ライフサイエンスコーパス: neurogenic inflammation

1 uous airway inflammation, a process known as neurogenic inflammation.

2 TRPV4 deletion attenuated PAR(2)-stimulated neurogenic inflammation.

3 d oil, demonstrating that NMB contributes to neurogenic inflammation.

4 ng increasingly blurred by new insights into neurogenic inflammation.

5 ies in primary afferents and are involved in neurogenic inflammation.

6 important role than DRRs in formalin-induced neurogenic inflammation.

7 heral chemosensory neurons, causing pain and neurogenic inflammation.

8 licated in somatosensory function, pain, and neurogenic inflammation.

9 plasma extravasation, which is a measure of neurogenic inflammation.

10 nduce a local inflammatory response known as neurogenic inflammation.

11 in nerves may indicate its participation in neurogenic inflammation.

12 y opposing the action of Substance P (SP) in neurogenic inflammation.

13 gered lipid mediators and may be relevant in neurogenic inflammation.

14 ther investigation in models of migraine and neurogenic inflammation.

15 nomedical use for disorders characterized by neurogenic inflammation.

16 g pain and release neuropeptides that induce neurogenic inflammation.

17 CGRP, which affect intraocular pressure and neurogenic inflammation.

18 tide (iCGRP), a neuropeptide associated with neurogenic inflammation.

19 n in sensory nerve endings can contribute to neurogenic inflammation.

20 s are important mediators of pain, itch, and neurogenic inflammation.

21 es of primary afferent neurons that initiate neurogenic inflammation and are required for the develop

22 kinin neuropeptide, has been associated with neurogenic inflammation and asthma; therefore, we chose

23 PV1 and TRPA1 are thought to be required for neurogenic inflammation and development of inflammatory

24 erapy may include antibodies to mediators of neurogenic inflammation and even treatment of bacteria i

25 Capsaicin causes neurogenic inflammation and has analgesic and anti-infla

26 PAR(2)) on primary sensory neurons to induce neurogenic inflammation and hyperalgesia.

27 (PAR2) on primary afferent neurons to cause neurogenic inflammation and hyperalgesia.

28 to sickle pain pathophysiology by promoting neurogenic inflammation and nociceptor activation via th

29 ssed in primary sensory neurons that mediate neurogenic inflammation and pain transmission, and PAR(2

30 As a mediator of neurogenic inflammation and pain, we hypothesized that l

31 flammatory proteases, is a major mediator of neurogenic inflammation and pain.

32 potential (TRP) ion channels, which amplify neurogenic inflammation and pain.

33 P) channels of nociceptive neurons to induce neurogenic inflammation and pain.

34 red ligand that excites nociceptors, causing neurogenic inflammation and pain.

35 ential vanilloid 1 (TRPV1) activation causes neurogenic inflammation and plays an important role in a

36 ation elicits robust pain behaviours without neurogenic inflammation and produces profound hypersensi

37 tors in airway sensory neurons, resulting in neurogenic inflammation and respiratory hypersensitivity

38 Neurogenic inflammation and the role of nerve growth fac

39 al tumor invasion of intrapancreatic nerves, neurogenic inflammation, and tumor metastases along extr

40 Substance P (SP), involved in neurogenic inflammation by acting through its receptor N

41 y was to determine the role of DRR and AR in neurogenic inflammation by examining the blood perfusion

42 nsequently, this work provides evidence that neurogenic inflammation can be induced in the human airw

43 n (1% in 25 microl), which is known to cause neurogenic inflammation, failed to produce edema formati

44 cetylcholine receptors prevents SCC-mediated neurogenic inflammation for both denatonium and the bact

45 e results suggest: (1) an important role for neurogenic inflammation in pancreatitis and pain-related

46 s experimental inflammatory hyperalgesia and neurogenic inflammation in rats and naturally occurring

47 he periphery and these signals can result in neurogenic inflammation in the innervated tissue.

48 primary mediator of an axon reflex mediating neurogenic inflammation in the intestine.

49 id 1 (TRPV1) receptors in the development of neurogenic inflammation in the pelvis and pelvic organ c

50 gate whether substance P (SP) contributes to neurogenic inflammation in the skeletal muscle tissue.

51 SP does not play a critical role in inducing neurogenic inflammation in the skeletal muscle tissue.

52 f trigeminal pain fibers by capsaicin evokes neurogenic inflammation in the surrounding epithelium.

53 skin (neurogenic spots), caused by cutaneous neurogenic inflammation, in the dermatome that overlaps

54 Neurogenic inflammation is believed to originate with th

55 Significantly, TRPA1-dependent neurogenic inflammation is greater in mice anesthetized

56 These data raise the possibility that neurogenic inflammation is not a major factor in headach

57 s innervating the bladder and resulting in a neurogenic inflammation localized to the bladder.

58 This new mechanism of protease-induced neurogenic inflammation may contribute to the proinflamm

59 n precipitated by stress and seem to involve neurogenic inflammation (NI) of the dura mater associate

60 ence debilitating headaches that result from neurogenic inflammation of the dura and subsequent sensi

61 flexes, including sneezing, apnea, and local neurogenic inflammation of the mucosa.

62 ere, we show that an acupoint is one form of neurogenic inflammation on the skin.

63 nal SP levels may be involved in maintaining neurogenic inflammation or the development of airway hyp

64 fense, drug-induced anaphylactoid reactions, neurogenic inflammation, pain, itch, and chronic inflamm

65 Using the rat model of neurogenic inflammation, the albumin extravasation ratio

66 tor calcitonin gene-related peptide mediates neurogenic inflammation via the calcitonin receptor-like

67 us pain, hyperalgesia/allodynia and signs of neurogenic inflammation were studied clinically and ther

68 perimentally as an inducer of acute pain and neurogenic inflammation, which are largely mediated by t

69 Neurogenic inflammation, which results from peripheral r

70 conduction of these spikes may contribute to neurogenic inflammation while orthodromic (centripetal)

71 This neurogenic inflammation within the meninges has been sug