乡土物种补播对青藏高原高寒草甸群落稳定性的影响

为了探究高寒草甸天然草地补播乡土物种对草地群落稳定性的影响，本试验以垂穗披碱草（Elymus nutans）、异针茅（Stipa aliena）、中华羊茅（Festuca sinensis）、溚草（Koeleria cristata）、星星草（Puccinellia tenuiflora）、扁蓿豆（Melissitus rutenica）、冷地早熟禾（Poa crymophila）为试验材料，设置5种混播组合，于2017年在青海省贵南县天然草地上进行补播。试验采用方差比率法（Variance ratio，VR）、M.Godron贡献定率法（Contribution law）以及生物量稳定性分析方法，结果表明：5种组合补播后使得群落联结性降低、生物量稳定性增大，群落整体稳定性增强，正向着稳定方向发展；5种组合中，组合D （扁蓿豆+星星草+垂穗披碱草+异针茅+溚草）的生物量稳定性最大，是对草地恢复最有效的物种组合。本试验筛选出了对草地生态修复最有效的物种组合，为草地保护及利用提供了科学依据。     

小麦山农4143抗黑胚病遗传分析及抗性遗传位点检测

 黑胚病是小麦生产的重要籽粒病害,麦根腐平脐蠕孢(Bipolaris sorokiniana)是黑胚病的主要致病菌。为分析小麦抗黑胚病遗传规律并检测抗性位点,本研究以抗黑胚病小麦品系山农4143与感病品系宛原白1号的F₇代重组自交系(RIL)群体为材料,于2018~2019年在3个试验点种植,采用“孢子液喷洒、套袋保湿”的方法进行接菌鉴定,用“主基因＋多基因混合遗传模型”进行遗传分析,并挑选极端抗、感自交系构建混池、结合小麦660K SNP芯片进行混合分组分析(BSA)。研究结果显示小麦品系山农4143对黑胚病抗性符合“4对主基因加性-上位性遗传模型”,主基因遗传力为0.88~0.95;通过BSA检测到黑胚病抗性位点36个,分别位于1A、2B(6)、2D(2)、3A、3B(2)、3D、4A(6)、4D、5A(4)、5B(6)、5D(3)、7A、7B和7D共14条染色体上,A、B、D染色组上分别为13、 15和8个,36个位点中有18个为抗黑胚病新鉴定位点。本研究结果为小麦抗黑胚病位点的精细定位和抗性育种中分子标记的开发奠定了基础。     

大数据视角下的食用菌电商发展路径

鉴于目前食用菌电商在发展过程中面临着食用菌电商流程亟待完善、缺乏食用菌安全体系、缺乏食用菌电商人才以及缺乏知名食用菌品牌等困境,从食用菌生产销售主体角度,基于大数据视角出发,利用大数据优化食用菌电商流程,建设以大数据为支撑的食用菌安全体系,以大数据应用能力为导向培养食用菌电商人才,依托大数据建设知名食用菌品牌。     

深圳市道路绿化管养标准体系构建浅析

城市道路绿化在改善城市生态环境、提升市民生活质量方面有重要作用。在道路绿化中，管养工作是维持道路绿化活力的重要内容。通过考察研究深圳市以及其他省市的道路绿化管养标准体系，分析对比每个城市的道路绿化管养标准体系现状，指出了深圳市道路绿化管养标准体系具有建立较早、内容较为全面的优势，以及存在体系架构不健全、部分标准标龄过长、可量化执行标准较少等方面的不足。并从系统性、指导性、先进性角度提出优化建议，将深圳市道路绿化管养标准体系划分为基础标准和道路绿化管养通用标准两大部分，其中基础标准分为术语标准等4个大类，道路绿化管养通用标准划分为质量技术等14个类别。     

从星球化到在地性：基于克莱因四元群模型的风景园林思潮研究计划

随着人类观察世界的能力大幅提升,设计与研究的尺度得到了极大拓展,星球化(planetarization)与在地性(locality)同时成为空间设计学科重点关注的议题,近年来涌现出多个新思潮。基于克莱因四元群模型构建的风景园林思潮研究计划旨在建立一套理论框架以对不同研究实践进行更系统的讨论分析,为国内风景园林学科与行业带来新的思考,并运用新理论框架重点介绍了4个风景园林思潮,包括星球城市化背景下的风景园林理论、新地理视角中的空间叙事、关注本土议题的风景园林研究以及直觉导向的在地探索。     

紫薇新品种‘彩霞’

‘彩霞’是由紫薇自然杂交种子实生选育得到的新品种。小乔木，新叶紫红色，成熟叶灰绿色，小枝的翅波状，花芽圆锥形，花芽顶端突起明显，花为绛紫红色。     

亚精胺浸种对番茄种子萌发及幼苗高温抗性的影响

以番茄品种合作903为试验材料,设置0、0.1、0.2、0.4 mmol · L~(-1 )亚精胺(Spd)浸种10 h,研究不同浓度Spd浸种对番茄种子萌发、幼苗生长及高温抗性的影响。结果表明:不同浓度Spd浸种处理均能显著提高番茄种子的发芽指数和活力指数,幼苗地下部干质量和壮苗指数明显提高,其中0.2 mmol · L~(-1 )Spd浸种处理发芽最快,活力指数最高。Spd浸种处理降低了高温胁迫下番茄叶片的相对电解质渗透率、丙二醛(MDA)和H_2O_2含量,其中0.2 mmol · L~(-1 )Spd处理的相对电解质渗透率、MDA和H_2O_2含量最低;抗氧化酶(SOD、APX、DHAR)活性增加,并在0.2 mmol · L~(-1)时达到最大值。综上,0.2 mmol · L~(-1 )Spd浸种能有效促进番茄种子萌发和幼苗生长,提高番茄幼苗高温抗性。     

茭白胡麻叶斑病研究进展

综述了近年来在茭白胡麻叶斑病上的病害发生、病原菌鉴定及其生物学特性、发病规律和病害防治等方面的研究成果，论述了胡麻叶斑病的防治措施如选用抗病品种、农业防治、药剂防治、植物免疫诱导剂防治等的研究进展，总结了茭白胡麻叶斑病研究上存在的问题，并指出未来需要加强茭白胡麻叶斑病病原物种群多样性、致病力分化以及于病原菌的浸染机制及致病机理方面的研究；进一步收集、筛选与鉴定茭白抗病种质资源，培育优良的抗性品种；开展茭白胡麻叶斑病抗药性监测及抗性机理研究；筛选新型生态友好的化学农药和低毒、高效的生防菌剂。     

Captopril exerts myocardial protective effect in coronary microembolization rats by inhibiting oxidative stress injury and alleviating inflammatory response

AIM: To investigate the effects of captopril (CAP) on oxidative stress injury and inflammatory response induced by coronary microembolization (CME) and its related molecular mechanisms. METHODS: The rat model of CME was established by clamping the rat artery and injecting blood microemboli. The rats were divided into control group, CME group and CME+CAP group, with 6 rats in each group. The myocardial tissues of each group were collected. The changes of myocardial structure and the degree of inflammatory response were analyzed by HE staining. Cardiomyocyte apoptosis was detected by TUNEL staining. The fluorescence intensity of cleaved caspase-3 was detected by immunofluorescence obervation. The protein levels of cleaved caspase-3 and Bax were determined by Western blot. The activity of superoxide dismutase (SOD) and catalase was measured by ELISA. The production of reactive oxygen species (ROS) was detected by DHE fluorescence staining. RESULTS: CAP significantly reduced the myocardial structural changes (P<0.05), inflammatory cell infiltration (P<0.01), number of apoptotic cardiomyocytes (P<0.01), the protein levels of cleaved caspase-3 and Bax (P<0.01), and ROS production levels (P<0.01), but promoted the activity of antioxidant markers SOD and catalase (P<0.01) in the CME rats.CONCLUSION: CAP attenuates CME-induced myocardial injury by resisting oxidative stress and alleviating inflammatory response.     

Ethanol extract from Cortex Albiziae attenuates mouse acute liver injury induced by carbon tetrachloride via modulation of NF-κB pathway

AIM:To investigate the protective effect of ethanol extract from Cortex Albiziae on acute liver injury, and to explore its possible mechanism. METHODS:Acute liver injury in mice was induced by single intraperitoneal injection of 25% carbon tetrachloride (olive oil solubilization). The effective parts of ethanol extract from Cortex Albizziae against acute liver injury were screened. The pathological changes of the liver tissues were examined by pathological sections with HE staining. The activity of total superoxide dismutase (T-SOD) and the content of malondialdehyde (MDA) of the liver tissues were detected, the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were mea-sured by ELISA, and the protein expression levels of NF-κB p65, Bcl-2 and Bax in the liver cells of the mice in each group were determined by Western blot. RESULTS:Compared with model group, the serum levels of AST and ALT in low-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-L, 4 mg·kg^-1·d^-1) group and high-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-H, 8 mg·kg^-1·d^-1) group were significantly decreased. The necrosis extent and degree of the hepatocytes and infiltration of inflammatory cells were significantly lower than that in model group. Compared with model group, the serum levels of TNF-α and IL-6 in AB-H group and AB-L group were significantly decreased (P<0.05). The protein level of NF-κB p65 in the nuclei of mouse liver cells in AB-H group and AB-L group were also decreased significantly (P<0.05). Compared with model group, the protein expression of Bax was decreased, the protein expression of Bcl-2 was increased, and the Bcl-2/Bax ratio was increased in AB-L group and AB-H group. CONCLUSION:The n-butanol phase of ethanol extract from Cortex Albiziae may protect the liver by reducing the activation of NF-κB p65, inhibiting the excessive release of inflammatory cytokines IL-6 and TNF-α, and decreasing hepatocyte apoptosis via regulating Bcl-2 and Bax expression.