ライフサイエンスコーパス: arthritic

1 investigated its anti-inflammatory and anti-arthritic activities in experimentally-induced RA.

2 demonstrated that MMPP exhibited potent anti-arthritic activity in a collagen antibody-induced arthri

3 Our study highlights the anti-arthritic activity of Celastrus-derived celastrol and th

4 strol derived from Celastrus has potent anti-arthritic activity.

5 xic natural plant products that possess anti-arthritic activity.

6 The fluorescence signal intensities of arthritic and normal joints were compared for significan

7 ked a larger inward current in neurones from arthritic animals than in control neurones, indicating a

8 In arthritic animals treated with MTX (35 mg of MTX/kg 48 h

9 cule inhibitor of IKK-2, was administered to arthritic animals, and disease activity was monitored.

10 ocessing of C-nociceptor inputs in naive and arthritic animals, but gains in effects on spinal A-noci

11 ptic component was recorded in neurones from arthritic animals, but not in control neurones, and was

12 70%) was observed as compared with untreated arthritic animals.

13 cision-making deficits and pain behaviors of arthritic animals.

14 nses to A-nociceptor activation, but only in arthritic animals.

15 isease revealed enhanced (18)F-FLT uptake in arthritic ankles (2.2 +/- 0.2 percentage injected dose p

16 -(18)F-fluorothymidine ((18)F-FLT) uptake in arthritic ankles and carcinomas between dynamic and stat

17 d cell proliferation and (18)F-FLT uptake in arthritic ankles and CT26 colon carcinomas.

18 Ki-67 immunohistochemical staining of the arthritic ankles and forepaws revealed a strong correlat

19 tly reduced (18)F-FLT uptake was measured in arthritic ankles and in CT26 colon carcinomas when the m

20 The prostanoid content of arthritic ankles was assessed in ankle homogenates, and

21 f measuring hypoxia noninvasively in vivo in arthritic ankles with PET/MRI using the hypoxia tracers

22 pimonidazole and expression of HIF-1alpha in arthritic ankles.

23 tely 60% of patients experience intermittent arthritic attacks, a condition that in some individuals

24 (-/-) mice were similar to those observed in arthritic B6 WT control mice.

25 ls directly correlated with the intensity of arthritic bone erosion, suggesting relevance in patholog

26 of arthritis was characterized by increased arthritic bone erosion, whereas cartilage damage remaine

27 ppressed inflammatory osteoclastogenesis and arthritic bone resorption.

28 d disease and suggesting a new genus of anti-arthritic bone-sparing therapeutics.

29 ad to the development of a new genus of anti-arthritic bone-sparing therapeutics.

30 In the PAG of arthritic, but not naive, rats, there is enhanced contro

31 FN-responsive genes was observed in severely arthritic C3H mice at 1 wk of infection, which was absen

32 Severely arthritic C3H mice possessed a naturally occurring hypom

33 remarkable due to its absence in the mildly arthritic C57BL/6 (B6) mice.

34 ment, as it was absent from infected, mildly arthritic C57BL/6 mice.

35 k of infection, which was absent from mildly arthritic C57BL/6 mice.

36 cent findings showed increased cell death in arthritic cartilage and linkage with extracellular matri

37 YKL-40 is expressed in arthritic cartilage and produced in large amounts by cul

38 s synovial fibroblasts (RASFs) contribute to arthritic cartilage degradation.

39 anti-ROS-modified CII scFv bound to damaged arthritic cartilage from patients with RA and OA but not

40 ity of anti-ROS-modified CII scFv to damaged arthritic cartilage was assessed in vitro by immunostain

41 ls and the expression of angiogenic genes in arthritic cells.

42 showed that VEGF-transduced MDSCs caused an arthritic change in the knee joint, and sFlt-1 improved

43 l changes were evaluated in conjunction with arthritic changes in the TMJ, assessed by histopathologi

44 on of splenic CXCR2(+) neutrophils in chGRKO arthritic compared to WT arthritic mice.

45 ach endocrine disorder may also have its own arthritic complaints, which can present as a definitive

46 lage injury may prevent serious and lifelong arthritic complications, early detection and treatment i

47 Osteoarthritis (OA), the most common arthritic condition in humans, is characterized by the p

48 rus affecting humans, resulting in a chronic arthritic condition that can persist for months or years

49 To date, there are at least 10 arthritic conditions for which specific genetic mutation

50 Under arthritic conditions, CD25(lo)Foxp3(+)CD4(+) T cells los

51 heumatoid arthritis and related inflammatory arthritic conditions.

52 sive fibroblast-like synoviocytes (FLS) from arthritic DA rats and from patients with rheumatoid arth

53 Clinical signs of disease were monitored in arthritic DBA/1 mice after therapeutic administration of

54 erging alphavirus that causes a debilitating arthritic disease and infects millions of people and for

55 Supporting this hypothesis, arthritic disease driven by exuberant TNF-alpha expressi

56 reasons) may also be at risk of exacerbated arthritic disease following alphaviral infection.

57 a significant cause of both encephalitic and arthritic disease in humans worldwide.

58 ing pain and restoring mobility in end-stage arthritic disease in the short-term.

59 uses, the pathogenesis of alphavirus-induced arthritic disease is not well understood.

60 Arthritic disease is usually characterized by high level

61 rther insights into the cause of this common arthritic disease over the next few months.

62 only marginal changes in antiviral immunity, arthritic disease was substantially increased and prolon

63 fact that Sucnr1(-/-) mice developed reduced arthritic disease, using two different in vivo models, i

64 hly novel link between epigenetic status and arthritic disease.

65 ce the burden of severe atypical and chronic arthritic disease.

66 es potential targets for future treatment of arthritic disease.

67 f healthy joints and pathogenic processes in arthritic disease.

68 icipate in the initiation and progression of arthritic disease.

69 opulation with different causes of end-stage arthritic disease.

70 TS protein family, is critically involved in arthritic diseases because of its direct role in cleavin

71 Excessive bone loss in arthritic diseases is mostly due to abnormal activation

72 loss of extracellular matrix due to chronic arthritic diseases such as osteoarthritis (OA).

73 idely recommended conservative treatment for arthritic diseases.

74 ts for developing therapeutic strategies for arthritic disorders and for culturing artificial cartila

75 d sensory, gastrointestinal, skin, limb, and arthritic disorders by self-reported impairment.

76 nd for developing therapeutic strategies for arthritic disorders.

77 insights for developing strategies to treat arthritic disorders.

78 inflammation are the targets of several anti-arthritic drugs.

79 We investigated the anti-arthritic effect of engineered MSCs in a collagen-induce

80 In arthritic effusions, however, HA concentration and osmot

81 can fall below C* (approximately 1 mg/ml) in arthritic effusions, promoting loss of HA.

82 eal lymph node (PLN) enlarges during the pre-arthritic 'expanding' phase, and then 'collapses' with a

83 ith decreased drainage from the joint during arthritic flare, and validate these biomarkers of RA pro

84 with the increased synovial fluids found in arthritic flares but was not found in the synovial fluid

85 We thus propose that arthritic FLS are mesenchymal stem cells whose different

86 models of rheumatoid arthritis, we show that arthritic FLS contain a substantial (>30%) fraction of b

87 osteogenic and adipogenic differentiation of arthritic FLS.

88 rotein, reacted with aurothiomalate, an anti-arthritic gold compound.

89 We injected arthritic, healthy, and CT26 colon carcinoma-bearing mic

90 to relieve pain and restore function to the arthritic hip joint.

91 This myeloid skewing was cell intrinsic, as arthritic HSPPCs up-regulate myeloid-specific transcript

92 s gene in the myeloid priming that occurs in arthritic HSPPCs.

93 e monocyte/macrophage-dominated inflammatory arthritic infiltrates seen after infection with arthrito

94 nous IFN-gamma/IL-27 successfully controlled arthritic inflammation and inhibited the defined mediato

95 Using an experimental model of arthritic inflammation, we demonstrate that the temporal

96 f IL-33-treated basophils suppressed induced arthritic inflammation.

97 matrix) have the potential to contribute to arthritic inflammation.

98 ck, cardiovascular disease, acute pelvic and arthritic inflammatory diseases, and various infections.

99 mpathetic nerve fibers occurs in the painful arthritic joint and may be involved in the generation an

100 selectively recruited and/or retained in the arthritic joint and may be playing a significant role in

101 Analysis of the different stages of arthritic joint disease revealed enhanced (18)F-FLT upta

102 ovial inflammation and tissue destruction in arthritic joint disease.

103 yptase association could also be detected in arthritic joint extracts by co-immunoprecipitation.

104 TCR-BV8 and BV14 T cells that migrate to the arthritic joint generally made up a single CDR3 length.

105 promising tool to investigate the extent of arthritic joint inflammation.

106 These findings demonstrate that the arthritic joint matrix is a major source of FSTL-1 and t

107 , but the inflammatory environment within an arthritic joint may also inhibit chondrogenesis and indu

108 ctions in monocyte and T cell recruitment to arthritic joint tissue compared to that observed in WT m

109 TSG-6 was present in arthritic joint tissue extracts together with the heavy

110 stable metabolite of PGI2) were detected in arthritic joint tissues, correlating strongly with the i

111 sion behavior in the synovial vessels of the arthritic joint upon administration of a compound that a

112 and appear to preferentially migrate to the arthritic joint, indicating a potential direct role of C

113 therapeutics can be targeted specifically to arthritic joints and suggest a new approach for the deve

114 ng confirmed marked synovial inflammation of arthritic joints and the absence of inflammation in cont

115 mammalian cells derived from blood vessels, arthritic joints and the immune and central nervous syst

116 nt and oxygenation between the unequivocally arthritic joints and the normal joints.

117 ne green, long-term enhanced fluorescence of arthritic joints can be achieved.

118 icant increase in the fluorescence signal of arthritic joints compared with baseline values (P < 0.05

119 Histologic analysis of arthritic joints from anti-NKG2D-treated mice demonstrat

120 Histologic assessment of arthritic joints from OPN-deficient mice revealed synovi

121 ritis, however, histological analysis of the arthritic joints from WT and IL-17-/- mice revealed a si

122 ntly, we found that CXCL14 is upregulated in arthritic joints in a mouse model of autoimmune arthriti

123 probes from synovial lesions within affected arthritic joints in an attempt to recapitulate disease-r

124 ase (JAK) signaling and structural damage to arthritic joints in rheumatoid arthritis (RA) is poorly

125 neutrophils were preferentially recruited to arthritic joints in the presence of CXCR2-deficient neut

126 The SPMs present in self-resolving arthritic joints include the D-series Rvs, for example,

127 Elevated coefficients of friction in arthritic joints occur concurrently with enhanced proteo

128 tent with this, neutrophils in the blood and arthritic joints of anti-G-CSF receptor-treated mice sho

129 the locus were significantly dysregulated in arthritic joints of congenic mice; expression of these g

130 pecific T cell response in the periphery and arthritic joints of DR1 transgenic mice.

131 Extensive destruction was observed in the arthritic joints of IL-4 (-/-) mice, with a correspondin

132 nrichment of CXCR2-expressing neutrophils in arthritic joints of mice with mixed CXCR2(+/+) and CXCR2

133 man mu-opioid receptor (HuMOR) expression in arthritic joints of mice, using the feline immunodeficie

134 Serial MRI scans of hMSC transplants in arthritic joints of recipient rats showed that the iron

135 rheumatoid human synovium and from normal or arthritic joints of wild-type and cytokine gene-deficien

136 tilage-derived aggrecan proteoglycans in the arthritic joints of wild-type B6 mice but not mMCP-6-nul

137 neutrophil recruitment, synovial fluid from arthritic joints showed a comparable proportion of Gr1+

138 The arthritic joints showed synovial hyperplasia and erosion

139 alpha are the two major cytokines present in arthritic joints that modulate the expression of many ge

140 r of pro-inflammatory Th17 cells in inflamed arthritic joints through TRAIL-induced apoptosis while i

141 ific T cell response in lymph nodes draining arthritic joints toward the Th17 phenotype without affec

142 ectly demonstrate that NF-kappaB activity in arthritic joints was reduced after ML120B administration

143 The fluorescence signal of arthritic joints was significantly higher compared with

144 ntibody (111)In-28H1 specifically visualized arthritic joints with high resolution, and tracer accumu

145 althy joints (healthy joints, 1.25 +/- 0.59; arthritic joints, 3.13 +/- 1.03; P < .001).

146 cally normal asymptomatic joints adjacent to arthritic joints, and 18 normal controls.

147 ses osteoclast-mediated structural damage to arthritic joints, and this effect is secondary to decrea

148 In synovial fluid of arthritic joints, MMR was expressed on CD11b(+)F4/80(+)

149 Because of the high expression of FAP in arthritic joints, radioimmunoimaging of activated fibrob

150 fy molecular targets of the Igs deposited in arthritic joints, which may activate local inflammation,

151 rexpressed by fibroblastlike synoviocytes in arthritic joints.

152 butes to vascularization of solid tumors and arthritic joints.

153 tant role in the destruction of cartilage in arthritic joints.

154 myloid plaques, atherosclerotic lesions, and arthritic joints.

155 , and specificity of T cells that infiltrate arthritic joints.

156 restricted to lymph nodes draining inflamed, arthritic joints.

157 uppressed IFN-gamma and CXCL10 production in arthritic joints.

158 murine synovial MC population in normal and arthritic joints.

159 dhere tightly to the synovial endothelium in arthritic joints.

160 4(+)/tetramer(+) T cells were present in the arthritic joints.

161 indicating specific uptake of all tracers in arthritic joints.

162 promising tool for cartilage regeneration in arthritic joints.

163 thus maintaining a state of inflammation in arthritic joints.

164 FMT was used to detect synovitis in all arthritic joints.

165 ge degeneration and the induction of pain in arthritic joints.

166 ility to track inflammatory cells in vivo in arthritic joints.

167 n of lymphatic draining and cell egress from arthritic joints.

168 Arthritic K/BxN mice were treated with B cell depletion

169 ritis was induced by injection of serum from arthritic K/BxN mice.

170 and sympathetic nerve fibers in the painful arthritic knee joint and whether nerve growth factor (NG

171 A painful arthritic knee joint was produced by injection of Freund

172 e evaluated by histopathological analysis of arthritic knee joints and immunostaining of aggrecan neo

173 the Enabling Self-Management and Coping with Arthritic Knee Pain through Exercise (ESCAPE-knee pain)

174 es (Enabling Self-management and Coping with Arthritic Knee Pain through Exercise [ESCAPE-knee pain])

175 as performed during 3 different pain states: arthritic knee pain, experimental knee pain, and pain-fr

176 owever, transfer of spleen cells from mildly arthritic KO donors to SCID hosts resulted in developmen

177 SPECT (SPECT/CT) was used to image arthritic lesions in the inflamed paws of 29 mice using

178 n CIA mice, (99m)Tc-NbV4m119 accumulation in arthritic lesions increased according to the severity of

179 Arthritic Lewis rats in the late phase of AA show divers

180 fter immunization, and identification of the arthritic limbs is not difficult.

181 In contrast, arthritic macrophages expressed many IFNgamma-inducible

182 , and the strength of induction was lower in arthritic macrophages for most genes.

183 The residual response of arthritic macrophages to IL-10 stimulation was qualitati

184 The number of genes induced by IL-10 in arthritic macrophages was markedly smaller than that ind

185 ms to be a link in humans between persistent arthritic manifestations post-antibiotic treatment and t

186 Cs decreases the proportion of Th17 cells in arthritic mice and simultaneously reduces the severity a

187 nd B, both of which were highly expressed in arthritic mice and treatment-naive RA patients, were sel

188 ter was detected in the cartilage tissues of arthritic mice as well as human osteoarthritic patients.

189 The lymph nodes of arthritic mice contain elevated numbers of inflammatory

190 hritis induction, and the cartilage of these arthritic mice contained deposits of C3.

191 Spleen myeloid cells from arthritic mice did not have suppressive effects.

192 ed FoxP3gfp mice with K/BxN mice to generate arthritic mice in which Treg cells express green fluores

193 Blockade of this pathway in arthritic mice reduced inflammation and restored tissue

194 o transfection of siRNA into joint tissue in arthritic mice to achieve local RNA interference.

195 erest, adoptive transfer of nTregs even from arthritic mice treated with atRA suppressed progression

196 In lymph node cells from the arthritic mice treated with BB-Cl-amidine, there was a d

197 lls isolated from spleens and lymph nodes of arthritic mice treated with CM-MSC or MSCs.

198 Finally, CD4+ T cells from arthritic mice treated with CM-MSC showed increases in F

199 stic analysis of CXCR2 involved treatment of arthritic mice with a CXCR2 antagonist, bone marrow (BM)

200 Treatment of arthritic mice with type II collagen-pulsed tolerogenic

201 of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotina

202 Fc, it significantly reduced inflammation in arthritic mice, as compared with the effects of mTNFRII-

203 PA-Her, when administered therapeutically to arthritic mice, controlled clinical and histologic signs

204 Therefore, our results indicate that in arthritic mice, HSPPCs adopt a pathologic state that fav

205 ontrol IL-6 production in spleen cultures of arthritic mice, providing an important link to the mecha

206 When systemically administered to arthritic mice, the anti-ROS-modified CII accumulated se

207 Upon intravenous injection into arthritic mice, tolerogenic DCs migrated to the spleen,

208 lls and extended this finding to the paws of arthritic mice.

209 ovial membrane tissue and in paw tissue from arthritic mice.

210 dation was up-regulated in chGRKO but not WT arthritic mice.

211 rine protease is abundant in the synovium of arthritic mice.

212 cells proliferated in both nonarthritic and arthritic mice.

213 was expressed in spleen and joint tissues of arthritic mice.

214 nover and bone mass remained unchanged in tg arthritic mice.

215 tracts of cells retrieved from the joints of arthritic mice.

216 ould be monitored by radionuclide imaging in arthritic mice.

217 antibody) was used to deplete Treg cells in arthritic mice.

218 utrophils in chGRKO arthritic compared to WT arthritic mice.

219 increased levels of CD4+CD39+FoxP3+ cells in arthritic mice.

220 et, and attenuated inflammatory reactions in arthritic mice.

221 l was seen in the knees, ankles, and toes of arthritic mice.

222 n of the up-regulated enzymes was studied in arthritic mice.

223 ccumulating in joint-draining lymph nodes of arthritic mice.

224 Joint damage was minimal in arthritic MKK-6(-/-) mice and intermediate in MKK-3(-/-)

225 els were modestly decreased in the joints of arthritic MKK6(-/-) mice compared with WT but were signi

226 ogenic role has been characterized in animal arthritic models.

227 e-stimulated fibroblasts from rheumatoid and arthritic mouse joints expressed higher levels of RANKL

228 ptom, the efficacy of an anti-G-CSFR mAb for arthritic pain and disease was compared with that of a n

229 ectly the brain areas involved in processing arthritic pain and experimental pain in a group of patie

230 supporting a population with high levels of arthritic pain and lack of health insurance.

231 activity, but at the cost of not controlling arthritic pain as effectively.

232 Inflammatory pain such as arthritic pain is typically treated with opioids and cyc

233 in conditions activated the pain matrix, but arthritic pain was associated with increased activity in

234 and mechanisms in the amygdala in a model of arthritic pain.

235 incomplete picture of brain activity during arthritic pain.

236 cellular and molecular levels in a model of arthritic pain.

237 nvolved in the generation and maintenance of arthritic pain.

238 dies may identify factors that contribute to arthritic pathology.

239 blood osteoclast precursor (OCP) numbers in arthritic patients and animals, which are reduced by ant

240 n was first described in synovial fluid from arthritic patients and later described as a structural a

241 s algorithm efficiently revealed subtypes of arthritic patients based on EV heterogeneity patterns.

242 Synovial macrophages collected from arthritic patients were found to bind and internalize fo

243 side neutrophils isolated from the joints of arthritic patients, and are found in neutrophils only in

244 shown to image inflamed joints of rheumatoid arthritic patients.

245 matrix protein (COMP) have been observed in arthritic patients.

246 on natural killer (NK) and CD4+ T cells, in arthritic paw cell isolates.

247 visible inspection (clinical index of 3 for arthritic paws and 0 for control paws) and histologic ex

248 gic examination (histologic score of 3-5 for arthritic paws and 0 for control paws).

249 terleukin-17 production from CD4+ T cells in arthritic paws and splenic NK cell cytotoxic effector fu

250 Additionally, analysis of the synovium from arthritic paws indicated that the same CD4(+)/BV8(+)/BV1

251 NKG2D expression in arthritic paws was demonstrated by immunohistochemistry.

252 nstrated that NF-kappaB activity in inflamed arthritic paws was inhibited by ML120B, resulting in sig

253 ences in metabolites between the control and arthritic paws.

254 induce autoantibodies in lung during the pre-arthritic phase, and SFB-dependent lung pathology requir

255 hogenicity studies associated lp28-1 with an arthritic phenotype and further studies may identify fac

256 -infected CD28(-/-)MHCII(-/-) mice, remained arthritic post-antibiotic treatment.

257 p a novel BHPH derivative with improved anti-arthritic properties and drug-likeness.

258 ecule with potent anti-inflammatory and anti-arthritic properties, mediated through the inhibition of

259 Six arthritic proximal interphalangeal (PIP) joints in six p

260 ot of total NR1, were measured in the CeA of arthritic rats compared to controls.

261 es in splenic regions distal to the hilus in arthritic rats compared with nonarthritic rats.

262 of the amygdala (CeLC) in brain slices from arthritic rats compared with normal controls.

263 However, arthritic rats exhibited a significantly higher CPP scor

264 d that secondary hindpaw hypersensitivity in arthritic rats results from spinal sensitization to peri

265 d synaptic facilitation in brain slices from arthritic rats through a postsynaptic mechanism.

266 The treatment of arthritic rats with celastrus/celastrol suppressed infla

267 Intriguingly, the treatment of arthritic rats with one such peptide resulted in efficie

268 In arthritic rats, blockade of vlPAG EP3R raised EMG thresh

269 In the gingival tissue of the untreated arthritic rats, gelatinase, collagenase, TNF-alpha, and

270 exes) and supraspinal pain behavior of awake arthritic rats, including affective responses such as ul

271 atory drug ibuprofen increased CPP scores in arthritic rats, suggesting that analgesia itself had a r

272 creased significantly (P <0.05) in untreated arthritic rats.

273 ) in brain slices from control rats and from arthritic rats.

274 ollagen type II), and studied its effects on arthritic rats.

275 -17)-driven inflammation are involved in the arthritic response to Borrelia burgdorferi infection.

276 r tryptase/heparin complexes have attenuated arthritic responses, with mMCP-6 as the dominant tryptas

277 nanoparticles without drugs exhibited a mean arthritic score of 9.0 +/- 0.3 and mean change in ankle

278 oup that received no treatment showed a mean arthritic score of 9.8 +/- 0.5 and mean change in ankle

279 Transfer of arthritic serum alone induced only mild and transient ar

280 This study shows that activated arthritic SFs from human patients and animal models expr

281 vivo imaging revealed more ROS in joints of arthritic SKG mice compared to wild-type mice, which lin

282 ion resulting in clustering of cells seen in arthritic states.

283 CD200R was found to be expressed in arthritic synovia and in lymph nodes, yet no changes in

284 etermined by histomorphometry in healthy and arthritic synovia.

285 Arthritic synovial fluid (SF) contains mesenchymal stem

286 in healthy and K/BxN serum transfer-induced arthritic synovial tissue was defined using immunohistoc

287 Whereas TSG-6 was broadly detectable in arthritic synovial tissue, the highest level of TSG-6 wa

288 ast cell (CTMC) phenotype in both normal and arthritic synovial tissue, which expresses mMCP-4, -5, -

289 ulature in SCID mice transplanted with human arthritic synovial xenografts.

290 e expressed in the microvasculature of human arthritic synovium and that has the potential to be deve

291 of lymphocyte-independent CTMCs and identify arthritic synovium as a model system by which to gain in

292 The arthritic synovium showed expression of uPA and uPAR in

293 pecificity for the microvasculature of human arthritic synovium.

294 es specific to the microvasculature of human arthritic synovium.

295 In addition, MC hyperplasia was seen in the arthritic synovium.

296 factor in arthritis and can be found in the arthritic temporomandibular joint (TMJ).

297 clinically applicable tool for detection of arthritic tissue.

298 ced the nociceptive response of rats with an arthritic TMJ and reduced the amount of the proinflammat

299 (+) IL-17(+) cells in the lymph node between arthritic wild-type and NOD2(-/-) mice.

300 ferred to SCID mice, using spleen cells from arthritic WT and CCR5(-/-) mice.