小麦保护性耕作技术研究与分析     

徐国强  孙国生  赵郑华 《农业科技与装备》2009,(2):121-122

小麦保护性耕作技术是以机械化作业为主要手段,采取少耕或免耕方法,保护土壤、降低生产成本、实现农业可持续发展的机械化耕作技术体系.将保护性耕作技术种植小麦的试验数据与常规耕作技术的试验数据相比较,结果表明:应用保护性耕作技术种植小麦的增温、保墒作用更为明显.麦田含水率较常规耕作的多2.52%,小麦个体发育健壮,平均增产1.6%,节约耕作费用450元/hm2,新增经济效益570元/hm2.  相似文献   

配电GIS图形转换系统的研究     

许童羽  蔡楠 《农业科技与装备》2009,(1):52-56

配电网地理图自动生成电气接线图是配电GIS图形转换的主要问题,要求生成的电气接线图与地理图信息完全一致,同时还要科学、美观.采用优化的节点提取拓扑分析方法分析配电地理图中网络拓扑结构.在常见处理方法的基础上提出一种快捷有效的算法,可根据配电网地理图中的地理信息自动生成电气接线图.  相似文献   

农村变电站选址规划方法     

许童羽  孙艳辉  刘泽浩 《农业科技与装备》2009,(2):44-46

农村变电站选址是电网规划的重要组成部分,在农网规划是起承上启下的作用,文中介绍最优化选址问题,并将优化选址的数学模型进行分类,又全面地比较分析应用于变电站选址方法的诸多算法,提出5项有利于电力市场环境下的农网变电站选址的建议.  相似文献   

金秋梨栽培技术   总被引：3，自引：0，他引：3  

徐应华  秦燕 《落叶果树》2000,32(5):36-37

介绍了金秋梨壮苗培育,科学建园,土壤管理和施肥技术以及整形修剪,花果管理和病虫害防治等栽培技术。  相似文献   

Inhibition of ICAM-1 expression on endothelial cells in hypoxia/reoxygenation by antisense oligodeoxynucleotides     

XIA Bin  XU Hong-shi  SHAO Fu-yuan  CHEN Lei 《园艺学报》2000,16(12):1267-1269

AIM: To investigate the effect of antisense oligodeoxynucleotides (AS-ODN) on the intercellsular adhesion molecule-1(ICAM-1) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R, the positive percentage of ICAM-1 expression was measured by flow cytometry before and after giving AS-ODN. RESULTS: The ICAM-1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group, it increased in 6 hours reoxygenation, and decreased by 40.6% after giving AS-OND. CONCLUSION: AS-ODN may decrease the expression of ICAM-1 on endothelial cells in H/R.  相似文献   

Role of leukotriene D₄ in promoting proliferation of cultured human airway smooth muscle cells     

LUO Ya-ling  WEN Jin-xu  XU Jian  ZHU Jian-jun 《园艺学报》2000,16(3):252-254

AIM: To investigate whether leukotriene D₄(LTD₄) would stimulates proliferation of cultured human airway smooth muscle (ASMC). METHOD: Human ASMC were isolated and subcultured, varying concentration of LTD₄ were added to the media. Cell counts were obtained, -thymidine([³H]-TdR) incorporation and inositol 1, 4, 5-trisphosphate (IP₃) accumulation were measured. RESULTS: LTD₄(0.1nmol·L^-1~10 nmol·L^-1) increased cell number and also increased incorporation of[³H]-TdR and accumulation of IP₃ in a concentration dependent manner(P＜0.01). The latter response was blocked by phospholipase C inhibition with neomycin (1 μmoL·L^-1(P＜0.01). However, neomycin had no effect on the promitogenic action of LTD₄. CONCLUSION: LTD₄ stimulates proliferation of cultured human ASMC and may play a role in airway remodeling of asthma.  相似文献   

Effects of glucose and Mg²⁺ in the neurons damaged by glutamate     

XING Hong  HE Qi-hua  YUAN Lan  XU Jia-ling  WU Ben-jie 《园艺学报》2000,16(6):508-511

AIM and METHODS: To observe the effects of glucose-free and Mg²⁺-free in the extracellular fluid on the changes of [Ca ²⁺]_i in the cerebro-cortical neurons damaged by 1mmol/L glutamate using laser confocal scanning microscope. RESULTS: Both frequency and amplitude of neuronal calcium oscillation induced by glutamate were lowered in glucose-free and Mg²⁺-free buffers. The basic [Ca²⁺]_i concentration was lowered in the former case , but it was elevated in the latter case. CONCLUSION: Mg²⁺-free aggravates [Ca²⁺]_i overload induced by 1mmol/L glutamate ,under certain conditions the glucose-free might resist damage role of glutamate and Mg²⁺-free.  相似文献   

Role and regulation of calcineurin in angiotensin Ⅱ-stimulated cardiac myocyte hypertrophy of rats     

FU Min-gui  CHEN Ya-hong  LI Shu-lian  XU Song  PANG Yong-zheng  LIU Nai-kui  TANG Chao-shu 《园艺学报》2000,16(7):588-591

AIM: To study the role and regulation of calcineurin(CaN) in angiotensin II(AngⅡ)-stimulated cardiacmyocyte hypertrophy of rats. METHODS: Using AngⅡ to induce the cultured cardiac myocyte hypertrophy of rats, and investigating the effect of CaN inhibitor on [³H]-leucine incorporation of AngⅡ-stimulated cardiomyocytes and the regulation of various factors on CaN activity in cardiomyocytes.RESULTS: AngⅡ can stimulate the CaN activity in cultured neonatal rat cardiomyocytes in a dose- and time-dependent manner. In cardiac myocytes incubated with 10, 100, 1000 nmol·L^-1 of AngⅡ for 12h, the CaN activities increased respectively by 13%,57%(P＜0.05) and 228%(P＜0.01) compared with that in non-stimulated cardiomyocytes. The CaN activities in AngⅡ-stimulated cardiomyocytes were significantly inhibited by losartan(50 μmol·L^-1), H₇(50 μmol·L^-1)and Fura-2/AM(4 μmol·L^-1),while no effect was observed with PD98059(50 μmol·L^-1).The [³H]-leucine incorporation in AngⅡ-stimulated cardiomyocytes increased by 46%(P＜0.01) compared with that in control group, which was dramatically inhibited by cyclosporin A(0.5~5μg/mL). CONCLUSIONS: Calcineurin, a Ca²⁺/calmodulin-dependent protein phosphatase, may play an important role in AngⅡ-induced cardiac myocyte hypertrophy. The activation of CaN may dependent on the sustained increases of [Ca²⁺]i and be regulated by some protein kinases (such as PKC,etc.).  相似文献   

Protective effect of C1q/tumor necrosis factor-related protein 3 on vascular endothelium in rats with hyperuricemia     

LIN Xue  ZHANG Jun-xia  XU Jin-xiu  TANG Feng  TAN Lu-pin 《园艺学报》2000,36(9):1551-1556

AIM To study whether C1q/tumor necrosis factor （TNF）-related protein 3 （CTRP3）protect vascular endothelium in rats with hyperuricemia and its potential mechanisms. METHODS An animal model of hyperuricemia was established by using male SD rats drinking 10% fructose water （n=10）. The rats drinking normal water served as normal controls （n=10）. After 12 weeks, the rats were given a single injection with Ad-CTRP3 or Ad-GFP. The experiment was ended at 14th day after transfection.The serum levels of uric acid and nitric oxide （NO） were evaluated. The serum contents of TNF-α and interleukin-6 （IL-6） were measured by ELISA. HE staining and TUNEL assay were used to assess the morphological changes of intima and apoptosis of endothelial cells in thoracic aorta, respectively. The mRNA levels of endothelial nitric oxide synthase （eNOS）, TNF-α and IL-6 were detected by RT-qPCR. The protein levels of CTRP3 and Toll-like receptor 4 （TLR4） were determined by Western blot. RESULTS Compared with normal control group, the rats with hyperuricemia showed lower CTRP3 and higher TLR4 protein levels in the thoracic aorta （P<0.05）. Hyperuricemic rats had higher serum contents of uric acid, TNF-α and IL-6 （P<0.05）. Also, the intima structure disturbance of thoracic aorta, increased apoptotic rate, higher mRNA levels of TNF-α and IL-6 as well as lower mRNA levels of eNOS were observed （P<0.05）. By contrast, CTRP3 over-expression decreased TLR4 protein levels, reduced inflammatory cytokines, and obviously improved the morphology and function of thoracic aorta in the rats with hyperuricemia. CONCLUSION CTRP3 protect vascular endothelium in rats with hyperuricemia maybe via down-regulation of TLR4- mediated inflammatory signaling pathway.  相似文献   

Activation of repair pathways after neuronal DNA damage induced by bupivacaine     

LUO Jia-ming  LI Ji  XU Shi-yuan  ZHAO Wei 《园艺学报》2000,36(9):1667-1672

AIM To investigate the activation of related repair pathways after bupivacaine-induced neuronal DNA damage by cDNA gene screening. METHODS The bupivacaine-induced SH-SY5Y neuronal damage and DNA damage model was established. The technique of cDNA microplate array was used to screen the 21 important regulatory factors in the DNA damage repair pathway. Post-analysis of these differentially expressed repair genes for the repair pathway enrichment and distribution was performed. The data were analyzed by GraphPad Prism 6 statistical software to compare differences between groups. RESULTS The viability of SH-SY5Y cells treated with bupivacaine at different concentrations （detected by CCK-8 assay） showed that the IC₅₀ value of bupivacaine was 1.5 mmol/L. The comet assay related index （the comet tail） was increased （P<0.05）, the phosphorylation level of γH2AX protein was increased （P<0.05）, indicating that DNA damage in the SH-SY5Y cells was significantly aggravated after bupivacaine treatment. The results of cDNA microplate assay showed that compared withcontrol group, the differentially expressed genes after bupivacaine treatment were DNA-PKcs, PTEN, NTH1, RAD9, CSB, GADD45, XPD, XPC-HR23B and P53. The analysis showed that these repair genes were mainly concentrated in the following 3 repair mechanisms： base excision repair, nucleotide excision repair, and non-homologous reconstitution. CONCLUSION The repair genes differentially expressed after neuronal DNA damage caused by local anesthetics are mainly concentrated in the pathways of non-homologous end-joining, base excision repair and nucleotide excision repair.  相似文献