ライフサイエンスコーパス: joint fluid

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1 clinical criteria rather than examination of joint fluid.

2 AKA were not selectively concentrated in the 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 ate administration, and were present in both joint fluid and blood implying they were candidate drive

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 or characterizing gelatinases from arthritic joint fluid is demonstrated.

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

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

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

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

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

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

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

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

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

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

36 Joint fluid samples were analyzed for the concentration

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

38 Immunoblotting of joint fluid showed that both treatments increased concen

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

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

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

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

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

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

45 Joint fluids were obtained from normal canine joints by

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

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