用于作物表型信息边缘计算采集的认知无线传感器网络分簇路由算法

随着无线终端数量的快速增长和多媒体图像等高带宽传输业务需求的增加，农业物联网相关领域可预见地会出现无线频谱资源紧缺问题。针对基于传统物联网的作物表型信息采集系统中存在由于节点密集部署导致数据传输过程容易出现频谱竞争、数据拥堵的现象以及固定电池的网络由于能耗不均衡引起监测周期缩减等诸多问题，本研究建立了一个认知无线传感器网络（CRSN）作物表型信息采集模型，并针对模型提出一种引入边缘计算机制的动态频谱和能耗均衡（DSEB）的事件驱动分簇路由算法。算法包括：（1）动态频谱感知分簇，采用层次聚类算法结合频谱感知获取的可用信道、节点间的距离、剩余能量和邻居节点度为相似度对被监控区域内的节点进行聚类分簇并选取簇头，构建分簇拓扑的过程对各分簇大小的均衡性引入奖励和惩罚因子，提升网络各分簇平均频谱利用率；（2）融入边缘计算的事件触发数据路由，根据构建的分簇拓扑结构，将待检测各区域变化异常表型信息触发事件以簇内汇聚和簇间中继交替迭代方式转发至汇聚节点，簇内汇聚包括直传和簇内中继，簇间中继包括主网关节点和次网关节点-主网关节点两种情况；（3）基于频谱变化和通信服务质量（QoS）的自适应重新分簇：基于主用户行为变化引起的可用信道改变，或分簇效果不佳对通信服务质量产生的干扰，触发CRSN进行自适应重新分簇。此外，本研究还提出了一种新的能耗均衡策略去能量消耗中心化（假设sink为中心），即在网关或簇头节点选取计算式中引入与节点到sink的距离成正比的权重系数。算法仿真结果表明，与采用K-medoid分簇和能量感知的事件驱动分簇(ERP)路由方案相比，在CRSN节点数为定值的前提下，基于DSEB的分簇路由算法在网络生存期与能效等方面均具有一定的改进；在主用户节点数为定值时，所提算法比其它两种算法具有更高频谱利用率。     

基于TRIZ理论的玉米果穗分配装置创新设计

研究了国内外玉米收获模式，分析了目前国内市场果穗类玉米收获机采用的果穗分配装置（在玉米收获机中，该装置被称为分配器）的结构特点，针对普遍存在的果穗分配不均，导致下一流程剥皮装置各剥皮通道负荷不等，造成的各组剥皮辊磨损程度不均衡，从而降低剥皮装置乃至整机可靠性等问题，采用TRIZ理论进行了创新设计，设计了一种新型果穗分配装置。      

4种杀菌剂防治草坪草夏季斑枯病研究

夏季斑枯病是危害冷季型草坪草的主要病害之一，严重影响草坪质量，目前我国仍未有登记药剂防治夏季斑枯病。本研究结合室内毒力测定及田间防效检验，分析比较了嘧菌酯、稻瘟灵、丙环唑和甲基硫菌灵4种杀菌剂对夏季斑枯病菌的抑制效果，评估了药剂的田间防病效果。结果表明，丙环唑对供试的夏季斑枯病菌3株靶标菌抑制效果最佳，EC50为0.09~0.16 μg/mL；嘧菌酯次之，EC50为0.14~0.28 μg/mL；稻瘟灵和甲基硫菌灵抑制效果再次之。4种杀菌剂对夏季斑枯病害均具有较好的防控效果；其中50%嘧菌酯水分散粒剂制剂用量800 g/hm2防控效果最佳，第4次药后17 d可达99.09%；25%丙环唑乳油制剂用量2 000 g/hm2防控效果次之，第4次药后17 d为93.14%。     

串番茄新品种红星302 的选育

红星302 是以抗病、耐低温弱光材料01-61 为母本，以01-23 为父本育成的串番茄一代杂种，无限生长类型，果实串收，果色亮红，果实椭圆形，酸甜适口，品质佳，VC 含量为364 mg · kg^-1，可滴定酸0.44%，可溶性糖4.25%，平均单果质量30.79 g，硬度为11.40×10⁵ Pa。单株结果数约为53个，产量4 900 kg ·（ 667 m²）^-1 左右，高抗蕨叶病毒病、青枯病，适宜河北地区冬季日光温室和早春保护地栽培。     

PGPR菌剂对辣椒的促生效应及根际土壤细菌的响应研究

研究田间条件下PGPR菌剂灌根对辣椒根际土壤细菌数量及群落结构的影响,为深入探究PGPR菌剂的田间促生机制提供理论依据。以4株PGPR菌株制成PGPR菌剂,对辣椒进行灌根,并采用Illumina-MiSeq平台对辣椒根际土壤细菌V3-V4区进行Paired-end测序,结合细菌及功能菌群数量、辣椒产量指标,比较分析菌剂灌根配施全量化肥(PGPR-CF1)、菌剂灌根配施80%化肥(PGPR-CF2)和全量化肥(CK)处理后对辣椒根际土壤细菌数量及群落结构特征的影响。结果表明:PGPR菌剂灌根后辣椒根际土壤细菌及包含固氮、解磷及解钾等功能菌群的数量显著提高,且物种丰度和多样性均高于对照,细菌优势度则表现为PGPR-CF1和CK组高于PGPR-CF2。所有土样共得到有效序列573 896条,在相似水平为97%下聚类分析得到OTUs数分别为2 153个(CK)、2 337个(PGPR-CF1)、2 358个(PGPR-CF2);各处理辣椒根际土壤中的优势门为酸杆菌门、放线菌门、拟杆菌门、绿弯菌门、浮霉菌门和变形菌门,相对丰度总占比分别为83.7%(PGPR-CF1)、79.55%(PGPR-CF2)和79.77%(CK)。PGPR菌剂灌根后增加了伯克霍尔德氏菌目、芽孢杆菌目、鞘脂单胞菌目等的相对丰度,降低了芽单胞菌目、酸杆菌目的相对丰度。Pearson指数表明,辣椒产量和单果重与根际土壤细菌多样性和丰度正相关。研究显示,PGPR菌剂处理,可以提高根际土壤细菌和功能菌群的数量,同时影响了物种多样性和群落结构,并促进了辣椒增产。     

基于问题导向的农业物料工程特性实验课教学探索

农业物料工程实验课程教学在农林类院校培养研究生科研、创新意识，以及提供农业物料基本工程数据等方面发挥着关键作用，传统实验教学大多为机械式照搬实验指导，重现数据，忽略了研究生的理论基础和主观能动性。该文提出在农业物料工程特性实验课程中以学生科研课题需求为导向，设置扫描电镜、原子力显微镜和红外光谱等实验内容，以农业物料的理化特性表征分析贯穿始终，最后通过撰写论文报告采用团队互评等形式可显著提升课程实效。      

水稻资源全生育期耐盐性鉴定筛选

对来自国内外不同地区的550份水稻资源进行全生育期耐盐性鉴定。设置淡水、0.3%和0.5%盐溶液浇灌3个处理,插秧10d后,通过浇灌不同体积的淡水与海水调至设计浓度对水稻进行不同浓度的盐胁迫处理。分别调查了淡水及0.3%盐处理下水稻株高、有效分蘖数、主穗长度、主穗结实率、单株产量、抽穗期6项农艺性状和0.5%盐处理下的水稻耐盐表型。与淡水浇灌相比,全生育期在0.3%盐溶液处理下,550份水稻(100%)株高显著降低;124份(22.55%)水稻有效分蘖数(90份增加, 34份减少)、414份(75.27%)水稻主穗长度(405份变短、9份增长)、145份(26.36%)水稻主穗结实率(84份减少, 61份增加)、375份(68.18%)水稻单株产量(343份减少, 32份增加)存在(极)显著差异;水稻资源的抽穗期无显著差异。主成分分析表明,主穗结实率、有效分蘖数及单株产量3项性状累计贡献77.25%的变异。根据产量耐盐系数筛选了121份耐盐水稻资源(产量耐盐系数≥0.8),在0.5%盐胁迫持续处理42 d后,筛选了78份耐盐水稻资源(耐盐表型为3级),其中25份水稻资源全生育期在0.3%盐处理下单株产量耐盐系数≥0.8,在0.5%盐胁迫持续处理42 d后的耐盐表型为3级。筛选的耐盐水稻资源为培育耐盐新品种及深入研究耐盐机制提供材料。     

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.     

ROCK promotes high glucose-induced cardiomyocyte apoptosis by inhi-biting PI3K/Akt signaling pathway

AIMTo investigate whether Rho-associated coiled-coil kinase (ROCK) is involved in high glucose-induced apoptosis of primary cardiomyocytes by regulating PI3K/Akt signaling pathway. METHODSPrimary Wistar rat cardiomyocytes were cultured and identified by α-sarcomeric actin (α-SCA) immunohistochemistry. Cardiomyocytes were treated with 5.5, 33 and 40 mmol/L glucose for 48 h. The cell viability was measured by MTT assay, and the mRNA expression of ROCK1 and ROCK2 in the cardiomyocytes was detected by RT-qPCR. Flow cytometry was used to analyze the apoptosis of the cardiomyocytes. The protein levels of ROCK1, ROCK2, cleaved caspase-3, Bcl-2, PI3K, Akt and p-Akt were determined by Western blot. In order to confirm the regulatory effect of ROCKs on PI3K/Akt signaling pathway, the cells were divided into control group (5.5 mmol/L glucose), high glucose group (33 mmol/L glucose) and high glucose+Y27632 (ROCK inhibitor) group. Western blot was used to detect the protein levels of ROCK1, ROCK2, PI3K, Akt and p-Akt. RESULTSAfter 48 h of high glucose exposure, the values of relative cell viability in 33 and 40 mmol/L glucose groups were (79.71±2.43)% and (68.41±7.49)%, respectively, both of which were significantly decreased compared with normal control group (P<0.05). After 48 h of high glucose exposure, the relative mRNA levels of ROCK1 and ROCK2 in 33 and 40 mmol/L glucose groups were significantly increased compared with normal control group (P<0.05). Compared with normal control group, the apoptotic rate in 33 and 40 mmol/L glucose groups was increased significantly (P<0.05). Compared with normal control group, the protein expression of ROCK1, ROCK2 and cleaved caspase-3 in 33 and 40 mmol/L glucose groups was increased (P<0.05), while the protein expression of Bcl-2 was decreased (P<0.05). No significant difference in the protein levels of PI3K and Akt among the 3 groups was observed, while the protein level of p-Akt in 33 and 40 mmol/L glucose groups was decreased compared with normal control group (P<0.05). Compared with high glucose group, the expression of ROCK1 and ROCK2 was decreased in high glucose+Y27632 group. No significant difference in the protein levels of PI3K and Akt among the 3 groups was observed. Compared with normal control group, the protein level of p-Akt in high glucose group was decreased, and the protein level of p-Akt in high glucose+Y27632 group was increased significantly compared with high glucose group. CONCLUSION Under high glucose environment, ROCK may reduce the level of p-Akt by inhibiting the PI3K/Akt signaling pathway， thus promoting the apoptosis of cardiomyocytes.