ライフサイエンスコーパス: CIA

1 CIA and EIA stenoses predominantly involved the distal a

2 CIA decreased the Hill coefficient of steady-state force

3 CIA model studies were performed with CIKS-deficient and

4 CIA was determined in dialysates obtained from wheat (2.

5 CIA was induced in DBA mice by immunization with collage

6 CIA was induced in DBA/1 mice by immunization with type

7 CIA was induced in DBA/1 mice by injection of collagen t

8 CIA was induced in DBA/1J mice by immunization with type

9 CIA(+)/RPR(-)/TP-PA(+) (n = 38) women were more likely t

10 CIA(+)/RPR(-)/TP-PA(-) serology in pregnancy is likely t

11 CIA, EIA, and femoral lesions were not randomly associat

12 CIA-positive, RPR-negative, TP-PA-negative serology may

13 Upon hip flexion, 23 CIA and 116 EIA stenoses showed kinking (mean amplitude,

14 After repeat testing, 7/31 (23%) CIA-positive, RPR-negative, TP-PA--negative patients ser

15 Among the 77 (49%) CIA(+)/RPR(-)/TP-PA(-) women who were retested, 53% beca

16 Whether this Ca2+-independent activation (CIA) occurs under physiological conditions remains uncle

17 olvation using collision induced activation (CIA), time-resolved hydrogen/deuterium back exchange (HD

18 ed, soluble CFA/I fimbriae protected against CIA as effectively as did Salmonella-CFA/I and found tha

19 -1(-/-)) mice were equally protected against CIA as were wild-type mice, suggesting a limited role fo

20 of IL-17 may explain the protection against CIA afforded by ES-62.

21 published by the Central Information Agency (CIA), including the per capita gross domestic product, t

22 A Compound Identification Algorithm (CIA) was previously developed for automated elemental fo

23 igh-resolution chemical index of alteration (CIA) records in the sediments of South China prior to th

24 However, the KO mice presented ameliorated CIA in terms of clinical scores, disease incidence, and

25 ap was also seen between CHIKV arthritis and CIA.

26 hat a regulatory circuit involving FBXL5 and CIA acts through both IRPs to control iron metabolism an

27 characteristics, prior syphilis history and CIA index values were compared for CIA-positive, RPR-neg

28 hylogenetic analyses reveal that the ISC and CIA pathways are predominantly bacterial, but their cyto

29 were generated and studied using the PIA and CIA models.

30 licly available microarray studies of RA and CIA.

31 on, baking and in vitro digestion on TIA and CIA were studied.

32 in collagen- and pristane-induced arthritis (CIA and PIA).

33 RA mouse models, collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA), via

34 e development of collagen-induced arthritis (CIA) and discover cellular and molecular mechanisms of I

35 as determined in collagen-induced arthritis (CIA) and local joint TLR5 ligation models.

36 the rat model of collagen-induced arthritis (CIA) and to evaluate the contribution of neuroimmune int

37 protects against collagen-induced arthritis (CIA) by eliciting two regulatory T cell (Treg) subsets:

38 KLH) study and a collagen-induced arthritis (CIA) disease model of rheumatoid arthritis.

39 nts of mice with collagen-induced arthritis (CIA) express RANKL.

40 Collagen induced arthritis (CIA) is an animal model of RA.

41 tion (MSCT) into collagen-induced arthritis (CIA) mice prevented arthritis progression by inhibiting

42 The collagen-induced arthritis (CIA) model and DR-1 transgenic mice were used to study t

43 cy in the murine collagen-induced arthritis (CIA) model for rheumatoid arthritis (RA) supported 14l a

44 op in the murine collagen-induced arthritis (CIA) model of inflammatory arthritis.

45 oss in the mouse collagen-induced arthritis (CIA) model of RA.

46 In the collagen-induced arthritis (CIA) model, while ectopic expression of FGF2 in vivo exa

47 neered MSCs in a collagen-induced arthritis (CIA) model.

48 nd damage in the collagen-induced arthritis (CIA) model.

49 model of RA, the collagen-induced arthritis (CIA) model.

50 eficiency in the collagen-induced arthritis (CIA) model.

51 g/kg) in the rat collagen induced arthritis (CIA) model.

52 ogression in the collagen-induced arthritis (CIA) mouse model to an extent just shy of disease abroga

53 e erosion in the collagen-induced arthritis (CIA) mouse.

54 g(-/-) mice with collagen-induced arthritis (CIA) or K/BxN serum transfer-induced arthritis (STIA).

55 ovial cells from collagen-induced arthritis (CIA) rats and RA patients.

56 Collagen-induced arthritis (CIA) was induced in male DBA/1J mice.

57 anism of action, collagen-induced arthritis (CIA) was therapeutically treated with anti-IL-7 Ab or Ig

58 with established collagen-induced arthritis (CIA) was undertaken to determine whether substitution of

59 ical features of collagen-induced arthritis (CIA) were significantly reduced in fXIII-deficient mice.

60 otective against collagen-induced arthritis (CIA), a model of rheumatoid arthritis (RA).

61 the progress of collagen-induced arthritis (CIA), a mouse model for RA.

62 inflammation in collagen-induced arthritis (CIA), a mouse model for RA.

63 sess its role in collagen-induced arthritis (CIA), a mouse model of human rheumatoid arthritis.

64 ities with RA or collagen-induced arthritis (CIA), a mouse model of RA.

65 C57BL/6 mice to collagen-induced arthritis (CIA), a well-established mouse model of RA.

66 pon induction of collagen-induced arthritis (CIA), tau-tg mice displayed an increased incidence and a

67 d into mice with collagen-induced arthritis (CIA), this T cell line specifically enhanced the severit

68 ion in mice with collagen-induced arthritis (CIA).

69 of inflammation, collagen-induced arthritis (CIA).

70 murine model of collagen-induced arthritis (CIA).

71 ced incidence of collagen-induced arthritis (CIA).

72 mmune arthritis, collagen-induced arthritis (CIA).

73 s on established collagen-induced arthritis (CIA).

74 itis (RA) and in collagen-induced arthritis (CIA).

75 luated in murine collagen-induced arthritis (CIA).

76 les of mice with collagen-induced arthritis (CIA).

77 challenged with collagen-induced arthritis (CIA).

78 e progression of collagen-induced arthritis (CIA).

79 arthritis model collagen-induced arthritis (CIA).

80 linical phase of collagen induced arthritis (CIA).

81 thritis, namely, collagen-induced arthritis (CIA).

82 and cytosolic iron-sulfur cluster assembly (CIA) machineries carry out biogenesis of iron-sulfur (Fe

83 tosolic iron-sulfur (Fe-S) cluster assembly (CIA) pathway functions to incorporate inorganic Fe-S cof

84 through the cytosolic FeS cluster assembly (CIA) pathway.

85 the cytosolic iron-sulfur cluster assembly (CIA) system in eukaryotes, with a focus on information g

86 A dedicated cytosolic Fe-S cluster assembly (CIA) system is required to assemble Fe-S clusters into c

87 the cytosolic iron-sulfur cluster assembly (CIA) system, converting it into cytosolic aconitase (c-a

88 ntified a cytoplasmic Fe-S cluster assembly (CIA) targeting complex composed of MMS19, CIAO1, and FAM

89 the cytosolic iron-sulfur protein assembly (CIA) machinery required for maturation of [4Fe-4S] clust

90 the cytosolic iron-sulfur protein assembly (CIA) machinery, is crucial for Fe/S cluster insertion in

91 equires the cytosolic Fe-S protein assembly (CIA) machinery.

92 the cytosolic iron-sulfur protein assembly (CIA) machinery.

93 inis cytosolic iron-sulfur protein assembly (CIA) pathway includes the essential Cfd1-Nbp35 scaffold

94 tes with most known cytosolic Fe-S assembly (CIA) components.

95 complex with the cytoplasmic Fe-S assembly (CIA) proteins CIAO1, IOP1, and MIP18.

96 nery and the cytosolic iron-sulfur assembly (CIA) system.

97 mAb to LAIR-1 also significantly attenuated CIA in the LAIR(+/+) mice.

98 TP-PA(-) women who were retested, 53% became CIA(-).

99 (-); more than half who were retested became CIA(-).

100 Our results indicated that the Boson CIA demonstrated strong discriminatory power in diagnosi

101 e damage and neutrophil infiltration in both CIA and CAIA models.

102 Sera were screened by CIA, and reactive samples underwent reflex testing with

103 The Advia-Centaur CIA and Trep-Sure EIA had signal strength cutoffs correl

104 uminescence immunoassay [CIA], Advia-Centaur CIA, and Trep-Sure EIA) and three manual assays (Trepone

105 S to 99.7% (99.0 to 99.9%) for Advia-Centaur CIA; negative agreement ranged from 86.3% (84.1 to 88.2%

106 ) and were categorized as "TP-PA confirmed" (CIA(+)/RPR(-)/TP-PA(+)) or "isolated CIA positive" (CIA(

107 Conversely, CIA joint inflammation and bone erosion are alleviated w

108 Similar to mutant plants with defective CIA components, grxs17 loss-of-function mutants showed s

109 he perfect correlation between the developed CIA and commercial ELISA for the detection of various co

110 The developed CIA detected HFA in the range of 0.3 pg mL(-1)-20 ng mL(

111 -62 in protecting DBA/1 mice from developing CIA and mirrored its mechanism of action in downregulati

112 stamine resulted in significantly diminished CIA pathology and local markers of osteoclastogenesis.

113 , anticollagen autoantibody responses during CIA did not differ among the genotypes.

114 h mice will develop clinical symptoms during CIA.

115 fied with traditional screening methods (eg, CIA-positive, rapid plasma regain (RPR)-negative).

116 Animals with either CIA or TNFalpha-induced paw edema were injected with ant

117 Blockade of NKG2D ameliorated established CIA, with significant reductions in clinical scores and

118 to, all flours, doughs, and breads exhibited CIA.

119 B6.DR1/LAIR-1(+/+) mice were challenged for CIA and mean severity scores were recorded thrice weekly

120 story and CIA index values were compared for CIA-positive, RPR-negative patients according to TP-PA s

121 rmularity with a user-friendly interface for CIA function and newly developed search function Isotopi

122 rin is expressed on synovial Th17 cells from CIA mice and its neutralization with a specific mAb sign

123 tic cells, was important for protection from CIA.

124 daptor that recruits apo-Rli1 to the generic CIA machinery.

125 s the potential utility of the developed HFA CIA for clinical diagnosis.

126 How CIA and FBXL5 collaborate to maintain cellular iron home

127 Abnormalities of the common iliac (CIA), external iliac (EIA), and femoral arteries were cl

128 d a new Boson chemiluminescence immunoassay (CIA) and evaluated its application with cross-sectional

129 um treponemal chemiluminescence immunoassay (CIA) specimens cause clinical uncertainty.

130 t such as the chemiluminescence immunoassay (CIA), followed by testing of CIA-positive (CIA(+)) speci

131 gram sensitive chemiluminescent immunoassay (CIA) was developed for the detection of human fetuin A (

132 BIA], Liaison chemiluminescence immunoassay [CIA], Advia-Centaur CIA, and Trep-Sure EIA) and three ma

133 h treponemal chemiluminescence immunoassays (CIA) identifies patients with discordant serology who ar

134 Impaired CIA activity, as noted by reduced c-acon activity, was a

135 In CIA mice, (99m)Tc-NbV4m119 accumulation in arthritic les

136 Ectopic expression of IL-27 in CIA mice ameliorated inflammation, lining hypertrophy, a

137 une responses and its mechanism of action in CIA pathogenesis.

138 stigate arthritis development in STIA and in CIA under dexamethasone treatment.

139 creased levels of IL-27 relieve arthritis in CIA mouse ankles.

140 fied by enzyme-linked immunosorbent assay in CIA mouse ankles locally expressing adenoviral IL-27 as

141 creased in mice that received the T cells in CIA, and levels of these T cells were increased in the s

142 gulator of inflammatory joint destruction in CIA.

143 phosphatase were significantly diminished in CIA-challenged and even unchallenged fXIIIA(-/-) mice re

144 dosomal TLR signaling, ameliorate disease in CIA, and suppress inflammatory cytokine production in hu

145 Arthritis subsided more efficiently in CIA mice injected with mcTNFR2MSCs than in those injecte

146 hed RANKL positive cells and bone erosion in CIA mice.

147 Furthermore, inhibition of HDAC1 in CIA resulted in reduced joint swelling, cartilage and bo

148 Tc-NbV4m119 visualizes joint inflammation in CIA.

149 mmunoregulatory effects of PAD inhibition in CIA are complex, but primarily mediated by transcription

150 joints and to a reduction of IL-17 levels in CIA mice.

151 cted periarticular and systemic bone loss in CIA mice by maintaining trabecular bone structure.

152 e inflammation-induced systemic bone loss in CIA mice by reducing osteoclast precursors and promoting

153 une and subsequent inflammatory processes in CIA.

154 oration of arthritis involves a reduction in CIA mouse serum and joint levels of IL-17 and results in

155 get molecules were greatly down-regulated in CIA mouse ankles receiving forced expression of IL-27.

156 indicate that SAP plays an essential role in CIA because of Fyn-independent and Fyn-dependent effects

157 d RA patients, whereas knockdown of Snail in CIA joints prevents cartilage invasion and joint damage.

158 It has been also shown that in CIA the concentration of 3-HAA was increased in the kidn

159 ction in RA, we used anti-TLR5 Ab therapy in CIA mice.

160 ibodies showed the same affinity as those in CIA.

161 al studies, flagellin postonset treatment in CIA and local TLR5 ligation in vivo provoke homing and o

162 Vascularization in CIA was determined by immunohistochemical analysis and d

163 differentiation and joint vascularization in CIA.

164 Chicken type II collagen was used to induce CIA in mice, which were then treated with an anti-human

165 y trypsin (TIA) and chymotrypsin inhibitory (CIA) activities were determined in the extracts of wheat

166 The purpose of this study was to investigate CIA using computational analysis.

167 ve on CIA, of which 133 (11.3%) had isolated CIA reactivity.

168 irmed" (CIA(+)/RPR(-)/TP-PA(+)) or "isolated CIA positive" (CIA(+)/RPR(-)/TP-PA(-)).

169 composition and interactions within the late CIA complex.

170 BioPlex MBIA and Liaison CIA had signal strength cutoffs correlating with >/=99%

171 syphilis (57% versus 9%), with higher median CIA index values (9.8 versus 1.6) (all P < .0001).

172 Compared to that in wild-type mice, CIA in Crp-/- mice progressed more rapidly and was more

173 They were mild (CIA and EIA mean severity, 19% +/- 7 and 26% +/- 11, res

174 (against U1), resembling human RA and murine CIA.

175 To identify new CIA proteins we employed systematic protein interaction

176 ively, viperin maturation represents a novel CIA pathway with a minimal requirement of the CIA-target

177 We found that a certain amount of CIA was essential for the model to reproduce reported ef

178 used to noninvasively monitor the course of CIA in mice.

179 s effective in inhibiting the development of CIA in DBA/1 mice.

180 nd that SAP was essential for development of CIA in response to collagen immunization.

181 ombin(WE) also suppressed the development of CIA in wild-type mice.

182 We found evidence of CIA, TPPA, and FTA Abs seroreversion.

183 clinical and histologic erosive features of CIA in mice.

184 before and up to 18 days after induction of CIA by immunization with type II collagen.

185 Furthermore, induction of CIA led to significantly elevated numbers of Iba-1-expre

186 f NK cells from mice before the induction of CIA reduces the severity of subsequent arthritis and alm

187 ion (early) and during development (late) of CIA strongly suppressed clinical and histological signs

188 treatment with flagellin after the onset of CIA exacerbated joint inflammation; in contrast, inflamm

189 hermore, treatment with ASCs at the onset of CIA significantly reduced clinical symptoms and joint pa

190 increased incidence and an earlier onset of CIA that was associated with a more pronounced inflammat

191 can amplify disease severity after onset of CIA.

192 Th17 cell activation in the pathogenesis of CIA, suggesting that its blockade can be beneficial for

193 filament model, which allowed predictions of CIA-dependent muscle behavior.

194 of twitch tension show that the presence of CIA increases peak tension while profoundly delaying rel

195 oval of SAP expression during progression of CIA attenuated disease severity.

196 partially interfered with the progression of CIA.

197 Strategies for reconciliation of CIA and IPA assignments were discussed.

198 This link might contribute to recovery of CIA machinery efficiency to mature cytosolic and nuclear

199 identifies CD73 as an important regulator of CIA in mice.

200 controlling the development and severity of CIA mostly depends on CD39/CD73 signals and partially de

201 The results demonstrated that suppression of CIA by A9 is dependent on T cells.

202 ce immunoassay (CIA), followed by testing of CIA-positive (CIA(+)) specimens with the rapid plasma re

203 und to be upregulated in synovial tissues of CIA mice.

204 erexpressed in synovial cells and tissues of CIA rats and RA patients, whereas knockdown of Snail in

205 Dexamethasone treatment of CIA mice reduced (99m)Tc-NbV4m119 accumulation as compar

206 Treatment of CIA with PLP-LCL significantly suppressed joint swelling

207 in Treg frequencies after IL-33 treatment of CIA.

208 sue inflammation and damage were assessed on CIA up to 47 days following immunization.

209 women considered susceptible to RV based on CIA results tested positive for RV antibodies by IB/Nt.

210 reversed the protective effect of G-MSCs on CIA.

211 261 specimens, 1171 (4.1%) were reactive on CIA, of which 133 (11.3%) had isolated CIA reactivity.

212 mutants defective in either Fe-S cluster or CIA targeting complex binding blocks Fe-S cluster assemb

213 19 revealed that CIA1, but none of the other CIA factors, is predominantly required for (55)Fe/S clus

214 tive serology may represent a false-positive CIA in low-prevalence populations.

215 (CIA), followed by testing of CIA-positive (CIA(+)) specimens with the rapid plasma reagin test (RPR

216 RPR(-)/TP-PA(+)) or "isolated CIA positive" (CIA(+)/RPR(-)/TP-PA(-)).

217 linical species and robust efficacy in a rat CIA model.

218 toff ratio was similar for isolated reactive CIA sera and sera that were reactive on either FTA Abs o

219 20 patients (55%) with an isolated reactive CIA specimen who underwent medical record review had pre

220 Isolated reactive CIA specimens may represent true T. pallidum infection a

221 ts (66 of 82 [80.5%]) with isolated reactive CIA specimens were from high-prevalence populations.

222 a subset of subjects with isolated reactive CIA specimens.

223 y on the CIA were deemed "isolated" reactive CIA samples.

224 Anti-IL-7 Ab treatment significantly reduces CIA monocyte recruitment and osteoclast differentiation

225 linical significance of discordant serology (CIA(+)/RPR(-)) for maternal and neonatal outcomes is unk

226 tected, developing significantly less severe CIA and PIA.

227 viously showed that A9 profoundly suppressed CIA and immune responses to type II collagen.

228 tment with stimulating LAIR-1 Abs suppresses CIA whereas B6.DR1/LAIR-1(-/-) mice develop more severe

229 Our analyses suggest that CIA is present in cardiac muscle under normal conditions

230 The CIA study in DBA/1J mice indicated that compounds led to

231 The CIA, EIA, and femoral lesion classification may help to

232 l iron-sulfur cluster assembly (ISC) and the CIA machineries.

233 idence of a possible direct link between the CIA machinery and the mitoNEET cluster transfer repair p

234 served C-terminal tryptophan for binding the CIA targeting complex, the deca-GX3 motifs in both Yae1

235 is in ApoE(-/-) mice was not affected by the CIA protocol.

236 rize how Fe-S assembly is facilitated by the CIA targeting complex.

237 n which XPD acquires a Fe-S cluster from the CIA targeting complex before assembling into TFIIH.

238 Angiography depicted 28 abnormalities in the CIA (27 stenoses, one dissection), 185 in the EIA (17 th

239 icantly reduced arthritis progression in the CIA and delayed-type hypersensitivity arthritis models.

240 racts with Fe-S apoproteins and MMS19 in the CIA complex but not with the individual proteins.

241 n of osteoclasts, and vascularization in the CIA effector phase.

242 locks the proteolytic capacity of uPA in the CIA model and the delayed-type hypersensitivity arthriti

243 tis and autoimmunity by treating mice in the CIA model with Cl-amidine on days 0-35.

244 In the CIA model, a 2.34-fold increase in E-selectin-targeted s

245 S during the development of arthritis in the CIA model, including in the formation of CII antibodies,

246 In the CIA model, the impact of anti-uPA treatment was on par w

247 In the CIA pathway, CIA1 cooperates with CIA2A, CIA2B, and MMS1

248 Fe/S target protein is unprecedented in the CIA pathway.

249 None of the CIA components downstream of Dre2 was required for RNR c

250 Fe-S cluster, or along with knockdown of the CIA factors NUBP2 or FAM96A, reduced cell viability.

251 rming that MMS19 is a central protein of the CIA machinery that brings Fe-S cluster donor proteins an

252 An important limitation of the CIA model is that the CII response and the disease are s

253 ins Yae1 and Lto1 as binding partners of the CIA targeting complex.

254 IA pathway with a minimal requirement of the CIA-targeting factors and represents a new paradigm for

255 hrough ubiquitination and degradation of the CIA-targeting protein MMS19.

256 ly depends on ISC machineries and not on the CIA or CIAPIN1.

257 Samples reactive only on the CIA were deemed "isolated" reactive CIA samples.

258 y exclusive fashion with either TFIIH or the CIA targeting complex.

259 GE-F1-NSE1 E3 ubiquitin ligase regulates the CIA pathway through ubiquitination and degradation of th

260 However, the mechanisms regulating the CIA pathway are unknown.

261 Thus, flux through the CIA pathway can be regulated by degradation of the subst

262 cytosolic monothiol GRXs associate with the CIA complex, as in other eukaryotes, and contribute to,

263 ndicate that the association of XPD with the CIA targeting complex occurs in the cytoplasm, whereas i

264 At the same time, CIA had minimal effect on the rate of force redevelopmen

265 ve, TP-PA--negative patients seroreverted to CIA-negative.

266 Susceptibility to CIA, a disease that resembles RA in humans, was compared

267 t mice are significantly more susceptible to CIA than wild-type mice.

268 one erosion as compared with control-treated CIA mice.

269 Of 21,623 assays, 439 (2%) were CIA-positive and 255/439 (58%) were RPR-negative; subseq

270 ere CIA(+)/RPR(-)/TP-PA(-) and 38 (20%) were CIA(+)/RPR(-)/TP-PA(+).

271 Of 194 pregnant women, 156 (80%) were CIA(+)/RPR(-)/TP-PA(-) and 38 (20%) were CIA(+)/RPR(-)/T

272 pregnant women with discordant serology were CIA(+)/RPR(-)/TP-PA(-); more than half who were retested

273 yphilis during pregnancy than women who were CIA(+)/RPR(-)/TP-PA(-) (all P < .005).

274 However, it had no effect on disease when CIA was clinically established.

275 horylation of IRP1 at Ser-138 increased when CIA was inhibited and was required for iron rescue.

276 importance of FBXL5 for regulating IRP1 when CIA is impaired.

277 ed more rapidly and was more severe, whereas CIA in CRP-Tg mice was dramatically attenuated.

278 While CIA assigns elemental formulas for compounds containing

279 ed joints of WT, but not CRIg(-/-) mice with CIA and STIA.

280 s indicate that ES-62 treatment of mice with CIA leads to unique multisite manipulation of the initia

281 Infusion of G-MSCs in DBA/1J mice with CIA significantly reduced the severity of arthritis, dec

282 Mice with CIA were treated with the TLR-5 agonist flagellin to doc

283 In the knees of mice with CIA, (99m)Tc-NbV4m119 was found to accumulate even befor

284 Moreover, in the livers from mice with CIA, concentration of tryptophan and kynurenine was decr

285 In mice with CIA, early intervention with APO866 inhibited synovial i

286 In mice with CIA, META060 significantly reduced the arthritis index a

287 In mice with CIA, MMR expression was detected on cells from the bone

288 human/mouse DR5-transgenic Ubc.Cre mice with CIA, transgenic DR5 was most highly expressed on CD11b+

289 s further examined using APO866 in mice with CIA, with effects on disease activity assessed using rad

290 obtained from various organs from mice with CIA.

291 o down-regulate IL-17 responses in mice with CIA.

292 ryptophan, kynurenine and 3-HAA in mice with CIA.

293 analysis of joint inflammation in mice with CIA.

294 an early and beneficial effect in mice with CIA.

295 njection of TNFalpha as well as in mice with CIA.

296 FAP antibody 28H1 was performed in mice with CIA.

297 From August 2007-October 2007, patients with CIA-positive, RPR-negative serology were tested with the

298 helped guide the management of patients with CIA-positive, RPR-negative serology.

299 Rats with CIA developed significant mechanical hypersensitivity, w

300 and spinal microglial response in rats with CIA.