ライフサイエンスコーパス: gouty

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1 Lead toxicity can lead to gouty arthritis (gout), but whether the low lead exposur

2 cid has been long recognized as the cause of gouty arthritis and kidney stones.

3 mechanism of action of ACTH in experimental gouty arthritis and points to a novel antiinflammatory t

4 s at MC3-R) for clinical management of human gouty arthritis and possibly other chronic inflammatory

5 of the drugs we use to manage patients with gouty arthritis have been in existence since the 1970s a

6 management, and pathophysiology of gout and gouty arthritis have been recently reviewed.

7 Gouty arthritis is associated with an excess risk of acu

8 neutrophil recruitment in experimental acute gouty arthritis of the rabbit knee.

9 has been incriminated in the pathogenesis of gouty arthritis, Alzheimer's, and silicosis.

10 Finally, in a model of gouty arthritis, direct injection of urate crystals into

11 This is a discussion of acute gouty arthritis, seen for over 50 years of engagement.

12 sis of a number of human diseases, including gouty arthritis, silicosis, atherosclerosis, and type 2

13 itis, such as juvenile chronic arthritis and gouty arthritis, that may have a variable appearance com

14 eutic approaches for hyperuricemia and acute gouty arthritis.

15 al of MSU crystal deposits and the course of gouty arthritis.

16 hilic response in this in vivo evaluation of gouty arthritis.

17 lcohol consumption may lead to a decrease in gouty arthritis.

18 ce of factors contributing to development of gouty attacks such as diuretic therapy, weight gain, and

19 may explain some of the uncertainties about gouty attacks.

20 tentially more effective strategies for both gouty inflammation and urate lowering.

21 appreciated centrality of IL-1beta in acute gouty inflammation has prompted studies of agents blocki

22 However, gouty inflammation is spontaneously self-limited, an occ

23 his study, we examined the potential role in gouty inflammation of CD14, a phagocyte-expressed patter

24 ium urate monohydrate (MSU) crystals promote gouty inflammation that is critically mediated by neutro

25 he factors that restrains the progression of gouty inflammation.

26 be noninflammatory and promote resolution of gouty inflammation.

27 al variability in the extent and duration of gouty inflammation.

28 nse protein 88 (MyD88) is required for acute gouty inflammation.

29 proinflammatory responses and trigger acute gouty inflammation.

30 crystals and key cellular components of the gouty inflammatory paroxysm, with new material on pathog

31 that the innate immune system may drive the gouty inflammatory response to MSU.

32 tudy could lead to a better understanding of gouty joint inflammation and help improve the treatment

33 and unsaturated fat diet was recommended for gouty patients since they all enhance insulin sensitivit

34 nto SCID mice while, simultaneously, diluted gouty SF containing CXCL16, or depleted of CXCL16 by ant

35 SCID mouse chimeras injected intragraft with gouty SF that had been depleted of CXCL16 during PMN tra

36 XCL16 concentrations were highly elevated in gouty SF, and PMNs were observed to migrate in response

37 Recruitment of PMNs to the gouty SF-injected normal human ST was then examined in t

38 as an active recruitment factor for PMNs in gouty SF.

39 h that after administration of sham-depleted gouty SF.

40 t mediator of in vivo recruitment of PMNs to gouty SF.

41 uced by neutralization of CXCL16 activity in gouty SF.

42 Gouty synovitis is driven and sustained by neutrophil in

43 ient referred to us for recurrent chest wall gouty tophus, but who was determined to actually have a

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