脂质、血红蛋白、胆红素标本对乙肝病毒DNA荧光定量测定的影响

目的:探讨脂血、高胆红素和溶血标本对乙肝病毒DNA(HBVDNA)荧光定量测定结果的影响。方法:将乙肝大三阳高脂血和非脂血、溶血血清和未溶血血清同时作HBVDNA荧光定量检测;将HBVDNA阴性黄疸血清和HBVDNA阴性正常血清与来自同一份乙肝大三阳血清混合,在相同条件下进行HBVDNA荧光定量。结果:乙肝大三阳溶血与未溶血样本HBVDNA含量都在同一数量级。乙肝大三阳高脂血的HBVDNA含量明显低于对照标本。高黄疸血清、正常对照血清与相同的HBVDNA阳性模板组合后所测得的HBVDNA结果无差异。结论:脂血对HBVD-NA定量测定有严重干扰;溶血样本、高胆红素样本对HBVDNA测定结果无影响。     

IL-12p40-overexpressing immature dendritic cells induce T cell hyporesponsiveness in vitro but accelerate allograft rejection in vivo: role of NK cell activation and interferon-gamma production

Infusion of genetically modified dendritic cells (DC) expressing immunosuppressive molecules is a potential therapy for organ rejection. IL-12p70, a cytokine produced mainly by DC and macrophages, consists of two subunits, p40 and p35. IL-12p70 is an activator of T cells, while the IL-12p40 subunit serves as a natural antagonist for IL-12p70 action. The primary aim of this study was to evaluate the effect of IL-12p40 gene-modification on both the T-cell stimulatory activity of immature DC (imDC) and their ability to prolong cardiac allograft survival. IL-12p40 gene-modified imDC (DC-p40) exhibited a phenotype characteristic of imDC and displayed impaired T-cell allostimulatory ability in vitro. However, to our surprise, for murine vascularized heterotopic heart transplantation (HHT), administration of donor-derived DC-p40 7 days prior to transplantation did not prolong allograft survival but instead significantly exacerbated cardiac allograft rejection. Further study showed that DC-p40 augmented NK cell activity both in vitro and in vivo and enhanced interferon-gamma (IFN-gamma) production in vivo, which might be due to the increased IL-23 production by DC-p40. Our data suggested that although IL-12p40 gene-modified immature DC can induce T cell hyporesponsiveness in vitro, their ability to activate NK cells and induce IFN-gamma production counterbalances this, exacerbating cardiac allograft rejection. The unexpected effects of DC-p40 limit their value in promoting allograft survival in vivo and likely reflect the complexity of IL-12p40 biology.     

显性遗传性聋─大家系研究

本文报告江苏省淮阴县运南地区方氏家族六代６８３人的系谱、皮纹学、染色体和ＡＢＯ血型等遗传学方法的调查与检测，确定属常染色体显性遗传性聋患者１３７例。经检索这是我国首例显性遗传性聋大家系，亦是国际上的第三例聋人大家系的报告。     

下颌骨的应力迹线与骨小梁构筑的关系

根据下頜光弹的等倾线图,描绘出主应力迹线规迹。在下颌侧位X线照片和去除唇侧及颊侧密质骨板的标本上,观察骨密质和松质的配布,以及骨小梁的排列和方向,试行探讨骨小梁方向与主应力迹线的关系。用光弹法求得的主应力迹线有两个系列:S_1系在下颌体近水平方向,在下颌支近垂直方向分布;S_2系力线与S_1系诸力线呈正交。在标本和X线照片上,主应力迹线规迹不同程度地在骨小梁的排列上有所反映。     

Integrated medical informatics with small group teaching in medical education

National Taiwan University College of Medicine (NTUCM) introduced small groups of teaching and basic-clinical integrated courses for medical students in 1992. By using computer network and multimedia techniques, this study tried to overcome barriers to learning in small group teaching. The Department of Medical Informatics of NTUCM established campus networking and computer classrooms and provided Internet and intranet network services including mail, netnews, bulletin board systems (BBS), world wide web (WWW), gopher, ftp and local file servers. To implement an interactive learning environment, the authors first tried mail lists, newsgroups and BBS. Next an integrated learning system prototype on the WWW was developed to provide functions including online syllabus, discussion boards simulated to BBS, online talk, interactive case studies, virtual classroom with video on demand (VOD) and Internet medical resources. The results showed that after the medical students completed the required course of medical informatics and had good network access using a network to communicate with each other became a daily practice. In the future, the system will extend to the tutoring of clinical practice and continuing medical education. The authors expect a national medical education network and more international cooperation and exchange.     

Induction of the human protein P56 by interferon, double-stranded RNA, or virus infection

P56 is the most abundant protein induced by interferon (IFN) treatment of human cells. To facilitate studies on its induction pattern and cellular functions, we expressed recombinant P56 as a hexahistidine-tagged protein in Escherichia coli and purified it to apparent homogeneity using affinity chromatography. A polyclonal antibody raised against this recombinant protein was used to show that P56 is primarily a cytoplasmic protein. Cellular expression of P56 by transfection did not inhibit the replication of vesicular stomatitis virus and encephalomyocarditis virus. P56 synthesis was rapidly induced by IFN-beta, and the protein had a half-life of 6 h. IFN-gamma or poly(A)(+) could not induce the protein, but poly(I)-poly(C) or an 85-bp synthetic double-stranded RNA efficiently induced it. Similarly, infection of GRE cells, which are devoid of type I IFN genes, by vesicular stomatitis virus, encephalomyocarditis virus, or Sendai virus caused P56 induction. Surprisingly, Sendai virus could also induce P56 in the mutant cell line P2.1, which cannot respond to either IFN-alpha/beta or double-stranded RNA. Induction of P56 in the P2.1 cells and the parental U4C cells by virus infection was preceded by activation of IRF-3 as judged by its translocation to the nucleus from the cytoplasm.     

Amphiphysin IIm, a novel amphiphysin II isoform, is required for macrophage phagocytosis

Phagocytosis of pathogens by macrophages initiates the innate immune response, which in turn orchestrates the adaptive immune response. Amphiphysin II participates in receptor-mediated endocytosis, in part, by recruiting the GTPase dynamin to the nascent endosome. We demonstrate here that a novel isoform of amphiphysin II associates with early phagosomes in macrophages. We have ablated the dynamin-binding site of this protein and shown that this mutant form of amphiphysin II inhibits phagocytosis at the stage of membrane extension around the bound particles. We define a signaling cascade in which PI3K is required to recruit amphiphysin II to the phagosome, and amphiphysin II in turn recruits dynamin. Thus, amphiphysin II facilitates a critical initial step in host response to infection.