ライフサイエンスコーパス: AIDP

1 AIDP predictions were confirmed neuropathologically in 4

2 AIDP was also paired with antemortem MRI to test against

3 ed by DNA-based technology in 34 control, 12 AIDP, and 31 AMAN cases.

4 AMAN and AIDP have an immunologic basis, and some cases are assoc

5 entiating the two disease entities (AMAN and AIDP) and focuses our attention on particular DR beta/DQ

6 Next, using SDCP-MS and AIDP-Wb, we rapidly identify multiple regulatory factors

7 ential application of Reel-seq, SDCP-MS, and AIDP-Wb can greatly help to translate large sets of GWAS

8 rometry) to identify fSNP-bound proteins and AIDP-Wb (allele-imbalanced DNA pulldown-Western blot) to

9 l distribution of DR13 allelic forms between AIDP and AMAN cases may suggest that there are different

10 s associated with protection (p = 0.05) from AIDP.

11 observed an identical diagnostic shift from AIDP to axonal GBS with modified criteria as that descri

12 In AIDP patients, the DRB1*1301 allele showed a significant

13 e, the search for the putative antibodies in AIDP and those that might be present in CNS diseases sho

14 he DRB1*1301 allele was not increased, as in AIDP patients.

15 The role of T-cell-mediated immunity in AIDP remains unclear and there is evidence for the invol

16 es were closely associated with AMAN but not AIDP.

17 greater than 1:100, 60% of AMAN versus 4% of AIDP patients had IgG anti-GD1a antibodies; with a cutof

18 ction was detected in 81% of AMAN and 50% of AIDP patients, and anti-ganglioside antibodies were comm

19 results suggest that at least some forms of AIDP are complement mediated.

20 ntal in understanding the pathophysiology of AIDP.

21 criteria, we identified comparable rates of AIDP (56.2% vs. 58.7%; p=0.70), axonal GBS (35.1% vs. 36

22 This prospective multicenter cohort study of AIDP met its primary end points.

23 e inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) being the

24 e inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).

25 e inflammatory demyelinating polyneuropathy (AIDP) pattern of Guillain-Barre syndrome.

26 e inflammatory demyelinating polyneuropathy (AIDP) type of GBS or in central nervous system (CNS) dis

27 e inflammatory demyelinating polyneuropathy (AIDP), the attack appears directed against a component o

28 matory demyelinating polyradiculoneuropathy (AIDP) (71.5% vs. 72%; p=1), axonal GBS (17.5% vs. 14.7%;

29 matory demyelinating polyradiculoneuropathy (AIDP) from acute motor axonal neuropathy (AMAN), as clas

30 matory demyelinating polyradiculoneuropathy (AIDP) subtype resembles experimental autoimmune neuritis

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

32 :1,000, 24% of AMAN patients and none of the AIDP patients had IgG anti-GD1a antibodies.

33 Three AIDP subjects who were autopsied had had symptoms for 3

34 topes were associated with susceptibility to AIDP (p = 0.009 and p = 0.004, respectively), and the DQ

35 Results suggest using AIDP in the diagnostic workup for common parkinsonian sy

36 ods, 47 patients with AMAN, 25 patients with AIDP, and 97 healthy controls were studied for the distr