Soil Physicochemical and Biological Properties of Paddy-Upland Rotation: A Review

Paddy-upland rotation is an unavoidable cropping system for Asia to meet the increasing demand for food. The reduction in grain yields has increased the research interest on the soil properties of rice-based cropping systems. Paddy-upland rotation fields are unique from other wetland or upland soils, because they are associated with frequent cycling between wetting and drying under anaerobic and aerobic conditions; such rotations affect the soil C and N cycles, make the chemical speciation and biological effectiveness of soil nutrient elements varied with seasons, increase the diversity of soil organisms, and make the soil physical properties more difficult to analyze. Consequently, maintaining or improving soil quality at a desirable level has become a complicated issue. Therefore, fully understanding the soil characteristics of paddy-upland rotation is necessary for the sustainable development of the system. In this paper, we offer helpful insight into the effect of rice-upland combinations on the soil chemical, physical, and biological properties, which could provide guidance for reasonable cultivation management measures and contribute to the improvement of soil quality and crop yield

Engineering HIV-Resistant Human CD4+ T Cells with CXCR4-Specific Zinc-Finger Nucleases

HIV-1 entry requires the cell surface expression of CD4 and either the CCR5 or CXCR4 coreceptors on host cells. Individuals homozygous for the ccr5Δ32 polymorphism do not express CCR5 and are protected from infection by CCR5-tropic (R5) virus strains. As an approach to inactivating CCR5, we introduced CCR5-specific zinc-finger nucleases into human CD4+ T cells prior to adoptive transfer, but the need to protect cells from virus strains that use CXCR4 (X4) in place of or in addition to CCR5 (R5X4) remains. Here we describe engineering a pair of zinc finger nucleases that, when introduced into human T cells, efficiently disrupt cxcr4 by cleavage and error-prone non-homologous DNA end-joining. The resulting cells proliferated normally and were resistant to infection by X4-tropic HIV-1 strains. CXCR4 could also be inactivated in ccr5Δ32 CD4+ T cells, and we show that such cells were resistant to all strains of HIV-1 tested. Loss of CXCR4 also provided protection from X4 HIV-1 in a humanized mouse model, though this protection was lost over time due to the emergence of R5-tropic viral mutants. These data suggest that CXCR4-specific ZFNs may prove useful in establishing resistance to CXCR4-tropic HIV for autologous transplant in HIV-infected individuals