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