Reduced protein kinase C activity and endogenous protein phosphorylation in ethionine-induced fatty liver in cows

Protein kinase C (PKC) activity was evaluated and the phosphorylation of its endogenous substrates was explored in fatty liver induced by administration of ethionine (an analogue of methionine) to cows in order to assess the relevance of PKC-dependent phosphorylation in the development of fatty liver. PKC activity was decreased in both the cytosolic and the total particulate fractions from fatty livers, compared to the corresponding fractions from control liver. The mode of activation by the PKC cofactors (1-oleoyl-2-acetyl-sn-glycerol, 12-O-tetradecanoylphorbol-13-acetate, phosphatidylserine and Ca²⁺) was similar in both control and fatty livers, suggesting a quantitative but not a qualitative change in PKC in fatty liver. At least three substrate proteins (34 kDa, 26 kDa and 19 kDa) were found in the cytosolic fraction and their phosphorylation was reduced in fatty liver. These results suggest that impairment of the signal transduction pathway mediated by PKC is involved in the pathogenesis of fatty liver in cows.Abbreviations ATP adenosine triphosphate - EGTA ethylene glycol bis(-aminoethylether)-N,N,N,N-tetraacetic acid - NEFA non-esterified fatty acid - OAG 1-oleoyl-2-acetyl-sn-glycerol - PKC protein kinase C - PS phosphatidylserine - SDS-PAGE sodium dodecyl sulphate-polyacrylamide gel electrophoresis - TG triglyceride - TPA 12-O-tetradecanoylphorbol-13-acetate     

Pathogenic mechanisms of caprine arthritis-encephalitis virus

Goats infected with caprine arthritis-encephalitis virus (CAEV) show chronic arthritis and cachexia, which are progressive in nature. The immunopathogenic mechanisms responsible for these progressive clinical symptoms have not been fully elucidated. Various haematological and immunological parameters were evaluated in experimentally-infected goats showing typical signs of CAEV-induced disease. Infected goats showed recurrent lymphocytosis that may be due to constant presentation of antigen by infected cells of a monocyte/macrophage lineage. The serum alkaline phosphatase and -glutamyl transferase concentrations were elevated in infected goats, a characteristic of hepatic and bone disorders. All other serum chemistry parameters were similar between infected and control goats. Importantly, the serum tumour necrosis factor- (TNF-) levels were higher in infected goats. The cachexia seen in infected goats may be at least partly due to altered metabolism as a result of prolonged elevation of serum TNF- levels. Depressed natural killer cell activity was observed in infected goats and may contribute towards the establishment of a persistent infection with CAEV.Abbreviations AIDS acquired immunodeficiency syndrome - CAEV caprine arthritis-encephalitis virus - GGT -glutamyl transferase - HBSS Hanks' balanced salt solution - HIV human immunodeficiency virus - NK natural killer - PBMC peripheral blood mononuclear cells - PCR polymerase chain reaction - SAP serum alkaline phosphatase - TNF tumour necrosis factor     

Chylous effusions revisited

Varying terms and criteria have been used in the veterinary literature to characterize milky opaque pleural effusions through the years. This article addresses ideas widely repeated in the veterinary and human literature upon which time, experience, diagnostic techniques, experimental data, and improved understanding of pathogenesis have cast doubt. Topics discussed include terminology, pathogenesis of chylous and pseudochylous effusions, criteria for differentiation of chylous from pseudochylous effusions, and clinicopathologic changes associated with drainage of chylous effusions.     

禽网状内皮组织增生病病毒和马立克氏病病毒共感染对鸡的致肿瘤作用

用禽网状内皮组织增生病病毒(REV)和马立克氏病病毒(MDV)共感染肉鸡，研究这2种病毒对鸡的致瘤作用，结果表明肉鸡共感染MDV和REV后13d即可发生死亡．接种后100d死亡率达84％。死亡鸡的肝脏、脾脏、肾脏和心脏等可以形成2种外观明显不同的散在的大肿瘤结节和弥漫性的小肿瘤结节。取发病鸡的肝脏、脾脏、肾脏、心脏和腺胃等组织样品做连续石蜡切片，HE染色后发现这些脏器均存在2种不同类型的肿瘤细胞增生。对这些连续切片分别用MDV和REV的单克隆抗体进行间接荧光试验，则同1份样品存在可以与REV和MDV分别呈现阳性反应的肿瘤细胞团，结果表明REV和MDV可以在感染鸡的体内分别诱发形成肿瘤。在接种后14、21、28和42d随机采集3只鸡的全血分离MDV和REV，均可以同时分离到MDV和REV。表明REV和MDV的共感染延长了病毒血症的时间。     

内毒素介导动物急性肾功能衰竭机理的试验研究

为了阐明内毒素介导急性肾功能衰竭的机理,观察了内毒素性肾功能衰竭家兔血液凝固性变化和肾脏的病理形态学变化。与对照组家兔比较,模型组家兔血小板计数和血浆纤维蛋白原含量极显著降低(P<0 01),出血时间、凝血时间、凝血酶原时间和白陶土部分凝血活酶生成时间显著或极显著延长(P<0 05,P<0 01)。另一方面,内毒素注射在全部模型组家兔导致了弥漫性血管内凝血,71.4%的肾小球中发现了微血栓,肾小球纤维素密度指数达60 6%。此外,96.2%的肾小管上皮细胞变性坏死,84.1%的肾小管中有管型形成。对照组家兔均未发现这些病理变化。上述试验结果揭示,内毒素引发了弥漫性血管内凝血,而肾小球毛细血管内广泛形成的微血栓阻断了肾小球毛细血管血流,从而导致肾小球滤过率降低,这是内毒素介导急性肾功能衰竭的首要机理。此外,肾小管上皮细胞的变性、坏死可损害其重吸收和分泌功能,管型形成可阻塞肾小管管腔并增大肾球囊内的压力,这些也都是在内毒素介导急性肾功能衰竭发生发展过程中起重要作用的因素。     

小麦矮缩病毒引起的植株矮化与赤霉素代谢的相关性分析

【目的】由异沙叶蝉(Psammotettix alienus)传播的小麦矮缩病毒病是近年来中国西北部麦区严重发生的小麦病毒病害之一。受侵染的小麦植株严重矮化,有效分蘖减少,产量损失严重。论文旨在明确小麦矮缩病毒(Wheat dwarf virus,WDV)侵染小麦植株后矮化症状形成与赤霉素代谢调控的关系,为该病害的防治打下基础。【方法】以小麦品种扬麦12为试验材料,以异沙叶蝉为传毒介体饲毒后转移到1叶期的健康幼苗(3头/株)上进行传毒,同时以无毒异沙叶蝉取食健康幼苗为对照。根据试验需要,不同时间取样备用。为保证试验的准确性,经PCR检测为阳性的作为处理组试验材料;采用间接酶联免疫吸附(ELISA)法,利用植物赤霉素(GA3)试剂盒测定分析侵染第21天取样的小麦叶片赤霉素含量;将带毒条沙叶蝉接种的小麦苗分为两个平行处理组,接种后第7天分别用GA3(浓度为50 mg·L-1)和H2O进行叶面喷施处理,每隔一周处理一次。以无毒叶蝉接种后长势一致的小麦苗作为对照组,根据株高统计结果分析外施赤霉素对受侵染小麦植株的表型变化;以山羊草(Aegilops tauschii)的内根-贝壳杉烯合成酶(ent-kaurene synthase-like 3,KSL3)的基因编码区序列为参考基因设计引物(KSL3-F:5′-ATGATGGTGAATCCGCCGC-3′;KSL3-R:5′-TTAATGGTTGATCTTTGTTT-3′),对扬麦12的KSL3进行克隆和序列分析;分别取接种后7、14和21 d的小麦植株叶片,提取RNA后反转录,以克隆得到的Ta KSL3基因序列设计引物(Ta KSL3-F:5′-GAGACATGTGCCATGGCGTTC-3′;Ta KSL3-R:5′-CGTGTCACTCAGATCGGTGGAG-3′),选择小麦翻译延伸因子1A(EF-1α)作为内参基因,利用荧光定量PCR方法分析赤霉素代谢相关基因的转录水平。【结果】经ELISA检测发现,接种21 d的发病植株赤霉素含量与健康植株相比降低了28.9%;通过施用浓度为50 mg·L-1的赤霉素后,发病植株的平均株高相比对照组显著增加35.9%;采用同源克隆得到了完整的小麦赤霉素合成途径关键酶KSL3的编码区序列,长度为1 827 bp,编码608个氨基酸,BLAST比对分析发现该DNA序列与山羊草KSL3编码区序列相似度为85.2%。经荧光定量检测发现受小麦矮缩病毒侵染后小麦KSL3表达量显著下降,接种14 d降低为对照组的35.7%,21 d降低为对照组的9.6%。【结论】小麦矮缩病毒的侵染导致赤霉素合成途径关键酶的表达量降低,可能使赤霉素合成受阻,赤霉素含量降低引发受赤霉素调节的细胞生物学过程异常,从而诱导矮化症状形成。研究结果为揭示小麦矮缩病毒侵染的致病机理和病害防控打下了基础。     

核桃黑斑病综合防治技术

通过对核桃黑斑病发病侵染规律及原因分析,采取加强水肥土管理,合理修剪,减少密蔽,改善通风透光条件;谨防蛀果害虫;越冬管理;药剂防治的综合措施防治,可有效控制核桃黑斑病的发生危害。     

桑椹菌核病研究进展

桑椹菌核病是由3种子囊菌真菌引起的相似症状病害的统称,为果桑生产中的毁灭性真菌病害,严重制约果桑产业的发展。这3种病原菌同为死体营养型病原菌,其侵染手段多样,侵染机制复杂。由于3种病原菌在人工培养上存在不同程度的困难(桑实杯盘菌和肉阜状杯盘菌难培养,核地杖菌在人工培养基上不能完成生活史),在一定程度上限制了病原菌的研究。本文综述了桑椹菌核病的侵染循环、病原菌、病害流行、病原菌与寄主互作等方面的研究进展,并对未来的研究进行了展望,以期对桑椹菌核病的深入研究提供参考。     

苹果抗轮纹病机制研究进展

在中国引起苹果轮纹病的病原菌为葡萄座腔菌（Botryosphaeria dothidea）,其主要通过自然孔口直接侵染苹果,并分泌细胞降解酶等使苹果组织降解以促进病菌的进一步侵染,而苹果可通过增强细胞壁的木质化、释放抗菌化合物以及产生免疫蛋白等抑制病菌。通过对苹果轮纹病的危害及病原菌种类、病菌侵染机制、苹果的抗性机制等方面的详细综述,为有效防治苹果轮纹病提供理论依据。