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1 Osteoarthritis (OA) is a low-grade chronic inflammatory joint disease.
2 s that are implicated in the pathogenesis of inflammatory joint disease.
3 We also determined TSG-6 expression in inflammatory joint disease.
4 novel target for therapeutic intervention in inflammatory joint disease.
5 t has been implicated in the pathogenesis of inflammatory joint disease.
6 , 49 of the 63 patients (78%) had persistent inflammatory joint disease.
7 is provide a window into the pathogenesis of inflammatory joint disease.
8 -1 gene products in initiating or amplifying inflammatory joint disease.
9 d their activation-induced microparticles in inflammatory joint diseases.
10 and juvenile idiopathic arthritis among the inflammatory joint diseases.
11 lpha) therapies for non-rheumatoid arthritis inflammatory joint diseases.
12 ing expression of the cartilage phenotype in inflammatory joint diseases.
13 tilage destruction that is characteristic of inflammatory joint diseases.
14 namics involved in tumor angiogenesis and in inflammatory joint diseases.
15 , a drug initially used for the treatment of inflammatory joint disease and only later in the treatme
16 receptor blockade in a therapeutic model of inflammatory joint disease and provide support for pursu
17 ajor advance in the treatment of a number of inflammatory joint diseases and have been widely availab
18 n rheumatoid arthritis (RA), the most severe inflammatory joint disease, autoantibodies against citru
20 thritis (RA), the severity of autoimmune and inflammatory joint disease correlates with large numbers
21 erantigens on the development of autoimmune, inflammatory joint disease in animals that are susceptib
22 significantly ameliorated the development of inflammatory joint disease in mice challenged with colla
26 nflammation is most commonly associated with inflammatory joint diseases, it also occurs in OA and is
27 ercise/joint mobilization is therapeutic for inflammatory joint diseases like rheumatoid and osteoart
28 lling effect on the development of Ag-driven inflammatory joint disease, possibly by mediating the re
29 t acquired lubricin degradation occurring in inflammatory joint diseases predisposes the cartilage to
30 ical agents for the treatment of the chronic inflammatory joint disease rheumatoid arthritis has rein
31 exRNA and its antagonist RNase1 in a chronic inflammatory joint disease, rheumatoid arthritis (RA).
32 ngiogenic treatment may reduce the burden of inflammatory joint diseases such as rheumatoid arthritis
33 orks represent common effector mechanisms in inflammatory joint diseases such as rheumatoid arthritis
34 y apoptosis contributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthriti
35 was grown) and controls (non-Lyme arthritis inflammatory joint disease, syphilis, multiple sclerosis
36 radative processes are better documented for inflammatory joint diseases than tendinopathy even thoug
37 xin are apparent in rheumatoid arthritis, an inflammatory joint disease that disables millions of peo
38 atment-resistant Lyme arthritis is a chronic inflammatory joint disease that follows infection with B
39 3 is a critical proinflammatory cytokine for inflammatory joint disease that integrates fibroblast ac
40 SM and highlight new therapeutic targets for inflammatory joint diseases that aim to repress the expr
41 To determine the effect of TSG-6 on chronic inflammatory joint disease, we induced CIA in DBA/1J mic
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