ライフサイエンスコーパス: danger

1 g able to choose stimuli not associated with danger.

2 gy in situations in which there is impending danger.

3 nt between the nidus and neural structure in danger.

4 es multiple body systems to escape impending danger.

5 n, when in fact the protein may pose no real danger.

6 siology, yet simultaneously pose a potential danger.

7 emotion that helps defend against potential danger.

8 ical structures critical to rapidly appraise danger.

9 ircuitry underlying more active responses to danger.

10 ess pathways that alert the immune system to danger.

11 Cigarette smoking is a major public health danger.

12 food was available, regardless of potential danger.

13 pattern recognition receptors for infectious danger.

14 damaged-self patterns as signs of potential danger.

15 e an animal to be ready and able to react to danger.

16 one component, benzyl acetate (BA), to avoid danger.

17 rely on learning systems encoding reward and danger.

18 mygdala may drive responding upon more acute danger.

19 lar parts, activating circuits to help avoid danger.

20 s as they monitor moving prey or approaching dangers.

21 e systems evolve to detect new environmental dangers.

22 Both species use alarm pheromones to warn of dangers.

23 poses substantial public health and economic dangers.

24 dual differences in the ability to cope with danger?

25 ects, of an alarm signal that encodes graded danger and attack context.

26 animals learn to recognize cues that signal danger and instantaneously initiate an adequate threat r

27 hat encodes information about the context of danger and its threat level.

28 e behavior: using the past to predict future danger and learning from errors in these predictions.

29 mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1beta a

30 lementary mechanisms to detect environmental danger and protect tissues from damage.

31 ing conflicting behavioral tendencies toward danger and reward, enabling adaptive responding under th

32 balances the competing behavioral demands of danger and reward, enabling adaptive responding under th

33 overcome emotional barriers in acknowledging danger, and engage in effective verbal and physical self

34 dents and humans, distinct from avoidance of danger, and reduced by anxiolytic drugs.

35 ompulsions are an attempt to avoid perceived dangers, and the intent of ERP is to extinguish compulsi

36 Instinctive reactions to danger are critical to the perpetuation of species and a

37 ndispensable for recognizing and eliminating danger arising from foreign invaders and tissue trauma.

38 (ATP) released by dying cells is sensed as a danger associated molecular pattern through P2 purinergi

39 However, chronic activation by danger associated molecular patterns (DAMPs) can be dele

40 e senses a variety of signals referred to as danger associated molecular patterns (DAMPs), including

41 These helicases reduce the dangers associated with replication blockage by protein-

42 and thereby assign a previously unidentified danger-associated function to a set of dark matter repet

43 ced inflammatory responses occur in part via danger-associated molecular pattern (DAMP) molecules, su

44 Thus, adenosine acts as a danger-associated molecular pattern (DAMP) that initiate

45 g hemoglobin and heme represent erythrocytic danger-associated molecular pattern (eDAMP) molecules, w

46 Over the last decade, danger-associated molecular pattern molecules, or alarmi

47 ion and induces membranolysis and release of danger-associated molecular pattern molecules.

48 ma nuclear DNA, used as a marker for general danger-associated molecular pattern release, and the spe

49 Extracellular RNAs act as novel danger-associated molecular pattern signals and potent c

50 Leukocytes sense extracellular ATP, a danger-associated molecular pattern, released during cel

51 Mitochondrial components are recognized as danger-associated molecular patterns (DAMPS) by cytosoli

52 hogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and the mo

53 sma membrane permeabilization and release of danger-associated molecular patterns (DAMPs).

54 molecular pattern release, and the specific danger-associated molecular patterns (EN-RAGE and heat s

55 t with recognition of different pathogen- or danger-associated molecular patterns and include identic

56 complexes that sense pathogen-associated and danger-associated molecular patterns and induce inflamma

57 the result of the intracellular presence of danger-associated molecular patterns and mediate the rel

58 obial ligands, but depends on the release of danger-associated molecular patterns and MyD88-dependent

59 a congenita (PC) and feature upregulation of danger-associated molecular patterns and skin barrier re

60 ate immunity and senses soluble pathogen and danger-associated molecular patterns as well as biologic

61 of pathogen-associated molecular patterns or danger-associated molecular patterns by a nucleotide-bin

62 f pathogen-associated molecular patterns and danger-associated molecular patterns by host cells is an

63 ng cardiac arrest and whether the release of danger-associated molecular patterns could be involved.

64 Release of danger-associated molecular patterns during the first da

65 pattern recognition receptors that recognize danger-associated molecular patterns expressed on stress

66 Inflammatory signals such as pathogen- and danger-associated molecular patterns have been hypothesi

67 Various danger-associated molecular patterns released from dying

68 to and suppresses inflammation triggered by danger-associated molecular patterns such as heat shock

69 acterial signals, but also to non-infectious danger-associated molecular patterns that activate the N

70 recognizing multiple pathogen-associated and danger-associated molecular patterns that contributes to

71 thogen-associated molecular patterns (PAMPs)/danger-associated molecular patterns, including di- and

72 T cells, reactive oxygen species, alarmins, danger-associated molecular patterns, purinergic recepto

73 IL-1beta and IL-18, alarmins and endogenous danger-associated molecular patterns, signifying the inf

74 asome pathway is triggered by cell death and danger-associated molecular patterns, we hypothesized th

75 activities lead to the formation of several danger-associated molecular patterns, which can activate

76 in response to a wide array of pathogens and danger-associated molecular patterns.

77 osol of cells upon detection of pathogen- or danger-associated molecular patterns.

78 sialic acid-bearing molecule can be either a danger-associated or self-associated signal through pair

79 ptors (TLR) recognize pathogen molecules and danger-associated signals that stimulate inflammatory pr

80 er inflammation in response to pathogen- and danger-associated signals.

81 Instead, it is time to confront the dangers at hand and rethink some fundamental features of

82 However, to what extent, and for whom, is danger avoided if this ambitious target is realized?

83 alled Boreal Forest Warming at an Ecotone in Danger (B4WarmED) that addresses the potential for proje

84 Cancer poses danger because of its unregulated growth, development of

85 earn which stimuli in the environment signal danger, but understanding how this learning is generaliz

86 eptor sensory neurons protect organisms from danger by eliciting pain and driving avoidance.

87 and may help to reinforce the perception of danger by plant cells.

88 nsitive and rapid detection of the potential danger caused by microbes and pests.

89 on recall (safety context) and fear renewal (danger context).

90 ey also showed impaired fear renewal; in the danger context, they had less skin conductance response

91 y context, and fear memory prevailing in the danger context.

92 d fear to stimuli resembling the conditioned danger cue as one of the more robust conditioning marker

93 H2O2 is an early danger cue required for innate immune cell recruitment t

94 ced conditioned stimulus (CS+, a conditioned danger cue) to resembling stimuli is widely accepted as

95 e, with extreme sizes serving as conditioned danger cues (CS+) and conditioned safety cues.

96 rocesses and attentional biases to potential danger cues in the environment.

97 some-associated immunostimulatory endogenous danger/damage associated molecular patterns (DAMPs) and

98 rmed (Boreal Forest Warming at an Ecotone in Danger) experiment.

99 There is great danger for the evolution of novel viruses, such as new s

100 need to protect themselves against potential dangers from their surroundings, yet they require consta

101 ning of private well water will identify the dangers hidden in America's drinking water supply and re

102 ted passive release models suggested by the "danger hypothesis," it was recently shown that alarmins

103 Transposon reactivation is an inherent danger in cells that lose epigenetic silencing during de

104 akes a mother rat willing to put her life in danger in order to protect her offspring.

105 l times for exploring resources and avoiding dangers in the environment.

106 h PTSD will be biased to attend to potential dangers in the environment.

107 ate immunity; the accurate identification of danger, including infection, injury, or tumor, is key to

108 aily global climate data sets and three fire danger indices to develop a simple annual metric of fire

109 of MCPT4 and human chymase to the control of danger-induced inflammation.

110 Successfully differentiating safety from danger is an essential skill for survival.

111 This is particularly important when danger is associated with stimuli that we ingest.

112 nd to instances of protection from impending danger is critical for preventing chronic stress and anx

113 late responses to the proximity of potential danger is critical to survival and imbalance in this sys

114 In acute pulmonary inflammation, danger is first recognized by epithelial cells lining th

115 Detecting danger is one of the foremost tasks for a neural system.

116 isms that underpin learning about reward and danger, little is known about how these interact to solv

117 hat provides no benefit for those in gravest danger: malnourished children and immunocompromised pati

118 Although necroptosis and release of danger molecule high-mobility group box 1 are eliminated

119 Necroptotic cell death and release of the danger molecule may promote inflammatory responses and t

120 maged red blood cells, functions as a potent danger molecule that induces sterile tissue injury and o

121 lular adenosine triphosphate (ATP), a potent danger molecule, is elevated in patients immediately aft

122 Innate recognition of microbial products and danger molecules by monocytes and macrophages has been w

123 Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA,

124 is is that dying cells in the graft release "danger" molecules that induce APC maturation and initiat

125 idely accepted view is that inflammatory or 'danger' molecules released by dying graft cells at the t

126 The work highlights the danger of assigning functional significance to small dif

127 y has a particularly chaotic orbit and is in danger of being lost within a few billion years.

128 Ps denote microbial viability, signaling the danger of cellular exploitation by intracellular pathoge

129 trong acidic or alkaline treatments bear the danger of degrading sensitive synthetic polymers.

130 of the world's around 6,000 languages are in danger of disappearing as people give up use of a minori

131 he ability to fast overturn could reduce the danger of dying.

132 uction practices and public awareness of the danger of eating raw or undercooked pork.

133 aken, our results suggest these reefs are in danger of extinction within this century, with significa

134 ing political diversity in academia bear the danger of imposing political interests on science.

135 warning governments and the public about the danger of nuclear war and the need to abolish nuclear we

136 city to a rate and volume that eliminate the danger of premature swelling rupturing the sutured area.

137 Generally, our approach allows to assess the danger of self-sustained epidemics from any viral sequen

138 Assessing the danger of transition of HIV transmission from a concentr

139 ing ever more accessible and affordable, the danger of transplantation-mediated helminth infections,

140 lopmental abnormalities, thus confirming the danger of unrepaired G/U mispairs in promoters.

141 esis based on quinone redox reactions face a danger of wasteful energy dissipation by diversion of th

142 lain-Barre syndrome alerted the world to the danger of ZIKV.

143 of such a process and conclude by noting the dangers of allowing controversy to ossify and the benefi

144 t highlighting factual information about the dangers of communicable diseases can positively impact p

145 In light of the potential dangers of IL-6-directed treatment, we studied the mecha

146 st for surgical change but also point to the dangers of inaccurate history in stymieing such advances

147 uences on decision making, and underline the dangers of increased behavioural predictability in other

148 eek food and energy against the accompanying dangers of injury and predation.

149 eek food and energy against the accompanying dangers of injury and predation.

150 There is now wide appreciation of the dangers of maternal smoking during pregnancy and the lif

151 tcomes seen in smokers while implicating the dangers of nCB exposure in non-smokers.

152 can be used to improve identification of the dangers of products used in gambling.

153 ity as clinicians increasingly recognize the dangers of prolonged invasive ventilation.

154 One of the dangers of ready accessibility of health care data and c

155 -cell therapy first highlighted the possible dangers of this new treatment.

156 Researchers should be aware of the dangers of unconscious investigator bias, all papers sho

157 problem of under-reporting eruptions and the dangers of underestimating the long-term risk of widespr

158 These studies highlight the dangers of using simple reference equilibria such as pKa

159 Activated danger or pathogen sensors trigger assembly of the infla

160 st-derived endogenous signals referred to as danger- or damage-associated molecular patterns (DAMPs),

161 elopment over a year, the method forecasts a danger over one month ahead of blockage.

162 tial fluid containing biomarkers without the dangers, pain, or expertise needed to collect blood.

163 flammasome component NLRP3 mutation, and ASC danger particles.

164 share the same signaling pathways evoked by danger/pathogen associated molecular pattern molecules.

165 We also found that the danger receptor galectin-8 detects damaged endomembranes

166 The inflammasome is a central danger recognition platform that triggers local and syst

167 eir foraging boundaries when confronted with danger remains largely unknown.

168 ined states of anxiety potential and unclear danger requires vigilant scanning of the environment and

169 , they can be detected and neutralized via a danger response mediated by tau-associated antibodies an

170 tly damages epithelial membranes, triggers a danger response signalling pathway and activates epithel

171 Increased understanding about danger sensing by the innate immune system has led to th

172 complex response raises the possibility that danger sensing is an evolutionarily conserved process.

173 We conclude that many bacteria possess danger sensing pathways composed of a danger signal rece

174 a an innate immune-like process that we term danger sensing.

175 We therefore targeted alternative danger-sensing pathways, focusing on a range of compound

176 ver, recognition of the lysed vacuole by the danger sensor galectin-8 initiates the uptake of bacteri

177 locking signaling by the putative endogenous danger signal adenosine, which can be released during in

178 x (MHC) class I-like molecules that act as a danger signal alerting the immune system to the presence

179 The proinflammatory danger signal ATP, released from damaged cells, is degra

180 be leveraged by immunomodulators such as the danger signal calreticulin.

181 were cellular damage, thereby releasing the danger signal HMGB-1 in the brain to prime microglia by

182 ced lung inflammation through release of the danger signal HMGB1.

183 spinal cord injury (SCI) rapidly produce the danger signal interleukin (IL)-1alpha, which triggers ne

184 al that extracellular ATP acting as an early danger signal is responsible for the activation of Duox1

185 nt study, we investigated how the endogenous danger signal monosodium urate (MSU) crystals can alter

186 L-33) is implicated as an epithelium-derived danger signal promoting Th2-dependent responses in asthm

187 ossess danger sensing pathways composed of a danger signal receptor and corresponding signal transduc

188 Necroptosis and subsequent danger signal release is a novel mechanism of injury fol

189 ssue types and detect extracellular ATP as a danger signal released from dying cells.

190 ansport in macrophages constitutes a general danger signal required for NLRP3-related inflammation.

191 with crystalline cholesterol, an endogenous danger signal that contributes to atherogenesis.

192 Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic in

193 Extracellular ATP is an endogenous danger signal that is known to activate inflammatory res

194 results identify tenascin-C as an endogenous danger signal that is upregulated in SSc and drives TLR4

195 ular adenosine triphosphate (ATP) binds as a danger signal to purinergic receptor P2X7 and promotes i

196 ndings identify IL-1alpha as a crucial early danger signal triggering post-MI inflammation.

197 iptional response to a microbial stimulus or danger signal with a high degree of cell type and stimul

198 lowing transplantation, the proinflammatory "danger signal" adenosine triphosphate (ATP) is released

199 tein in myeloid cells, acts as an endogenous danger signal, driving inflammation and aggravating tiss

200 Thus, in addition to its role as a danger signal, which occurs when the cytokine is passive

201 In premature infants, danger signal-induced DC activation may promote proinfla

202 adipocytes may function as an immunological "danger signal." Here we show that endogenous oils of hum

203 s to abnormal tissue turnover or damage as a danger signal; the signaling indicator ligands would ref

204 l damage/disease and so P2X7Rs respond to a "danger" signal and are not normally active.

205 Kidney injury implies danger signaling and a response by the immune system.

206 s of sterile inflammation, which established danger signaling via pattern recognition receptors as a

207 nt domain)), caspase-1 activation by another danger-signaling sensor NLRP1 does not require ASC becau

208 For this study, we used representative danger signals (elicitors) belonging to the classes of t

209 rganisms (i.e., intra-amniotic infection) or danger signals (i.e., sterile IAI) has been implicated i

210 Pathogens and cellular danger signals activate sensors such as RIG-I and NLRP3

211 rations, but importantly also in response to danger signals and cytokines.

212 he Western lifestyle and diet promote innate danger signals and immune responses through production o

213 s cells (LCs) are epithelial APCs that sense danger signals and in turn trigger specific immune respo

214 complexes that sense intracellular microbial danger signals and metabolic perturbations.

215 essive release of inflammatory cytokines and danger signals are linked to an increasing spectrum of i

216 Pathogen- and injury-related danger signals as well as cytokines released by immune c

217 nd release of pro-inflammatory cytokines and danger signals as well as pyroptosis in response to infe

218 ic protein complexes that respond to diverse danger signals by activating caspase-1.

219 epend on timely recognition of pathogenic or danger signals by multiple cell surface or cytoplasmic r

220 NLRP3 inflammasome responds to microbes and danger signals by processing and activating proinflammat

221 inal cord injury (SCI) causes the release of danger signals by stressed and dying cells, a process th

222 olesterol crystals acted both as priming and danger signals for IL-1beta production.

223 inhibiting the release of self antigens and danger signals from apoptotic cell-derived constituents

224 ceptors are present in nociceptors to detect danger signals from infections.

225 nse against infection after host cells sense danger signals from microbes.

226 of actin polymerization can remove potential danger signals from the system and prevents monocyte IL-

227 rols inflammatory responses to intracellular danger signals generated by pathogens, is both activated

228 ugh cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1beta

229 in chemotherapeutic drugs elicit immunogenic danger signals in dying cancer cells that can incite pro

230 operty of HSPCs that enables them to convert danger signals into versatile cytokine signals for the r

231 Therefore, danger signals may drive sterile inflammation, such as t

232 t does not require the presence of microbial danger signals or alarmins associated with cytopathic da

233 ts as an alarmin, initiating and propagating danger signals resulting from tissue injury or inflammat

234 e initiation phase of acute GvHD, endogenous danger signals such as ATP are released and inform the i

235 amma and suggest a revised paradigm in which danger signals such as IL-33 are crucial amplifiers of i

236 med toward excess nutrients and the numerous danger signals that appear in a variety of chronic infla

237 Viral infection activates danger signals that are transmitted via the retinoic aci

238 communication pathways involving endogenous danger signals that have recently been argued to facilit

239 neutrophils and macrophages via signaling of danger signals through NETs.

240 vHD, which could be exploited when targeting danger signals to prevent GvHD.

241 death that causes the subsequent release of danger signals to propagate and perpetuate inflammatory

242 tal immune sensor that recognizes endogenous danger signals triggering sterile inflammation.

243 much attention as the sensor of endogenous "danger signals" and mediator of "sterile inflammation" i

244 macrophages are activated by lipid derived "danger signals" such as ceramides and palmitate and prom

245 Necrotic cells release danger signals, activating innate immune pathways and tr

246 iosis surgery, this study shows that soluble danger signals, among them interleukin-1beta, increase b

247 contact with peripheral antigens, cytokines, danger signals, and immune cells travelling from periphe

248 -1beta release, even in the presence of both danger signals, are needed to protect from collateral da

249 iles were regulated by external and internal danger signals, as well as whether bacteria were membran

250 ts memory CD8(+) T cells as early sensors of danger signals, mediating protective immunity both throu

251 Endogenous danger signals, or damage-associated molecular patterns

252 NLRP3 inflammasome activation in response to danger signals, such as a hypotonic environment, largely

253 al lymphopoietin, and GM-CSF, and endogenous danger signals, such as high-mobility group box 1, uric

254 active oxygen species stress associated with danger signals, such as induction of cell-surface calret

255 NLRP3 inflammasome assembles in response to danger signals, triggering self-cleavage of procaspase-1

256 uence their basal functions and responses to danger signals.

257 nized Staphylococcus aureus and inflammatory danger signals.

258 (NODs) can also recognize a broader array of danger signals.

259 eath in response to pathogens and endogenous danger signals.

260 vated in response to microbial infection and danger signals.

261 ialylated receptors that recognize exogenous danger signals.

262 olled and typically requires two consecutive danger signals.

263 d NLRP3 to sense pathogen invasion and other danger signals.

264 to initiate inflammatory response to various danger signals.

265 lycan fragments in the host cell cytosol, as danger signals.

266 e variety of endogenous and pathogen-derived danger signals.

267 receptor that senses microbes and endogenous danger signals.

268 nts of inflammatory cytokines in response to danger signals.

269 ated in response to microbial and endogenous danger signals.

270 ead cells, and other substances perceived as danger signals; efflux cholesterol to high-density lipop

271 inels for the immune system, MG also detect "danger" signals (pathogenic or traumatic insult), become

272 n of immature IL-1beta, and then endogenous "danger" signals activate innate immune signaling complex

273 y was ascribed primarily to dsDNA and other "danger" signals released from laser-damaged skin cells.

274 There was a reduction in children with danger signs from 24.7% before to 18.1% during the inter

275 te by RDT and microscopy among children with danger signs in the 3 countries was 67.9% and 41.8%, res

276 setting and could be termed "danger signs." Danger signs may be suitable for the basis of routines t

277 tries of sub-Saharan Africa because they had danger signs preventing them from being able to take ora

278 hic data, speed of accessing treatment after danger signs were recognized, clinical symptoms, malaria

279 to algorithms that incorporate screening for danger signs.

280 system in this setting and could be termed "danger signs." Danger signs may be suitable for the basi

281 n-like receptor (NLR) family, detect stress, danger stimuli, and pathogen-associated molecular patter

282 In reply to internal or external danger stimuli, the body orchestrates an inflammatory re

283 en-associated molecular patterns, stress, or danger stimuli.

284 after changes in the position of the visual danger stimulus smaller than 1 degrees .

285 trates the long-underestimated public health danger that filoviruses pose as natural human pathogens.

286 ow behavioral competition between reward and danger: the opportunity to seek food reward negatively m

287 against foreign pathogens and other types of dangers through their role in Toll-like receptor (TLR) a

288 e an animal to be ready and able to react to danger, thus assisting in survival.

289 iate statistical evaluations, minimizing the danger to compare artifacts generated on either platform

290 Larval parasitoids constitute clear danger to Drosophila, as up to 80% of fly larvae become

291 Space radiation is a great danger to electronics and astronauts onboard space vesse

292 strongly suggest that LCs pose a more severe danger to human health than cigarettes.

293 However, rapid evolution can also be a danger to our health and a stumbling block for biotechno

294 multidrug-resistant strains is an increasing danger to public health.

295 ving the ability of infected cells to signal danger to the surrounding tissue.

296 sents a complex palette of opportunities and dangers to animals, which have developed surveillance an

297 Among the dangers to astronauts engaging in deep space missions su

298 These dangers urgently compel the development of agents for am

299 nflammatory mediators, rapidly communicating danger via cytokine secretion, and functioning as guardi

300 natural environments to balance avoidance of danger with approach to things of value.