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。

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。

Two human pancreatic carcinoma cell lines, PC-1 and PC-2, were establishen from nude mice xenogrfts derived from metastatic panereatic carcinomas of two patients. The two cell lines propagated continuously in vitro over 19 and 19.5 moths. The cells grow in a monolayered sheet with doubling times of 47 hours for PC-1 and 58 hours for PC-2, The cells exhibited epithelial morphology and were confirmed to be malignant cpithelial cell lies by morphological study, CEA and cytokeration immunocytochemisry, flow cytometry and Con A test. The tumors caused by inoculation of eultured PC-1 and PC-2 into unde mice retained the histological and ultrastructural features of the original tumors. The findings proved that the two cell lines were human exocrine pancreatic adenocarcinoma cell lines. Chormosomal analysis together with flow cytomertyr data revealed that the two cell lines had the human ancuploid karyotypic fcarues with model chromosome numbers of 48 and 66.