ライフサイエンスコーパス: danger

1 val (e.g., detect deviant sounds that signal danger).

2 isual inputs that are predictive of imminent danger.

3 ballistic escape reactions to avoid imminent danger.

4 Memories of painful events protect us from danger.

5 tivity vlPAG neurons that decrease firing to danger.

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

7 food was available, regardless of potential danger.

8 involving the amygdala detect and respond to danger.

9 pattern recognition receptors for infectious danger.

10 damaged-self patterns as signs of potential danger.

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

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

13 rely on learning systems encoding reward and danger.

14 mygdala may drive responding upon more acute danger.

15 lar parts, activating circuits to help avoid danger.

16 g able to choose stimuli not associated with danger.

17 more intense eruptions can present a serious danger.

18 ion and contact-seeking are key responses to danger.

19 ills, such as walking, talking, and avoiding danger.

20 s are associated with enhanced learning from danger.

21 face to contact inhaled irritants and report danger.

22 ay fear responses to a context that predicts danger.

23 oposed to mediate fear responses to imminent danger.

24 s as they monitor moving prey or approaching dangers.

25 poses substantial public health and economic dangers.

26 e systems evolve to detect new environmental dangers.

27 ct to the presence and location of potential dangers.

28 ose of transplantation in times of increased danger?

29 appropriately respond to stimuli that signal danger(1).

30 should be implemented to reduce the risk of danger: 1) preintubation assessment for potential diffic

31 to risks to study participants, but serious dangers accrue to nonparticipants, including sex partner

32 One cue-inhibited population flipped danger activity from early inhibition to late excitation

33 ons constitute a judgment about the relative danger and benefits of those locations.

34 pathogens; however, OSNs' ability to detect danger and initiate immune responses is unclear.

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

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

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

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

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

40 ned stimulus (CS) as a signal for reward (or danger) and then transformed the same CS into a signal f

41 s) progeny that may be better able to escape danger, and the combination of these factors improves th

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

43 Educational programs to inform of the danger are now required, as public perception has grown

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

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

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

47 Host DNA can, however, also act as a danger-associated molecular pattern (DAMP) and elicit st

48 y acts as an acute response to any perceived danger-associated molecular pattern (DAMP) in primary ad

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

50 Cytosolic DNA acts as a universal danger-associated molecular pattern (DAMP) signal; howev

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

52 ity results in a tissue-specific increase of danger-associated molecular pattern molecules (DAMPs) an

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

54 tacking in fibrillar alphaSN creates a known danger-associated molecular pattern of stretches of anio

55 iated B-1a immune responses via pathogen- or danger-associated molecular pattern recognition exerts a

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

57 ride, respectively, as well as an endogenous danger-associated molecular pattern.

58 Cells treated with the inhibitor secreted danger-associated molecular patterns (DAMP), including A

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

60 New insights reveal major contributions from danger-associated molecular patterns (DAMPs) in the init

61 ) on immune and parenchymal cells can detect danger-associated molecular patterns (DAMPs) released fr

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

63 ven by release of endogenous alarmins called danger-associated molecular patterns (DAMPs), which init

64 lated in psoriasis, are known to function as danger-associated molecular patterns (i.e., DAMPs) to ac

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

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

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

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

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

70 The recognition of microbial or danger-associated molecular patterns by complement prote

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

72 is circuit and accompanying release of other danger-associated molecular patterns expands BM myeloid-

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

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

75 t are engulfed during phagocytic process and danger-associated molecular patterns that are mainly byp

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

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

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

79 sterile inflammation through the release of danger-associated molecular patterns, which are recogniz

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

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

82 duce pyroptosis in response to intracellular danger-associated signals.

83 Here, we review the danger-associated stimuli that have been reported to act

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

85 of food while also weighing relative risk of danger based on group size and predation risk.

86 How does a stimulus never associated with danger become frightening?

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

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

89 owing short-latency increases in firing to a danger cue - the presumed neural substrate for fear outp

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

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

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

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

94 siology, as opposed to adaptive responses to danger/damage situations, is unclear.

95 that the amygdala is of vital importance for danger detection and fear processing.

96 ls of leukaemia, we show that ligands of the danger detector NKG2D-a critical mediator of anti-tumour

97 he benefits (e.g., in research settings) and dangers (e.g., privacy implications, psychological targe

98 the size of extinct animals is fraught with danger, especially when they were much larger than their

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

100 simultaneously acting as a learned source of danger for its S2 associate (whose consolidation require

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

102 Predicting danger from previously associated sensory stimuli is ess

103 involving the amygdala detect and respond to danger has contributed to the 'amygdala fear center' mem

104 ting emotion, including inhibiting fear when danger has passed.

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

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

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

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

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

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

111 e, relapsing fear behavior in the absence of danger is a hallmark of disabling anxiety disorders that

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

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

114 From an evolutionary perspective, sensing danger is essential for organismal survival.

115 Learning to fear danger is essential for survival.

116 nosine is a signal of stress, damage, and/or danger, it is less important for baseline regulation of

117 ferential firing with greatest inhibition to danger, less to uncertainty and no inhibition to safety.

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

119 the brain engages the periphery at times of danger may offer new perspectives for detecting and trea

120 -light memory formed in stage 1 with a light-danger memory formed in stage 2, as they show fear when

121 was inhibited during formation of the light-danger memory, rats no longer showed fear when tested wi

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

123 Heme is a critical danger molecule liberated from hemeproteins in various c

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

125 ies, which can jointly regulate host-derived danger molecule signaling and integrate specific global

126 h as Porphyromonas gingivalis, through small danger molecule signaling.

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

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

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

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

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

132 This case highlights the danger of complacency in patients with SCT, offering a l

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

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

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

136 th at least 2,000 species estimated to be in danger of extinction [1, 2].

137 y of unknown structures is possible, and the danger of inferring unsubstantiated image details.

138 ty to remodel the underlying chromatin and a danger of losing epigenetic information.

139 ercial DLS instrumentation comes an inherent danger of misinterpretation or misapplication at the bor

140 cs datasets, in order to avoid the potential danger of misinterpreting an association between a predi

141 and polymer groups to determine the fate and danger of plastic contamination.

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

143 assemble productively, while minimizing the danger of protein aggregation.

144 , especially in high-current cables, and the danger of quenches.

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

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

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

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

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

150 citing opportunities for SMBs that avoid the dangers of flammable liquids.

151 drug resistant S. Typhi only highlights the dangers of ignoring this threat.

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

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

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

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

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

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

158 ocial distancing, these models highlight the dangers of relaxing nonpharmaceutical public health inte

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

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

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

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

163 Activated danger or pathogen sensors trigger assembly of the infla

164 en transformed the same CS into a signal for danger (or reward).

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

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

167 s predicted unique foot shock probabilities: danger (p=1.00), uncertainty (p=0.375) and safety (p=0.0

168 fatal if untreated, and a clear and present danger posed by nerve agent OPs has become palpable in r

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

170 or bacterial ligands, or indirectly, through danger receptors that bind host molecules displayed in a

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

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

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

174 anonical roles of other intracellular innate danger sensing systems and argue that a "location-centri

175 etails its escape strategy to a key cellular danger-sensing mechanism, 2) indicate that transcription

176 NKG2D is a danger sensor expressed on different subsets of innate a

177 Not having any WHO danger sign or consolidation on chest radiograph had an

178 0.82; 1.5% died if no danger signs, 10% if 1 danger sign, and 33% if >=2 danger signs).

179 myelin on BCVs may therefore act as an early danger signal alerting the cell to imminent bacterial in

180 dsRNA in biochemical assays to eliminate the danger signal and inhibit the innate immune response.

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

182 The epithelial cell-derived danger signal mediators thymic stromal lymphopoietin (TS

183 mobility group protein 1 (HMGB1), a sterile danger signal molecule, and osteopontin (OPN), a multifu

184 ating of the intestine may be perceived as a danger signal that activates an immune fight-and-flight

185 rom the nucleus or mitochondria represents a danger signal that alerts the host immune system(1).

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

187 hat TLR9 can respond to mitochondrial DNA, a danger signal that is released upon tissue injury, we ex

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

189 ndogenous, concentration-dependent pulmonary danger signal that primes and activates the NLPR3 inflam

190 eflex action that is sufficient to provide a danger signal that triggers regional immunity to fight a

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

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

193 owever, murine macrophages require a second "danger signal" for the inflammasome-driven maturation of

194 ll fusion through micronuclei formation as a danger signal, and consequently limits aberrant cell div

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

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

197 onents by acting as a molecular glue between danger-signal sensors and procaspase-1.

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

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

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

201 Together, these danger signals activate antigen-presenting cells (APCs)

202 ress TLRs and other PRRs that directly sense danger signals after injury or during infection, leading

203 lf-derived autoantigens and pathogen-derived danger signals and antigens.

204 broad range of microbial motifs, endogenous danger signals and environmental irritants, resulting in

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

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

207 RNA sensors recognize virus-derived dsRNA as danger signals and initiate innate immune responses.

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

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

210 unctions, the local release of cytokines and danger signals by dying radiosensitive cells, and altere

211 immune cells and the release of antigens and danger signals by malignant cells killed by chemotherapy

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

213 T cell homeostasis and responses to external danger signals from "sterile" inflammation remain poorly

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

215 the cell surface facilitate the detection of danger signals from diverse pathogens and initiate a ser

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

217 Release of molecular danger signals from injured cell mitochondria (mitochond

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

219 tilize TLRs and other PRR pathways to detect danger signals in their environment.

220 ested to promote immunogenicity by acting as danger signals recognized by dendritic cells (DC) facili

221 lts reveal that in addition to their role as danger signals released from dead cells, IL-1 family cyt

222 s on the cell surface to detect host-derived danger signals released in response to attacks by pathog

223 nctions, have evolved extracellular roles as danger signals released in response to cell lysis, apopt

224 At the same time, danger signals released into the circulation by damaged

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

226 ress or injury induces release of endogenous danger signals such as ATP, which plays a central role i

227 ent and discriminate between homeostatic and danger signals such as modified components of the extrac

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

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

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

231 T cells can also directly recognize danger signals through the expression of TLRs.

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

233 Intracellular pathogens and danger signals trigger the formation of inflammasomes, w

234 s related to innate immunity and response to danger signals triggered by activating transcription fac

235 These agonists offer a means of providing "danger signals" in order to activate the immune system t

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

237 (TLRs) are critical receptors to respond to danger signals, and their functions are relevant in the

238 o pathogens, microbial toxins, or endogenous danger signals, EC responses are polymorphous, heterogen

239 Following recognition of pathogens and danger signals, inflammasomes assemble and recruit and a

240 Endogenous danger signals, or damage-associated molecular patterns

241 Taken together, inflammatory cues and danger signals, such as bone and implant particles exace

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

243 receptor that senses microbes and endogenous danger signals.

244 nts of inflammatory cytokines in response to danger signals.

245 ated in response to microbial and endogenous danger signals.

246 uence their basal functions and responses to danger signals.

247 ates the capacity of monocytes to respond to danger signals.

248 nized Staphylococcus aureus and inflammatory danger signals.

249 phages provide defence against pathogens and danger signals.

250 microbial capacity, which is up-regulated by danger signals.

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

252 Inflammasomes respond to pathogen or tissue "danger" signals and assemble into multiprotein "machiner

253 Mammalian immune responses are initiated by "danger" signals--immutable molecular structures known as

254 ed inpatients with World Health Organization danger signs and cough.

255 eastfeeding initiation time on early newborn danger signs and severe illness.

256 2 < 90% predicted death independently of WHO danger signs compared with SpO2 >= 90%: HC Risk Ratio (R

257 he number of World Health Organization (WHO) danger signs demonstrated the highest discrimination (C

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

259 The number of WHO danger signs on presentation to hospital could be the mo

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

261 Severe illness was defined using newborn danger signs reported by The Young Infants Clinical Scie

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

263 ) respiratory symptoms and signs and general danger signs with ancillary tests (such as chest imaging

264 signs, 10% if 1 danger sign, and 33% if >=2 danger signs).

265 ination (C statistic = 0.82; 1.5% died if no danger signs, 10% if 1 danger sign, and 33% if >=2 dange

266 because of using mothers' report of newborn danger signs.

267 to algorithms that incorporate screening for danger signs.

268 fear that accrues to a stimulus paired with danger simultaneously spreads to its past associates, th

269 response to pathogen patterns and endogenous danger stimuli.

270 isting genetic variation in populations, the danger that adaptation by breaking genes will, over long

271 s experimental design, and we illustrate the dangers that uncorrected stimuli pose to receptive field

272 To be able to adapt to different modes of danger, the brain needs to recognize these features, int

273 for food-seeking competes with avoidance of danger, the PFC likely plays a role in selecting the opt

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

275 e damage, as well as efforts to manage these dangers through emerging hybrid, bioelectronic device ar

276 ponding to a variety of external stimuli and dangers through the regulation of specific built-in mole

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

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

279 s disease and represents a clear and present danger to global health as new tools for vaccination, tr

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

281 without obvious signs of their considerable danger to human health.

282 ogues such as carfentanil pose a significant danger to opioid users due to their high potency and rap

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

284 rt to the conclusion that these gases pose a danger to public health and welfare.

285 rt to the conclusion that these gases pose a danger to public health and welfare.

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

287 Since energetic electrons pose a potential danger to satellite operations, our findings demonstrate

288 ch may indicate physiological dysfunction or danger to the organism.

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

290 els of antimicrobial resistance pose serious dangers to patients, population health, food security, a

291 r weapons that constitute one of the biggest dangers to the world.

292 s received fear discrimination consisting of danger, uncertainty and safety cues.

293 ing a discrimination procedure consisting of danger, uncertainty, and safety cues, we have found rapi

294 g fear discrimination consisting of cues for danger, uncertainty, and safety.

295 These dangers urgently compel the development of agents for am

296 n damage as mechanical stress, which signals danger via TRPV4, calcium, and calcineurin to initiate a

297 l defense mechanism to protect the body from danger, which becomes potentially harmful if it turns ch

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

299 he advantage of being able to migrate out of danger with more ease, but energy needed for wing produc

300 ramework can reveal the presence of 'sensory danger zones', hotspots of conservation concern where se