高锌对仔猪肝脏脂肪代谢的影响

本研究旨在探讨高浓度硫酸锌对仔猪肝脏脂肪代谢的影响.试验选用120头平均始重为(26.66±2.45)kg的杜×长×大三元杂交仔猪,随机分成4组(对照组、试验组Ⅰ、试验组Ⅱ和试验组Ⅲ),每组3个重复,每个重复10头猪,分别饲喂添加60、300、1 000和3 000 mg/kg锌的基础饲粮.预试期7 d,正试期16 d.结果表明,与对照组相比,1)各试验组血清总甘油三酯和低密度脂蛋白胆固醇含量均显著提高(P<0.05);2)试验组Ⅲ血清总胆固醇、C18:1脂肪酸含量显著升高(P<0.05),肝脏C18:0、C18:2脂肪酸含量显著降低(P<0.05),而C16:0脂肪酸含量无显著变化(P>0.05);3)试验组Ⅱ和试验组Ⅲ肝脏硬脂酰辅酶A去饱和酶1(SCD1)mRNA水平、血浆瘦素和胰岛素含量都显著升高(P<0.05).随着锌浓度的升高,血浆四碘甲状腺原氨酸(T4)含量显著降低(P<0.05),三碘甲状腺素原氨酸(T3)和胰高血糖素含量有上升趋势,但差异不显著(P>0.05).由此可知,饲粮中添加1 000和3 000 mg/kg锌上调了仔猪肝脏SCD1转录水平,促进了机体饱和脂肪酸(C18:0)的去饱和化,增加了机体甘油三酯和胆固醇的合成,且高锌可通过促进瘦素和胰岛素的分泌调节机体的脂肪代谢.     

芥蓝二氢黄酮醇4–还原酶基因BoaDFR的克隆与功能鉴定

以白花芥蓝‘四季粗条’为材料克隆了Boa DFR基因,Gen Bank登录号为MT472647,CDS序列长为1158 bp,编码385个氨基酸,与甘蓝型油菜、甘蓝和白菜等具有高度同源性。Boa DFR表达水平在芥蓝不同发育时期、不同器官中存在显著差异,随植株发育总体呈现先下降后上升的趋势,在幼嫩种子中表达量最高。芥蓝原生质体的亚细胞定位结果显示Boa DFR定位在细胞核上。构建了农杆菌介导的芥蓝瞬时过表达体系,将Boa DFR转入白花芥蓝‘四季粗条’和黄花芥蓝‘福州黄花’中,发现Boa DFR在两种芥蓝中均高水平表达,转基因植株叶片颜色明显变紫,花青素苷显著积累,总含量最高达461.43μg·g-1 FW,而野生型和转空载体芥蓝叶片中几乎检测不到花青素苷。通过HPLC在转基因植株叶片中共检测到8种花青素苷,均为矢车菊花青素苷,其中矢车菊–3–阿魏酰–丙二酰–槐糖苷–5–葡萄糖苷占比最高。     

高温条件下复合抗应激剂对肉鸡的影响

本文研究了高温条件下复合抗应激剂对肉鸡的影响。结果表明：经历３２ ℃一周的５ ～８ 周龄肉鸡采食量、增重、饲料转化率均显著下降（Ｐ＜ ０ ．０１） ,饮服复合抗应激剂显著改善增重和饲料转化率（Ｐ＜ ０ ．０１） , 采食量未见明显改变,饲料转化率达到常温水平。３２ ℃１６ 小时血浆皮质酮、Ｔ３ 显著下降（Ｐ＜ ０ ．０１） 、Ｔ４ 显著升高（Ｐ＜ ０ ．０１） ;３２ ℃１２０ 小时血浆皮质酮、Ｔ３ 升高并超出常温组（Ｐ＜ ０ ．０５） 、Ｔ４ 较１６ 小时下降但仍高出常温组（Ｐ＜ ０ ．０５） 。饮服复合抗应激剂时血浆皮质酮、Ｔ３ 、Ｔ４ 显现相同变化规律,但这种变化得到显著缓解     

黄皮洋葱新品种连葱4号的选育

连葱4号是以连引洋葱1号为母本、富永中生为父本配组杂交后,经多代系统选择育成.具有优质、高产、抗病等优点.平均每667 m2产量5000～6 500kg,适于长江流域地区种植.     

饲料添加剂双乙酸钠的5P营销策略

基于产品(product)、价格(price)、地点(place)和推广(promotion)等市场营销4P策略的内容,结合双乙酸钠的特征、应用和市场现状,整合融入营销平台(platform),即从4P策略过渡到5P策略,并对双乙酸钠市场营销的5P策略实施进行了分析与探讨.     

传染性支气管炎病毒结构蛋白免疫鸡对CD4+CD8+T淋巴细胞亚群的影响

为了比较传染性支气管炎病毒3种主要结构蛋白免疫鸡后对CD4+、CD8+T淋巴细胞亚群的不同影响.本试验以pVAX1载体为携带工具,制备分别含有IBV主要结构蛋白基因的质粒免疫健康雏鸡,采用流式细胞仪(FACS)对免疫鸡外周血中CD4+、CD8+T淋巴细胞数进行检测.结果显示:各试验组间,携带N蛋白基因的质粒在免疫后3周内CD4+T淋巴细胞数和CD8+T淋巴细胞数均高于其他组,且差异极显著(P＜0.01).由此可见,IBV的N蛋白可明显诱导CD8+T淋巴细胞的CTL免疫作用和CD4+T淋巴细胞的辅助性免疫作用,其细胞免疫原性高于S1蛋白和M蛋白.     

Characterization of an intravenous lipopolysaccharide inflammation model in calves with respect to the acute-phase response

Our objective was to develop a lipopolysaccharide (LPS) inflammation model in calves to evaluate the acute-phase response with respect to the release of pro-inflammatory cytokines and acute-phase proteins, fever development and sickness behaviour. Fourteen 4-week-old male Holstein Friesian calves were included and randomly assigned to a negative control group (n = 3) and an LPS-challenged group (n = 11). The latter received an intravenous bolus injection of 0.5 μg of LPS/kg body weight. Blood collection and clinical scoring were performed at 0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 5, 6, 8, 12, 18, 24, 28, 32, 48, 54 and 72 h post LPS administration (p.a.). In the LPS group, the following clinical signs were observed successively: tachypnoea (on average 18 min p.a.), decubitus (29 min p.a.), general depression (1.75 h p.a.), fever (5 h p.a.) and tachycardia (5 h p.a.). Subsequent to the recovery from respiratory distress, general depression was prominent, which deteriorated when fever increased. One animal did not survive LPS administration, whereas the other animals recovered on average within 6.1 h p.a. Moreover, the challenge significantly increased plasma concentrations of tumour necrosis factor-α, interleukin 6, serum amyloid A and haptoglobin, with peaking levels at 1, 3.5, 24 and 18 h p.a., respectively. The present LPS model was practical and reproducible, caused obvious clinical signs related to endotoxemia and a marked change in the studied inflammatory mediators, making it a suitable model to study the immunomodulatory properties of drugs in future research.     

Involvement of TLR4/NLRP3 inflammasome in contrast medium-induced inflammation and injury in renal tubular epithelial cells

AIM: To investigate whether Toll-like receptor 4 (TLR4) and Nod-like receptor protein 3 (NLRP3) inflammasome were involved in contrast medium (CM)-induced inflammation and injury in renal tubular epithelial cells. METHODS: Iopromide was used to injure NRK-52E cells in the study. The cell viability was measured by CCK-8 assay. The protein levels of TLR4, NLRP3, apoptosis-associated speckle-like protein (ASC), caspase-1 and cleaved caspase-3 were determined by Western blot. The releases of interleukin (IL)-1β and IL-18 were detected by ELISA. The apoptotic rate was evaluated by Hoechst staining, and mitochondrial membrane potential (MMP) was analyzed by JC-1 staining. siRNA was transfected into the NRK-52E cells to silence NLRP3 expression. RESULTS: CM decreased the viability of NRK-52E cells (P<0.05). CM also elevated the protein levels of cleaved caspase-3, TLR4, NLRP3, IL-1β and IL-18 (P<0.05). Silencing NLRP3 attenuated CM-induced releases of inflammatory cytokines. Moreover, treatment with TLR4 inhibitor TAK-242 or knockdown of NLRP3 by siRNA transfection both attenuated cell apoptosis and loss of MMP caused by CM. CONCLUSION: TLR4/NLRP3 inflammasome takes part in the pathogenesis of CM-induced acute kidney injury, and mediates CM-induced injury and inflammation in renal tubular epithelial cells.