalp hair follicles) against redox insult.

15 ons in the peri-infarct cortex 65d after the insult.

16 ishment following inflammatory or thrombotic insult.

17 vulnerability (ICV) triggered by the initial insult.

18 photoreceptor rods and cones after a retina insult.

19 nesis and valvulogenesis upon a pathological insult.

20 y relevant time point after an epileptogenic insult.

21 ensatory neuroprotection against excitotoxic insult.

22 al description of the response to mechanical insult.

23 o the nature, magnitude, and duration of the insult.

24 f the engineered lung microtissue upon MWCNT insult.

25 ainst a subsequent, more prolonged, ischemic insult.

26 ral immunity produce Igs to match pathogenic insult.

27 ression of disease regardless of the primary insult.

28 ic diabetic heart following an acute hypoxic insult.

29 PCNs induced by blood exposure or hemoglobin insult.

30 ophagosome within approximately 45 min after insult.

31 d deductions about the extent of the initial insult.

32 ation, timing and severity of the hypoxaemic insult.

33 jury when exposed to an ischemic-reperfusion insult.

34 minished remyelination after a demyelinating insult.

35 y on cells to repair DNA lesions and survive insult.

36 d gave rise to exacerbated liver injury upon insult.

37 s protection to the host encountering immune insult.

38 sm, and an increased sensitivity to ischemic insults.

39 tive immunodominant epitopes from pathogenic insults.

40 of the intestinal epithelium following toxic insults.

41 defense to combat oxidative or electrophilic insults.

42 ) generated by both exogenous and endogenous insults.

43 ions as a first-line defense against noxious insults.

44 orrecting cellular homeostasis after various insults.

45 e genome is constantly attacked by genotoxic insults.

46 e are protected from heart failure-promoting insults.

47 able effects of liver fibrosis against acute insults.

48 ory responsiveness to sterile and infectious insults.

49 ar cell integrity and plasticity on cellular insults.

50 inflammasomes during pathogenic and sterile insults.

51 es cell wall integrity against environmental insults.

52 l cell types subjected to the same oncogenic insults.

53 c inhibition or stress-induced mitochondrial insults.

54 shes rDNA as a genomic target of nutritional insults.

55 logical lymphangiogenesis induced by various insults.

56 the response to endogenous and environmental insults.

57 tic activity as a consequence of excitotoxic insults.

58 ysfunction triggered by immune and nonimmune insults.

59 on, whereby cells compete through mechanical insults.

60 patients exposed to potential epileptogenic insults.

61 cardium to diverse genetic and environmental insults.

62 defense against pathogens and environmental insults.

63 n developmental anomalies and/or early brain insults.

64 al neurons highly susceptible to excitotoxic insults.

65 of life that is dysregulated by inflammatory insults.

66 eration pathway that is activated by diverse insults.

67 rotection to liver cells exposed to chemical insults.

68 been found to cause resistance to genotoxic insults.

69 idative stress from endogenous and exogenous insults.

70 nt neuronal cell death following excitotoxic insults.

71 ibed consequences of other early nutritional insults.

72 damage and neutralizing potentially harmful insults.

73 anges in osmotic pressure and small molecule insults.

74 ic behavior at rest and in response to renal insults.

75 state and in response to pathophysiological insults.

76 fork stabilization in response to genotoxic insults.

77 E) is a devastating sequela of various brain insults.

78 aging neurons vulnerable to disease-related insults.

79 n individual responses to exogenous cellular insults.

80 on changes in functional demands and diverse insults.

81 in host protection against pro-inflammatory insults.

82 st responses to infectious and environmental insults.

83 As epileptogenic insult, a status epilepticus (SE) was induced in rats by

84 selective injury but more likely by systemic insults, a humanized xenograft model of FSGS resulted in

85 ponse to physical damage and/or inflammatory insult, affects nearly every tissue in the body and can

86 These changes are often reversible if the insulting agent is removed early, with the exception of

87 chromatin, making it more accessible to DNA insulting agents, and by its ability to become a barrier

88 pffer cell p38 activation relative to either insult alone, and this corresponded to a 43% (p < 0.05)

89 e that a sublethal ischaemic preconditioning insult also leads to Kv2.1 redistribution in a ryanodine

90 xplored an alternative hypothesis that these insults alter the maturational trajectory of SPNs.

91 lls to arrive at the site of an inflammatory insult and are among the first to die.

92 derlying etiology based on the timing of the insult and causal factor.

93 o characterize the pattern of the mechanical insult and estimate the extent of brain injury to direct

94 one of the earliest sensors of environmental insult and have been shown to play a role in ENM-mediate

95 neurodegeneration after a cerebral ischemic insult and highlights the significant potential of chemi

96 ests that differences exist in the microbial insult and inflammatory responses leading to gingivitis

97 ated molecular patterns to contextualize the insult and inform a tailored adaptive response via T and

98 hemical processes beginning with the initial insult and lasting for days, months and even years post-

99 tive damages caused by arsenic-induced liver insult and pressure overload heart injury.

100 inues to represent an important, incremental insult and risk modifier of acute and longer-term outcom

101 tes reflect the severity of an epileptogenic insult and that a panel of plasma VD3 metabolites may be

102 mpromise intestinal regeneration upon tissue insult and/or promote tumor growth.

103 ing a physical barrier against environmental insults and allergens and providing a tissue interface b

104 cells to survey tissues and sense pathologic insults and deviations makes them a unique platform for

105 a function as barriers against environmental insults and express the transcription factor aryl hydroc

106 protection of tissues from various types of insults and for cancer prevention.

107 air to facilitate survival against genotoxic insults and found that FASN suppresses NF-kappaB but inc

108 to outline the contribution of developmental insults and genes in the occurrence and pathogenesis of

109 ation to protect probiotics against GI tract insults and improve their adhesion and growth on the int

110 which recognize exogenous or endogenous CNS insults and initiate an immune response.

111 To protect against these insults and maintain genome integrity, cells have evolve

112 izophrenia is associated with prenatal brain insults and premorbid cognitive deficits, we tested the

113 d to confer protection against environmental insults and prevent disease or inhibit the progression o

114 hat underlie its susceptibility to metabolic insults and then discuss the pathways that contribute to

115 entering a quiescent state to avoid genomic insults and to prevent exhaustion caused by excessive pr

116 n conferred cellular resistance to genotoxic insults and was required for the recruitment of BLM and

117 ic tumors, characterized by very few somatic insults and, possibly, important epigenetic changes.

118 hen faced with mutational and non-mutational insult, and elucidates the dynamic cellular behaviours u

119 lood CitH3 was detected 30 minutes after LPS insult, and remained elevated for 24 hours (period of th

120 is and ER stress during ischemia/reperfusion insult, and the infarct size was reduced.

121 c release of cytokines after an inflammatory insult, and this was further increased by estrogen.

122 apid degeneration following a range of toxic insults, and also involutes as part of the aging process

123 engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms.

124 microbial substances, sterile environmental insults, and molecules derived from host cells.

125 lin D/Cdk4/pRb activation following ischemic insult are presently not clear.

126 s in a rat model of major burn and endotoxin insults are ameliorated by resolvin D2.

127 As similar insults are known to activate hyaluronan synthesis we ex

128 Environmental insults are often detected by multiple sensors that acti

129 neous melanoma, where hundreds of exonic DNA insults are usually detected.

130 nisms for repairing several forms of genomic insults are well understood, the upstream signalling pat

131 ain, among other vital organs, often suffers insults as a result of HF, and both anatomic and functio

132 This cell-autonomous genetic insult attenuated neuronal spiking by increasing the aft

133 During times of environmental insult, Bacillus subtilis undergoes developmental change

134 ct "danger" signals (pathogenic or traumatic insult), become activated, produce proinflammatory cytok

135 are immunologic challenges and environmental insults, both of which associate with changes in epigene

136 When unanticipated insults breach epithelial barriers, dormant programmes o

137 uli prepares the body against future massive insult by activating endogenous protective responses.

138 Conversely, FoxO1 responded to Abeta insult by binding to the Trib3 gene promoter, enhancing

139 the behavioral effects of developmental MeHg insult by exposing parental generations of zebrafish to

140 mation and survival in the setting of septic insult by targeting MyD88- and Toll/IL-1R domain-contain

141 protective effect (13-62%) on SH-SY5Y cells insulted by H2O2 at a concentration of 50mug/mL by DCFH-

142 ediates neuronal death in response to neural insults by activating a caspase apoptotic pathway.

143 gitis sensitizes cholangiocytes to apoptotic insults by activating sAC, which may play a crucial role

144 ression after ischemic and obstructive renal insults by not only attenuating inflammation but also, d

145 egulates cellular response against genotoxic insults by up-regulating PARP-1 and DNA repair via NF-ka

146 ell production before an epileptogenic brain insult can mitigate epileptogenesis.

147 injury (TBI), neurons surviving the initial insult can undergo chronic (secondary) degeneration via

148 Genetic, environmental, or metabolic insults can induce overly restrictive or overly permissi

149 lls by genetic, environmental, or biological insults can initiate complex signaling mechanisms that p

150 This insult caused a delayed loss of mitochondria from astroc

151 Pathomechanistically, amyloid-beta insult caused cofilin activation and F-actin remodeling

152 aumatic brain injury (rmTBI), resulting from insults caused by an external mechanical force that disr

153 In the case of H2O2 insult, cells treated with 3-amino-1,2,4-triazole (a cat

154 tasis in the face of intrinsic and extrinsic insults, cells have evolved elaborate quality control ne

155 anisms sensitizing other modalities after an insult, cold allodynia is mediated exclusively by a sing

156 T cells showed higher tolerance to genotoxic insults compared with their TERT-negative counterparts.

157 A variety of neurological insults compromise sound processing, particularly in com

158 nocytes to the injured brain early after the insult contribute to long-term functional recovery after

159 euroinflammation, triggered by epileptogenic insults, contributes to seizure development.

160 dies and brain imaging can identify an acute insult contributing to the presentation.

161 ophages in control mice protected from acute insult; conversely, depleting macrophages in fibrotic li

162 vironmental, physiological, and pathological insults disrupt protein-folding homeostasis in the endop

163 gical environment and we show that oncogenic insults drive this MB subgroup in different cerebellar l

164 ime points after perturbation by environment insults, drugs and chemicals.

165 (TLE) generally takes years after an initial insult during which maladaptation of hippocampal circuit

166 ological genetic variation and environmental insults during sensitive periods in brain development ha

167 ut it is exquisitely sensitive to a range of insults during the transplant period, including conditio

168 Additionally, persistent microbial insult (e.g. LPSs) induces cyclin-dependent kinase inhib

169 thology, repeated focal seizures, and global insults each contribute to atrophy in specific tracts.

170 , increased expression of GRK2 after cardiac insult exacerbates injury and speeds progression to hear

171 reduction in seizures, suggesting that peri-insult generated cells mediate epileptogenesis, but that

172 treated with diphtheria toxin to ablate peri-insult generated newborn granule cells, which were born

173 effectively stimulated after an excitotoxic insult has been delivered, and may identify a new therap

174 sure of the child to the index environmental insult has sparked interest in transgenerational inherit

175 taining vesicles in response to inflammatory insults has not been studied.

176 function in the face of multiple proteotoxic insults, holding open the possibility of targeting these

177 did not alter their response to inflammatory insult; however, injecting purified Abs from CV animals

178 uring homeostatic turnover and immunological insults; however, the metabolic requirements for this pr

179 roorganisms as well as physical and chemical insults; however, the physiological mechanisms that main

180 y related to some combination of environment insults (i.e. abnormal physiology), donor-specific antib

181 adaptively respond to chronic, low-level NP insults; (ii) the cell stress response is not reversible

182 ellular protection against hydrogen peroxide insult in a pentose phosphate pathway and GSH-dependent

183 The in situ control of redox insult in human organs is of major clinical relevance, y

184 s, lesions in AMN may result from a vascular insult in the choriocapillaris.

185 s R-837 and R-848 were used to mimic a viral insult in the upper airways represented by primary human

186 vitro following hypoxia and global ischemic insult in vivo Finally, we show that shRNA targeting Cdc

187 (LV) viability and function after ischaemic insults in vitro, but its long-term cardioprotective act

188 steady state and following myelosuppressive insult, in which inhibition of EC NF-kappaB promotes imp

189 During gestation, prenatal insults including maternal infection and subsequent immu

190 sease and dementia and after global cerebral insults including stroke and epilepsy.

191 that are poised to respond to environmental insults including viral infections with the potential fo

192 also be used to assess the effects of airway insults, including coinfections by recognized respirator

193 he aged brain and vulnerability to secondary insults, including infections and psychological stress.

194 mely hydrophobic and impermeable to external insults, including many antibiotics.

195 devastating long-term risk of various brain insults, including trauma, stroke, infections, and statu

196 as the severity of the infectious pulmonary insult increased, without recovery at 6 weeks.

197 natal exposure to infectious or inflammatory insults increases the risk of neurodevelopmental disorde

198 All of these insults induce hepatocyte death and subsequent inflammat

199 osidase staining in a culture-based model of insult-induced senescence.

200 reased in number after relevant pathological insults (infarcts), suggesting a similar expansion of ce

201 In response to ischemic insult, injured tissues secrete several chemo-cytokines,

202 on the pathophysiology of chronic metabolic insults involving both the airways and the cardiovascula

203 terial infection, or by sterile inflammatory insult is a primary trigger of spontaneous preterm birth

204 However, when the tissue insult is chronic, the ongoing release of multiple pro-i

205 tive diseases, cell death induced by primary insult is followed by a wave of secondary loss.

206 y respond transcriptionally upon the initial insult is incompletely understood.

207 perturbed and that a critical developmental insult is key to the afferent pathology.

208 ns that are protective against such cellular insults is a potentially valuable therapeutic approach.

209 inct B cell subsets during neuroinflammatory insults is critical for preventing and managing acute en

210 After ischemic, oxidative, or inflammatory insults, Kv2.1 mediates a pronounced, delayed enhancemen

211 Procalcitonin reacted to LPS insult late.

212 ar signaling by which hypoxia and some other insults lead to upregulation of VEGF has been elucidated

213 regulation may be sensitive to environmental insult leading to altered phenotypes.

214 could be a major consequence of chronic EtOH insult leading to fatty liver.

215 NLRP3 senses exogenous and endogenous insults, leading to inflammasome activation, which occur

216 ng first to the hypothesis that carcinogenic insults leave characteristic imprints on the DNA sequenc

217 ar hair cells are vulnerable to a variety of insults like acoustic trauma and ototoxic drugs.

218 increased susceptibility to secondary immune insults like infections.

219 des into extracellular space is triggered by insults like wounding and ultraviolet radiation, resulti

220 ective in protecting old liver from ischemic insults, mainly owing to its ability to induce circulati

221 ure, and it has implications for how genetic insults may contribute to psychiatric disorders.

222 regulatory T cells (Tregs) during autoimmune insults may have therapeutic efficacy in autoimmune dise

223 of persistent susceptibility to excitotoxic insult mediated by neurovirulent virus effects on other

224 on of patients survive their initial cardiac insult, medical systems worldwide are being faced with a

225 s, did not induce persistent disease in MPTP-insulted mice.

226 ferent genetic deficits and/or environmental insults, neural computations and the behaviors that rely

227 gulated differently than the acute, one time insult of axotomy.

228 irs of samples before and after the ischemic insult of cardiopulmonary bypass.

229 of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors

230 p 1-1 carriers may be more vulnerable to the insults of poor glycemic control.

231 these patients as a result of an autoimmune insult on the kidney collecting duct cells.

232 can be useful for assessing other cytotoxic insults on cultures of hESC.

233 cert to mediate axonal responses to external insult or injury in mammalian CNS neurons.

234 Due to environmental insult or innate genetic deficiency, protein folding env

235 al capacity that has been lost through brain insult or musculoskeletal injury.

236 Environmental insults or increased protein synthesis often lead to pro

237 , protecting itself from harm (environmental insults or infections), to ultimately, death by apoptosi

238 such as excessive inflammation, a second-hit insult, or an imbalance between pro- and anti-inflammato

239 ic cells and their terminations against MPTP insult, particularly in animals that developed few clini

240 in patients who had experienced major immune insults, particularly prior immunosuppressive drug expos

241 ministered at fixed time intervals after the insult, perhaps ignoring the inherent variability in mag

242 h we interpret as a consequence of bilateral insults (potentially generalized seizures and/or medicat

243 free window, with or without a demyelinating insult, provides a favorable environment for SVZ-derived

244 Here we show that a proteostatic insult, provoked by persistent expression of the secreto

245 We find that DLK-activating insults ranging from nerve injury to neurotrophin depriv

246 sevoflurane administered after the ischemic insult reduced brain infarct percentage and neurological

247 t mechanisms of injury development following insult remain ill-defined and there are no FDA approved

248 Hemodynamic insults secondary to increased intraabdominal pressure i

249 Understanding of insults should enable decades of morbidity-free survival

250 e occur after the initial acute haemorrhagic insult subsides, and represent one of its most feared lo

251 However, the contribution of insults such as dietary factors that can also activate t

252 ad, poorly defined, and frequently occurring insults such as inflammation.

253 share several altered cellular responses to insults such as oxidative stress, extracellular matrix r

254 natal periods as vulnerable to environmental insults such as stress.

255 ystem and is also a hallmark of pathological insult, such as injury [1, 2].

256 pathogenetic hallmark after different brain insults, such as ischemia and status epilepticus (SE).

257 ells into the nigra was found on 1 d of MPTP insult, T cell infiltration decreased afterward, becomin

258 s (hemodynamic, biological, renal, and liver insults) than donors without extracorporeal membrane oxy

259 al circuit remodeling after an epileptogenic insult that generates prominent excitatory monosynaptic

260 ome is a whole-body reaction to a triggering insult that often results in life-threatening illness.

261 h preterm birth may result from neurological insults that begin in utero.

262 dulates protein folding in reply to cellular insults that lead to endoplasmic reticulum (ER) stress.

263 Hence, despite the resistance of SPNs to insults that trigger white matter injury, transient hypo

264 an lead to abnormal responses to a secondary insult, these results suggest that chronic sleep loss, t

265 levels, and upon BA- or drug-induced biliary insults, these mice exhibit exacerbated cholestatic path

266 lls in S-phase sensitizes cells to apoptotic insult, this study suggests novel therapeutic approaches

267 exert the protective effects against lethal insults through conferring apoptosis resistance to hepat

268 re key steps in the continuum from allograft insult to chronic allograft dysfunction.

269 ult of severe periodontal disease acts as an insult to the endothelium.

270 mpal recordings of epileptogenesis (from the insult to the first spontaneous seizure) from two labora

271 eroxidation were similar irrespective of the insult to the livers that resulted in fatty liver.

272 A primary insult to the pancreatic islets of Langerhans, leading t

273 he data may also help to explain why genetic insults to alpha4 subunits are associated with working m

274 athway activated by a wide range of cellular insults to elicit innate immune defenses through the act

275 Insults to the airway epithelium play a key role in cons

276 th PAMPs and DAMPs can be liberated by early insults to the allograft, including ischemia/reperfusion

277 er cognition and help to explain why genetic insults to the alpha4 subunit weaken cognitive and atten

278 in inhibition on the BBB following traumatic insults to the brain.

279 isease occurring after years of inhalational insults to the lungs, pinpointing abnormalities or disru

280 We determined SPN responses to two common insults to the preterm brain: hypoxia-ischemia and hypox

281 ane potential recovery after a mitochondrial insult together with alterations in lysosomes and autoph

282 argely unclear and presumably depends on the insult types and responding components.

283 unclear how the consequences of this genetic insult unfold to impair neurodevelopment.

284 ewly generated cells after the epileptogenic insult using a conditional, inducible diphtheria-toxin r

285 Here, the bacterial insult was of focal nature and led to changes in tight j

286 bly, within weeks after the initial ischemic insult, we observed functional cardiac recovery, which t

287 in order to deliver a localized excitotoxic insult, we replicate secondary spreading toxicity and de

288 ction against tissue damage by environmental insults, we identified artemisitene as a novel Nrf2 acti

289 epilepsy development after an acquired brain insult, which represents a feasible therapeutic target t

290 Sestrin2 is induced by different stress insults, which diminish ATP production and induce energe

291 pocampal neuronal cells from the excitotoxic insult, while efavirenz (EFV) did not contrast the neuro

292 In response to an oxidative insult, wild-type p53 has been implicated as a central r

293 red haemostasis could exacerbate the primary insult with risk of initiation or aggravation of bleedin

294 oxidation assays, as well as, SH-SY5Y cells insulted with H2O2.

295 them to respond rapidly to perceived tissue insults with a view to initiating a co-ordinated program

296 least-squares-path modeling we found that WM insult within the optic radiations, V1, and cuneus is a

297 eant neuroprotective agent against oxidative insults without interacting with P-gp efflux system.

298 ways that allow effective responses to acute insults, without descending into chronic inflammation.

299 e environments and against many inflammatory insults, yet the tissue-enriched factor(s) that influenc

300 aging that sensitizes the heart to ischemic insults, young C57BL/6 mice (age 3-4 mo), middle-aged mi