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1 the spinal cord in animals with and without joint inflammation.
2 ed the highly variable nature of TNF-induced joint inflammation.
3 ith a mouse model of spontaneous, autoimmune joint inflammation.
4 at in some individuals progresses to chronic joint inflammation.
5 unity against mouse cartilage PG and chronic joint inflammation.
6 kine IL-10 to profoundly attenuate localized joint inflammation.
7 nhibitor SzV-1287 in chronic mouse models of joint inflammation.
8 al target for treatment of acute and chronic joint inflammation.
9 ES as a preventative reduced the severity of joint inflammation.
10 not significantly up-regulate RvTs or reduce joint inflammation.
11 cking B1R results in significantly increased joint inflammation.
12 nduce Ets-1 and HIF-1alpha expression during joint inflammation.
13 eukin-1 (IL-1) may dominate the drive toward joint inflammation.
14 isms and bypass the need for IL-1 in chronic joint inflammation.
15 ll predominance correlated with the level of joint inflammation.
16 beta4 and Valpha1 segments, failed to induce joint inflammation.
17 in a model of collagen-induced arthritis and joint inflammation.
18 velopment of serum anti-GPI autoantibody and joint inflammation.
19 with a potential role in the perpetuation of joint inflammation.
20 a direct contribution of type 2 response to joint inflammation.
21 rrow and spleen before the onset of systemic joint inflammation.
22 erimentally induced autoimmunity and chronic joint inflammation.
23 the role of P-selectin in the development of joint inflammation.
24 ng its utility for assessing the severity of joint inflammation.
25 T-cell responses leads to an exacerbation of joint inflammation.
26 eam walk test, and microscopic assessment of joint inflammation.
27 may play a role in cartilage remodeling and joint inflammation.
28 rsistent immune responses that cause chronic joint inflammation.
29 pared to wild-type mice, which links ROS and joint inflammation.
30 el, JNJ-54271074 dose-dependently suppressed joint inflammation.
31 opulation and is characterized by widespread joint inflammation.
32 tool to investigate the extent of arthritic joint inflammation.
33 ng the systemic immune response required for joint inflammation.
34 interaction for osteoclast formation during joint inflammation.
35 RA begin long before the onset of detectable joint inflammation.
36 ber of ACPAs may be associated with signs of joint inflammation.
37 nd systemic host immune responses and elicit joint inflammation.
38 rochetes, bba57 mutants are unable to induce joint inflammation.
39 ry of autoantibodies and may thereby promote joint inflammation.
40 secreting cells, inflammatory cytokines, and joint inflammation.
41 eund's complete adjuvant were used to induce joint inflammation.
42 m to limit the degree of bone erosion during joint inflammation.
43 ein reduces the clinical signs of autoimmune joint inflammation.
44 al injury and bone erosion during autoimmune joint inflammation.
45 en Toll-like receptor 2 (TLR-2) and NOD-2 in joint inflammation.
46 ents with OA or patients with periprosthetic joint inflammation.
47 ntrast, inhibited both lymphangiogenesis and joint inflammation.
48 ted T lymphocytes sustain tissue-destructive joint inflammation.
49 cytokines, and MMPs, which may contribute to joint inflammation.
50 ting a potential role in the pathogenesis of joint inflammation.
51 tihyperalgesia produced by TENS in rats with joint inflammation.
52 dentified PAR-2 as a key mediator of chronic joint inflammation.
53 evelopment of arthritis at the peak of acute joint inflammation (14 d) and in the resolution phase (6
55 Th2 cytokine therapy at the time of maximum joint inflammation also suppressed symptoms of disease.
56 ss tenascin-C show rapid resolution of acute joint inflammation and are protected from erosive arthri
59 y of purified recombinant rat SLPI inhibited joint inflammation and cartilage and bone destruction.
61 in synovium and articular cartilage initiate joint inflammation and cartilage degradation in large pa
62 matoid arthritis, the contribution of MCs to joint inflammation and cartilage loss remains poorly und
63 report demonstrating effective prevention of joint inflammation and clinical signs of CIA with an I-A
64 ibition on both RASF phenotype in vitro, and joint inflammation and damage in the collagen-induced ar
68 ssion of NF-kappaB-regulated genes mediating joint inflammation and destruction, including chemokines
72 ould lead to a better understanding of gouty joint inflammation and help improve the treatment and ca
73 Splenectomy dramatically decreased chronic joint inflammation and histopathologic damage as well as
76 -control studies including participants with joint inflammation and no previous definitive gout diagn
77 -control studies including participants with joint inflammation and no previous definitive gout diagn
78 ay provide insights into the pathogenesis of joint inflammation and noninvasive monitoring of disease
79 leted of essential oils profoundly inhibited joint inflammation and periarticular joint destruction i
80 lds promise for control of temporomandibular joint inflammation and prevention of associated morbidit
81 gnaling in osteoblasts significantly reduces joint inflammation and prevents structural bone and cart
82 a critical role for CD44 in the pathology of joint inflammation and reveals a unique mechanism of rec
84 s important for the prevention of persistent joint inflammation and spirochete clearance, and they co
85 and Sl/Sld, were resistant to development of joint inflammation and that susceptibility was restored
88 bone destruction, shows evidence of reducing joint inflammation, and may be mediated by high local le
89 to ameliorate arthritis in animal models of joint inflammation, and preliminary studies have suggest
90 side of the MCP joints in early RA, and that joint inflammation appears to drive the inherent tendenc
93 matoid arthritis, which are characterized by joint inflammation as well as periarticular and systemic
94 ignalling, are involved in the regulation of joint inflammation as well as systemic fuel metabolism.
95 neutralizing antibodies to gp96 ameliorated joint inflammation, as determined by clinical and histol
96 on to TLR-2 signaling events, NOD-2 mediated joint inflammation, as evidenced by the fact that mice d
98 of Th1-associated chemokine receptors reduce joint inflammation, bone destruction, and cell recruitme
99 doptive transfer, and chemotaxis, we defined joint inflammation, bony destruction, neutrophil and mac
100 T-PCR, and Western blot analysis, we defined joint inflammation, bony erosion, monocyte migration, pr
101 ts indicates that IL-18 may contribute to RA joint inflammation by enhancing the recruitment of leuko
102 mportance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum i
104 ze that chondrocytes actively mitigate local joint inflammation, cartilage degradation and systemic n
106 e subcutaneous air pouch in mice and chronic joint inflammation characteristic of adjuvant disease in
107 e arthritis in response to Bb infection, the joint inflammation clears after 2 wk, despite continuous
111 orrelated strongly with 2 indicators of knee joint inflammation: early-phase bone scintigraphic findi
112 deficiency did not alter the TLR-2-dependent joint inflammation elicited by the synthetic TLR-2 agoni
113 e was assessed at 3 years, using measures of joint inflammation, functional disability, and radiologi
114 s assessed at 2 years in terms of persistent joint inflammation, functional disability, and radiologi
115 nclusion, this study suggests that long-term joint inflammation has an impact on DRG neurons that res
116 We evaluated the effect of splenectomy on joint inflammation, histopathology, leukocyte subtypes i
117 rate to severe psoriasis can reduce skin and joint inflammation; however, their effects on vascular i
120 sts during the steady state and during acute joint inflammation in a model of inflammatory arthritis.
122 howed that Mtb DNA was necessary for maximal joint inflammation in adjuvant arthritis but could be re
124 cate that TNFalpha, a cytokine that mediates joint inflammation in arthritis, induces cathepsin B-med
125 suggest that IL-10 limits the development of joint inflammation in both arthritis-resistant and -susc
127 e immunologic events that lead to persistent joint inflammation in certain patients with Lyme arthrit
129 a useful tool for monitoring and quantifying joint inflammation in collagen-induced arthritis (CIA),
130 intracellular cAMP have been shown to reduce joint inflammation in experimental arthritis, presumably
134 indicate that DEK can contribute directly to joint inflammation in JIA by generating ICs through high
135 indicate that DEK can contribute directly to joint inflammation in JIA by generating immune complexes
137 istence of uveitis with axial and peripheral joint inflammation in mice immunized with cartilage prot
141 id (GLA), an unsaturated fatty acid, reduces joint inflammation in patients with rheumatoid arthritis
143 cells were previously shown to contribute to joint inflammation in the course of CHIKV infection in m
146 DEK-targeted aptamers significantly reduces joint inflammation in vivo and greatly impairs the abili
147 a-articular injection of tenascin-C promotes joint inflammation in vivo in mice, and addition of exog
148 flagellin after the onset of CIA exacerbated joint inflammation; in contrast, inflammation in control
149 centrations in animals with and without knee joint inflammation induced by intra-articular injection
152 is was studied in IL-6-deficient mice, since joint inflammation is influenced by the T helper cell re
155 s of FLS, leading to significant decrease in joint inflammation, joint damage, and bone loss with imp
156 th CAIA demonstrated significantly increased joint inflammation, joint destruction, and expression of
158 eutrophils are prominent participants in the joint inflammation of human rheumatoid arthritis (RA) pa
161 e-dependent symptoms of arthritis, including joint inflammation, primary mechanical hyperalgesia in t
163 n contrast to rheumatoid arthritis (RA), the joint inflammation referred to as Jaccoud's arthritis th
167 me points, MyD88(-/-) mice display decreased joint inflammation, swelling, and proinflammatory cytoki
168 so revealed that TWEAK inhibition diminished joint inflammation, synovial angiogenesis, as well as ca
169 eventative and/or therapeutic manner reduced joint inflammation, synovial cellularity, levels of proi
170 patients and is characterized by continuous joint inflammation that does not resolve with antibiotic
171 orrelia burgdorferi, the etiology of chronic joint inflammation that ensues in a subset of patients r
173 nt arthritis, detection of temporomandibular joint inflammation using contrast-enhanced magnetic reso
176 del of anti-collagen Ab-triggered arthritis, joint inflammation was not affected by LTbetaR-Ig treatm
178 nflammatory reaction in mice with persistent joint inflammation was restricted to the joints, since t
180 e, both clinical and histological indexes of joint inflammation were significantly mitigated in anima
181 igned to inhibit TNFalpha strongly inhibited joint inflammation, whereas electroporation of irrelevan
182 a sensitive method for detecting sacroiliac joint inflammation, which is useful in predicting the de
183 (RA) is characterized by autoimmune chronic joint inflammation, which is worsened by mechanical stre
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