INT8388
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In dorsal root ganglia, RIA disclosed a 21% increase in VIP-LI, although no VIP-positive cells could be detected. | |||||||||||||||
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We tested the hypothesis that increases in the spinal levels of vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY) were related to the development of neuropathic pain. | |||||||||||||||
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Furthermore, VIP10-28, the C-terminal fragment that inhibits VIP stimulation of adenylate cyclase, reduced the number of surviving RGCs. | |||||||||||||||
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In addition, c-jun AS-ODN also suppressed the remarkable elevations of VIP and NPY mRNAs and the percentages of phosphorylated c-Jun-, VIP-, and NPY-immunoreactive neurons observed in DRGs following CCI. | |||||||||||||||
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In contrast, SRIF seems to inhibit the VIP stimulation of prolactin release. | |||||||||||||||
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The spinal content of CGRP and SP decreased significantly 4 h after CRD, while galanin and VIP levels increased gradually and reached highest level at 24 h (p<0.05). | |||||||||||||||
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Vasoactive intestinal polypeptide (VIP), a marker of the cranial parasympathetic system, is increased during acute attacks of some primary headaches, and with its expression in the pituitary may link some pituitary tumours to their headache presentations. | |||||||||||||||
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In cats, bilateral electrical stimulation of the sciatic nerve at high, but not low intensity, resulted in a 218% and 132% increase above prestimulation baseline in the levels of CCK and VIP, respectively. | |||||||||||||||
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In rats, the addition of potassium (40 mM in excess) resulted in a 138% and 46% increase in the levels of CCK and VIP, respectively above resting levels (3.7 +/- 1.2 fmol/ml/10 min and 1.7 +/- 0.5 fmol/ml/10 min, respectively). | |||||||||||||||
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These observations suggest that NPY is primarily induced in myelinated primary afferent neurons, while VIP and GAL mRNA induction occurs in a mixed population, a sizeable percentage of which has unmyelinated axons. | |||||||||||||||
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Following the nerve cut, RNA blot analysis demonstrated a dramatic induction of NPY, VIP, and GAL mRNA levels from the undetectable constitutive level of expression. | |||||||||||||||
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Plasma VIP is increased in active physical exercise and in transcutaneous nerve stimulation. | |||||||||||||||
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No significant increase in the plasma VIP was found. | |||||||||||||||
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V(mean MCA) decreased (16.3 +/- 5.9%) and diameter of STA increased significantly after VIP (45.9 +/- 13.9%). | |||||||||||||||
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Increases in circulating VIP are known to stimulate secretion of renin. | |||||||||||||||
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Asbestos-related increase in pulmonary levels of vasoactive intestinal peptide (VIP). | |||||||||||||||
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Asbestos-related increase in pulmonary levels of vasoactive intestinal peptide (VIP). | |||||||||||||||
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PACAP and VIP are known to be upregulated in primary sensory neurons following nerve injury, implying that these neuropeptides could be mediators of sensory transmission in neuropathic pain states. | |||||||||||||||
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Studies on the additional involvement of an active local vasodilator have demonstrated a moderate increase in plasma vasoactive intestinal polypeptide (VIP) but excluded a series of known dilators. | |||||||||||||||
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Vasoactive intestinal polypeptide (VIP), a marker of the cranial parasympathetic system, is increased during acute attacks of some primary headaches, and with its expression in the pituitary may link some pituitary tumours to their headache presentations. | |||||||||||||||
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General Comments
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