ライフサイエンスコーパス: autoantibody-negative

1 yopathy who previously were considered to be autoantibody negative.

2 /IA-2 autoantibody-positive but anti-phogrin autoantibody-negative.

3 let autoantibodies and controls who remained autoantibody-negative.

4 ctional and longitudinal analyses of healthy autoantibody-negative (AA(-)) high HLA-risk siblings (HR

5 dies (Ab(+)) and 40 age-matched persistently autoantibody negative (Ab(-)) control subjects.

6 We observed that autoantibody negative (Ab-) type 2 diabetic patients (n

7 in insulin sensitivity and secretion between autoantibody-negative (Ab-) and -positive (Ab+) youth wi

8 conventional autoantibodies and a utility in autoantibody-negative AIH.

9 ndrocyte glycoprotein-IgG-positive or double autoantibody-negative) and two control groups (healthy d

10 pond to corticosteroid therapy and represent autoantibody-negative autoimmune hepatitis.

11 nd the United Kingdom and enrolling 25 islet autoantibody-negative children aged 2 to 7 years with a

12 etes-associated autoantibodies (n = 18) with autoantibody-negative children matched for age, sex, ear

13 en cases of BCA were detected; 153 unrelated autoantibody-negative children were selected from the co

14 here was a greater proportion who were islet autoantibody negative compared with those T1D DQB1*06:02

15 re not significantly different from those of autoantibody-negative control subjects.

16 ee relatives of the IDDM subjects, and in 28 autoantibody-negative control subjects.

17 ties, and air trapping, compared with 33% of autoantibody-negative controls (P = 0.005).

18 (a profile that is 96% specific for RA), 15 autoantibody-negative controls, and 12 patients with est

19 ependent diabetes syndrome, characterized by autoantibody-negative diabetes mellitus and skin deformi

20 evident both in autoantibody-positive and in autoantibody-negative disease.

21 tibody-positive RA but also with the risk of autoantibody-negative disease.

22 ty over its potential use in, and impact on, autoantibody-negative diseases.

23 e at-risk first-degree relatives (FDRs) from autoantibody-negative FDRs and persisted through clinica

24 red with concentrations in age-matched islet autoantibody-negative first-degree relatives of patients

25 ell cytoplasmic autoantibody- and/or insulin autoantibody-negative first-degree relatives of the IDDM

26 ibody positive group (P = 0.010) than in the autoantibody negative group.

27 hed control children who remained islet cell autoantibody-negative in follow-up.

28 Autoantibody-negative individuals (n = 171) served as a

29 o diabetes-predictive autoantibodies and 366 autoantibody-negative matched control children.

30 iabetes (progressors) and those who remained autoantibody negative, matched by age, sex, sample perio

31 e found in 26% of T1D subjects classified as autoantibody-negative on the basis of existing markers [

32 lizumab-treated recipients compared with GAD autoantibody-negative or ATG-treated recipients.

33 nterval [95% CI] 0.39-0.76) as compared with autoantibody-negative patients (OR 0.90, 95% CI 0.41-1.9

34 ible interval [CrI], 1.2-103.6) than that of autoantibody-negative patients, and the increased odds w

35 isease severity in autoantibody-positive and autoantibody-negative patients, respectively.

36 IDDM (6 of 9 [66%]; 3.9+/-3.2) compared with autoantibody-negative relatives (1 of 15 [7%]; 1.8+/-1.0

37 A comparison with 60 autoantibody-negative relatives suggested protection fro

38 The response in healthy control subjects, autoantibody-negative relatives, and IDDM patients, resp

39 o T1D (progressors) (n = 25), reverted to an autoantibody-negative stage (reverters) (n = 47), or mai

40 mokine (C-X-C motif) ligand 10 compared with autoantibody-negative subjects.

41 Among islet autoantibody-negative women, breastfeeding was associate