Expert consensus on organizing the multidisciplinary team (MDT) diagnosis and treatment of hepato-pancreato-biliary diseases in China

Science China Life Sciences -     

行道树叶绿素变化的高光谱神经网络模型

采样分析了城市行道树（长春市主要街道）与对比区（净月潭国家森林公园）相应树种的叶绿素变化,并对由叶绿索变化引起的光谱反射率以ASD光谱仪进行了测试,并对二者之间的关系进行了单波段回归分析、V1植被指数与叶绿素含量的模型分析以及神经网络模型分析。结果表明,1）城市环境对行道树叶绿素有重要影响,但是对针叶树种响应较小,而阔叶树种响应较大;2）光谱反射率与测试树种叶绿素含量关系密切,在740～760nm附近确定性系数达0．72以上;3）PSSR植被指数与测试树种的叶绿素含量关系密切,幂函数回归的决定系数R^2为0．82左右。3）神经网络模型能够提高光谱反射率模型反演植被叶绿素含量的水平,模型的决定系数R^2高达0．97。表明高光谱遥感可以用来监测因城市环境引起的植被叶绿素变化。     

Association of p73 G4C14‐to‐A4T14 polymorphism at exon 2 with the response of human lung adenocarcinoma cell lines to chemotherapy

In order to assess the effect of p73 gene polymorphism G4C14‐A4T14 on cisplatin‐based chemosensitivity of human lung adenocarcinoma cell lines, we examined the differences in biological character and drug sensitivity affected by cisplatin between human lung adenocarcinoma cell lines A549 and P15. The allelic expression ofp73 in A549 and P15 was studied by Sty I polymorphism analysis. MTT [3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide] assay was used to analyse the response of these two cell lines to cisplatin. The changes in the biological behaviour of the cells were observed by colony formation assay. The drug‐induced apoptosis of cells was measured by Hoechst and TUNEL techniques. Homozygous allelic expression was demonstrated in the two cell lines. AT/AT genotype appeared in A549, GC/GC genotype was detected in P15. Although the colony formation number decreased with an increasing cisplatin dose (P<0.05), there was no significant difference in colony‐formation rate in these two cell lines (P>0.05). MTT assay also determined that the 50% inhibitory concentration (IC₅₀) for A549 and P15 was 8.9 and 11.6 μmol/l, respectively; the IC₅₀ value did not differ significantly between A549 and P15 (P>0.05). The cell apoptosis induced by cisplatin was demonstrated in both A549 and P15. P73 G4C14‐A4T14 polymorphisms at exon 2 existed in human NSCLC (non‐small‐cell lung cancer) cell lines. Our data in vitro suggest that p73 G4C14‐A4T14 polymorphism has no significant relationship to the cisplatin‐based chemosensitivity in human lung adenocarcinoma.     

Downregulation of miR-200a Induces EMT Phenotypes and CSC-like Signatures through Targeting the β-catenin Pathway in Hepatic Oval Cells

Hepatocellular carcinoma (HCC) can be derived from malignant transformed adult hepatic progenitor cells. However, the regulatory factors and molecular mechanisms underlying the process are not well defined. Our previous microRNA (miRNA) microarray analysis revealed a significant decrease of miR-200a level in F344 rat HCC side population (SP) fraction cells versus their normal counterparts. In the present study, we further investigated the effect of miR-200a on hepatic oval cell (HOC) phenotypes. We first confirmed downregulated miR-200a levels in rat hepatoma cells compared with WB-F344 cells. Next, by lentivirus-mediated loss-of-function studies, we showed that stable knockdown of miR-200a confers a mesenchymal phenotype to WB-F344 cells, including an elongated cell morphology, enhanced cell migration ability and expression of epithelial mesenchymal transition (EMT)-representative markers. Concomitantly, several cancer stem cell (CSC)-like traits appeared in these cells, which exhibit enhanced spheroid-forming capacity, express putative hepatic CSC markers and display superior resistance to chemotherapeutic drugs in vitro. Furthermore, bioinformatics analysis, luciferase assays and western blot analysis identified β-catenin (CTNNB1) as a direct and functional target of miR-200a. Knockdown of miR-200a partially activated Wnt/β-catenin signaling, and silencing of β-catenin functionally attenuated anti-miR-200a effects in vitro in WB-F344 cells. At length, in vivo xenograft assay demonstrated the acquisition of tumorigenicity of WB-F344 cells after miR-200a siliencing. Collectively, our findings indicate that miR-200a may function as an important regulatory factor in neoplastic transition of HOCs by targeting the β-catenin pathway.     

Notch is the key factor in the process of fetal liver stem/progenitor cells differentiation into hepatocytes

Cell transplantation is efficient method to therapy end-stage liver disease (ESLD). How to punctually induce stem cell differentiation into hepatocyte is still a challenge. Notch plays important roles in embryonic development and cell differentiation. However, during the differentiation process from fetal liver stem/progenitor cells (FLSPCs) to mature hepatocytes, the contribution of Notch, especially which Notch receptor is primarily responsible, is unknown. First, specific Notch receptor responsible for FLSPCs differentiation was identified. On both tissue level and cell level, we found that Notch3 was the only receptor greater expressed in liver tissue at embryonic day (ED) 14 and FLSPCs, compared with the adult liver and BRL cells, respectively. Second, morphological phenotypic and functional aspects were analyzed to evaluate whether Notch inhibition by GSIs (γ-secretase inhibitors, inhibitor of Notch) promotes the differentiation of FLSPCs into hepatocytes. Results showed that N-[N-(3, 5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) as GSIs was able to induce FLSPCs differentiation into hepatocytes. The differentiated FLSPCs showed similar morphology to mature hepatocytes, expressed hepatic markers indicative of a mature developmental stage, and displayed similar functionality to mature hepatocytes. The differentiation efficiency by GSIs was similar to that by hepatocyte growth factor (HGF) induction. More specifically, as the differentiation of FLSPCs progressed towards hepatocytes, the expression of Notch3 was gradually down-regulated, consistent with the down-regulation of other stem cell markers. These findings imply that Notch3 may not only be a regulator of FLSPCs differentiation into hepatocytes, but also be a potential marker of FLSPCs.     

新开河流域土地利用格局变化及其生态学意义

基于利用不同时期的地形图和TM遥感数据,运用ARC/INFO软件,以马尔柯夫空间概率模型为基础,对新开河流域的土地利用格局变化及驱动因素进行的分析,论证新开河流域土地利用结构日趋不合理：不仅林地占地最小,而且土地盐碱化、沙化严重,草地退化严重,生态环境质量整体向恶化方向发展,分析了生态环境恶化的原因,探讨了土地利用格局变化的生态学意义,提出了治理措施和方法.     

吉林省镇赉县近10年景观格局变化

以吉林省镇赉县2000年、2005年、2009年三期TM遥感影像为信息源,在小尺度下通过RS解译,对GIS建立的空间数据模型叠加分析和景观特征指数计算,结合自然与人文要素,具体分析镇赉县土地利用景观格局的变化情况。分析结果表明:近10a间研究区景观斑块面积和斑块的数量发生明显变化,水体景观类型斑块数量呈现大幅度增加,研究区各景观面积动态度变化显著,耕地面积大幅度增加,而草地和未利用土地面积大幅度减少。研究区景观破碎化程度较低、景观分维数较小且变化不大、景观异质性低,景观较为完整,该地区生态表现出明显的脆弱性和易恢复性。自然环境的制约、人为活动的干扰、政策的导向等因素决定和影响了该地区景观格局的变化趋势。     

Loss of heterozygosity of the tumor suppressor gene Tg737 in the side population cells of hepatocellular carcinomas is associated with poor prognosis

Analysis of loss of heterozygosity (LOH) is a useful method for finding genetic alterations in tumor and precancerous lesion tissues. In this study, we analyzed LOH of the tumor suppressor gene Tg737 in side population cells of human hepatocellular carcinomas. Side population cells were sorted and identification by flow cytometry from suspensions of hepatocarcinoma or normal liver cells generated from 95 hepatocellular carcinoma and normal tissues, respectively. DNA was extracted from the two groups of side population cells and peripheral blood specimens. Five microsatellite markers on the Tg737 gene were used to analyze the frequency of loss of heterozygosity in the side population cells of the hepatocellular carcinoma. Twenty-four (25.30%) tumor samples had a large deletion in more than three microsatellite markers. The highest frequency of loss of heterozygosity was observed with the G64212 marker (78.75%) and the SHGC-57879 marker (75.95%). Statistical analysis of the correlation between loss of heterozygosity of Tg737 and clinicopathological features indicated a strong correlation between the two markers associated with the highest frequency of loss of heterozygosity and survival. The results indicate that loss of heterozygosity of the tumor suppressor gene Tg737 may play an important role in the carcinogenetic mechanism of liver cancer stem cells. In addition, the independent association between loss of heterozygosity at the SHGC-57879 and G64212 markers and worsened short-term survival in patients could be used as a novel prognostic predictor. Further studies of side population cells may contribute to the establishment of novel therapeutic strategies for hepatocellular carcinoma.     

Role and Variation of the Amount and Composition of Glomalin in Soil Properties in Farmland and Adjacent Plantations with Reference to a Primary Forest in North-Eastern China

The glycoprotein known as glomalin-related soil protein (GRSP) is abundantly produced on the hyphae and spores of arbuscular mycorrhizal fungi (AMF) in soil and roots. Few studies have focused on its amount, composition and associations with soil properties and possible land-use influences, although the data hints at soil rehabilitation. By choosing a primary forest soil as a non-degraded reference, it is possible to explore whether afforestation can improve degraded farmland soil by altering GRSP. In this paper, close correlations were found between various soil properties (soil organic carbon, nitrogen, pH, electrical conductivity (EC), and bulk density) and the GRSP amount, between various soil properties and GRSP composition (main functional groups, fluorescent substances, and elements). Afforestation on farmland decreased the EC and bulk density (p < 0.05). The primary forest had a 2.35–2.56-fold higher GRSP amount than those in the plantation forest and farmland, and GRSP composition (tryptophan-like and fulvic acid-like fluorescence; functional groups of C–H, C–O, and O–H; elements of Al, O, Si, C, Ca, and N) in primary forest differed from those in plantation forest and farmland (p < 0.05). However, no evident differences in GRSP amount and composition were observed between the farmland and the plantation forest. Our finding highlights that 30 years poplar afforestation on degraded farmland is not enough to change GRSP-related properties. A longer period of afforestation with close-to-nature managements may favor the AMF-related underground recovery processes.