Objective To investigate the relationship between hepatitis B virus (HBV) basic core promoter(BCP)/precore(PreC) mutations and severity of liver dis ease. Methods In 113 patients chronically infected with HBV, do uble mutations in BCP(T1762/A1764) and PreC mutation(A1896) were determined by INNO-LiPA and HB V genotype was determined by S gene sequencing. Results Whether in all patients or in patients infected by single genotype C, compared with AsC, the prevalence of double mutations in BCP(T1762/A1764) was higher in patients with CHB, LC and HCC[(24.1% vs 2.8%,? 2=5.93, P0.05). Conclusions The doubl e mutations in BCP(T1762/A1764 ) may be related to progressive liver disease in patients with chronic HBV infec tion.

Objective:To investigate the influence of hepatocyte growth factor(HGF)on the expression of vascular endothelial growth factor C(VEGF-C)and the mechanism of HGF-induced VEGF-C expression in tongue squamous cell carcinoma Tca8113 cells.Methods:Tca8113 cells were cultured and exposed to HGF with various concentrations.The expression level of VEGF-C was assessed by ELISA.Signaling transduction inhibitors LY294002,U0126,SP600125,SB203580 was used to block PI3K/Akt,P44 /P22MAPK,JNK,P38MAPK signaling pathways,respectively.Then,the expression level of VEGF-C was detected by ELISA.Re-sults:The VEGF-C expression of Tca8113 cells increased at the beginning and decreased later with the increase of HGF concentra-tion.When the concentration of HGF was 40 ng/ml,VEGF-C expression level was the highest.Inhibitor LY294002 of PI3K/Akt and Inhibitor U0126 of P44 /P22MAPK significantly blocked the effects on HGF-induced VEGF-C up-regulation(P ＜0.01 ).Inhibitor SP600125 of JNK and inhibitor SB203580 of P38MAPK didn't interfere HGF-induced VEGF-C expression(P >0.05).Conclusion:HGF contributed to the expression of VEGF-C,PI3K/Akt and P44 /P22MAPK signaling pathways may be involved in HGF-induced VEGF-C up-regulation,and may play potential roles in lymphatic metastasis of oral squamous cell carcinoma.

Objective To investigate the signaling pathway and the key signal molecules of protein kinase (RIPK)3 in SH-SY5Y cells. Methods SH-SY5Y cells were transfected with RIPK3 expression plasmid vector to upregulate intracellular RIPK3, while the SH-SY5Y cells were transfected with empty vector plasmid, which was considered as control group. Western blot assay was used to check the expression of exogenous RIPK3 in cells. The proliferation rate of SH-SY5Y cells was determined by MTT assay at designated time to detect exogenous RIPK3 activity. Whole transcriptome sequencing (RNAseq) was used to detect the transcription of genes. Whole-transcriptomic gene transcription was measured by following Ingenuity Pathway Analysis (IPA) to obtain downstream signaling pathways and the key molecule, which were partly confirmed by following droplet digital PCR (ddPCR). Results Exogenous RIPK3 showed biological activity in SH-SY5Y, which inhibited the proliferation of cells. IPA showed that znic finger protein 36 (ZFP36) was significantly up-regulated as compared with that of the control group. The tran?scription levels of ZFP36 downstream genes such as tumor necrosis factor (TNF), brain derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and mRNA-decapping enzyme 2 (DCP2) were affected at the same time. Conclusion Within the limitations of this study, it seems that RIPK3 is notable for the development, inflammation and tumorigenesis of the nervous system as an independent regulator of ZFP36 gene and downstream effectors.