ライフサイエンスコーパス: joint inflammation

1 en Toll-like receptor 2 (TLR-2) and NOD-2 in joint inflammation.

2 ents with OA or patients with periprosthetic joint inflammation.

3 ntrast, inhibited both lymphangiogenesis and joint inflammation.

4 ted T lymphocytes sustain tissue-destructive joint inflammation.

5 A depend on neutrophils for the induction of joint inflammation.

6 cytokines, and MMPs, which may contribute to joint inflammation.

7 ting a potential role in the pathogenesis of joint inflammation.

8 tihyperalgesia produced by TENS in rats with joint inflammation.

9 dentified PAR-2 as a key mediator of chronic joint inflammation.

10 the spinal cord in animals with and without joint inflammation.

11 ed the highly variable nature of TNF-induced joint inflammation.

12 ith a mouse model of spontaneous, autoimmune joint inflammation.

13 at in some individuals progresses to chronic joint inflammation.

14 unity against mouse cartilage PG and chronic joint inflammation.

15 kine IL-10 to profoundly attenuate localized joint inflammation.

16 novial fibroblasts, enabling amelioration of joint inflammation.

17 al target for treatment of acute and chronic joint inflammation.

18 ES as a preventative reduced the severity of joint inflammation.

19 cking B1R results in significantly increased joint inflammation.

20 nduce Ets-1 and HIF-1alpha expression during joint inflammation.

21 eukin-1 (IL-1) may dominate the drive toward joint inflammation.

22 isms and bypass the need for IL-1 in chronic joint inflammation.

23 ll predominance correlated with the level of joint inflammation.

24 beta4 and Valpha1 segments, failed to induce joint inflammation.

25 in a model of collagen-induced arthritis and joint inflammation.

26 s distinctly protective in colitis and ankle joint inflammation.

27 velopment of serum anti-GPI autoantibody and joint inflammation.

28 with a potential role in the perpetuation of joint inflammation.

29 a direct contribution of type 2 response to joint inflammation.

30 rrow and spleen before the onset of systemic joint inflammation.

31 erimentally induced autoimmunity and chronic joint inflammation.

32 the role of P-selectin in the development of joint inflammation.

33 hypernociception without obvious concurrent joint inflammation.

34 ng its utility for assessing the severity of joint inflammation.

35 T-cell responses leads to an exacerbation of joint inflammation.

36 eam walk test, and microscopic assessment of joint inflammation.

37 may play a role in cartilage remodeling and joint inflammation.

38 is known about the role of the SF glycome in joint inflammation.

39 redisposed mice not only to skin but also to joint inflammation.

40 epidermally triggered lymphocytes in driving joint inflammation.

41 (RA), an autoimmune disease characterized by joint inflammation.

42 sensory neurons without measurably altering joint inflammation.

43 tected from the development of allodynia and joint inflammation.

44 ompanied by enhanced psoriasis-like skin and joint inflammation.

45 e of glycosylation in stromal immunology and joint inflammation.

46 A) is an autoimmune disease characterized by joint inflammation.

47 MRL/Mp-lpr/lpr, and extended to alleviating joint inflammation.

48 eund's complete adjuvant were used to induce joint inflammation.

49 nhibitor SzV-1287 in chronic mouse models of joint inflammation.

50 n state that evolves secondary to persistent joint inflammation.

51 not significantly up-regulate RvTs or reduce joint inflammation.

52 rsistent immune responses that cause chronic joint inflammation.

53 pared to wild-type mice, which links ROS and joint inflammation.

54 t with FGF-2 and FGF-8 was found to suppress joint inflammation.

55 el, JNJ-54271074 dose-dependently suppressed joint inflammation.

56 opulation and is characterized by widespread joint inflammation.

57 tool to investigate the extent of arthritic joint inflammation.

58 ng the systemic immune response required for joint inflammation.

59 interaction for osteoclast formation during joint inflammation.

60 RA begin long before the onset of detectable joint inflammation.

61 ber of ACPAs may be associated with signs of joint inflammation.

62 ry Th1 responses in the development of CHIKV joint inflammation.

63 nd systemic host immune responses and elicit joint inflammation.

64 rochetes, bba57 mutants are unable to induce joint inflammation.

65 ry of autoantibodies and may thereby promote joint inflammation.

66 secreting cells, inflammatory cytokines, and joint inflammation.

67 m to limit the degree of bone erosion during joint inflammation.

68 ein reduces the clinical signs of autoimmune joint inflammation.

69 al injury and bone erosion during autoimmune joint inflammation.

70 evelopment of arthritis at the peak of acute joint inflammation (14 d) and in the resolution phase (6

71 analyzed IL-8 levels, leukocyte influx, and joint inflammation 24 hours later.

72 Th2 cytokine therapy at the time of maximum joint inflammation also suppressed symptoms of disease.

73 nd IL-13 protect mice from antibody-mediated joint inflammation, although the mechanism is not unders

74 id arthritis is characterized by progressive joint inflammation and affects ~1% of the human populati

75 ss tenascin-C show rapid resolution of acute joint inflammation and are protected from erosive arthri

76 escence, affording a distinct way to control joint inflammation and arthritis.

77 induced arthritis protected mice from severe joint inflammation and bone destruction.

78 Conversely, CIA joint inflammation and bone erosion are alleviated when

79 y of purified recombinant rat SLPI inhibited joint inflammation and cartilage and bone destruction.

80 Chondrocalcinosis, which can promote joint inflammation and cartilage degeneration, is highly

81 in synovium and articular cartilage initiate joint inflammation and cartilage degradation in large pa

82 e most common joint disease characterized by joint inflammation and cartilage deterioration.

83 matoid arthritis, the contribution of MCs to joint inflammation and cartilage loss remains poorly und

84 et their collective impact on injury-induced joint inflammation and catabolism is poorly understood.

85 report demonstrating effective prevention of joint inflammation and clinical signs of CIA with an I-A

86 ibition on both RASF phenotype in vitro, and joint inflammation and damage in the collagen-induced ar

87 hysical activity in smokers) which may limit joint inflammation and damage.

88 is a chronic autoimmune disorder that causes joint inflammation and damage.

89 cal disability, in addition to the burden of joint inflammation and damage.

90 rticoid signaling in chondrocytes attenuates joint inflammation and damage.

91 new framework to understand T(reg) cells in joint inflammation and define potential strategies for T

92 Monocytes are the key regulators of joint inflammation and destruction in rheumatoid arthrit

93 prototypical autoimmune disease that causes joint inflammation and destruction(1).

94 ssion of NF-kappaB-regulated genes mediating joint inflammation and destruction, including chemokines

95 switched pathogenic Abs and the evolution of joint inflammation and destruction.

96 ly blocked the LPS-triggered acceleration of joint inflammation and destruction.

97 st glucose-6-phosphate isomerase, leading to joint inflammation and destruction.

98 c inflammatory arthritis results in rhythmic joint inflammation and drives major changes in muscle an

99 ould lead to a better understanding of gouty joint inflammation and help improve the treatment and ca

100 Splenectomy dramatically decreased chronic joint inflammation and histopathologic damage as well as

101 t of swelling but required for resolution of joint inflammation and infection.

102 , IL-6, and IL-8, gene products important in joint inflammation and joint destruction.

103 Joint inflammation and metabolism were evaluated by mult

104 -control studies including participants with joint inflammation and no previous definitive gout diagn

105 -control studies including participants with joint inflammation and no previous definitive gout diagn

106 ay provide insights into the pathogenesis of joint inflammation and noninvasive monitoring of disease

107 Dex, resulting in sustained amelioration of joint inflammation and pain in rodent models of inflamma

108 leted of essential oils profoundly inhibited joint inflammation and periarticular joint destruction i

109 lds promise for control of temporomandibular joint inflammation and prevention of associated morbidit

110 gnaling in osteoblasts significantly reduces joint inflammation and prevents structural bone and cart

111 rce of naive macrophages capable of reducing joint inflammation and producing molecules essential for

112 a critical role for CD44 in the pathology of joint inflammation and reveals a unique mechanism of rec

113 wide in the past decade, causes debilitating joint inflammation and severe pain.

114 s important for the prevention of persistent joint inflammation and spirochete clearance, and they co

115 and Sl/Sld, were resistant to development of joint inflammation and that susceptibility was restored

116 induced arthritis model markedly accentuated joint inflammation and tissue damage.

117 DEK is thus key to joint inflammation, and anti-DEK aptamers hold promise f

118 tein in the context of cartilage protection, joint inflammation, and associated pain behavior.

119 bone destruction, shows evidence of reducing joint inflammation, and may be mediated by high local le

120 to ameliorate arthritis in animal models of joint inflammation, and preliminary studies have suggest

121 side of the MCP joints in early RA, and that joint inflammation appears to drive the inherent tendenc

122 result from inflammation, arthritis pain and joint inflammation are at least partially uncoupled.

123 The mechanisms by which aberrant NOD2 causes joint inflammation are poorly understood.

124 but rather improves only certain aspects of joint inflammation as assessed histologically.

125 matoid arthritis, which are characterized by joint inflammation as well as periarticular and systemic

126 ignalling, are involved in the regulation of joint inflammation as well as systemic fuel metabolism.

127 phenotype is defined by the lack of ongoing joint inflammation, as confirmed through clinical assess

128 neutralizing antibodies to gp96 ameliorated joint inflammation, as determined by clinical and histol

129 on to TLR-2 signaling events, NOD-2 mediated joint inflammation, as evidenced by the fact that mice d

130 Mice lacking T-bet had markedly reduced joint inflammation at both early and late time points an

131 of Th1-associated chemokine receptors reduce joint inflammation, bone destruction, and cell recruitme

132 doptive transfer, and chemotaxis, we defined joint inflammation, bony destruction, neutrophil and mac

133 T-PCR, and Western blot analysis, we defined joint inflammation, bony erosion, monocyte migration, pr

134 at IDO2 mediates autoantibody production and joint inflammation by acting as a repressor of Runx1 fun

135 ts indicates that IL-18 may contribute to RA joint inflammation by enhancing the recruitment of leuko

136 mportance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum i

137 el, mechanical hypersensitivity outlasts the joint inflammation by weeks.

138 ze that chondrocytes actively mitigate local joint inflammation, cartilage degradation and systemic n

139 The histological appearance of joint inflammation (cellular inflammation and bone erosi

140 e subcutaneous air pouch in mice and chronic joint inflammation characteristic of adjuvant disease in

141 e arthritis in response to Bb infection, the joint inflammation clears after 2 wk, despite continuous

142 kin inflammation but exhibited no changes in joint inflammation compared with wild-type mice.

143 lacking Rsad2 had higher viremia and severe joint inflammation compared with wild-type mice.

144 When the particle challenge caused local joint inflammation, decreased peri-implant bone volume,

145 Subclinical joint inflammation detected by imaging techniques explai

146 Thus, our data demonstrate that localized joint inflammation drives a time-of-day-dependent build-

147 ed gut barrier breakdown and exacerbation of joint inflammation during inflammatory arthritis.

148 mice with B. burgdorferi resulted in altered joint inflammation during murine Lyme arthritis.

149 orrelated strongly with 2 indicators of knee joint inflammation: early-phase bone scintigraphic findi

150 deficiency did not alter the TLR-2-dependent joint inflammation elicited by the synthetic TLR-2 agoni

151 stem remodeling, tissue tolerance erodes and joint inflammation ensues as tissue-invasive effector T

152 In contrast, during joint inflammation, fibroblasts contribute to disease pa

153 e was assessed at 3 years, using measures of joint inflammation, functional disability, and radiologi

154 s assessed at 2 years in terms of persistent joint inflammation, functional disability, and radiologi

155 nclusion, this study suggests that long-term joint inflammation has an impact on DRG neurons that res

156 We evaluated the effect of splenectomy on joint inflammation, histopathology, leukocyte subtypes i

157 ion in SpA initiates in the gut and leads to joint inflammation; however, although conceptually attra

158 rate to severe psoriasis can reduce skin and joint inflammation; however, their effects on vascular i

159 Multiple joint inflammation in a distal distribution in the hands

160 Losartan inhibited acute joint inflammation in a dose-dependent manner, with 15 m

161 sts during the steady state and during acute joint inflammation in a model of inflammatory arthritis.

162 Multiple joint inflammation in a proximal distribution in the han

163 isingly, Elmo1-deficient mice showed reduced joint inflammation in acute and chronic arthritis models

164 howed that Mtb DNA was necessary for maximal joint inflammation in adjuvant arthritis but could be re

165 burgdorferi, the Lyme disease agent, causes joint inflammation in an experimental murine model.

166 cate that TNFalpha, a cytokine that mediates joint inflammation in arthritis, induces cathepsin B-med

167 suggest that IL-10 limits the development of joint inflammation in both arthritis-resistant and -susc

168 NA expression increased substantially during joint inflammation in both models of arthritis.

169 e immunologic events that lead to persistent joint inflammation in certain patients with Lyme arthrit

170 /CT imaging with (99m)Tc-NbV4m119 visualizes joint inflammation in CIA.

171 a useful tool for monitoring and quantifying joint inflammation in collagen-induced arthritis (CIA),

172 intracellular cAMP have been shown to reduce joint inflammation in experimental arthritis, presumably

173 phages, has promising potential to visualize joint inflammation in experimental arthritis.

174 rgets for suppression of neutrophil-mediated joint inflammation in gout.

175 Moreover, autoantibodies contribute to joint inflammation in inflammatory arthritis by triggeri

176 indicate that DEK can contribute directly to joint inflammation in JIA by generating ICs through high

177 indicate that DEK can contribute directly to joint inflammation in JIA by generating immune complexes

178 Joint inflammation in juvenile rheumatoid arthritis (JRA

179 istence of uveitis with axial and peripheral joint inflammation in mice immunized with cartilage prot

180 nt cell populations, and in situ analysis of joint inflammation in mice with CIA.

181 ey effector cells in IL-23-mediated skin and joint inflammation in mice.

182 IRE1alpha-specific inhibitor 4U8C attenuated joint inflammation in mice.

183 emained infected were infectious and induced joint inflammation in naive hamsters.

184 id (GLA), an unsaturated fatty acid, reduces joint inflammation in patients with rheumatoid arthritis

185 tial mediator of autoantibody production and joint inflammation in preclinical models of autoimmune a

186 crophage MS4A4A may represent a biomarker of joint inflammation in RA and a target to amplify the the

187 pression of MS4A4A represents a biomarker of joint inflammation in RA and that its upregulation in co

188 ysophosphatidic acid (LPA) is linked to both joint inflammation in RA patients and to neuropathic pai

189 ssociation and dissociation between pain and joint inflammation in RA.

190 lated autoantibody generation and subsequent joint inflammation in RA.

191 ically reduced clinical signs of disease and joint inflammation in rats with a model of rheumatoid ar

192 To define the cell populations that drive joint inflammation in rheumatoid arthritis (RA), we appl

193 cells were previously shown to contribute to joint inflammation in the course of CHIKV infection in m

194 tibiotics suppressed IL-23-mediated skin and joint inflammation in the WD-fed mice.

195 the chronic, self-perpetuating character of joint inflammation in this autoimmune model.

196 RANKL inhibition prevents joint inflammation in TNF-mediated arthritis.

197 DEK-targeted aptamers significantly reduces joint inflammation in vivo and greatly impairs the abili

198 a-articular injection of tenascin-C promotes joint inflammation in vivo in mice, and addition of exog

199 ced bacterial colonization and LD-associated joint inflammation in vivo.

200 flagellin after the onset of CIA exacerbated joint inflammation; in contrast, inflammation in control

201 limit cartilage degeneration in settings of joint inflammation including advanced age.

202 centrations in animals with and without knee joint inflammation induced by intra-articular injection

203 Joint inflammation is characterized by bone erosions, os

204 Joint inflammation is detectable as early as 1 day posti

205 is was studied in IL-6-deficient mice, since joint inflammation is influenced by the T helper cell re

206 selectin to the initiation and chronicity of joint inflammation is not well understood.

207 The role of CCR6, however, in IL-23-mediated joint inflammation is unclear.

208 tent of their role in the inductive phase of joint inflammation is unknown.

209 s of FLS, leading to significant decrease in joint inflammation, joint damage, and bone loss with imp

210 th CAIA demonstrated significantly increased joint inflammation, joint destruction, and expression of

211 ts ~1% of the global population and leads to joint inflammation, local bone erosions and systemic bon

212 Chronic joint inflammation may persist despite spirochetal killi

213 and systemic administration of AAT reversed joint inflammation, nociception, and cartilage degradati

214 eutrophils are prominent participants in the joint inflammation of human rheumatoid arthritis (RA) pa

215 The impact of chronic joint inflammation on articular vascular function in rat

216 severity and incidence of CIA as measured by joint inflammation or histology.

217 Furthermore, the role of underlying joint inflammation, or synovitis, is often not considere

218 e-dependent symptoms of arthritis, including joint inflammation, primary mechanical hyperalgesia in t

219 In osteoarthritis (OA), low-grade joint inflammation promotes altered chondrocyte differen

220 n contrast to rheumatoid arthritis (RA), the joint inflammation referred to as Jaccoud's arthritis th

221 Mice null for Ido2 display decreased joint inflammation relative to wild-type mice owing to a

222 disease severity by assessing skin scaling, joint inflammation, serum cytokine profiles, and changes

223 rget patient population includes adults with joint inflammation suspected to be gout.

224 rget patient population includes adults with joint inflammation suspected to be gout.

225 me points, MyD88(-/-) mice display decreased joint inflammation, swelling, and proinflammatory cytoki

226 so revealed that TWEAK inhibition diminished joint inflammation, synovial angiogenesis, as well as ca

227 eventative and/or therapeutic manner reduced joint inflammation, synovial cellularity, levels of proi

228 s cause human disease, with sudden fever and joint inflammation that can persist for long periods.

229 patients and is characterized by continuous joint inflammation that does not resolve with antibiotic

230 orrelia burgdorferi, the etiology of chronic joint inflammation that ensues in a subset of patients r

231 MSU crystals produced a knee joint inflammation that was time dependent and was chara

232 ed macrophages, which actively contribute to joint inflammation, these epithelial-like CX(3)CR1(+) li

233 nt arthritis, detection of temporomandibular joint inflammation using contrast-enhanced magnetic reso

234 K cells, and neutrophils mediates persistent joint inflammation via production of IL-18 and GM-CSF.

235 Joint inflammation was assessed by near-infrared fluores

236 However, continued joint inflammation was dependent on the presence of WT n

237 del of anti-collagen Ab-triggered arthritis, joint inflammation was not affected by LTbetaR-Ig treatm

238 A and by an LPA(1/3) receptor inhibitor, but joint inflammation was not affected.

239 icant reduction in PsA-like skin scaling and joint inflammation was observed in DC-TNFR2KO mice.

240 rpassed WT joint swelling, and resolution of joint inflammation was prolonged.

241 nflammatory reaction in mice with persistent joint inflammation was restricted to the joints, since t

242 Joint inflammation was robust and proceeded even in the

243 e, both clinical and histological indexes of joint inflammation were significantly mitigated in anima

244 igned to inhibit TNFalpha strongly inhibited joint inflammation, whereas electroporation of irrelevan

245 a sensitive method for detecting sacroiliac joint inflammation, which is useful in predicting the de

246 (RA) is characterized by autoimmune chronic joint inflammation, which is worsened by mechanical stre

247 Locally administered PG resulted in joint inflammation, which was markedly reduced in mice d

248 Strikingly, reduced skin and joint inflammation with a partial reversion of the gut m

249 Consequently, imaging of joint inflammation with CRIg-specific Nanobodies offers