Using unsupported lead-210 measurements to investigate soil erosion and sediment delivery in a small Zambian catchment

Journal ArticleTraditional techniques used to assemble information on rates of erosion and soil redistribution possess many important limitations. As a result, the use of environmental radionuclides, and more particularly 137Cs measurements, has attracted increasing attention in recent years as a means of obtaining spatially distributed information on rates of erosion and deposition. The application of the 137Cs approach is, however, hampered in some areas of the world where 137Cs inventories are low and the low concentrations of 137Cs found in soils and sediments cause problems for laboratory analysis. These problems will increase as time progresses due to the radioactive decay of the existing inventory, most of which was deposited as fallout ca. 40 years ago. This contribution explores the potential for using another fallout radionuclide, namely unsupported 210Pb, as an alternative to 137Cs, in the small (63 km2) Upper Kaleya catchment in southern Zambia where 137Cs inventories are already very low. The approach employed with unsupported 210Pb is similar to that used for 137Cs, although the essentially constant fallout of unsupported 210Pb through time means that the resulting estimates of erosion and soil redistribution rates reflect a longer period of time (ca. 100 years rather than ca. 40 years). The estimates of erosion and deposition rates derived from the unsupported 210Pb measurements are used to construct typical sediment budgets for the three main land-use types in the Upper Kaleya catchment, namely, commercial cultivation, communal cultivation and bush grazing. The results obtained from the unsupported 210Pb are compared with equivalent results based on 137Cs measurements provided by a previous investigation undertaken in the study catchment. The two sets of results are highly consistent. The study reported confirms the viability of using unsupported 210Pb as an alternative to 137Cs in this environment and demonstrates that conjunctive use of both radionuclides can provide additional information on the erosional history of a study area

Epstein-Barr virus: clinical and epidemiological revisits and genetic basis of oncogenesis

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancie