The impacts of rapid industrialization on agricultural soil cadmium (Cd) accumulation and their potential risks have drawn major attention from the scientific community and decision-makers, due to the high toxicity of Cd to animals and humans. A total of 812 topsoil samples (0–20 cm) was collected from the southern parts of Jiangsu Province, China, in 2000 and 2015, respectively. Geostatistical ordinary kriging and conditional sequential Gaussian simulation were used to quantify the changes in spatial distributions and the potential risk of Cd pollution between the two sampling dates. Results showed that across the study area, the mean Cd concentrations increased from 0.110 mg/kg in 2000 to 0.196 mg/kg in 2015, representing an annual average increase of 5.73 μg/kg. Given a confidence level of 95%, areas with significantly-increased Cd covered approximately 12% of the study area. Areas with a potential risk of Cd pollution in 2000 only covered 0.009% of the study area, while this figure increased to 0.75% in 2015. In addition, the locally concentrating trend of soil Cd pollution risk was evident after 15 years. Although multiple factors contributed to this elevated Cd pollution risk, the primary reason can be attributed to the enhanced atmospheric deposition and industrial waste discharge resulting from rapid industrialization, and the quick increase of traffic and transportation associated with rapid urbanization.

Supplementary Table 2 from <i>In vitro</i> Modeling of Human Pancreatic Duct Epithelial Cell Transformation Defines Gene Expression Changes Induced by K-<i>ras</i> Oncogenic Activation in Pancreatic Carcinogenesis

Supplementary Table 3 from <i>In vitro</i> Modeling of Human Pancreatic Duct Epithelial Cell Transformation Defines Gene Expression Changes Induced by K-<i>ras</i> Oncogenic Activation in Pancreatic Carcinogenesis

Supplementary Table 1 from <i>In vitro</i> Modeling of Human Pancreatic Duct Epithelial Cell Transformation Defines Gene Expression Changes Induced by K-<i>ras</i> Oncogenic Activation in Pancreatic Carcinogenesis

<div>Abstract<p>Genetic analysis of pancreatic ductal adenocarcinomas and their putative precursor lesions, pancreatic intraepithelial neoplasias (PanIN), has shown a multistep molecular paradigm for duct cell carcinogenesis. Mutational activation or inactivation of the K-<i>ras</i>, <i>p16</i>^INK4A, <i>Smad4</i>, and <i>p53</i> genes occur at progressive and high frequencies in these lesions. Oncogenic activation of the K-<i>ras</i> gene occurs in >90% of pancreatic ductal carcinoma and is found early in the PanIN-carcinoma sequence, but its functional roles remain poorly understood. We show here that the expression of K-<i>ras</i>^G12V oncogene in a near diploid HPV16-E6E7 gene immortalized human pancreatic duct epithelial cell line originally derived from normal pancreas induced the formation of carcinoma in 50% of severe combined immunodeficient mice implanted with these cells. A tumor cell line established from one of these tumors formed ductal cancer when implanted orthotopically. These cells also showed increased activation of the mitogen-activated protein kinase, AKT, and nuclear factor-κB pathways. Microarray expression profiling studies identified 584 genes whose expression seemed specifically up-regulated by the K-<i>ras</i> oncogene expression. Forty-two of these genes have been reported previously as differentially overexpressed in pancreatic cancer cell lines or primary tumors. Real-time PCR confirmed the overexpression of a large number of these genes. Immunohistochemistry done on tissue microarrays constructed from PanIN and pancreatic cancer samples showed laminin β3 overexpression starting in high-grade PanINs and occurring in >90% of pancreatic ductal carcinoma. The <i>in vitro</i> modeling of human pancreatic duct epithelial cell transformation may provide mechanistic insights on gene expression changes that occur during multistage pancreatic duct cell carcinogenesis.</p></div>