中国杧果科学研究70年

新中国成立70年来,我国杧果科学研究在人才培养与团队建设、硬件平台、基础理论创新与技术研发等方面均取得了重要进展,有力支撑了我国杧果产业的创建和可持续发展。本文在概述世界和我国杧果地位、分布、规模的基础上,从科学研究发展历程、种质资源与遗传育种、土壤与肥水管理、耕作模式与花果管理、病虫害防控、采后贮运保鲜、产业经济等方面全面梳理了我国杧果研究取得的成就,分析了存在的不足并提出了未来的重点发展方向。     

黄蝉花素抑制斜纹夜蛾生长发育作用

室内测定了黄蝉花素对斜纹夜蛾幼虫的抑制生长发育活性。结果表明,黄蝉花素对斜纹夜蛾幼虫的抑制生长发育活性与其处理浓度具有一定的相关性。与对照相比,处理组食物消耗量减少,幼虫生长发育被抑制,发育历期延长。处理组幼虫在蛹期不能正常化蛹而形成畸形蛹,羽化后的成虫表现为形态畸形。在预蛹期和蛹期由于不能正常蜕皮导致死亡率较高。研究显示黄蝉花素作为一类新型的昆虫生长发育控制剂或害虫田间种群管理的先导化合物值得进一步研究。     

适宜机插的优质籼稻品种筛选及其评价指标体系

为了筛选适宜贵州稻区机插的优质籼稻品种，建立适宜机插优质籼稻品种的评价关键指标体系，以近年选育的34个优质籼稻品种为试验材料，在贵州省遵义市湄潭县进行机插试验，对各品种的秧苗素质以及机插条件下水稻分蘖生长、干物质积累、抗倒伏性、产量及其构成因素进行研究。结果表明，机插条件下34个优质籼稻的产量变幅为6.1~10.5 t·hm-2，结合两步聚类算法，以产量为依据将参试品种划分为适宜机插和不适宜机插两类。适宜机插优质籼稻类型主要表现为产量均高于8.25 t·hm-2，其成苗率高、秧苗均匀性好、幼苗健壮；分蘖早生快发，易形成充足的有效穗数；植株能获得较高的花前和花后干物质积累量，并重新分配到籽粒；茎秆粗壮，基部3个节间平均抗折力强，倒伏指数小。综合来看，F优498、晶两优534和蓉18优2348等15个优质籼稻品种适宜贵州地区机插，且适宜机插优质籼稻关键评价指标为：成苗率>85%，秧苗均匀性>1.5苗·cm-2；倒伏指数<150%，基部3个节间平均抗折力>1 500 g；产量>8.25 t·hm-2，有效穗数225×104～300×104 hm-2，每穗粒数>140粒，结实率>75%，成熟期干物质积累量>15 t·hm-2，收获指数>0.45。研究为机插专用优质籼稻品种选育及应用提供理论依据。     

旋转脱膜式残膜回收机的设计与试验

【目的】针对弹齿式残膜回收机残膜回收作业后自动脱膜困难的问题,设计一种旋转脱膜式残膜回收机具。【方法】采用田间试验确定了搂膜弹齿的最佳入土角范围、曲率半径和排布方式,通过理论研究设计残膜回收机的脱膜机构,用正交试验方法对残膜回收率的影响因素进行优化,以残膜回收率最高为优化目标确定最优参数组合,并对修正后的最优参数组合进行试验验证。【结果】综合田间试验数据,得出搂膜弹齿最佳入土角为18°～35°,主弹齿直径10 mm,副弹齿直径5 mm,3排搂膜弹齿交错排布;正交优化试验表明,各因素对残膜回收率影响的表现为作业深度作业速度搂膜弹齿曲率半径,当作业速度为7 km/h、主搂膜弹齿曲率半径190 mm、副搂膜弹齿曲率半径160 mm、作业深度50 mm时,对应的残膜回收率最高;验证试验表明,在该参数组合条件下残膜回收率为84.86%,与预测的残膜回收率(85.56%)十分接近。【结论】设计的旋转脱膜式残膜回收机收膜效果好、脱膜率高、制造成本低、调整使用便捷。     

Progress in relationship between epithelial sodium channel and related respiratory diseases

Epithelial sodium channel (ENaC) is an ion channel widely distributed in various tissues and organs of human. It is composed of 3 homologous subunits and allows the flow of sodium ion across epithelial cells, maintain?ing water-salt balance in the cells. Recent studies show that abnormal expression or dysfunction of ENaC in the respiratory system affects water-salt balance, fluid transportation and cell mobility, and causes abnormal changes of the airway surface liquid level and impaired clearance. ENaC is closely related to the development of respiratory diseases, such as cystic fibrosis, asthma and chronic obstructive pulmonary disease. This article reviews the progress in ENaC structure, function and roles in related respiratory diseases in order to provide a reference for the treatment of the diseases.     

Roles of protein phosphatase 4 in down-regulation of eNOS Ser633 phosphorylation induced by palmitic acid in human umbilical vein endotheli?al cells

AIMTo investigate the roles of protein phosphatase 4 (PP4) in down-regulation of endothelial nitric oxide synthase (eNOS) Ser633 phosphorylation induced by palmitic acid (PA). METHODSHuman umbilical vein endothelial cells (HUVECs) were treated with PA at 25 μmol/L, 50 μmol/L, 100 μmol/L and 200μmol/L for 36 h, or treated with PA at 100 μmol/L for 12 h, 24 h, 36 h and 48 h. Protein phosphatase 2A (PP2A) family inhibitor fostriecin (FST, 20 nmol/L) or okadaic acid (OA, 5 nmol/L) was selected to pretreat the HUVECs for 30 min. Protein phosphatase 4 catalytic subunit (PP4c) siRNA or protein phosphatase 2A catalytic subunit (PP2Ac) siRNA was transfected into the HUVECs. The protein expression levels of of eNOS, PP4c and PP2Ac, as well as the level of eNOS Ser633 phosphorylation, were detected by Western blot. The intracellular nitric oxide (NO) content was measured by DAF-FM DA. RESULTS(1) Compared with control group, the levels of eNOS Ser633 phosphorylation were decreased in PA groups in which the HUVECs were treated with 25 μmol/L, 50 μmol/L, 100 μmol/L and 200 μmol/L PA for 36 h (P<0.05) and 100 μmol/L PA for 24 h, 36 h and 48 h (P<0.05). No significant difference in the level of total eNOS protein expression among all the groups was observed. (2) Compared with control group, both FST and OA pretreatment reversed the reduction of eNOS Ser633 phosphorylation (P<0.05) and the decrease in intracellular NO content (P<0.05) induced by PA. No significant difference in the level of total eNOS protein expression among all the groups was observed. (3) Compared with si-Control group, the PP4c protein expression was significantly reduced (P<0.05), while the level of eNOS Ser633 phosphorylation was significantly increased in si-PP4c group (P<0.05). Although the levels of PP2Ac protein expression declined significantly (P<0.05), the level of eNOS Ser633 phosphorylation remained unchanged in si-PP2Ac group. No significant differencein the level of total eNOS protein expression among all the groups was found. CONCLUSION PA significantly reduces the level of eNOS Ser633 phosphorylation and the content of NO in the HUVECs, which may be due to PA inducing the activation of the PP2A family member PP4 rather than PP2A.     

Molecular mechanisms of Belinostat inhibiting viability of osteosarcoma cells

AIM: To observe the effect of histone deacetylase inhibitor (HDACi) Belinostat on the viability of osteosarcoma cells and to study the underlying mechanism. METHODS: Osteosarcoma cell lines SAOS-2 and U2OS were incubated with Belinostat at different concentrations in vitro. The viability of the cells was measured by MTT assay. The activity of caspase-3/-7 and the DNA fragmentation were detected by fluorescence probe and ELISA, respectively. Western blot was used to detect the levels of histone acetylation, expression of PTEN, caspase-3, Bcl-xL and Akt, and phosphorylation of glycogen synthetase kinase 3β (GSK-3β) and Akt. Finally, the cells were incubated with Belinostat and doxorubicin at different concentrations, and then the combination index (CI) was calculated by MTT. RESULTS: Belinostat at 0.5, 1, 2.5 and 5 μmol/L inhibited the viability of U2OS cells and SAOS-2 cells in a dose-dependent manner, induced DNA fragmentation, enhanced caspase-3/-7 activity, and promoted the activation of caspase-3. At the same time, in the SAOS-2 cells, the expression of Bcl-xL was reduced, and the acetylation of histones H3 and H4 was increased. The results of Western blot showed that phosphorylation levels of Akt and GSK-3β in U2OS cells and SAOS-2 cells were decreased significantly after treatment with Belinostat (P<0.05). MTT results showed that combination of Belinostat and doxorubicin further reduced the viability of U2OS and SAOS-2 cells (CI<1). CONCLUSION: Belinostat inhibits the viability of osteosarcoma cells treated with doxorubicin, and the mechanism may be related to the inhibition of Akt signaling pathway.