ライフサイエンスコーパス: substance P

1 sion of preprotachykinin-A (the precursor of substance P).

2 reased number of neurons expressing CGRP and substance P.

3 equency response to exogenous application of substance P.

4 kinin is another tachykinin with homology to substance P.

5 glucagon, glucagon-like peptide 1 (GLP1) and substance P.

6 tes at sites of intestinal inflammation make substance P.

7 encoding the precursor for the neuropeptide substance P.

8 ptive neuronal markers IB4, TRPV1, CGRP, and substance P.

9 tes modulatory responses to the neuropeptide substance P.

10 highly correlated to the process elicited by substance P.

11 one that resembled degranulation induced by substance P.

12 alized within 48 hours, including release of substance P.

13 by the striosomally enriched neuromodulator substance P.

14 (p = 0.001) and thiobarbituric acid reactive substances (p = 0.001) as well as the mean percent chang

15 as a small and high affinity ligand for the substance P 1-7 (SP(1-7), H-Arg-Pro-Lys-Pro-Gln-Gln-Phe-

16 ollowing TTX application, carbachol (1 muM), substance P (1 muM) and an NKI agonist (GR73632, 100 nM)

17 d to the endothelium-dependent vasodilators, substance P (10(-8) M) and adenosine 5diphosphate (10(-5

18 200, 2 mum) antagonists and mimicked by NK1 (substance P, 100 nm) and NK3 (neurokinin B [NKB], 100 nm

19 on increases in flow evoked by intracoronary substance P (20 pmol/min).

20 y excitatory interneurons and many coexpress substance P, a marker for a discrete subset of nocicepti

21 In this study, we test the role of substance P, a neuroinflamatory peptide, in RLB-induced

22 Substance P, a peptide derived from the TAC1 gene, media

23 isms in the mouse preBotzinger complex using substance P, a potent excitatory modulator of breathing

24 ormed rapid quantification of serum level of substance P, a potential biomarker of acute neuroinflamm

25 nction with capillary LC for the analysis of substance P, a tryptic digest of bovine serum albumin, a

26 Intrathecal injection of Substance P activated this cascade (increased phosphoryl

27 ars critical, nerve growth factor, CGRP, and substance P all appear to be required.

28 Intradermal administration of substance P, an activator of skin mast cells, and challe

29 Neurokinin-1 antagonists compete with substance P, an endogenous ligand with a high density of

30 potential (TRP)V1, TRPA1, and neuropeptides (substance P and calcitonin gene-related peptide) using g

31 type 1, the small peptidergic neuron markers substance P and calcitonin gene-related peptide, and the

32 emonstrate that glutamate together with both substance P and CGRP mediate tissue-injury associated pa

33 a(2+) transients to KCl, caffeine, nicotine, substance P and GR 64349 (an NK2 agonist), suggesting th

34 We hypothesize substance P and its receptor, the neurokinin 1 receptor

35 Substance P and its truncated receptor exert oncogenic e

36 re-embedding immunoelectron microscopy using substance P and Met-/Leu-enkephalin antibodies to label

37 muscle afferents excite NTS GABA neurons via substance P and microinjection of a substance P-neurokin

38 ERK, and MMP-1; p <= 0.039) and spinal cord (substance P and MMP-1; p <= 0.041).

39 o demonstrate TAC1 (encoding the tachykinins substance P and neurokinin A) to be strongly activated b

40 pocampal and ventral tegmental area neurons, substance P and neurotensin activate a channel complex c

41 These include peptides, such as substance P and neurotensin, as well as acetylcholine an

42 n of mass/charge peak expression levels with substance P and proenkephalin A (218-228).

43 itively correlated with expression levels of substance P and proenkephalin A (amino acids 218-228), r

44 The spatial expression patterns of substance P and proenkephalin, marker neuropeptides of t

45 mmatory-cell infiltration, and the pulmonary substance P and pulmonary Th2 cytokine levels that occur

46 Colonic IL-6 levels as well as substance P and S100beta density in myenteric ganglia of

47 ed levels of the stem cell chemoattractants, substance P and SDF-1, in both the injured cornea and bl

48 V-1 Gp120-induced calcium influx mediated by substance P and significantly decreased the permeability

49 to such nociceptors, through the release of substance P and the activation of the cationic molecule

50 odilators adenosine 5'-diphosphate (ADP) and substance P and the endothelium-independent vasodilator

51 functional maturation via angiotensin II and substance P and through the angiotensin II receptor type

52 wn Prep substrates, such as the neuropeptide substance P and thymosin-beta4, the precursor to the bio

53 egulate the transmission of pain messages by substance P and TRPV1-expressing pain fibers.

54 xicant reactions increase skin sensory nerve substance P and, in turn, increase itching responses.

55 Substance-P and hemokinin-1 are proinflammatory neuropep

56 tive for calcitonin gene-related peptide and substance P) and myelinated non-nociceptive fibers (posi

57 nerve-derived dilator neuropeptides CGRP and substance P, and also nNOS-derived NO.

58 that expressed choline acetyltransferase and substance P, and in inhibitory motoneurons and interneur

59 e under resting conditions, independently of substance P, and internalized following activation by DO

60 kers calcitonin gene-related peptide (CGRP), substance P, and isolectin B4.

61 lapse, including the urocortins, nociceptin, substance P, and neuropeptide S.

62 The baseline responses to ADP, substance P, and SNP of arterioles from the UDM patients

63 thase (nNOS), vasoactive intestinal peptide, substance P, and tyrosine hydroxylase to quantify nerves

64 , stimulated with carbachol, stimulated with substance P, and, as a test for synergy, stimulated with

65 Together, substance P- and enkephalin-positive terminals represent

66 mining the well-characterized model peptides substance P, angiotensin II, and bradykinin.

67 as not only a critical pharmacophore for the substance P antagonist activities, but as an address reg

68 ifunctional peptides with opioid agonist and substance P antagonist bioactivities were designed with

69 ak clusters in mass spectra of reserpine and substance P are measured using Fourier transform ion cyc

70 uction by the toxin [Sar(9), Met (O(2))(11)]-substance P as the rest of the RTN Phox2b(+)/TH(-) cells

71 [M + 2H](2+) or [M + 3H](3+) charge state of substance P as well as individual trisaccharide isomers

72 receptor-capture experiments to identify the substance P-binding receptor via liquid chromatography-t

73 iatal matrix, whose axons corelease GABA and substance P, both at synapses with GABAergic neurons in

74 with secretion elicited by compound 48/80 or substance P but not by FcepsilonRI aggregation.

75 cid (GABA)-ergic striatal neurons expressing substance P, but it is also influenced by indirect basal

76 Gq, Gs, and beta-arrestin when stimulated by substance P, but it lacks any sign of constitutive activ

77 id-mediated depression, and the neuropeptide Substance P, but not blockade of inhibitory synaptic tra

78 of dynorphin and prodynorphin with CGRP and substance P, but not with isolectin B4.

79 d glycation end-products-in the neuropeptide substance P by ultrahigh-resolution Fourier transform io

80 No apparent differences were observed in substance P, calcitonin gene-related peptide, or neurope

81 ed by vagal sensory axons expressing Phox2b, substance P, calcitonin-gene related peptide, and the se

82 1,4,5-trisphosphate-dependent signaling with substance P causes idiosyncratic changes in dynamic Ca(2

83 per type 2 cells, IL-17(+) cells, basophils, substance P(+) cells, and dermal deposition of periostin

84 relationship between central nervous system substance P containing neural circuits and aggression in

85 ts correlated with a significant increase in substance P content of the cutaneous nerves and an accom

86 ay a role in the pathogenesis of IBD include substance P, corticotropin-releasing hormone, neurotensi

87 t calcitonin gene-related peptide (CGRP) and substance P could neutralise their actions.

88 y activation of the neurokinin-1 receptor by substance P decreases sepsis survival through multiple m

89 IgE-dependent and substance P-dependent activation in vivo also induced di

90 Consistent with the substance P-dependent synaptic potentiation in the LIPN,

91 opical corticosteroid, alcohol delamination, substance P-derived peptide and ILGF-I drops, botulinum

92 Topical treatment with the MC trigger substance P does not affect wound healing in MC-deficien

93 We find that substance P does not alter the balance of excitation and

94 ing product-ion spectra of doubly protonated substance P, doubly protonated gramicidin S, doubly prot

95 te, GABA, thyrotropin releasing hormone, and substance P encoded by the Tachykinin-1 (Tac1) gene.

96 aboratory demonstrated that the neuropeptide substance P enhances the striatal METH-induced productio

97 lutamatergic synapses in LIPN neurons, while substance P enhances this plasticity.

98 xons and terminals overlap with cholinergic, substance P-ergic, and glutamatergic markers.

99 confirmed that preBotC neurons responsive to substance P exhibited similar responsiveness to bradykin

100 these receptors are expressed on polymodal, substance P-expressing neurons.

101 n of Gad65, dopamine receptor D1 (Drd1), and substance P expression at different phases of prenatal d

102 production, while TGF-beta blocks macrophage substance P expression.

103 Siebenharr et al. demonstrate that substance P fibers are increased in early lesions, and t

104 y requires release of the excitatory peptide substance P from D1-MSNs and robust cholinergic interneu

105 They also suggest that any release of substance P from injured Abeta afferents is unlikely to

106 ted inflammation, suggesting that release of substance P from nerve fibers triggers the inflammatory

107 f HXA(3) correlated with enhanced release of Substance P from primary sensory afferents.

108 facilitates the release of the neuropeptide substance P from TRPM8(+) cold-sensing neurons to signal

109 sis, it was found that IL-12 and IL-23 drive substance P gene expression and peptide synthesis in mur

110 Substance P had bidirectional effects on dopamine releas

111 Tachykinin/Substance P has been implicated in aggression in mammals

112 modulation of aggression, but no studies of substance P have yet been reported with regard to human

113 gic and surrounded by terminals with intense substance P immunoreactivity.

114 ncreased calcitonin gene-related peptide and substance P immunoreactivity.

115 The high production of substance P in breast cancer cells (BCCs) is caused by t

116 sm in the LIPN and a region-specific role of substance P in fear extinction.

117 lated peptide but increases the neuropeptide substance P in LPS-treated mice.

118 lts demonstrate the relative contribution of substance P in regulating the clinical severity of HSK l

119 and nociceptor activation via the release of substance P in the skin and dorsal root ganglion.

120 horns revealed increased immunoexpression of Substance P in week 8 and neurokinin-1 in weeks 8 and 12

121 Substance P induced CD301b(+) DC migration to the dLN wh

122 P<0.01) but, in contrast to SMTC, inhibited substance P-induced increases in flow (P<0.01).

123 Overall, substance P-induced vasorelaxation corresponded poorly w

124 and without RLB revealed an increase of the substance P-inducible neurokinin 1 receptor (NK1-R) in t

125 A spontaneous IPSCs (sIPSCs), (2) endogenous substance P influence on sIPSC frequency, and (3) sIPSC

126 Exogenous PACAP and substance P initiated a slow depolarization in the neuro

127 uence on the signal intensities of molecular substance P ions.

128 Substance P is a tachykinin that enhances pathways of in

129 with the potential to release both 5-HT and substance P is necessary for normal respiratory dynamics

130 , we show that the neurokinin 1 receptor for substance P is required for SCC-mediated inflammation, s

131 Substance P is the prototype tachykinin peptide and trig

132 Substance P knockout (KO) mice retained their ability to

133 -2, iNOS, and VGSC was investigated by using substance P, l-arginine, and veratrine, respectively, as

134 uch as up-regulation of the NK1 receptor and substance P, lead to antiopioid effects in ascending or

135 Substance P-like immunoreactive free nerve endings were

136 immunoreactive en plaque motor endplates and substance P-like immunoreactive, thin and varicose free

137 Substance P-like immunoreactivity (SPL-IR) was semiquant

138 The cerebrospinal fluid substance P-like immunoreactivity levels were directly c

139 subjects with personality disorder (PD) and substance P-like immunoreactivity was measured and corre

140 complex, the patterns of calbindin-like and substance P-like immunoreactivity, and the organization

141 T2 in the Trpv1-Cre population together with substance P mediate acute cold pain, whereas glutamate t

142 ls and neurokinin receptors are important in substance P-mediated inhibition of ductal bicarbonate se

143 ferent weighting of dopamine transmission by substance P modified the apparent center-surround contra

144 rough the angiotensin II receptor type 1 and substance P neurokinin 1 receptors.

145 rons via substance P and microinjection of a substance P-neurokinin 1 receptor (NK1-R) antagonist int

146 Substance P neuropeptide and its receptor, neurokinin-1

147 obe did not interfere substantially with the substance P-NK(1) receptor interaction.

148 data suggest that an interaction between the substance P NK1-R and GABAergic transmission in the NTS

149 uorescence labeling in NTS show an increased substance P NK1-R internalization on GABA neurons.

150 tion channel subfamily V, receptor 1 (TRPV1)-substance P nociceptive signaling pathway.

151 es, calcitonin gene-related polypeptide, and substance P, occurred at variable density throughout the

152 ough TACR1 (a G-protein-coupled receptor for substance P) occurs by means of a unique mechanism: it d

153 in the same region, microinjections of 1 mum substance P or 1 mm nicotine into the pTRG restored rhyt

154 urthermore, by pharmacological inhibition of substance P or calcitonin gene-related peptide (CGRP) si

155 cient mice, we evaluated the contribution of substance P or CGRP to these sensory modulations, with o

156 ross-sectional area-and some co-labeled with substance P or isolectin B4.

157 id not prevent modulation of RTN activity by Substance P or thyrotropin-releasing hormone, previously

158 d NS309-induced vasodilatation and abolished substance P- or adenosine 5 diphosphate-induced relaxati

159 or Gal, Penk, and Adcyap1, and receptors for substance P, orexin, serotonin, and ATP.

160 e possibility is raised that blocking of the substance P pathway with NK1-R antagonists postocular tr

161 Drift field application frequency scans of substance P peptide ions show that it is possible to sep

162 ures of ions produced by electrospraying the substance P peptide, as well as a mixture of tryptic pep

163 IL-31 when stimulated with a combination of substance P, periostin, and red blood cell lysate (repre

164 e mediators were increased in the periphery (substance P, pERK, and MMP-1; p <= 0.039) and spinal cor

165 d in an increased labeling of CGRP-, but not substance P-positive cells in the lumbar dorsal root gan

166 studies in mice reveal that an activation of substance P-positive dorsomedial habenula (dMHb) neurons

167 in corneal epithelial nerve regeneration and substance P-positive nerve density in both wounded and u

168 treatment also targeted the regeneration of substance P-positive nociceptive axons but had no effect

169 hat proposed for basic neuropeptides such as substance P, possibly involving Mas-related gene 2 (MrgX

170 IL-10 inhibits T-cell substance P production, while TGF-beta blocks macrophage

171 tor beta (TGF-beta) in controlling leukocyte substance P production.

172 Pro-substance P (ProSP) is a stable surrogate marker for lab

173 a subset of dissociated neurons responded to substance P, putatively corresponding to inspiratory pre

174 cribes an asymmetric synthesis of the potent substance P receptor antagonist (+)-CP-99,994 from 4-phe

175 Administration of a substance P receptor antagonist in mice.

176 anisms responsible for this improvement, the substance P receptor was blocked in mice after traumatic

177 ify NALCN as the cation channel activated by substance P receptor, and suggest that UNC-80 and Src fa

178 We focused on substance P receptor-expressing (NK1R+) projection neuro

179 not elicit degranulation of human skin MC or substance P release from NT2N cells in vitro.

180 by noxious heat and mechanical stimulations, substance P release was measured in the spinal cord by v

181 vasodilatation caused by CGRP (and possibly substance P) released from sensory-motor nerves and vaso

182 stellation pharmacology, we found that these substance P-responsive neurons also responded to histami

183 lood-brain barrier impermeable toxin, stable substance P-saporin (SSP-SAP), which ablates cells expre

184 otrapezoid nucleus region was destroyed with substance P-saporin prior to lentivirus injection into t

185 a neurokinin-1-receptor antagonist to block substance P signaling eliminated the improved survival o

186 des illustrated how many of these, including substance P, somatostatin, and neurotensin have actions

187 x/POU domain protein 3b, Ets variant gene 1, substance P, somatostatin, vasoactive intestinal polypep

188 ions, and 10 chloride and contains a single Substance P (SP) [SP + 3H](3+) ion (SP(3+); amino acid s

189 Substance P (SP) activation of the neurokinin-1 receptor

190 in joint disease including the production of Substance P (SP) affecting local inflammatory responses

191 we investigated the role of the neuropeptide substance P (SP) and cognate neurokinin 1 (NK1) nocicept

192 Substance P (SP) and hemokinin-1 (HK-1) are neuropeptide

193 peptides of the tachykinin family, including substance P (SP) and hemokinin-1 (HK-1), bind the neurok

194 We have shown that substance P (SP) and its neurokinin-1 receptor (NK-1R) r

195 ting evidence suggests that the neuropeptide substance P (SP) and its principal receptor neurokinin 1

196 Substance P (SP) and its receptors are involved in anxie

197 eloped a combination of systemic delivery of substance P (SP) and local release of stromal-derived fa

198 factor, and endogenous pruritogens, such as substance P (SP) and serotonin.

199 The peptide substance P (SP) and the cytokine tumor necrosis factor

200 n-converting enzyme-1 (ECE-1) in controlling substance P (SP) and the neurokinin 1 receptor (NK(1)R)

201 Substance P (SP) and the neurokinin-1 receptor (NK-1R) a

202 IL-33 augments VEGF release induced by substance P (SP) and tumor necrosis factor (TNF) release

203 Studies have shown that blocking substance P (SP) binding to neurokinin 1 receptor with s

204 e is increasing evidence that the tachykinin substance P (SP) can augment inflammatory immune respons

205 he structural evolution of the undecapeptide substance P (SP) during the final stages of ESI.

206 kephalinergic striatal neurons, and enhanced substance P (SP) expression by SP striatal projection ne

207 Release of substance P (SP) from nociceptive nerve fibers and activ

208 The peptide substance P (SP) has been implicated in inflammatory con

209 othelin-converting enzyme-1 (ECE-1) degrades substance P (SP) in early endosomes of epithelial cells

210 he nasal mucosa and higher concentrations of substance P (SP) in nasal secretions than HCs.

211 nd superresolution microscopy, we found that substance P (SP) induces the association of the neurokin

212 gh some work has suggested that intracranial substance P (SP) infusion reinstates cocaine seeking fol

213 To determine the effects of blocking substance P (SP) interactions with its major receptor (N

214 Substance P (SP) is a neuropeptide that mediates numerou

215 Substance P (SP) is a proinflammatory mediator implicate

216 Substance P (SP) is a prominent neuromodulator, which is

217 Substance P (SP) is a tachykinin neuropeptide, implicate

218 Substance P (SP) is also involved in inflammatory diseas

219 Substance P (SP) is an 11-amino acid peptide that belong

220 Substance P (SP) is an undecapeptide present in the CNS

221 Substance P (SP) is involved in wound healing, but its e

222 Substance P (SP) is linked to itch and inflammation thro

223 Substance P (SP) is thought to play a cardinal role in e

224 Substance P (SP) mediates colitis.

225 In chronic pain, the substance P (SP) neurokinin 1 receptor (NK(1)R) redistri

226 in part, by inhibiting GABAergic input onto substance P (SP) neurons in the ventral tegmental area (

227 U73,122 did not interfere with the effect of Substance P (SP) on cellular morphology and cellular imp

228 Furthermore, by pharmacologic inhibition of substance P (SP) or calcitonin gene-related peptide (CGR

229 ved cultured mast cells were stimulated with substance P (SP) or IgE/anti-IgE with or without preincu

230 To determine whether substance P (SP) plays a role in LH-induced antinocicept

231 ne PanIN cells that express the neuropeptide substance P (SP) receptor neurokinin 1-R (NK1-R).

232 Substance P (SP) regulates important intestinal function

233 ct, while the delayed phase occurs following substance P (SP) release in the brainstem.

234 , we report a strain divergence of total and substance P (SP) sensory corneal nerves in uninjured mic

235 Restoration of substance P (SP) signaling in denervated KC-Tie2 skin pr

236 Substance P (SP) specifically triggered intracellular ca

237 d paw edema and the anterograde transport of substance P (SP) that occur following formalin injection

238 The current study examined the effect of substance P (SP) upon intestinal epithelial cells and th

239 The role of substance P (SP) was investigated by pretreating animals

240 GFAP), tyrosine receptor kinase B (TrkB) and substance P (SP) were significantly increased in the col

241 ivery (RMD) technology utilizes a variant of substance P (SP), a neuropeptide that is rapidly interna

242 Substance P (SP), a pleotropic neuropeptide implicated i

243 rons expressed and secreted higher levels of substance P (SP), a proinflammatory neuropeptide.

244 network via simultaneous release of 5-HT and substance P (SP), acting at 5-HT(2A/2C), 5-HT(4), and/or

245 We also found that the neuropeptide substance P (SP), an endogenous agonist of Mrgprb2, faci

246 d by soluble factors, such as neuropeptides, substance P (SP), and neurokinin A (NK-A), which mediate

247 Approximately 50% of MSNs corelease substance P (SP), but how this neurotransmitter controls

248 Neuropeptides, such as substance P (SP), have long been seen as mediators of wi

249 Substance P (SP), involved in neurogenic inflammation by

250 The tachykinin, substance P (SP), is well known to augment inflammatory

251 ins are a family of neuropeptides, including substance P (SP), neurokinin A (NKA), and neurokinin B (

252 ioid peptide cholecystokinin, pronociceptive Substance P (SP), Neurokinin B, and a late wave of somat

253 ers: calcitonin gene-related peptide (CGRP), substance P (SP), neuronal nitric oxide synthase (nNOS),

254 IP), calcitonin-gene related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), and the n

255 Substance P (SP), one of the most widely expressed pepti

256 Substance P (SP), S100beta, GFAP, and phosphorylated mit

257 PY), nitric oxide synthase (NOS), serotonin, substance P (SP), vasoactive intestinal peptide (VIP) or

258 ther calcitonin gene-related peptide (CGRP), substance P (SP), vesicular glutamate transporter 1 (VGl

259 al levels of the antiapoptosis neuropeptide, substance P (SP), were treated with the SP antagonist, S

260 renergic and delta-opioid receptors (DOP) on substance P (SP)-immunoreactive (-ir) varicosities in th

261 noreactive (IR) varicosities; 20 +/- 4.3% of substance P (SP)-IR varicosities and 9 +/- 1.3% vasoacti

262 issue of Blood, Janelsins et al report that substance P (SP)-treated dendritic cells (DCs) efficient

263 uch information to the spinal cord expresses substance P (SP).

264 s calcitonin gene-related peptide (CGRP) and substance P (SP).

265 mesis model which also vomits in response to substance P (SP).

266 rtebrates is modulated by neuropeptides like Substance P (SP).

267 Activation of the substance P (SP)/neurokinin 1 receptor (NK1R) axis trigg

268 The lower limit of detection was 30pM Substance P (SP, 2pg/50microl), and reproducible respons

269 lcitonin gene-related peptide (CGRP) without substance P (SP; CGRP(+) SP(-) ).

270 The selective NK1R agonist, GR73632, and Substance-P (SP) inhibited NE transport and reduced plas

271 ) reveal that MrgprB2/MrgprX2 is a mast cell substance-P-specific receptor that critically links neur

272 the NK1 receptor agonist [Sar9,Met(O(2))11]-substance P (SSP), and fully blocked by the NK1 receptor

273 Injection of the neurotoxin saporin-substance P (SSP-SAP) into the retrotrapezoid nucleus (R

274 n the NTS while SAP conjugated to stabilized substance P (SSP-SAP) selectively killed neurons with NK

275 in the human coronary vascular bed, whereas substance P-stimulated vasodilatation is eNOS mediated.

276 od antagonist activity in the GPI assay with substance P stimulation ( K e = 26 nM) and good affinity

277 study examined possible mechanisms by which Substance P (Sub P) assumes a pronociceptive role in the

278 This study investigated the ability of substance P (Sub P) to induce dendritic varicosities (DV

279 Intestinal macrophages also produce substance P, subject mostly to IL-23 and TGF-beta regula

280 us secretion by sensory neurons that release substance P (SubP).

281 Laboratory animal studies of substance P suggest a facilitory role for this undecapep

282 Cytokine induction of substance P synthesis both in T cells and in macrophages

283 Certain signals, including substance P, the complement anaphylatoxins C3a and C5a,

284 Substance P, the principal ligand for the neurokinin-1 r

285 The activation by substance P through TACR1 (a G-protein-coupled receptor

286 pression of GABA(B) receptor activity allows substance P to induce a long-lasting increase in glutama

287 by protease allergens stimulates release of substance P to induce migration of Th2-skewing CD301b(+)

288 These data support the postulate that substance P transmits early inflammatory signals from th

289 ers are increased in early lesions, and that substance P treatment induces catagen follicles along wi

290 pendent microvascular relaxation response to Substance P was diminished in HCC swine, which was rescu

291 Although substance P was not detected in terminals of injured aff

292 itonin gene-related peptide (CGRP-alpha) and substance P was significantly increased in ETR compared

293 an inducible manner, and the peptidic ligand substance P was used as a test system.

294 ferently in striosome-matrix compartments by substance P.We paired detection of evoked dopamine relea

295 The post-CPB relaxation responses to ADP and substance P were significantly decreased in all 3 groups

296 oSP) is a stable surrogate marker for labile substance P, which has pro-inflammatory effects, increas

297 gh traumatic brain injury-induced release of substance P, which improves innate immunity to decrease

298 ed sensory neurons released the neuropeptide Substance P, which stimulated proximally located CD301b(

299 onfirmed successful coupling of the probe to substance P, while inositol monophosphate accumulation a

300 d RTN neuron activation by the neuropeptide, substance P, without affecting pH-sensitive background K