DCC基因蛋白在大肠癌中的表达及意义

目的探讨DCC基因在大肠癌中的蛋白表达及其生物学行为的关系.方法应用免疫组化方法检测46例大肠癌及相应癌旁正常组织和41例正常人大肠组织的DCC基因蛋白表达.结果正常大肠粘膜组织全部表达,大肠癌组织部分表达,阳性率为28%(13/46),两组差异显著(P＜0.01),且与肿瘤浸润转移(Dukes分期)及分化程度有明显相关(P＜0.05),5例伴肝转移组织全部表达缺失.结论DCC基因与大肠癌的发生发展有关,与其浸润转移(Dukes分期)呈负性相关.DCC基因蛋白表达可作为形态学之外判断大肠癌生物学行为的一种指标.     

石杉碱甲-亚油酸酯的合成及其性质的初步研究

目的 合成石杉碱甲(huperzine A，HUP)-亚油酸(1inoleic acid，LA)酯(HUP—LA)，并对其性质进行初步探讨。方法 利用二环己基碳酰二亚胺(DCC)法制备HUP—LA；考察了其在不同pH值、不同温度的缓冲液及小鼠血浆和不同脏器组织匀浆中的降解情况。结果 HUP—LA经^1H—NMR，^13C—NMR，IR，MS，UV证实为目标化合物。目标化合物在不同的体外环境中稳定性差异大。结论 该研究对于石杉碱甲的结构改造有参考意义。     

国人大肠肿瘤与DCC基因mRNA表达缺失的相关性研究

应用逆转录聚合酶链反应（ＲＴ－ＰＣＲ）技术检测了３４例大肠肿瘤及其相应正常粘膜中ＤＣＣ基因ｍＲＮＡ表达情况。结果：５例大肠腺瘤和２９例大肠癌组织中分别有１例（２０％）、１５例（５１．７％）ＤＣＣ基因ｍＲ－ＮＡ表达发生缺失。其中高、中、低分化的大肠癌组织中该基因ｍＲＮＡ表达缺失率分别为２５．０％（２／８）、４４．４％（４／９）、７５．０％（９／１２）（Ｐ＜０．０５）。而有转移者为７６．９％（１０／１３），无转移者３１．２％（Ｐ＝０．０１８）。ＤＣＣ基因ｍＲＮＡ表达缺失与性别、肿瘤大小及部位无关。提示：对大肠癌原发病灶ＤＣＣ基因ｍＲＮＡ表达的检测将有助于识别高度恶性的大肠癌及判断大肠癌的转移潜能。     

Characteristics and sputum conversion of tuberculosis (TB) patients in Kalutara,Sri Lanka

Background

Tuberculosis (TB) is an infectious bacterial disease; remains as one of the important public health problem affecting every part of the world. Substantial number of TB cases are reported from Sri Lanka every year irrespective of its strong preventive health system. The aim of this analysis is to describe the characteristics of TB patients and to assess the factors associated with sputum conversion. This analysis was based on the data from the District Chest Clinic of Kalutara district, Sri Lanka.

大肠癌组织APC／MCC和DCC基因杂合缺失的研究

为评估ＡＰＣ／ＭＣＣ和ＤＣＣ基因在大肠癌发生和发展中的作用，采用聚合酶链反应（ＰＣＲ）技术，并配合限制性片段长度多态现象（ＲＦＬＰ）分析，对４１例大肠癌患者的组织ＡＰＣ／ＭＣＣ（位于染色体５ｑ２１）和ＤＣＣ基因（位于染色体１８ｑ２１．３）杂合缺失（ＬＯＨ）进行研究。ＡＰＣ基因ＬＯＨ率为２８．０％（７／２５），ＭＣＣ基因ＬＯＨ率为３６．４％（８／２２），两者综合分析ＬＯＨ率为３８．９％（１４／３８）。ＤＣＣ基因ＬＯＨ率为５５．３％（２１／３８）。ＤＣＣ基因在有淋巴结转移组的ＬＯＨ率（８０．０％）显著高于无淋巴结转移组（３９．１％）（Ｐ＜０．０５），在ＤｕｋｅｓＣ、Ｄ期组的ＬＯＨ率（７１．４％）显著高于Ａ、Ｂ期组（３５．３％）。以上结果提示，ＡＰＣ／ＭＣＣ和ＤＣＣ基因的ＬＯＨ是大肠癌常见的基因改变，ＤＣＣ基因ＬＯＨ的测定有可能成为大肠癌病人预后估计的指标。     

No association between the Arg201Gly polymorphism of the DCC gene and colorectal cancer.

BACKGROUND AND AIMS: In one small study, the DCC Arg201Gly polymorphism has been observed more frequently in colorectal cancer cases compared with controls. We wondered whether these results could be replicated in a much larger study. METHODOLOGY: The DCC Arg201 Gly polymorphism was genotyped in 625 unselected Caucasian colorectal cancer patients and 220 controls. Association analysis was used to search for a difference between patients and controls. Subgroup analyses were performed for site of tumour, gender, age at diagnosis, family history of colorectal cancer and modified Dukes classification. RESULTS: The association analyses revealed no difference in Arg201Gly genotype frequency between patients and controls, neither overall nor for different subgroups according to site of tumour, gender, age at diagnosis, family history of colorectal cancer and modified Dukes classification. CONCLUSION: No association was observed between the Arg201Gly polymorphism of DCC and colorectal cancer risk.     

Molecular lesions in colorectal cancer: impact on prognosis? Original data and review of the literature

BACKGROUND: In the Dukes' B and C stages of colorectal carcinoma there are considerable variations in the observed courses of the disease. Since post-operative chemotherapy in patients with Dukes' C (node-positive) colon carcinoma has been demonstrated to be effective in improving overall-survival, a more exact prognosis assessment gains additional significance and therapeutic relevance. DISCUSSION: One also hopes to derive improved prognostic factors from the clarification of the molecular pathogenesis. Because of its frequency and the accessibility and recognizability of its developmental stages colorectal carcinoma is among the best investigated of all solid tumors. Despite a multitude of suggested molecular candidate markers none of these changes has yet been able enter the everyday life of the clinic. However, it is to be expected that some of the molecular alterations presently discussed will gain importance before long in the clinical treatment of patients with colorectal carcinoma. CONCLUSION: Considering also our own findings, this review presents the latest developments in the scientific discussion of the tumor suppressor/oncogenes p53, k-ras, and DCC, biochemical determinants of the 5-fluorouracil metabolism, and defects of the DNA repair system.     

UNC5H3和DCC在胃癌中的表达与增殖的关系及其预后

目的 探讨UNC5H3和DCC在胃癌组织的表达,与临床病理特征和增殖的关系以及与患者生存和预后的关系。 方法 应用组织芯片和免疫组织化学技术,分析60例胃癌组织中UNC5H3、DCC和Ki-67的表达,并对其表达进行相关分析。利用图像分析软件Image-Pro Plus 6.0测量切片积分吸光度,对结果进行验证。采用Kaplan-Meier限乘法计算生存率。建立Cox回归模型,评价UNC5H3和DCC作为胃癌患者预后的独立影响因素的可行性。结果 在60例胃癌组织中,UNC5H3、DCC和Ki-67的阳性表达率分别为43.3%、53.3%和60.0%。UNC5H3和DCC与淋巴转移和远处转移之间,差异有显著性(P<0.05)。UNC5H3和DCC表达与Ki-67表达相互之间无相关性（P>0.05）。用Kaplan-Meier生存曲线经 Log-rank检验发现,UNC5H3的阳性表达与胃癌患者生存之间存在相关性（P<0.05）。DCC的阳性表达与胃癌患者生存之间无相关性（P>0.05）。经Cox回归分析,UNC5H3和DCC的表达与胃癌患者预后无明显相关性。结论 依赖性受体UNC5H3和DCC共同参与了胃癌的发生进展,检测UNC5H3和DCC可作为反映胃癌临床病理学特点的指标,检测UNC5H3可作为胃癌患者生存期的指标,但UNC5H3和DCC的表达不是判断胃癌患者预后的独立影响因素。     

Neuroprotective effect of gold nanoparticles composites in Parkinson's disease model

Parkinson’s disease (PD) is second most common neurodegenerative disorder worldwide. Although drugs and surgery can relieve the symptoms of PD, these therapies are incapable of fundamentally treating the disease. For PD patients, over-expression of α-synuclein (SNCA) leads to the death of dopaminergic neurons. This process can be prevented by suppressing SNCA over-expression through RNA interference. Here, we successfully synthesized gold nanoparticles (GNP) composites (CTS@GNP-pDNA-NGF) via the combination of electrostatic adsorption and photochemical immobilization, which could load plasmid DNA (pDNA) and target specific cell types. GNP was transfected into cells via endocytosis to inhibiting the apoptosis of PC12 cells and dopaminergic neurons. Simultaneously, GNP composites are also used in PD models in vivo, and it can successfully cross the blood-brain barrier by contents of GNP in the mice brain. In general, all the works demonstrated that GNP composites have good therapeutic effects for PD models in vitro and in vivo.     

原发性胃癌中DCC抑癌基因杂合性丢失的研究

目的：探讨原发性胃癌组织中结直肠癌缺失基因（deleted in colorectal carcinoma.DCC)杂合性丢失（loss of heterozygosity,LOH)的情况及其与胃癌临床病理学间的关系。方法：用多聚酶链反应－单链构相多态性（PCR－SSCP）银染法分析49例原发性胃癌组织中DCC的杂合性丢失。结果：D18S484位点发生LOH的频率为26．6％（12／45），D18S487为23．9％（11／46），DCC发生LOH的频率为36．7％（18／49）。36．8％（7／19）的肠型胃癌发生DCC LOH，24．0％（6／25）的弥漫型胃癌发生DCC LOH，而100％（5／5）的混合型胃癌为DCC LOH（P＜0．05）。在淋巴结有转移的胃癌中，52％（13／25）的原发性胃癌发生DCC LOH，无转移者中为20．8％（5／24）（P＜0．05）；发生远处转移者，原发性胃癌DCC LOH为100％（3／3），而无转移者为32．6％（15／46）（P＜0．05）；在TNM Ⅲ、Ⅳ期中DCC LOH为50．0％（12／24），有高于TNM I、Ⅱ期（24％，6／25）的趋势（P＝0．059）。DCC LOH与病人的性别、年龄、肿瘤发生部位、大小、组织学分级均无统计学意义（P＞0．05）。结论：DCC的杂合性丢失可能在胃癌的发展和转移中起重要作用，是胃癌发展后期的重要分子事件。