小熊猫犬瘟热继发大肠杆菌的诊治

1病理学诊断心外膜疏松、水肿,毛细血管扩张、充血、出血,心肌纤维变性,肌横纹不清,胞浆均质红染。肝小叶中央静脉扩张瘀血,肝细胞体积增大,发生“气球样”病变,严重者发生破裂溶解,肝窦扩张瘀血。脾窦扩张瘀血、出血,白髓发生凝固性坏死。肺支气管上皮变性、坏死、脱落,管腔和肺泡腔内充满大量黏液和各种细胞,在部分上皮细胞的胞浆内可见嗜酸性的球形包涵体。肺泡壁增厚,毛细血管扩张、充血。肾小球肿大,网状内皮细胞增生,肾小囊内充满红细胞和浆液。肾小管上皮细胞肿胀,发生颗粒变性,甚至坏死。间质内可见局灶性的出血和炎症细胞的浸润,呈…     

猪繁殖障碍与呼吸道综合征的组织病理学研究

作者对广东部分猪场确诊为猪繁殖障碍与呼吸道综合征（PRRS）的病例，通过病理切片观察发现，肝灶性充血，呈空泡样变性，核内有包涵体，巨噬细胞周边有含铁血黄素；肺充血严重，肺泡面积显著缩小，血管壁变薄，毛细血管内皮细胞肿胀，有少量含铁血黄素颗粒出现；淋巴结皮髓质界限不清楚，细胞排列松散，以网状细胞增生为主，巨噬细胞有核内包涵体出现；肾小球扩张淤血，肾小管管腔狭窄，近曲小管细胞肿胀并有颗粒变性；心组织无明显病理变化。     

实验性家兔蜱传回归热病理形态学观察

向家兔腹腔中注入含蜱传回归热螺旋体血液０．８～１．０ｍＬ。１０ｄ后全部处死，剖检发现其内脏器官均普遍充血、肿大，尤以肝脾为著。镜下各实质器官细胞浊肿，有较多淋巴细胞浸润和散在点状出血，其特征性病变是网状内皮细胞增生和形成肉芽肿结节     

2例藏獒犬传染性肝炎的诊断

为了对两例疑似感染犬传染性肝炎的藏獒进行诊断和分析,研究藏獒的犬传染性肝炎的病理特征,试验通过快速检测试纸卡、解剖学和组织学方法进行诊断。结果表明:两例病犬的病料经犬传染性肝炎快速诊断试剂盒检测,结果犬传染性肝炎均为阳性。解剖学观察,病犬皮下均有不同程度的水肿,多器官有充血、出血,胃、肠、胆囊和横膈膜出血明显。肝脏肿大,淤血,呈紫黑色,表面有浅灰色针尖状病灶;胆囊肿大,胆汁较黏稠,胆囊壁增厚,浆膜有纤维素样渗出物。组织学观察,肝脏有坏死灶,肝细胞肿胀,有明显的包涵体,肝窦萎缩;胆囊上皮细胞变性、坏死和脱落,固有层水肿,黏膜肌层萎缩变形;大脑血管内皮细胞增生,核内有包涵体,血管周围淋巴鞘出血;脾脏被膜和小梁充血、出血,红髓、白髓坏死,中央动脉内皮细胞肿胀,脾静脉窦淤血。说明藏獒患犬传染性肝炎能够引起全身性病变。     

鸡马立克氏病（MD）与淋巴细胞糖皮质激素受体（GR）相关性研究：II.…

运用ＢＡ免疫组化技术与ＨＥ染色进行对比研究，探讨了实验性攻击马立克氏病病毒（ＭＤＶ）后鸡体内病毒抗原分布与病变特点之间的关系。结果表明，ＭＤＶ能引起胸腺髓质区、脾动脉周围淋巴鞘、法氏囊生发中心淋巴细胞坏死、网状细胞增生，开逐渐在全身各部位产生多发性淋巴样细胞增生灶。病毒抗原阳性反应与网状细胞增生明显相关。ＭＤＶ抗原阳性细胞主要包括网状细胞，浓缩碎裂的淋巴细胞及浸润的淋巴样细胞，这些细胞浆和胞核均哇     

贵州山羊关节炎脑炎调查研究——山羊关节炎脑炎病理组织学及超微结构的研究

本研究采用光镜和透视电镜研究,关节炎脑炎(CAE)病的病理学特征,其证病性的病理变化特征,主要表现:消瘦拉稀,跛行或瘫痪、精神不振、关节膜增厚质硬、关节囊内有多量混浊或淡色液体。脑膜充血、出血。病理组织学变化,主要表现在,大小脑内血管充血、出血,淋巴细胞浸润呈结节状、脑实质具有筛状软化,胶质细胞、呈弥慢性或灶性分布,可见卫星现象。神经细胞肿胀、变性、坏死、或消灭。关节囊间质及结缔组织增生。超微结构变化:大,小脑:分子层的星形细胞,水平细胞以及多形细胞层的细胞和大、小锥体细胞、哺金野氏细胞浆中,线粒体肿胀变成圆形或不规则形,渐进变性、坏死、溶解,形成空腔。核膜结构消失,核孔扩大,染色质边移,或团块状。电子密度中度或较高。     

鸡马立克氏病（MD）与淋巴细胞糖皮质激素受体（GR）相关性研究Ⅱ．病毒抗原定位与病变特点相关性研究

运用ＢＡ免疫组化技术与ＨＥ染色进行对比研究，探讨了实验性攻击马立克氏病病毒（ＭＤＶ）后鸡体内病毒抗原分布与病变特点之间的关系。结果表明，ＭＤＶ能引起胸腺髓质区、脾动脉周围淋巴鞘、法氏囊生发中心淋巴细胞坏死、网状细胞增生，并逐渐在全身各部位产生多发性淋巴样细胞增生灶。病毒抗原阳性反应与网状细胞增生明显相关。ＭＤＶ抗原阳性细胞主要包括网状细胞、浓缩碎裂的淋巴细胞及浸润的淋巴样细胞。这些细胞胞浆和胞核均呈强阳性着染。     

鸡腺胃型传染性支气管炎的病理变化

对１９９５年以来在江苏一些县市养鸡场和养鸡专业户蛋鸡群发生的鸡腺胃型传染性支气管炎的自然病例和人工感染病例进行了系统的病理学观察。自然病例和人工感染病例的病理变化基本相同。其主要眼观病理变化为腺胃显著肿大,小肠充血、出血和炎症;主要组织学变化为腺胃粘膜充血、出血、炎性水肿和浅层坏死,小肠粘膜急性炎症变化,肝、心、肾等实质细胞变性以至局灶性坏死,脾、胸腺及法氏囊的淋巴组织萎缩。     

养殖大鲵蛙病毒自然感染的病理形态学观察

对经PCR确诊为蛙病毒感染的养殖大鲵自然病例进行病理形态学变化观察。剖检发现病鲵腹部膨大,皮肤上出现白点、出血斑,溃疡,头部与四肢肿胀;肝肿大,呈灰白色或斑点状出血;脾、肾肿大,淤血、斑点状出血;肠壁变薄,肠腔内充满大量含血的或淡黄色的液体。镜检主要见全身组织器官广泛性水肿、出血、变性、坏死和炎症细胞浸润,特别是肾、肝、胃肠道、脾和皮肤肌肉的损伤较为严重,并在病变组织细胞见圆形或椭圆形嗜酸性胞浆包涵体。肾表现为渗出性肾小球肾炎及肾小管上皮的空泡变性与坏死;肝细胞广泛性空泡变性与灶性坏死;脾淋巴细胞坏死,数量减少;胃肠道为卡他性一出血性炎;皮肤水肿,表皮细胞空泡变性,坏死脱落,形成渍疡。电镜显示肝、脾、肾的细胞发生明显的病变,线粒体肿胀,嵴断裂,溶解,粗面内质网扩张,核糖体颗粒脱落,细胞核染色质浓缩,边集,并在一些病变细胞浆内见晶格状排列或散在的虹彩病毒样颗粒。     

布鲁氏菌羊型5号菌苗气雾免疫牛、羊的病理组织学观察

用布鲁氏菌羊型5号菌苗气雾免疫牦牛16头、绵羊20隻。病理标本固定于10％的中性福尔马林,石蜡切片,苏木紫伊红染色。观察免疫后动物的组织反应和变化情况时,结果两种动物的组织器官都有一些基本相似的反应和改变,即(1)主要为淋巴网状内皮系统的增生反应。这种反应在免疫后35日内随着时间的延长逐渐明显;(2)其中3/16的牦牛和4/20的绵羊伴有局部淋巴网状组织变性和溶解;经过5次免疫的个别绵羊(1/7)出现坏死灶;(3)母畜发生子宫内膜炎;(4)实质器官细胞轻度变性,间或伴有炎症。一例绵羊大脑白质有增生性胶质细胞结节。     

LLO对大鼠肠黏膜微血管内皮细胞分泌NO和ET-1的影响

为探讨李斯特菌溶血素(LLO)导致大鼠肠黏膜微血管内皮细胞(RIMVECs)损伤的作用机制,将体外培养的RIMVECs分为对照组和LLO组,观察细胞形态变化,测定细胞生长情况,并检测细胞培养上清液中NO、ET-1浓度变化。结果表明:LLO组RIMVECs的细胞间隙变大,有大量细胞碎片漂浮;当LLO浓度达到50ng/m L以上时,测得细胞增殖(OD值)均呈极显著下降(P0.01);12 h内,NO、ET-1分泌量高于正常水平。试验表明,LLO引起RIMVECs细胞因子NO、ET-1分泌量升高,导致细胞微环境紊乱,是LLO导致肠黏膜微血管内皮细胞损伤的机制之一。     

PPARγ对猪血管内皮细胞增殖、迁移及小管形成的影响

试验旨在研究过氧化物酶体增殖物激活受体γ（peroxisome proliferator-activated receptors γ,PPARγ）对猪血管内皮细胞增殖、迁移及小管形成的影响,并探讨PPARγ在猪体外血管生成中的作用。设置PPARγ激动剂组（5、10、15、20 μmol/L罗格列酮）、抑制剂组（5、10、15、20 μmol/L T0070907）及对照组,通过iCelligence细胞功能分析、划痕试验和Matrigel基质胶三维培养,构建猪体外血管生成的模型,模拟猪体内血管生成的环境,分别对猪血管内皮细胞的增殖、迁移、小管形成能力进行测定,同时根据NCBI已有的相关序列,应用Primer Premier 5.0软件设计PPARγ基因特异性引物,利用SYBR GreenⅠ实时荧光定量PCR检测PPARγ基因mRNA相对表达量,对PPARγ的体外作用效果进行验证。结果显示,5、10 μmol/L罗格列酮能促进猪血管内皮细胞增殖、迁移及小管形成,T0070907的抑制效果在试验浓度区间内（5~15 μmol/L）随浓度升高而加强,较高浓度（20 μmol/L）的两种药物均由于药物毒性的影响对细胞活动产生干扰。此外,5~20 μmol/L罗格列酮和5~20 μmol/L T0070907能分别提高和降低PPARγ基因mRNA相对表达量,且浓度趋势与增殖、迁移、小管形成的试验结果一致。综上所述,通过激活PPARγ可以对猪血管内皮细胞的增殖、迁移及小管形成产生促进效果,提示其在猪体外血管生成中具有积极作用,可为研究PPARγ对猪胎盘血管发生的影响提供参考依据。     

A comparative study of the interaction of Bartonella henselae strains with human endothelial cells

Bartonella henselae can cause a wide range of clinical outcomes and may lead to severe disease, especially in patients with acquired immunodeficiency syndrome. It is well-known that B. henselae-induced cell proliferation is mediated by anti-apoptotic activity; however, the detailed mechanism is still unclear. In this study, the cellular responses of endothelial cells after infection with four B. henselae strains were compared and protein candidates that may be involved in the interaction between cells and bacteria were determined. The Houston-1 strain elicited the fastest response in terms of stimulating endothelial cell proliferation, and the JK-40 strain had the strongest ability to induce cell proliferation. By Western blot analysis, it was demonstrated that B. henselae-induced cell proliferation involved the mitochondria intrinsic apoptotic pathway. In addition, the adhesion abilities of the U-4 and JK-40 strains were much greater than those of the Houston-1 and JK-47 strains; however, the ability of Houston-1 to invade host cells was high. By two-dimensional gel electrophoresis analysis, it was found that succinyl-CoA synthetase subunit beta, phage-related protein, and ATP synthase subunit alpha might be involved in the invasion process. The expression of superoxide dismutase [Cu-Zn] precursor increased with infection time for all four strains but was significantly higher in the Houston-1 strain, which may increase the competitive advantage of Houston-1 in terms of survival in host cells and render it successful in invading host cells and stimulating cell proliferation. Our data suggest that the interaction of B. henselae and endothelial cells differed between strains, and the results indicated possible candidate proteins that may play a role in the pathogenesis of B. henselae infection.     

巴马小型猪骨髓来源内皮祖细胞的培养鉴定及生物学特性分析简

为探索并建立巴马小型猪骨髓来源内皮祖细胞(EPCs)的体外培养及鉴定方法,本研究在健康猪髂后上棘取骨髓,采用密度梯度分离法分离单个核细胞,按2×10⁷个/孔的密度加入预先包被人纤维连结素（HFN）的6孔细胞培养板中,用含内皮细胞生长因子的选择性培养基诱导培养,逐日在倒置相差显微镜下观察,MTT法检测EPCs增殖情况;流式细胞术（FACs）检测EPCs中AC133和vWF的表达纯度;免疫荧光法双染检测EPCs表面相关抗原ac-LDL和UEA-1。结果发现,从巴马小型猪骨髓分离的EPCs具有增殖能力;MTT结果显示细胞于48 h换液二次贴壁后3～5 d增殖明显,7～10 d增殖加速并出现条索状结构;FACs检测结果显示,二次贴壁细胞vWF阳性细胞百分率74.91%,AC133阳性细胞百分率79.54%,而未经诱导的二次贴壁细胞vWF和AC133阳性率分别是33.65%和39.87%;细胞经免疫荧光双染后Dil-ac-LDL和FITC-UEA-1表达呈阳性,vWF和AC133免疫荧光染色阳性。由此可见,分离培养的细胞具有自我增殖和分化潜能,是内皮祖细胞。     

Cutaneous vascular malformation in a guinea pig (Cavia porcellus)

Abstract   A skin lesion classified as a vascular malformation is reported in a young-adult, female guinea pig. The physical examination revealed a 3 × 2-cm irregularly shaped violaceous plaque located on the left caudal flank. The surface of the plaque was ulcerated and bled intermittently, resulting in fatal blood loss. On histology the mass consisted of variably sized vascular spaces filled with red blood cells and variable amounts of extramedullary haematopoietic cells, lined by well-differentiated endothelial cells often surrounded by one layer of spindle-shaped cells. Based on immunohistochemistry, the spindle cell population was confirmed to be smooth muscle cells and no proliferation of endothelial cells was found with the Ki67 proliferation marker. Histological and immunohistochemical findings were consistent with a vascular malformation. Classification of vascular malformations and potential treatments are discussed. To the authors' knowledge, this is the first reported case of a cutaneous vascular lesion in a guinea pig.     

一氧化氮、内皮素-1对体外培养大鼠心肌膜微血管内皮细胞增殖影响的对比研究

对比研究一氧化氮（NO）供体亚硝基乙酰青酶胺（SNAP）和内皮素-１（ET-1）对体外培养大鼠心肌膜微血管内皮细胞（RMMVECs）增殖的影响。应用不同浓度的SNAP及ET-1作用于RMMVECs,通过MTT法检测SNAP及ET-1对RMMVECs增殖的影响。与对照组细胞相比,对RMMVECs作用12 h后,浓度为125～1500 μmol/L的SNAP均可明显抑制细胞的增殖（P<0.05）,抑制率在10.74%～18.80%之间,浓度为0.125～1.5 μmol/L的ET-1组有显著的促增殖作用（P<0.05或P<0.01）,增殖率在20%～42%之间。在体外,SNAP能够在一定程度上抑制RMMVECs的增殖,而ET-1则能够促进RMMVECs的增殖,结果提示,调节二者在体内的平衡可能对疾病的发生及治疗起着一定的作用。     

Hepatic lymphangiomatosis in a young dog

A 9-month-old intact male American cocker spaniel was referred because of hepatomegaly and ascites. Ultrasonographic evaluation of the liver revealed congestion and increased parenchymal echogenicity with focal and more hyperechoic nodules. Histopathology of the hepatic lesion revealed diffuse, ill-defined vascular proliferation. A single layer of endothelial cells, which showed signs of minimal cellular atypia, lined the irregular vessels. On immunohistochemistry, the proliferative endothelial cells lining the irregular vessels were positive for an antiserum to factor VIII related antigen. Based on these findings, the dog was diagnosed with hepatic lymphangiomatosis.     

Production of heparin-binding angiogenic factor(s) by bovine corpora lutea during pregnancy.

Effects of luteal-conditioned media (LCM) on proliferation and migration of endothelial cells were used to assess angiogenic activity of corpora lutea (CL) obtained from cows on d 100 (n = 5), 150 (n = 6), 200 (n = 6), and 250 (n = 6) of gestation. Explants of CL (200 mg) were incubated for 6 h in 3 mL of serum-free media containing no hormone, LH (1 microgram/mL), prostaglandin F2 alpha (PGF2 alpha; 3 microM), or both hormones. Media from the four stages of gestation were subjected to the following procedures: 1) ultrafiltration, 2) high-salt (3.0 M NaCl) treatment and then ultrafiltration, 3) heat treatment, 4) heparin-Sepharose affinity chromatography, 5) immunoneutralization with specific antibodies against heparin-binding growth factor (HBGF)-1 and against HBGF-2, and 6) dot immunoblot assay for HBGF-2. Fractions from the first five procedures were evaluated in the endothelial cell proliferation bioassay. In addition, progesterone concentration of LCM was determined by RIA. Across all days of gestation and hormone treatments, LCM stimulated (P less than .05) proliferation and migration of endothelial cells, but activities did not differ among stages of gestation or hormone treatments. Both mitogenic and migration-stimulating fractions seemed to have Mr greater than 100,000. The mitogenic activity fraction had an apparent Mr greater than 100,000 even after treatment with high salt and was heat-labile. This endothelial mitogen was retained on heparin-Sepharose columns and was eluted with 2.0 M NaCl. Mitogenic activity was partly neutralized (P less than .05) by antibodies against HBGF-2 but not HBGF-1. Presence of HBGF-2 in LCM was detected by dot immunoblot assay.(ABSTRACT TRUNCATED AT 250 WORDS)     

Synovial hemangioma in the stifle joint of a dog

Synovial hemangioma was diagnosed in an 8-year-old castrated male Belgian Sheepdog with lameness of 3 months' duration. Pain, soft-tissue swelling, and hemarthrosis were localized to the left stifle joint. Projections of synovial membrane with reddish-purple nodules, excised via arthrotomy, were composed histologically of variably sized vascular channels that were lined by well-differentiated endothelial cells and separated by fibrous septa. Distension of some channels resulted in endothelial disruption, thrombosis, hemorrhage, necrosis, and focal spindle-cell proliferation. The limb was amputated to remove remaining neoplastic tissue. The hemangioma extended focally into the joint capsule and popliteal soft tissue but did not invade skeletal muscle or bone. The dog was free of detectable neoplasia 6 months after amputation. Synovial hemangioma is a rare benign vascular proliferation in people, most commonly in the knee, and should be included in the differential diagnosis for canine synovial tumors.