目的研究DPC4（deleted in pancreatic cancer locus 4）基因在胰腺癌中的改变。方法用多聚酶链反应2单链构象多态性分析（PCR2SSCP）银染技术及PCR产物直接测序法检测胰腺癌细胞系P1、P2、P3、P4、P7，11例新鲜冷冻胰腺癌组织中DPC4基因第1，2，3，4，8，11外显子的缺失和突变。结果5株人胰腺癌细胞系中，3株（P1、P2、P3）存在DPC4基因突变,DPC4 基因改变率为3/5。11例新鲜冷冻胰腺癌组织中，3例有DPC4基因的纯合性缺失，2例有基因突变，DPC4基因改变率为5/11(45.5%)。结论DPC4作为一种抑癌基因，其改变在胰腺癌的形成中可能起重要作用。

We report here the two-dimensional protein database of human pancreas. The proteins were analyzed by two-dimensional electrophoresis followed by matrix-assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS). Totally, 302 proteins were identified, of which about 27% were enzymes with a broad range of catalytic activities. Several of these are specifically expressed in pancreas, such as pancreatic amylase, pancreatic stone protein, pancreatitis-associated protein, pancreatic lipase, pancreatic elastase, etc. Structural and cytoskeletal proteins are also strongly represented on the gels. Thus, the pancreatic proteome reflects the organ's function. This work paves the way for further studies on pancreatic protein expression in health and disease, such as diabetes and pancreatic cancer.

通过研究严重急性呼吸综合征（severe acute resplratory svyndrome, SARS）患者的尸检肺部标本，总结SARS的肺部病变特点及发病机制。方法详细检查SARS患者肺脏标本的大体特点，并用常规方法研究显微光镜下SARS累及各肺叶的病变特点。结果7例SARS患者的双肺均明显膨胀，镜下表现以弥漫性肺泡损伤（DAD）不同时期的病变为主。7例均有肺水肿及透明膜形成，肺水肿尤以早期明显。病程超过3周者开始有肺泡内机化及肺间质纤维化，造成肺泡的纤维性闭塞。几乎每例部可见到小血管内的微血栓和肺出血、散在的小叶性肺炎、肺泡上皮脱落、增生等病变。2例可见曲霉菌感染，1例累及左全肺及右肺部分区域，1例出现在肺门淋巴结。肺门淋巴结多表现为充血、出血及淋巴组织减少，窦组织细胞增多。结论SARS肺可能为SARS病毒造成的弥漫性肺泡损伤，表现为肺泡上皮及毛细血管的严重损伤导致肺水肿和肺泡及细支气管的纤维素性渗出性炎症，出现透明膜，继而出现肺泡内机化及肺泡间隔的成纤维细胞增生，共同使肺泡萎陷、机化，最终形成纤维化实变。肺门淋巴组织的减少可能是此病影响免疫系统的又一形态学表现。

Gene amplification and enhanced expression of the epidermal growth facor receptor (EGFR) represent the major moiecular genetic alteration in glioblastomas and it may play an essential role in cell growth and in the carcinogenic process, On the other hand, the nuclear suppressor proteins PML and p53 are also known to play critical roles in cancer edveiopment and in suppressing cell growth. Here we report that, in glioblastoma cells with cefectivw EGFR function, the expressions of both promyetocytic leukaernia (PML) and p53 were altered. Cells that were transfected with the antisense-cDNA of EGFR were found to have more cells in G1 and fewer cells in Sphase, In Addition, the transfceted cells were found to be non-responsive to EGF-induced cell growth, Inteerestingly, the expression of the suppressors p53 and PML were found to be signillcantly increased by immunohistochemical assay in the antisense-EGFR cells. Moreover, the PML expression in many of the cells was converted from the nucleal dot pattern imto fine-granulated staining pattern, In contrast, the expressions of other cell cycle regulated geries and proto-oncogene, including the cycli-dependent kinase 4(cocik4), retinblastoma, p16 think and p21bjone, were not altered. These data indicate that there are specific inductions of PML and p53 proteins which may account for the increase in G1 and growth arrest in antisense-EGFR treated cells, It also indicates that the EGF, p53 and PML transduction pathways were liked and they may constifulte arrest in an ntegral part of an alterred growth reguiaory programme .The interactions and cross-talks of these critical molecules may be very importtant in regulating cell growth, differentiation and cellular resporise to treatment in glioblastomas.