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Spatial variability of soil has an important influence on the structure and function of soil. The spatial distribution of soil physical properties provides basic and useful information relevant to soil management and ecological protection. A typical red beds basin was selected for this study, soil samples at 0-20 cm were taken from 150 locations in the northeast part of Nanxiong Basin, in which GIS and geostatistics were used to analyze the spatial variability of the soil physical properties. The results show that the coefficients of variation of soil bulk density, total porosity and capillary porosity are 9.82%, 4.47%, and 3.72%, respectively, which indicate weak variation. Pearson correlation indicated that soil bulk density was significantly positively correlated with soil moisture and capillary water capacity (p<0.01), with correlation coefficients of 0.85 and 0.91, respectively, but was significantly negatively correlated with total porosity, capillary porosity and non-capillary porosity, with correlation coefficients of 0.82, 0.71 and 0.94, respectively (p<0.01). The spatial distributions of soil physical properties using ordinary kriging (OK) and empirical bayesian kriging (EBK) methods were subjected to comparative analysis. In addition, different cross-validation indicators were applied to assess the performance of different interpolation methods. Cross-validation demonstrated that EBK performed better than OK. And EBK produced smaller regions of predicted soil physical properties than OK, highlighting the necessity of choosing the appropriate methods in studying the spatial distribution of soil properties.
Angiogenesis plays a crucial role in the growth, invasion and metastasis of breast cancer. Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are the key regulators of tumor angiogenesis. VEGFR-2, known as the kinase insert domain receptor (KDR), is a key receptor involved in malignant angiogenesis. We previously showed that knocking down KDR with short interference RNA (KDR-siRNA) markedly decreased KDR expression and suppressed tumor growth in a xenograft model. However, the mechanisms underlying the anti-cancer effects of KDR-siRNA are not clearly understood. This study aimed to elucidate the molecular mechanisms that induce apoptosis in human breast cancer MCF-7 cells after transfection with KDR-siRNA. We studied the effects of KDR-siRNA on proliferation, apoptosis, antiapoptotic and pro-apoptotic proteins, mitochondrial membrane permeability, cytochrome c release and caspase-3 activity. The results indicated that KDR-siRNA treatment significantly inhibited the proliferation and induced the apoptosis of MCF-7 cells, reduced the levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xl, and increased the level of the pro-apoptotic protein Bax, resulting in a decreased Bcl-2/Bax ratio. KDR-siRNA also enhanced the mitochondrial membrane permeability, induced cytochrome c release from the mitochondria, upregulated apoptotic protease-activating factor-1 (Apaf-1), cleaved caspase-3, and increased caspase-3 activity in MCF-7 cells. Furthermore, KDR-siRNA-induced apoptosis in MCF-7 cells was blocked by the caspase inhibitor Z-VAD-FMK, suggesting a role of caspase activation in the induction of apoptosis. These results indicate that the Bcl-2 family proteins and caspase-related mitochondrial pathways are primarily involved in KDR-siRNAinduced apoptosis in MCF-7 cells and that KDR might be a potential therapeutic target for human breast cancer treatments.
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