鹅源H5N1亚型禽流感病毒感染SPF雏鸡免疫球蛋白含量的变化研究

以7日龄SPF雏鸡为试验动物,采用常规间接酶联免疫吸附试验(IELISA)法,对鹅源H5N1亚型禽流感病毒(AIV)感染SPF雏鸡后,其泪液、气管液、肠液、胆汁的IgA、IgG、IgM含量的动态变化进行了检测.结果发现,鹅源H5N1亚型中强毒AIV感染SPF雏鸡后,其泪液、气管液、肠液、胆汁的免疫球蛋白IgA、IgM含量均在1～3 d或1～4 d显著低于相应对照雏鸡(P＜0.05),而感染后第5天,上述被检指标开始升高,并于5～8 d或5～14 d,病毒感染雏鸡的IgA和IgM显著高于对照雏鸡(P＜0.05或P＜0.01).表明7日龄SPF雏鸡感染AIV后的早期,其消化道和呼吸道的体液免疫功能降低.     

新疆兵团昭苏垦区家畜包虫病防控情况调查

为了解新疆昭苏垦区包虫病防控工作近况,对新疆生产建设兵团农四师76团和77团饲养的家犬和家畜进行包虫病调查。结果表明,两个团场分别饲养犬1 004条和620条,养殖家畜58 253头(只)和64 848头(只);犬感染细粒棘球绦虫感染率为9.76%(98/1 004)和15.98%(81/507);77团家畜感染包虫病感染率26.45%(338/1 278)。     

日粮中添加不同浓度吡啶甲酸铬对生长肥育猪氧化作用的影响

本研究旨在观察日粮中持续添加不同浓度吡啶甲酸铬对生长肥育猪氧化作用的影响.选取30头(30±1)kg三元杂交型(杜×长×大)生长肥育猪,按体重、遗传基础和性别随机平均分成5个处理.5个处理分别饲喂铬的添加水平为0、200、800、1 600、3 200 ug/kg(以吡啶甲酸铬的形式添加)的日粮,试验期为80 d.试验第35天和第80天时,测定吡啶甲酸铬对动物血清中超氧化物歧化酶(SOD),过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GSH-Px)的活力和丙二醛(MDA)的含量,以及动物尿液中8-羟基脱氧鸟苷(8-OHdG)的水平.试验结束时,屠宰动物并取肝脏和肾脏样品,分别测定这些组织中的SOD、GSH-Px、CAT的活力和MDA的水平.结果表明,日粮中长期添加高剂量(≥800 ug Cr/kg)的吡啶甲酸铬显著降低第80天时肥育猪血清中的SOD和肾脏中CAT的活性(P<0.05),但对其他指标都没有显著影响(P>0.05).结果提示,在生产肥育期全程(80 d)添加适宜量(200 ug Cr/kg)的吡啶甲酸铬不会造成猪的氧化损伤;添加16倍适宜量的吡啶甲酸铬导致猪血清SOD和肾CAT活性降低,但不引起脂质过氧化和DNA损伤.     

Research on the Antioxident Function of Sulforaphane on the Leydig Cells of Cadmium Exposured Mice

The study was aimed to explore the antioxident function of sulforaphane (SFN) on the leydig cells of cadmium (Cd) exposured mice.Cd and SFN were added to the cell culture medium of TM3 cell, half inhibitory concentration (IC₅₀) of Cd and SFN safe dose range were determined.The tested model was set up,and the relative survival rate of TM3 cells, lactate dehydrogenase (LDH) activity and cell antioxidant levels were determined to study the antioxident function of SFN to cadmium exposured mice.The results showed that:①With the increase of Cd concentration,the relative survival rate of TM3 cells was decreased,and the IC₅₀ of Cd was 51.4 μmol/L;Within a certain concentration range,SFN could increased the cells survive rate,but there was toxicity when the SFN concentration was more than the scope,and the greater the concentration,the greater the toxicity. At experimental condition,SFN safety concentration were 2.5,5 and 10 μmol/L.②Compared with the control group,the GSH content,the T-SOD and GSH-Px activities in Cd group were significantly or extremely significantly decreased (P < 0.05;P < 0.01),and the LDH activity,the MDA content were increased.Additionally,the LDH activity and MDA content of SFN groups were decreased,while others three indexes were increased. Compared with Cd group,the GSH content,the T-SOD and GSH-Px activities of Cd+SFN groups were significantly or extremely significantly increased (P < 0.05;P < 0.01),however,the LDH activity,MDA content were decreased. The result indicated that SFN had the antagonism effect on toxicity of Cd in TM3 cell.     

Inductive expression of the NOD1 signalling pathway in chickens infected with Salmonella pullorum

1. The aim of this study was to describe the role of Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) receptor signalling in chicken.

2. Tissue-specific expression analysis of NOD1, receptor-interacting serine-threonine kinase 2 (RIPK2), nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase 11 (MAPK11 or p38) by quantitative real-time PCR (qRT-PCR) revealed their wide distribution in various organs and tissues.

3. Salmonella pullorum infection activated NOD1 receptor signalling in vivo and in vitro, resulting in significant induction of downstream signalling molecules RIPK2, NF-κB/p65, MAPK11/p38 and the effector molecules IL-1b and IL-8.

4. Activation of NOD1 by its agonist bacterial γ-D-glutamyl-meso-diaminopimelic acid (iE-DAP) in HD11 cells induced the adapter molecular RIPK2 and activated the NF-κB/p65 and MAPK11/p38 pathways, resulting in an increase in IL-8 but not IL-1β. Additionally, inhibition of NOD1 using NOD1-shRNA resulted in downregulation of RIPK2, MAPK11 and IL-8, while NF-κB/p65 and IL-1β were unaltered.

5. These results highlight the important role of NOD1 receptors in eliciting the innate immune response following pathogenic invasion in chicken.     

断奶对仔猪肠道屏障的影响及营养调控

在集约化养殖中,3~4周龄早期断奶是仔猪生命周期中一个非常紧张的时期,此时仔猪胃肠道还未发育成熟。肠道屏障由上皮、免疫和肠神经系统组成,这些系统控制上皮屏障的完整性以及肠道功能,包括肠腔营养物质、水和电解质的运输。早期断奶导致肠道通透性增加,出现胃肠功能紊乱的情况,可能对猪只一生产生长期的影响。因此,仔猪断奶饲粮需要正确水平的营养素、营养源和高质量的添加剂,鼓励仔猪快速进食,减轻或消除断奶应激综合症,降低死亡率和发病率。养猪就是养肠道,合理使用功能性氨基酸、植物化学物质和有机酸等添加剂,能够修复由于断奶应激综合症导致的肠道屏障功能障碍。     

羊草草原群落初级生产力动态研究

在锡林郭勒盟南部羊草草原对群落初级生产力动态进行11年的定位研究,结果表明:群落地上生物量有着显著的波动,在11年中遇丰年3个、平年7个、欠年1个。群落地上生物量季节积累动态符合Compertz曲线B_t＝B_max·e^-ea-kt,其高峰值出现在返青后的125.2～162.7天。制约群落地上生物量波动的限制因素是水分条件。建立了群落地上生物量与水热因子关系的数学模型。根据这些规律作者对畜牧业生产提出了合理建议。     

我国茸鹿育种研究进展及现代茸鹿育种探讨

综述了我国茸鹿育种自 1 958年始至今历经 42年 3个阶段 ,成绩显著 ,取得了令世界瞩目的成就     

Spatiotemporal heterogeneity of PPARγ expression in porcine uteroplacenta for regulating of placental angiogenesis through VEGF-mediated signalling

Non-infectious prenatal mortality severely affects the porcine industry, with pathological placentation as a likely key reason. Previous studies have demonstrated that peroxisome proliferator-activated receptor gamma (PPARγ) deficiency causes defects in the uteroplacental vasculature and induces embryonic losses in mice. However, its role in porcine placental angiogenesis remains unclear. In the present study, PPARγ expression was investigated in porcine uteroplacental tissues at gestational day (GD) 25, GD40 and GD70 via quantitative polymerase chain reaction (qPCR), Western blot and immunohistochemistry (IHC). Moreover, the roles of PPARγ in porcine placental angiogenesis were investigated using a cell model of porcine umbilical vein endothelial cells (PUVECs) to conduct proliferation, migration and tube formation assays in vitro and a mouse xenograft model to assess capillary formation in vivo. The results showed that PPARγ was mainly located in the glandular epithelium, trophoblast, amniotic chorion epithelium and vascular endothelium, as indicated by the higher expression levels at GD25 and GD40 than at GD70 in endometrium and by higher expression levels at GD40 and GD70 than at GD25 in placenta. Moreover, PPARγ expression was significantly downregulated in placenta with dead foetus. In PUVECs, knocking out PPARγ significantly inhibited proliferation, migration and tube formation in vitro and inhibited capillary formation in mouse xenografts in vivo by blocking S-phase, promoting apoptosis and downregulating the angiogenic factors of VEGF and its receptors. Overall, the spatiotemporal heterogeneity of PPARγ expression in porcine uteroplacental tissue suggests its vital role in endometrial remodelling and placental angiogenesis, and PPARγ regulates placental angiogenesis through VEGF-mediated signalling.