摘要:目的:探讨左半结肠癌合并肠梗阻Ⅰ期手术切除肠吻合的方法和注意事项。〖HTH〗方法:〖HTSS〗分析36例左半结肠癌合并肠梗阻患者Ⅰ期行手术切除肠吻合手术及术后恢复情况。结果:36例左半结肠癌并肠梗阻患者,Ⅰ期手术切除、肠吻合无一例吻合口瘘,术后恢复良好。〖HTH〗结论:〖HTSS〗只要围手术期、术中处理得当,左半结肠癌合并肠梗阻患者选择Ⅰ期手术切除肠吻合,可以减少患者痛苦、节约医疗费用,同时也是安全的。
The results of 2389 patients exmained by colonofiverscope in past nine years are reported. Polyps were found in 561 cases, including 1256 polyps in the large intestine and 82 polyps in the terminal ileum. All 1299 polyps were removed with biopsy forceps. Pathology demonstrated that there were 406 adenomas, including 89 atypical hyperplasia and 23 cases with malignant change and 932 non-canerous polyps with 102 atypical hyperplasia. Since adenoma is seen to be a precancerous change, the polypectomy by colonofiberscope , ecpecially atypical hyperplastic polyps may decrease morbidity of large intestinal cancer. Cancer associated with adenoma may be as high as 51.28%, so the recrudescence of polyps may possibly be found even afer the cancer removal. These data showed that an early discovery of small malignant adenoma is key to improve efficiency.
目的 探讨结肠癌和直肠癌并发肠穿孔的外科诊治方法。方法 分析13例结直肠癌并发肠穿孔患者的临床资料。结果 13例患者中4例行肿瘤所在肠段一期切除吻合术； 4例行一期病灶切除吻合术，近端肠段行外置双管造瘘术； 2例切除肿瘤所在肠段，近端行端式结肠造瘘术，远端行封闭（Hartmann）术； 3例行单纯肠造瘘术。术后并发症发生率为46.15%（6/13），手术死亡率为15.38%（2/13）。结论 重视对结直肠癌并发肠穿孔的认识及选择合适的手术方式是减少并发症、提高疗效的重要措施。
ObjectiveTo improve the efficacy of colon doublecontrast barium enema examination by using digital gastrointestinal machine and modified enema techniques. MethodsSixtyfour patients were examined on digital remote controlled gyration table, with oral coloncleansing preparation and selfmade disposable plastic bag. Results In 64 patients, up to 93.8% were found with none or little fecal materials in the cecum and ascending colon. 80% of the results were scored excellent, and 95% were accurate for making diagnosis. All the patients underwent the examination successfully. ConclusionDigital gastrointestinal machine examination combined with modified hypotonic doublecontrast barium enema is a simple, convenient and efficient way to clearly demonstrate colonic mucosa, and help increase the detection and diagnosis rate.
ObjectiveTo investigate the effects of overexpression of alpha/beta hydrolase domain-containing protein 5 (ABHD5) on the invasion and migration of human colon cancer cell line HCT116 and the pathway of adenosine monophosphate-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR).MethodsThe expression of ABHD5 in colon cancer tissues and its relationship with clinicopathological features was analyzed by UALCAN database. HCT116 cells were cultured in vitro and transfected with ABHD5 recombinant plasmid, then they were divided into control group, negative transfection group and ABHD5 transfection group. Real time quantitative PCR (qRT-PCR) was used to detect the expression of ABHD5 mRNA in HCT116 cells. The proliferation of HCT116 cells was detected by CCK-8 method. Transwell assay was used to detect the invasion and migration of HCT116 cells. The expression of matrix metalloprotein 9 (MMP-9), E-cadherin, Snail, and AMPK/mTOR pathway proteins p-AMPK, AMPK, p-mTOR and mTOR were detected by Western blot.ResultsThe results of the UALCAN showed that compared with normal colon tissues, the expression of ABHD5 mRNA in colon cancer tissues was decreased (P<0.05), and which in the adenocarcinoma and the N1 stage was lower than that of the mucinous adenocarcinoma (P<0.05) and N0 stage (P<0.05), respectively. Compared with the control group and the negative transfection group, the expression of ABHD5 mRNA in the ABHD5 transfection group was increased (P<0.05), the proliferation inhibition rate of HCT116 cells in the ABHD5 transfection group was increased (P<0.05), the numbers of migration and invasion cells in the ABHD5 transfection group were decreased (P<0.05), the expressions of MMP-9, Snail, p-mTOR and mTOR were reduced, and the expressions of E-cadherin, p-AMPK and AMPK were increased (P<0.05).ConclusionsThe overexpression of ABHD5 can inhibit the invasion and migration of colon cancer HCT116 cells, activate AMPK, and inhibit the expression of mTOR. It suggests that ABHD5 may play a role in inhibiting colon cancer by affecting AMPK/mTOR pathway.