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1 tage), thickness of the synovial lining, and joint swelling.
2 as highly effective at reversing established joint swelling.
3 pressive effect of CD44-specific antibody on joint swelling.
4 of CIA with PLP-LCL significantly suppressed joint swelling.
5  prinomastat were arthralgia, stiffness, and joint swelling.
6 s global assessment of disease activity, and joint swelling.
7 joint tenderness, despite improvement of the joint swelling.
8       The 7 ACR Core Data Set measures of 1) joint swelling, 2) joint tenderness, 3) physician global
9 derness, 56% versus 41% (P = 0.021), and for joint swelling, 54% versus 39% (P = 0.023); by Paulus cr
10  but that its deficiency resulted in earlier joint swelling and an inability to resolve arthritis as
11 tion of C3H IL-10(-/-) mice led to increased joint swelling and arthritis severity scores over those
12 rence of arthritis, as assessed by measuring joint swelling and by the gross-observation score, and a
13 ficantly reduced inflammation as assessed by joint swelling and clinical inflammation scores.
14 hronic erosive disease typified by disabling joint swelling and deformity (articular index = 8.17+/-0
15 inase (JNK) 1, but not JNK2, is critical for joint swelling and destruction in a serum transfer model
16 se of systemic SCW, virtually eliminated the joint swelling and destruction typically observed during
17                       Efficacy in preventing joint swelling and destruction was determined clinically
18  mice interleukin (IL)-1 plays a key role in joint swelling and destruction, as suggested by the abil
19                                              Joint swelling and disability peaked at 2 weeks of infec
20 h B. burgdorferi developed higher degrees of joint swelling and higher anti-B. burgdorferi immunoglob
21     Arthritis was assessed by measurement of joint swelling and histology of joints collected at d 14
22 s by administration of PG-PS, causing tarsal joint swelling and histopathologic changes characteristi
23 erall severity of arthritis as determined by joint swelling and histopathology.
24 a, as measured by laser Doppler imaging, and joint swelling and hyperemic responses to recombinant hu
25 0 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progressio
26                              Within a trial, joint swelling and joint tenderness or patient and physi
27 and inflammation was determined by measuring joint swelling and macrophage percentage area.
28                     The effects of IL-1Ra on joint swelling and radiographic bone damage in patients
29 tor-alpha and interleukin-1 beta, abrogating joint swelling and reducing destruction of bone and cart
30                                              Joint swelling and serum levels of hyaluronan (HA) and s
31 contributes to the generation of early-onset joint swelling and suggests that arp expression has a ne
32 l synthetic PAR-2 agonist, induced prolonged joint swelling and synovial hyperemia.
33 n B. burgdorferi infection, showed increased joint swelling and synovial inflammation compared with n
34 eta-tryptase resulted in dose-dependent knee joint swelling and synovial vasodilatation in PAR-2(+/+)
35 s (patient and physician global assessments, joint swelling and tenderness counts, and global pain as
36 tient pain assessment than to changes in the joint swelling and tenderness counts.
37   Clinical outcomes evaluated included pain, joint swelling and tenderness, activities of daily livin
38 patient-centered) outcomes, such as pain and joint swelling and tenderness; and adverse effects of th
39  in rats was investigated to address whether joint swelling and the associated vascular dysfunction a
40                      The maximum severity of joint swelling and the duration of Lyme arthritis after
41                           In conclusion, the joint swelling and vascular dysfunction associated with
42           In both arthritis models clinical (joint swelling) and histologic indices of inflammatory a
43 s intraarticular accumulation of leukocytes, joint swelling, and bone erosion.
44  expression, pannus formation, bone erosion, joint swelling, and pain.
45 , swelling of MyD88(-/-) joints surpassed WT joint swelling, and resolution of joint inflammation was
46 s, as evidenced by significant reductions in joint swelling at wk 5, 6, and 7 postinfection, and in t
47 t in joint tenderness and 50% improvement in joint swelling, based on joint scores).
48 hibition of HDAC1 in CIA resulted in reduced joint swelling, cartilage and bone damage and lower tumo
49                      The maximum severity of joint swelling correlated directly with the response to
50 ria (20% improvement in joint tenderness and joint swelling counts, and in 3 of 5 other measures: phy
51 monstrated significantly reduced tibiotarsal joint swelling during the first 6 weeks of infection com
52 tic-refractory arthritis, who had persistent joint swelling for a median duration of 10 months despit
53 although substitution of metacarpophalangeal joint swelling for erosion produced a higher RA prevalen
54         Serotype B-infected mice had greater joint swelling, functional disability, and leukocytic in
55 receptors displayed protective phenotypes in joint swelling, histologic changes in inflammation, and
56  CM-MSC treatment significantly reduced knee-joint swelling, histopathological signs of AIA, cartilag
57 ively prevents arthritis onset and abrogates joint swelling in established disease.
58 mg/kg of losartan substantially reduced knee joint swelling in rats with adjuvant monarthritis (> or
59 ody (versus control antibody) did not affect joint swelling in SCW-treated animals.
60 rthritis, Ifitm3(-/-) mice sustained greater joint swelling in the ipsilateral ankle at days 3 and 7
61                   After i.v. PG-PS treatment joint swelling increased 2.1 +/- 0.3 mm in controls but
62 y indices (patient or physician assessment), joint swelling, joint pain or tenderness, erythrocyte se
63 e suggests that targeting PAR-2 helps reduce joint swelling observed in animal models of arthritis.
64 se, as assessed clinically by measurement of joint swelling on day 1 (P < 0.0001), day 2 (P < 0.01),
65 tor activator of NF-kappaB ligand, and block joint swelling, osteoclast recruitment, and osteolysis.
66 culoskeletal stiffness, cramps, weakness and joint swelling (P < .001), cataract surgery (P < .001),
67 nduced arthritis model in rats, 37 prevented joint swelling partially at 10 mg/kg.
68 ivity, erythrocyte sedimentation rate [ESR], joint swelling, radiographic changes, RA nodules, RA com
69 ations, and joint pain/tenderness scores and joint swelling scores in patients with peripheral articu
70 in 4 of 6 measures: joint tenderness scores, joint swelling scores, physician's and patient's global
71 idence interval [CI], 78%-90%), a history of joint swelling (sensitivity, 78%; 95% CI, 71%-85%), and
72 e, including a reduction in inflammation and joint swelling, suggesting that PPS is a promising candi
73                  We previously reported that joint swelling, synovial thickening, and cartilage matri
74 ) mice exacerbated anti-collagen/LPS-induced joint swelling that was abolished by neutrophil depletio
75 ith antibiotic-responsive arthritis, in whom joint swelling usually resolved during a 1-month course
76         While COX-1/COX-2 inhibition reduced joint swelling, vascular dysfunction in AIA is independe
77 n-site AEs from days 1 to 5, and joint pain, joint swelling, vesicular lesions (blisters), and rashes
78                                              Joint swelling was measured and histologic analysis was
79 ion halted, but a significant improvement in joint swelling was observed within 2 days of treatment.
80 n, appeared early after immunization, before joint swelling was observed.
81                              The severity of joint swelling was restored to wild-type levels in mice
82                                              Joint swelling was similarly attenuated by indomethacin
83 monoarthritis model of chronic inflammation, joint swelling was substantially inhibited in PAR-2-defi
84 T cells are essential for the development of joint swelling without any effect on virus replication a

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