枯草芽孢杆菌B—916防治水稻纹枯病的田间试验

１９９２～１９９４年在田间小区试验比较两个拮抗细菌（Ｂ－９１６、Ｐ－９１）和井岗霉素对水稻纹枯病的防治效果。１９９４～１９９５年在江苏省３个基点上进行了Ｂ－９１６防治纹枯病的大面积示范试验。Ｂ－９１６发酵液在田间对水稻纹枯病的为害有较强的控制能力，发酵含菌量为２．５４×１０１１～２．５４×１０１２ｃｆｕ／ｍＬ时，用量３．７５Ｌ／ｈｍ２的防治效果为５０．０％～８１．０％。     

生、炒酸枣仁镇静催眠作用的比较研究

采用两种催眠试验方法,观察生、炒酸枣仁煎剂对阈下剂量戊巴比妥钠入睡的影响及对阈剂量戊巴比妥钠睡眠的影响.结果阈下剂量戊巴比妥钠的入睡试验中,不同炮制酸枣仁处理差异不明显;同一炮制中高剂量作用大于低剂量;在睡眠试验中亦获得类似的结果.结果表明:生、炒酸枣仁在同一剂量下药理作用无差异,但同种炮制存在一定的剂量效应关系.     

花粉多糖注射剂质量标准中几个项目测定

根据中国药典对注射剂的要求,对花粉多糖的蛋白质、鞣质、树脂、草酸盐、炽灼残渣、钾离子、砷盐、重金属含量进行测定,均符合规定,达到质量标准。     

花粉多糖注射剂临床前抗肿瘤药效学预试

花粉多糖对小鼠Lewis肺癌(足趾接种)模型以200mg/kg,100mg/kg,50mg/kg三个剂量iv×10qd方案给药,实验显示高、中、低三个剂量组抑瘤率分别为48.01%,43.09%,31.38%。免疫实验以上述相同的给药方案,花粉多糖对荷Lweis肺癌小鼠NK细胞活性具有明显的提高和促进作用。     

检测猪流行性腹泻病毒的R-PCR方法的建立

根据猪流行性腹泻病毒 (PEDV)的N基因自行设计和合成了一对可扩增长度为 641bp目的片段的引物 ,成功地建立了检测的猪流行性腹泻病毒的RT PCR方法。对猪轮状病毒 (PRV)、猪传染性胃肠炎病毒 (TGEV)的RT PCR检测结果均呈阴性。对PEDV JS株的RT PCR产物的序列分析表明 ,与CV777株的同源性为 97 3 %。     

闭锁群体BLUP选择下遗传方差和近交系数的变化

采用计算机随机模拟方法模拟了在一个闭锁群体内连续对单个性状进行 1 5个世代选择的情况。选择过程中世代不重叠 ,每个世代的种畜根据动物模型最佳线性无偏预测 (BLUP)法估计的育种值进行选留 ,并在此基础上系统地比较了不同群体规模、公母比例和性状遗传力对群体遗传方差和近交系数变化的影响。结果表明 ,扩大育种群规模、增加公畜比例以及对低遗传力性状进行选择时 ,群体遗传方差降低的速度和近交系数上升的速度会更慢 ,在长期选择时可望获得更大的持续进展和适宜的近交增量     

利用体外培养法建立饲料营养成分与瘤胃丙酸产量的回归模型

根据美国康乃尔净碳水化合物和蛋白质体系 (CNCPS) ,分析测定了 4类 2 4种饲料的营养成分 ,利用体外批次培养技术测定了它们在体外培养一定时间后的丙酸产量 ,并由此建立了饲料中产丙酸的营养成分和瘤胃丙酸产量的回归方程     

山楂叶螨抗药性及混配增效作用

采用载玻片浸渍法测定了山西省忻州、晋中、运城地区山楂叶螨种群对9种杀螨剂的抗药性水平.测定结果表明:忻州地区种群对甲氰菊酯和三氯杀螨醇表现中抗,抗性指数FR分别为17.79和31.93倍,对水胺硫磷和毒死蜱表现低抗,FR值分别为7.74和5.35倍;晋中地区种群对水胺硫磷、甲氰菊酯和三氯杀螨醇均表现中抗,FR值为22.42～33.00倍,而运城地区种群对这3种药剂产生了高抗,FR值分别为135.05、41.53和1714.01倍;运城地区种群对毒死蜱表现中抗,FR值为34.49倍;晋中和运城地区种群对双甲脒表现低抗,FR值分别为5.15和6.89倍;3个种群对阿维菌素、苯丁锡、三唑锡和四螨嗪仍相对敏感.混配增效作用测定结果表明,阿维菌素与甲氰菊酯1:20、1:10、1:5组合以及阿维菌素与三氯杀螨醇1:20、1:10组合均具有明显增效作用,共毒系数为189.63～363.30,其中阿维菌素与甲氰菊酯1:20和1:10组合以及阿维菌素与三氯杀螨醇1:20组合是比较理想的混配组合.     

Nitric oxide-mediated the cardioprotection of tumor necrosis factor-alpha on cultured neonatal rat cardiomyocytes during hypoxia/reoxygenation

AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (10⁵ U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC.     

Effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium

AIM: In order to study the relationship between the ERK and p38 MAPK activation and the protection of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) and ischemia preconditioning (IP), the effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium were examined. METHODS: The rat heart was subjected to ischemia for 5 min by ligating the left anterior descending coronary artery followed by reperfusion for 5 min (two times) to undergo ischemia preconditioning. The rats were divided into 5 groups: (1) control; (2) sham group; (3) ischemia/reperfusion (I/R) group, in which the rat heart suffered from 60 min ischemia followed by 30 min reperfusion; (4) IP plus I/R group; (5) EET plus I/R group, in which 6.28×10^-8 mol/L 11, 12-EET was injected intravenously 20 min before I/R. The heart function was examined, and phosphorylated ERK and p38 MAPK were detected by Western blot. RESULTS: At 30 min reperfusion, +dp/dt_max, -dp/dt_max and LVDP decreased significantly in I/R group compared with sham group, IP plus I/R group and EET plus I/R group; Phosphorylated ERK1/2 level was higher in I/R group than sham group, but was lower in I/R group than IP plus I/R group and EET plus I/R group; Phosphorylated p38 MAPK level was lower in control, sham, IP plus I/R and EET plus I/R group than I/R group. CONCLUSION: 11,12-EET protects rat heart against ischemia/reperfusion injury, the mechanism may be related to activation of ERK1/2 and inhibition of p38 MAPK.