Optimization of experimental infection protocols for the estimation of genetic parameters of resistance to White Spot Syndrome Virus (WSSV) in Penaeus (Litopenaeus) vannamei

Two infection protocols, individual oral (IO) and waterborne infection (WB), were evaluated to challenge Penaeus (Litopenaeus) vannamei with White Spot Syndrome Virus (WSSV). Five different batches of full and half-sib families were infected experimentally and tested for growth performance under commercial growth conditions. The genetic variance for WSSV resistance was estimated using a linear sire-dam repeatability model that considers test-day survival as the dependent variable. The heritability estimates using the IO protocol ranged from 0.01 ± 0.00 to 0.02 ± 0.01, whereas the heritability estimates using the WB infection protocol were not significantly different from zero. The genetic correlations measured as the product moment correlation between full-sib family breeding values for resistance to WSSV and harvest body weight in ponds were unfavourable in three of the five batches and favourable in one of them. The dosage of WSSV was better controlled with IO oral infection than with other methods, with all animals being exposed to approximately the same risk of infection at the same time. This should improve the accuracy of the genetic parameters and hence improve the accuracy of the breeding values. It should, however, be noted that once the outbreak was established and the mortalities began, the shape and the magnitude of the slope of the mortality curves showed little difference in the infection pattern between batches irrespective of the dosage and infection protocol, and in most of the cases the cumulative mortality was greater than 80%. The main reason for this is probably the high densities of animals in the tanks needed for the genetic evaluations.     

甜菜碱对热应激肉鸡生长性能、十二指肠消化酶活性及盲肠微生物区系的影响

本试验通过在饲粮中添加不同剂量的甜菜碱研究其对热应激肉鸡生长性能、十二指肠消化酶活性及盲肠微生物区系的影响。选取270只14日龄爱拔益加(AA)肉鸡随机分成6组:常温组、热应激组,常温+0.1%甜菜碱组、热应激+0.1%甜菜碱组、热应激+0.2%甜菜碱、热应激+0.4%甜菜碱组。热应激肉鸡饲养在(32±1)℃的高温环境中。每组3个重复,每个重复15只。预试期7 d,正试期21 d。结果表明:1)饲粮添加甜菜碱可极显著增加28~42日龄热应激肉鸡的体重(P<0.01),极显著降低22~35日龄肉鸡料重比(P<0.01);2)除添加0.1%和0.2%甜菜碱饲粮对28日龄热应激肉鸡胰蛋白酶活性无显著影响(P>0.05)和添加0.1%甜菜碱对35日龄热应激肉鸡淀粉酶活性无显著影响(P>0.05)外,不同浓度的甜菜碱均能显著或极显著增加28、35、42日龄热应激肉鸡十二指肠胰蛋白酶、淀粉酶和胰脂肪酶活性(P<0.05或P<0.01);3)饲粮添加甜菜碱极显著提高了28、35、42日龄热应激肉鸡盲肠内乳酸杆菌的数量(P<0.01),极显著降低了产气荚膜梭菌的数量(P<0.01)。由此可见,热应激状态下,在基础饲粮中添加甜菜碱可改善AA肉鸡生长性能,提高十二指肠消化酶的活性,维持盲肠内微生物区系平衡,从而减轻热应激对肉鸡的危害。     

持续高温应激对肥育猪生产性能、胴体性状、背最长肌营养物质含量及肌纤维特性的影响

本试验旨在研究持续30℃的环境高温应激对肥育猪生产性能、胴体性状、背最长肌质构分析、营养物质含量及肌纤维特性的影响.试验选取8窝共24头体重为(79.0±1.5) kg的“杜长大”三元阉公猪,其中每3头来自同一窝的猪只随机分到3组,每组8个重复,每个重复1头,3组分别为对照组(22℃适温+自由采食)、高温应激组(30℃高温+自由采食)和采食量配对组(22℃适温+采食量配对),试验期21d.结果表明:1)持续高温应激显著降低肥育猪平均日增重(ADG) (P＜0.05),极显著降低肥育猪平均日采食量(ADFI) (P＜0.01).2)3组之间的肥育猪胴体重、胴体长、平均背膘厚和皮厚均差异不显著(P＞0.05),高温应激组肥育猪背最长肌大理石花纹评分在宰后24 h有低于对照组的趋势(P＜0.10).3)高温应激组肥育猪背最长肌的剪切力极显著高于对照组和采食量配对组(P＜0.01).与采食量配对组相比,高温应激组肥育猪背最长肌胶黏性和硬度有降低的趋势(P＜0.10).4)高温应激组和采食量配对组肥育猪背最长肌粗蛋白质含量显著高于对照组(P＜0.05),且2组的背最长肌肌内脂肪(IMF)含量极显著低于对照组(P＜0.01).5)高温应激组肥育猪背最长肌Ⅰ型肌纤维含量有低于采食量配对组的趋势(P＜0.10),采食量配对组的Ⅱx型肌纤维含量显著低于对照组(P＜0.05).由此可见,肥育后期高温应激会改变猪表观肉品质和肌肉营养物质含量.     

表达产肠毒素性大肠埃希菌STa-K99融合蛋白重组腺病毒的免疫学特性研究

为研究表达产肠毒素性大肠埃希菌(ETEC)耐热性肠毒素STa与粘附素K99融合蛋白重组腺病毒rAd.STa-K99的免疫学特性,本实验将rAd.STa-K99经肌肉注射免疫小鼠,采用ELISA法分别检测了特异性IgG、SIgA、脾脏淋巴细胞增殖活性水平及CD4+、CD8+T淋巴细胞分型比值;并通过攻毒保护试验对其免疫效果进行评价.结果表明,免疫后小鼠特异性IgG、SIgA及脾脏淋巴细胞增殖活性水平显著升高;CD4+/CD8+值显著增大;动物攻毒保护率达到70％.结果表明rAd.STa-K99可以刺激小鼠机体产生较高水平的体液免疫、特异性细胞免疫和肠道粘膜免疫反应,并对小鼠提供有效保护.本实验为研制预防由ETEC引起的新生动物腹泻重组腺病毒疫苗奠定了基础.     

中药“救必应”水提取物对产ESBLs大肠杆菌耐药性的影响

“救必应”为冬青科植物铁冬青的树皮或根皮水浸出物制备,具有广谱的抗菌作用.为研究中药“救必应”对产超广谱β-内酰胺酶(ESBLs)大肠杆菌耐药性的影响,本研究将产ESBLs的E.coli在亚抑菌浓度的中药“救必应”中传代,采用微量稀释法测定抗生素对产ESBLs的E.coli最小抑菌浓度(MIC),并通过透射电镜观察中药作用后细菌形态学变化.结果显示,中药“救必应”可以显著降低产ESBLs的E.coli对阿莫西林、加替沙星、诺氟沙星、盐酸左旋氧氟沙星、乙酰甲喹、磺胺间甲氧嘧啶钠、克林沙星、氟苯尼考的MIC值,并且MIC均降低4倍;此外,中药作用后可以引起细菌细胞壁的皱裂、干瘪、折叠、缩短等形态变化.     

湛江东海岛对虾育苗场水体细菌的抗生素耐药性

利用K-B纸片扩散法研究分离自湛江东海岛6个对虾育苗场(分别编号为YF,JD,DC,HM,SD,XR)水体中的217株细菌菌株对12种抗生素的耐药性。研究结果表明,参试的12种抗生素之间的细菌耐药性差异显著(ANOVA,P0.05),6个育苗场内细菌对多粘菌素B、左氟沙星和环丙沙星高度敏感,对氨苄西林、甲氧苄胺嘧啶、复方新诺明和四环素则高度耐药;多重耐药菌株在每个育苗场中均有发现,52.07%的菌株呈现多重耐药性,未发现对参试的12种抗生素100%耐药的菌株。统计分析结果显示,尽管HM和XR育苗场的细菌耐药性比其他育苗场高,但6个对虾育苗场之间水体细菌的抗生素耐药性无显著差异(ANOVA,P0.05)。     

水稻OsNHO1基因cDNA序列分离及表达分析

OsNHO1是一种甘油激酶,受多种因素的诱导,在植物先天免疫反应中起着重要的作用。笔者采用同源序列法,根据已报道的拟南芥NHO1基因序列结合水稻基因组测序结果,筛选水稻OsNHO1基因,采用RT-PCR获得水稻OsNHO1基因全长cDNA(1 590 bp,529AA),并通过半定量RT-PCR方法分析OsNHO1基因在SA,PXO99刺激下的表达模式,结果显示OsNHO1基因的表达受SA,PXO99的诱导,为进一步研究OsNHO1的具体功能和作用机理奠定了基础。     

鹤蕉种质资源抗寒性和农艺性状的鉴定与评价

针对抗寒性、花期和观赏特性等几个农艺性状,对引进的67个鹤蕉品种进行了连续3年的大田圃鉴定与评价,筛选出适合在海南不同区域栽培的8个有应用价值的品种。旨在为鹤蕉的品种改良、栽培和开发利用提供参考。     

Inhibition of c-Myc by 10058-F4 overcomes imatinib resistance in chronic myeloid leukemia cells

AIM：To investigate the effect of c-Myc inhibitor 10058-F4 on human chronic myeloid leukemia (CML) K562 cells and imatinib-resistant K562/G cells. METHODS：The protein expression of c-Myc was detected by Western blotting. Cell proliferation was evaluated by MTT assay and colony formation assay. PI staining was used to determine the cell cycle distribution. Annexin V-PI staining was applied for apoptosis detection. RESULTS：Imatinib-resistant K562/G cells displayed lower sensitivity to imatinib than K562 cells with high expression of c-Myc. Treatment with specific c-Myc inhibitor 10058-F4 inhibited the cell proliferation in a dose- and time-dependent manner, and K562/G displayed more sensitivity to 10058-F4 than K562 cells. 10058-F4 also induced cell cycle arrest in G0/G1 phase and induced apoptotic cell death in the 2 cells. Importantly, 10058-F4 suppressed the colony formation ability in K562 and K562/G cells. CONCLUSION：c-Myc is a novel target to overcome imatinib-induced drug resistance, and c-Myc inhibitor provides a new approach in CML therapy.     

Is the metabolic syndrome a useful clinical concept in dogs? A review of the evidence

The metabolic syndrome is a set of risk factors for the development of type 2 diabetes, atherosclerosis, coronary heart disease and stroke in human beings. The term has recently been applied to dogs that exhibit components of the human metabolic syndrome, specifically visceral obesity, hypercholesterolaemia, hypertriglyceridaemia, hypertension and fasting hyperglycaemia. Obese dogs, like obese humans, are known to develop resistance to the glucose-lowering effects of insulin, and develop increased circulating concentrations of triglycerides, cholesterol and blood pressure. Unlike humans, however, obese dogs do not develop fasting hyperglycaemia or atherogenic hyperlipidaemia. Importantly, there is no evidence that dogs develop type 2 diabetes. Atherosclerosis, coronary heart disease and stroke are rare and not known to be associated with obesity in dogs. On the basis of current knowledge, the use of the term ‘metabolic syndrome’ in dogs does not appear to have merit.