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Gold mine tailing is an important source of arsenic pollution. There are great differences in the arsenic forms of mine tailings formed by different smelting processes. Different arsenic form directly affects its migration and transformation in the environment. Confirming the existing form of arsenic is an important method in the study of repairing arsenic contamination sites. Based on mine tailings generated by two different leaching methods (flotation process and biological oxidation process) for gold, pH meter and Eh meter was used to measure the physical properties of mine tailings (pH, Eh), X-ray Diffraction and X-ray Fluorescent to analyze the mineral phases and main compositions of the mine tailings and Electro-probe Microanalysis to analyze the arsenic existing form. The characterization result shows that the physical properties of flotation mine tailing and biological oxidation mine tailing change with the stacking environment. pH, Eh and pHpzc are almost equal, ie pH≈8.5 and pHpzc≈8.5. The choice of repair method is also restricted because both min tailings belong to the alkaline condition. For example, the electric repair method is only suitable for the acid condition but not for the two main mine tailings. Meanwhile the choice of repair reagent must be alkaline substance and iron oxide (hydroxide). The main mineral compositions of flotation mine tailing are quartz, dolomite and clay minerals and their chemical components are mainly Si and Al. The color of mine tailing is off-white. The arsenic content of this mine tailing is about 754 μg/g, mainly existing in the form of arsenopyrite (FeAsS). However, the main mineral type of biological oxidation mine tailing is gypsum. The main chemical components are Fe, Ca and S with a reddish-brown colour. The arsenic content is about 26350 μg/g. The existing forms of arsenic of this mine tailing are mainly arsenopyrite (FeAsS) and arsenic pentoxide (As2O5). There are many differences in mineral phase, main chemical components and arsenic forms of two kinds of mine tailings because every procedure step of the two-gold leaching processes is different. Therefore, in the in-situ repair work of mine tailings, it should be considered that different methods of gold leaching will influence the piled-up environment of mine tailings and arsenic forms and should be taken into consideration in order to choose a more appropriate, cheap and efficient repair method and choice of reagents.

PTEN/MMAC1/TEP1 is a tumor suppressor that possesses intrinsic phosphatase activity. Deletions or mutations of its encoding gene are associated with a variety of human cancers. However, very little is known about the molecular mechanisms by which this important tumor suppressor regulates cell growth. Here, we show that PTEN expression potently suppressed the growth and tumorigenicity of human glioblastoma U87MG cells. The growth suppression activity of PTEN was mediated by its ability to block cell cycle progression in the [G.sub.1] phase. Such an arrest correlated with a significant increase of the cell cycle kinase inhibitor [p27.sup.KIP1] and a concomitant decrease in the activities of the [G.sub.1] cyclin-dependent kinases. PTEN expression also led to the inhibition of Akt/protein kinase B, a serine-threonine kinase activated by the phosphatidylinositol 3-kinase (PI 3-kinase) signaling pathway. In addition, the effect of PTEN on [p27.sup.KIP1] and the cell cycle can be mimicked by treatment of U87MG cells with LY294002, a selective inhibitor of PI 3-kinase. Taken together, our studies suggest that the PTEN tumor suppressor modulates [G.sub.1] cell cycle progression through negatively regulating the PI 3-kinase/Akt signaling pathway, and one critical target of this signaling process is the cyclin-dependent kinase inhibitor [p27.sup.KIP1].

The lats gene encodes a family of proteins conserved from insects to humans. Drosophila carrying lats mutant cells or mice deficient for Lats1 develop tumors in various tissues. The mammalian LATS1 protein was previously shown to bind to CDC2, suggesting that LATS1 may modulate G2/M cell cycle progression by affecting CDC2 activity. In this study, we introduced human LATS1 into LATS-/- MEF cells by adenovirus-mediated gene transfer. Overexpression of LATS1 causes G2/M arrest through inhibition of CDC2 kinase activity. Furthermore, overexpression of LATS1 significantly suppressed the human tumor cell growth in vitro and tumorigenicity in vivo by inducing either cell cycle arrest in G2/M or apoptosis. These observations suggest that LATS1 is a potent growth suppressor and, like other tumor suppressors, it suppresses growth by inducing cell cycle arrest or apoptosis. Oncogene (2001) 20, 6516–6523. [ABSTRACT FROM AUTHOR]