Tono Reservoir fishery contribution to poverty reduction among fishers in northern Ghana

Fishery characteristics and livelihood status of fishers at Tono Reservoir, Ghana, were investigated between January 2015 and June 2016. Data on fisher demography, fishing gears, fishing methods, perceptions of the state of fish stocks, management practices, income and consumption of fishers were obtained through structured interviews. Censuses of fishers and fishing gears were conducted through direct observation and counts. The population of fishers was 950 and the majority (74%) of the sampled respondents fell within the ages of 24–41 years. Gillnet, cast net, trap and hook and line were the four main gears utilised. Illegal methods of fishing observed included the use of mosquito nets (nets with mesh <1.0 cm) and the use of brewer’s waste (pito mash) as bait. Brycinus nurse, Synodontis spp., Parailia spiniserrata and Chrysichthys spp. were perceived to have disappeared from the reservoir. The fishers were unaware of the existence of any fisheries regulations, hence there was no adherence to management practices. Their daily income was derived mainly from fishing. The incidence of poverty among fishers was low (8%). The Tono Reservoir has a great potential for supporting livelihood if it is properly managed.     

Adhesion of phospholipid vesicles to Chinese hamster fibroblasts: Role of cell surface proteins

The adhesion of artificially generated lipid membrane vesicles to Chinese hamster V79 fibroblasts in suspension was used as a model system for studying membrane interactions. Below their gel-liquid crystalline phase transition temperature, vesicles comprised of dipalmitoyl lecithin (DPL) or dimyristoyl lecithin (DML) absorbed to the surfaces of EDTA- dissociated cells. These adherent vesicles could not be removed by repeated washings of the treated cells but could be released into the medium by treatment with trypsin. EM autoradiographic studies of cells treated with[(3)H]DML or [(3)H]DPL vesicles showed that most of the radioactive lipids were confined to the cell periphery. Scanning electron microscopy and fluorescence microscopy further confirmed the presence of adherent vesicles at the cell surface. Adhesion of DML or DPL vesicles to EDTA-dissociated cells modified the lactoperoxidase-catalyzed iodination pattern of the cell surface proteins; the inhibition of labeling of two proteins with an approximately 60,000- dalton mol wt was particularly evident. Incubation of cells wit h (3)H-lipid vesicles followed by sodium dodecyl sulfate (SDS)- polyacrylamide gel electrophoresis showed that some of the (3)H-lipid migrated preferentially with these approximately 60,000-mol wt proteins. Studies of the temperature dependence of vesicle uptake and subsequent release by trypsin showed that DML or DPL vesicle adhesion to EDTA- dissociated cells increased with decreasing temperatures. In contrast, cells trypsinized before incubation with vesicles showed practically no temperature dependence of vesicle uptake. These results suggest two pathways for adhesion of lipid vesicles to the cell surface-a temperature-sensitive one involving cell surface proteins, and a temperature-independent one. These findings are discussed in terms of current models for cell-cell interactions.     

Hydroquinone inhibits PMA-induced activation of NFκB in primary human CD19+ B lymphocytes

Hydroquinone (HQ), a reactive metabolite of benzene, is known to inhibit mitogen-stimulated activation of both T and B lymphocytes. Despite extensive study, the underlying mechanism for the immunotoxicity of the HQ is not clear. We have previously demonstrated that 1 μmol/L HQ inhibits TNF-induced activation of NFκB in CD4⁺ T cells, resulting in decreased IL-2 production. NFκB, known to be important in T lymphocytes, also plays a critical role in normal B cell development and activation. We therefore hypothesized that alterations in NFκB might be involved in HQ-induced B cell immunosuppression as well. In this study, we demonstrate that 1–10 μmol/L HQ inhibits PMA/ionomycin-induced activation of NFκB in primary human CD19⁺ B cells. Inhibition of NFκB is accompanied by a dose-dependent decrease in PMA-stimulated production of TNF with no corresponding loss in viability or increased apoptosis. HQ also does not appear to alter NFκB directly, as preincubation of B cell nuclear extracts with HQ does not diminish DNA binding activity of this protein. In contrast to T cells, inhibition of NFκB by HQ in B cells is not reversible after 72 h in culture, suggesting a long-term functional suppression. These data support our original findings in T cells and indicate that NFκB is particularly susceptible to inhibition by HQ. We further hypothesize that inhibition of NFκB in lymphocytes, and perhaps other cell types as well, may play a significant role in the observed toxicity of HQ. This revised version was published online in July 2006 with corrections to the Cover Date.