ライフサイエンスコーパス: AMAN

1 AMAN and AIDP have an immunologic basis, and some cases

2 assical Golgi alpha-mannosidase II (AMAN-2), AMAN-3 displayed a cobalt-dependent alpha1,6-mannosidase

3 ed technology in 34 control, 12 AIDP, and 31 AMAN cases.

4 ution of DR13 allelic forms between AIDP and AMAN cases may suggest that there are different immunolo

5 Binding of anti-GD1a mAbs and AMAN sera with anti-GD1a Abs to these derivatives was ex

6 with predominant motor neuropathies such as AMAN.

7 or differentiating the two disease entities (AMAN and AIDP) and focuses our attention on particular D

8 to the classical Golgi alpha-mannosidase II (AMAN-2), AMAN-3 displayed a cobalt-dependent alpha1,6-ma

9 In AMAN patients, alleles DRB1*1301-03 and DRB1*1312, taken

10 neuromuscular junction is a major factor in AMAN.

11 nation for preferential motor axon injury in AMAN.

12 hy (AIDP) and acute motor axonal neuropathy (AMAN) being the most common forms observed.

13 The acute motor axonal neuropathy (AMAN) form of the Guillain-Barre syndrome is a paralytic

14 mpatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disease (median d

15 Campylobacter acute motor axonal neuropathy (AMAN) variant of GBS, and immunization of rabbits with G

16 The acute motor axonal neuropathy (AMAN) variant of Guillain-Barre syndrome (GBS) is associ

17 sociated with acute motor axonal neuropathy (AMAN), a form of Guillain-Barre syndrome that selectivel

18 rre syndrome, acute motor axonal neuropathy (AMAN), and acute motor and sensory axonal neuropathy (AM

19 y (AIDP) from acute motor axonal neuropathy (AMAN), as classified by electrophysiology (sensitivity 1

20 drome subform acute motor axonal neuropathy (AMAN), Campylobacter jejuni enteritis triggers the produ

21 In acute motor axonal neuropathy (AMAN), the attack appears directed against the axolemma

22 hy (AIDP) and acute motor axonal neuropathy (AMAN).

23 cutoff titer of greater than 1:1,000, 24% of AMAN patients and none of the AIDP patients had IgG anti

24 a cutoff titer of greater than 1:100, 60% of AMAN versus 4% of AIDP patients had IgG anti-GD1a antibo

25 mpylobacter infection was detected in 81% of AMAN and 50% of AIDP patients, and anti-ganglioside anti

26 In 7 fatal cases of AMAN, immunocytochemistry demonstrated the presence of I

27 of rabbits with GM1 has produced a model of AMAN.

28 odies may be involved in the pathogenesis of AMAN.

29 To elucidate the pathophysiology of AMAN, we have developed several monoclonal antibodies (m

30 The GD1a-derivative binding patterns of AMAN sera resembled those with motor-specific mAbs.

31 Enzymatic characterization of recombinant AMAN-3 and confocal microscopy studies using a knock-in

32 Our data demonstrated that AMAN-3 is a Golgi alpha-mannosidase required for core fu

33 These results suggest that AMAN is a novel disorder caused by an antibody- and comp

34 tal GlcNAc of N-glycans, which suggests that AMAN-3 is the relevant mannosidase on whose action FUT-6

35 tibodies (> 1:100) were detected in both the AMAN and the AIDP forms (57% vs 35%, NS).

36 anti-GM1 (>1:1,000) were more common in the AMAN form (24% vs 8%, NS).

37 The typical AMAN-associated anti-ganglioside antibodies were rarely

38 Using AMAN-3 and other C. elegans glycoenzymes, we were able t

39 GD1a antibodies were closely associated with AMAN but not AIDP.

40 II HLA associations were not identified with AMAN, suggesting a different immunological mechanism of

41 g DNA-based typing methods, 47 patients with AMAN, 25 patients with AIDP, and 97 healthy controls wer