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1 ypic plasticity in response to infectious or noxious agents, characterized by substantially lower exp
2 nal mucus layer protects the epithelium from noxious agents, viruses, and pathogenic bacteria present
3      Unsaturated oxidative formaldehyde is a noxious aldehyde in cigarette smoke that causes edematou
4  become more toxic after consumption of this noxious alga.
5 nd that TMC-1 is required for worms to avoid noxious alkaline environment.
6                                 Avoidance of noxious ambient heat is crucial for survival.
7  utility in the storage and capture of other noxious and corrosive gases.
8 s aquatic organisms that potentially include noxious and harmful taxa.
9 orn play critical roles in the processing of noxious and innocuous sensory information.
10 PA1, known to function as chemical sensor of noxious and irritant signaling.
11 o light touch without affecting responses to noxious and itch stimuli.
12      TRPV1 channels support the detection of noxious and nociceptive input.
13 asive evidence for a lateralized response to noxious and non-noxious stimuli in the human spinal cord
14 l horn; they may represent mediators between noxious and pruritic pathways, and allow scratch to inhi
15 time task and provided perceptual ratings of noxious and tactile stimuli.
16 ral basis for designing drugs to counter the noxious and vasorelaxant properties of general anestheti
17                                        These noxious anesthetics activate transient receptor potentia
18 persistence of male C. elegans copulation in noxious blue light.
19  antinociceptive relief against a subsequent noxious challenge from formalin injection into the same
20 um is continuously exposed to a multitude of noxious challenges in inhaled air.
21 own as the wasabi receptor) is a detector of noxious chemical agents encountered in our environment o
22 sitive TRPV1 ion channel responds to various noxious chemical and thermal stimuli, causing pain and i
23 aintaining a role for TRPV1 as a detector of noxious chemical cues.
24 8 and functions as a potent inhibitor of the noxious chemical receptor TRPA1.
25 cation channel has a conserved function as a noxious chemical sensor throughout much of Metazoa.
26 gonists suppress the overall withdrawal from noxious chemical stimuli through a pathway requiring an
27 l)), which still require, for the most part, noxious chemicals for processing.
28 tter warns against the intake of potentially noxious chemicals.
29    Ablated animals showed little aversion to noxious cold and did not distinguish between cold and a
30  in mammals, whether TRPA1 is a receptor for noxious cold is highly controversial, as channel activat
31              The basic mechanisms underlying noxious cold perception are not well understood.
32           We developed Drosophila assays for noxious cold responses.
33  completely insensitive to temperatures from noxious cold to painful heat (-5 to 55 degrees C) by abl
34 ber of dorsal horn neurons that responded to noxious cold.
35 stration of linaclotide reduced signaling of noxious colorectal distention to the spinal cord.
36 rn neurons in the spinal cord in response to noxious colorectal distention.
37  permeation barrier to protect the cell from noxious compounds (1)(,)(2) .
38  non-replicating infections or non-microbial noxious compounds in tissues.
39 imilar to that seen when they are exposed to noxious compounds such as mustard oil.
40 tinal pathogen Vibrio cholerae must overcome noxious compounds that damage the bacterial outer membra
41 ality of such water sources is threatened by noxious contaminants, of which heavy metals represents a
42 s, whereas ASH nociceptive neurons integrate noxious cues over several seconds to reach a threshold f
43 1.7 in resected human appendix stimulated by noxious distending pressures.
44 igins, it is likely that they share the same noxious effect on the brain.
45  if OPN could limit LPS availability and its noxious effects in the liver, binding studies were perfo
46 1-deficient mice are more susceptible to the noxious effects of bee and snake venoms, suggesting that
47 s titrate their nicotine intake to avoid its noxious effects, sensitivity to which may influence vuln
48 luate brain activation to an innocuous and a noxious electrical stimulus on healthy human subjects (n
49 tudy, energy consumption, greenhouse gas and noxious emissions for five after-market dual fuel config
50 ties that is induced in response to multiple noxious environmental stimuli and disease states.
51  scratching, to expel invading pathogens and noxious environmental stimuli.
52 as an important role in host defence against noxious environmental substances, including venoms, haem
53 ts, activate bacterial adaptive responses to noxious environments.
54 y metal ions, facilitating their survival in noxious environments.
55  improved discrimination between tactile and noxious events occurs [2, 11, 12].
56 s, infants display a distinct, long latency, noxious evoked 18-fold energy increase in the fast delta
57 tivity is concomitant with the refinement of noxious-evoked limb reflexes.
58 at spinal administration of JWH133 inhibited noxious-evoked responses of spinal neurones in the model
59 ts in a subgroup of rats despite delivery of noxious foot shocks.
60      However, site-specific delivery of this noxious gas presents a major challenge in hospital setti
61 results reveal the potential binding mode of noxious general anesthetics at TRPA1.
62 um and vasculature to a range of potentially noxious haemodynamic, metabolic, and inflammatory stimul
63  V of the spinal cord lost responsiveness to noxious heat (whether generated by a contact heat probe
64 rs are necessary and probably sufficient for noxious heat activation of dorsal horn neurons and that,
65 ain reports during meditation in response to noxious heat and administration of the opioid antagonist
66 anipulation control condition in response to noxious heat and intravenous administration of the opioi
67                            Here we show that noxious heat and irritant chemicals elicit robust escape
68 imary afferents in the activation of DNIC by noxious heat and mechanical stimulations, substance P re
69 ciceptors where they inhibit pain induced by noxious heat and mechanical stimuli, respectively.
70 ificantly reduced the sensitivity of mice to noxious heat and PregS-induced chemical pain.
71 -)/(-) mice display an impaired sensation of noxious heat and thermal hyperalgesia.
72 eat, activation of TRPV1 in these neurons by noxious heat did not alter pain behavior.
73                           We find that after noxious heat exposure, quiescence-defective animals show
74 d receptor TRPV2 is involved in detection of noxious heat in a subpopulation of high-threshold nocice
75 sible to use fMRI to assess pain elicited by noxious heat in healthy persons.
76 .7 (in NaV 1.8-expressing neurons) regulates noxious heat pain threshold and that this can be recapit
77 quirement for NaV 1.7 in regulating somatic (noxious heat pain threshold) but not in visceral pain si
78 odality-dependent manner, modulating somatic noxious heat pain, but is not required for visceral pain
79  eIF2alpha is instrumental in the control of noxious heat sensation.
80 essential for sustaining the transmission of noxious heat signals.
81 f function as shown by paw withdrawal from a noxious heat source.
82 s essential for avoidance behavior following noxious heat stimulation by modifying the forward-to-rev
83       Only CFA-treated rats that experienced noxious heat stimulation exhibited a significant increas
84 ed in saline- and CFA-treated rats following noxious heat stimulation of the hind paws.
85 d the membrane localization of Nav1.7 during noxious heat stimulation, enabling the sustained firing
86                                          The noxious heat stimuli could not evoke the sustained actio
87 t glia) of the superficial dorsal horn after noxious heat stimuli.
88 our data reveal a core function for TRPA1 in noxious heat transduction, demonstrate its conservation
89 etector of pain-producing stimuli, including noxious heat, acid, inflammatory mediators, and vanilloi
90 lthough MrgprA3(+) neurons were sensitive to noxious heat, activation of TRPV1 in these neurons by no
91 prD+ afferents did not alter the response to noxious heat, but reduced the firing of superficial dors
92 ssing sensory neurons reduced sensitivity to noxious heat, capsaicin, and itch (histamine and chloroq
93    TRPV1 is a polymodal channel activated by noxious heat, capsaicin, and protons.
94 der conditions of cellular stress, including noxious heat, cold, hypertonicity, and tissue damage, th
95 ts endogenous activators, such as low pH and noxious heat, is a key factor in hyperalgesia during tis
96 persensitivity, but reflex responsiveness to noxious heat, nerve injury-induced heat hypersensitivity
97 ve ligand-gated cation channel responding to noxious heat, protons, and chemicals such as capsaicin.
98 2alpha(+/S51A)) exhibit reduced responses to noxious heat.
99 whereas glutamate together with CGRP mediate noxious heat.
100 nd remarkably, is also robustly activated by noxious heat.
101 ctural elements sufficient for activation by noxious heat.
102 em, where it is involved in the detection of noxious heat; however, owing to the lack of potent and s
103  either planarian or human TRPA1 can restore noxious-heat avoidance to TRPA1-mutant Drosophila, altho
104 utant Drosophila flies are also defective in noxious-heat responses.
105 iceptive synapse and enhance the transfer of noxious information to higher brain regions, thus contri
106 othesise that the human infant brain encodes noxious information with different neuronal patterns com
107                      In this respect diffuse noxious inhibitory controls (DNIC) are a unique form of
108 eat-induced and mechanically induced diffuse noxious inhibitory controls (DNICs).
109 n second-order neurons (SONs), developmental noxious input modifies transmission from nociceptors to
110             This pathway was unresponsive to noxious input, and has been broadly implicated in valuat
111                     Coordinated responses to noxious inputs manifest from a balance of descending fac
112 e parasitism for the efficient management of noxious insects in the field.
113 ases triggered by disparate genetic lesions, noxious insults, or both.
114 e in response to a variety of infectious and noxious insults.
115 nd functions as a first-line defense against noxious insults.
116 erior cingulate cortex (ACC) correlated with noxious intensities, and optogenetic modulation of ACC n
117                   The gastric refluxate is a noxious material that injures the esophagus and elicits
118 defense mechanism that removes particulates, noxious material, and microorganisms from the lung.
119 d determination of the pesticides (and other noxious materials) in different real food samples.
120 NaV 1.7 did not affect afferent responses to noxious mechanical and chemical stimuli in nerve-gut pre
121 mutants exhibit diminished responsiveness to noxious mechanical and thermal stimuli.
122  possess nociceptors that selectively encode noxious mechanical but not heat stimuli, and that show l
123 f mGlu4 in mice alters sensitivity to strong noxious mechanical compression and accelerates the onset
124 selective cationic channels for detection of noxious mechanical impact.
125 s produced a marked and specific decrease in noxious mechanical pain sensitivity, whereas sensitivity
126 e microRNA cluster continuously scales acute noxious mechanical sensitivity in nociceptive neurons an
127  laser), with no change in their response to noxious mechanical stimulation.
128 in class IV neurons is essential for sensing noxious mechanical stimuli but is not involved in gentle
129 ity and wind up ratio (temporal summation of noxious mechanical stimuli).
130 rong candidate for a channel that transduces noxious mechanical stimuli.
131 els may be used to sense gentle touch versus noxious mechanical stimuli.
132                     These findings suggest a noxious mechanism by which P2X7 receptor leads to enhanc
133 tration is a widespread strategy to detoxify noxious metabolites, frequently for the insect's own ben
134 l dysfunction, all of which may perpetuate a noxious microenvironment leading to pain.
135 their model is absent, avoidance learning of noxious models is disrupted (Batesian mimicry [3]), or r
136 ies, or pumps, determine the efflux of small noxious molecules, such as detergents, heavy metals, and
137    In these deaf mice, we found responses to noxious noise, which damages hair cells, but not to inno
138 we studied the impact of the invasion of two noxious nonnative species, Polygonum cuspidatum, which p
139 ut an individual whose actions led to either noxious or neutral consequences for the subject did inde
140 pically display sensitized responses to both noxious or normally innocuous stimuli.
141  regulation that extends beyond avoidance of noxious or suboptimal temperatures.
142  most amphibian species produce or sequester noxious or toxic secretions in the granular glands of th
143 ly activated ion channel(s) must account for noxious (painful) mechanosensation.
144 ble for the transduction and transmission of noxious (painful) stimuli and innocuous stimuli that do
145          In visceral organs of mammals, most noxious (painful) stimuli as well as innocuous stimuli a
146 mbrane damage inflicted by the pathogens and noxious particles they ingest.
147 f the opioid antagonist naloxone potentiates noxious peripheral input into the spinal cord and dramat
148 populations based on their responsiveness to noxious peripheral stimulation and neurochemical profile
149 Sub P in the RVM is increased in response to noxious peripheral stimulation in a persistent inflammat
150  Atypical CR-expressing neurons responded to noxious peripheral stimulation, the excitatory drive ont
151                                              Noxious pH triggers pungent taste and nocifensive behavi
152  play a central role in sensory responses to noxious physical and chemical stimuli.
153 s, we found that afferent activity evoked by noxious pinch in these preparations was conveyed to cent
154 trast, the ongoing activity and responses to noxious pinches in nociceptive VTT neurons were frequent
155 tivity in response to a clinically essential noxious procedure.
156 sage-like stroking of hairy skin, but not by noxious punctate mechanical stimulation.
157 n pregenual anterior cingulate cortex during noxious rectal distensions, compared to controls and nor
158  forward and feed even when presented with a noxious repellant, with AIB inhibition decreasing the re
159                                     However, noxious sensory signals from visceral organs produce hyp
160  treat dyslipidemic conditions is limited by noxious side effects, most commonly facial flushing.
161 mpared EEG responses to the same time-locked noxious skin lance in infants aged 0-19 days (n = 18, cl
162 ncluding tail autotomy, colour patterns, and noxious skin secretions.
163 our and specific cortical activity following noxious skin stimulation, but it is not known whether br
164  out of a series of oriented gratings with a noxious sound stimulus.
165 deceitfully imitating the warning signals of noxious species (models), generates striking cases of ph
166 targeting of the pathways that lead to these noxious species may result in valuable therapeutic strat
167 ndergraduates were tested for sensitivity to noxious stimulation alone and/or together (dyads).
168 avioural activity following graded intensity noxious stimulation and clinical heel lancing in 30 term
169 neurons in the spinal cord during peripheral noxious stimulation and recruits microglial cells to pro
170 rain regions that are active following acute noxious stimulation in newborn infants, and compared the
171 rons of the spinal cord and, upon peripheral noxious stimulation in the presence of spinal TNF-alpha,
172                     Brain activity evoked by noxious stimulation is therefore enhanced by stress, but
173                            We tested whether noxious stimulation of the corneal surface can alter ner
174  pain circuit, is activated more strongly by noxious stimulation of the face than of the hindpaw.
175 d responses to chemoreceptor stimulation and noxious stimulation were blunted compared to WT mice.
176            A- and C-fibre nociceptors detect noxious stimulation, and have distinct and independent c
177 ty in the inferior orbital cortex, and, like noxious stimulation, increased activity in temporal cort
178  well as enhanced release of Sub P following noxious stimulation, underlie the pronociceptive role of
179 ion in sensitivity to mechanical and thermal noxious stimulation.
180 ent SA being induced in primary afferents by noxious stimulation.
181 hese neurons become responsive to peripheral noxious stimulation.
182 ics at rest and autonomic dysreflexia during noxious stimulation.
183                       The temperature of the noxious stimulations was determined individually to cont
184 on, in healthy mice increases sensitivity to noxious stimuli (referred to as 'pain') without general
185 are responsive to a variety of modalities of noxious stimuli and can signal pain even when activated
186 rsal root ganglion (DRG) neurons that detect noxious stimuli and elicit pain.
187 cortex potently suppresses SpVc responses to noxious stimuli and produces behavioral hypoalgesia.
188    Spinal cord neurons respond to peripheral noxious stimuli and relay this information to higher bra
189 olution are critical in ensuring disposal of noxious stimuli and return to homeostasis.
190 orsal root ganglia (DRG) neurons that detect noxious stimuli and signal pain.
191  and mark dying cells in response to diverse noxious stimuli and suggest that elaborate, multilayered
192 e disorder characterized by insensitivity to noxious stimuli and variable intellectual disability (ID
193             Aggression and responsiveness to noxious stimuli are adaptable traits that are ubiquitous
194 ulation and nocifensive responses to thermal noxious stimuli are not modified.
195 the ACC to increase the aversive response to noxious stimuli at anatomically unrelated sites.
196 he response of the brain reward circuitry to noxious stimuli at baseline before opioid administration
197                The ion channel TRPA1 detects noxious stimuli at the plasma membrane of neurons and el
198  whereby noradrenaline may suppress incoming noxious stimuli at the primary synaptic afferents in the
199 redicted by the neuronal response to painful noxious stimuli before infusion in key structures of the
200  distal limbs have a high spatial acuity for noxious stimuli but a low density of pain-sensing neurit
201 espond to beta-alanine, heat, and mechanical noxious stimuli but do not respond to histamine.
202 peripheral and spinal nociceptive neurons to noxious stimuli but only when the joint was inflamed.
203 fit trait that defends against pathogens and noxious stimuli but whose overactivation can result in i
204 within the vasculature and tissue respond to noxious stimuli by sending out coordinated signals that
205 underlying the detection and transmission of noxious stimuli by the peripheral nervous system.
206                           All three types of noxious stimuli caused a depletion of CGRP from corneal
207          The nociceptive system of detecting noxious stimuli comprises two classes of peripheral affe
208 nent of the cellular mechanism through which noxious stimuli evoke pain.
209 al nerves, indicating that all modalities of noxious stimuli evoked peptide release.
210 he mechanisms underlying the transduction of noxious stimuli from the viscera, suggest that the inves
211 ascending pain pathway occurred during acute noxious stimuli in healthy individuals.
212 anism for noradrenaline to modulate incoming noxious stimuli in the dorsal horn of the spinal cord.
213 or a lateralized response to noxious and non-noxious stimuli in the human spinal cord.
214 vel NPVF-vRN functional circuit modulated by noxious stimuli in vertebrates.
215   Hyperalgesia is an exaggerated response to noxious stimuli produced by peripheral or central plasti
216             We also observed that repetitive noxious stimuli resulted in adaptation of the signal.
217 in, and suppress the overall withdrawal from noxious stimuli through a pathway requiring the opioid-l
218 n sensation is initiated by the detection of noxious stimuli through specialized transduction ion cha
219                      All animals must detect noxious stimuli to initiate protective behavior, but the
220                                              Noxious stimuli usually cause pain and pain usually aris
221 sture (e.g., escape behaviors in response to noxious stimuli vs freezing in response to fear-evoking
222                    Many organisms respond to noxious stimuli with defensive maneuvers.
223                    Many organisms respond to noxious stimuli with defensive maneuvers.
224  the preinfusion period neuronal response to noxious stimuli within the ventral tegmentum.
225   Finally, we show that the neural coding of noxious stimuli, and consequent experience of pain, are
226  encounters with predators, competitors, and noxious stimuli, animals have evolved defensive response
227 ally cause pain and pain usually arises from noxious stimuli, but exceptions to these apparent truism
228 hibited normal behavioral responses to acute noxious stimuli, but subsequent to partial sciatic nerve
229 b neurons augments the autonomic response to noxious stimuli, ensuring sufficient glucose mobilizatio
230 1, a channel implicated in detecting several noxious stimuli, exhibiting a 50% effective concentratio
231 hronic pain: it is initiated by a variety of noxious stimuli, has indefinite duration, and pain appea
232           The TRPV1 channel is a detector of noxious stimuli, including heat, acidosis, vanilloid com
233 that detect odors, tastants, pheromones, and noxious stimuli, including receptors of the odor recepto
234 creasingly greater pain evoked by repetitive noxious stimuli, is highly variable between individuals.
235            In response to invading microbes, noxious stimuli, or tissue injury, an acute inflammatory
236                        The ability to detect noxious stimuli, process the nociceptive signal, and eli
237 eurons and vRN are suppressed and excited by noxious stimuli, respectively.
238  is normally attenuated after elimination of noxious stimuli, restoration of homeostasis and initiati
239                                       During noxious stimuli, serotonergic neurons activation was due
240 o recorded L-ITCcs are strongly activated by noxious stimuli, such as hindpaw pinches or electrical f
241                              As a sensor for noxious stimuli, TRPV1 channel has been described as a k
242                       For both innocuous and noxious stimuli, we observed a signal change in the prim
243                               Application of noxious stimuli, which often signal the need to mobilize
244 or cell viability during exposure to various noxious stimuli.
245 sent a way for dopamine to modulate incoming noxious stimuli.
246 unicate to us their perceived levels of such noxious stimuli.
247 or for heat, acidic pH, capsaicin, and other noxious stimuli.
248 v1.7 plays a crucial role in transmission of noxious stimuli.
249 rain region mediating affective responses to noxious stimuli.
250 ment neuronal sensitivity (sensitization) to noxious stimuli.
251 racolumbar skin and is selectively driven by noxious stimuli.
252 ferent nociceptors and is activated by other noxious stimuli.
253  retinal cells die in response to a range of noxious stimuli.
254 o associated with the perception of pain and noxious stimuli.
255 ating homeostatic responses against external noxious stimuli.
256 n the magnitude and duration of responses to noxious stimuli.
257 ses hyperalgesia, an enhanced sensitivity to noxious stimuli.
258 arly stage of lung inflammatory responses to noxious stimuli.
259 O mice responded normally to a wide array of noxious stimuli.
260 ugmented glucose mobilization in response to noxious stimuli.
261          Additionally, we show that, after a noxious stimulus (intradermal capsaicin injection), thes
262 ere examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute la
263 nctional ASICs, are insensitive to acid as a noxious stimulus and show diminished avoidance of acidic
264 ggests that movement of the limb away from a noxious stimulus is a sensitive indication of nociceptiv
265 ty.SIGNIFICANCE STATEMENT The intensity of a noxious stimulus is encoded by the frequency of action p
266                To fulfill these functions, a noxious stimulus might induce a percept which, in turn,
267 hieved optogenetically, without any external noxious stimulus or injury.
268  prolonged (up to 48 h) stress response to a noxious stimulus such as UVB.
269 t reprogram mouse and human fibroblasts into noxious stimulus-detecting (nociceptor) neurons.
270        Off food, animals reverse away from a noxious stimulus.
271 rsion to formalin injection, an inflammatory noxious stimulus.
272 atory, we identified and selectively labeled noxious-stimulus-activated PBL neurons and performed com
273 eal lumen, and therefore greater exposure to noxious substances in refluxate.
274 nmental factors, including diet, exposure to noxious substances, and microorganisms.
275 appropriate defense against parasitic worms, noxious substances, toxins, venoms, and environmental ir
276 ls and IgE can help protect the host against noxious substances.
277 ty barrier to prevent unrestricted access of noxious substances.
278 t function in protection of the host against noxious substances.
279 ccurs as a result of nonspecific adhesion of noxious substrates to the surface.
280 ociceptive activity, but also facilitate non-noxious tactile activity in the healthy adult rat spinal
281 ific bursts of activity occur in response to noxious, tactile, visual, and auditory stimulation [7-10
282 exhibits a high-temperature threshold in the noxious temperature range above 50 degrees C.
283 s involvement was significantly stronger for noxious than for tactile stimuli.
284 dal ion channel involved in the detection of noxious thermal and chemical stimuli by primary afferent
285 ally in keratinocytes, are less sensitive to noxious thermal and mechanical stimuli than control anim
286              Nociceptive responses to select noxious thermal and mechanical stimuli were enhanced fol
287                 Behavioral responses to some noxious thermal and mechanical stimuli were enhanced in
288 uitination affects TrkA activation following noxious thermal stimulation and inflammatory pain.
289                              Main effects of noxious thermal stimulation were observed across several
290 tients and 18 healthy individuals exposed to noxious thermal stimulations administered in a functiona
291  that the AWC(OFF) signals adapt to repeated noxious thermal stimuli and quantify the corresponding b
292  or methadone antinociception in response to noxious thermal stimuli.
293 fect motor activity, anxiety or responses to noxious thermal stimulus.
294 with the behavioral observation of increased noxious thermal thresholds and enhanced inflammatory the
295 lt of short-term low-grade interactions with noxious thermal, chemical, or mechanical sources to more
296  a variety of nociceptive stimuli, including noxious touch and temperature, with stereotyped escape r
297      The duration of excitatory responses to noxious UBD during acute colonic inflammation (3 days po
298 hermal grill illusion (TGI), alternating non-noxious warm and cold temperatures cause a paradoxical,
299 sitivity to heat stimuli, and a normally non-noxious warm stimulus induces activity-dependent Fos exp
300 eceptor (EP3R) antagonism in vlPAG modulated noxious withdrawal reflex (EMG) thresholds to preferenti

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