Objective To detect the expression of EIF5A2 in hepatocellular carcinoma(HCC) and to explore its relation with clinicopathological characters and prognosis of HCC patients. Methods The expression of EIF5A2 mRNA and protein in 12 pairs of fresh HCC and corresponding non-tumor tissues adjacent to the cancer was examined by qRT-PCR and Western blot. The expression level of EIF5A2 in 284 pairs of HCC and adjacent non-tumor tissues was detected by IHC staining. Then we analyzed between EIF5A2 expression and clinical pathological parameters and prognosis of HCC patients. Results The relative expression levels of EIF5A2 mRNA and protein in fresh HCC tissues were significantly higher than those in the corresponding adjacent non-tumor tissues (t=5.305, P=0.0003; t=10.120, P < 0.001); EIF5A2 expression in 284 HCC tissues was significantly higher than that in the corresponding adjacent non-tumor tissues (z=-12.186, P < 0.001). The expression of EIF5A2 was significantly correlated with tumor size (χ²=13.079, P < 0.001), tumor multiplicity (χ²=4.589, P=0.032) and differentiation degree (χ²=4.844, P=0.028). The 3- and 5-year overall survival time and disease-free survival time of the patients with high expression of EIF5A2 were significantly shorter than those with low expression of EIF5A2 (P < 0.001). EIF5A2 was an independent prognostic factor affecting the 3- and 5-year overall survival time and disease-free survival time of HCC patients (P < 0.05). Conclusion The up-regulation of EIF5A2 expression may be related with the occurrence and development of hepatocellular carcinoma. The high expression of EIF5A2 is an independent influence factor for poor prognosis and EIF5A2 can be used as a potential molecular marker for predicting the prognosis of HCC patients.

Objective:To detect the expression of Myc-induced nuclear antigen 53 (Mina53) and liver tissue >5 cm from the edge of the tumor (LTM5), and analyze its relationship with tumorigenesis, clinicopathological characteristics, and patient survival and prognosis in hepatocellular carcinoma (HCC).Methods:The expression levels of Mina53 mRNA and protein in 18 pairs of fresh HCC and LTM5 were assessed by qRT-PCR and Western blot, respectively. The expression of Mina53 in 284 pairs of HCC and LTM5 sample was determined by immunohistochemistry. Paired-sample t-test was used for the comparison of measurement data among groups, and heterogeneity of variance was tested using Wilcoxon rank-sum test. χ2 test was used for the comparison of measurement data among groups. Kaplan-Meier method and log-rank test were used for survival analysis. Cox regression model was used for single factor and multi factor analysis. Results:The relative expression levels of Mina53 mRNA and protein in 18 fresh HCC tissues were significantly higher than those in LTM5 tissues (mRNA: -4.41 ± 1.48 and -5.93 ± 1.65, t = 3.100, P = 0.007; protein: 1.12 ± 0.29 and 0.46 ± 0.21, t = 10.616, P < 0.001). The relative expression level of Mina53 in 284 HCC tissues was higher than that of LTM5 ( z = -18.739, P < 0.001). The expression level of Mina53 was associated with tumor size ( χ2 = 5.474, P = 0.019), vascular invasion ( χ2 = 8.965, P = 0.003), pathological grade ( χ2 = 12.006, P = 0.002), and TNM stage ( χ2 = 16.686, P < 0.001). The overall postoperative survival time and disease-free survival time of patients with high expression of Mina53 (28.5 months and 22.7 months, respectively) were shorter than those with low expression (33.0 months and 31.8 months, respectively) ( P < 0.05) in HCC. Cox multivariate regression analysis showed that Mina53 and multiple tumors were independent prognostic factors affecting the overall postoperative survival time and disease-free survival time of HCC patients ( P < 0.05). Conclusion:Mina53 may play an important role in the occurrence of HCC and participate in the process of tumor growth as well as invasion and metastasis. The high expression of Mina53 signifies that the patient has a poor prognosis and thus can be used as a potential marker for judging the prognosis of HCC patients.

Objective To construct a prokaryotic expression vector of of the long QT syndrome(LQTS)associated C-terminal lobe of calmodulin(CaM)mutant E141G(C-lobeE141G)and to identify the expression,purification,and activity of C-lobeE141G.Methods A cDNA fragment was inserted into a PGEX-6p-3 plasmid vector and transferred into Escherichia coli BL21 receptor cells,and glutathione-S-trans-ferase(GST)fusion protein was induced by isopropyl thio-β-D galactoside(IPTG).Glutathione-Sepharose 4B beads were used to separate and purify GST-C-lobeE141G.After removing the GST label with protease,the purity and concentration of purified C-lobeE141G were detected using SDS-PAGE and BCA,respectively.The activity of purified C-lobeE141G was detected using the GST pull-down method and patch clamp technique.Results GST-C-lobeE141G fusion protein was highly expressed,and C-lobeE141G with high purity and concentration was obtained.The purified C-lobeE141G protein not only bound to CaV1.2 calcium channels,but also rescued the channel activity from run-down in the ventricular myocytes of rat hearts.Conclusion This study successfully constructed a prokaryotic expression vector of C-lobeE141G,which provides a material basis for the study of the mechanism of LQTS mediated by C-lobe mutations in CaM.

Fibroblast growth factors (FGF) are a group of structurally related polypeptides which constitute an elaborate signaling system with their receptors. Evidence accumulated in the years suggests that the FGF family plays a key role in the repair of central nervous system injury. The main protective mechanisms include activating the expression of PI3K-Akt, peroxisome proliferator-activated receptor (PPARγ) and other signals; inhibiting NF-κB-mediated inflammatory response, oxidative stress and apoptosis; regulating neuronal differentiation and neuronal excitability as well as participating in protection of neurovascular units and nerve function repair. This paper comprehensively summarizes the latest research progress in FGF signaling related to diseases of the central nervous system such as cerebral infarction, cerebral hemorrhage, traumatic brain injury, Alzheimer's disease, Parkinson's disease, epilepsy and depression, aiming to provide scientific basis and reference for the development of innovative FGF drugs for the prevention and treatment of neurological diseases.
Humans ; Fibroblast Growth Factors ; Phosphatidylinositol 3-Kinases/metabolism* ; Central Nervous System/metabolism* ; Signal Transduction/physiology* ; Alzheimer Disease