ライフサイエンスコーパス: autoantibody-positive

1 gative first-degree relatives who were never autoantibody positive.

2 wly diagnosed IDDM patients tested were IA-2 autoantibody positive.

3 ually diminished in alpha-cells of NOD mice, autoantibody-positive (AA(+)) and overtly type 1 diabeti

4 ne and endocrine pancreas of T1D and at-risk autoantibody-positive (AAb(+)) donors, along with its ta

5 ranscriptomics in up to 32 nondiabetic (ND), autoantibody-positive (AAB(+)), and T1D pancreas donors.

6 In contrast, autoantibody positive (Ab+) type 2 diabetic patients (n

7 time in situ, that in pancreas sections from autoantibody-positive (Ab+) donors, insulin area and bet

8 e predictive power of autoantibodies because autoantibody-positive (AbP) children have heterogeneous

9 b in the treatment of acetylcholine receptor autoantibody-positive (AChR+) generalized MG.

10 (HLA) alleles for anti-citrullinated-protein-autoantibody-positive (ACPA(+)) rheumatoid arthritis (RA

11 e polymorphisms (SNPs) were genotyped in 556 autoantibody-positive African Americans with RA and 791

12 d diabetes risk among those who are multiple autoantibody positive, although substantial false positi

13 No differences between anti-islet cell autoantibody-positive and -negative children were found

14 ent of juvenile DM in both myositis-specific autoantibody-positive and -negative patients.

15 children with new-onset type 1 diabetes and autoantibody-positive and -negative siblings by ELISA.

16 The magnitude of association was assessed in autoantibody-positive and -negative subgroups.

17 be useful in predicting disease severity in autoantibody-positive and autoantibody-negative patients

18 ucleatum) were significantly associated with autoantibody-positive and high-risk status (P < 0.05).

19 ears, associations that were evident both in autoantibody-positive and in autoantibody-negative disea

20 We compared anti-U11/U12 RNP autoantibody-positive and negative SSc patients on demog

21 Examination of human pancreas samples from autoantibody-positive and T1D donors with residual beta-

22 markers MxA, PKR, and HLA-I in the islets of autoantibody-positive and T1D donors.

23 n of CD8 T cells in pancreata from T1D, T2D, autoantibody-positive, and healthy control subjects.

24 of AnnoSpat to type 1 diabetic, non-diabetic autoantibody-positive, and non-diabetic organ donor coho

25 in children with newly diagnosed T1D and in autoantibody-positive at-risk children with impaired glu

26 s; namely, early features that differentiate autoantibody-positive at-risk first-degree relatives (FD

27 the expression of these genes in human T1D, autoantibody-positive (autoantibody+), and control pancr

28 eving complete and durable remissions in the autoantibody-positive autoimmune diseases as a group, ir

29 atives followed to diabetes were ICA512/IA-2 autoantibody-positive but anti-phogrin autoantibody-nega

30 In preclinical autoantibody-positive cases, the number of elevated cyto

31 ntribute to type 1 diabetes (T1D) risk among autoantibody-positive children in The Environmental Dete

32 tetramer staining in 6 patients and 10 islet autoantibody-positive children showed large diversity wi

33 gorithm allows refined grouping of beta-cell autoantibody-positive children who distinctly progressed

34 7-CD8+ memory T cells, was observed in islet autoantibody-positive children who later progressed to T

35 We studied 28 autoantibody-positive children, out of which 22 progress

36 gnificantly higher in pretransplantation GAD autoantibody-positive daclizumab-treated recipients comp

37 Autoantibody-positive diabetic subjects (n = 1,384) and

38 hat T1D is more similar genetically to other autoantibody-positive diseases, significantly most simil

39 ws early Golgi alteration in beta-cells from autoantibody-positive donors, which persists in residual

40 ut diabetes, donors who were type 1 diabetes autoantibody positive, donors with type 1 diabetes, and

41 levels of interleukin-4 (IL-4) in anti-islet autoantibody-positive first-degree relatives of patients

42 Of 171 relatives previously tested single autoantibody positive for autoantibodies to full-length

43 complement factor H-related (CFHR) genes and autoantibody-positive form of hemolytic uremic syndrome

44 ptor (AChR) or muscle-specific kinase (MuSK) autoantibody-positive generalised myasthenia gravis (Mya

45 ons were higher in high-risk (P = 0.011) and autoantibody positive group (P = 0.010) than in the auto

46 uremic syndrome, in FHR1:FHR3 deficient and autoantibody-positive hemolytic uremic syndrome form and

47 on-diabetic organ donors, non-diabetic islet autoantibody-positive individuals (AAb), and age-matched

48 alysis suggested that the gut microbiomes of autoantibody-positive individuals and seronegative FDRs

49 beta-cells in pancreatic sections from GAD65 autoantibody-positive individuals who have not yet progr

50 ide association study meta-analysis of 5,539 autoantibody-positive individuals with rheumatoid arthri

51 is known about the disposition index (DI) in autoantibody-positive individuals, we have assessed whet

52 ign for MuSK-CAART for the treatment of MuSK autoantibody-positive MG.

53 Individuals were considered autoantibody positive (n = 113) if they had >/=1 RA-rela

54 applied this assay to 78 subjects, including autoantibody positive (n = 20) and new-onset type 1 diab

55 ed whether immunoglobulin G from aquaporin-4-autoantibody-positive neuromyelitis optica patients has

56 sues of non-diabetic control (ND), beta cell autoantibody-positive non-diabetic (AAb+), and T1D donor

57 antibodies on 2 consecutive visits and still autoantibody positive or having diabetes at last follow-

58 toantibodies were identified in 561 PLA(2)R1 autoantibodies-positive patients, 27 THSD7A autoantibodi

59 autoantibodies-positive patients, 27 THSD7A autoantibodies-positive patients, and 77 patients with o

60 h focal accumulation in the muscle fibers of autoantibody-positive patients compared with a homogeneo

61 Immunoglobulin G from autoantibody-positive patients induced hyperpolarization

62 estive evidence of a stronger association in autoantibody-positive patients with RA (OR 0.55, 95% con

63 ellent immunotherapy-independent outcomes of autoantibody-positive patients without encephalitis sugg

64 In autoantibody-positive patients, multiparametric characte

65 In autoantibody-positive populations, insulin secretion is

66 king is associated not only with the risk of autoantibody-positive RA but also with the risk of autoa

67 enome-wide association study (GWAS) of 5,539 autoantibody-positive RA cases and 20,169 controls.

68 of 33 [42%]; 3.8+/-4.5 at 10 microg/ml) and autoantibody-positive relatives at increased risk for ID

69 l insulin delays onset of type 1 diabetes in autoantibody-positive relatives of patients with type 1

70 Among autoantibody-positive relatives of patients with type 1

71 We examined a cohort of 3,358 autoantibody-positive relatives of T1D patients in the P

72 ly regulated (interleukin-10-positive, pauci-autoantibody-positive) responses.

73 ritis in an independent replication of 3,929 autoantibody-positive rheumatoid arthritis cases and 5,8

74 toantibodies in 88 dual (ICA512 and phogrin) autoantibody-positive sera could be completely blocked b

75 to identify patients with so-called 'active, autoantibody-positive SLE'.

76 No autoantibody-positive subject had inflammatory arthritis

77 ed from whole genome sequencing of 160 islet autoantibody positive subjects, including 87 who had pro

78 HRCT revealed that 76% of autoantibody-positive subjects had airways abnormalities

79 The median age of autoantibody-positive subjects was 54 years, 52% were fe

80 valence and type of lung abnormalities among autoantibody-positive subjects were similar to those amo

81 In 2 autoantibody-positive subjects with airways disease, inf

82 e consistent with inflammation are common in autoantibody-positive subjects without inflammatory arth

83 lls in early stages of T1D (i.e., in healthy autoantibody-positive subjects) and in more advanced pha

84 edicts a low first-phase insulin response in autoantibody-positive subjects.

85 cestry; T1D (n = 262 clinically defined, 200 autoantibody positive), T2D (n = 345) and controls (n =

86 iagnosed patients ages 1-18 years with islet autoantibody-positive type 1 diabetes (n = 970) and cont