国宝--金梅枣

金梅枣为河南省南时大枣研究所培育的特晚熟鲜食极品。金梅枣果实特别大,近圆形,成熟期为金红色,形似李梅。平均单果重30克左右,最大过重65克,色泽光洁美丽,皮薄肉脆,细嫩多汁,甜似蜂蜜,枣味香浓郁,品质顶级。可食率93.8%,含水率65.4%,含糖量32.2%,维生素C含量352mg,蛋白质1.65%,含人体所需的氨基酸19种。金梅枣药用价值也特别高,每百克果肉中含环磷酸腺苷50mg,这种物质对人体癌细胞具有极强的破坏和抑制作     

Spatial simulation of landscape changes in Georgia: A comparison of 3 transition models

Spatial simulation models were developed to predict temporal changes in land use patterns in a piedmont county in Georgia (USA). Five land use categories were included: urban, cropland, abandoned cropland, pasture, and forest. Land use data were obtained from historical aerial photography and digitized into a matrix based on a 1 ha grid cell format. Three different types of spatial simulation were compared: (1) random simulations based solely on transition probabilities; (2) spatial simulations in which the four nearest neighbors (adjacent cells only) influence transitions; and (3) spatial simulations in which the eight nearest neighbors (adjacent and diagonal cells) influence transitions. Models and data were compared using the mean number and size of patches, fractal dimension of patches, and amount of edge between land uses. The random model simulated a highly fragmented landscape having numerous, small patches with relatively complex shapes. The two versions of the spatial model simulated cropland well, but simulated patches of forest and abandoned cropland were fewer, larger, and more simple than those in the real landscape. Several possible modifications of model structure are proposed. The modeling approach presented here is a potentially general one for simulating human-influenced landscapes.     

Effect of luteolin on TGF-β1-induced epithelial-mesenchymal transition in lung cancer A549 cells

AIM:To investigate the effects of luteolin on the invasion and epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1) in lung cancer A549 cells. METHODS:The effect of luteolin at 5, 10, 20, 40, 80 and 160 μmol/L on the viability of A549 cells was measured by MTT assay. The invasion ability was analyzed by Transwell method. The morphological changes of the A549 cells were observed under microscope.The protein expression of E-cadherin and vimentin in the A549 cells were determined by Western blot. RESULTS:The viability of the A549 cells was significantly inhibited by luteolin in a dose-time dependent manner (P<0.05). The IC₅₀ of luteolin for the A549 cells (24 h) was 68.79 μmol/L, while that (48 h) was 47.86 μmol/L. TGF-β1 induced morphological alteration of the A549 cells from epithelial to mesenchymal forms. Luteolin significantly inhibited TGF-β1-induced invasion of the A549 cells (P<0.01). The protein expression of E-cadherin was significantly down-regulated and the protein expression of vimentin was significantly up-regulated in the presence of TGF-β1 at 5 μg/L (P<0.01). However, luteolin reversed TGF-β1-induced EMT, up-regulation of E-cadherin and down-regulation of vimentin (P<0.01). CONCLUSION:Lu-teolin reverses TGF-β1-induced EMT in the lung cancer A549 cells.     

A 3D cell culture system to study epithelial-mesenchymal transition and drug resistance of lung cancer

AIM To explore the molecular mechanism of transforming growth factor-β1 （TGF-β1）-induced epithelial-mesenchymal transition （EMT） and cisplatin resistance in three-dimensionally cultured lung cancer cells. METHODS Under three-dimensional culture condition, the morphological changes and protein expression changes of human non-small-cell lung cancer 95D cells were observed by inversed fluorescence microscopy, scanning electron microscopy, laser scanning confocal microscopy and Western blot before or after TGF-β1 stimulation. The cisplatin sensitivity was determined by MTT assay. RESULTS Under the three-dimensional culture condition, the structure of 95D cell spheroids after TGF-β1 stimulation collapsed, the cells were dispersed and migrating, and the spheroids merged with each other. The results of laser confocal microscopy showed that E-cadherin protein expression in the 95D cells did not changed after TGF-β1 stimulation, and the protein expression of N-cadherin and vimentin was significantly up-regulated. The results of Western blot showed that the expression of E-cadherin was down-regulated after TGF-β1 stimulation, and the protein levels of N-cadherin, vimentin, phosphorylated AKT and phosphorylated mTOR were up-regulated. LY294002 and rapamycin reversed TGF-β1-induced expression of the above proteins. The results of MTT assay showed that TGF-β1 reduced the sensitivity of three-dimensionally cultured 95D cells to cisplatin, while LY294002 and rapamycin reversed the cisplatin resistance of the 95D cells stimulated by TGF-β1. CONCLUSION TGF-β1 induces the EMT and cisplatin resistance of three-dimensionally cultured lung cancer cells through the activation of PI3K/AKT/mTOR signaling pathway.     

Pathogenesis of endothelial-mesenchymal transition in pulmonary arterial hypertension

Endothelial-mesenchymal transition (EndMT) is a biological process through which endothelial cells change their endothelial phenotype into a mesenchymal or myofibroblastic phenotype with the expression of mesenchymal markers such as α-smooth muscle actin (α-SMA) and vimentin. When the pulmonary vascular endothelial cells are exposed to hypoxia and inflammatory stimulation, vascular smooth muscle cells in the outer and middle membrane accumulate through EndMT process, leading to pulmonary vascular remodeling and pulmonary arterial hypertension (PAH). Transforming growth factor β (TGF-β)/bone morphogentic protein (BMP) signaling pathways promote EndMT process by bone morphogentic protein receptor 2 (BMPR2) gene mutation which up-regulates high mobility group protein A1 (HMGA1) gene and contributes to protein expression such as Slug and Snail, thus resulting in PAH. In brief, TGF-β/BMP signaling pathways and related regulators play an important role in pulmonary vascular reconstruction and the formation of PAH.     

Assessment of the state of oxidative stress

Oxidative stress, an imbalance toward the pro-oxidant side of the pro-oxidant/antioxidant homeostasis, occurs in several human diseases. The assessment of the state of oxidative stress could be done by measuring the concentration of various pro-oxidants, i.e., reactive oxygen and nitrogen species, and measuring various kinds of metabolites of the biological molecules damaged by ROS and/or RNS, such as nuclear acids, lipids and protein. It also can be done by detecting the antioxidant agents including enzymes such as catalase, superoxide dismutase, glutathione peroxidase, and numerous non-enzymatic antioxidants, including vitamins A, E and C, glutathione, ubiquinone, metallothionein and thioredoxin. As redox reaction is associated with oxidative stress, the apparent redox potential reflecting the redox state of the body can also be used to judge the overall state of oxidative stress. The combination of the redox potential and reduction capacity for various redox pairs, e.g. GSSG/GSH redox pair, may be a useful approach for the assessment of the state of oxidative stresss.     

Renal tubular epithelial-mesenchymal transition in kidney fibrosis

Epithelial-mesenchymal transition (EMT), a process by which differentiated epithelial cells undergo a phenotypic conversion that gives rise to the matrix-producing fibroblasts and myofibroblasts, is increasingly recognized as an integral part of tissue fibrogenesis after injury. However, the degree to which renal tubular epithelial EMT contributes to kidney fibrosis remains a matter of intense debate and is likely to be context-dependent. Renal tubular EMT is an adaptive response of epithelial cells to a hostile or changing microenvironment and is regulated by many factors. Several intrace-llular signal transduction pathways such as transforming growth factor-β (TGF-β)/Smad and Wnt/β-catenin signaling are essential in controlling the process of renal tubular epithelial EMT which are potential targets of antifibrotic therapy presently. This review highlights the current understanding of renal tubular epithelial EMT and its underlying mechanisms to stimulate further discussion on its role in the pathogenesis of renal interstitial fibrosis.     

日本果树生产现状

日本当前果树栽培总面积225 760hm2,其中柑桔占24.7%,苹果19.4%,栗11.2%,柿11.1%。果树生产中支出与收益比例良性化发展。果园管理中推行机械化作业,实行省力化栽培。农协在果树生产、加工和销售以及服务中发挥着重要作用。生产机械化水平不断改进和提高,标准化、区域化生产已成为日本果树生产的特色。     

枣产业转型期面临的挑战与对策

枣是我闰原产果树、第一大干果和五大优势经济林之一。改革开放以来发展迅猛,面积和产量分别增加了10多倍和20多倍,达200万hm~2和800万t,成为我国特色果品大产业。近年来,我国枣产业整体上进入从卖方市场向买方市场、从传统果业向现代果业转型的关键期。分析转型期枣产业面临的严峻挑战和历史性新机遇,并从高效新理念、目标新导向、发展新模式、品种新布局、栽培新技术、科技新支撑诸方面提出了对策建议。     

Role of HMGA2 in epithelial-mesenchymal transition of gastric cancer cells

AIM:To investigate the role of HMGA2 in the epithelial-mesenchymal transition (EMT) in gastric cancer cells. METHODS:The expression of HMGA2 in human gastric cancer cell lines with different degrees of differen-tiation (MKN45, MKN28 and SGC7901) and immortalized human gastric epithelial cell line GES-1 was determined by Western blot and RT-qPCR. pcDNA3.0-HMGA2 plasmid was transfected into the MKN28 cells by liposome method. Transfection of si-HMGA2 interference fragments into MKN45 cells was also performed. The transfection efficiency was evaluated by Western blot and RT-qPCR. The effects of HMGA2 over-expression in the MKN28 cells and knock-down in the MKN45 cells on the cell viability were measured by CCK-8 assay. The effects of HMGA2 over-expression in the MKN28 cells on the cell migration and invasion abilities were detected by wound healing and Transwell invasion assays. The effects of HMGA2 over-expression in the MKN28 cells and knock-down in the MKN45 cells on the expression of EMT-related markers E-cadherin, N-cadherin, vimentin at mRNA and protein levels were determined by RT-qPCR and Western blot. The changes of Wnt/β-catenin signaling pathway-related molecules in the MKN28 cells with HMGA2 over-expression were also determined by RT-qPCR. RESULTS:The expression levels of HMGA2 were quite different in different differentiation levels of gastric cancer cells (P<0.05). The increased expression level of HMGA2 in MKN28 cells inhibited the cell viability (P<0.05), while the decreased expression level of HMGA2 in MKN45 cells promoted the cell viability (P<0.05). The increased expression level of HMGA2 in MKN28 cells promoted cell migration and invasion (P<0.05), changed the expression of EMT-related markers (P<0.05), while the decreased expression level of HMGA2 in the MKN45 cells changed the expression of EMT-related markers (P<0.05). The increased expression level of HMGA2 in the MKN28 cells significantly increased the mRNA levels of β-catenin in the Wnt/β-catenin pathway and the downstream molecules c-Myc and cyclin D1 (P<0.05). CONCLUSION:HMGA2 is closely related to the migration and invasion abilities of gastric cancer cells. Moreover, it promotes the EMT process of gastric cancer cells by activating Wnt/β-catenin pathway.     

Effect of c-SKI on coronary endothelial cell proliferation and endothelial-mesenchymal transition

AIM: To investigate the effect of cellular Sloan-Kettering Institute (c-SKI) on the proliferation and endothelial-mesenchymal transition of human coronary artery endothelial cells (HCAECs). METHODS: HCAECs were treated with transforming growth factor-β1 (TGF-β1) at varying concentrations for different time points. Western blot was used to test the expression of c-SKI and mesenchymal markers such as α-smooth muscle actin (α-SMA) and vimentin. Meanwhile, the endothelial marker E-cadherin was also detected. HCAECs were transfected with c-ski gene mediated by lentivirus (LV), the efficiency of LV-SKI transfection was detected by RT-qPCR. The HCAECs were divided into 4 groups:control group, TGF-β1 (5 μg/L) group, LV-SKI+ TGF-β1 group, LV-NC+ TGF-β1 group. The cell viability and colony formation were measured by MTT assay and colony formation assay. The protein levels of vimentin, α-SMA, E-cadherin, Smad2, Smad3, p-Smad2 and p-Smad3 were determined by Western blot. RESULTS: The expression of c-SKI was down-regulated in the HCAECs treated with TGF-β1 (P<0.01). Over-expression of c-SKI inhibited the proliferation of HCAECs (P<0.01). Compared with LV-NC group, over-expression of c-SKI down-regulated the expression of α-SMA and vimentin (P<0.01), up-regulated the expression of E-cadherin (P<0.01), and inhibited the protein phosphorylation of Smad2 and Smad3 (P<0.01), reversed the endothelial-mesenchymal transition induced by TGF-β1. CONCLUSION: The expression of c-SKI in the HCAECs is down-regulated in the process of endothelial-mesenchymal transition. Over-expression of c-SKI inhibits proliferation and endothelial-mesenchymal transition of HCAECs, the mechanism may be related to regulation of the TGF-β1/Smad signaling pathway.     

Inhibitory effect of oxymatrine on high glucose-induced rat renal tubular epithelial-mesenchymal transition

AIM:To investigate the inhibitory effect of oxymatrine (OM) on high glucose-induced rat renal tubular epithelial-mesenchymal transition (EMT). METHODS:The rat renal tubular epithelial NRK52E cells were cultured in vitro. The cells were divided into control group, high glucose group, high glucose+different concentrations of OM groups and high glucose+0.50 g/L OM dynamic observation group. The expression of TGF-β1, Smad7, α-SMA and E-cadherin at mRNA and protein levels was detected by real-time PCR and Western blotting. The viability of NRK52E cells was determined by MTT assay. RESULTS:(1) Compared with control group, the expression of TGF-β1 and α-SMA at mRNA and protein levels in high glucose group gradually increased, and Smad7 protein and E-cadherin mRNA and protein gradually reduced, but the mRNA expression of Smad7 gradually increased. (2) Compared with high glucose group, as increases in OM doses, the expression of TGF-β1 and α-SMA at mRNA and protein levels in high glucose+different concentrations of OM groups gradually reduced, and Smad7 protein and E-cadherin mRNA and protein gradually increased, but the mRNA expression of Smad7 had no significant change. (3) Compared with high glucose group, the expression of TGF-β1 and α-SMA at mRNA and protein levels was significantly reduced, the expression of E-cadherin at mRNA and protein levels significantly increased, and the protein expression of Smad7 significantly increased, but the mRNA expression of Smad7 had no significant change in high glucose+0.50 g/L OM dynamic observation group. CONCLUSION: In NRK52E cells, oxymatrine inhibits high glucose induced EMT by down-regulating TGF-β1 and up-regulating Smad7, thus preventing the fibrosis effect of TGF-β1/Smads signaling.     

Forecasting the spatial dynamics of gypsy moth outbreaks using cellular transition models

A series of cellular transition probability models that predict the spatial dynamics of gypsy moth (Lymantria dispar L.) defoliation were developed. The models consisted of four classes: Simple Markov chains, Rook's and Queen's move neighborhood models, and distance weighted neighborhood models. Historical maps of gypsy moth defoliation across Massachusetts from 1961 to 1991 were digitized into a binary raster matrix and used to estimate transition probabilities. Results indicated that the distance weighted neighborhood model performed better then the other neighborhood models and the simple Markov chain. Incorporation of interpolated counts of overwintering egg mass counts taken throughout the state and incorporation of historical defoliation frequencies increased the performance of the transition models.     

贵州威宁苹果产业现状与发展措施

概述威宁县苹果产业发展的现状,分析威宁发展苹果产业的气候资源、竞争优势以及存在的主要问题,并提出相应的发展对策和措施     

韩国的果树生产和育种进展

介绍了韩国果树生产的基本情况和果树育种工作的成就韩国高度重视果树资源的收集和品种选育,有目的、有针对性地培育了适合韩国条件的苹果、梨、桃等品种、韩国对国外果树科研、生产和市场情况的深入了解,对果树科研的思路和方法,以及生产模式等均值得学习借鉴。     

Effects of Snail1 siRNA on tubular epithelial-to-mesenchymal transition induced by high glucose

AIM: To explore the effect of Snail1 siRNA on high-glucose induced tubular epithelial-to-mesenchymal transition (TEMT). METHODS: Subconfluent renal tubular epithelial cells were incubated in serum-free DMEM for 24 h to arrest and synchronize the cell growth. Then cells were treated with normal glucose (5.5 mmol/L D-glucose) or high glucose (25 mmol/L D-glucose) for 72 h. Meanwhile 19.5 mmol/L D-manntiol was used as high osmotic control. Snail1 siRNA was transfected into tubular epithelial cells. In parallel, cells were transfected with non-specific siRNA which served as the control data sets. Cells were then treated with 25 mmol/L D-glucose for 72 h. RNA and cell lysates were collected to determine the protein and mRNA levels of Snail1, TGF-β1, α-SMA, vimentin and E-cadherin. RESULTS: Transfection caused the decreases in Snail1 at mRNA and protein levels by 62% and 68% respectively as compared to those in untransfected cells cultured in high glucose medium. Western blotting exhibited that Snail1 siRNA transfection restored E-cadherin protein expression by 61% compared to that in high-glucose-treatment cells, whereas it inhibited high-glucose-induced induction of α-SMA protein by 58%. Similarly, RT-PCR revealed that Snail1 siRNA transfection dramatically suppressed the high-glucose-induced mRNA expressions of α-SMA and vimentin by 72% and 61%, respectively, while E-cadherin mRNA increased by 53%. CONCLUSION: Our study provides direct evidence that Snail1 is able to control TEMT.     

Role of connective tissue growth factor in high glucose-induced epithelial-mesenchymal transition in podocytes

AIM: To investigate the role of connective tissue growth factor (CTGF) in high glucose-induced epithelial-mesenchymal transition (EMT) in podocytes. METHODS: The differentiated podocytes cultured under different conditions for 24 h at 37 ℃ were divided into 4 groups: control (5 mmol/L glucose solution), 5 mmol/L glucose solution supplemented with 50 μg/L CTGF, high glucose (30 mmol/L glucose solution) and high glucose supplemented with CTGF (50 μg/L). The morphology of cultured podocytes was observed under phase-contrast microscope. To study the relevant markers of EMT, the mRNA and protein expression was analyzed by real-time RT-PCR and Western blotting, respectively. In addition, the effect of CTGF inhibition with anti-CTGF antibody on high glucose-induced EMT in podocytes was investigated. RESULTS: High glucose induced phenotypic transition in the podocytes from an arborization morphology to a cobblestone morphology. After addition of CTGF to high glucose culture, the podocytes developed a feature of spindle. Under high glucose condition, podocytes underwent EMT, as the epithelial marker (nephrin) was decreased and the mesenchymal marker (desmin) was increased. Exogenous CTGF showed the effect of synergy on high glucose-induced EMT. Moreover, high glucose-induced EMT in podocytes was prevented by CTGF inhibition with anti-CTGF antibody. CONCLUSION: CTGF is involved in high glucose-induced EMT in podocytes. Inhibition of CTGF might prevent podocytes from injury in diabetes.     

Derivation of a yearly transition probability matrix for land-use dynamics and its applications

Transition matrices have often been used in landscape ecology and GIS studies of land-use to quantitatively estimate the rate of change. When transition matrices for different observation periods are compared, the observation intervals often differ because satellite images or photographs of the research site taken at constant time intervals may not be available. If the observation intervals differ, the transition probabilities cannot be compared without calculating a transition matrix with the normalized observation interval. For such calculation, several previous studies have utilized a linear algebra formula of the power root of matrices. However, three difficulties may arise when applying this formula to a practical dataset from photographs of a research site. We examined the first difficulty, namely that plural solutions could exist for a yearly transition matrix, which implies that there could be multiple scenarios for the same transition in land-use change. Using data for the Abukuma Mountains in Japan and the Selva el Ocote Biosphere Reserve in Mexico, we then looked at the second difficulty, in which we may obtain no positive Markovian matrix and only a matrix partially consisting of negative numbers. We propose a way to calibrate a matrix with some negative transition elements and to estimate the prediction error. Finally, we discuss the third difficulty that arises when a new land-use category appears at the end of the observation period and how to solve it. We developed a computer program to calculate and calibrate the yearly matrices and to estimate the prediction error.     

Chronic alcohol intake-induced epithelial-mesenchymal transition contri-butes to hepatic fibrogenesis in mice

AIM：To evaluate the effect of chronic alcohol intake on the histopathological changes of the liver and to determine the contribution of epithelial-mesenchymal transition (EMT) to hepatic fibrogenesis. METHODS：Thirty male C57BL/6 mice were randomly divided into 3 groups as following: the mice in control group was given (ig) water; the mice in low-dose alcohol group (2.0 g·kg -1·d -1) and high-dose alcohol group (4.0 g·kg -1·d -1) were given (ig) alcohol for 5 months. Alcohol-induced histopathological changes of the liver or development of hepatic fibrosis were evaluated using the histological methods with HE and Masson trichrome staining. The apoptosis of the liver was detected by TUNEL fluorometric staining (counterstained with DAPI). The activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) was measured by an automated biochemical analyzer. The expression of fibroblast-specific protein 1 (FSP-1), α-smooth muscle actin (α-SMA) and E-cadherin in the hepatic tissues was detected by immunofluorescence examination. The protein levels of E-cadherin, α-SMA, FSP-1, transforming growth factor β 1 (TGF-β 1) and hypoxia-inducible factor 1α (HIF-1α) were analyzed by Western blotting. RESULTS：Compared with control, the activity of serum ALT and AST, and apoptotic index of liver tissues were increased in the mice treated with alcohol for 5 months. The histopathological changes of the livers in the mice of low-dose alcohol group included steatosis and mild liver fibrosis, while severe liver fibrosis was observed in the high-dose alcohol-treated mice. Chronic alcohol consumption induced the increase in malondialdehyde (MDA) level, and the decreases in the activity of superoxide dismutase (SOD) and catalase (CAT) in the livers. It also reduced E-cadherin expression and increased α-SMA expression. FSP-1 immunostaining and albumn immunostaining positive cells were co-localized in the hepatocytes of low-dose alcohol group, but only FSP-1 positive hepatocytes were observed in high-dose alcohol group. Chronic alcohol consumption decreased E-cadherin expression and increased α-SMA, FSP-1, TGF-β 1 and HIF-1α expression in a dose-dependent manner, but the HIF-1α expression was not altered between the 2 alcohol-treated groups. CONCLUSION：Chronic alcohol intake induces the progression of hepatic fibrosis. Some fibroblasts derive from hepatocytes in liver fibrosis via EMT. The underlying mechanism is associated with the changes of the redox state, and increased TGF-β 1 generation and HIF-1α expression.