ライフサイエンスコーパス: small fiber

1 ost patients have impaired function of these small fibers.

2 brane of the soma, axon initial segment, and small fibers.

3 mprises over 20 large muscle fibers and four small fibers.

4 s between large/small fibers and sympathetic/small fibers.

5 tients had functional abnormalities of these small fibers; 29 patients (60%) had abnormal sweat test

6 t permitted rapid, noninvasive evaluation of small-fiber alterations in patients and could be used to

7 hat premium products release more amounts of small fibers and disintegrate more slowly than average o

8 s; and abnormal communications between large/small fibers and sympathetic/small fibers.

9 This loss was accompanied with loss of small fiber axon counts and declining metabolic reserve

10 (+) and anti-HMGCR(+) Abs, a large number of small fibers corresponding to both atrophic and regenera

11 However, CCM quantifies small fiber damage rapidly and noninvasively and detects

12 eal confocal microscopy (IVCCM) can quantify small fiber damage.

13 s (n = 46, 54.8%), patients with significant small fiber deficits (n = 38, 45.2%) reported higher ave

14 on, compared to patients without significant small fiber deficits (n = 46, 54.8%), patients with sign

15 rtion of former critically ill patients show small fiber deficits which seem to be associated with in

16 s, we aimed to identify associations between small fiber deficits, pain, health-related quality of li

17 ng, and numbness are generally attributed to small fiber dysfunction.

18 ema, and abnormal sweating-are explicable by small-fiber dysfunction.

19 against pre-equilibrium SPME (using multiple small fibers), equilibrium SPME, and liquid extraction m

20 Secondary measures included functional small fiber evaluation, such as autonomic (heart rate, b

21 mportant clinical implications for assessing small-fiber function in neuropathies and neuropathic pai

22 alues in thermal testing, indicating reduced small fiber functioning.

23 ve patient care and broaden our knowledge of small-fiber functions.

24 Similar to small fibers, Ia axons are vulnerable to diabetes, and t

25 ullary cores that have a structure and dense small-fiber innervation resembling that of tooth pulp.

26 fibers is reduced by 50%, and the number of small fibers is also occasionally reduced.

27 Small-fiber lesions are easily missed on examination and

28 howed length-dependent somatic and autonomic small fiber loss, more severely expressed in patients wi

29 Small fiber neuropathy (SFN) is an important feature of

30 data are available on the natural history of small fiber neuropathy (SNF).

31 n, topical application of capsaicin causes a small fiber neuropathy and is associated with a delay in

32 hese mice develop sensory loss with a distal small fiber neuropathy and peripheral myelinopathy.

33 Patients with small fiber neuropathy for which no other cause has been

34 Objective quantification of small fiber neuropathy in patients with human immunodefi

35 This report describes 2 patients with small fiber neuropathy in whom vasculitis was found to b

36 e wound healing that isolated the effects of small fiber neuropathy on the healing process.

37 suggesting a patchy manifestation pattern of small fiber neuropathy.

38 studies were consistent with a dysautonomic small fiber neuropathy.

39 Idiopathic small-fiber neuropathy (I-SFN), clinically characterized

40 Small-fiber neuropathy (SFN) is a disorder of peripheral

41 Small-fiber neuropathy (SFN) is characterized by injury

42 nful disorders inherited erythromelalgia and small-fiber neuropathy (SFN).

43 with recordings from 17 female patients with small-fiber neuropathy and 9 female controls.

44 iceptors in the fibromyalgia group, 114 from small-fiber neuropathy patients, and 66 from controls.

45 f silent nociceptors in fibromyalgia, 34% in small-fiber neuropathy, and 2.2% in controls.

46 silent nociceptors in fibromyalgia, 22.7% in small-fiber neuropathy, and 3.7% in controls.

47 exhibit hyperexcitability resembling that in small-fiber neuropathy, but high activity-dependent slow

48 oximately 30% of cases of idiopathic painful small-fiber neuropathy.

49 s of 104 patients with painful predominantly small-fiber neuropathy.

50 w (Bcl-2l2) is required for the viability of small fiber nociceptive sensory neurons.

51 hile oxidative stress has been implicated in small-fiber painful peripheral neuropathies, antioxidant

52 tolerated is limited by the development of a small-fiber painful peripheral neuropathy.

53 ibromyalgia population demonstrates signs of small fiber pathology as measured by CCM.

54 Spinal inhibitory dysfunction and peripheral small fiber pathology may contribute to the clinical phe

55 Small fiber pathology was detected in the cornea of 51%

56 h outcomes of skin biopsies in patients with small fiber pathology.

57 for 12/15-lipoxygenase in diabetic large and small fiber peripheral and autonomic neuropathies.

58 al changes characteristic for both large and small fiber peripheral diabetic neuropathies and axonal

59 nsgenes resulted in restoration of large and small fiber peripheral nerve function.

60 nerves from chronic CRPS-I patients confirm small-fiber-predominant pathology.

61 Indeed, small-fiber-predominant polyneuropathies cause CRPS-like

62 Small fibers sense pain and temperature but also regulat

63 hat the animals had some normally conducting small fiber sensory nerves.

64 trophic factor that promotes the survival of small fiber sensory neurons and sympathetic neurons in t

65 ablish bcl-w(-/-) mice as an animal model of small fiber sensory neuropathy and provide new insight r

66 hies that affect large nerve fibers; painful small fiber sensory neuropathy has not previously been d

67 Small fiber sensory neuropathy is a common disorder in w

68 In the majority of patients, the cause of small fiber sensory neuropathy is unknown, and treatment

69 nation, pressure threshold, and quantitative small fiber sensory testing.

70 everity, and distribution of both large- and small-fiber sensory loss and which approaches and techni

71 s/1 mm may be used as a surrogate measure of small-fiber sensory loss but appear not to correlate clo

72 In contrast, P2X3 mRNA is localized to small-fiber sensory neurons and produces less mechanosen

73 performing functional rather than structural small fiber studies when evaluating erythromelalgia.

74 rge-fiber topography, but was not changed in small-fiber topography with these inhibitors.

75 lgia is associated with a structural loss of small fibers using the ENFD technique and to compare thi

76 lgia is associated with a structural loss of small fibers using the ENFD technique and to compare thi

77 In addition, small fibers were initially detected in most of the samp