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HBV infection is an important clanger factor in the occurrence of HPC and it indicates that PHC patients are often accompanied by active HBV replication.

因此，积极预防和控制HBV感染流行，恰当治疗、保肝和护肝措施，是减少原发性肝癌发生的关键所在。

Oxidative stress, a known activator of HIV replication in vitro, has a potential role as a cofactor of HIV disease progression.

氧化压力已知可以催化在体外复制 HIV ，对于辅助 HIV 疾病发展扮演着重要的角色。

Finally, we demonstrated that EBNA2-induced polyploidy is due to both DNA endo-replication and cytokinesis failure.

最后我们也证明了EBNA2诱发的多套体是由於DNA的内复制以及细胞质分裂失败所造成的。

In contrast, cancer cells lacking functional P53 would be expected to be sensitive to viral replication and subsequent cytolysis. However P53 defections wildly exist in most of human cancer cell, deletion of E1B-55kD gene can make the adenovirus target at p53 mutation tumor cell.

以往的研究表明，大部分人类肿瘤中均存在p53基因突变，因此E1B55kD蛋白缺失的重组病毒只能在P53功能异常的肿瘤细胞中复制，而在正常细胞中该重组病毒由于缺乏对抗P53蛋白的病毒产物，不能有效复制，因此具有肿瘤靶向治疗的特点。

Methods: Virus proliferation assay, cell viability assay and Western blot were performed to assess the selective replication and cytolysis of CNHK500 in telomerase positive liver cancer cells Hep3B, HepGⅡ, SMMC7721 and in normal cells.

方法利用病毒增殖实验、细胞活力实验、蛋白印迹分析来检测增殖病毒CNHK500在端粒酶阳性的肝癌细胞株HepGⅡ、Hep3B、SMMC7721及正常细胞中选择性增殖和溶解细胞的特性。

Antitumor efficacy of replication-competent adenovirus CNHK500 in vivo was associated with increased dosage of CNHK500. Conclusions: The results prove that CNHK500 has highly proliferation selectivity and potent cytolysis effect on breast cancer.

肿瘤选择性增殖腺病毒CNHK500可选择性在端粒酶阳性的乳腺癌细胞中复制，并产生体内外杀伤作用。

Because different cell lines may show various levels of susceptibility to adenovirus infection and virus production, non-selectively replicating wtAd5 was used to be a comparison with the tested conditionally replicating adenovirus CNHK500.ONYX-015, the first replication-competent adenovirus entered into clinical trials was also used to be a comparison. We used virus proliferation assay, cell viability assay and western blot to evaluate the proliferation and cytolysis selectivity of CNHK500. Results demonstrated that the CNHK500 virus proliferation multiples in breast cancer cell lines after 48 hours is similar to that of wtAd5, ONYX-015 virus proliferation ability is less than that of CNHK500 in cancer cells.

然后，通过与ONYX-015（E1B 55 KD a蛋白缺失的2型和5型嵌和型腺病毒，美国ONYX生化制药公司研制）、wtAd5进行对比，利用病毒增殖实验和细胞生长抑制实验，验证了CNHK500选择性增殖能力和肿瘤特异性杀伤作用；利用Western Blot检测CNHK500腺病毒E1A和E1B在乳腺癌细胞和正常成纤维细胞中的表达差异，揭示了腺病毒肿瘤靶向性的机制；利用携带绿色荧光蛋白的CNHK500-EGFP感染乳腺癌细胞株和正常成纤维细胞株，直观地观察其感染乳腺癌细胞的能力和在乳腺癌细胞中的增殖过程。

In addition to humans than chimpanzees are the only primates infected with HIV, but HIV-maneuvers in the human body to body like a chimpanzee was Danian of the same low level of replication does not cause any symptoms of HIV.

黑猩猩是除人类之外唯一能感染HIV的灵长类动物，但在人体内纵横捭阖的HIV到了黑猩猩体内却像被打蔫了一样，复制水平很低，不会引起任何艾滋病症状。

Contribution of asymmetric cytosine deamination was found to be weak to TAP in most phyla, and strong to RAP in all the Proteobacteria but weak in most of the Firmicutes. This possibly reflects the differences in their chromosomal replication machineries.

不对称的cytosine deamination作用对大多数的门中的TAP贡献很小，对Proteobacteria的RAP贡献显著，而对大多数Firmicutes的RAP贡献很小，这可能反映了这两门物种间染色体复制机制的不同。

These skew reflect mainly those in protein coding sequences, which are driven by asymmetric mutation pressures during replication and transcription (notably asymmetric cytosine deamination) plus subsequent selection for preferred structures, signals, amino acid or codons.

这些不对称性主要反应在蛋白质编码序列上，并且主要是受到复制与转录期间复制双股之间的不对称突变压力加上之后为了偏好的结构、信号、胺基酸或转录子的筛选所驱使。

What are your goals and strategies for growth?

你的成长目标和策略是什么？

And unto the angel of the church in Sardis write; These things saith he that hath the seven irits of God, and the seven star I know thy works, that thou hast a name that thou livest, and art dead.

3：1 你要写信给撒狄教会的使者，说，那有神的七灵和七星的，说，我知道你的行为，按名你是活的，其实是死的。