Gastric dysplasia may be an independent risk factor of an advanced colorectal neoplasm

AIM: To evaluate the relationship between gastric dysplasia and Helicobacter pylori (H pylori) and the occurrence of colorectal adenoma, and to defi ne the necessity for colonoscopy in patients with gastric dysplasia or H pylori infection.METHODS: From May 2005 to February 2008, 133 patients with established gastric dysplasia by gastroduo-denoscopy (EGD) were additionally investigated by colonoscopy. The authors compared results with those of 213 subjects who underwent both EGD and colonoscopy during the same period at the author’s Health Promotion Center as a control group. H pylori infection was evaluated in both the gastric dysplasia and control groups.RESULTS: The mean age of all 346 study subjects was 54.1 ± 10.5 years, and there were 258 (73%) men and 87 (27%) women. No signif icant difference was found between the H pylori positive and negative subjects in terms of the prevalence of colorectal adenoma and advanced colorectal adenoma (P = 0.261). Patients with gastric dysplasia showed no elevated risk of colorectal adenoma (OR = 0.910, 95% CI: 0.587-1.411, P = 0.738), but had a signif icantly higher risk of having advanced colorectal adenoma (OR = 3.382, 95% CI: 1.700-6.342, P = 0.000).CONCLUSION: The study emphasizes the need for colon surveillance in patients with gastric dysplasia, regardless of H pylori infection.

Trans-10,cis-12, not cis-9,trans-11, conjugated linoleic acid decreases ErbB3 expression in HT-29 human colon cancer cells

瞄准：检验是否 trans-10， cis-12 CLA (t10c12 ) 或 cis-9， trans-11 CLA (c9t11 ) 禁止 heregulin (HRG )-beta-stimulated 细胞生长并且 HRG-beta-ErbB3 在 HT-29 细胞发信号。方法：我们在 CLA 异构体或 ErbB3 ligand HRG 贝它的缺席或存在的有教养的 HT-29 房间。MTT 试金，[3H ] 胸腺嘧啶核甙加入，染色的 Annexin V， RT-PCR，西方的弄污，免疫降水，和在试管内激酶试金被执行。结果：HRG 贝它增加了房间生长，但是没阻止导致 t10c12 的生长抑制。T10c12 禁止了 DNA 合成并且导致了 HT-29 房间的 apoptosis，而 c9t11 没有效果。T10c12 减少了以一种剂量依赖者方式的 ErbB1， ErbB2，和 ErbB3 蛋白质和抄本的层次，而 c9t11 没有效果。Immunoprecipitation/Western 污点研究表明 t10c12 禁止了 ErbB3，到 ErbB3 的 phosphoinositide 3-kinase (PI3K ) 的 p85 子单元的招募，联系 ErbB3 的 PI3K 活动，和 Akt 的磷酸化的 HRG-beta-stimulated 磷酸化。然而， c9t11 没在 phospho Akt 层次上有效果。既不 t10c12 也不 c9t11 在 ERK-1/2 的 HRG-beta-induced 磷酸化上有任何效果。结论：这些结果显示由 t10c12 的 HT-29 细胞生长的抑制可以经由它发信号导致 Akt 激活的抑制的 ErbB3 的调整被导致。