Effect of recent alcohol intake on acceptor properties of high-density lipoproteins and their interaction with liver cells

Institute of Therapy, Siberian Branch, Academy of Medical Sciences of the USSR, Novosibirsk. All-Union Preventive Medicine Research Center, Ministry of Health of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR Yu. P. Nikitin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 110, No. 12, pp. 611–613, December, 1990.     

Differential Anatomical Expression of Transplantation Antigens Within the Normal Human Placental Chorionic Villus*

ABSTRACT: The expression of transplantation antigens by cells of the placenta was examined by immunohistological and immunoprecipitation procedures with defined conventional and monoclonal antisera to beta₂-microglobulin, DR and DC gene products, and H-Y antigen. Cells of the mesenchymal stroma within chorionic villi were positive by immunofluorescence for major histocompatibility complex antigens, and in male pregnancies for H-Y antigen, but the trophoblast was consistently negative for all antigen systems examined. Immunohistological examination of viable suspensions of cultured diploid trophoblast and of isolated membranes also gave negative results, and after radioiodination and solubilization of membranes, no detectable radioactive material was immunoprecipitated. These results provide further evidence that transplantation antigens are not expressed by human trophoblast. Since this is a fetal structure exposed directly to immunologically competent cells of the mother in the intervillous spaces, this observation may be relevant to the apparent lack of damaging maternal immune responses directed against the fetal homograft.     

A monoclonal antibody (RH1-38) which inhibits multiple systems of cell-mediated cytotoxicity--II. Evidence that the epitope recognized is involved in a late step in the cytolytic mechanism

A monoclonal antibody (RH1-38) which blocks multiple systems of cell-mediated cytotoxicity was functionally characterized. RH1-38 specifically blocks, in the absence of complement, natural killer (NK) activity (K562 targets) without any effect on NK-K562 conjugate formation. Kinetic studies suggested that the antibody blocks a step that occurs 30-120 min after effector populations are mixed with target cells. Single-cell cytotoxicity assays in agarose, combined with standard 51Cr release assays and Michaelis-Menten analysis revealed that RH1-38 markedly decreases Vmax and the number of active NK cells, again without any effect on the number of target-binding cells. The maximum recycling capacity was usually decreased, but in some experiments unchanged, in the presence of the monoclonal antibody. RH1-38 inhibited equally well whole peripheral blood mononuclear leukocytes (PBML), Percoll-fractionated lymphocytes enriched for NK activity, and interferon (IFN)-boosted NK activity. PBML exposed to RH1-38 and then washed mediated depressed NK activity which was partially reversed by subsequent treatment with IFN. These studies are most consistent with the hypothesis that RH1-38 inhibits a step late in the NK cytolytic mechanism rather than through an effect on conjugate formation. The primary effect is probably not on the IFN-generating or boosting mechanism, but a secondary effect on IFN-related mechanisms cannot be ruled out. Inhibition through an effect on a small lymphocyte modulator of NK activity is also unlikely but not rigorously excluded. Thus, RH1-38 appears to inhibit NK activity through a direct effect on NK effector cells, probably by interfering with a cell-surface molecule which is important in the expression of NK activity. The companion paper demonstrates that this monoclonal antibody immunoprecipitates a molecule which is very similar or identical to the LFA-1 antigen. Thus, RH1-38 recognizes either a novel epitope on the LFA-1 molecule or alternatively a distinct, functional killer cell surface molecule. The epitope appears to be involved in a late step in the cytolytic mechanism, possibly part of the effector cell lytic machinery.     

大鼠肝再生中糖代谢相关基因的表达变化

目的了解糖类代谢相关基因在大鼠肝再生中的表达变化。方法本研究用搜集网站资料和查阅相关论文等方法获得糖类代谢相关基因,用大鼠基因组230 2.0芯片检测它们在大鼠再生肝中的表达情况,用比较手术组和假手术组中基因表达的差异性确定肝再生相关基因。结果初步证实上述基因中118个基因与肝再生相关。肝再生早期[部分肝切除(PH)后0.5~4h]、前期(PH后4~12h)、中期(PH后16~66h)和后期(PH后72~168h)等4个阶段起始表达的基因数为33、6、68和7;基因的总表达次数为68、44、210和83。表明肝再生相关基因主要在肝再生启动阶段起始表达,在不同阶段发挥作用。它们共上调205次,下调200次,分为12种表达方式,表明肝再生中糖代谢活动多样和复杂。其中,单糖和糖原代谢、糖蛋白和糖脂(主要为神经节苷脂)合成相关基因几乎在整个肝再生中表达增强,寡糖和糖胺聚糖合成及糖蛋白和糖脂分解相关基因表达下调。结论肝再生与糖代谢密切相关。     

脂类代谢和运输涉及的基因与大鼠肝再生的相关性分析

目的在基因转录水平了解脂类代谢和运输相关基因在大鼠肝再生(LR)中的表达变化和模式。方法用搜集网站资料和查阅相关论文等方法获得参与脂类代谢和运输基因,用大鼠基因组230 2.0芯片检测它们在大鼠再生肝中的表达情况,用比较手术和假手术中基因表达的差异性确定肝再生相关基因。结果初步证实上述基因中193个基因与肝再生相关。肝再生早期[部分肝切除(PH)后0.5~4h]、前期(PH后6~12h)、中期(PH后12~66h)、后期(PH后72~168h)等4个阶段起始表达的基因数为113、20、66和1;基因的总表达次数为250、205、796和293。共上调852次,下调630次,分为27种表达方式。肝再生早期和前期胆汁酸代谢相关基因转录减弱;早期和后期糖皮质激素分解相关基因转录增强;前期和中期磷脂合成相关基因转录增强,磷脂分解相关基因转录减弱;中期脂肪酸、白三烯和鞘糖脂合成相关基因转录增强,甘油三酯和磷脂酰肌醇代谢相关基因转录增强,鞘糖脂分解相关基因转录减弱;中期和后期前列腺素合成和脂肪酸分解相关基因转录增强;几乎在整个肝再生中性激素、糖皮质激素和孕酮合成相关基因转录增强,鞘磷脂代谢相关基因转录增强,脂类运输相关基因转录增强,胆固醇代谢相关基因转录减弱。结论肝再生中脂类代谢和运输变化较大,与肝再生密切相关。     

两袖套法大鼠同种异体减体积肝移植模型的建立

目的探讨建立稳定大鼠减体积原位肝移植模型的方法。方法利用两袖套法连接肝下下腔静脉及门静脉,单线连续吻合肝上下腔静脉。共完成120例大鼠减体积原位肝移植模型。结果顺利完成模型建立,移植术后大鼠均能自由活动,进食活跃。其2d和7d存活率分别为85.8%和83.3%。结论利用改进的两袖套法,可以建立稳定的大鼠同种异体减体积原位肝脏移植模型。     

人胚胎大脑海马发育过程中凋亡神经元超微结构观察

本文借助电子显微镜技术对 4月胎龄组及 6月胎龄组水囊引产胎儿海马中段部位的凋亡神经元超微结构进行观察、拍照 ,并对结果进行了分析讨论。结果显示 :两组对象中均可见凋亡神经元 ,所见的凋亡神经元的超微结构变化基本相同 ,即细胞核内有明显的染色质边集和凝结成块的现象 ,并可见核膜皱缩和扭曲。另外 ,6月组凋亡细胞的结构变化较 4月组更为明显。在 6月组细胞质内和核内均有小体出现 ,其他细胞器无显著变化。从而更进一步说明在胚胎海马发育中存在着神经元不同性质的死亡现象 -即正常死亡和凋亡。而且提出 6月组显现出更为明显的凋亡神经元形态变化     

脂肪肝与胰岛素抗性的关系

目的探讨脂肪肝与胰岛素抗性的关系。方法对30例诊断为脂肪肝患者作回顾性分析。结果多数患者合并胰岛素抗性综合征(高血压、肥胖症、糖尿病、高脂血症),18例接受口服葡萄糖耐量试验(OGTT)中,1例确诊为Ⅱ型糖尿病,17例患者中3例空腹血糖减损(IFG),1例糖耐量减退(IGT)及13例糖耐量正常(NGT)具有较正常人为高的血浆胰岛素(INS)浓度,胰岛素抗性脂数为8.91±1.52%。结论脂肪肝与胰岛素抗性所致的代谢紊乱关系紧密,呈正相关系。     

Small epithelial cells in human liver cirrhosis exhibit features of hepatic stem-like cells: immunohistochemical,electron microscopic and immunoelectron microscopic findings

AIMS: To investigate whether cells with features similar to those of the oval cells of rodents and the small epithelial cells (SEC) recently described in certain human liver diseases, i.e. hepatic progenitor cells, also occur in human liver cirrhosis. METHODS AND RESULTS: Surgical specimens from 35 cases of hepatitis B virus-positive cirrhosis (30 cases containing hepatocellular carcinoma) were investigated by immunohistochemical staining for cytokeratin 7 and albumin. Electron microscopic investigations, and immunoelectron microscopic investigations using the same antibodies and a double-labelling technique were performed in 15 and seven cases, respectively. SEC were observed in proliferated bile ductules, at the margins of regenerating nodules and in the fibrous septa in all cases of cirrhosis. The SEC were morphologically similar to the SEC described previously, and to the oval cells seen in experimental hepatocarcinogenesis. They were characterized by their small size, oval shape, scanty electron-dense or electron-lucent cytoplasm, a high nucleo-cytoplasmic ratio, tonofilaments and intercellular junctions. Immunoelectron microscopy revealed that the SEC co-expressed cytokeratin 7 and albumin. Both relatively undifferentiated SEC and SEC with morphological and immunophenotypical signs of differentiation towards biliary epithelial cells and hepatocytes were found. CONCLUSIONS: SEC that exhibit morphological and immunophenotypical features of the SEC seen in certain other liver diseases are found in cirrhosis. These findings further support the hypothesis that a bipotent hepatic stem cell that may give rise to biliary epithelial cells and hepatocytes exists in the human liver.