Abnormal expression of glypican-3 and ubiquitin D in hepatocellular carcinoma and the associated interaction / 解剖学报

Objective To explore the abnormal expression of ubiquitin D (UBD) and glypican-3 (GPC3) among patients of hepatocellular carcinoma (HCC) by using analysis tools of genomics and epigenetics, so as to study their prognostic effects. Methods The online tools called ULCAN( http://ualan.path.uab.edu) and Gene Expression Profiling Interative Analysis (GEPIA) were used to perform expression analysis in genomics and epigenetics of UBD and GPC3. Moreover, GEPIA was conducted to evaluate the survival effects on HCC patients. The GeneCards was used to find the localization of UBD and GPC3 in tumor tissue and normal tissue. The STRING was utilized to perform the construction of PPI network and gene annotation. The correlation between UBD and GPC3 in progress of HCC was revealed based on Pearson correlation coefficient. Results UBD and GPC3 were dramatically up-regulated in HCC tissues, with downregulation of methylation level. UBD was located in 6p22. 1 with primary expression in the nucleus, while GPC3 was located in Xq26. 2 with main expression in the plasma membrane, extracellular matrix, endoplasmic reticulum, lysosome and golgi apparatus. The enrichment analysis showed that, UBD was enriched in activities involving proteasome, such as post-translation protein modification, ubiquitination and deubiquitination. GPC3 was enriched in the biosynthetic and catabolic process of glycosaminoglycan, possessed relationship with proteoglycans in cancer, ECM-receptor interaction, cell adhesion molecules (CAMs). Both of UBD and GPC3 were shown to exhibit a positive linear correlation, which suggested that GPC3 and UBD mediated the pathological process of HCC in cooperation. The survival analysis showed that, GPC3 exhibited a critical effect on survival of HCC patients. Conclusion UBD and GPC3 represent up-regulation in tumor tissue, in which GPC3 possesses a greater impact on the prognosis of HCC. GPC3 could be potential to serve as a practical biomarker for early diagnosis and medical intervention.

Integrated Analysis of Hub Genes and Pathways In Esophageal Carcinoma Based on NCBI's Gene Expression Omnibus (GEO) Database: A Bioinformatics Analysis.

BACKGROUND Esophageal carcinoma (ESCA) is a health challenge with poor prognosis and limited treatment options. Our aim is to screen for hub genes and pathways associated with ESCA pathology as diagnostic or therapeutic targets. MATERIAL AND METHODS We downloaded 2 ESCA-related datasets from the Gene Expression Omnibus (GEO) database. Subsequently, differentially expressed genes (DEGs) of ESCA were determined by statistical analysis. Both Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs were performed using online analytic tools. Network analysis was employed to construct a protein-protein interaction (PPI) network and to filter hub genes. We evaluated the expression level and impact of hub genes on survival of ESCA patients using the OncoLoc webserver. RESULTS A total of 210 DEGs were identified. The GO analysis showed that the DEGs were enriched in cell division. The KEGG pathway analysis showed DEGs that were enriched in cell cycle regulation, known cancer pathways, the PI3K-Akt signaling pathway, and the cGMP-PKG signaling pathway. The top 10 hub genes were markedly upregulated in ESCA tissue compared with normal esophageal tissue. Moreover, the expression level of the hub genes was different at different pathological stages of ESCA. Further prognostic analysis identified that the top 10 hub genes were related to late survival of ESCA patients, while exhibiting few associations with early survival time. CONCLUSIONS The signaling pathways involving the DEGs probably represent the pathological mechanism underlying ESCA. The hub genes were associated with survival of ESCA patients, and as such have the potential to serve as diagnostic indicators and therapeutic targets.

Effect of NAD+ against radiation injury and its dose-effect relationship / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the effect of NAD+ against radiation injury and its dose-effect relationship.</p><p><b>METHODS</b>L02 liver cells cultured in RPMI 1640 medium containing 10% fetal calf serum were exposed to X-ray irradiation followed by immediate application of NAD+. The cellular viability was analyzed by MTT assay and the apoptotic cells were detected by TUNEL methods to observe the damages of L02 liver cells induced by X-ray exposure and analyze the dose-effect relationship of NAD+.</p><p><b>RESULTS</b>The viability of L02 liver cells was decreased with increasing dose of X-ray irradiation. The most obvious growth inhibition of L02 cells occurred 24 h after the irradiation. NAD+ significantly increased the cell survival rate after irradiation, and this effect was gradually increased within the concentration range of 100-1000 microg/ml; at higher concentrations, the survival rate of the irradiated L02 cells showed no significant increase.</p><p><b>CONCLUSION</b>NAD+ provides partial protection of the liver cells against radiation injury, and the effect is positively correlated to NAD+ concentration within a certain range.</p>

Advances in Applications of Bacterial Cellulose in Biomedical Materials / 中国生物工程杂志

Bacterial cellulose (BC) is a natural polymer that has bioactivity, biodegradability and biocompatibility. It displays unique physical, chemical and mechanical properties including high crystallinity, high water holding capacity, nanofibre-network structure, high tensile strength and elastic modulus. Due to its unusual material properties, BC has recently become a kind of attractive biomedical material in the international research.Describes BC's properties, study history and its applications as biomedical materials, especially gives emphasis to introduce the applications of BC on scaffold tissue engineering, artificial blood vessels, artificial skin and the treatment of skin wound, as well as the present study status.