ライフサイエンスコーパス: dysautonomia

1 mpathetic dysfunction similar to humans with dysautonomia.

2 esponsible for the milder course in familial dysautonomia.

3 uanylate cyclase coupling to cGMP in cardiac dysautonomia.

4 nt disorders, reduction in consciousness and dysautonomia.

5 r Ca(2+) impairment underpinning sympathetic dysautonomia.

6 ion abnormalities and profound physiological dysautonomia.

7 and this syndrome and others with associated dysautonomia.

8 (AAN) is an acquired, often severe, form of dysautonomia.

9 tically and pathophysiologically in acquired dysautonomia.

10 ic dysfunction and more frequent cholinergic dysautonomia.

11 ic function, both can be considered forms of dysautonomia.

12 nguishes these disorders from other types of dysautonomia.

13 from 157 patients with a variety of types of dysautonomia.

14 laints, connective tissue abnormalities, and dysautonomia.

15 , we assess CG-2 as a candidate for familial dysautonomia.

16 of 6-[18F]fluorodopamine in 26 patients with dysautonomia.

17 pathetic neurons leading to diabetes-induced dysautonomias.

18 ent clinical manifestation (64%) followed by dysautonomia (16 patients [8%]) and encephalopathy (15 p

19 ated to increased autonomic symptoms, making dysautonomia a plausible therapeutic target.

20 it of human Elongator (Elp1) causes familial dysautonomia, a severe recessive neuropathy.

21 Migraine, post-concussional syndrome, and dysautonomias also cause persistent dizziness and may be

22 In MSA, severe dysautonomia and early development of combined autonomic

23 otype resembles that of the adults, although dysautonomia and hypoventilation are less frequent or se

24 midodrine supports the hypothesis of partial dysautonomia and indicates that the use of alpha1-agonis

25 its strong link with chronic pain, fatigue, dysautonomia and the adverse impact on quality of life.

26 spectrum disorders, schizophrenia, familial dysautonomia, and Alzheimer's disease.

27 , reduced accessibility of cardiac reserves, dysautonomia, and hypertrophy.

28 her syndromes such as Klippel-Feil, familial dysautonomia, and Marfan syndrome demonstrate high rates

29 Prevention of pain and dysautonomia are also clinical targets.

30 Dysautonomias are an important subject in clinical neuro

31 y with clinical features similar to familial dysautonomia as well as contractures, we identified a de

32 clinical pathophysiologic classification of dysautonomias, based on the occurrence of sympathetic ne

33 Methods for detecting dysautonomia can be as simple as performing a history an

34 G-2 (C9ORF5), was isolated from the familial dysautonomia candidate region on 9q31 using a combinatio

35 direct genomic sequencing from the familial dysautonomia candidate region on 9q31.

36 gene DYS, which is responsible for familial dysautonomia (FD) and has been mapped to a 0.5-cM region

37 The autosomal recessive disorder familial dysautonomia (FD) has recently been demonstrated to be c

38 Familial dysautonomia (FD) is a debilitating disorder that affect

39 Familial dysautonomia (FD) is a devastating developmental and pro

40 Familial dysautonomia (FD) is a rare but fatal peripheral neuropa

41 Familial dysautonomia (FD) is a severe hereditary sensory and aut

42 Familial dysautonomia (FD) is a severe neurodegenerative disorder

43 Familial dysautonomia (FD) is an autosomal recessive neurodegener

44 Familial dysautonomia (FD) is caused by mutations in IKBKAP, and

45 Familial dysautonomia (FD) is characterized by severe and progres

46 Familial dysautonomia (FD) is the best-known and most common memb

47 ed to generate and purify iNCs from familial dysautonomia (FD) patient fibroblasts.

48 Familial dysautonomia (FD), a devastating hereditary sensory and

49 ere generated from individuals with familial dysautonomia (FD), a rare, fatal genetic disorder affect

50 (IKBKAP) gene as the major cause of familial dysautonomia (FD), a recessive sensory and autonomic neu

51 Familial dysautonomia (FD), also known as HSAN type III, is an au

52 to the high morbidity/mortality of familial dysautonomia (FD), the mechanisms remain unclear.

53 n Elp1p (IKAP) are a known cause of familial dysautonomia (FD).

54 erature and sweating dysfunction in familial dysautonomia (FD).

55 Familial dysautonomia (FD; also known as "Riley-Day syndrome"), a

56 d autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian Inheritance in Man (O

57 s including cutaneous flushing and pruritus, dysautonomia, functional gastrointestinal symptoms, chro

58 Dysautonomia has also been recognised in other movement

59 The classification of dysautonomias has been confusing, and the pathophysiolog

60 sing fibroblasts from patients with familial dysautonomia (hereditary sensory and autonomic neuropath

61 65.5%, amnesia 55.6%, hallucinations 51.9%), dysautonomia (hyperhidrosis 86.2%, cardiovascular 48.3%)

62 Dysautonomia in degenerative disorders also affect respi

63 are common manifestations of cardiovascular dysautonomia in Parkinson's disease and related synuclei

64 Although the clinical presentation of dysautonomia in these two disorders may overlap, yet pat

65 this apparently disease specific peripheral dysautonomia is unknown and would be the subject of much

66 Dysautonomia may occur during hemiplegia or in isolation

67 at it may have a role in some forms of human dysautonomia, most of which have no known cause.

68 frequent focal seizures, prominent amnesia, dysautonomia, neuromyotonia and neuropathic pain.

69 Patients with dysautonomia often have unpredictable and paradoxical ph

70 thophysiologies include hypovolemia, partial dysautonomia, or a primary hyperadrenergic state.

71 ificantly more abundant in cells of familial dysautonomia patients with IKBKAP (I-kappa-B kinase comp

72 on were detected for either gene in familial dysautonomia patients.

73 The term dysautonomia refers to a change in autonomic nervous sys

74 tion of ASIC2 recapitulates the pathological dysautonomia seen in heart failure and hypertension and

75 Here, we describe a novel syndrome of pain, dysautonomia, small hands and small feet in a kindred ca

76 out detectable cardiac pathology, as well as dysautonomia, some specific features, and the principles

77 inical manifestation of primary degenerative dysautonomias such as multiple system atrophy (MSA) and

78 es like spinal muscular atrophy and familial dysautonomia that allowed partial modeling of the diseas

79 heart in patients with acquired, idiopathic dysautonomias using thoracic positron-emission tomograph

80 Patients with dysautonomia who did not have sympathetic neurocirculato

81 igrostriatal system of the brain, but also a dysautonomia, with norepinephrine loss in the sympatheti

82 vascular disease associated with sympathetic dysautonomia would have significant therapeutic utility.