油梨嫁接苗分级标准探讨

通过逐步聚类分析方法，初步探讨了油梨嫁接苗的分级标准。分析得出以苗高和茎粗为油梨嫁接苗的分级质量指标，将油梨嫁接苗分为三级，即Ⅰ级苗：苗高≥74cm，茎粗≥1.13cm；Ⅱ级苗：74cm＞苗高≥66 cm，1.13cm＞茎粗≥0.93cm；Ⅲ级苗：苗高＜66cm，茎粗＜0.93cm。     

云南省德宏州发现3种草地贪夜蛾幼虫寄生蜂

重大迁飞性害虫草地贪夜蛾Spodoptera frugiperda(J.E.Smith)自2019年1月入侵我国以来,已对我国粮食安全构成重大威胁。为加速对我国草地贪夜蛾寄生性天敌资源的发掘与防治潜能的评估,我们于2019年9月-11月对云南省德宏州玉米和小麦上草地贪夜蛾的寄生性天敌开展田间调查并对采集到的天敌进行分子鉴定。共发现3种草地贪夜蛾幼虫寄生蜂,分别为斯氏侧沟茧蜂Microplitis similis Lyle、半闭弯尾姬蜂Diadegma semiclausum Hellen和斜纹夜蛾长距姬小蜂Euplectrus laphygmae Ferrière,田间最高自然寄生率分别为12.00%、22.30%和5.33%。另外,田间调查发现在玉米和大豆上斯氏侧沟茧蜂还可寄生与草地贪夜蛾同属的斜纹夜蛾S.litura幼虫;在大豆和杂草上斜纹夜蛾长距姬小蜂可寄生甜菜夜蛾S.exigua幼虫。本研究将为今后开展草地贪夜蛾天敌昆虫的保护和利用提供重要参考。     

甜樱桃花芽不同发育时期内参基因的筛选与验证

为了筛选甜樱桃花芽不同发育时期均稳定表达的内参基因,以甜樱桃桑提娜和黔樱一号不同发育时期花芽为材料,通过qRT-PCR技术检测28S rRNA、EF1-a1、EF1-a2、UBC、RPL13、18S rRNA、RSP3、CYP40、ACT2和α-TUB3等10个常用看家基因的表达水平,并利用GeNorm、NormFinder和BestKeeper综合评价其表达稳定性。结果表明,EF-1a2和RSP3在所有样品中稳定性最好。分别以EF-1a2、RSP3及EF-1a2+RSP3作为内参基因检测不同发育时期花芽生长素运输载体AUX1基因及生长素响应因子ARF基因的表达模式,该2个基因在不同内参基因标定下表达模式相同。表明EF-1a2、RSP3及EF-1a2+RSP3可作为甜樱桃花芽不同发育时期的内参基因。     

优化施肥下长江流域冬小麦产量及肥料增产效应

【目的】针对长江流域冬小麦不合理施肥带来的肥料利用率低的现状,探讨冬小麦产量分布特征及施用氮、磷和钾肥料的增产效应,为长江流域冬小麦肥料减施增效和优化养分管理措施提供依据。【方法】本文数据来源于国际植物营养研究所（IPNI）于2000—2018年在我国长江流域开展的田间试验,以及在中国知网（CNKI）数据库通过检索字段或字段组合（冬小麦、冬小麦+产量及冬小麦产量+肥料利用率等）得到的此期间关于长江流域冬小麦田间试验的论文,共1 732个田间试验。试验处理包括：优化施肥处理,农民习惯施肥,以及在优化施肥和农民习惯施肥基础上的不施氮肥、不施磷肥和不施钾肥处理,以探究长江流域各省（市）（四川、云南、贵州、重庆、湖北、安徽、江苏、浙江和上海）冬小麦在优化施肥下的可获得产量、产量反应、相对产量、农学效率和偏生产力特征。【结果】我国长江流域冬小麦优化施肥处理下的平均产量为6.6 t·hm^-2,其中安徽省平均产量水平最高,为7.3 t·hm^-2,重庆市最低,为3.6 t·hm^-2。施用氮、磷和钾肥的平均产量反应分别为2.3、0.9和0.6 t·hm^-2,但变异范围较大。氮、磷和钾肥平均相对产量分别为0.6、0.8和0.9,氮是小麦产量的主要限制因子。优化施肥处理的氮、磷和钾肥的平均农学效率分别为12.6、11.6和7.7 kg·kg^-1,平均偏生产力分别为34.0、78.9和73.4 kg·kg^-1。与农民习惯施肥措施相比,优化施肥处理平均增产0.5 t·hm^-2,增幅为8.8%;氮、磷、钾肥的农学效率分别提高了41.1%、121.1%和84.6%;偏生产力分别提高了42.4%、23.5%和25.4%。【结论】优化施肥有效提高了长江流域冬小麦的产量和养分利用率,但各省（市）间存在一定差异且省（市）内变异较大。四川、云南、湖北和江苏省的部分地区具有较低的产量反应,说明具有较高的土壤养分供应,应因地制宜地制定养分优化管理方案。分析长江流域优化养分管理措施下的小麦产量反应和肥料利用率等参数,可以确定氮为小麦产量的第一限制因子。     

添加槐花粉对白三叶青贮发酵品质的影响

采用单因子随机设计，研究添加不同比例的槐(Sophora japonica)花粉对白三叶 (Trifolium repens)青贮发酵品质的影响，以期为槐花应用于青贮饲料生产提供科学依据。分别设置白三叶单独青贮(C)、95%白三叶 + 5%槐花粉青贮(T1)、90%白三叶 + 10%槐花粉青贮(T2)、85%白三叶 + 15%槐花粉青贮(T3)、80%白三叶 + 20%槐花粉青贮(T4)共5个处理。结果表明，白三叶单独青贮品质较差，添加槐花粉提高了青贮原料的干物质、水溶性碳水化合物含量和发酵系数，降低了缓冲能值，使得青贮后的感官评分、乳酸、乳酸 ? 乙酸、干物质、水溶性碳水化合物、粗蛋白质含量显著提高(P ≤ 0.05)，pH、氨氮 ? 总氮、乙酸、丁酸含量显著降低(P ≤ 0.05)。综合考虑，80%白三叶 + 20%槐花粉青贮能获得良好的青贮品质。     

Reversing effect of naringin on cisplatin resistance in human lung cancer A549/DDP cells

AIM: To investigate the effect of naringin (NRG) on cisplatin (DDP) resistance in human lung cancer A549/DDP cells and its possible mechanism. METHODS: A549/DDP cells were cultured in vitro and treated with NRG and/or DDP at different concentrations for 24 h, and then the cell viability were measured by CCK-8 assay. The combination index (CI) of NRG and DDP were analyzed by Chou-Talalay method. The apoptosis rate was analyzed by flow cytometry. Western blot was performed to detect the protein levels of P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1), p-Akt, CXC chemokine receptor 4 (CXCR4), cleaved caspase-3, Bcl-2 and Bax.RESULTS: The protein levels of P-gp, MRP1, p-Akt and CXCR4 in the A549/DDP cells were higher than those in the A549 cells (P<0.05). The cell viability was remarkably reduced in a dose-dependent manner when A549/DDP cells were exposed to NRG and/or DDP (P<0.05), and the IC₅₀ values of NRG and DDP were 36.92 μmol/L and 129.77 μmol/L, respectively. When the inhibition rate exceeded 15%, NRG in combination with DDP produced a synergistic effect (CI<1). Combination treatment with NRG and DDP significantly induced apoptosis (P<0.05), up-regulated the protein levels of cleaved caspase-3 and Bax, and down-regulated the protein level of Bcl-2 (P<0.05). Meanwhile, NRG remarkably down-regulated the protein levels of P-gp, MRP1, p-Akt and CXCR4 in a dose-dependent manner (P<0.05). CONCLUSION: NRG may enhance the sensibility of A549/DDP cells to DDP most likely via up-regulating the protein level of Bax and down-regulating the protein levels of Bcl-2, P-gp, MRP1, p-Akt and CXCR4.     

沙柳多元醇液化产物流变性能的研究

沙柳木粉在液化剂和催化剂的作用下制成的液化产物可生产制作聚氨酯、环氧树脂、胶黏剂等。研究沙柳液化产物的流变性能,可探索宏观流变性质与液体微观内部反应机理之间的关系,优化设备结构和加工工艺条件,对其高效利用有着重大意义。本试验将沙柳木粉在浓硫酸催化条件下进行多元醇液化,通过改变液化处理条件(反应时间、反应温度和催化剂用量)制备具有不同流变性能的沙柳液化产物。利用旋转型流变仪对所制备的沙柳液化产物进行流变性能测试和分析。沙柳木粉液化条件的单因素试验和正交试验分析结果表明:影响沙柳液化产物黏度的主要因素是反应时间,其次是反应温度和催化剂用量,最佳工艺条件为反应时间70 min、反应温度170℃、催化剂用量5%。在最佳工艺条件下,剪切速率为78.87 s-1时,黏度为0.26 Pa·s。红外光谱(FT-IR)分析得出,液化物中纤维素被大量降解,半纤维素和木质素部分降解,羟基增加,生成更多的反应活性官能团,此条件下液化反应更加充分,流体黏度较大。流变性能测试结果显示:稳态扫描测试时,黏度随剪切速率的增加逐渐减小,表现出剪切变稀的现象;剪切应力随着剪切速率的增加逐渐升高,表现出假塑性流体的性质。通过动态频率扫描曲线变化规律分析,储能模量和损耗模量随着角频率的升高而逐渐增加,复数黏度却随之减小。     

Role of PERK pathway in morphine-induced myocardial protection of H9c2 cells

AIM: To explore whether morphine protects oxidative stress-damaged myocardial cells by inhibiting the PERK pathway to reduce endoplasmic reticulum stress and prevent mitochondrial permeability transition pore (mPTP) opening. METHODS: Rat myocardial H9c2 cells were cultured to establish an oxidative stress model, and then randomly divided into control group, H₂O₂ group, H₂O₂+morphine group, H₂O₂+morphine+PERK pathway inhibitor GSK2656157 group, morphine group and GSK2656157 group. Immunohistochemical method was used to detect the effects of morphine on expression of glucose-regulated protein (GRP) 78 and GRP94 induced by oxidative stress. The protein levels of PERK signaling pathway-related molecules were determined by Western blot. Confocal microscopy was used to observe the effects of morphine on mPTP opening and endoplasmic reticulum induced by oxidative stress. Cellular toxicity was detected by lactate dehydrogenase (LDH) kit and cell viability was measured by MTT assay. RESULTS: Compared with control group, GRP78 and GRP94 proteins in H₂O₂ group were strongly expressed, and the brown-yellow particles were significantly increased, but morphine significantly inhibited this process. Compared with control group, the phosphorylation of PERK was significantly reduced with GSK2656157 treatment at different concentrations, among which 2 μmol/L had the most significant effect (P < 0.05). Oxidative stress significantly increased the protein levels of GRP78, GRP94, p-PERK and CHOP, but significantly decreased p-GSK-3β level. These changes were inhibited by morphine, and the effects of morphine were further enhanced by GSK2656157 (P < 0.05). Compared with control group, oxidative stress significantly reduced the fluorescence intensity of mitochondrial TMRE and ER-Tracker Red. Morphine significantly inhibited this effect even when mitochondrial membrane potential was reduced, mPTP was open, and endoplasmic reticulum was damaged, while GSK2656157 further enhanced the effect of morphine (P < 0.05). Compared with control group, H₂O₂ significantly increased cellular toxicity and decreased the cell viability. Morphine inhibited this effect and GSK2656157 significantly enhanced the effect of morphine (P < 0.05). CONCLUSION: Morphine protects cardiac H9c2 cells under oxidative condition by inhibiting endoplasmic reticulum stress through PERK pathway and preventing the mPTP opening via GSK-3β inactivation.     

Sulodexide protects against hyperglycemia-induced retinal vascular injury via suppressing NOX4/NLRP3 pathway

AIM To investigate the effect of sulodexide (SDX) on high glucose-induced damage in retinal microvascular endothelial cells. METHODS (1) High-fat diet combined with intraperitoneal injection of streptozocin were used to induce type 2 diabetes mellitus (DM) followed by injection of saline or SDX in C57BL/6J male mice. Retinal microvascular leakage and density, and the protein levels of NLRP3 inflammasome-related proteins, zonula occludens-1 (ZO-1) and NADPH oxidase 4 (NOX4) were measured. (2) Human retinal microvascular endothelial cells (HRMECs) were treated with normal glucose or high glucose with or without SDX, and were further transfected with siRNA to knock down NOX4, or infected by adenovirus to over-express NOX4. The protein levels of ZO-1, VE-cadherin (VE-Cad), NOX4 and NLRP3 inflammasome-related proteins as well as the level of reactive oxygen species (ROS) were detected. RESULTS Treatment with SDX increased the protein level of ZO-1, attenuated retinal leakage and NLRP3 inflammasome activation, and enhanced the density of microvasculature and the number of ganglion cells in diabetic retinas. The protein levels of ZO-1 and VE-Cad were decreased, while the levels of NOX4, NLRP3 inflammasome-related proteins and ROS generation were increased in high glucose-treated HRMECs. Silencing of NOX4 inhibited high glucose-induced increases in NLRP3 inflammasome and ROS generation, and decreases in the protein levels of ZO-1 and VE-Cad. Over-expression of NOX4 significantly increased the levels of NLRP3 inflammasome-related proteins and ROS generation in HRMECs, and reduced the protein levels of ZO-1 and VE-Cad. Treatment with SDX partly reversed NOX4 over-expression-induced changes. CONCLUSION SDX alleviates hyperglycemia-induced retinal microvascular endothelial injury via inhibiting NOX4/ROS/NLRP3 pathways.     

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.