INT397
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
OBJECTIVE: It has been established in animals that somatostatin (SST) is released from pain-activated sensory nerve endings and exerts systemic antinociceptive and anti-inflammatory actions. | |||||||||||||||
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OBJECTIVE: It has been established in animals that somatostatin (SST) is released from pain-activated sensory nerve endings and exerts systemic antinociceptive and anti-inflammatory actions. | |||||||||||||||
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We have previously shown in animals that somatostatin released from capsaicin-sensitive afferents in response to inflammation and tissue damage exerts systemic anti-nociceptive and anti-inflammatory actions. | |||||||||||||||
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Somatostatin release by human gastric mucosa. | |||||||||||||||
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These results imply possible impairments of the paracrine release of somatostatin in peptic ulcer disease and in pernicious anemia. | |||||||||||||||
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Somatostatin release by antral and fundic mucosa of patients with pernicious anemia was also significantly decreased (20 +/- 8 pg/mg tissue, n = 12, and 7.6 +/- 2 pg/mg tissue, n = 12, respectively) (P less than 0.05). | |||||||||||||||
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Somatostatin was found to be released at a constant rate by antral explants during 3 h of incubation. | |||||||||||||||
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In active duodenal ulcer antral and fundic 2-h somatostatin release (18.7 +/- 2.6 pg/mg tissue (means + SE), n = 75; and 27 +/- 3 pg/mg tissue, n = 94, respectively) was significantly lower than release by control antral and fundic mucosa (83 +/- 17 pg/mg tissue, n = 39, and 72 +/- 16 pg/mg tissue, n = 42, respectively) (P less than 0.01). | |||||||||||||||
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We applied the organ culture technique to examine somatostatin release by explants of human gastric mucosa taken from patients with active duodenal ulcer, from control subjects, and from patients with pernicious anemia. | |||||||||||||||
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Carbamazepine and phenytoin inhibit somatostatin release from dispersed cerebral cells in culture. | |||||||||||||||
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Phenytoin, another anticonvulsant with many similar properties, also blocked picrotoxin-induced somatostatin release at a concentration of 10(-4) M, and its effects were also reversed by veratridine at a concentration of 10(-5) M. | |||||||||||||||
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Concentrations of carbamazepine within the therapeutic range (4 x 10(-5) M) inhibited spontaneous release of somatostatin and blocked secretory responses to the epileptogen, picrotoxin, and to the cyclic cAMP stimulator forskolin. | |||||||||||||||
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Some of its effects may involve release of somatostatin (SST) and actions on enteric neurons. | |||||||||||||||
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Some of its effects may involve release of somatostatin (SST) and actions on enteric neurons. | |||||||||||||||
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The beta3-adrenoceptor agonist GW427353 (Solabegron) decreases excitability of human enteric neurons via release of somatostatin. | |||||||||||||||
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SST release from human primary adipocytes was measured with enzyme-linked immunoabsorbent assay. | |||||||||||||||
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Effects of various types of natural skin stimuli on the in situ release of immunoreactive substance P and somatostatin from the rabbit dorsal horn were examined. | |||||||||||||||
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The release of gastric and pancreatic somatostatin is regulated by ingested and circulating nutrients and is modulated by neural mechanisms (cholinergic, adrenergic, dopaminergic) histamine, prostaglandins, opiates and gastrointestinal hormones. | |||||||||||||||
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The present communication summarises the evidence for the release of somatostatin into the gastrointestinal lumen and the potential action of luminally released somatostatin. | |||||||||||||||
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The present communication summarises the evidence for the release of somatostatin into the gastrointestinal lumen and the potential action of luminally released somatostatin. | |||||||||||||||
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General Comments
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