ライフサイエンスコーパス: joint disease

1 tis (OA) is a low-grade chronic inflammatory joint disease.

2 c phenotype may protect against degenerative joint disease.

3 aetiology and possible treatment of synovial joint disease.

4 rthritis or osteoarthritis, or those without joint disease.

5 plicated in the pathogenesis of inflammatory joint disease.

6 estruction of connective tissue resulting in joint disease.

7 may be an effective therapy for degenerative joint disease.

8 el therapeutics for the treatment of chronic joint disease.

9 m by which antibodies to GPI may precipitate joint disease.

10 cessfully treated infections or degenerative joint disease.

11 nd may serve as an indicator of degenerative joint disease.

12 turbances in these processes are involved in joint disease.

13 3 patients (78%) had persistent inflammatory joint disease.

14 e and fluid-and subsequently contributing to joint disease.

15 e, joint laxity and early-onset degenerative joint disease.

16 ggested an entheseal-based pathology for the joint disease.

17 denstrom's macroglobulinemia who do not have joint disease.

18 window into the pathogenesis of inflammatory joint disease.

19 by it can potentially initiate or accelerate joint disease.

20 , and in cartilage from adults with no known joint disease.

21 joints and hip, but the runners had more PF joint disease.

22 cts in initiating or amplifying inflammatory joint disease.

23 hemarthroses can prevent the development of joint disease.

24 drome of autoimmunity manifested by lung and joint disease.

25 ly in macrophages, ameliorated both skin and joint disease.

26 therapeutic target for treating degenerative joint disease.

27 atic arthritis or unmasked previously occult joint disease.

28 ) is an age-related progressive degenerative joint disease.

29 ental animal model of immune complex-induced joint disease.

30 s (OA), a chronic and degenerative articular joint disease.

31 gnal in driving adaptive immunity in erosive joint disease.

32 resolvins (RvTs), and significantly reduced joint disease.

33 g complications and progression to end-stage joint disease.

34 plicated in the pathogenesis of inflammatory joint disease.

35 cytokine-independent mechanisms involved in joint disease.

36 determined TSG-6 expression in inflammatory joint disease.

37 ammation and tissue destruction in arthritic joint disease.

38 c factors, autoantibodies, inflammation, and joint disease.

39 nd cartilage degradation during degenerative joint disease.

40 ture study of inflammation in this prevalent joint disease.

41 for therapeutic intervention in inflammatory joint disease.

42 with other inflammatory and noninflammatory joint diseases.

43 n of the cartilage phenotype in inflammatory joint diseases.

44 ate cartilage mineralization in degenerative joint diseases.

45 ction that is characteristic of inflammatory joint diseases.

46 ly event in the pathogenesis of degenerative joint diseases.

47 n, in a way that is different from all other joint diseases.

48 her development of gene treatments for human joint diseases.

49 function in patients with degenerative knee joint diseases.

50 ed in tumor angiogenesis and in inflammatory joint diseases.

51 new physical or pharmacologic therapies for joint diseases.

52 ation-induced microparticles in inflammatory joint diseases.

53 idiopathic arthritis among the inflammatory joint diseases.

54 es for non-rheumatoid arthritis inflammatory joint diseases.

55 ociated comorbidities were 6/14 degenerative joint disease, 9/10 gastroesophageal reflux disorder, 2/

56 regression analyses adjusted for baseline 28 joint disease activity score (DAS28), baseline health as

57 her serum ACPA concentration (P = 0.004), 28-joint Disease Activity Score (P = 0.023), health assessm

58 int counts and the activity scores on the 28-joint Disease Activity Score assessment.

59 aire-Disability Index (HAQ-DI) score, the 28-joint Disease Activity Score based on C-reactive protein

60 d the stable low disease activity target (28-joint disease activity score with C-reactive protein [DA

61 ge of Rheumatology 20% response criteria, 28-joint Disease Activity Score, DeltaHAQ, DeltaRAQoL, and

62 graphic and functional outcomes, although 28-joint Disease Activity Score-based measures of remission

63 ine kinase (CK) level, as well as muscle and joint disease activity.

64 r a patient with significant nail, skin, and joint disease, adalimumab, etanercept, ustekinumab, infl

65 teoarthritis (OA) is a complex heterogeneous joint disease affecting more than 35 million people worl

66 OA is the most common joint disease, affecting 10-15% of people over 60 years

67 Degenerative joint disease, also known as osteoarthritis, is the most

68 y levels correlated modestly with muscle and joint disease, an association confirmed by a custom ELIS

69 with early RA with clinically diagnosed MCP joint disease and 28 healthy controls were examined by m

70 Osteoarthritis is the most prevalent joint disease and a common cause of joint pain, function

71 Osteoarthritis is the most prevalent joint disease and a frequent cause of joint pain, functi

72 to virus-host interactions and mechanisms of joint disease and connective tissue disease.

73 Osteoarthritis (OA) is the most common joint disease and involves progressive degeneration of a

74 Osteoarthritis (OA) is the most common whole-joint disease and is characterized by progressive loss o

75 rapidly developed rheumatoid arthritis-like joint disease and large-vessel vasculitis.

76 ially used for the treatment of inflammatory joint disease and only later in the treatment of inflamm

77 of an effective therapy in the treatment of joint disease and other pathologies involving the action

78 ckade in a therapeutic model of inflammatory joint disease and provide support for pursuing this ther

79 The syk(f/f) MRP8-cre(+) mice display absent joint disease and reduced deposition of pathogenic anti-

80 synovitis could develop in both degenerative joint disease and spondylarthritis.

81 rtant role of TLR4 signaling in MPS bone and joint disease and suggest that targeting TNF-alpha may h

82 proliferative changes observed in hemophilic joint disease and that aberrant expression of c-myc may

83 Osteoarthritis (OA) is the most common joint disease and typically begins with an aging-related

84 in the treatment of a number of inflammatory joint diseases and have been widely available in clinica

85 in which surviving mice acquire degenerative joint diseases and tumors in multiple organs.

86 es mellitus, hypogonadotrophic hypogonadism, joint disease, and cardiomyopathy.

87 r patents tend to manifest enthesitis, axial joint disease, and persistent oligoarthritis.

88 pathway in the pathogenesis of MPS bone and joint disease, and the use of the anti-TNF-alpha drug, R

89 (OA) is the most prevalent and debilitating joint disease, and there are currently no effective dise

90 clinical efficacy of adrenocorticotropin in joint diseases, AP1189 was tested in experimental inflam

91 we observe no clinical signs of degenerative joint disease apart from mild, or in one case moderate,

92 he factors that control T cell activation in joint disease are not well understood.

93 The manifestations of joint disease are usually clinically apparent, but the e

94 Joint diseases are often characterized by inflammatory p

95 s, genitals, face, or nails, and concomitant joint disease, are also important when considering treat

96 ne cells play a central role in degenerative joint disease associated with osteoarthritis (OA) and pa

97 arthritis (RA), the most severe inflammatory joint disease, autoantibodies against citrullinated prot

98 Osteoarthritis is a joint disease characterized by a nonsymptomatic, preradi

99 Osteoarthritis is a degenerative joint disease characterized by a progressive and irrever

100 Psoriatic arthritis (PsA) is an inflammatory joint disease characterized by extensive bone resorption

101 the severity of autoimmune and inflammatory joint disease correlates with large numbers of CD4+CD28-

102 Patients with liver disease, joint disease, diabetes mellitus and other endocrinopath

103 Secondary end points were measures of joint disease, disability, and quality of life in all pa

104 TMJ) disc displacement (DD) and degenerative joint disease (DJD) has never been conclusively describe

105 t reduction (DDwR and DDwoR) to degenerative joint disease (DJD), and patient-reported outcomes of ja

106 In osteoarthritic joint disease, expression of bFGF and MMP-13 in chondroc

107 Osteoarthritis is a common degenerative joint disease for which no disease-modifying drugs are c

108 Chronic joint disease from repeated bleeding into joints is a se

109 dity in these patients included degenerative joint disease, gastroesophageal reflux disease, hyperten

110 major role in the pathogenesis of hemophilic joint disease (HJD).

111 hibitors have proved effective in rheumatoid joint disease; however, their effect on the tenosynovium

112 inumab for treatment of psoriatic arthritis, joint disease improved.

113 gh very effective, do not completely prevent joint disease in a long-term perspective.

114 pain symptoms, disability, and more serious joint disease in American Indian patients.

115 the development of autoimmune, inflammatory joint disease in animals that are susceptible to the dev

116 ameliorated the development of inflammatory joint disease in mice challenged with collagen-induced a

117 ern that ustekinumab may unmask or aggravate joint disease in selected patients.

118 Joint disease in Smad3-knockout (Smad3(-/-)) mice was ex

119 c therapies in the treatment of degenerative joint disease in the future.

120 ight into the complex processes that mediate joint disease in the inflammatory arthritides through th

121 arthritis (RA) is an inflammatory autoimmune joint disease in which the complement system plays an im

122 trogens may ameliorate bone and inflammatory joint diseases in patients infected with HTLV-I by repre

123 useful information that may help understand joint diseases in the general population and how therapi

124 tionship with meniscal tear and degenerative joint disease independent of effusion was also demonstra

125 significant association between severity of joint disease, induced with distinct protocols and volum

126 litions also can be acquired by degenerative joint disease, inflammatory arthritis, infection, and cl

127 s, and one mechanism linking fibrin(ogen) to joint disease is coupled to alphaMbeta2-mediated inflamm

128 e both with and without chronic inflammatory joint disease is emerging.

129 with clinical problems, but the severity of joint disease is only weakly related to that of the clin

130 The end stage of inflammatory joint diseases is characterized by excessive ECM catabol

131 ritis (OA), the most prevalent aging-related joint disease, is characterized by insufficient extracel

132 s most commonly associated with inflammatory joint diseases, it also occurs in OA and is thus relevan

133 mobilization is therapeutic for inflammatory joint diseases like rheumatoid and osteoarthritis, but t

134 This suggests that the anatomic basis for joint disease localization differs between RA and PMR.

135 The anatomic basis for joint disease localization in polymyalgia rheumatica (PM

136 previous 6 months (mCSA), temporomandibular joint disease (mCSA and section modulus), functional dis

137 of disease between patients with neuropathic joint disease (NJD) and patients with degenerative arthr

138 ecruited at New York University Hospital for Joint Diseases (NYUHJD), and 1 cohort (a validation coho

139 tic manifestations of osteoarthrosis (OA), a joint disease of major economic importance.

140 ndon, enthesis, and adjacent bone in the DIP joint disease of PsA patients.

141 flammation (100%) experienced improvement in joint disease, only 6 of 16 with ocular inflammation (38

142 descriptors did not distinguish the type of joint disease or pain intensity.

143 The pathophysiology of the most common joint disease, osteoarthritis (OA), remains poorly under

144 on the development of Ag-driven inflammatory joint disease, possibly by mediating the recruitment and

145 Although it is not clear whether joint disease precedes or follows a decline in muscular

146 bricin degradation occurring in inflammatory joint diseases predisposes the cartilage to damage.

147 one of the most common and most debilitating joint diseases, producing high personal, social, and eco

148 mmation, which might improve on treatment of joint disease, remains to be determined.

149 sculoskeletal and Skin Diseases/Hospital for Joint Diseases Research Registry for Neonatal Lupus.

150 on 8 (Smad3(ex8/ex8)) developed degenerative joint disease resembling human osteoarthritis, as charac

151 n and results in development of degenerative joint disease resembling osteoarthritis in humans.

152 nalysis of the different stages of arthritic joint disease revealed enhanced (18)F-FLT uptake in arth

153 or the treatment of the chronic inflammatory joint disease rheumatoid arthritis has reinvigorated res

154 antagonist RNase1 in a chronic inflammatory joint disease, rheumatoid arthritis (RA).

155 Serum COMP levels correlated with total-body joint disease severity as determined by late-phase bone

156 adian rhythm disruption is a risk factor for joint diseases such as OA.

157 meostasis and its disturbance contributes to joint diseases such as osteoarthritis (OA).

158 tion of the cartilage matrix in degenerative joint diseases such as osteoarthritis.

159 of the cartilage matrix during degenerative joint diseases such as osteoarthritis.

160 from articular cartilage during degenerative joint diseases such as osteoarthritis.

161 differentiation and may have implications in joint diseases such as osteoarthritis.

162 atment may reduce the burden of inflammatory joint diseases such as rheumatoid arthritis by facilitat

163 t common effector mechanisms in inflammatory joint diseases such as rheumatoid arthritis.

164 py offers a novel approach to treating human joint diseases such as rheumatoid arthritis.

165 Degenerative joint diseases, such as arthritis, cause loss of normal

166 ontributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthritis (RA).

167 ch as age and sex; description of ocular and joint disease; surgical and other complications; medical

168 nsion, gastroesophageal reflux, degenerative joint disease symptoms, type 2 diabetes mellitus, pseudo

169 nd controls (non-Lyme arthritis inflammatory joint disease, syphilis, multiple sclerosis, and nondise

170 esses are better documented for inflammatory joint diseases than tendinopathy even though the pathoge

171 ent in rheumatoid arthritis, an inflammatory joint disease that disables millions of people worldwide

172 ant Lyme arthritis is a chronic inflammatory joint disease that follows infection with Borrelia burgd

173 al proinflammatory cytokine for inflammatory joint disease that integrates fibroblast activation with

174 Osteoarthritis (OA) is a degenerative joint disease that involves the destruction of articular

175 Osteoarthritis is a degenerative joint disease that ranks among the leading causes of adu

176 ght new therapeutic targets for inflammatory joint diseases that aim to repress the expression of col

177 ation, gastroesophageal reflux, degenerative joint disease, urinary incontinence, venous stasis, and

178 Although joint disease was prevented or cured in five of five amo

179 the effect of TSG-6 on chronic inflammatory joint disease, we induced CIA in DBA/1J mice by immuniza

180 ukocyte protease inhibitor (SLPI) in erosive joint diseases, we cloned, sequenced, and expressed acti

181 ither inflammatory eye disease or associated joint disease were studied retrospectively to determine

182 ic arthritis (PsA) is a chronic inflammatory joint disease which develops in patients with psoriasis.

183 Degenerative joint disease, which affects one-fifth of the US populat

184 eumatoid arthritis is a chronic inflammatory joint disease, which can cause cartilage and bone damage

185 ombination leads to early onset degenerative joint disease, which is revealed by simultaneous enlarge

186 Osteoarthritis is a degenerative joint disease whose molecular mechanism is currently unk

187 (OA) is a prevalent, heritable degenerative joint disease with a substantial public health impact.

188 oid arthritis (RA) is a chronic inflammatory joint disease with episodic flares.

189 K/BxN mice develop an inflammatory joint disease with many features characteristic of rheum

190 oid arthritis (RA) is one of the major human joint diseases with unknown etiology, the early diagnosi

191 rmation regarding how these pathogens elicit joint disease, with emphasis on C. trachomatis in its ro