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High hepatotoxic dose of paracetamol produces generalized convulsions and brain damage in rats. A counteraction with the stable gastric pentadecapeptide BPC 157 (PL 14736)

100%

Ilic S., Drmic D., Zarkovic K., Kolenc D., Coric M., Brcic L., Klicek R., Radic B., Sever M., Djuzel V., Ivica M., Boban Blagaic A., Zoricic Z., Anic T., Zoricic I., Djidic S., Romic Z., Seiwerth S., Sikiric P.

Journal of Physiology and Pharmacology

2010

tom 61

nr 2

We focused on stable gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, MW 1419, an anti-ulcer peptide efficient in inflammatory bowel disease trials (PL 14736), no toxicity reported) because of its hepatoprotective effects. We investigate a particular aspect of the sudden onset of encephalopathy with extreme paracetamol overdose (5 g/kg intraperitoneally) so far not reported: rapidly induced progressive hepatic encephalopathy with generalized convulsions in rats. BPC 157 therapy (10 µg, 10 ng, 10 pg/kg, intraperitoneally or intragastrically) was effective (µg-ng range) against paracetamol toxicity, given in early (BPC 157 immediately after paracetamol, prophylactically) or advanced stage (BPC 157 at 3 hours after paracetamol, therapeutically). At 25 min post-paracetamol increased ALT, AST and ammonium serum values precede liver lesion while in several brain areas, significant damage became apparent, accompanied by generalized convulsions. Through the next 5 hour seizure period and thereafter, the brain damage, liver damage enzyme values and hyperammonemia increased, particularly throughout the 3-24 h post-paracetamol period. BPC 157 demonstrated clinical (no convulsions (prophylactic application) or convulsions rapidly disappeared (therapeutic effect within 25 min)), microscopical (markedly less liver and brain lesions) and biochemical (enzyme and ammonium serum levels decreased) counteraction. Both, the prophylactic and therapeutic benefits (intraperitoneally and intragastrically) clearly imply BPC 157 (µg-ng range) as a highly effective paracetamol antidote even against highly advanced damaging processes induced by an extreme paracetamol over-dose.

Vivax malaria presenting with cerebral malaria and convulsions

80%

Anvikar A. R., Singh D. K., Singh R., Dash A. P., Valecha N.

Acta Parasitologica

2010

tom 55

nr 1

96-98

A patient was admitted with fever, vomiting, restlessness and convulsions. He was febrile and unconscious. Laboratory tests showed a low platelet count and ruled out enteric fever and dengue. His peripheral blood smear was positive for Plasmodium vivax. The presence of P. vivax monoinfection was confirmed by polymerase chain reaction and DNA sequencing. The report highlights the importance of considering the possibility of complications even in P. vivax malaria and formulation of strategies accordingly.

The effect of lead on dopamine, GABA and histidine spontaneous and KCI-dependent releases from rat brain synaptosomes

70%

Struzynska L., Rafalowska U.

Acta Neurobiologiae Experimentalis

1994

tom 54

nr 3

Ograniczanie wyników

1 Acta Neurobiologiae Experimentalis

1 Acta Parasitologica

1 Journal of Physiology and Pharmacology

1 Anic T.

1 Anvikar A. R.

1 Boban Blagaic A.

1 Brcic L.

1 Coric M.

1 Dash A. P.

1 Djidic S.

1 Djuzel V.

1 Drmic D.

1 Ilic S.

1 Ivica M.

1 Klicek R.

1 Kolenc D.

1 Radic B.

1 Rafalowska U.

1 Romic Z.

1 Seiwerth S.

1 Sever M.

1 Sikiric P.

1 Singh D. K.

1 Singh R.

1 Struzynska L.

1 Valecha N.

1 Zarkovic K.

1 Zoricic I.

1 Zoricic Z.

2 2010

1 1994

Wyniki wyszukiwania

High hepatotoxic dose of paracetamol produces generalized convulsions and brain damage in rats. A counteraction with the stable gastric pentadecapeptide BPC 157 (PL 14736)

Vivax malaria presenting with cerebral malaria and convulsions

The effect of lead on dopamine, GABA and histidine spontaneous and KCI-dependent releases from rat brain synaptosomes