Molecular cloning and multifunctional characterization of GRIM-19 (gene associated with retinoid-interferon-induced mortality 19) homologue from turbot (Scophthalmus maximus)

GRIM-19 (gene associated with retinoid-interferon-induced mortality 19), a novel cell death regulatory gene, plays important roles in cell apoptosis, embryogenesis, mitochondrial respiratory chain and immune response. To date, little information is known about fish GRIM-19 characteristics except orange-spotted grouper (Epinephelus coioides). Here a new GRIM-19 gene is identified and characterized from turbot (Scophthalmus maximus), an economic marine fish in China and Europe. Briefly, turbot GRIM-19 is a 595-bp gene encoding a 144 amino acids protein, which shares the closest relationship with Atlantic halibut (Hippoglossus hippoglossus). The expression of turbot grim-19 in liver, spleen and kidney is up-regulated by the infection of Vibrio anguillarum and LCDV (lymphocystis disease virus). Subsequently, a recombinant protein of turbot GRIM-19 is acquired and the anti-bacterial function is proved by liquid culture inhibition experiment. The subcellular location indicates that turbot GRIM-19 is co-localized with STAT3 in the cytoplasm, which is mainly determined by GRIM-19 41–84 amino acids and STAT3 1–321 amino acids. Finally, the involvements of turbot GRIM-19 in cell apoptosis and NF-κB pathway are investigated. All these data help to understand GRIM-19 function in fish, as well as provide the application possibility of GRIM-19 in fish disease resistance breeding.     

Imidacloprid Affects <Emphasis Type="Italic">Pardosa Pseudoannulata</Emphasis> Adults and Their Unexposed Offspring

Imidacloprid is a nicotine-based, systemic, widely used insecticide. In order to investigate the effects of imidacloprid on the spider Pardosa pseudoannulata (Araneae: Lycosidae), specimens were exposed to different concentrations of imidacloprid (12.5, 25, 50, 100, 200 mg/L) by the dipping method. Surviving spiders were used to determine the fecundity, development time of unexposed offspring, predation, and the activities of detoxification enzymes. Significant reductions were observed in survival rate and fecundity of spiders exposed to imidacloprid. The development times of unexposed offspring (F₁) were prolonged significantly with increased concentrations of imidacloprid. Spiders exposed to concentrations of imidacloprid above 25 mg/L showed significantly weaker predation on Drosophila melanogaster than the control group, but a low dose of imidacloprid (12.5 mg/L) increased predation ability. The activities of carboxyl esterase, acetyl cholinesterase, and the mixed-function oxidase were significantly inhibited by imidacloprid. With increasing concentrations of imidacloprid, the activities of all three kinds of enzymes were decreased significantly. These results suggest that imidacloprid can stimulate the performance of spiders (in low concentration) and has chronic toxicity to the spiders.     

独立学院化工与制药类专业实验教学体系建设研究与实践

培养企业需要的应用型工程技术人才是独立学院工程专业的主要任务,实验和实践教学是培养应用型工程技术人才的重要教学环节。本文对产学研结合建设实验教学中心、按照专业共性构建资源共享的实验教学平台、根据人才培养定位,改革实验教学内容和实验教学模式,构建高效的实验中心管理体制和实验教师团队建设等进行了探索,实践效果明显。     

f因子法考察萘普生胶囊溶出度

目的:考察2种市售萘普生胶囊的溶出曲线,研究《中国药典》和《日本药局方》规定的溶出务件下溶出度的差异,分析现行溶出方法的质量可控性.方法:采用溶出仪测定萘普生胶囊在水,pH1.2,pH4.0,pH6.8,pH7.4等5种介质中的溶出曲线,对试验结果进行分析并用f因子法评估溶出曲线的相似性.结果:2种市售萘普生胶囊溶出曲线与日本标准溶出曲线相比存在较大差异,且国产萘普生制剂溶出较慢.2种市售萘普生胶囊的溶出度均符合《中国药典》的规定,但不同厂家生产的萘普生胶囊之间溶出曲线差异较大,不同厂家产品存在质量差异.结论:现行药典的溶出限度(Q值)不能反映制剂质量的内在差异,建议生产企业采用溶出曲线对制剂产品进行生产工艺、处方、质量评估.     

Dissolution Determination of Metronidazole Tablets from Different Manufacturers by f Factor and AV Method

目的：考察国产三个不同厂家生产的甲硝唑片在四种介质中的溶出曲线,并与日本厚生省《医疗用药品品质情报集》中溶出标准曲线进行比较,分析我国溶出度检查方法对质量的可控性及AV法的适用性。方法：在pH 1.2、pH 4.0、pH6.8、水四个溶出介质中,以紫外-可见分光光度法测定药物在不同时间的累积溶出百分率,对实验结果用f因子法和AV法评价溶出曲线间相似度。结果：f因子法显示三种市售甲硝唑片在pH 1.2的介质中溶出曲线间非常相似,但较日本标准溶出曲线存在差异。国产甲硝唑片在其余三种介质溶出行为与日本标准溶出曲线相似。AV法分析结果在纯水和pH 4.0基本相同,但在其他情况下与f因子法分析结果不同。结论：不同溶出介质对甲硝唑片溶出行为影响较大,我国现行工艺及处方有利于药物在胃中溶出。AV法是否可广泛用于溶出曲线相似度上还有待进一步考察。     

槲皮素-羟丙基-β-环糊精包合物对柔红霉素心脏毒性的保护作用

目的：研究槲皮素-羟丙基-β-环糊精包合物（QUE-HP-β-CD）对柔红霉素（DNR）心脏毒性的保护作用。方法：将实验小鼠分为6组：正常组每天腹腔注射等量生理盐水;DNR组从实验第9~19天每2日1次腹腔注射3 mg·kg^-1 DNR;包合物不同剂量组于实验第1~17天每日1次分别灌胃50,100,200 mg·kg^-1包合物,并于第9天用与DNR组相同的剂量和方式给予DNR;QUE组用100 mg·kg^-1QUE代替包合物,其余处理方法与包合物组完全相同。结果：QUE和不同剂量包合物均能抑制小鼠体质量降低,但100~200 mg·kg^-1包合物可显著改善DNR所致心肌肥大和心室重构,并使各项心肌酶恢复到正常水平;切片显示100 mg·kg^-1包合物能显著改善DNR所致心肌损伤。结论：QUE-HP-β-CD（100 mg·kg^-1）对抑制DNR所致小鼠心脏毒性效果最好。