Human activities significantly alter ecosystems and their services; however, quantifying the impact of human activities on ecosystems has been a great challenge in ecosystem management. We used the Universal Soil Loss...Human activities significantly alter ecosystems and their services; however, quantifying the impact of human activities on ecosystems has been a great challenge in ecosystem management. We used the Universal Soil Loss Equation and county-level socioeconomic data to assess the changes in the ecosystem service of soil conservation between 2000 and 2010, and to analyze its spatial characteristics and driving factors in the southwestern China. The results showed that cropland in the southwestern China decreased by 3.74%, while urban land, forest, and grassland areas increased by 46.78%, 0.86%, and 1.12%, respectively. The soil conservation increased by 1.88 × 10^(11) kg, with deterioration only in some local areas. The improved and the degraded areas accounted for 6.41% and 2.44% of the total land area, respectively. Implementation of the Sloping Land Conversion Program and urbanization explained 57.80% and 23.90% of the variation in the soil conservation change, respectively, and were found to be the main factors enhancing soil conservation. The 2008 Wenchuan earthquake was one of the factors that led to the degradation of soil conservation. Furthermore, industrial adjustment, by increasing shares of Industry and Service and reducing those of Agriculture, has also promoted soil conservation. Our results quantitatively showed and emphasized the contributions to soil conservation improvement made by implementing ecological restoration programs and promoting urbanization. Consequently, these results provide basic information to improve our understanding of the effects of ecological restoration programs, and help guide future sustainable urban development and regional industrial restructuring.展开更多
AIM： To analyse αv integrin expression induced by gas- trin in pancreatic cancer models.METHODS： αv integrin mRNA expression in human pan- creatic cancer cells was analysed using a ＂cancer genes＂ array and confi...AIM： To analyse αv integrin expression induced by gas- trin in pancreatic cancer models.METHODS： αv integrin mRNA expression in human pan- creatic cancer cells was analysed using a ＂cancer genes＂ array and confirmed by real-time reverse transcription- polymerase chain reaction （PCR）. Western blotting and semi-quantitative immunohistochemistry were used to examine protein levels in human pancreatic cancer cell lines and pancreatic tissues, respectively, The role of αv integrin on gastrin-induced cell adhesion was examined using blocking anti-αv integrin monoclonal antibodies. Adherent cells were quantified by staining with crystal violet.RESULTS： Using a ＂cancer genes＂ array we identi- fied c^v integrin as a new gastrin target gene in human pancreatic cancer cells. A quantitative real-time PCR approach was used to confirm αv integrin gene expression. We also demonstrate that Src family kinases and the PI 3-kinase, two signalling pathways specifically activated by the CCK-2 receptor （CCK2R）, are involved in gastrin-mediated αv integrin expression. In contrast, inhibition of the ERK pathway was without any effect on αv integrin expression induced by gastrin. Our results also show that gastrin modulates cell adhesion via αv integrins. Indeed, in vitro adhesion assays performed on fibronectin show that gastrin significantly increases adhesion of pancreatic cancer cells. The use of blocking anti-αv integrin monoclonal antibodies completely reversed the increase in cell-substrate adhesion induced by gastrin. In addition, we showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, leads to the overexpression of αv integrin. This process may contribute to pancreatic turnout development observed in these transgenic animals.CONCLUSION： αv integrin is a new gastrin target in pancreatic cancer models and contributes to gastrin effects on cell adhesion.展开更多
Objective： To investigate the effects of rAdinbitor on the adhesion and proliferation of human hepatoma cell strain 8MMC-7721. Methods： Cell adhesion assay was used to observe the effect of rAdinbitor on the adhesio...Objective： To investigate the effects of rAdinbitor on the adhesion and proliferation of human hepatoma cell strain 8MMC-7721. Methods： Cell adhesion assay was used to observe the effect of rAdinbitor on the adhesion of 8MMC-7721 cells to fibronectin （FN）. Crystal violet staining was performed to detect the influence of rAdinbitor on the adhesion of 8MMC- 7721 cells. MTT assay was employed to detect the inhibitory effects of different concentration of rAdinbitor on the proliferation of 8MMC-7721 cells. The morphologic changes of the control 8MMC-7721 cells and the apoptotic cells induced by 200μg/mL rAdinbitor for 36 h were observed under light microscope after HE staining. Flow cytometry analysis was applied to determine the apoptosis rate of 8MMC-7721 cells. Results： （1） FN promoted the adhesion of human hepatoma cell strain 8MMC-7721 in a dose-dependent manner. （2） rAdinbitor could dose-dependently inhibit the adhesion of SMMC-7721 cells to FN. The higher the concentration was, the stronger the inhibition was. There was significant difference among the groups （P 〈 0.05）. （3） rAdinbitor had a strong inhibition on the proliferation of 8MMC-7721 cells and showed a dose-dependent manner （P 〈 0.05）. After a 48 h exposure, the IC50 value of rAdinbitor was 177.83 μg/mL. （4） After exposure of 8MMC-7721 cells to 200μg/mL rAdinbitor for 36 h, the early morphologic changes appeared and the apoptosis rate was 20.68%, significantly higher than that of the control group （2.38%, P 〈 0.05）. Conclusion： rAdinbitor can dose-dependently inhibit the 8MMC-7721 cells adhesion to FN, and can inhibit the proliferation in dose-dependent manner and promote their apoptosis.展开更多
基金Under the auspices of National Key Technology Research and Development Program of China(No.2011BAC09B08)Special Issue of National Remote Sensing Survey and Assessment of Eco-Environment Change between 2000 and 2010(No.STSN-04-01)
文摘Human activities significantly alter ecosystems and their services; however, quantifying the impact of human activities on ecosystems has been a great challenge in ecosystem management. We used the Universal Soil Loss Equation and county-level socioeconomic data to assess the changes in the ecosystem service of soil conservation between 2000 and 2010, and to analyze its spatial characteristics and driving factors in the southwestern China. The results showed that cropland in the southwestern China decreased by 3.74%, while urban land, forest, and grassland areas increased by 46.78%, 0.86%, and 1.12%, respectively. The soil conservation increased by 1.88 × 10^(11) kg, with deterioration only in some local areas. The improved and the degraded areas accounted for 6.41% and 2.44% of the total land area, respectively. Implementation of the Sloping Land Conversion Program and urbanization explained 57.80% and 23.90% of the variation in the soil conservation change, respectively, and were found to be the main factors enhancing soil conservation. The 2008 Wenchuan earthquake was one of the factors that led to the degradation of soil conservation. Furthermore, industrial adjustment, by increasing shares of Industry and Service and reducing those of Agriculture, has also promoted soil conservation. Our results quantitatively showed and emphasized the contributions to soil conservation improvement made by implementing ecological restoration programs and promoting urbanization. Consequently, these results provide basic information to improve our understanding of the effects of ecological restoration programs, and help guide future sustainable urban development and regional industrial restructuring.
文摘AIM： To analyse αv integrin expression induced by gas- trin in pancreatic cancer models.METHODS： αv integrin mRNA expression in human pan- creatic cancer cells was analysed using a ＂cancer genes＂ array and confirmed by real-time reverse transcription- polymerase chain reaction （PCR）. Western blotting and semi-quantitative immunohistochemistry were used to examine protein levels in human pancreatic cancer cell lines and pancreatic tissues, respectively, The role of αv integrin on gastrin-induced cell adhesion was examined using blocking anti-αv integrin monoclonal antibodies. Adherent cells were quantified by staining with crystal violet.RESULTS： Using a ＂cancer genes＂ array we identi- fied c^v integrin as a new gastrin target gene in human pancreatic cancer cells. A quantitative real-time PCR approach was used to confirm αv integrin gene expression. We also demonstrate that Src family kinases and the PI 3-kinase, two signalling pathways specifically activated by the CCK-2 receptor （CCK2R）, are involved in gastrin-mediated αv integrin expression. In contrast, inhibition of the ERK pathway was without any effect on αv integrin expression induced by gastrin. Our results also show that gastrin modulates cell adhesion via αv integrins. Indeed, in vitro adhesion assays performed on fibronectin show that gastrin significantly increases adhesion of pancreatic cancer cells. The use of blocking anti-αv integrin monoclonal antibodies completely reversed the increase in cell-substrate adhesion induced by gastrin. In addition, we showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, leads to the overexpression of αv integrin. This process may contribute to pancreatic turnout development observed in these transgenic animals.CONCLUSION： αv integrin is a new gastrin target in pancreatic cancer models and contributes to gastrin effects on cell adhesion.
文摘Objective： To investigate the effects of rAdinbitor on the adhesion and proliferation of human hepatoma cell strain 8MMC-7721. Methods： Cell adhesion assay was used to observe the effect of rAdinbitor on the adhesion of 8MMC-7721 cells to fibronectin （FN）. Crystal violet staining was performed to detect the influence of rAdinbitor on the adhesion of 8MMC- 7721 cells. MTT assay was employed to detect the inhibitory effects of different concentration of rAdinbitor on the proliferation of 8MMC-7721 cells. The morphologic changes of the control 8MMC-7721 cells and the apoptotic cells induced by 200μg/mL rAdinbitor for 36 h were observed under light microscope after HE staining. Flow cytometry analysis was applied to determine the apoptosis rate of 8MMC-7721 cells. Results： （1） FN promoted the adhesion of human hepatoma cell strain 8MMC-7721 in a dose-dependent manner. （2） rAdinbitor could dose-dependently inhibit the adhesion of SMMC-7721 cells to FN. The higher the concentration was, the stronger the inhibition was. There was significant difference among the groups （P 〈 0.05）. （3） rAdinbitor had a strong inhibition on the proliferation of 8MMC-7721 cells and showed a dose-dependent manner （P 〈 0.05）. After a 48 h exposure, the IC50 value of rAdinbitor was 177.83 μg/mL. （4） After exposure of 8MMC-7721 cells to 200μg/mL rAdinbitor for 36 h, the early morphologic changes appeared and the apoptosis rate was 20.68%, significantly higher than that of the control group （2.38%, P 〈 0.05）. Conclusion： rAdinbitor can dose-dependently inhibit the 8MMC-7721 cells adhesion to FN, and can inhibit the proliferation in dose-dependent manner and promote their apoptosis.
