BAP31 is frequently overexpressed in patients with primary colorectal cancer and correlates with better prognosis

We previously showed that B cell receptor associated protein 31(BAP31) was significantly upregulated in colorectal cancer compared with normal mucosa epithelia. However, its expression pattern and pathological role in colorectal cancer are not clearly understood. In this study, we investigated whether the expression of BAP31 was associated with the clinicopathological parameters of colorectal cancer. The expression pattern of BAP31 was detected by immunohistochemistry on a tissue microarray in both primary ...     

PCR检测白血病患者外周血中EB病毒的DNA

目的：了解白血病患者ＥＢ病毒感染情况。方法：收集２１例急性淋巴细胞白血病、１例慢性淋巴细胞白血病、１５例急性粒细胞白血病、８例慢性粒细胞白血病患者及３２例正常对照组的外周血,分离单个核细胞,提取ＤＮＡ,应用ＰＣＲ方法检测ＥＢ病毒ＤＮＡ。结果：在１例初诊慢性粒细胞白血病病人样本中发现ＥＢ病毒阳性,余均为阴性。结论：白血病患者存在ＥＢ病毒感染情况,但并不普遍。     

高龄食管贲门癌围手术期处理

目的探讨高龄食管、贲门癌病人围手术期处理,提高老年患者手术成功率和疗效。方法回顾性分析212例高龄食管、贲门癌患者的临床资料。结果本组212例患者,探查无法切除8例,治愈出院196例,术后死亡6例,2例术后死于心脏骤停,4例死于呼吸衰竭,近期吻合口瘘8例,胸腔积液6例,肺不张8例。结论高龄食管、贲门癌患者如围手术期给予很好、恰当的处理,大部分病人可恢复如愿。     

老年与青年肺癌的临床特征及预后比较

目的:为了解老年与青年肺癌的临床特征及预后的差异。方法:回顾性收集近7年来在我院肿瘤科经病理学证实的住院肺癌患者,其中符合条件的老年(≥70岁)组188例,青年(≤40岁)组68例,对患者的年龄、性别、组织分类、临床症状、治疗经过及预后等指标进行比较。结果:(1)老年组中女性患者的比例较青年组低,鳞癌类型较高;(2)老年组中胸痛症状的比例较青年组低,而阻塞性肺炎或肺不张等合并症多见;(3)老年组中远处转移较多见,临床分期较晚;(4)老年组接受综合治疗方案比例与青年组相仿。结论:老年人肺癌相比于青年人肺癌,以男性、鳞癌比例较高,合并症、远处转移更多见,易误诊和漏诊,分期较晚,预后较差。早期诊断、积极治疗能提高老年人肺癌的生存期。     

Amplification of specific DNA sequences correlates with multi-drug resistance in Chinese hamster cells

Mammalian cells selected for resistance to certain cytotoxic drugs frequently develop cross-resistance to a broad spectrum of other drugs unrelated in structure to the original selective agent. This phenomenon constitutes a major problem in cancer chemotherapy. Multi-drug resistance arises from decreased intracellular drug accumulation, apparently due to an alteration of the plasma membrane. The observation of double minute chromosomes or homogeneously staining regions in some of the multi-drug-resistant cell lines suggests that gene amplification underlies this phenomenon. We have used the technique of DNA renaturation in agarose gels to detect, compare and clone amplified DNA sequences in Adriamycin- and colchicine-resistant sublines of Chinese hamster cells. We show that both Adriamycin- and colchicine-resistant cells contain amplified DNA fragments, some of which are amplified in both of these independently derived cell lines. Furthermore, loss of the multi-drug resistance phenotype on growth in the absence of drugs correlates with the loss of amplified DNA. These results strongly suggest that the DNA sequences which are amplified in common in multi-drug-resistant cell lines include the gene(s) responsible for a common mechanism of multi-drug resistance in these cells. We have cloned one of the commonly amplified DNA fragments and show that the degree of amplification of this fragment in the cells correlates with the degree of their drug resistance.     

IL-17在胃癌组织中的表达及其与微血管生成的相关性分析

为探讨胃癌患者肿瘤组织中IL-17的表达及其与微血管生成的关系,采用免疫组织化学染色检测IL-17在30例胃癌患者石蜡包埋肿瘤组织中的表达,分析IL-17阳性细胞的形态学特征;对上述胃癌组织进行CD34免疫组织化学染色,计数微血管生成;统计学分析胃癌组织中IL-17表达与微血管生成的关系。结果在人类胃癌组织中IL-17阳性细胞多呈淋巴细胞样特征,且其表达水平较高组微血管生成增多。说明胃癌组织中IL-17表达水平与微血管生成正相关。     

Premature ageing in mice expressing defective mitochondrial DNA polymerase

Point mutations and deletions of mitochondrial DNA (mtDNA) accumulate in a variety of tissues during ageing in humans, monkeys and rodents. These mutations are unevenly distributed and can accumulate clonally in certain cells, causing a mosaic pattern of respiratory chain deficiency in tissues such as heart, skeletal muscle and brain. In terms of the ageing process, their possible causative effects have been intensely debated because of their low abundance and purely correlative connection with ageing. We have now addressed this question experimentally by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase. Here we show that the knock-in mice develop an mtDNA mutator phenotype with a threefold to fivefold increase in the levels of point mutations, as well as increased amounts of deleted mtDNA. This increase in somatic mtDNA mutations is associated with reduced lifespan and premature onset of ageing-related phenotypes such as weight loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis (curvature of the spine), osteoporosis, anaemia, reduced fertility and heart enlargement. Our results thus provide a causative link between mtDNA mutations and ageing phenotypes in mammals.