ライフサイエンスコーパス: narcoleptic

1 r, behaviours that induce cataplexy in human narcoleptics.

2 Hcrt receptor 2, which is mutated in canine narcoleptics.

3 o show intense axonal degeneration in canine narcoleptics.

4 cides with symptom onset and increase in the narcoleptics.

5 o show intense axonal degeneration in canine narcoleptics.

6 ular formation and ventral tegmental area of narcoleptic and control Doberman pinchers.

7 mptom onset and compare hypocretin levels in narcoleptic and normal dogs.

8 lso significantly higher than those in adult narcoleptic and normal dogs.

9 explanations of the difference between human narcoleptics and animal models of narcolepsy, including

10 (69.86 +/- 5.31 and 68.36 +/- 4.74 years in narcoleptics and controls, respectively), because class

11 epsy with cataplexy, with no overlap between narcoleptics and controls.

12 explain the lack of light-induced arousal in narcoleptics and its presence in normal individuals.

13 s similar to those that trigger cataplexy in narcoleptic animals.

14 neurons in the mesolimbic dopamine system of narcoleptics are hypersensitive to dopaminergic autorece

15 ed, along with uncertainties concerning the 'narcoleptic borderland', including narcolepsy type 2 (NT

16 Hcrt receptor 2, which is mutated in canine narcoleptics, but lack the Hcrt receptor 1 mRNA.

17 Cataplexy in the narcoleptic canine may be modulated by systemic administ

18 fects of monoaminergic drugs on cataplexy in narcoleptic canines when perfused locally via microdialy

19 increased wakefulness and decreased sleep in narcoleptic canines, whereas TRH (400 and 1600 microg/kg

20 lopride produced a decrease, in cataplexy in narcoleptic canines.

21 The vast majority of narcoleptic-cataplectic individuals have low or undetect

22 We have previously reported that, in the narcoleptic dog, noradrenergic cells of the locus coerul

23 esponding neuronal populations in normal and narcoleptic dogs (Doberman Pinscher) by using choline ac

24 may be operative in spontaneous cataplexy in narcoleptic dogs as well as in narcoleptic humans.

25 humans; yet, unlike narcoleptic humans, the narcoleptic dogs have normal hypocretin levels.

26 date microdialysate dopamine measurements in narcoleptic dogs revealed that the wake-promoting antina

27 ugs that reduce or increase cataplexy in the narcoleptic dogs, greatly increase and decrease, respect

28 es the symptoms of narcolepsy in genetically narcoleptic dogs.

29 tified in the LDT, PPT, and LC of normal and narcoleptic dogs.

30 c to catecholaminergic cells in the brain of narcoleptic dogs.

31 Moreover, modafinil, an anti-narcoleptic drug with ill-defined mechanisms of action,

32 Altogether, 24 of 89 (27%) narcoleptics exhibited pattern A or B or C.

33 Here we show that human narcoleptics have an 85%-95% reduction in the number of

34 aplexy as do narcoleptic humans; yet, unlike narcoleptic humans, the narcoleptic dogs have normal hyp

35 cataplexy in narcoleptic dogs as well as in narcoleptic humans.

36 gs that increase or decrease cataplexy as do narcoleptic humans; yet, unlike narcoleptic humans, the

37 were used to detect histamine cells in human narcoleptics, hypocretin (Hcrt) receptor-2 mutant dogs,

38 oducing cells in postmortem hypothalami from narcoleptic individuals was reported.

39 1N1 virus have the potential to cause per se narcoleptic-like sleep disruption.

40 this or any other brain region have produced narcoleptic-like sleep, suggesting that specific neurons

41 ctivating gene 1-deficient mice) can lead to narcoleptic-like sleep-wake fragmentation and sleep stru

42 In addition to fragmented wakefulness, narcoleptic mammals also display sleep fragmentation, a

43 ding, drinking and energy expenditure in the narcoleptic mice under unperturbed conditions.

44 new mouse model for studying GABA neurons in narcoleptic mice, which could serve as a useful tool for

45 xpenditure were significantly reduced in the narcoleptic mice.

46 upon awakening at a greater rate than in the narcoleptic mice.

47 wever, considered unimpaired in patients and narcoleptic mice.

48 t and manipulate CeA activity selectively in narcoleptic (orexin(-/-)) mice to determine its function

49 ient type 1 and tended to decrease in type 2 narcoleptic patients although the levels with the regula

50 CSF was collected from healthy controls, narcoleptic patients of type 1 with hcrt-1 deficiency, t

51 colepsy diagnosis, although some portions of narcoleptic patients show normal hcrt-1 levels.

52 Sera from 89 narcoleptic patients, 52 patients with other sleep-relat

53 s novel potential therapeutic approaches for narcoleptic patients.

54 As reported elsewhere, almost all narcoleptic subjects were positive for both HLA-DQA1*010

55 In this work, 1,087 control subjects and 420 narcoleptic subjects with cataplexy, from three ethnic g

56 significantly different between control and narcoleptic subjects.

57 etion of orexins is not necessary to prevent narcoleptic symptoms.

58 of Hcrt neurons and Hcrt-null mice also have narcoleptic symptoms.

59 n was studied in the CNS of human and canine narcoleptics using immunohistochemistry and Northern ana

60 a marker of neuronal activity changes in the narcoleptic VGAT-Cre mice by expressing the calcium sens

61 n (hypocretin), a peptide lost in most human narcoleptics, was delivered into the brains of the orexi

62 c silver stain on brain sections from canine narcoleptics, we found elevated levels of axonal degener