Cysticercosis as a major risk factor for epilepsy in Burundi,east Africa

PURPOSE: Human cysticercosis is a direct consequence of infection by Taenia solium larvae (Cysticercus cellulosae). Results of studies on the impact of neurocysticercosis on epilepsy in Africa are inconsistent. The objective was to evaluate the role of cysticercosis in epilepsy in Burundi. METHODS: A prevalent matched case-control design was used in the Kiremba area, Burundi, between March and April 2001. One case with epilepsy was matched to two control subjects, according to their age. Cases were subjects who had shown at least two unprovoked epileptic seizures within a 24-h time range and who lived in the Kiremba area. The control subjects also lived in Kiremba and had neither neurologic illness nor kinship with the people with epilepsy. Seropositivity for cysticercosis was the exposure variable. Three hundred twenty-four prevalent cases, with onset of epilepsy between 1950 and 2000, and 648 age-matched controls were included. RESULTS: This study found a link between cysticercosis infestation and the occurrence of epilepsy (odds ratio, 3.8; 95% confidence interval, 2.5-5.1). CONCLUSIONS: The study highlighted the importance of cysticercosis in the area of Kiremba, as 31.5% of the control subjects screened positive for this parasite. The attributable risk for cysticercosis was 50% (95% confidence interval, 42-57) in this population.     

Neutrophils do not contribute to infarction,oxidative stress,and NO synthase activity in severe brain ischemia

Polymorphonuclear leukocytes (PMNs) were reported to contribute to ischemia-reperfusion-induced brain damage. The present work examined whether PMN infiltration is deleterious in a severe model of transient focal cerebral ischemia and in which part PMNs contribute to oxidative stress and nitric oxide (NO) production. A 20-min occlusion of the left middle cerebral artery and both common carotid arteries was performed in rats. Infarction was maximal 24 h after reperfusion, while accumulation of PMNs in infarcted tissue was not significant before 48 h. Moreover, neutropenia induced by vinblastine (0.5 mg/kg iv) significantly decreased by 60-80% PMN infiltration 48 h after reperfusion but did not reduce the infarct volume. Thus PMNs do not contribute to cerebral injury in our model. Furthermore, decreased PMN infiltration modified neither oxidative stress evaluated by glutathione concentrations nor NO synthase activities 48 h after reperfusion. In conclusion, our results suggest that PMNs are not involved in severe cerebral ischemia and that anti-PMN strategies may be inefficient in some pathological conditions.     

Treatment of slow-channel congenital myasthenic syndrome with fluoxetine

The authors found that fluoxetine significantly shortens at 5 microM/L and nearly normalizes at 10 microM/L the prolonged opening bursts of slow-channel congenital myasthenic syndrome (SCCMS) acetylcholine receptors (AChR) expressed in fibroblasts. Prompted by this observation, they treated two SCCMS patients allergic to quinidine with up to 80 to 120 mg of fluoxetine per day over 3 years (serum fluoxetine + norfluoxetine levels 8 to 11 microM/L). Both patients showed marked subjective and objective improvement by quantitative muscle strength testing and electromyography.     

Vasoactive intestinal peptide stimulates proliferation in HT29 human colonic adenocarcinoma cells: concomitant activation of Ras/Rap1-B-Raf-ERK signalling pathway

The vasoactive intestinal peptide (VIP) has been shown to regulate cell proliferation and differentiation in many cell types. We previously reported that this neuropeptide inhibited proliferation in HT29 adenocarcinoma cells cultured in serum-containing medium. In addition, it has been demonstrated that VIP induced a potent stimulation of intracellular cAMP production in these cells cultured either in the absence or in the presence of serum. We also demonstrated that VIP induced phosphorylation of the small GTPase Rap1 in these cancerogenous cells. In the present study, the effects of VIP on the proliferation of HT29 cells cultured in the absence of growth factors and various concomitant signalling events were investigated. Under serum-free conditions VIP stimulates HT29 cell proliferation and induced a time- and concentration-dependent ERK activation. Furthermore, VIP induced the activation of the small GTPase Rap1 and of a 95 kDa isoform of the serine/threonine kinase B-Raf. Ras GTPase is also activated in VIP-stimulated cells. We hypothesize that VIP-induced proliferation in HT29 adenocarcinoma cells may involve a cAMP-Rap1/Ras-B-Raf-ERK signalling pathway.