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Heavy metal(loid)s are natural constituents of the Earth's crust, and apportionment of their sources in surface soils is a challenging task. This study evaluated the application of positive matrix factorization (PMF) model, assisted with regression modeling and geospatial mapping, in the quantitative source apportionment of heavy metal(loid)s in the agricultural soils of Handan, a region covering >12,000 km2. Obvious enrichment of As, Cd, Cu, Pb, and Zn was found in the surface soils, with Cd alone accounted for 73 % of the overall potential ecological risk. PMF model revealed that Cd (56.9 %) and Pb (47.8 %) in the region's agricultural soils were predominantly contributed by industrial sources, Fe (71.8 %), Cr (60.0 %), V (52.9 %), Cu (50.7 %), Ni (42.2 %), and Mn (41.4 %) were primarily of lithogenic origin, while Co (54.1 %), As (42.9 %), and Zn (40.0 %) mainly came from the mixed sources of natural background, agricultural sources, and vehicle emissions. Uncertainty analysis showed that the contributions of pollution sources to the soil heavy metal(loid)s estimated by PMF model had considerable variations. While quantitative source apportionment of heavy metal(loid)s in soils could be achieved with PMF based on their spatial distributions, combination with emission inventory and reactive transport are probably necessary to obtain more accurate results.

The traditional industrial operations are well recognized as an important source of heavy metal pollution, while that caused by the e-waste recycling activities, which have sprouted in some developing countries, is often overlooked. This study was carried out to compare the status of soil heavy metal pollution caused by the traditional industrial operations and the e-waste recycling activities in the Pearl River Delta, and assess whether greater attention should be paid to control the pollution arising from e-waste recycling activities. Both the total contents and the chemical fractionation of major heavy metals (As, Cr, Cd, Ni, Pb, Cu, and Zn) in 50 surface soil samples collected from the e-waste recycling areas and 20 soil samples from the traditional industrial zones were determined. The results show that the soils in the e-waste recycling areas were mainly polluted by Cu, Zn, As, and Cd, while Cu, Zn, As, Cd, and Pb were the major heavy metals in the soils from the traditional industrial zones. Statistical analyses consistently show that Cu, Cd, Pb, and Zn in the surface soils from both types of sites were contributed mostly by human activities, while As, Cr, and Ni in the soils were dominated by natural background. No clear distinction was found on the pollution characteristic of heavy metals in the surface soils between the e-waste recycling areas and traditional industrial zones. The potential ecological risk posed by heavy metals in the surface soils from both types of sites, which was dominated by that from Cd, ranged from low to moderate. Given the much shorter development history of e-waste recycling and its largely unregulated nature, significant efforts should be made to crack down on illegal e-waste recycling and strengthen pollution control for related activities.

Objective: To observe the effects of the new anticancer drug taxol on different types of lymphoma cells and explore the value of its clinical application. Methods: Inverted microscopy, light microscopy, electron microscopy, flow cytometry (FCM) assay and DNA gel electrophoresis were used to observe the effects taxol on three different types of lymphoma cell lines, i.e., Jurkat (T cell lymphoma), B JAB (B cell lymphoma, EBV negative ) and Raji (B cell lymphoma, EBV positive). Results: Taxol was able to inhibit the growth of and induce apoptosis in all of the three cell lines. Jurkat cells were the most sensitive, apoptosis being the main effect; B JAB was the second sensitive showing G2/M arrest first and then apoptosis; Raji was the least, showing G2/M arrest in most of the cells and entering apoptosis in only a few of them. Conclusion: Taxol is a valuable chemotherapeutic agent for lymphoma therapy. The senstivity to the agent may vary with the tumor type, the existence of EBV infection or not and the extent of induced apoptosis.

To study the reversal effect of nomegestrol acetate (NOM) on mutidrug resistance (MDR) in MCF7/ADR and its mechanism.Using tetrazolium dye assay, effects of various concentrations of NOM on sensitivity to ADR in MCF7/ADR was studied. Expression of MDR related genes MDR1, glutathoine S-transferase Pi (GSTpi), Topoisomerase II alpha (Topo II alpha) and MDR related protein (MRP) were assayed by reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry assay. Using flow cytometry (FCM), intracellular ADR concentration effects on cell cycle were observed.NOM significantly reversed MDR in MCF7/ADR. After NOM 20, 10 and 5 micromol/L treatment, the chemosensitivity to ADR increased to 21, 12 and 8 times. The reversal activity of NOM was stronger than that of the precursor compound megestrol acetate, and was comparable to that of verapamail. After treatment with NOM 5 micromol/L both MDR1 and GSTpi mRNA genes expression began to decline on D2 (P0.05,P0.01) and reached the lowest level on D3 (both P0.01), but the expression levels began to rise on D6 again (both P0.05). The expression of MRP and Topo II alpha gave no significant change. Changes of P-gp and GSTpi protein expressions were similar to those of their mRNA expressions, showing early decline and late rise. Two hours after NOM 20, 10, and 5 micromol/L treatment, intracellular ADR concentration increased 2.7, 2.3 and 1.5 times, respectively. FCM data showed that after forty-eight hours, combined administration of NOM (20 micromol/L) and ADR (from low concentration to high concentration), MCF7/ADR cells showed gradual arrest in the G(2)M phase with the increase of ADR dose.NOM has strong reversal effects on MDR in MCF7/ADR. The reversal takes place via different routes, i.e. down regulating mRNA and protein expression levels of MDR1 and GSTpi, increasing intracellular drug concentration, and enhancing the arrest of ADR in cells at G(2)M phase.