The influence of socio-economic factors on Helicobacter pylori infection rates of students in rural Zambia.

OBJECTIVES: Although prevalence of disease in sub-Saharan Africa is often quite high and attracts much research, relatively little is known about less critical maladies. We examined Helicobacter pylori infected students in rural Zambia. We attempted to determine if any socio-economic or co-occurring diseases were correlated to H. pylori infection. Understanding the context in which H. pylori infections occur may increase our understanding of this organism. DESIGN: We conducted a screening survey with diagnostic tests of primary and secondary school students to determine rates of H. pylori infection. We then correlated these rates to socio-economic factors such as income and tobacco use. We also explored the correlation of H. pylori to HIV and malaria. SETTING: Zimba, Zambia. SUBJECTS: Eighty seven primary and secondary school students. MAIN OUTCOME MEASURE: Correlation of H. pylori to socio-economic factors. RESULTS: H. pylori infection was common (60.9%) and was consistent with rates found in other African countries. We found no significant correlation between H. Pylori and disease and socio-economic variables. CONCLUSION: In the studied population H. pylori infection does not appear to be correlated with the measured socio-economic or disease variables.

Binding characteristics of the selective alpha 2-adrenoceptor antagonist [3H]idazoxan to rat olfactory cortex membranes.

[3H]Idazoxan binding to membranes prepared from rat olfactory cortex obeyed saturation kinetics and was to a single population of sites. Although the density of sites was dependent on the incubation medium, binding was of high affinity (KD approximately 5.5 nM) with a Hill coefficient close to unity. Competition studies with a range of adrenoceptor agonists and antagonists confirmed that [3H]idazoxan binding was to alpha 2-adrenoceptors. Neither chemical lesions with the neurotoxin kainic acid nor chronic unilateral bulbectomy significantly altered any of the [3H]idazoxan binding parameters. These findings suggest that alpha 2-adrenoceptors are not located on the lateral olfactory tract terminals or pyramidal cells of the olfactory cortex.

Prostacyclin synthesis and deacylation of phospholipids in human endothelial cells: comparison of thrombin, histamine and ionophore A23187.

Thrombin, histamine and ionophore A23187 stimulated human endothelial cells to release arachidonic acid and synthesize prostaglandins. To compare the activation of arachidonic acid release by these three stimuli in endothelial cells, we examined the intracellular lipid metabolism by prelabeling the cells with [14C]stearic acid and [3H]arachidonic acid. Thrombin stimulated the loss of 3H and 14C label from intracellular phospholipids. At the same time [3H]arachidonic acid and prostaglandins were released into the incubation medium. Thin layer chromatography analysis indicated that prostacyclin is the major metabolite formed followed by PGF2 alpha, PGE2, HHT and PGD2. In addition, several intracellular lipid metabolites were accumulated. These include: phosphatidic acid and 1,2-diacylglycerol detected by increase of both 14C and 3H radioactivity; lysophosphatidylinositol, lysophosphatidylethanolamine, and to a smaller extent lysophosphatidylcholine and lysophosphatidylserine detected by increase of 14C radioactivity. Like thrombin, both histamine and ionophore A23187 also stimulated release of arachidonic acid and synthesis of prostaglandins. Despite the different nature of the agonists, the type and the relative amount of prostaglandins synthesized in response to histamine and A23187 were similar to that stimulated by thrombin. The relative extents of hydrolysis of phospholipids and the accumulation of phosphatidic acid, 1,2-diacylglycerol and lysophospholipids are similar to that of 3H radioactivity and prostacyclin released into the medium and follow the order: ionophore A23187 greater than thrombin greater than histamine. These results suggest that in human endothelial cells, histamine, thrombin and ionophore A23187 directly or indirectly activated both phospholipase C and phospholipase A2 and these activations most likely involve mobilization of Ca2+.

Excitatory and inhibitory effects of noradrenaline on synaptic transmission in the rat olfactory cortex slice.

An investigation has been made of the effects of noradrenaline on excitatory transmission at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the rat olfactory cortex slice by measuring the effects of bath-applied noradrenaline on the amplitudes and latencies of the field potentials evoked on LOT stimulation. Low concentrations of noradrenaline (0.1-5 microM) facilitate transmission whereas higher doses (20-250 microM) depress transmission. Both these effects were completely blocked by non-selective alpha- and beta-adrenoceptor antagonists, by 2-amino-5-phosphonovaleric acid (an antagonist of excitatory amino acid receptors of the N-methyl-D-aspartate type) and by the methylxanthine theophylline. The depressant effects of noradrenaline were mimicked by bath application of GABA or adenosine and specifically antagonized by bicuculline and picrotoxin. In parallel experiments, noradrenaline (100 microM) significantly increased the potassium-evoked release of endogenous aspartate, glutamate and GABA, proposed transmitters of the olfactory cortex, although the effect on GABA release was specifically antagonized by 2-amino-5-phosphonovaleric acid. Noradrenaline (100 microM) also significantly increased the potassium-evoked release of D-[3H]aspartate, an effect antagonized by a number of alpha- and beta-adrenoceptor antagonists. It is concluded that at low concentrations, noradrenaline facilitates transmission at the LOT-superficial pyramidal cell synapse by increasing excitatory amino acid neurotransmitter release. This effect is mediated by both alpha- and beta-adrenoceptors although the primary site of release is unknown. At higher concentrations of noradrenaline, the increased levels of excitatory transmitters release sufficient endogenous GABA (and possibly adenosine) to cause an overall depression of transmission. These conclusions are supported by the results of a series of experiments in which the effects of noradrenaline on stimulus input-evoked field potential output relationships were assessed. It is not possible to exclude additional direct effects of noradrenaline on membrane excitability.