TGF-β1和Collagen-Ⅲ在牦牛感染细粒棘球蚴肝纤维化中的表达

研究转化生长因子β1(TGF-β1)、Ⅲ型胶原(Collagen-Ⅲ)在牦牛感染细粒棘球蚴导致肝纤维化中的表达及其意义。收集西藏地区40例细粒棘球蚴感染的牦牛肝组织和血清样本,同时收集未感染的肝组织和血清进行对照。采用苏木素-伊红(HE)染色法和天狼猩红染色法观察牦牛肝脏病理变化和肝纤维化程度;酶联免疫吸附试验(ELISA)和免疫组化法(IHA)分别检测肝组织和血清中TGF-β1、Collagen-Ⅲ的表达水平及分布;RT-PCR检测肝细胞内TGF-β1和Collagen-Ⅲ基因mRNA的相对表达水平。HE染色和天狼猩红染色结果显示,与未感染细粒棘球蚴病牦牛肝组织相比,感染棘球蚴周围的肝组织肝界板细胞破坏,呈虫蚀状,感染肝组织外围纤维化,细粒棘球蚴寄生的牦牛肝脏组织引起组织增生,纤维化;ELISA结果显示感染细粒棘球蚴牦牛血清样中细胞因子TGF-β1、Collagen-Ⅲ的含量明显超过未感染组(P<0.05),且免疫组化的结果显示它们的表达主要存在于细胞基质中;RT-PCR显示细粒棘球蚴感染肝组织中TGF-β1、Collagen-Ⅲ的mRNA相对表达量超出未感染组(P<0....     

试管孵化六钩蚴制备抗原,免疫羔羊预防细粒棘球蚴感染的效果

不使绵羊感染细粒棘球蚴,就要着重在细粒棘球绦虫生活史的两个阶段,即包囊形成前期和后期来预防。用细粒棘球蚴包囊制备的抗原所产生的免疫,对包囊形成后期起预防作用,阻止包囊生长,钙化虫体。但是,对包囊形成前期阶段,无免疫力,象对照组一样,形     

细粒棘球蚴感染对小鼠肝纤维化的影响

采用门静脉注射法建立细粒棘球蚴BALB/c小鼠高、低剂量(2 000、500原头蚴)肝脏模型,1、3及8个月后采集小鼠肝脏标本,Masson染色鉴定纤维化程度,免疫组化法检测α-平滑肌肌动蛋白(α-SMA)和Ⅲ型胶原蛋白(CollagenⅢ)的表达。Masson染色结果显示,病灶边缘带肝脏组织的胶原染色比正常肝脏组织明显增多并形成了致密的环状结构,在囊壁周围广泛分布,且与对照组相比,试验组纤维化程度具有统计学差异(P<0.01);免疫组化(α-SMA)染色显示,试验组小鼠肝脏中α-SMA主要表达在炎症浸润及肉芽组织增生区域,与对照组相比,试验组α-SMA的表达量具有统计学差异(P<0.01);免疫组化(CollagenⅢ)染色结果显示,正常肝脏组织中CollagenⅢ主要表达在血管周围,而在低剂量和高剂量细粒棘球蚴感染组小鼠肝脏中主要表达在病灶周围,且与对照组相比,不同时间点高剂量组和低剂量组具有统计学差异(P<0.001)。综上细粒棘球蚴感染小鼠可导致肝纤维化,且不同时间点不同剂量细粒棘球蚴感染小鼠肝脏中α-SMA、CollagenⅢ的表达水平随着胶原面积的增加而升...     

棘球蚴病病理及形态图

肝脏最易受棘球蚴的传染,受染之肝常甚肿大,显微镜下检查,则见棘球蚴周围有一层纤维组织,其中有嗜酸性的白血球及其它种类的炎性细胞之侵润,棘球蚴周围及附近之肝细胞则呈压迫性萎缩。     

青海玉树牦牛棘球蚴病的感染情况调查

棘球蚴病(俗称包虫病)是由寄生于犬狼等野生食肉类动物小肠内的细粒棘球蚴绦虫的幼虫所引起的.幼虫中绦期寄生在多种食草动物和人的肝肺等脏器中形成包囊,由于棘球蚴的类型不同,形成的包囊数量和形状也不同,此病是严重威胁食草动物和人类健康的人兽共患寄生虫病.呈世界性分布.我国是棘球蚴病发病率最高的国家之一,尤其是西北及青藏高原牧区生产生活方式及防病知识的欠缺,造成了动物和人畜间棘球蚴病的高度流行.为了摸清青海省玉树县放牧绵羊棘球蚴病的感染情况和危害程度,笔者于2008年11月进行调查,报道如下.     

共和地区绵羊棘球蚴病调查

为了掌握共和地区绵羊棘球蚴病的感染情况 ,为防治工作提供依据 ,笔者于 1 999年 9～ 1 0月利用海南州肉联厂屠宰检疫之机 ,对共和县收购的部分绵羊 (铁盖乡、英德尔乡、廿地乡、黑马河乡、恰卜恰乡、曲沟乡 )进行了调查 ,检查方法肉眼观察和用手触摸。检查结果 :棘球蚴病羊的肝、肺表面包囊数一般在 2个以上 ,有的达 40个 ,大的有鹅蛋大 ,小的豌豆大 ,感染严重的羊肝 ,肺全部被棘球蚴包囊覆盖 ,详见附表。附表 :绵羊棘球蚴病感染情况调查乡调查羊数 (只 )感染数 (只 )感染率 ( % )包囊数 (个 )平均感染强度感染范围肝脏感染数 (个 )肺脏感…     

绵羊细粒棘球蚴全血金标渗滤检测方法的建立

为建立一种快速、高效的诊断家畜细粒棘球蚴病方法,提取绵羊细粒棘球蚴包囊新鲜囊液,盐析囊液抗原,点样于硝酸纤维膜,以胶体金-驴抗羊IgG和胶体金-兔抗鼠IgG为检测标记物,采用垂直流渗滤装置检测绵羊与人工感染细粒棘球蚴小鼠血清和全血特异性抗体。患病绵羊阳性血清及全血检出率在90.91%~94.4%,细粒棘球蚴感染小鼠血清及全血检出率均为100%;细粒棘球蚴阴性羊血清和全血假阳性率为4.00%~4.59%;与脑多头蚴病血清交叉反应率为28.57%(2/7)。研究结果表明细粒棘球蚴全血金标渗滤法(DIGFA)可应用于绵羊棘球蚴病的诊断与检疫。     

新疆博州牛、羊棘球蚴病的调查与分析

棘球蚴病（包虫病）是人畜共患寄生虫病，成虫寄生犬、狼等肉食动物的小肠，绦蚴寄生在人、畜的肝、肺。棘球蚴病严重危害人体健康和畜牧业发展。新疆博州是棘球蚴病危害的重灾区，据《博州动物疫病志》记载：1988年全州羊的平均感染率为88．73％，牛为91．1％，感染强度羊肝为1—247个包囊，羊肺为1～47个包囊；牛肝为7～89个包囊，牛肺为1—2个包囊；此后再未对本病进行过调查。2004年4月～5月。我们再次对本病在我州的感染情况进行了调查，现将结果报告如下。     

新疆和静县绵羊细粒棘球蚴流行株基因分型研究

为了解新疆和静县绵羊细粒棘球蚴病的感染情况及流行株基因分型,对和静县屠宰场的1 115只1岁以上绵羊的细粒棘球蚴病感染情况进行调查和统计,并利用PCR技术对包囊病灶进行了基因分型鉴定。结果表明:有88只绵羊脏器表面发现棘球蚴包囊,感染率为7.89%(88/1115),其中来自农区的感染率为3%(10/331),来自牧区的感染率为9.9%(78/784)。通过线粒体细胞色素氧化酶基因1(mtCO1)特异性引物对剖检的感染病料进行PCR扩增、克隆、测序和NCBI中的Blast比对,发现新疆和静县绵羊细粒棘球蚴流行株基因型均为G1型。本研究为和静县绵羊细粒棘球蚴病的防控提供了科学依据。     

民和县屠宰羊棘球蚴感染情况调查

细粒棘球蚴病是由细粒棘球绦虫(Echinococcus granuloslls)的幼虫棘球蚴(echinococcus)寄生于哺乳动物脏器所引起的疾病。其成虫寄生于犬、狼、狐等肉食动物的小肠中,幼虫中绦期主要寄生在多种动物和人的脏器中,形成包囊俗称包虫     

Morphologic aspects and morphogenesis of blood cysts on canine cardiac valves

We investigated retrospectively the morphologic aspects of blood cysts of the atrioventricular valve in eight Beagle dogs and clarified the morphogenesis of the lesions. Study of serial sections revealed that the cysts communicate with the blood vessels; however, they showed no connection with the valve surface. Immunohistochemically, the thin endothelium of the lesions showed positive staining for factor VIII-related antigen. Histologic studies of a variety of sizes of blood cysts revealed four basic stages of blood cyst formation: 1) initially, the involved blood vessel undergoes only a slight enlargement that is not grossly detectable; 2) next, the vessel becomes moderately or markedly dilated and contains a large number of erythrocytes. The changes of this stage are macroscopically detectable; and 3) then, blood flow is arrested partly in the cystic lesion, followed by degeneration and necrosis of the cyst. At this third stage, fibrous tissue or dense collagenous connective tissue is usually seen surrounding the cyst; 4) and finally, metaplastic bone is formed within the lesion. Colloidal carbon infusion into the valves of normal canine hearts revealed the presence of an extensive, dense arrangement of blood vessels in the septal leaflet of the tricuspid valve, which usually is the recognized site to develop blood cysts.     

CD44 expression in the bile duct epithelium is related to hepatic fibrosis in nonalcoholic steatohepatitis rats induced by a choline-deficient,methionine-lowered, L-amino acid diet

Nonalcoholic steatohepatitis is a lifestyle-related disease and an increasing threat worldwide. Hepatic fibrosis, which results from chronic hepatic diseases including nonalcoholic steatohepatitis, is closely correlated with mortality among hepatic lesions, such as steatosis and inflammation. Thus, it is important to identify factors that can serve as diagnostic and therapeutic targets for hepatic fibrosis. In this study, we examined the function of CD44 in the development of hepatic fibrosis in choline-deficient, methionine-lowered, L-amino-acid diet-fed rats, especially with respect to the proliferation of bile duct epithelium. Male Fischer 344 rats were fed a choline-deficient, methionine-lowered, L-amino-acid diet for 2, 4, 13, or 26 weeks. This diet decreased the body weight; increased the levels of serum parameters indicating liver injury, such as aspartate and alanine aminotransferase; upregulated inflammation- and fibrosis-related gene expression in the liver; and resulted in the development of hepatic lesions, including fatty changes in hepatocytes, inflammatory cell infiltration, and fibrosis. Hepatic hyaluronan was synthesized and deposited in the liver tissue. The expression of both CD44 mRNA and protein was significantly increased throughout the experimental period. CD44 protein was observed in some of the bile duct epithelium, around which hyaluronic acid was deposited, and these bile duct lesions were concordant with the area of hepatic fibrosis. Thus, CD44 expressed in the bile duct epithelium may be a target for controlling nonalcoholic steatohepatitis-related hepatic fibrosis.     

Effect of Luteolin on Blood Indexes,Liver and Kidney in Mice with Acute Mercury Poisoning

To study the effect of luteolin on blood indexes,liver and kidney in mice with acute mercury poisoning,28 mice were randomly divided into four groups:Control group (intraperitoneal injection 0.9% saline),luteolin group (lavage 100 mg/kg luteolin),mercuric chloride group (intraperitoneal injection 4 mg/kg mercury chloride) and mercury chloride+luteolin group (intraperitoneal injection 4 mg/kg mercuric chloride,lavage 100 mg/kg luteolin).The activities of ALT in serum,AST,CREA and BUN contents,blood WBC,RBC,HGB content and GSH and MDA contents of liver tissue were detected.Morphological changes of liver and kidney tissues were observed.The results showed that compared with the control group,the activities of ALT and AST of mercuric chloride group were extremely significantly increased (P < 0.01),serum CREA,BUN,blood WBC and liver tissue MDA contents were significantly increased (P < 0.05) while blood RBC,HGB and liver tissue GSH contents were significantly decreased (P < 0.05).Liver,kidney pathological changes were obviously.Compared with mercuric chloride group,the activities of ALT,AST in serum,CREA,BUN,blood WBC and liver tissue MDA contents of mercuric chloride+luteolin group were significantly decreased (P < 0.05),while blood RBC,HGB and liver tissue GSH contents were significantly elevated (P < 0.05).Liver,kidney pathological changes were attenuated obviously.The poisoning were characterized by inflammation and the occurrence of anemia when acute mercury poisoning occurred,liver and kidney showed different degrees of injury in mice.Luteolin could reduce the toxic effects of acute mercury poisoning on blood,liver and kidney.     

木犀草素对急性汞中毒小鼠血液生化指标、肝脏及肾脏的影响

试验旨在研究小鼠急性汞中毒后血液、肝脏及肾脏的中毒表现及木犀草素对急性汞中毒小鼠血液指标、肝脏及肾脏的影响。将28只小鼠随机分成4组,分别为对照组(腹腔注射0.9%生理盐水)、木犀草素组(灌胃100 mg/kg木犀草素)、氯化汞组(腹腔注射4 mg/kg氯化汞)和氯化汞+木犀草素组(腹腔注射4 mg/kg氯化汞,灌胃100 mg/kg木犀草素)。检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,肌酐(CREA)和尿素氮(BUN)水平,血液白细胞(WBC)、红细胞(RBC)和血红蛋白(HGB)水平及肝脏组织谷胱甘肽(GSH)和丙二醛(MDA)水平,并观察肝脏、肾脏组织形态学改变。结果显示,与对照组相比,氯化汞组的血清ALT、AST活性极显著升高(P < 0.01),血清CREA、BUN,血液WBC及肝脏组织MDA含量均显著增加(P < 0.05),血液RBC、HGB及肝脏组织GSH水平均显著降低(P < 0.05),肝脏、肾脏病理变化明显。与氯化汞组相比,氯化汞+木犀草素组的血清ALT、AST活性,CREA和BUN,血液WBC及肝脏组织MDA含量均显著降低(P < 0.05);血液RBC、HGB及肝脏组织GSH含量均显著升高(P < 0.05),肝脏、肾脏病理变化减轻。小鼠急性汞中毒后,其中毒表现为炎症和贫血的发生及肝脏、肾脏不同程度的损伤,木犀草素可减弱急性汞中毒小鼠血液、肝脏和肾脏的毒性作用。     

不同剂量环磷酰胺对昆明小鼠肝肾组织的损伤作用研究

为研究不同剂量的环磷酰胺对小鼠肝肾组织及功能的损害程度,试验选取40只5周龄健康雌性昆明小鼠,随机分为5组,除对照组外,其余4组小鼠连续3 d分别腹腔注射40、80、120及160 mg/（kg·BW）环磷酰胺溶液,注射后第7天采集肝脏和肾脏组织样品及血清,制备石蜡组织切片及透射电镜切片,观察肝脏和肾脏的组织学变化,检测血清中甘胆酸（CG）、胆碱酯酶（ChE）、血清前白蛋白（PA）、总胆汁酸（TBA）、谷丙转氨酶（ALT）、谷草转氨酶（AST）、尿素氮（BUN）、血清肌酐（SCr）、尿酸（UA）含量/活性。结果显示,环磷酰胺可引起小鼠肝肾组织病理损害,呈剂量依赖性,肝脏比肾脏更早出现损伤。石蜡切片及透射电镜切片观察结果显示,环磷酰胺对肝脏的毒性作用主要表现在肝索紊乱、肝血窦扩张、微胆管淤胆、门管区及中央静脉周围炎性细胞浸润及纤维增生、组织间出血、肝细胞出现脂肪变性及气球样变性,凋亡及坏死细胞增多。肾脏组织损伤主要表现在出血及纤维增生,肾小管上皮细胞胞浆空泡样变、线粒体损伤、核固缩,上皮细胞基底膜增厚。环磷酰胺对膀胱的损害不严重。与对照组相比,40~160 mg/（kg·BW）剂量组小鼠血清中ChE活性及PA水平,120~160 mg/（kg·BW）剂量组AST活性,80~160 mg/（kg·BW）剂量组BUN水平及80 mg/（kg·BW）剂量组UA水平均显著升高（P<0.05）;其余生化指标与对照组差异不显著（P>0.05）。以上结果表明,环磷酰胺注射剂量在80~120 mg/（kg·BW）时可引起昆明小鼠肝脏和肾脏组织及细胞明显的病理损伤。该研究结果可为选择合适的环磷酰胺注射剂量用以制备动物肝脏免疫抑制模型提供试验依据。     

活血疏肝健脾汤对犬实验性肝损伤血清学和组织学影响

观察活血疏肝健脾汤对 CCl4诱导的犬肝纤维化的血清学指标和病理组织学变化影响 ,以探讨中药复方防治犬肝纤维化的机制。采用皮下多点注射和口服 CCl4菜籽油的方法制作动物实验性肝损伤模型。对照组仅给予 CCl4,中药组在给予 CCl4的同时口服中药复方煎剂 ;西药组在给予 CCl4的同时口服秋水仙碱。每周采集血样测定犬血清中 AL B、AST、AL T与羟脯氨酸 ( HYP)含量 ;8周后处死动物 ,观察肝脏组织的病理学变化 :1从试验开始到第 8周结束 ,对照组犬血清中的 AL B降低 ,AL T、AST升高 ,而中药组犬在试验的前 5周 ,血清白蛋白含量明显降低 ,自第 6周开始回升 ,第 7周时升至试验前的水平 ,血清 ALT和 AST活性无明显变化 ;2中药组犬的血清 HYP含量从第 5周开始显著高于对照组 ( P <0 .0 5 ) ,试验结束时其肝脏胶原含量显著低于对照组 ( P <0 .0 1) ;3对照组犬肝细胞变性、坏死 ,胶原纤维大量增生 ,中药组犬胶原纤维数量明显少于对照组。活血疏肝健脾汤具有减轻 CCl4对肝脏的损伤 ,保护肝细胞的功能和抗肝纤维化的作用     

Histopathology of Five Species of Didymocystis spp. (Digenea: Didymozoidae) in Cage-reared Atlantic Bluefin Tuna (Thunnus thynnus thynnus)

The first parasitological examinations of Atlantic bluefin tuna Thunnus thynnus thynnus reared in the Adriatic Sea revealed high numbers of different digenean trematodes, belonging to family Didymozoidae. Five species were the most frequently isolated: Coeliodidymocystis, abdominalis, Didymocystis wedli, Koellikerioides internogastricus, K. intestinalis and K. apicalis. Parasites were isolated from gills, gill rakers, intestine, serosa of pyloric caeca, and inner layers of the fundic region of stomach, encysted in pairs in connective tissue capsules originating from host tissue. Gross pathology revealed no pathological changes. Histological alterations comprised tissue reaction resulting in lymphocyte infiltration and formation of a collagenous envelope around the parasite cysts; the intensity of observed reaction depended on the size of the cyst and on the tissue infected. The most notable changes were observed in the intestine under provocation by K. intestinalis, while the most potentially pathogenic didymozoid under fish rearing conditions is D. wedli, which if present in high abundance can induce secondary bacterial infections.     

犬瘟热自然病例脱髓性脑病发生的机理

为了进一步调查脑组织的髓鞘脱失与神经胶质细胞等成份的关系,用12只犬瘟热自然病例通过病理组织学和免疫组织化学染色法进行了本试验.结果表明:髓鞘脱失部位的脑组织伴有明显的血液循环障碍,即淤血、水肿、血栓形成和弥漫性血管内凝血;少突胶质细胞发生代谢紊乱和凋亡;用抗犬瘟热病毒(CDV)抗体染色,星状胶质细胞呈现强阳性反应;用抗GFAP染色,纤维性星状胶质细胞在脱髓区呈较强阳性反应,用TUNEL染色可检出发生凋亡的星状胶质细胞;一些室管膜细胞也被CDV感染,许多含有包涵体币口凋亡的室管膜细胞在脑室壁被发现;少数神经元变性和皱缩,其核发生浓缩.据此认为,脑组织的髓鞘脱失主要与血液循环障碍和少突胶质细胞的代谢紊乱及凋亡有关;脑组织的髓鞘脱失是许多病因共同作用的结果,并非是一种病因所致.     

大肠杆菌病患鸡肝、脾结构的病理学研究

为了更好地了解大肠杆菌病患鸡肝、脾结构的病理变化,从云南省昆明地区养鸡场采集发病鸡,通过对其进行细菌分离鉴定,确诊为感染鸡大肠杆菌病后,采集发病鸡的肝、脾等制作组织切片,显微观察其病理变化。结果发现,肝脏组织的病理学变化主要为肝组织发生水肿、凝固样坏死,病变严重区域发生玻璃样变;脾组织的病理学变化主要为脾脏组织间隙增大,脾脏淋巴细胞稀疏,脾组织中间质细胞发生增生,出现大量长杆状细胞,脾组织中淋巴细胞出现皱缩,吞噬细胞数量增多。     

Clinico-pathological studies in cattle experimentally infected with Taenia saginata eggs

Calves 1-2 months old were experimentally infected with eggs of Taenia saginata and clinical and haematological deviations, development and distribution of cysticerci and pathological changes were recorded. The calves infected with 5,000, 10,000 or 50,000 eggs showed an increase in pulse and respiratory rates. The animals that received 50,000 eggs had significantly increased pulse (p < 0.05) and respiratory rates (p < 0.005). The symptoms were more severe in young, 30-day-old calves infected with 50,000 eggs. Haemoglobin concentration, haematocrit values and red blood cell count decreased, but white blood cell count increased slightly. Lymphocytes and eosinophils also increased up to 88% and 14% (p < 0.05), respectively. Most of the cysticerci were not fully formed 1 month post-infection, but at 2 months the cysts were fully mature and at 4 months, some cysts had degenerated. There was no uniform pattern of distribution of cysticerci in the body of infected calves, but the most commonly affected sites were masseter and heart muscles, followed by diaphragm, tongue and other skeletal muscles. The maximum concentration of 8-14 cysticerci per 10 g of tissue was recorded in masseter muscles and heart. The affected parts revealed tissue reactions that included pressure atrophy, necrosis and fibrosis. Microscopically, the lesions comprised infiltration with lymphocytes, plasma cells, eosinophils and macrophages, fibrosis, necrosis and calcification. The tissue reaction was severe in calves infected with 50,000 eggs. The severity of clinical signs, haematological and pathological changes depended mostly on the age of the animals and dose of infection.