60Co辐射诱变姬松茸突变株J3子实体不同部位的氨基酸分析研究

测定并比较了60Co辐射诱变姬松茸突变株J3与原菌株J1子实体不同部位的氨基酸含量.结果表明,除菌柄和盖皮外,姬松茸突变株J3子实体其它部位的必需氨基酸、儿童氨基酸、硫氨酸、支链氨基酸、鲜味氨基酸、芳香族氨基酸和甜味氨基酸均高于原菌株J1.姬松茸突变株J3子实体中谷氨酸含量占氨基酸总量的比例分别比原菌株J1、α-酪蛋白和卵清蛋白提高34.88%、56.68%和122.32%.     

不同砧木嫁接网纹甜瓜试验

为预防网纹甜瓜枯萎病等土传病害,以新土佐、灰甘瓜、全能铁甲南瓜,甬砧3号甜瓜为砧木,以当地主栽的拿玻里网纹甜瓜为接穗,进行嫁接试验。结果表明:拿玻里网纹甜瓜嫁接后,植株的抗病性有了显著提高,对枯萎病的防效高达100%,对白粉病的防效也有所提高,综合抗性增强。其中甬砧3号在4个参试砧木品种中,与接穗拿玻里网纹甜瓜的亲和性最好,抗病性提高明显,品质也较自根苗好。     

八珍汤对乳牛产后免疫状态的影响

为了探索提高乳牛产后期免疫状态的新方法，对试验乳牛分4组（产前第30d至产前第1d灌喂组、产前第15d至产后第15d灌喂组、产后第1d至第30d灌喂组、不灌喂中药对照组）灌喂中药八珍汤，检测产后期淋巴细胞及其亚群数量和淋巴细胞增殖活化功能。结果发现，产前组CD3细胞数量在产后第1d升高；产前产后组CD3、CD4和CD8细胞数量在产后第1d和第15d升高；产后组CD3细胞数量在产后第15d和第30d升高，CD4细胞数量也在产后第30d升高。淋巴细胞对ConA的反应能力，产前产后组在产后第1～30d明显提高，产后组在产后第15d和第30d明显提高。各组乳牛产后期CD21细胞数量的变化相近。结果表明，从产前第15d开始到产后第15d每日喂八珍汤，能明显提高乳牛产后期T细胞及其亚群数量和增加淋巴细胞增殖活化功能，而对B细胞数量增加的作用不明显。     

鸡传染性腔上囊病病毒VP2基因在昆虫细胞中的表达

为了深入研究鸡传染性腔上囊病病毒（IBDV）VP2基因的结构和功能,利用Bac-to-Bac系统研制出含有VP2基因的重组杆状病毒rBac-VP2,将rBac-VP2感染Sf9细胞,并用抗IBDV VP2特异性单克隆抗体经间接免疫荧光试验检测,证实感染重组病毒Sf9细胞能高效表达IBDV VP2基因产物;Western-blotting分析结果表明,VP2基因表达产物的分子质量约为40 ku.     

Analysis of gene expression profile of multidrug resistant MCF/DOX cell line after benflumetol derivative LY980503 treatment

AIM:To investigate the effect of LY980503(a benflumetol derivative)on multidrug resistance of tumor cell line using DNA microarray.METHODS:Total RNA was extracted from multidrug resistant MCF/DOX cell line. cDNA microarray containing 320 cDNAs was used to detect the gene expression profile.RESULTS:9 down-regulated genes and 1 up-regulated gene were identified after multidrug resistant MCF/DOX cells were treated with LY980503.CONCLUSION:LY980503 can effectively reverse the resistance of MCF/DOX to DOX in vitro by adjusting the expression of multi-genes.     

Effects of matrix metalloproteinases on ventricular remodelingfollowing myocardial ischemia in the rat

AIM:To examine the relationship between the activity of matrix metallproteinases(MMPs) and ventricular remodeling following myocardial ischemia in the rat.METHODS:The model of myocardial ischemia(MI) in the rat was established by isoprenaline(ISP). The activity of MMPs was measured by zymography and collagen concentration was assessed by the method of chloramine T, so did I/III collagen ratio by immunohistochemical staining. The microstructure of myocardium was also observed by electron microscope.RESULTS:The activity of MMP-2 in myocardial ischemia group (group M) increased by 5.8 folds at 1 st week(P＜0.01), 2.3 folds at 2 nd week(P＜0.01) and 1.7 flods at 4 th week(P＜0.05) compared with control group (group C) and MMP-9's activity in group M increased by 4.9 folds (P＜0.01), 1.9 flods(P＜0.01) and 1.4 folds(P＜0.05), respectively. Collagen amount and I/III collagen ratio in group M increased compared with that in group C at 2 nd week and 4 th week. It showed that cardiac myocytes in group M were necrosed and collagen grew abundantly in interstitium under electron microscope.CONCLUSION:The activity of MMPs in the myocardial interstitium increased following myocardial ischemia, then collagen amount and I/III collagen ratio increased, which may be the major causes of ventricular remodeling.     

The basic mechanism of increased microvascular permeability

The increased microvascular permeability appears mainly in venule during inflammation, shock, and burns. Endothelial cells play an important role in venule permeability enhancement. There are two kinds of pathway for macromolecule extravasation. One is paracellular pathway and another is transcellular pathway, which are related to the formation of endothelial gap or transcellular openings seperately. The alteration of intercellular related protein, such as occludin, claudin, zona occludens (ZO), junctional adhesion molecule (JAM), VE cadherin, catenin, integrin, etc, and the alteration of endothelial cytoskeleton, such as rearrangement of actin filament, formation of stress fiber and focal adhesion, etc, involve in the pathogenesis of increased microvascular permeability.     

Protective effect of onychin on the human umbilical vein endothelial cells injured by menadione

AIM: To investigate the protective effect of onychin on the endothelial cells injured by oxidative stress. METHODS: The injured model was established by endothelial cells treated with menadione. The growth inhibitory rate of endothelial cell was determined by MTT assay; NO₂^-／NO₃^- concentration in the medium was determined by nitrate reductase assay; eNOS and caveolin-1 protein levels were determined by Western blot. RESULTS: Onychin significantly decreased the growth inhibitory rate of endothelial cells injured by menadione, increased NO₂^-／NO₃^- concentration in the medium and eNOS activity and up-regulated caveolin-1 expression. CONCLUSION: Onychin possesses a protective effect against endothelial cell injury induced by menadione via caveolin-1/eNOS pathway.     

Effects of Sini decoction on atherosclerosis and ceramide content of aorta in rabbits

AIM:To observe the effects of Sini decoction on atherosclerosis(AS) and ceramide content of aorta in rabbits. METHODS:28 rabbits were randomly divided into three groups. Control group was fed with a normal diet; High cholesterol group was fed 1% cholesterol and 5% fat diet; Sini decotion+ high cholesterol group was fed 1% cholesterol and 5% fat diet plus Sini decotion (4.2 g·kg^-1·d^-1). At the end of study, the plaque area were measured, the atorta ceramide and cell apoptosis were also detected. RESULTS:Sini decotion diminished lipid plaque area on the aortic endothelium, reduced the levels of aorta ceramide and the apoptosis index. CONCLUSION:Sini decoction has an inhibitory effect on AS, the mechanism may be that Sini decotion reduces concentration of ceramide in aorta.     

Effect of cocaine on caspase-3 in myocardiac cells of male rats in different age

AIM: To study the effect of cocaine on caspase-3 in myocardiac cells of male rats in different age. METHODS: Three-week-old(n=16), six-week-old(n=16) and twelve-week-old (n=16) male Sprague-Dawley rats were all divided into control groups and experiment groups randomly, each group had eight animals, experiment groups were given cocaine hydrochloride (15 mg·kg^-1 body weight) subcutaneously daily for four weeks. The ratio of heart weight to body weight (HW/BW, mg/g) were measured. DNA fragmentation of myocardia cells was determined by gel electrophoresis, and caspase-3 activity in myocardia cells was tested by flow cytometry (FCM). RESULTS: In three experiment groups, the DNA isolated from myocardial cells displayed clear ladder pattern. The HW/BW and the caspase-3 activity were increased significantly than those of control groups (P<0.01). CONCLUSIONS: Cocaine induced apoptosis in rat myocardial cells. The increase in caspase-3 activity may be the one of important pathways related to the induction of apoptosis.