红腹锦鸡肝脏的显微结构观察

用组织学方法对3只红腹锦鸡（Chroysolophus pictus）的肝脏进行了显微结构观察，结果如下：红腹锦鸡的肝脏由许多肝小叶组成；中央静脉位于其纵轴中央，围绕中央静脉，两层肝细胞组成的肝细胞索（肝板）不连续的呈放射状排列，肝血窦呈辐射网状排列；肝血窦的窦壁由一层内皮细胞和枯否氏细胞组成，内皮细胞不连续，枯否氏细胞常见于肝血窦，有几个突起；肝细胞索的两层肝细胞之间见有胆小管，另外，对红腹锦鸡的肝脏与其它动物的肝脏进行了比较。     

虎皮鹦鹉肝脏结构的光镜和透射电镜观察

利用生物显微技术和透射电镜技术观察了虎皮鹦鹉(Melopsittacus undulates)肝脏的显微和超微结构.结果表明,虎皮鹦鹉的肝小叶不规则且分界模糊,肝细胞3～8个聚集成团或成不规则的索状围绕中央静脉呈放射状排列.肝细胞内富含线粒体、内质网、核糖体和溶酶体等细胞器;双核肝细胞较多.胆小管由相邻的肝细胞围成,相邻肝细胞间有连接复合体封闭胆小管.肝血窦内有巨噬细胞和浆细胞,窦周隙明显.肝细胞向胆小管面与窦周隙面伸出许多微绒毛.     

短耳鹗和雉鸡肝脏组织结构的比较研究

利用生物显微技术和透射电镜技术对短耳鹗(Asio flammeus)和雉鸡(Phasianus colchicus)的肝脏进行了比较.结果 显示:与大多数鸟类相似,短耳鹗和雉鸡的肝小叶分界模糊,肝细胞成索状或团块状围绕中央静脉呈放射状排列,门管区较明显.短耳鹗肝小叶的肝细胞排列较为规则,雉鸡的肝细胞大多3～6个聚集成团,雉鸡肝血窦较短耳鹗的丰富.短耳鹗肝细胞内线粒体、内质网的数量多于雉鸡,但雉鸡肝细胞内糖原颗粒、溶酶体的数量及胆小管切面的微绒毛数目明显多于短耳鹗.这表明短耳鹗和雉鸡肝脏组织结构存在差异,这种差异可能与其食性不同有关.     

鳖肝脏的基本病理组织学初步观察

鳖肝脏的基本病理组织学主要表现为肝细胞的变性坏死,肝血窦的扩张淤血和炎性细胞浸润,肝细胞以颗粒变性和水样变性为主,肝血窦的扩张淤血导致肝细胞受压而萎缩坏死,炎性细胞浸润现象普遍。     

赤腹松鼠消化腺组织学观察

研究了赤腹松鼠消化腺组织学结构.结果表明:消化腺由小消化腺和大消化腺组成.小消化腺由单管泡状腺的舌腺,单管状腺的胃腺、小肠腺和大肠腺以及管泡状腺的十二指肠腺构成;食管内未见食管腺,大肠内可见大量杯状细胞.大消化腺有大唾液腺、肝和胰腺.大唾液腺由腮腺、舌下腺和颌下腺组成,均为复管泡状腺.肝脏分为5叶,由肝小叶和门管区组成.肝小叶包括中央静脉、肝细胞索和肝血窦,门管区内有小叶间动脉、小叶间静脉和小叶间胆管.胰由外分泌部的复管泡状腺胰腺和内分泌部的胰岛构成.研究结果表明赤腹松鼠消化腺结构与其食性是相适应的.     

大鼠肝肿瘤成模过程中肝组织结构变化

为了解大鼠肝肿瘤成模过程中肝组织结构变化,用二乙基亚硝胺（diethylnitrosamine,DENA）灌胃法构建大鼠肝肿瘤模型,按常规方法制备肝组织石蜡切片和镜检.建模第1周大鼠肝脏的肝小叶结构完整,肝细胞排列整齐.从第5周起肝窦扩张,肝细胞变性肿胀并有不同程度的脂肪变性,同时出现炎症细胞浸润.第8周时肝窦充血,肝细胞脂肪变性严重,并出现纤维组织增生和明显的肝细胞增生.第10周时肝小叶结构受到破坏,出现肝细胞增生性结节.第12周时门管区内有不同程度的卵圆细胞增生及结缔组织增生,伴随胆管增生.第16周时肝小叶结构消失,可见典型的假小叶结构,结节内肝细胞异常增生明显,出现“结中结”,病理性核分裂相亦较多.第17周时肝肿瘤形成,且主要是肝细胞癌,癌细胞排列为索状、腺状、实片状.根据上述结果得出如下结论：用二乙基亚硝胺灌胃法构建大鼠肝肿瘤模型方便有效,肝组织结构和病理变化有规律,易于观察分析,值得推广应用.     

山斑鸠肝脏组织结构观察

目的:研究山斑鸠肝脏解剖学和组织学结构特点,并与其他鸟类和哺乳动物进行对比.方法:本实验通过解剖学观察和石蜡切片技术对山斑鸠肝脏的结构进行了研究.结果:山斑鸠的肝脏位于胸腔内分为左右两叶,无胆囊;肝脏占体质量比例约为(3.21±0.14)%;肝小叶间结缔组织很不发达,同时门管区也不是很明显;肝细胞呈圆形或卵圆形,各个肝细胞的界限不清楚,多由几个肝细胞形成肝细胞团块,大多数是单核的,但也有少数具有双核;肝血窦数量比较少;小叶间动脉不易观察.结论:山斑鸠肝脏组织结构与其功能密切联系,这是由这一物种的生活习性所决定.     

中华鳖腐皮病的病理组织学初步研究

取病鳖的肝，肠，脾，肾和溃烂处皮肤等组织数块，Ｚｅｎｋｅｒ‘ｓ液固定，石蜡包埋，ＨＥ染色。观察结果显示，病鳖肝细胞发生不同程度的变性以至坏死，肝血窦淤血，肠粘膜溃疡，肠壁结构被破坏。     

中华鳖腐皮病的病理组织学初步观察

取病鳖的肝、肠、脾、肾和溃烂处皮肤等组织数块,Zenker's液固定,石蜡包埋,HE染色.观察结果显示,病鳖肝细胞发生不同程度的变性以至坏死,肝血窦淤血.肠粘膜溃烂,肠壁结构被破坏.脾脏的红髓、白髓分界不清.肾脏的小管上皮细胞变性,毛细血管扩张.溃烂处皮肤表皮细胞坏死,真皮结缔组织中有大量红细胞和淋巴细胞存在.     

肝脏小叶的双重介质渗流模型及渗流模式

将肝脏内的肝血窦和窦周间隙当作多孔介质处理,采用多重连续介质生物渗流的理论,建立了一个基于双重介质渗流理论的生物力学模型,通过有限元法求解了特定情况下的渗流场,并分析了肝小叶区域内血液、组织液的流动规律与物质交换特征.     

几种鸟类肝脏的组织学比较

利用生物显微技术对虎斑地鸫Zoothera dauma、白眉地鸫Siberian thrush、戴胜Upupa epops、大山雀Pa-rus major、绿背山雀P.monticolus、黑冠山雀P.rubidiventris、山斑鸠Streptopelia orientalis和灰斑鸠S.decaocto的肝脏进行了比较.结果显示:与大多数鸟类相似,虎斑地鸫、白眉地鸫、戴胜、山斑鸠和灰斑鸠肝小叶分解不清,肝细胞成索状或团块状围绕中央静脉呈放射状排列,门管区数量少或不明显.大山雀、绿背山雀和黑冠山雀肝小叶的肝细胞排列较为规则,肝细胞索呈索状围绕中央静脉呈放射状排列,门管区的小叶间动脉、小叶间静脉和小叶间胆管清晰可见.从佛法僧目、鸽形目和雀形目来看,鸟肝占体质量的比例呈减小的趋势,肝细胞直径呈增大的趋势.结果表明:大山雀、绿背山雀和黑冠山雀的肝脏与虎斑地鸫、白眉地鸫、戴胜、山斑鸠和灰斑鸠的肝脏相比可能较为完善.     

Malaria parasites--discovery of the early liver form

Infections of mammalian malaria parasites start when sporozoites from an infected anopheline mosquito are injected into the bloodstream of the host. The sporozoites enter the hepatocytes and become transformed into exoerythrocytic schizonts. Since the discovery of the primate parasite Plasmodium cynomolgi in monkey hepatocytes and the rodent parasite Plasmodium berghei in hamster hepatocytes, the ultrastructure of these stages has been extensively studied both in primate and rodent plasmodia. These observations relate only to the development of the exoerythrocytic schizont 25 h after sporozoite injection until the final maturation (of P. berghei) 50 h post-inoculation. Recently, we have studied the route of entry of sporozoites across the cellular lining of liver sinusoids and invasion of the liver parenchymal cells by using transmission electron microscopy. The results of these studies in combination with other physiological experiments strongly suggested that the sporozoite was initially harboured by the Kupffer cell, from which the parasite escaped into the neighbouring hepatocyte. The migration of sporozoites from liver sinusoids to hepatocytes can be achieved within a few minutes. We present here the first ultrastructural observations on the natural transformation of intrahepatocytic sporozoites into exoerythrocytic forms in vivo, using the rodent malaria parasite P. berghei in a laboratory host, the Brown Norway rat. These observations complete the search for the final link in the life cycle of malaria parasites.     

胎儿肝脏的形态学研究

187例河南地区胎儿肝重、体重被测量,并用光镜观察肝的组织发生。结果表明:肝重(y)与体重(x)有显著的正相关关系,相关系数为0.9861,回归方程 =-0.0367+0.0417x;肝重随胎龄(x)变化的回归方程 =1.772e~(0.4359x);15-20周肝细胞渐排列为细长的索;23周以前肝中造血细胞(HC)甚多,24周肝血窦中HC数量减少,故肝中HC量减少时的顺序是先血窦后窦周隙;35周时各处HC数量大大减少,这提示,肝造血功能于35周急骤下降。     

肝脏干细胞的来源与潜能

肝干细胞是肝脏内具有自我更新能力和多分化潜能的细胞,包括卵圆细胞、小型肝细胞和小肝细胞样前体细胞.其中,卵圆细胞可能来源于胚胎干细胞和/或骨髓干细胞.肝干细胞能分化为肝实质细胞和胆管上皮细胞,在一定条件下,还能分化为胰腺细胞、肠上皮细胞、肌细胞或转化为肝肿瘤细胞.     

Cultivation of the liver forms of Plasmodium vivax in human hepatocytes

The blood schizogonic cycle of human malaria parasites has thus far been the most exhaustively studied phase of parasite development. However, before entering red blood cells (RBCs), the parasite undergoes its first multiplication not in blood, but in hepatic cells. These hepatic stages were the last to be discovered and only a few studies have been performed in humans and other primates. Despite recent advances, in vivo studies have limitations and other approaches such as cultures of these liver forms may be necessary to investigate their chemosensitivity and their biochemical or immunological properties. Recently, sporozoites of species of rodent malaria have been made to infect cultured cell lines or primary hepatocyte cultures. We report here that the complete cycle of the human malaria parasite Plasmodium vivax can be obtained in primary cultures of human hepatocytes up to release of merozoites able to penetrate RBCs.     

Ultrastructural localization of factor VIII procoagulant antigen in human liver hepatocytes

Factor VIII is generally believed to circulate in blood as a multimeric complex of two glycoproteins which are physiologically and immunologically distinct. One component of the factor VIII complex is factor VIII procoagulant activity (FVIII:C) which is associated with factor VIII/procoagulant antigen (FVIII:Ag, formerly FVIII/CAg). The second, larger unit of the complex is factor VIII/von Willebrand factor (vWF:Ag, formerly factor VIII-related antigen or FVIIIRAg). FVIII:C has anti-haemophilic activity and is defective or deficient in patients with classical haemophilia, and vWF:Ag is absent in patients with von Willebrand disease. FVIII:Ag was demonstrated recently in endothelial cells lining hepatic sinusoids, by using immunoperoxidase staining and light microscopy, whereas biochemical data had indicated its presence predominantly in the hepatocyte fractions and in lesser amounts in endothelial cells. Moreover, recent hybridization experiments detected FVIII:C messenger RNA in liver and kidney tissues. Despite several efforts, the cells responsible for FVIII:C synthesis have not been unequivocally identified. Here we use protein A-gold complex labelling to demonstrate the ultrastructural localization of FVIII:C in human liver cells; the results indicate that hepatocytes may synthesize FVIII:Ag.     

囊型肝包虫囊周肝细胞病理形态学观察

观察囊型肝包虫囊周肝细胞的病理形态学变化（肝细胞萎缩、坏死、凋亡）,初步探讨囊型肝包虫病肝细胞“消失”机制。对30例肝包虫囊肿周围肝组织及10例正常肝组织通过光镜观察肝细胞的病理形态学变化,透射电镜观察6例肝包虫囊肿周围肝细胞超微结构改变,运用TUNEL法测定肝细胞凋亡并采用免疫组化技术检测30例肝包虫囊肿周围肝组织及10例正常肝组织中Bcl-2及Bax蛋白的表达。结果显示TUNEL法测定囊周肝细胞凋亡发生极少（0．12％）与正常肝（0．16％）比较无显著差异,囊周肝组织Bcl-2及Bax蛋臼呈低表达,分别为6．6％和13．3％,病理学观察囊周肝细胞明显萎缩,肝细胞坏死。因此,肝细胞萎缩、坏死、凋亡共同参与囊型肝包虫囊周肝细胞“消失”,肝细胞萎缩、坏死可能是引起肝细胞“消失”的主要机制,肝细胞凋亡可能不是引起肝细胞“消失”的主要机制。     

Advances in studies on hepatic stem cells

The question whether hepatic stem cells exist or not has been debated for several decades. Current researches confirm that there are hepatic stem cells in the liver. Oval cells, putative bipotential hepatic stem cells, are probably located within canals of Hering, portal tracts or branches of biliary trees. Bone marrow is a potential source of oval cells, indicating that there exists a close relationship between liver and hematopoiesis in adulthood. Hepatic stem cells are able to proliferate in vitro and can be induced to differentiate into hepatocytes. This will provide a promising approach of cell transplantation, tissue engineering and gene therapy for liver diseases. In this review, the evidence of their presence, origin, identification, proliferation in vitro, differentiation by induction, application prospects of hepatic stem cells and future directions for the field are discussed.