抑癌基因CpG岛甲基化与结直肠癌关系的研究进展

CpG岛甲基化可导致抑癌基因的表观遗传学转录失活,在某些情况下可能是抑癌基因失活的惟一机制,直接导致肿瘤的发生.笔者对Syk,p15,hMLH1,APC,DCC,p16等抑癌基因CpG岛甲基化与结直肠癌的关系进行简要综述,并提出存在的问题和展望.     

抑癌基因异常甲基化与肿瘤发病的关系(文献综述)

抑癌基因失活存在于多种肿瘤中,5′CpG岛高甲基化导致抑癌蛋白表达的减少与肿瘤发病率密切相关.本文总结了抑癌基因5′CpG岛高甲基化的形成机制、在人类肿瘤中的发生率及相应的治疗对策.     

抑癌基因异常甲基化与肿瘤发病的关系

抑癌基因失活存在于多种肿瘤中 ,5′CpG岛高甲基化导致抑癌蛋白表达的减少与肿瘤发病率密切相关。本文总结了抑癌基因 5′CpG岛高甲基化的形成机制、在人类肿瘤中的发生率及相应的治疗对策     

抑癌基因异常甲基化与肿瘤发病的关系

抑癌基因失活存在于多种肿瘤中，5′CpG岛高甲基化导致抑癌蛋白表达的减少与肿瘤发者率密切相关。本文总结了抑癌基因5′CpG岛高甲基化的形成机制、在人类肿瘤中的发生率及相应的治疗对策。     

抑癌基因启动子区域CpG岛甲基化与膀胱癌的研究进展

膀胱癌是我国泌尿系最常见的肿瘤,抑癌基因的失活在膀胱肿瘤的发生过程中起重要作用,而基因的异常甲基化是抑癌基因失活的第三种机制.目前发现抑癌基因启动子区域CpG岛甲基化与膀胱癌分期、分级、进展、预后相关.本文就抑癌基因启动子区域CpG岛甲基化与膀胱癌的研究进展作一综述.     

胰腺癌中基因的CpG岛甲基化异常

基冈CpG岛甲基化异常包括甲基化过度和甲基化不足，以甲基化过度为主。在恶性肿瘤中甲基化过度主要发生在抑癌基因，从而使抑癌基因不能表达，细胞发生转化并向恶变发展。另一方面，一些原癌基因甲基化不足或去甲基化，癌蛋白大量表达，进一步使抑癌基因甲基化过度导致的恶变加剧。     

DNA甲基化异常与大肠癌发生的关系研究之进展

细胞恶变的分子机制主要包括遗传学改变和表观遗传学异常.在大肠癌中,表观遗传学变异主要表现为DNA甲基化异常--包括甲基化酶表达异常、基因CpG岛甲基化异常、癌基因及抑癌基因甲基化异常等.笔者就上述问题以及它们与大肠癌发生之间的关系的研究进展进行综述.     

胰腺癌中基因的CpG岛甲基化异常(文献综述)

基因CpG岛甲基化异常包括甲基化过度和甲基化不足 ,以甲基化过度为主。在恶性肿瘤中甲基化过度主要发生在抑癌基因 ,从而使抑癌基因不能表达 ,细胞发生转化并向恶变发展。另一方面 ,一些原癌基因甲基化不足或去甲基化 ,癌蛋白大量表达 ,进一步使抑癌基因甲基化过度导致的恶变加剧     

膀胱癌DBCCR1、p16、p15、p14基因甲基化检测的意义

膀胱肿瘤患者9号染色体改变占60%以上,该染色体上分布着候选抑癌基因DBCCR1和抑癌基因p16、p15、p14.我们对4种基因5＇CpG岛甲基化状态进行了研究,现报告如下.     

肝癌细胞NFAT2基因启动子区甲基化与其mRNA表达的关系

目的:探讨肝癌细胞中NFAT2基因启动子CpG岛甲基化状态及与其mRNA表达的关系。方法:用重硫酸盐测序法检测肝癌组织与癌旁组织及不同肝细胞系与正常肝细胞中NFAT2启动子甲基化状态,用qRT-PCR检测肝癌组织与癌旁组织NFAT2 mRNA表达,并分析肝癌组织NFAT2启动子甲基化与mRNA水平的相关性。结果:肝癌组织中NFAT2基因CpG岛甲基化率明显高于癌旁组织(33.0%vs.21.6%,P=0.003);人肝癌细胞系HuH7、HepG2、Hep3B中NFAT2基因CpG岛甲基化率分别为34.8%、40.4%、37.0%,均明显高于人正常肝细胞系L02中NFAT2基因CpG岛甲基化率(16.2%)(均P0.05)。肝癌组织NFAT2 mRNA相对表达量明显低于与癌旁组织(0.000 602 4 vs.0.001 469,P0.05),肝癌组织中NFAT2 mRNA水平与其启动子甲基化程度呈明显负相关(r=-0.661,P=0.027)。结论:肝癌细胞中NFAT2基因表达下调可能与其启动子区CpG岛高甲基化状态有关     

Body composition assessment and methodology in nonathletic and athletic adolescent and adult males and females

The purpose of this review is to outline methodology for assessing body composition utilizing anthropometric and densitometric techniques. The objective of body composition assessment is to measure body fat and lean body mass. The quantity of these components varies due to growth, physical activity, dietary regimens, and aging. Anthropometric techniques incorporate selected skinfolds, circumferences, skeletal widths, or other variables to estimate body composition within k2.0-4.0%. These techniques are adequate for field testing of groups or individuals, but are population specific. Densitometry measures body volume irrespective of physique, sex, or age. This laboratory technique estimates body composition within 1.0-2.0%, is more difficult to administer, but is not population specific. Some limitation exists with any present technique due to biological variability and incomplete research of reference body composition in children, females, and the aged. J Orthop Sports Phys Ther 1984;5(6):336-347.     

Perioperative and long-term morbidity and mortality after above-knee and below-knee amputations in diabetics and nondiabetics

We performed a retrospective review of a vascular surgery quality assurance database to evaluate the perioperative and long-term morbidity and mortality of above-knee amputations (AKA, n = 234) and below-knee amputations (BKA, n = 720) and to examine the effect of diabetes mellitus (DM) (181 of AKA and 606 of BKA patients). All patients in the database who had AKA or BKA from 1990 to May 2001 were included in the study. Perioperative 30-day cardiac morbidity and mortality and 3-yr and 10-yr mortality after AKA or BKA were assessed. The effect of DM on 30-day cardiac outcome was assessed by multivariate logistic regression and the effect on long-term survival was assessed by Cox regression analysis. The perioperative cardiac event rate (cardiac death or nonfatal myocardial infarction) was at least 6.8% after AKA and at most 3.6% after BKA. Median survival was significantly less after AKA (20 mo) than BKA (52 mo) (P < 0.001). DM was not a significant predictor of perioperative 30-day mortality (odds ratio, 0.76 [0.39-1.49]; P = 0.43) or 3-yr survival (Hazard ratio, 1.03 [0.86-1.24]; P = 0.72) but predicted 10-yr mortality (Hazard ratio, 1.34 [1.04-1.73]; P = 0.026). Significant predictors of the 30-day perioperative mortality were the site of amputation (odds ratio, 4.35 [2.56-7.14]; P < 0.001) and history of renal insufficiency (odds ratio, 2.15 [1.13-4.08]; P = 0.019). AKA should be triaged as a high-risk surgery while BKA is an intermediate-risk surgery. Long-term survival after AKA or BKA is poor, regardless of the presence of DM.     

Postoperative nausea and vomiting and opioid-induced nausea and vomiting: guidelines for prevention and treatment

Postoperative nausea and vomiting (PONV) causes patient discomfort, lowers patient satisfaction, and increases care requirements. Opioid-induced nausea and vomiting (OINV) may also occur if opioids are used to treat postoperative pain. These guidelines aim to provide recommendations for the prevention and treatment of both problems. A working group was established in accordance with the charter of the Sociedad Espa?ola de Anestesiología y Reanimación. The group undertook the critical appraisal of articles relevant to the management of PONV and OINV in adults and children early and late in the perioperative period. Discussions led to recommendations, summarized as follows: 1) Risk for PONV should be assessed in all patients undergoing surgery; 2 easy-to-use scales are useful for risk assessment: the Apfel scale for adults and the Eberhart scale for children. 2) Measures to reduce baseline risk should be used for adults at moderate or high risk and all children. 3) Pharmacologic prophylaxis with 1 drug is useful for patients at low risk (Apfel or Eberhart 1) who are to receive general anesthesia; patients with higher levels of risk should receive prophylaxis with 2 or more drugs and baseline risk should be reduced (multimodal approach). 4) Dexamethasone, droperidol, and ondansetron (or other setrons) have similar levels of efficacy; drug choice should be made based on individual patient factors. 5) The drug prescribed for treating PONV should preferably be different from the one used for prophylaxis; ondansetron is the most effective drug for treating PONV. 6) Risk for PONV should be assessed before discharge after outpatient surgery or on the ward for hospitalized patients; there is no evidence that late preventive strategies are effective. 7) The drug of choice for preventing OINV is droperidol.