ライフサイエンスコーパス: capsaicin

1 tive following id histamine, chloroquine, or capsaicin.

2 mpared with the prototypical soluble agonist capsaicin.

3 ting the redox reaction for the detection of capsaicin.

4 to better understand the redox mechanism of capsaicin.

5 arge cells, most of which did not respond to capsaicin.

6 mal similar to that of the aromatic group of capsaicin.

7 let and mechanisms of binding site access by capsaicin.

8 eal a preferred interfacial localization for capsaicin.

9 ductance, and EC50 value toward its agonist, capsaicin.

10 subjects (HCs) were treated with intranasal capsaicin.

11 l alters its ability to be gated directly by capsaicin.

12 that exhibited enhanced tussive responses to capsaicin.

13 noxious heat, protons, and chemicals such as capsaicin.

14 ar bases of IR and the therapeutic action of capsaicin.

15 s like TRPV1, a molecular sensor of heat and capsaicin.

16 can activate TRPV1 with efficacy similar to capsaicin.

17 ma and burning sensation with pregabalin and capsaicin.

18 , which transduces a nociceptive response to capsaicin.

19 cyanate (AITC; also known as mustard oil) or capsaicin.

20 ricyclic antidepressants (TCAs) than topical capsaicin 0.075%.

21 Perivagal application of capsaicin (1% solution) is considered to cause a selecti

22 y responses to intralaryngeal application of capsaicin (10 microg/ml, 50 microl), a selective stimula

23 increasing rheobase, decreasing responses to capsaicin (2 mum) and reducing action potential discharg

24 d samples at different concentration ranges: capsaicin (28.23-2322.35microg/g), vitexin (2.93-33.46mi

25 was expressed in hADSC, and the TRPV1 ligand capsaicin (5uM) stimulated proliferation, which could be

26 ransient receptor potential (TRP) V1 agonist capsaicin, a clinically relevant tussive stimulant.

27 ONALE: Heightened cough responses to inhaled capsaicin, a transient receptor potential vanilloid 1 (T

28 Noradrenaline or clonidine inhibited the capsaicin-activated current by approximately 60%, and th

29 Inhibition of capsaicin-activated current by noradrenaline was mediate

30 Inhibition of the capsaicin-activated current by SKF 81297 was mediated by

31 opamine receptor agonists were tested on the capsaicin-activated current recorded from acutely dissoc

32 radrenaline and clonidine were tested on the capsaicin-activated current recorded from acutely dissoc

33 3, the inhibitory effect of SKF 81297 on the capsaicin-activated current was greatly reduced, suggest

34 he inhibitory effect of noradrenaline on the capsaicin-activated current was greatly reduced, suggest

35 he inhibitory effect of noradrenaline on the capsaicin-activated current was not affected either by b

36 The inhibitory effect of SKF 81297 on the capsaicin-activated current was not affected when the pr

37 receptors) had no significant effect on the capsaicin-activated current.

38 let of the plasma membrane but inhibition of capsaicin-activated currents when PI(4,5)P2 was in both

39 We observed potentiation of capsaicin-activated TRPV1 currents by PI(4,5)P2 in the i

40 e preassociated in resting live cells, while capsaicin activation induced both the formation of more

41 only validate our current working model for capsaicin activation of TRPV1 but also should help guide

42 exosomal fraction of cultured DRG following capsaicin activation of TRPV1 receptors.

43 stin was increased at 1 and 3 days following capsaicin administration as shown by BrdU incorporation.

44 reatment were compared with those induced by capsaicin after placebo antitussive administration.

45 elated with responses to the algesic markers capsaicin, AITC and alpha, beta-methylene ATP.

46 of mean force (i.e., free energy profile) of capsaicin along the bilayer normal confirms that it pref

47 orometry, and we assessed the sensitivity to capsaicin, an agonist of the TRPV1 receptor.

48 ds were evaluated for their ability to block capsaicin and acid-induced calcium influx in CHO cells e

49 nsory neurones have displayed sensitivity to capsaicin and brainstem microinjections of these neurope

50 and -T469I variants were more responsive to capsaicin and coal fly ash.

51 AT3 expression and also with the content of capsaicin and dihydrocapsacin during fruit development.

52 The Caco-2 cells incorporated capsaicin and dihydrocapsaicin (8.4% and 10.9%, respecti

53 and IBS were used in a mixed linear model of capsaicin and dihydrocapsaicin content and fruit weight

54 tem has been tested for the determination of capsaicin and dihydrocapsaicin from fresh chilli and swe

55 ietary fat increased the bioaccessibility of capsaicin and dihydrocapsaicin in digestions with red pe

56 ocessing on the in vitro bioaccessibility of capsaicin and dihydrocapsaicin was studied in the absenc

57 saicinoids present in the Cayenne pepper are capsaicin and dihydrocapsaicin, which represent between

58 Capsaicin and four flavonoids were quantified in studied

59 The actions of both capsaicin and GI neuropeptides may not be restricted to

60 H. armigera, but insignificantly inhibited (capsaicin and gossypol) or induced (nicotine) it in H. a

61 e activation and desensitization of TRPV1 by capsaicin and heat can be modulated differentially and d

62 Our BRET study also confirmed that: (1) capsaicin and heat promoted distinct transitions, indepe

63 lanine insensitive but vigorously respond to capsaicin and histamine with distinct discharge patterns

64 Superficially applied capsaicin and intradermal injection of beta-alanine, an

65 d varicosities that were also seen following capsaicin and menthol stimulation.

66 mmation, we stimulated lung nociceptors with capsaicin and observed increased neuropeptide release an

67 linositol lipids occupy the binding site for capsaicin and other vanilloid ligands, suggesting a mech

68 Deep biopsies in the capsaicin and placebo areas healed at similar rates at b

69 d the transient receptor vanilloid 1 agonist capsaicin and placebo creams topically applied to contra

70 essfully introduced high-affinity binding of capsaicin and resiniferatoxin to the vanilloid-insensiti

71 r only to capsaicin (COR neurons) or to both capsaicin and the endogenous TRPV1 and CB1 receptor liga

72 ensitization of nerve fibres (in the case of capsaicin) and postsynaptic blockade of calcium channels

73 ultured DRG neurons also sensitive to TRPV1 (capsaicin) and/or TRPA1 (AITC) agonists.

74 ociception induced by formalin, acetic acid, capsaicin, and cinnamaldehyde.

75 PM8-positive small neurons also responded to capsaicin, and had significantly larger menthol-induced

76 tivated by heat and pungent agents including capsaicin, and has been extensively studied in nocicepti

77 We used concentrations of menthol, capsaicin, and hypertonic saline that evoked comparable

78 neurons reduced sensitivity to noxious heat, capsaicin, and itch (histamine and chloroquine) and impa

79 lymodal cellular sensor for heat, acidic pH, capsaicin, and other noxious stimuli.

80 ue-Dawley rats received a neurotoxic dose of capsaicin, and proliferation was quantified and characte

81 polymodal channel activated by noxious heat, capsaicin, and protons.

82 ified two segments that distinctly regulated capsaicin- and heat-induced desensitization.

83 hat B5-I neurons are innervated by menthol-, capsaicin-, and mustard oil-responsive sensory neurons a

84 by stepwise trials of topical agents (e.g., capsaicin), antiepileptic drugs (e.g., gabapentin), inje

85 Capsaicin application for 48 hours induces cutaneous fib

86 tive primary sensory neurons by burn injury, capsaicin application or sustained electrical activation

87 the bioavailability and therapeutic index of capsaicin are discussed in detail.

88 sensory neuron-derived exosomes released by capsaicin are readily phagocytosed by macrophages in whi

89 t improvement in cough reflex sensitivity to capsaicin at 2 hours and a borderline significant improv

90 We used this capsaicin axotomy technique to examine the effects of ex

91 nd 30-day cutaneous regeneration after thigh capsaicin axotomy were compared for participants with ty

92 but surmountable barrier to the flipping of capsaicin between opposing leaflets of the bilayer.

93 er confirm that Y511, known to be crucial to capsaicin binding, has a distribution along the bilayer

94 s in mice by interacting with the vanilloid (capsaicin)-binding pocket and promoting the stabilizatio

95 onal quantification revealed the location of capsaicin-binding site and critical residues mediating l

96 te adjacent to or overlapping with the TRPV1 capsaicin-binding site.

97 We found that menthol and capsaicin both caused a significant reduction in corneal

98 with COPD had heightened cough responses to capsaicin but reduced responses to prostaglandin E2 comp

99 obility decreased upon channel activation by capsaicin, but only in the presence of extracellular Ca(

100 TRPV1 agonists including capsaicin (CAP) and the eCBs anandamide and N-arachidono

101 HA diminishes heat, pH and capsaicin (CAP) responses, thus reducing the opening pro

102 a coarse characterization of the location of capsaicin (CAPS) and resiniferatoxin (RTX).

103 Consistent with these findings, capsaicin caused a greater number of coughs in CS-expose

104 Rats undergoing PMV deafferentation via capsaicin, celiac-superior mesenteric ganglionectomy (CS

105 cacy and potency in preclinical and clinical capsaicin challenge studies; despite this improved pharm

106 ronic cough and also the predictive value of capsaicin challenge testing in the assessment of novel a

107 ces where C-fiber activation was mimicked by capsaicin challenge.

108 Cough reflex sensitivity to capsaicin (concentration of capsaicin inducing at least

109 -mediated pain perception leading to altered capsaicin consumption and sensitivity to heat.

110 of diverse accessions are in agreement with capsaicin content (CA) and fruit weight (FW) classificat

111 acologically, neurons respond either only to capsaicin (COR neurons) or to both capsaicin and the end

112 Two novel capsaicin cough challenges were compared in patients wit

113 d-effects modeling demonstrates that maximal capsaicin cough responses better discriminate health fro

114 The pungent molecule capsaicin (CP) has a similar effect as AEA; however, CP

115 ocomotor adaptation task with pain on Day 1 (capsaicin cream around the ankle), while the task was pe

116 Surgical removal of the periosteum, capsaicin denervation of sensory nerves or knockdown in

117 Capsaicin did not alter c-KIT expression or nasal epithe

118 TAC1 neuropeptide precursor and decreased in capsaicin-diet fed mice.

119 The relative content of capsaicin differs from the evolution of the other four c

120 ve major capsaicinoids: nordihydrocapsaicin, capsaicin, dihydrocapsaicin, homocapsaicin and homodihyd

121 nornordihydrocapsaicin, nordihydrocapsaicin, capsaicin, dihydrocapsaicin, homocapsaicin and homodihyd

122 he contents of the four major capsaicinoids: capsaicin, dihydrocapsaicin, nordihydrocapsaicin, and ho

123 ny concentration of capsaicin (Emax) and the capsaicin dose inducing half-maximal response (ED50).

124 We sought to investigate capsaicin dose responses in different disease groups.

125 d negative voltages, which is reminiscent of capsaicin effects.

126 Inhaled capsaicin elicits cough reproducibly in human subjects a

127 ough response evoked by any concentration of capsaicin (Emax) and the capsaicin dose inducing half-ma

128 Accordingly, the reduction of the capsaicin-evoked [Ca(2+)]i rise and of the frequency of

129 nts with stable asthma exhibited exaggerated capsaicin-evoked cough responses consistent with neurona

130 We sought to investigate capsaicin-evoked cough responses in a group of patients

131 on awake cough frequency (primary outcome), capsaicin-evoked cough, and patient-reported outcomes.

132 these patients, despite small reductions in capsaicin-evoked cough.

133 se from hindpaw skin biopsies, and increased capsaicin-evoked inward current and membrane expression

134 TRPV1 activity, as demonstrated by increased capsaicin-evoked nocifensive responses, increased calcit

135 1 receptor only reduces both anandamide- and capsaicin-evoked responses in ACR neurons.

136 of G618W and M644I were recapitulated in the capsaicin-evoked YO-PRO1 uptake assay.

137 n resulted in a loss, rather than a gain, in capsaicin-evoked YO-PRO1 uptake.

138 ical excitation of trigeminal pain fibers by capsaicin evokes neurogenic inflammation in the surround

139 Capsaicin exerts its therapeutic action by ablating the

140 ochemical biosensor for the determination of capsaicin extracted from chilli fruits, based on a novel

141 Our analysis revealed that capsaicin failed to activate TRPV2_Quad likely due to st

142 We discuss the significance of capsaicin flipping from the extracellular to the intrace

143 s produced by intraplantar administration of capsaicin, formalin or complete Freund's adjuvant.

144 neurons express Fos after cheek injection of capsaicin, formalin, or chloroquine.

145 ptive responses to intraplantar injection of capsaicin, formalin, or complete Freund's adjuvant more

146 These results revealed that capsaicin forms hydrogen bonds with GLU355, GLU541, GLU5

147 gion of India evaluated showed variation for capsaicin from 0.27% (CHF-CA-1) to 3.03% (CHF-CA-21), ol

148 renal nerves, renal afferent disruption with capsaicin had no effect on blood pressure or renal infla

149 Capsaicin has also been used as an analgesic, and its to

150 On a more basic research level, capsaicin has been used as a ligand to activate several

151 oposal as second line for lidocaine patches, capsaicin high-concentration patches, and tramadol; and

152 lease and enacarbil; and 10.6 (7.4-19.0) for capsaicin high-concentration patches.

153 simulations were used to explore behavior of capsaicin in a 1-palmitoyl-2-oleoyl phosphatidylcholine

154 EN-D0501 and SB-705498 were profiled against capsaicin in a sensory nerve activation assay and in viv

155 highly improved the voltammetric process of capsaicin in comparison to the CNTs/GCE and bare GCE.

156 ic afferents, and sensitization responses to capsaicin in dorsal root ganglia (DRGs) following applic

157 oster the hope of innovative applications of capsaicin in human disease.

158 (CNTs) was applied for the determination of capsaicin in pepper samples.

159 n of submucosal neurons by the TRPV1 agonist capsaicin in rectal biopsy specimens collected from 9 pa

160 In contrast, direct gating of TRPM1 by capsaicin in RGS7(-/-)/RGS11(-/-) and WT rod BCs is simi

161 tein was seen for simulations initiated with capsaicin in the bilayer.

162 as successfully been applied for quantifying capsaicin in various pepper samples including Isot.

163 orresponded to reduced sensitivity to 100 nM capsaicin in vitro (IC50 = 230 +/- 20 nM, 76 +/- 4.4% wi

164 ntraduodenal capsaicin infusion (1.5 mg pure capsaicin) in healthy volunteers on hunger, satiety, and

165 In functional assays the TRPV1 agonist capsaicin induced dose-dependent IL-8 release, which cou

166 Investigations of Swiss Albino mice through capsaicin induced paw lickings and dextran induced infla

167 dependent signaling plays a dominant role in capsaicin-induced ablation of nociceptive terminals and

168 Ca(2+) influx through TRPV1 is necessary for capsaicin-induced ablation of nociceptive terminals.

169 ice showed that EGTA and MDL28170 diminished capsaicin-induced ablation.

170 of reactive oxygen species did not attenuate capsaicin-induced ablation.

171 lipid bilayers consisting of neutral lipids, capsaicin-induced activity depended on phosphatidylinosi

172 The mechanisms underlying capsaicin-induced analgesia likely involve reversible ab

173 ombinant human TRPV1 channels, 4 antagonized capsaicin-induced Ca(2+) influx, with an IC50 value of 4

174 Moreover, EREG application potentiated capsaicin-induced calcium influx in a subset of sensory

175 as none of the mutations selectively altered capsaicin-induced changes in NMDG permeability, the loss

176 ssay and in vivo potency established against capsaicin-induced cough in the guinea pig.

177 Theophylline inhibits capsaicin-induced cough under both normal and "disease"

178 In vivo XEN-D0501 completely inhibited capsaicin-induced cough, whereas 100 times more SB-70549

179 old more potent than SB-705498 at inhibiting capsaicin-induced depolarization of guinea pig and human

180 and primary afferent cultures, we monitored capsaicin-induced effects on afferent terminals in real

181 hibited nociceptive transmission by reducing capsaicin-induced internalization of NK-1 and phosphoryl

182 imilarly, clonidine reduced the frequency of capsaicin-induced mEPSCs by approximately 60%.

183 rons from stg/stg mice, but the amplitude of capsaicin-induced mEPSCs from C-fiber synapses was unalt

184 itch in the current-voltage relationships of capsaicin-induced mEPSCs, from linear to inwardly rectif

185 d slices, clonidine reduced the frequency of capsaicin-induced miniature EPSCs in the presence of tet

186 Although capsaicin-induced mitochondrial Ca(2+) uptake was TRPV1-

187 responses in formalin-induced tonic pain, in capsaicin-induced neurogenic pain, and notably in oxalip

188 We hypothesized that capsaicin-induced neuronal death would increase prolifer

189 ration within adult nodose ganglia following capsaicin-induced neuronal death.

190 nduced pruritus (itch) and additionally in a capsaicin-induced nociception model of pain without any

191 atorin significantly inhibited formalin- and capsaicin-induced nocifensive responses but did not alte

192 compound 30 rescued albino mice by 80% from capsaicin-induced paw licking and recovered it by 60% fr

193 Furthermore, capsaicin-induced spontaneous pain, inward currents in D

194 Moreover, MDL28170 prevented capsaicin-induced thermal hypoalgesia.

195 e TRPA1 mutant D477A) still showed increased capsaicin-induced TRPV1 activity.

196 ons, demonstrating that tiotropium inhibited capsaicin-induced, but not TRPA1-induced, calcium moveme

197 dy was to test the hypothesis that perivagal capsaicin induces degeneration of vagal efferents contro

198 We hypothesized that capsaicin induces satiety through the release of gastroi

199 x sensitivity to capsaicin (concentration of capsaicin inducing at least 5 coughs) and 24-hour cough

200 investigate the effects of an intraduodenal capsaicin infusion (1.5 mg pure capsaicin) in healthy vo

201 gallbladder volumes were observed after the capsaicin infusion compared with after the placebo infus

202 The intraduodenal capsaicin infusion significantly increased satiety (P-tr

203 he resultant brain responses associated with capsaicin inhalation without any treatment were compared

204 Capsaicin inhalational challenge was performed, and coug

205 Sensory neuron ablation by neonatal capsaicin injection prevented perineural invasion (PNI),

206 est stimulus because the coughing induced by capsaicin interfered with measurements.

207 Histamine, chloroquine, and capsaicin intradermally elicited similar distributions o

208 Capsaicin is an ingredient in spicy peppers that produce

209 The dietary compound capsaicin is responsible for the "hot and spicy" taste o

210 The response to intraplantar capsaicin is substantially reduced, as expected.

211 As a consequence, the efficacy of capsaicin is unknown in a significant number of IR patie

212 -articular injection of HA in rats decreases capsaicin joint nociceptor fibres discharge.

213 The pharmacological activity of capsaicin-like compounds is dependent on several factors

214 In contrast, channel activations by capsaicin, low pH, divalent cations, and even heat are m

215 challenged recombinant rTRPV1 receptors with capsaicin, low pH, or heat.

216 tantially reduced maximal cough responses to capsaicin (mean change from baseline, XEN-D0501, -19.3 +

217 TLR5-mediated Abeta-fiber blockade, but not capsaicin-mediated C-fiber blockade, also reduced chemot

218 The generation of novel capsaicin-mimetics and improved drug delivery methods wi

219 We also observed a capsaicin molecule flipping from the extracellular to th

220 We have no idea about the efficacy of capsaicin nasal spray in these patients nor about the ti

221 We report here that capsaicin nasal spray is effective in a broader group of

222 itis (IR) is a prevalent condition for which capsaicin nasal spray is the most effective treatment.

223 We sought to study the effects of capsaicin nasal spray on the afferent innervation of the

224 nd, placebo-controlled randomized trial with capsaicin nasal spray was performed involving 33 patient

225 ture is convincing regarding the efficacy of capsaicin nasal treatment in idiopathic rhinitis (IR).

226 aneous HA injection in mice reduces heat and capsaicin nocifensive responses, whereas the intra-artic

227 lecular mechanisms underlying the effects of capsaicin on nociceptors.

228 st days, an intraduodenal infusion of either capsaicin or a placebo (physiologic saline) was performe

229 estricted to temperature and does not affect capsaicin or acid responses, thereby maintaining a role

230 strategy, we report that TRPV1 activation by capsaicin or by the endocannabinoid anandamide depresses

231 sponse to intracolonic application of either capsaicin or mustard oil, stimuli known to evoke sustain

232 In contrast, exposure to the TRPV1 agonist capsaicin or the TRPM8 agonist icilin had no effect on i

233 cals of the tested hostplants significantly (capsaicin) or insignificantly (gossypol and nicotine) in

234 d) microinjection of histamine, chloroquine, capsaicin, or vehicle into the left cheek.

235 We suggest that histamine itch and capsaicin pain are peripherally encoded in C-MIAs, and t

236 es, application of extracellular QX-314 with capsaicin persistently reduces C-fiber but not A-fiber c

237 -S4 transmembrane helices in the presence of capsaicin placed in the aqueous phase, in the lipid, or

238 ramers correlates with channel activation by capsaicin, providing an optical marker of conformational

239 ectrometry we show that upon activation with capsaicin, QX-314 selectively accumulates in the cytosol

240 vars is highly variable, with the content of capsaicin ranging from 31% to 71% of the total capsaicin

241 he cannabinoid type 1 (CB1) receptor and the capsaicin receptor (TRPV1) exhibit co-expression and com

242 through the activation of the heat-sensitive capsaicin receptor TRPV1 by magnetic nanoparticles.

243 The capsaicin receptor TRPV1 ion channel is a polymodal noci

244 threshold temperature of the heat-sensitive capsaicin receptor TRPV1 ion channel, leading to its act

245 cules that serve as ligands of the "heat and capsaicin receptor" TRPV1.

246 The capsaicin receptor, TRPV1, is regulated by phosphatidyli

247 ne structures of two activated states of the capsaicin receptor, TRPV1.

248 underlying IR and the therapeutic action of capsaicin remain unknown.

249 arting from the cytosolic aqueous phase, and capsaicin remained stable in the majority of simulations

250 s elicited by id histamine, chloroquine, and capsaicin, respectively, 3.7%, 4.3%, and 4.1% were retro

251 1(+) neurons allowed allyl isothiocyanate or capsaicin, respectively, to evoke itch, implying that ce

252 id injection of histamine, chloroquine, and capsaicin, respectively.

253 (IC50 = 230 +/- 20 nM, 76 +/- 4.4% wild-type capsaicin responders vs. 56.9 +/- 4.7% HDAC4 cKO respond

254 without any effect on the overall number of capsaicin-responding cells.

255 diating PRL-induced transient enhancement of capsaicin responses in both male and female TG neurons.

256 lly similar muscarinic antagonist, inhibited capsaicin responses in isolated guinea pig vagal tissue,

257 tential vanilloid subtype 1 (TRPV1)-mediated capsaicin responses via Toll-like receptor 4 (TLR4) in m

258 d histamine activate distinct populations of capsaicin-responsive neurons in primate dorsal root gang

259 We found that in small-diameter, capsaicin-sensitive dorsal root ganglia neurons correspo

260 show that GRP directly activates small-size capsaicin-sensitive DRG neurons, an effect that translat

261 al inhibition of the TRP vanilloid-1 (TRPV1) capsaicin-sensitive subunit accelerates degeneration of

262 hibition of SDH neurons after stimulation of capsaicin-sensitive, nociceptive primary afferent fibers

263 An intraduodenal infusion of capsaicin significantly increases satiety but does not a

264 (SMD, -1.36 [CrI, -1.77 to -0.95]), topical capsaicin (SMD, -0.91 [CrI, -1.18 to -0.08]), TCAs (SMD,

265 er, interactions were seen between TRPV1 and capsaicin starting from the cytosolic aqueous phase, and

266 tidergic CGRP/somatostatin+ nociceptors upon capsaicin stimulation exert a tonic inhibitory control o

267 e Fos-positive neurons following pruritic or capsaicin stimuli, approximately 1-2% were retrogradely

268 Oral administration of the TRPV1 agonist, capsaicin, suppressed ligature-induced bone loss in mice

269 gene expression and neofunctionalization of capsaicin synthase have shaped capsaicinoid biosynthesis

270 einstate channel expression and responses to capsaicin, temperature, and voltage.

271 acids are better tolerated for activation by capsaicin than for activation by hot temperature, sugges

272 ecent studies have shown a metabolic role of capsaicin that may be mediated via the transient recepto

273 that responds to various stimuli, including capsaicin (the pungent compound found in chili peppers),

274 d in pain sensation, and is the receptor for capsaicin, the active ingredient of hot chili peppers.

275 Inhalation of capsaicin, the extract of hot chili peppers, induces cou

276 The best known agonist of TRPV1 channels is capsaicin, the pungent component of "hot" chili peppers.

277 subtype 1 (TRPV1), an irritant receptor for capsaicin, the pungent ingredient of chili peppers.

278 while completing a series of inhalations of capsaicin to induce the urge-to-cough.

279 Similarly, topical application of capsaicin to skin innervated by the saphenous nerve incr

280 e is relatively unstable, whereas binding of capsaicin to TRPV2_Quad antagonizes resiniferatoxin-indu

281 In Young MAs, capsaicin (to inhibit sensory neurotransmission) blocked

282 Fos expression was suppressed by 65-92% in capsaicin-treated animals, as was epinephrine (74%), nor

283 316,243 were attenuated by 50% in intra-BAT capsaicin-treated mice.

284 Shallow wounds in capsaicin-treated sites healed more slowly than in place

285 showed a trend to being better responders to capsaicin treatment compared with patients with IR but w

286 patients with IR and symptom reduction after capsaicin treatment demonstrates the clinical relevance

287 The therapeutic action of capsaicin treatment in patients with idiopathic rhinitis

288 s and the increased threshold for AITC after capsaicin treatment in patients with IR demonstrate the

289 Capsaicin treatment of IR patients increased the thresho

290 However, the functional consequences of capsaicin treatment on nasal nerve activation and the as

291 nasal hyperreactivity (NHR) and response to capsaicin treatment remain unknown.

292 observed in 11 of 14 patients with IR after capsaicin treatment.

293 5 was only reduced in patients with IR after capsaicin treatment.

294 ses in 36% of OA-NO2-sensitive neurons while capsaicin (TRPV1 agonist) or allyl-isothiocyanate (AITC,

295 When activated by capsaicin, TRPV1 recruits more glutamatergic, but not GA

296 The effects of capsaicin were also tested in vitro on human nasal epith

297 Concentrations of flavonoids and capsaicin were simultaneously quantified for the first t

298 al rhizotomy nor an intrathecal injection of capsaicin, which completely eliminated spinal cord TRPV1

299 Capsaicin, which is the major pungent principle in chili

300 rdic response to intralaryngeal perfusion of capsaicin, which was associated with up-regulation of TR