芳基卤的Suzuki交叉偶联反应

空间位阻、对空气稳定的单氧氯化膦与Pd2（dba）3反应原位形成复合物，可促进芳基硼酸与芳基卤的Suzuki交叉偶联反应。芳基卤上有吸电子基时反应性更高，羰基及氰基无需保护。13例收率66％～93％。     

血清HBV-DNA水平的变化与慢性乙型活动性肝炎的关系

目的:研究慢性肝炎患者HBV-DNA水平与病情变化的关系. 方法:采用荧光标记定量PCR的方法,测定慢性乙型肝炎急性发作患者(HBeAg阳性45例,抗HBe阳性30例)其活动期和恢复期的血清HBV-DNA含量. 结果:HBeAg阳性组血清HBV-DNA含量(Logarrithm copy/mL)在活动期显著高于恢复期[(10.2±1.6) vs (5.3±2.1), P<0.05],抗-HBe阳性组血清HBV-DNA含量(Logarrithm copy/mL)在活动期显著高于恢复期[(7.6±1.3) vs (4.0±2.0), P<0.05]. 另外,活动期血清HBV-DNA含量(Logarrithm copy/mL)在HBeAg阳性组显著高于抗HBe阳性组[(10.2±1.6) vs (7.6±1.3), P<0.05]. 血清HBV-DNA水平与丙氨酸转氨酶(ALT)、门冬氨酸转氨酶(AST)及总胆红素(T-BLLI)之间无相关性. 结论:HBV-DNA复制水平与慢性乙型病毒性肝炎的活动密切相关.     

Mutation analysis of the Smad2 gene in human colon cancers using genomic DNA and intron primers

In mammals, one of the Mad homologues, Smad2, was reported to be a mediator of TGF-beta signaling, and was found mutated in some cases of colon and lung cancers. To extend the analysis of this gene, we previously investigated the genomic organization of the human Smad2 gene and defined the structure of 12 exons and flanking introns. In this study, we designed 11 sets of intron-based primers to examine the entire coding region of the Smad2 gene. By the PCR-SSCP method using these primers, we screened genomic DNA sequences of colorectal cancers for mutations of the Smad2 gene. Though there was no mutation within all exons of the Smad2 gene, two of 60 sporadic colorectal cancers displayed deletions in the polypyrimidine tract preceding exon 4. Deletions of this region were also detected in colon cancer cell lines, and were clustered within cells exhibiting microsatellite instability. Deletions in the polypyrimidine tract had various effects on pre-mRNA splicing, but had no effect on the splicing of the Smad2 gene in these cases. However, our data support the idea that the polypyrimidine tract in the splicing acceptor site is a target of mutations in mismatch repair-deficient tumors.      

Cooperativity between the polyamine pathway and HER-2neu in transformation of human mammary epithelial cells in culture: Role of the MAPK pathway

Our experiments were designed to test the cooperativity between the polyamine pathway and HER-2neu in inducing transformation of human mammary epithelial cells in culture. Using the MCF-10A breast epithelial cell line, we observed that induction of overexpression of ornithine decarboxylase (ODC) (the first rate-limiting enzyme in polyamine biosynthesis) markedly potentiated the anchorage-independent growth stimulating effect of the β2 isoform of neu differentiating factor (NDF) known to activate HER-2neu in MCF-10A cells. ODC overexpression, on the other hand, did not enhance growth in liquid culture, thus pointing to a specific effect on transformation rather than proliferation. ODC-overexpressing MCF-10A cells exhibited increased MAPK phosphorylation in response to administration of NDF and/or epidermal growth factor (EGF). In contrast, the phosphorylation of the members of the stress-activated protein kinase cascade p38 and SEK were not affected by ODC overexpression. Of note, in the absence of EGF and NDF, ODC overexpression failed to induce both clonogenicity and MAPK activation. These results suggest that increased polyamine biosynthetic activity critically interacts with HER-2neu in promoting human mammary cell transformation in culture and that the MAPK cascade is an important mediator of this interaction. If confirmed in future in vivo<0R> studies, our results may identify important new targets for the chemoprevention of human breast cancer. Int. J. Cancer 76:563–570, 1998.© 1998 Wiley-Liss, Inc.     

血管性痴呆发病机制研究进展

血管性痴呆发病率日益增高, 但发病机制不明确, 缺乏有效治疗手段, 因此各方面研究日益受重视, 本文主要对血管性痴呆的危险因素、病理类型、发病机制等方面做一综述.