人居环境视角下居民垃圾分类意愿实证研究及政策建议——基于河南省郑州、洛阳、商丘和漯河四地市的调研

基于河南省人居环境现状,分别对郑州、洛阳、商丘和漯河四地市进行了实地调研,通过建立二元Logistic模型,分析了影响居民垃圾分类意愿高低的因素。结果表明:文化程度、经济发展、政策支持对提高居民垃圾分类意愿具有较强的正相关影响,而居民人居环境满意度对提高垃圾分类意愿具有负相关影响;女性相比男性的垃圾分类意愿更高,城市居民相比农村居民的垃圾分类意愿更高。基于此结论,从政府和社会两个方面分别提出了相关建议,以供参考。     

SIRT1 promotes autophagy of pancreatic cancer cells induced by hypoxia via regulating FOXO1/RAB7 signaling pathway

AIM: To investigate the effect of SIRT1 on the autophagy of pancreatic cancer cells under hypoxia condition, and to analyze the underlying mechanism of regulating FOXO1/RAB7 signaling pathway. METHODS: Western blot and immunofluorescence methods were used to determine the expression of SIRT1 in the pancreatic cancer cells. The small interfering RNA targeting SIRT1 and SIRT1 over-expression plasmid were transfected into the pancreatic cancer Panc-1 cells. Confocal microscopy was used to detect the LC3 expression. Western blot was used to analyze the protein levels of LC3, p62 and FOXO1/RAB7 signaling pathway-related molecules. Co-immunoprecipitation was used to detected the protein interaction between SIRT1 and FOXO1. RESULTS: The expression level of SIRT1 in the nucleus of Panc-1 cells was increased under hypoxia condition. Compared with negative control under hypoxia condition, knock-down of SIRT1 expression attenuated the autophagy flux in the pancreatic cancer Panc-1 cells (P<0.05). Over-expression of SIRT1 increased the protein levels of FOXO1 and RAB7. On the contrary, knock-down of SIRT1 expression inhibited the protein levels of FOXO1 and RAB7. The protein interaction between SIRT1 and FOXO1 in the pancreatic cancer cells was observed. CONCLUSION: SIRT1 in pancreatic cancer Panc-1 cells under hypoxia condition is over-expressed in the nucleus. Down-regulation of SIRT1 inhibits autophagy and its mechanism may be related to FOXO1/RAB7 signaling pathway.     

Effect of beclin-1 gene silencing on TuAKe-injured gastric cancer SGC-7901 cells

AIM: To observe the effect of beclin-1 silencing by the technique of RNA interference on the injury of human gastric cancer SGC-7901 cell by Sheliugu extract (the extract from tuber of Amorphophallus konjac, TuAKe). METHODS: To knock down the expression of beclin-1 gene, SGC-7901 cells were transfected with lentiviral vector carrying beclin-1-shRNA. The beclin-1 gene knock-down and non-knock-down SGC-7901 cells were treated with TuAKe. The cell viability was analyzed by CKK-8 assay. The percentages of apoptotic cells were detected by flow cytometry. The expression of beclin-1 and LC3 was detected by Western blot. RESULTS: The beclin-1 gene silencing decreased the protein expression of beclin-1 and increased the protein expression of LC3 in the SGC-7901 cells, leading to the decrease in cell viability and the increase in apoptotic rate (P<0.05). TuAKe increased the protein expression of beclin-1 and LC3 in the SGC-7901 cells, and decreased the protein expression of LC3 in the SGC-7901 cells with beclin-1 gene silencing, thus inhibiting the cell viability and increasing the apoptotic rate (P<0.05). CONCLUSION: Beclin-1 gene silencing inhibits the activation of beclin-1-related signaling pathway in gastric cancer SGC-7901 cells, and aggravates the injury of cell viability induced by TuAKe.     

27-Hydroxycholesterol modulates lung cancer cell proliferation by activation of LXR signaling pathway

AIM:To investigate the effect of cholesterol metabolite 27-hydroxycholesterol (27-OHC) on the proliferation of lung cancer cells. METHODS:Human lung cancer A549 cells were treated with 27-OHC at different concentrations (0, 0.3125, 0.625, 1.25, 2.5, 5 and 10 μmol/L) for 24~48 h. The cell viability, cell cycle, cell prolife-ration, the intracellular cholesterol levels and cholesterol metabolism-related molecule expression were subsequently assessed by CCK-8 assay, flow cytometry, EdU staining, tissue total cholesterol detection kit, real-time PCR and Western blot. RESULTS:27-OHC decreased the viability of the A549 cells in a dose-and time-dependent manner (P<0.01) and inhibited the cell proliferation (P<0.05). The expression of typical liver X receptor (LXR) downstream target proteins including ATP-binding cassette transporter A1 (ABCA1), low-density lipoprotein receptor (LDLR), and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CR) were modulated, which promoted the efflux of intracellular cholesterol, and reduced cholesterol influx and de novo synthesis, resulting in decreased intracellular cholesterol levels and cell viability. Furthermore, the inhibitory effect of 27-OHC on A549 cell viability was significantly attenuated after the LXR pathway was partially blocked by 5 μmol/L GSK2033 treatment (P<0.05). CONCLUSION:27-OHC inhibits A549 cell prolife-ration via activation of LXR signaling pathway.     

人地协调视角下农村居民点利用质量评价与提升策略

农村居民点高质量利用是乡村振兴的一种具体表现，综合开展农村居民点质量评价、全面改善质量障碍要素是科学编制村庄规划和优化农村要素配置的基础。该研究以北京市平谷区为例，从土地集约利用和人居环境品质相互协调的视角界定农村居民点利用质量内涵并构建评价体系，综合运用熵权-TOPSIS法、变异系数修正的弹性系数法和障碍度诊断模型，对农村居民点利用质量进行评价并提出相应的提升策略。结果表明：1）平谷区农村居民点土地集约利用水平中等偏高，人居环境品质和农村居民点利用综合质量则中等偏低。2）平谷区农村居民点类型表现为中等质量主导、高质量次之、低质量偏少，对应着从脱钩F弱型、脱钩T弱型、正向挂钩F强型、负向挂钩F弱型、正向挂钩T强型、负向挂钩T弱型、正向挂钩T-F同强型、负向挂钩T-F同弱型的村庄数量依次降低。3）平谷区农村居民点高质量利用的障碍要素主要体现在规模强度、空间布局、生活环境和生产环境4个维度，从高质量到低质量利用类型，障碍因素数量增多、作用程度逐渐增大。4）平谷区应充分发挥生态环境优势，在"整体化、集约化、人本化和善治化"战略导向下，按照"高质量利用类适当优化、中等质量利用类同步调控、低质量利用类系统整治"策略，分类有序地推进农村居民点质量提升。     

关中-天水经济区人类活动对植被覆盖变化的影响

为探究植被覆盖变化及人类活动对改善关中地区及西北地区的生态环境影响,利用植被覆盖和地表温度数据,结合Sen趋势与Mann-Kendall检验分析关中-天水经济区2001—2016年的植被覆盖变化趋势,并根据估算的土壤湿度因子,应用残差法评价人类活动对植被覆盖变化的影响程度及影响方向。结果表明:1)从时间变化维度来看,2001—2016年关中-天水经济区植被覆盖变化总体呈良好趋势,且整体表现为在不断波动中递增,表明关天经济区进行的生态环境建设工程正在慢慢凸显它的生态效应。2)从空间变化维度来看,关中-天水经济区植被覆盖显著增长的区域面积占35.87%,主要集中在研究区南北两侧。而显著下降的面积区域占3.21%,主要分布在城市中心,即经济发展活跃的地区,如西安市区,宝鸡市区,天水市区,铜川市区等。3)关中-天水经济区植被覆盖受自然因素影响较小,受其他因素影响大。其正相关区域占13.43%,不显著相关区域占85.26%。4)关中-天水经济区人类活动对植被覆盖变化的正作用大于负作用。其中,正作用区域主要分布在研究区北部和东南地区,其主要原因是人类活动不频繁,建设生态屏障、加强退耕还林、三北防护林保护以及水土保持等生态工程促进植被NDVI增长。负作用区域主要分布在渭河沿线、经济活动较高地区,其主要原因有:人类活动频繁、过度城市化、工业化等抑制植被生长。5)植被覆盖的增长和下降区域与人类活动对植被影响的正作用和负作用区域大致相同。这也从侧面反映了关天经济区植被覆盖情况受人类活动影响大。总之,在负作用区域,在经济建设发展的同时也要注重植被建设、以及对植被乃至生态环境的保护。     

MicroRNA-145 inhibits epithelial-mesenchymal transition in human renal cancer A-498 cells by ADAM28

AIM: To investigate the inhibitory effect of microRNA-145 (miR-145) on epithelial-mesenchymal transition (EMT) in renal cancer A-498 cells. METHODS: The A-498 cells were transfected with miR-145 mimics (M145) and mimic negative control(MNC), which served as M145 group and MNC group, respectively. Mock control (MC) group was set up using untreated A-498 cells. The expression level of miR-145 in each group was detected by RT-qPCR. Transwell assay was used to detect the invasion ability of the cells. The protein expression of vimentin, E-cadherin and ADAM28 was determined by Western blot. Bioinformatic method was used to predict the target genes of miR-145. Antagonistic effect of ADAM28 over-expression on the inhibition of EMT by miR-145 was detected by Western blot. The relationship between miR-145 and ADAM28 was analyzed by dual-luciferase reporter assay. RESULTS: The expression level of miR-145 in M145 group was significantly up-regulated than that in MC group (P<0.05). The number of invasive cells in M145 group was 12.78±3.37, which was significantly lower than that in MC group (P<0.05). ADAM28 may be the target gene of miR-145. Compared with MC group, the protein expression of vimentin and ADAM28 in M145 group was significantly decreased (P<0.05), while the protein expression of E-cadherin was significantly increased (P<0.05).After ADAM28 over-expression, the protein expression of vimentin in the A-498 cells of M145 group was significantly increased (P<0.05), and the protein expression of E-cadherin was significantly decreased (P<0.05). The results of dual-lucife-irasei reporter assay showed that ADAM28 was a downstream target gene of miR-145. CONCLUSION: miR-145 may inhibit the expression of EMT-related proteins through the downstream target gene ADAM28 and inhibit the EMT process of renal cancer A-498 cells.     

Metformin sensitizes human breast cancer MDA-MB-231 cells to tamo-xifen through down-regulation of c-Myc

AIM: To investigate whether metformin enhances the sensitivity of human breast cancer MDA-MB-231 cells to tamoxifen by down-regulating c-Myc. METHODS: The cell viability, colony formation, apoptosis, and migration and invasion abilities of MDA-MB-231 cells were detected by CCK-8 assay, colony formation experiment, flow cytometry and Transwell assay. The expression level of c-Myc was quantified by Western blot and immunohistochemical analysis. The antitumor effects of metformin and tamoxifen were investigated in vivo in a MDA-MB-231 triple-negative breast cancer xenograft model in the SCID mice. RESULTS: Metformin in combination with tamoxifen exerted synergistic effects on inhibition of the viability, colony formation, migration and invasion, and induced the apoptosis compared with the controls and either agent treatment alone in the MDA-MB-231 cells. The levels of c-Myc was down-regulated in vitro by treatment with metformin and/or tamoxifen (P<0.01). Moreover, metformin or in combination with tamoxifen also reduced the growth of MDA-MB-231 breast cancer tumors in the SCID mice by down-regulation of c-Myc in vivo. CONCLUSION: Metformin in combination with tamoxifen exerts synergistic effects on inhibition of the proliferation, migration, invasion and tumor growth of human triple-negative breast cancer MDA-MB-231 cells by down-regulating c-Myc expression, suggesting that metformin in combination with tamoxifen merits further evaluation as a target.     

F-box domain is involved in regulating the proliferation of MCF-7 cells by FBXO39 protein

AIM: To investigate the effect of F-box domain on the regulation of MCF-7 cell proliferation by FBXO39 protein. METHODS: The effect of F-box domain on the localization of FBXO39 protein in the MCF-7 cells was investigated. MCF-7 cell cDNA library was used as the template resource. The full-length cDNA sequence of FBXO39 was amplified by PCR method and subcloned into eukaryotic expression vector pEGFP-C2. The pEGFP-FBXO39ΔF (F-box domain deletion mutation) plasmid was successfully constructed with the template resource of pEGFP-FBXO39 plasmid. The recombinant plasmids were transfected into the MCF-7 cells, and then the expression of FBXO39 and FBXO39ΔF were determined by Western blot. The cellular localization of FBXO39 and FBXO39ΔF were observed by confocal microscopy. The localization of endogenous FBXO39 in the MCF-7 cells was detected by immunofluorescence staining. In addition, MTT and EdU assays were used to measure the cell proliferation, flow cytometry was used to measure the cell cycle distribution, and immunohistochemical staining was used to observe the expression of FBXO39 in the breast cancer and para-carcinoma tissues. RESULTS: The eukaryotic expression vector pEGFP-FBXO39 and pEGFP-FBXO39ΔF were constructed successfully. F-box domain had no effect on the cell localization of FBXO39. FBXO39 promoted MCF-7 cell proliferation but FBXO39ΔF did not. FBXO39 was highly expressed in the breast cancer tissues. CONCLUSION: F-box domain had no effect on the cellular localization of FBXO39 protein. However, it plays an important role in the biological function of FBXO39. FBXO39 may be related to breast cancer tumorigenesis.