ライフサイエンスコーパス: joint fluid

1 AKA were not selectively concentrated in the joint fluid.

2 clinical criteria rather than examination of joint fluid.

3 an and albumin normally coexist, however, in joint fluid.

4 A compared with nonangiogenic osteoarthritic joint fluid.

5 assessed for disk position, bone status, and joint fluid.

6 Although found in some RA joint fluids, AKA were not selectively concentrated in t

7 ominantly limited to X-ray, MRI and invasive joint fluid analysis, all of which lack chemical or mole

8 ate administration, and were present in both joint fluid and blood implying they were candidate drive

9 infections including inoculation of infected joint fluid and bone in blood-culture bottles should be

10 arthrography in the objective evaluation of joint fluid and lateral subluxation (r = 0.80, P < .01).

11 les in patients' inflamed synovial tissue or joint fluid and tested each epitope for autoreactivity.

12 lysis showed that C1s was being activated in joint fluid and that its activation was inhibited by the

13 tals are common components of osteoarthritic joint fluids and tissues.

14 e leukocyte esterase (LE) in human synovial (joint) fluid and urine.

15 GAGs), a major component of joint cartilage, joint fluid, and other soft connective tissue, causes th

16 ical irregularity, cartilage interface sign, joint fluid, and subacromial-subdeltoid bursal fluid.

17 of intact IGFBP-5 and IGF-1 in cartilage and joint fluid, and whether C1s inhibition would be associa

18 greater tuberosity cortical irregularity and joint fluid, are most valuable in the diagnosis of supra

19 such as sinus tracts and ulcers, as well as joint fluid aspirates, can be used for microbiological c

20 solates were piliated, while the majority of joint fluid, bone, and endocarditis blood isolates were

21 Serum and joint fluid levels of urea and joint fluid concentrations of glucose, lactate, cartilag

22 OFIRE Joint Infection (JI) Panel compared to joint fluid culture and/or 16S rRNA PCR, followed by San

23 (1,303/1,307) compared to detection by SOCj, joint fluid culture only, or 16S PCR/S only, respectivel

24 ed by standard-of-care joint (SOCj) studies (joint fluid culture with or without 16S PCR/S, as ordere

25 istence of concentration polarisation during joint fluid drainage was supported by the demonstration

26 ed joints (62% vs 21%, P < .001) and diffuse joint fluid enhancement was more common with infection (

27 forms of inflammatory arthritis, but not in joint fluid from patients with osteoarthritis.

28 sicles elaborated by activated platelets--in joint fluid from patients with rheumatoid arthritis and

29 e complement component C1s is present in dog joint fluid in an activated state.

30 rmed quickly, and was effective for sampling joint fluid in patients with hip prostheses.

31 or characterizing gelatinases from arthritic joint fluid is demonstrated.

32 Serum and joint fluid levels of urea and joint fluid concentration

33 was prepared from whole peripheral blood and joint fluid obtained from patients with PsA and rheumato

34 ynthesis of 15d-PGJ2 is not augmented in the joint fluid of patients with arthritis, nor is its urina

35 erum of patients with erythema migrans (EM), joint fluid of patients with Lyme arthritis, and superna

36 y OspC type K (RST2), were identified in the joint fluid of patients with Lyme arthritis, and the gen

37 Additionally, the joint fluid of these patients had markedly elevated leve

38 d drainage( 8d s) was measured at controlled joint fluid pressure (Pj) in knees of anaesthetized rabb

39 T genotypes were identified in 49 of the 124 joint fluid samples (40%).

40 We tested the proposed system by using human joint fluid samples and found its limit of detection for

41 Joint fluid samples from 124 patients seen over a 30-yea

42 Joint fluid samples were analyzed for the concentration

43 Analysis of the aspirated joint fluid showed that 31 +/- 0.07 % (s.e.m.) of dextra

44 Immunoblotting of joint fluid showed that both treatments increased concen

45 y (peak titers after 90 days), and only some joint fluids showed chemotactic activity, which on avera

46 An additional 104 residual joint fluid specimens were de-identified and prospective

47 Sixty-three frozen, residual joint fluid specimens were retrospectively tested using

48 es and with four real-matrix samples of knee joint fluid spiked with live pathogenic bacterial cells.

49 In joint fluid the polymer hyaluronan (HA) confers viscous

50 rheumatoid arthritis patients, of blood and joint fluid Tph cells as well as circulating plasmablast

51 greater tuberosity cortical irregularity and joint fluid was most important in the diagnosis of full-

52 Urea concentrations in joint fluid were directly proportional to those in serum

53 Total IGF-1 concentrations in joint fluid were increased 5.6-5.8-fold by these two tre

54 Joint fluids were obtained from normal canine joints by

55 The test is performed directly on joint fluids with a fast turnaround time of 1 hour.

56 rtook to determine whether inhibiting C1s in joint fluid would result in an increase in the amount of