The natural history of chronic HBV infection is diverse and variable, ranging from inactive carriers to progressive chronic hepatitis B ( CHB), cirrhosis and hepatocelluar carcinoma.It is estimated that 93 million people are chronically infected with HBV and 20 million cases suffering from chronic hepatitis B in China.Hepatocelluar carcinoma has been the second leading cause of death for male in China.Liver cirrhosis and HCC which have high mortality and morbidity have become the heavy burden for the limited medication resource of China.Here the current clinical applications and consensus progression based on antigen and nuclear acid detection were acknowledged.The reasonable application as well as appropriate clinical interpretation are emphasized indicating that laboratory medicine practitioners should be more actively involved in clinical diagnosis and treatment.More efforts and contributions should be made by the laboratory medicine practitioner for optimizing clinical management of HBV-related diseases in future.

China is among the middle-high endemic regions of HBV infection.The pathological outcomes of chronic HBV infection have been shown to be greatly influenced by several important factors,including HBV genotype,sub-genotype and gene viability mutation.HBV genome mutation,on the one hand,could alter its replication and secretion and thus change viral pathogenicity.In addition,host immune microenvironment and host-virus interaction,disease progression and the effect of antiviral therapy could be adapted at the same time.The detection of HBV genotypes,genetic subtypes and the key hotspot mutation is helpful to clinical risk assessment and prognosis prediction of HBV-related end-stage liver diseases (cirrhosis and hepatocellular carcinoma),it is also helpful to auxiliary predict the liver diseases recurrence and metastasis after treatment.Thus persistent care should be taken on the HBV mutation and its clinical translation so as to provide solid evidences for the personalized,standardized and fine management of HBV-related liver diseases.

Objective To observe the expression and distribution of IL 10 in local vessel after balloon injury in rat and study its significance in the response of artery injury Methods RT PCR and Western Blot as well as immunohistochemical method were used to assay the changes of IL 10′s mRNA as well as expression and distribution of protein Results There is no expression of IL 10 in vascular wall of normal rat After Balloon injury, the level of IL 10 mRNA and product of IL 10 was up regulated, and immunohistochemiscal staining showed immunoreactive IL 10 mainly in smooth muscle cells Conclusion IL 10 is expressed in balloon injured aorta and may contribute to the modulation of the local inflammatory response

To evaluate the feasibility of using polyethyleneimine (PEI) coated magnetic iron.oxide nanoparticles (polyMAG-1000) as gene vectors. The surface characteristics of the nanoparticles were observed with scanning electron microscopy. The ability of the nanoparticles to combine with and protect DNA was investigated at different PH values after polyMAG-1000 and DNA were combined in different ratios. The nanoparticles were tested as gene vectors with in vitro transfection models. Under the scanning electron microscope the nanoparticles were about 100 nm in diameter. The nanoparticles could bind and condense DNA under acid, neutral and alkaline conditions, and they could transfer genes into cells and express green fluorescent proteins (GFP). The transfection efficiency was highest (51%) when the ratio of nanoparticles to DNA was 1:1 (v:w). In that ratio, the difference in transfection efficiency was marked depending on whether a magnetic field was present or not: about 10% when it was absent but 51% when it was present. The magnetic iron oxide nanoparticles coated with PEI may potentially be used as gene vectors.
Breast Neoplasms/metabolism ; Breast Neoplasms/*pathology ; Cell Line, Tumor ; Ferric Compounds/*chemistry ; Ferric Compounds/metabolism ; Gene Targeting ; Genetic Vectors ; Green Fluorescent Proteins ; Magnetics ; Nanotechnology ; Particle Size ; Polyethyleneimine/chemistry ; Transfection/methods

The aim of this study was to evaluate the feasibility and efficacy of using TRAIL gene to treat breast cancer mediated with a novel carrier - magnetic iron oxide nanoparticles (poly-MAG-1000) coated with PEI. The magnetic iron oxide nanoparticles were used as gene carrier to transfect TRAIL gene into MCF-7 cells. The polyMAG-1000 without TRAIL gene was transfected into the tumor cells as negative control. TRAIL gene transfection with liposome as carrier served as positive control. The apoptosis of cells was detected with TUNEL method. The apoptosis ratio of tumor cells was measured with flow cytometry (FCM). It was found that the apoptosis occurred in the tumor cells after transfection of TRAIL gene mediated by both polyMAG-1000 and liposome. The apoptosis ratio in the group with polyMAG-1000 as gene carrier was (25.11+/-2.85) %, whereas it was (5.06+/- 1.05) % in the control group with polyMAG-1000 (P<0.01). The apoptosis ratio was as low as (18.31+/-2.44) % in the group with liposome as gene carrier (P<0.05, as compared with the group with polyMAG-1000 as gene carrier). It is suggested that TRAIL gene may induce apoptosis in MCF-7 breast cancer cells. The magnetic iron oxide nanoparticles coated with PEI may be a potential gene carrier with high transfection efficacy for cancer gene therapy..

Objective To investigate the oxidative mechanism of homocysteine ( Hey) -induced apoptosis in endothelial progenitor cells( EPCs). Methods Total mononuclear cells were isolated from mouse bone marrow by Ficoll density gradient centrifugation and were cultured in vitro for 7 d. Adherent cells were harvested and identified by fluorescence microscopy. EPCs were cultured with Hey (0, 50, 100 and 500 μmol/L) for 12, 24 and 48 h, or pretreated with NAC (1 mmol/L), DPI( 10 μmol/L) or SB203580 (10 μmol/L) for 30 min, then cultured with 500 μmol/L Hey for 24 h. Apoptosis was detected by Annexin-V/PI flow cytometry, levels of reactive oxygen species (ROS) in cells were measured using H2DCF-DA as a fluorescence probe, NADPH oxidases were evaluated with lucigenin-enhanced chemilumine9cence, and NO in the supernatant was determined by nitrate reductase assay. Results Hey induced EPCs apoptosis, ROS accumulation, NADPH oxidase activation and decrease of NO in a time-dose dependent manner( P <0.05 or P < 0.01). Pretreatment with NAC, DPI and SB203580 could inhibit these effects (P < 0.05 or P < 0.01). Conclusion Hey could activate NADPH oxidase, induce ROS increase and NO decrease, and activate p38MAPK to enhance EPCs apoptosis.

BACKGROUND: Carbamylated erythropoietin (CEPO) cannot only remarkably promote the prognosis of cerebral infraction, but also improve the microcirculation. OBJECTIVE: To explore the underlying mechanism of CEPO promoting the microcirculation following cerebral infraction. METHODS: 150 Wistar rats were selected, and 120 rats were used for establishing the models of cerebral infarction, followed by allotted into four groups. The model rats were treated with 500, 1000 and 2000 u/kg CEPO as experimental groups, and those received no treatment as model group. The other 30 rats were as controls. Vascular endothelial cells were isolated and cultured in vitro, and the cell proliferation was detected by cell counting kit-8 assay. The expression levels of proliferation-related genes (Ki67 and p16) and vascular endothelial growth factor (VEGF) were detected using western blot assay. After selective silencing of VEGF through RNA interference, all above indicators were detected again. RESULTS AND CONCLUSION: Cell counting kit-8 assay results showed that the proliferation ability of vascular endothelial cells was increased with CEPO concentration increasing. Western blot assay results showed a significant upregulation of Ki67, p16 and VEGF. After shRNA-VEFG interference, these indicators had no positive correlation with the increased concentration of CEPO. Our findings indicate that CEPO can improve the proliferation of vascular endothelial cells in an animal model of cerebral infarction via upregulating the VEGF expression.

Aim To study the effect of TSA on vascular smooth muscle cells(VSMC)proliferation and apoptosis in vitro.Methods VSMC proliferation was analyzed by MTT assay and BrdU incorporation assay.Cell cycle phase distributions were determined by flow cytometer.The expressions of cyclin D1 and cyclin A were assessed by western blot.Cell apoptosis was quantified by detecting cytoplasmic histone-associated DNA-fragments and the level of cleaved caspase-3.Results TSA at a low concentration was adequate to inhibit serum-induced VSMC proliferation without significant cytotoxity.High concentration of TSA activated caspase-3 and induced VSMC apoptosis.TSA treatment reduced expressions of cyclin D1 and cyclin A,and blocked VSMC entry into S phase.Conclusions TSA inhibits serum-induced VSMC proliferation and G1→S phase progression of cell cycle.Histone deacetylase(HADC)inhibitors may constitute a novel therapy for vascular proliferative diseases.

AIM:To investigate the effect of trichostatin A(TSA)on p27kip1 gene expression in vascular smooth muscle cells.METHODS:Reverse transcription-polymerase chain reaction(RT-PCR)was used to measure the level of p27kip1 mRNA.The protein levels of p27kip1 and S-phase kinase-associated protein-2(skp2)were determined by Western blotting.20S proteasome activity was quantified by using a fluorogenic proteasome-specific substrate.RESULTS:TSA did not affect mRNA level of p27kip1 in VSMCs,but attenuated serum-induced downregulation of p27kip1 through stabilizing p27kip1 turnover.In addition,TSA decreased the expression of skp2,an F-box protein that targets p27kip1 for degradation,but had no effect on proteasome activity.CONCLUSION:TSA regulates p27kip1 expression at the post-translational level in VSMCs.

Objective To study the differentially expressed genes in the vascular tissue of diabetic gangrene toot and the possible mechanism of diabetic gangrene.Methods The differentially expressed genes in the vascular tissue of diabetic gangrene foots were screened by the functional classific gene chip.Reverse transcription polymerase chain reaction(RT-PCR) detection was used to verify the differentially expressed 3 genes.Results In the detected 113 genes,13 of the gene expression level increased more than 2 times,3 of the gene expression level decreased more than 2 times.Three genes were verified with RT-PCR detection,which were results similar to those with chip testing.Conclusions The abnormal expression in a variety of genes in tissues of vascular lesions plays an important role in the course of development and progression of diabetic gangrene.Analysis of differential gene expression can contribute to understanding of the possible mechanisms of diabetic gangrene.