ライフサイエンスコーパス: EAN

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1 EAN was induced in Lewis rats (n = 116, in three indepen

2 tion of peripheral nerves that characterizes EAN.

3 lective upregulation of specific MMPs during EAN and their varied cellular localization suggests that

4 ur MMPs were differentially regulated during EAN.

5 localization in sciatic nerve tissue during EAN, using a semiquantitative competitive reverse transc

6 isease accelerated the rate of recovery from EAN.

7 macrophages as pathogenic effector cells in EAN, these data suggest that M2-differentiated macrophag

8 te the P0106-125-specific immune response in EAN.

9 nce of the macrophage polarization status in EAN.

10 amage and may even protect neural tissues in EAN.

11 sensory neuropathy type la, can also induce EAN.

12 The clinical course of P0106-125-induced EAN in mice deficient for IL-10(0/0), IL-4(0/0), or STAT

13 work (DMN), the executive attention network (EAN), and the medial visual network (MVN), with the MVN

14 Experimental allergic neuritis (EAN) is considered the in vivo model of Guillain-Barre s

15 Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barre syndrome.

16 can induce experimental autoimmune neuritis (EAN), a model of human inflammatory neuropathy.

17 B-1101, in experimental autoimmune neuritis (EAN), an animal model of Guillain-Barre syndrome.

18 mal model, experimental autoimmune neuritis (EAN), are typically acute monophasic diseases of the PNS

19 me, namely experimental autoimmune neuritis (EAN), induced in Lewis rats by immunization with bovine

20 ced murine experimental autoimmune neuritis (EAN).

21 protic ionic liquid (ethylammonium nitrate, EAN).

22 ay a multifactorial role in the aetiology of EAN.

23 cantly increased early in the development of EAN and continued to rise, peaking at day 15 coincident

24 ase (MMP) inhibitor, prevents development of EAN when given from the day of immunization and, more im

25 of immunization prevented the development of EAN, and when given from the onset of symptoms, it signi

26 tological examination of the tibial nerve of EAN animals revealed that flecainide provided significan

27 NF-alpha are involved in the pathogenesis of EAN, and that drugs of this type may have potential as n

28 ement of MMP activity in the pathogenesis of EAN.

29 relating to the effector phase of Lewis rat EAN that may be relevant to C. jejuni-induced GBS are di

30 reater connectivity within the DMN and right EAN (corrected P [P(corr)] < 0.05 versus controls), and

31 etween the insula and both the DMN and right EAN (P(corr) < 0.05).

32 egeneration in the periphery in animals with EAN.

33 previously in the pathology associated with EAN.

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