目的:应用脉冲场凝胶电泳技术(pulsed field gel electrophoresis,PFGE)对由原料乳和牛粪中分离的肠致病性大肠杆菌EPEC O128∶K67(B12)进行基因分型,了解来自天津市9个奶牛场和保定市9个奶牛场的原料乳样品和牛粪样品分离株的遗传相关...目的:应用脉冲场凝胶电泳技术(pulsed field gel electrophoresis,PFGE)对由原料乳和牛粪中分离的肠致病性大肠杆菌EPEC O128∶K67(B12)进行基因分型,了解来自天津市9个奶牛场和保定市9个奶牛场的原料乳样品和牛粪样品分离株的遗传相关性。方法:对7株肠致病性大肠杆菌EPEC O128∶K67(B12)按照脉冲场凝胶电泳方法进行基因分型。结果:用XbaI限制性内切酶对分离株的基因组DNA进行酶切,经PFGE可形成17～20条清晰条带的分离株DNA指纹图谱,由聚类分析树状图可将7株分离株分为3个基因群。结论:7株肠致病性大肠杆菌EPEC O128∶K67(B12)分离株存在3个图谱类型,各型之间不紧密相关,未发现单个基因型菌株流行的迹象。研究发现,脉冲场凝胶电泳分型技术分辨率高、可靠、应用性强、技术先进,对原料乳的致病菌溯源有较大的应用前景。展开更多
AIM： To examine surgical specimens of pancreas with either chronic pancreatitis or pancreatic cancer in order to study whether ductal hyperplasia and dysplasia in pancreas represent precursor lesions for pancreatic c...AIM： To examine surgical specimens of pancreas with either chronic pancreatitis or pancreatic cancer in order to study whether ductal hyperplasia and dysplasia in pancreas represent precursor lesions for pancreatic cancer. METHODS： We examined expression of Ki-67, CEA, p53, and K-ras, in the surgical specimens of pancreas with adenocarcinomas （n = 11） and chronic pancreatitis （n = 12）. Cellular proliferation was assessed by Ki-67 proliferation index using the proliferation marker Ki-67. In specimens with pancreas cancer, we divided pancreas epithelium into normal （n = 7）, ductal hyperplasia （n = 3）, dysplasia （n = 4）, and cancerous lesion （n = 11） after hematoxylin and eosin staining, Ki-67, and CEA immunohistochemical staining. In cases with chronic pancreatitis, the specimen was pathologically examined as in cases with pancreas cancer, and they were also determined as normal （n = 10）, ductal hyperplasia （n = 4）, or dysplasia （n = 5）. p53 and K-ras expression were also studied by immunohistochemical staining. RESULTS： In pancreatic cancer, the Ki-67 index was 3.73±3.58 in normal site, 6.62±4.39 in ductal hyperplasia, 13.47：1：4.02 in dysplasia and 37.03±10.05 in cancer tissue, respectively. Overall, p53 was positive in normal ducts, ductal hyperplasia, dysplasia, and carcinoma cells in 0 of 14 （0%）, 0 of 7 （0%）, 7 of 9 （78%）, and 10 of 11 （91%）, respectively, and K-ras was positive in 0 of 8 （0%）, 1 of 3 （33%）, 4 of 6 （67%）, 4 of 5 （80%）, respectively. CONCLUSION： Our results favorably support the hypothesis that ductal hyperplasia and dysplasia of the pancreas might be precursor lesions for pancreas cancer. Further evaluation of oncogenes by the molecular study is needed.展开更多
文摘目的:应用脉冲场凝胶电泳技术(pulsed field gel electrophoresis,PFGE)对由原料乳和牛粪中分离的肠致病性大肠杆菌EPEC O128∶K67(B12)进行基因分型,了解来自天津市9个奶牛场和保定市9个奶牛场的原料乳样品和牛粪样品分离株的遗传相关性。方法:对7株肠致病性大肠杆菌EPEC O128∶K67(B12)按照脉冲场凝胶电泳方法进行基因分型。结果:用XbaI限制性内切酶对分离株的基因组DNA进行酶切,经PFGE可形成17～20条清晰条带的分离株DNA指纹图谱,由聚类分析树状图可将7株分离株分为3个基因群。结论:7株肠致病性大肠杆菌EPEC O128∶K67(B12)分离株存在3个图谱类型,各型之间不紧密相关,未发现单个基因型菌株流行的迹象。研究发现,脉冲场凝胶电泳分型技术分辨率高、可靠、应用性强、技术先进,对原料乳的致病菌溯源有较大的应用前景。
基金Supported by the Inha University Research Grant 2005
文摘AIM： To examine surgical specimens of pancreas with either chronic pancreatitis or pancreatic cancer in order to study whether ductal hyperplasia and dysplasia in pancreas represent precursor lesions for pancreatic cancer. METHODS： We examined expression of Ki-67, CEA, p53, and K-ras, in the surgical specimens of pancreas with adenocarcinomas （n = 11） and chronic pancreatitis （n = 12）. Cellular proliferation was assessed by Ki-67 proliferation index using the proliferation marker Ki-67. In specimens with pancreas cancer, we divided pancreas epithelium into normal （n = 7）, ductal hyperplasia （n = 3）, dysplasia （n = 4）, and cancerous lesion （n = 11） after hematoxylin and eosin staining, Ki-67, and CEA immunohistochemical staining. In cases with chronic pancreatitis, the specimen was pathologically examined as in cases with pancreas cancer, and they were also determined as normal （n = 10）, ductal hyperplasia （n = 4）, or dysplasia （n = 5）. p53 and K-ras expression were also studied by immunohistochemical staining. RESULTS： In pancreatic cancer, the Ki-67 index was 3.73±3.58 in normal site, 6.62±4.39 in ductal hyperplasia, 13.47：1：4.02 in dysplasia and 37.03±10.05 in cancer tissue, respectively. Overall, p53 was positive in normal ducts, ductal hyperplasia, dysplasia, and carcinoma cells in 0 of 14 （0%）, 0 of 7 （0%）, 7 of 9 （78%）, and 10 of 11 （91%）, respectively, and K-ras was positive in 0 of 8 （0%）, 1 of 3 （33%）, 4 of 6 （67%）, 4 of 5 （80%）, respectively. CONCLUSION： Our results favorably support the hypothesis that ductal hyperplasia and dysplasia of the pancreas might be precursor lesions for pancreas cancer. Further evaluation of oncogenes by the molecular study is needed.
