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Epigenetics is defined as a heritable change occurring in gene expression and phenotype without altering the underlying primary DNA sequence itself. Epigenetic variation consists of DNA methylation repatterning, posttranslational modification of histone proteins, and non-coding RNAs (ncRNAs). Epigenetic modifications are deeply involved in tumorigenesis and tumor development. Epigenetic abnormalities can be therapeutically reversed, and three families of epigenetic marks, including "readers", "writers" and "erasers", could be modulated by epi drugs. Over the past decade, ten small-molecule epi drugs (e.g., inhibitors of DNA methyltransferases and histone deacetylases) have been approved by FDA or CFDA for the treatment of different cancers. Epigenetics therapy has been most effective in oncology and has become an attractive area in cancer treatment. Pulmonary hypertension (PH) encompasses a set of multifactorial diseases of progressive cardiopulmonary disorder. WHO classifies PH into five groups based on similar pathophysiological mechanisms, clinical presentation, haemodynamic characteristics, therapeutic management, and underlying etiology. Since PH shows many similarities with cancer, such as proliferation, resistance to apoptosis, and dysregulation of tumor suppressor genes, the current epigenetics therapeutic strategies used in cancer might be considered for the treatment of PH. The role of epigenetics in the setting of PH is a fast-growing field of research. In this review, we have summarized the up-to-date articles on the role of epigenetic mechanisms in the context of PH. The aim of this review is to provide a comprehensive insight from the epigenetics perspective and introduce the potential role of approved epi drugs in PH treatment.

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<p><b>OBJECTIVE</b>To observe the effectiveness and safety of electrothermal acupuncture in the prevention and treatment of chemotherapy-induced nausea and vomiting (CINV) in the cancerous patients of phlegm-stasis interaction in cisplatin-containing chemotherapy.</p><p><b>METHODS</b>Sixty cases of phlegm-stasis interaction in cisplatin-containing chemotherapy were randomized into a trial group and a control group, 30 cases in each one. In the control group, the intravenous drip of granisetron hydrochloride injection was adopted, 3 mg before and after cisplatin-containing chemotherapy 30 min, continuously for 3 days. 43 to 45℃ electrothermal acupuncture at zusanli(ST 36) for 30 min was used on the basis of the treatment as the control group in the trial group,once a day for 3 days. CINV, anti-nausea effects, Karnofsky score, the syndrome score of phlegm-stasis interaction, and relevant indices of safety were observed on the 1st and 7th days of cisplatin-containing chemotherapy separately.</p><p><b>RESULTS</b>1.Regarding CINV and anti-nausea effect, CINV did not occur before chemotherapy in the patients of the two groups. On the 1st and 7th days of chemotherapy, CINV in the trial group were milder than those in the control group (both<0.05).The anti-nausea effects in the trail group were better than those of the control group.2.Regarding Karnofsky score and the syndrome score of phlegm-stasis interaction, the improvements on the 7th days of chemotherapy in the trial group were better than those in the control group, indicating the significant differences (both<0.05). 3.Regarding the safety indies, there was no adverse reaction during the treatment in the two groups.</p><p><b>CONCLUSIONS</b>The electrothermal acupuncture effectively relieves CINV, and improves self-care dbility and the symptoms of phlegm-stasis interaction.</p>

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The objective of this study was to construct and express recombinant prokaryotic plasmid pET32a (+)- ast1 in E. coli BL21(DE3). Amastin gene was amplified from genomic DNA of Leishmania Donovani and its transmembran region was predicted by the methods of SOSUI and Tmpred; astl located in N-terminus of amastin gene was amplified and cloned into prokaryotic plasmid pET32a(+), which was named pET32a(+)-ast1, and then rAST1 was expressed in E. coli BL21(DE3). The results of SDS-PAGE and immunobloting assay showed that a fusion protein rAST1 (relative molecular mass about 27 kDa) was able to express in BL21. The recombinant prokaryotic plasmid pET32a(+)- ast1 was successfully constructed, and noted to be efficiently expressed in E. coli BL21(DE3).

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In order to clone lvgA gene (Legionella virulence gene) of Legionella pneumophila and detect its expression in prokaryotic cell, we amplified the lvgA gene from the total cell DNA of Legionella pneumophila with PCR,and then inserted it into the coloning vector pUC18. The recombinant plasmid pUlvgA was obtained. After the recombinant plasmid pUlvgA was identified with restriction enzyme analysis, polymerase chain reaction and nucleotide sequencing analysis, the lvgA gene was subcloned into the prokaryotic expression vector pGEX-4T-1. The prokaryotic expression recombinant plasmid pGlvgA was constructed. After IPTG induction, the E. coli JM109 containing the recombinant plasmid pGlvgA expressed fusion protein. The expression of lvgA was subsequently detected by SDS-polyacrylamine gel electrophoresis and Western-blot analysis. The results indicated that the lvgA gene of 627 bp long was amplified, the recombinant plasmids pUlvgA and pGlvgA were constructed successfully, and the GST-LvgA fusion protein of approximately 36 KDa in size was expressed in prokaryotic cell efficiently as expected.

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