The presence of oocysts was determined by light microscopy after 7 days, and the presence

of sporozoite by ELISA after 14 days. Mosquito species and molecular forms were identified by PCR.

Results: The oocyst rate was significantly higher in the molecular S form (79.07%) than in the M form (57.81%, Fisher’s exact test p < 0.001) and in Anopheles arabiensis (55.38%, Fisher’s exact test vs. S group p < 0.001). Mean +/- s.e. m. number of oocyst was greater in the An. gambiae S form (1.72 +/- 0.26) than in the An. gambiae M form (0.64 +/- 0.04, p < 0.0001) and in the An. arabiensis group (0.58 +/- 0.04, vs. S group, p < 0.0001). Sporozoite rate was also higher in the molecular

form S (83.52%) than in form M (50.98%, Fisher’s exact test p < 0.001) and Anopheles arabiensis Selleckchem Cyclopamine 50.85%, Fisher’s exact test vs. S group p < 0.001).

Conclusion: Infected in the same experimental conditions, the molecular form S of An. gambiae is PFTα ic50 more susceptible to infection by P. falciparum than the molecular form M of An. gambiae and An. arabiensis.”
“Neural mechanisms underlying the onset and maintenance of epileptic seizures involve alterations in inhibitory and/or excitatory neurotransmitter pathways. Thus, the prospecting of novel molecules from natural products that target both inhibition and excitation systems has deserved interest in the rational design of new anticonvulsants. We isolated the alkaloids (+)-erythravine and ( +)-11-alpha-hydroxyerythravine from the flowers of Erythrina

mulungu and evaluated the action of these compounds against chemically induced seizures in rats. Our results showed that the administration of different doses of (+)-erythravine inhibited seizures evoked by bicuculline, pentylenetetrazole, and kainic acid at maximum of Z-IETD-FMK Apoptosis inhibitor 80, 100, and 100%, respectively, whereas different doses of (+)-11-alpha-hydroxy-erythravine inhibited seizures at a maximum of 100% when induced by bicuculline, NMDA, and kainic acid, and, to a lesser extent, PTZ (60%). The analysis of mean latency to seizure onset of nonprotected animals, for specific doses of alkaloids, showed that (+)-erythravine increased latencies to seizures induced by bicuculline. Although (+)-erythravine exhibited very weak anticonvulsant action against seizures induced by NMDA, this alkaloid increased the latency in this assay. The increase in latency to onset of seizures promoted by (+)-11-alpha-hydroxy-erythravine reached a maximum of threefold in the bicuculline test. All animals were protected against death when treated with different doses of (+)-11-alpha-hydroxy-erythravine in the tests using the four chemical convulsants. Identical results were obtained when using (+)-erythravine in the tests of bicuculline, NMDA, and VIZ, and, to a lesser extent, kainic acid.