Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Noxious stimulation can suppress epileptic seizures in humans and epileptiform activity in laboratory animals. Using as a model system the focal epileptiform activity (FEA) induced by the pneumophoresis of penicillin, the role of 5-hydroxytryptamine (5HT) in suppression of this activity by noxious stimulation was investigated. Drugs known to depress dorsal raphe unit activity, (+/-)-8-hydroxydipropylaminotetralin (DPAT), imipramine, and fluoxetine prevented suppression of FEA induced by noxious stimulation. Desimipramine, which depresses locus ceruleus but not dorsal raphe unit activity, was ineffective in blocking the suppression. Quipazine, an agonist at 5-HT receptors, in part restored the suppression that had been blocked by DPAT or imipramine. Several serotonin antagonists effective at 5-HT1 and 5-HT2 receptors blocked suppression, but an unequivocal determination of the serotonin receptor subtype mediating suppression could not be made. We conclude that 5-HT mediates suppression of FEA induced by noxious stimulation.
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PMID:Serotonin mediates suppression of focal epileptiform activity induced by noxious stimulation. 249 71

In this case, we report a patient with a known seizure disorder who develops an increased frequency of his seizures concommitant with severe depression. When the seizures failed to respond to the usual management, Desipramin was added to the treatment and, contrary to the idea that Desipramin lowers the seizure threshold, we found that this drug was not only effective in improving the depressive symptoms but it appeared to contribute to a rather dramatic decrease in the number of seizures being suffered by this patient.
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PMID:The use of a tricyclic antidepressant in epilepsy. 1789 89

The pathogenesis of portal hypertension (PH) involves venous congestion with gastric mucosal capillary dilatation. The formation of new blood vessels, as was shown in experimental models of PH, is pathological hallmark of PH. Generation of new blood vessels is stimulated by vascular endothelial growth factor (VEGF), the regulator of angiogenesis. The aim of the study was to investigate changes in gastric microvessels in patients with liver cirrhosis complicated with PH in different stages, and the factors influencing the development of portal hypertensive gastropathy. We studied the relation between gastric mucosal capillary parameters, measured morphometrically, and endoscopic appearances in 56 patients with PH. The gastric biopsy was obtained from antrum and corpus of the stomach. We determined expression and localization of Fit-1 receptor for VEGF in human gastric mucosa by immunohistochemistry. Mucosal capillary network assessed on histological sections immunostained for CD34, a specific marker for endothelial cells and revealed proliferating endothelial cells by Ki-67 antibodies. Nicon CP 995 camera and digital image analyzing system (DMI-1) was used for morphometry. The number, size and relative volume of vessels in gastric mucosa were evaluated. Helicobacter pillory-positive patients were excluded from study. The number of vessels in gastric mucosa was significantly higher in groups with PH (p < 0.05) compared with patients without PH. The mean size of vessels in gastric mucosa was decreased in patients with PH (212 +/- 20 vs 282 +/- 25 mkm2, p < 0.05) in atrum and (155 +/- 12 vs 198 +/- 13 mkm2, p < 0.039) in corpus. The majority of the vessels were presented by newly formed small sized capillaries. Meanwhile the relative volume of vessels in gastric mucosa was not changed significantly in groups with PH. These observations have not supported the view that PH is usually associated with a prominent dilatation of gastric mucosal capillaries. Our data have shown intensifying of neoangiogenesis in human gastric mucosa at PH. The anti-angiogenic therapeutic approach could be taken into consideration for patients suffering from PH.
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PMID:[Morphological features of the gastric mucosa capillary network in patients with portal hypertension]. 2216 32