稀土壳聚糖螯合盐对水产颗粒饲料性能的影响

研究了在饲料中添加稀土壳聚糖螯合盐（ＲＥＣＣ）对水产颗粒饲料性能的影响。根据鲫（Ｃａｒａｓｓｉｕｓａｕｒａｔｕｓ）鱼苗的营养需求配制４种类型的ＲＥＣＣ试验日粮,即１号饲料（０．００％）、２号饲料（０．０８％）、３号饲料（０．１６％）和４号饲料（０２４％）。测定４种饲料的粉化率和溶失率。结果显示,添加稀土壳聚糖螯合盐后可以降低饲料的 粉化率,饲料中添加０．１６％的稀土壳聚糖螯合盐效果尤其明显（Ｐ＜０．０１）;在饲料中添加ＲＥＣＣ可以显著降低饲料的溶失率（Ｐ＜０．０５）,并可以提高和改善水产颗粒饲料的性能。     

MicroRNA-142-3p modulates atherosclerosis-associated endothelial cell apoptosis via targeting Rictor

AIM To investigate the role of microRNA-142-3p （miR-142-3p） in endothelial cell apoptosis during atherosclerosis （AS） and the underlying mechanism. METHODS Human aortic endothelial cells （HAECs） were treated with oxidized low-density lipoprotein （ox-LDL）. The expression level of miR-142-3p was detected by RT-qPCR. Apoptosis was determined via flow cytometry （FCM） and caspase-3 activity assay. Prediction of the binding site between miR-142-3p and 3’-UTR of Rictor mRNA was performed by bioinformatics analysis and confirmed by dual-luciferase reporter assay. RESULTS The expression of miR-142-3p was substantially up-regulated during the ox-LDL-elicited apoptosis in HAECs （P<0.05,P<0.01）. Forced expression of miR-142-3p exacerbated apoptosis in HAECs whereas inhibition of miR-142-3p partly alleviated apoptotic cell death mediated by ox-LDL. Further analysis identified Rictor as a direct target gene of miR-142-3p, and Rictor knock-down abolished the anti-apoptotic effect of miR-142-3p inhibitor. Moreover, the Akt/endothelial nitric oxide synthase （eNOS） signaling pathway was found to mediate the beneficial effect of miR-142-3p inhibitor on endothelial cells apoptosis. CONCLUSION Down-regulation of miR-142-3p inhibits endothelial cell apoptosis and atherosclerotic development by up-regulating the expression of Rictor and activating the Akt/eNOS signaling pathway.     

Effect of lncRNA FEZF1-AS1 on viability and apoptosis of LPS-induced vascular endothelial cells by regulating miR-363-3p expression

AIM To investigate the mechanism of long noncoding RNA （lncRNA） FEZF1-AS1 regulating microRNA-363-3p （miR-363-3p） on the viability and apoptosis of lipopolysaocharide （LPS）-induced vascular endothelial cells. METHODS Human umbilical vein endothelial cells （HUVECs） were cultured in vitro. pcDNA-NC, pcDNA-FEZF1-AS1, anti-miR-NC, anti-miR-363-3p, miR-NC and miR-363-3p mimics were transfected into the HUVECs and LPS stimulation was applied for 24 h. RT-qPCR was used to detect the expression of FEZF1-AS1 and miR-363-3p. The cell viability was measured by MTT assay. The apoptotic rate was analyzed by flow cytometry. The dual-luciferase reporter experiment was used to verify the targeted regulation of FEZF1-AS1 and miR-363-3p. Western blot was used to determined the expression of cyclin D1, Ki67 and cleaved caspase-3. RESULTS Compared with control group, the expression level of FEZF1-AS1 in LPS group was significantly reduced （P<0.05）, and the expression level of miR-363-3p was significantly increased （P<0.05）. Compared with pcDNA-NC+LPS group, the cell viability in pcDNA-FEZF1-AS1+LPS group was significantly increased （P<0.05）, the apoptotic rate was significantly reduced （P<0.05）, the protein levels of cyclin D1 and Ki67 were significantly increased （P<0.05）, and the protein level of cleaved caspase-3 was significantly reduced （P<0.05）. Compared with anti-miR-NC+LPS group, the cell viability in anti-miR-363-3p+LPS group was significantly increased （P<0.05）, the apoptotic rate was significantly reduced （P<0.05）, the protein levels of cyclin D1 and Ki67 were significantly increased （P<0.05）, and the protein level of cleaved caspase-3 was significantly reduced （P<0.05）. Dual-luciferase reporter experiment confirmed that FEZF1-AS1 targeted miR-363-3p. Compared with miR-NC+pcDNA-FEZF1-AS1+LPS group, the cell viability in miR-363-3p+pcDNA-FEZF1-AS1+LPS group was significantly reduced （P<0.05）, the apoptotic rate was significantly increased （P<0.05）, the protein levels of cyclin D1 and Ki67 were significantly reduced （P<0.05）, and the protein level of cleaved caspase-3 was significantly increased （P<0.05）. CONCLUSION Over-expression of FEZF1-AS1 promotes the viability and inhibits apoptosis of LPS induced vascular endothelial cells by inhibiting the expression of miR-363-3p.     

小麦TaNIP4-1基因的克隆及生物信息学分析

水通道蛋白不仅控制着水分和一些小分子溶质的跨膜运输,也是植物体应对非生物胁迫的重要组成部分。为了进一步研究小麦水通道蛋白的功能,本研究以NCBI和Ensemble Plant数据库中查找出的已报道的小麦水通道蛋白基因序列为模板,针对其保守区设计了19对引物,应用PCR的方法从5个小麦品种中克隆出19个基因片段。通过比对鉴定到一个此前未曾报道的新基因,并对其进行生物信息学分析,将其命名为TaNIP4-1。理化特性分析表明,该基因位于3A染色体短臂,基因全长1 315bp,CDS序列长度864bp,含有3个外显子和2个内含子,编码含有288个氨基酸的多肽,含有保守的沙漏模型,有6个跨膜区和2个保守的NPA基序。亚细胞定位预测结果表明该基因位于质膜上。该基因启动子序列含有与逆境响应相关的顺式调控元件,而对7日龄的麦苗进行干旱和盐胁迫处理后,其qRT-PCR结果显示,干旱和盐处理5h后,TaNIP4-1基因在小麦叶片中的表达量明显上调;盐处理7d后,TaNIP4-1基因在小麦根部的表达量显著上调。由此可见,TaNIP4-1基因参与了小麦应对逆境的过程。     

Inhibition study of red rice polyphenols on pancreatic α-amylase activity by kinetic analysis and molecular docking

This study sought to investigate the possible inhibition mechanism of red rice polyphenols (RRP) on pancreatic α-amylase (PA) activity. RRP showed strong inhibition against PA activity and the half-inhibitory concentration (IC₅₀) value was 3.61 μg/mL. The fluorescence quenching of PA by RRP was a combination of static quenching and dynamic quenching. RRP could aggregate with PA and the physiochemical properties of the aggregates were closely related to the concentration of RRP. Kinetic analysis suggested that the inhibition mode of RRP on PA was reversible inhibition, which was a mixing of competitive inhibition and noncompetitive inhibition. Molecular docking speculated that RRP could form hydrogen bonds with PA by binding to the catalytic active sites (ASP197, GLU233 and ASP300) and the microenvironments of TRP58 and TRP59 were altered, thus inhibiting PA activity.     

硼对平邑甜茶幼苗硝态氮吸收、利用及分配特性的影响

以平邑甜茶幼苗为试材,运用~(15)N同位素示踪和非损伤微测技术,研究了不同供硼(硼酸0、1.0、2.0、3.0、4.0、5.0和6.0 mg·L~(-1))水平对平邑甜茶根系生长及氮素吸收、利用和分配特性的影响。结果表明,3.0 mg·L~(-1)硼酸处理的幼苗根系活力及根系形态指标显著高于其他处理,幼苗的全氮量及~(15)N吸收量增幅最大,分别比对照提高了19.4%和75.0%。随供硼水平的增加,植株氮素利用率呈现先增高后降低的趋势,在3.0 mg·L~(-1)硼酸处理时最大,为14.8%,是对照的1.8倍。施硼处理对幼苗的~(15)N分配率有一定的影响,3.0 mg·L~(-1)硼酸处理的根系~(15)N分配率达到最大,且显著高于对照。非损伤微测结果显示,3.0 mg·L~(-1)硼酸处理时,平邑甜茶根系对NO_3~-有强烈吸收且内流速度达到最大,在缺硼和高硼(硼酸0和6.0 mg·L~(-1))处理时有明显外排趋势。因此,3.0 mg·L~(-1)硼酸处理最有利于平邑甜茶根系的生长、根系活力的提高和氮素的吸收利用,而低硼和过量供硼均会抑制根系生长及氮素的吸收利用。     

散叶莴苣灰霉病药剂筛选试验

为筛选出散叶莴苣灰霉病防治药剂,本文进行了10%多抗霉素可湿性粉剂、45%异菌腺悬浮剂、20%丁子香酚水乳剂、50%啜酰菌胺水分散粒剂不同浓度对散叶莴苣的田间药效试验。结果表明,于莴苣灰霉病发生初期连续防治2次,药后7、14d45%异菌腺悬浮剂、50%喘酰菌胺水分散粒剂效果表现优越,最终病指防效均达80%以上,且对莴苣生长安全,无残留。     

miR-140-3p inhibits viability,invasion and migration of non-small-cell lung cancer A549 cells by targeting PD-L1

AIM: To explore the target relationship between microRNA-140-3p (miR-140-3p) and programmed cell death ligand 1 (PD-L1) and their effect on the viability, migration and invasion of non-small-cell lung cancer A549 cells.METHODS: RT-qPCR was used to detect the miR-140-3p expression in HLF-1, A549 and H1299 cells, and then the A549 cells with the most significant difference were selected as the subsequent research object. TargetScan software and dual-luciferase reporter assay were performed to predict and confirm the target relationship between miR-140-3p and PD-L1. RT-qPCR and Western blot were used to determine the effects of miR-140-3p mimic and inhibitor on PD-L1 expression level. MTT assay was used to detect the viability of A549 cells. Transwell assay was performed to detect the migration and invasion abilities of the A549 cells.RESULTS: miR-140-3p was significantly down-regulated in the A549 cells and H1299 cells (P<0.05). Transfection with miR-140-3p mimic decreased the expression of PD-L1 and inhibited the viability, migration and invasion of the A549 cells. Transfection with pcDNA3.0-PD-L1 reversed the inhibitory effect of miR-140-3p on the viability, migration and invasion of the A549 cells.CONCLUSION: miR-140-3p inhibits the viability, migration and invasion of A549 cells by targeting PD-L1.     

闽引圆叶决明辐射变异后代新品系(86134-32-3)的若干特性

从60Coγ射线辐射闽引圆叶决明86134牧草种子种植后代中筛选出性状稳定的优良变异后代新品系86134-32-3。M4代田间小区品比试验表明,与原品种86134相比,新品系植株叶子生长数、干物质含量、粗脂肪含量、氨基酸总量和单位产量都有大幅度的提高,达到显著或极显著水平;其植株茎叶比大幅度下降。新品系植株的其余营养成分、包括生殖生长期在内的农艺性状均保持原品种特性。     

欧盟27国小水电的发展对我国的战略思考

详细介绍和分析了欧盟27国发展小水电的现状和战略规划、欧盟可再生能源和分布式能源的结构比例,以及欧洲小水电协会系统推进小水电发展所起的作用.根据国家水利部颁发的《＂十二五＂全国水电新农村电气化规划》,介绍和分析了我国小水电的发展现状和战略规划;对我国发展小型和微型水电中存在的突出问题进行了详细的分析,例如：小水电的权责不清晰;小水电站数量多和管理难;小水电开发产业的延续性差和未来趋势不清晰;小水电设备的制造企业面临的问题,例如技术水平低、技术储备不足、科研投入少和科研能力差、管理程度浅等;小水电站年利用小时数偏低和径流式电站的问题.提出了5点建议：明晰小水电的权责关系,规范小水电的开发和经营;建立小流域发展综合管理委员会,采取＂电站群＂的管理方式;把握我国和国际市场的小水电发展趋势,把小水电产业做大做强并保持可持续发展;提出了从＂一个科研中心、两个方向＂出发,提升小水电设备制造企业技术水平低的思路;提高小水电站年满发小时数即设备的利用率,增加小水电的发电效益.