大型猪场传染病流行的新特点与免疫程序设计

当前大型猪场疫病流行的新特点有九大类,主要是防疫好口蹄疫、猪瘟、蓝耳、伪狂犬、乙脑、细小病毒及气喘病等.猪群只要疫苗免疫得当,加上合理的药物保健程序,控制好一些继发感染(主要是副猪嗜血杆菌、传染性胸膜肺炎、弓形体、附红细胞体等),猪群则会处于较好的保护状态下,没有必要做很多的疫苗.     

湘黄鸡马立克氏病(MD)临床免疫方法及效果研究

通过本次临床试验得出；湘黄鸡马立克氏病(MD)的免疫以CVI988 HVT苗或Rispens CVI988苗为最佳效果，可使该病的临床发病率分别控制在1．33％和1．67％以下，致瘤率为34％左右．用中药进行预防达不到免疫的效果．所以认为用血清I型疫苗是目前衡阳地区湘黄鸡马立克氏病(MD)的唯一有效的免疫方法．     

高速冲击下多胞材料细观结构中波传播规律

目的 获取安全防护结构中细观多胞材料在高速冲击下的波传播规律.方法 采用基于3D-Voronoi细观多胞结构数值仿真和基于最小二乘法的局部应变梯度法,研究细观多胞结构在高速冲击下的冲击波波阵面传播规律.通过细观多胞结构数值仿真提取的位移场数据,结合局部应变梯度法得到界面清晰的冲击波波阵面.结果 冲击端和支撑端分别诱发右行和左行冲击波波阵面.冲击波波阵面传播过程分为3个阶段,即冲击端诱发右行冲击波阶段、支撑端诱发左行冲击波且未压缩区刚性向右运动阶段和右行冲击波压缩区域与未压缩区域一体刚性向右运动阶段.通过冲击波波速的演化规律研究,分别获取了右行和左行冲击波波阵面的拉氏位置和拉氏波速,通过严格理论推导解释了右行冲击波波阵面具有恒定减加速度的结论.最后对冲击波波阵面划分阶段的合理性进行了验证.结论 基于3D-Voronoi细观多胞结构数值仿真和基于最小二乘法的局部应变梯度法可以获取界面清晰的冲击波波阵面,细观多胞结构在高速冲击下的冲击波波阵面传播规律可为安全防护结构的设计和研究提供参考依据.     

加氯消毒过程中纯细菌物质生成消毒副产物研究

按照UFC方法对水体中3种常见细菌Acinetobacter junii、Staphylococcussciuri和Escherichia coli进行纯细菌加氯消毒处理,同时考察水中溴离子对纯细菌物质生成DBPs的影响.结果表明,3种细菌均为DBPs前体物,加氯消毒生成的DBPs除水合三氯乙醛(CHD)外,生成的三卤甲烷(THMs)物质主要为氯仿(TCM),卤乙腈(HANs)物质主要为二氯乙腈(DCAN).氯仿的生成量与细菌物质TOC浓度无明显关系,但HANs和CHD生成量均随细菌TOC浓度增大而增加.其中革兰氏阳性细菌Staphylococcus sciuri生成的DCAN和CHD比革兰氏阴性细菌Acinetobacter junii和Escherichia coli生成的要高,说明细胞壁的化学组分可能是DCAN和CHD生成的影响因素之一.Escherichia coli细菌反应液中溴离子(Br-)存在时,除生成CHD、TCM及DCAN外,THMs和HANs中的溴代种类CHBr3随Br-增多而持续增加,相反TCM持续减少.当Br-浓度为4mg.L-1时,TBM浓度增至最高127.9μg.L-1;HANs和CHD生成量随Br-浓度增加先有所增加,随后持续降低至低于检测限;Br离子存在时THMs为主要DBPs种类.     

基于元胞自动机的极端降雨下地铁疏散模拟*

为研究地铁系统在极端降雨灾害下的人员疏散过程,分析人员疏散过程影响因素和改善方法,将数值模拟方法与模糊逻辑理论相结合,在传统元胞自动机疏散模型中引入人员疏散行为选择机制,模拟地铁隧道遭受洪水侵入以及采取改善措施后的疏散情况。研究结果表明:引入人员疏散行为选择机制可以较真实地模拟极端降雨下受限空间中的人员疏散过程;采取改善方案后,人员被迫改变疏散行为的比例下降53.95%,人群疏散安全度由0.201提升至0.633;当采取与防洪能力不适应的疏散平台高度时,疏散安全度较采取合理设施时平均下降30%且差异较大;硬件设施满足安全度达到0.6为宜,按照最终安全度为1设计疏散方案,可使硬件设施设计与疏散方案制定更加合理配套。研究结果可为地铁系统防洪设计与管理提供参考。     

持久性有机污染物致胰岛素抵抗及其潜在病理机制

胰岛素抵抗综合症目前在全世界以惊人的速度增长,成为21世纪公共健康的严重挑战。多例流行病学调查结果已经显示持久性有机污染物与胰岛素抵抗的关联。胰岛素信号传递受损是胰岛素抵抗的本质原因。考察机制发现,可在机体脂肪组织中贮存积累的持久性有机污染物,如二噁英、多氯联苯、溴代阻燃剂、有机氯农药等,可干扰细胞内受体如环芳烃受体、过氧化物酶体增殖物激活受体、导致氧化损伤、线粒体功能障碍并通过慢性炎症介质TNFα的释放及其相关信号调控;进而可能阻扰胰岛素信号传递中关键蛋白InsR或IRS-1/2正常磷酸化,导致胰岛素抵抗。     

长期饲喂钬对鲤鱼非特异性免疫酶活性的影响

以鲤鱼为研究对象,进行为期60 d的饲喂试验,研究了硝酸钬对其非特异性免疫的影响。结果表明:与对照组相比,在实验剂量范围内,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)在肝脏中呈先升高后降低的趋势,SOD、GSH-Px酶活性在20 mg·kg~(-1)时,升高显著(P0.05),三者在65 mg·kg~(-1)时都被显著抑制(P0.05);在肾中都被诱导,在65 mg·kg~(-1)升高显著(P0.05)。肝肾中丙二醛(MDA)含量都变化不显著(P0.05)。抗超氧阴离子自由基、抑制羟自由基能力和单胺氧化酶(MAO)活性都降低,且在65 mg·kg~(-1)时降低显著(P0.05或P0.01)。因此,在饲料中添加稀土元素钬20、42、65 mg·kg~(-1),能够影响非特异性免疫力,且鲤鱼肝组织比肾脏反应更敏感。     

The plausibility of a role for mercury in the etiology of autism: a cellular perspective

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.     

Electron microscopy documenting the cellular metabolic fate of Zn IONS∗

In vertebrates and invertebrates Zn exist as complexed compounds with metallothioneins. However, its cellular level effects and metabolic fates are scantly documented. In the elucidation of this fact, EM results on hepatic cellular alterations in fish under lethal dose exposure at 4.0 ppm over a week is illustrated.

A large number of lysosomes in hepatic cells prevailed on exposure to Zn in its sulfate form. Evidently, due to metal compound stress and cellular damage lysosomal activity is augmented. The lysosomes harboured digestible material, presumably the aforementioned substrates. Contrary to it, fat droplets prevailed while glycogen depletion is noticeable. Unlike the effects of Hg, the nuclei were normal with granular chromatin and prominent nucleoli. However, the mitochondria contained some small intramitochondrial bodies. Similar to the effects of Hg, the cell membrane remained intact.

In vivo enzymatic studies indicated augmentation in catalase, acid‐ and alkaline‐phosphatases, while glucose‐6‐phosphatase is inhibited. However, only alkaline‐ and glucose‐6‐phosphatases are inhibited under in vitro conditions.

Thus, it is evident that Zn enhances cellular bioenergetic requirements culminating in glycogen depletion owing to stress, concomitantly envisaging inhibition of oxidative phosphorylation in the electron transport system.     

缺氧对贝类的胁迫效应及对其免疫系统的影响

基于缺氧对贝类养殖的危害,从贝类免疫系统角度总结了近年来围绕缺氧胁迫对其细胞免疫和体液免疫系统的相关因子影响的研究。从缺氧对与细胞免疫功能相关的血细胞总数(THC)、吞噬活性和细胞活性氧(ROS)含量、以及参与体液免疫的溶酶体酶、抗氧化物酶、抗氧化因子、酚氧化酶等多种免疫因子的影响,概括了缺氧对贝类免疫系统影响的一般规律。本文不仅能为衡量贝类所在水域的环境变化提供科学依据,还能为围绕贝类在缺氧胁迫下生理适应性机制的相关研究奠定基础。