Hepatitis B virus (HBV) infection and the subsequent persistent inflammation are the important factors that facilitate the development of liver cirrhosis and hepatocellular carcinoma. Both HBV infection and persistent inflammation can affect carcinogenesis via regulating microRNA expression. Aberrant expression of microRNAs plays an important role in regulating the malignant transformation of chronic inflammation. Some microRNAs can aggravate inflammation via increasing HBV replication or expression of inflammatory factors, some can promote fibrosis process via activating hepatic stellate cells or producing collagen proteins, and some can promote cancer progression by affecting the balance between cancer promoting factors and tumor suppressor factors. Proinflammatory molecules can promote Evo-Dev of HBV-induced hepatocellular carcinoma through epigenetic regulation including regulating the expression of microRNAs. Here in this review we discussed the potential mechanisms by which persistent inflammation induces aberrant expression of microRNAs and the role of dysregulated microRNAs in the development of chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma.

Background Rapamycin(RAPA)is a specific inhibitor of the mammalian target of rapamycin (mTOR).Researches showed that RAPA inhibits the proliferation of lens epithelium cells(LECs)and tumor cells and induces apoptosis of tumor cells.To investigate whether rapamycin has the inhibitory effect on retinal pigment epithelium(RPE)cells is very important for the prevention and management of proliferative vitreoretinopathy (PVR).Objective This study was to investigate the effects of RAPA on the proliferation and apoptosis of human RPE cells in vitro.Methods Human RPE cells(D407 strain)were cultured and passaged and then divided into regular culture group(blank control group),DMSO control group(0.1‰ DMSO +regular culture),and different concentrations RAPA-treatment groups(5,10,20,40,80,160,320 nmol/L).The proliferation(A490)of human RPE cells was detected using MTT,and the inhibitory rates of RAPA on the proliferation of RPE cells were calculated and compared among different groups at 12,24 and 48 hours.The apoptosis rates of the cells were analyzed among various groups by Hoechst staining after 12,24,48 hours.Results The inhibitory rates of RAPA on RPE cells were significantly different among various groups(F=484.451,P＜0.01)and evidently elevated in 20-320 nmol/L RAPA groups compared with DMSO control group(P ＜ 0.01).The inhibition of RAPA on the cells was considerably enhanced as the lapse of time(F=232.262,P＜0.01)with more dominant effects in 24 and 48 hours compared to 12 hours after addition of RAPA(P＜0.05-0.01).Compared with blank control group and DMSO control group,the apoptotic rates of the cells were evidently increased in 12,24,48 hours in 10 nmol/L RAPA group(all P＜0.05),and higher cellular apoptotic rates were found in 20-320 nmol/L RAPA groups(all P＜0.01).The alteration of cellular apoptotic rate showed a gradually incremental trend as the acting time of RAPA(F =625.584,P＜0.01).Karyorrhexis and mass-like density staining and chromatin substance were seen in RPE cells under the fluorescence microscope in ≥ 10 nmoL/L RAPA groups.Conclusions RAPA suppresses the proliferation and induces the apoptosis of human RPE cells in concentration-and time-dependent manner in vitro.

Objective To explore the relationship between obesity phenotypes and adipocytokines in children.Methods Based on the Beijing child and adolescent metabolic syndrome (BCAMS) study,3 508 children (1 788 boys and 1 720 girls) aged 6-18 were recruited.In this study,participants were categorized into four groups:226 cases in general obese group,192 cases in abdominal obese group,1 004 cases in combined obese group and 2 086 cases in non-obese group,according to the sex,age,specific body mass index(BMI),and waist circumference (WC) equal to or greater than the 90th percentile for age and gender of school children in Beijing in 2004.The levels of plasma insulin,serum leptin,resistin and adiponectin were measured by sensitive,specific double-antibody sandwich enzyme-linked immunosorbent assays (ELISA).Analysis of covariance,multivariate linear regression and binary logistic regression analysis were performed.Results There were highest plasma insulin and serum leptin,and lowest adiponectin levels in combined obese group than those in other obese groups and non-obese group and resistin level in abdominal obese group was highest than those in other obese groups or non-obese group.Among subjects with general obesity and conbined obesity,WC was more important factor than BMI for plasma insulin[?(WC)=0.158 P0.05].With covariates adjusted,the odds ratios(OR)and 95% confidence intervals of general obesity,abdominal obesity and combined obesity were 3.46(2.44-4.91),5.41(3.87-7.57) and 10.10(8.26-12.35) for predicting hyperinsulinemia,respectively,5.83(4.02-8.45),7.07(4.97-10.05)and 20.82(16.49-26.28) for hyperleptinaemia,respectively,1.47(1.05-2.07),2.0(1.42-2.80) and 2.66(2.23-3.18) for hypoadiponectinaemia,respectively.Serum resistin was highest in abdominal obesity.Conclusion The levels of adipocytokines in children were correlated with the phenotypes of obesity,especially for abdominal obesity.

To observe the expression of N - cadherin and fibronectin in retinal pigment epithelium ( RPE) cells in vitro under high glucose conditions, furthermore, to explore the effects of high glucose on epithelial -mesenchymal transition (EMT) in RPE cells.
●METHODS: Human RPE (hRPE) cells were cultured in vitro. Containing a final concentration of 60mmol/ L glucose was used for high glucose treatment. The cells were divided into normal glucose group (5. 5mmol/ L, NG) and high glucose group (24, 48 and 72h) respectively. The expression of N - cadherin and fibronectin in hRPE cells were evaluated by immunofluorescence and real -time PCR.
●RESULTS:RPE cells became disorganized and swollen over time under high glucose conditions, especially in 72h subgroup. lmmunohistochemical analysis revealed that the expression of N - cadherin in RPE cells under high glucose conditions was decreased compared with that in the control group, while the expression of fibronectin was increased. Real - time PCR results showed that the expression of N - cadherin mRNA in high glucose group was decreased at 24h compared with that in the control group, and declined markedly at 72h ( F = 12. 252, P =0. 000). There were no significant differences between the control group and the high glucose group at 24h, while the differences between the control group and the high glucose group (48 and 72h) were significant respectively (P < 0. 05 ). Meanwhile, the expression of fibronectin mRNA in RPE cells was increased in high glucose group at 24h, and reached the peak at 72h (F = 50. 543, P = 0. 000). There were no significant differences between the control group and the high glucose group at 24h. Compared with the control group, the expression of fibronectin mRNA in hRPE cells was increased significantly in high glucose group (48 and 72h) respectively (P= 0. 000, P= 0. 000).
●CONCLUSlON: The expression of epithelium marker N-cadherin is down - regulated under high glucose conditions in hRPE cells in vitro. Meanwhile, the expression of mesenchymal maker fibronectin is induced and appeared to EMT changes. Results of this study will enrich our growing understanding in proliferative diabetic retinopathy and hopefully lead to novel insights for the pathogenesis and therapeutic treatments.

Angiogenesis Inhibitors ; pharmacology ; therapeutic use ; Animals ; Antimetabolites, Antineoplastic ; therapeutic use ; Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; Deoxycytidine ; analogs & derivatives ; pharmacology ; therapeutic use ; Drug Therapy, Combination ; Female ; Ginsenosides ; pharmacology ; therapeutic use ; Lung Neoplasms ; drug therapy ; pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation

AIM : To construct and analyze eukaryotic expression plasmid inserted by Cx50 with V64G mutation through bioinformatics software.METHODS: The full coding domain sequence of Cx50 with V64G mutation was acquired from the blood of patients with cataract and was cloned into pcDNA3.1 /Amp (+).The constructed plasmid was identified with PCR , enzyme digestion and sequencing. The analysis of Cx50 with V64G mutation was performed with bioinformatics software.RESULTS : Cx50 with V64G mutation was successfully amplified and its eukaryotic expression plasmid was constructed. Valine-64 is well conserved in the first extracellular loop of connexin 50 in different species and also in different human α -type gap junctional proteins.CONCLUSION : The successive reconstruction and verification of eukaryotic expression plasmid containing Cx50 with V64G mutation established the foundation for further studying the mechanism of cataract.

Objective To observe toxic effect of deoxynivalenol(DON)on articular cartilage and synovium of New Zealand rabbits's knee ioints.Methods Fifteen male rabbits were divided randomly into 3 groups:control, high-dosage,and low-dosage group.In high-dosage and low-dosage group,saline solution of DON was injected with a dose of 0.10 and 0.05 ms/kg every 48 h into ear vein of rabbits.Specimen of articular cartilage and synovium were through pathologY methods,and IL-1β,TNF-α,NO levels were assayed in joint liquid,after 20 days. Results Morphological changes were observed, such as synovium inflammative infiltration, chondrocytes deformation and necrosis under light microscope.The levels of IL-1β,TNF-α and NO had statistical significance in comDarison between 3 grouPs(F=19.396,18.195,22.136,P＜0.05).The levels of IL-1β,TNF-α and NO were significantly higher(all P＜0.05),high-dosage[(0.451±0.091),(0.575±0.122)μg/L;(70.27±11.53)μmol/L] and low-dosage group[(0.295±0.107),(0.387±0.131)μg/L;(45.32±12.24)μmol/L]compared with control ((0.1 13±0.049),(0.138±0.087)μg/L;(23.56±9.35)μmoL/L],and high-dosage compared with low-dosage group Conclusions DON results in articular and synovial impairment,which has the symptom similar to osteoarthritis. DON probably causes osteoarthritis.

OBJECTIVETo investigate the clinical and pathological features, differential diagnosis of granulocytic sarcoma.

METHODSThe clinical manifestations, histopathological features, immunohistochemistry, treatment and prognosis were analyzed retrospectively in 10 cases of granulocytic sarcoma.

RESULTSThe age of patients ranged from 10 to 56 years (means = 35.8 years). The male-to-female ratio was 1.5:1. Histologically, the malignant cells of granulocytic sarcoma grew in a diffuse pattern. The cytoplasm was scanty, with eosinophilic fine granularity in some cells. The nuclei were round or focally irregular, and had finely dispersed chromatin. The mitotic figures were visible. Immunohistochemical stains for MPO, CD43, CD117, CD34 and CD99 were positive.

CONCLUSIONSGranulocytic sarcoma can occur in patients of all ages with a male predominance. The diagnosis of granulocytic sarcoma is assisted by the cytochemical stain for naphthol-ASD-chloroacetate esterase and/or immunophenotypic analyses for MPO, CD43, CD117, CD34, CD99. These stains aid in the distinction of granulocytic sarcoma from: lymphoblastic lymphoma, Burkitt lymphoma, diffuse large B-cell lymphoma, small round cell tumours, particularly in children, and blastic plasmacytoid dendritic cell neoplasm.

12E7 Antigen ; Adolescent ; Adult ; Antigens, CD ; metabolism ; Antigens, CD34 ; metabolism ; Burkitt Lymphoma ; metabolism ; pathology ; Cell Adhesion Molecules ; metabolism ; Child ; Dendritic Cells ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Leukosialin ; metabolism ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Male ; Middle Aged ; Peroxidase ; metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; metabolism ; pathology ; Proto-Oncogene Proteins c-kit ; metabolism ; Retrospective Studies ; Sarcoma, Myeloid ; metabolism ; pathology ; Skin Neoplasms ; metabolism ; pathology ; Young Adult

Objective:To investigate the underlying mechanism of histone deacetylase (HDAC) inhibitor FK228-in- duced apoptosis of the prostate cancer cell line DU145.Methods:The inhibitory effect of FK228 on DU145 cell growth and its cytotoxicity were determined by MTT assay;cell cycle arrest was detected by flow cytometry assay;morphological change was observed by Giemsa staining;and defined kinase protein levels were determined by Western blot analysis.Re- suits:FK228 obviously inhibited DU145 cells growth,arrested cell cycle at G_0/G_1 phase,induced cells morphological changes and degraded several kinase proteins,including EGFR,Her2,Raf-1,Src,Cdk4 and IAP member Survivin.The degradation of these kinases blocked Raf-Mek-Erk and PI3K/Akt survival signal pathways,inducing apoptosis.Condu- sion:FK228 may induce DU145 cell apoptosis through depletion of multiple kinase proteins and blockade of survival sig- nal pathways of DU145 cells.

OBJECTIVETo study the effect of RNA interference (RNAi) targeting E6AP on the proliferation and apoptosis of HeLa cells.

METHODSHeLa cells were cultured and divided into 3 groups: blank control group, cells transfected with nonsense siRNA (small interference RNA), and cells transfected with specific E6AP siRNA. The expressions of E6AP mRNA and protein were detected by RT-PCR and Western blot before and after the transfection respectively. Cell proliferation was determined by methylthiazolyl tetrazolium (MTT). The cell apoptosis index was assessed by flow cytometry.

RESULTSUpon treatment with E6AP siRNA for 24, 48 and 72 h, the expression level of E6AP mRNA decreased 33%, 72% and 70% than siRNA treated group. The protein expression levels in 48 h and 72 h E6AP siRNA groups decreased 38%, 59% comparing with those of the nonsense siRNA treated group (P < 0.05). The proliferative capacity of cells transfectd with E6AP siRNA was significantly lower than blank control group (F = 101.38, P < 0.05) and siRNA treated group (F = 38.64, P < 0.05). The apoptosis index of HeLa cells treated with E6AP siRNA was significantly higher than that of the nonsense siRNA (F = 41.48, P < 0.05) and the blank control group (F = 86.36, P < 0.05).

CONCLUSIONSiRNA targeting can effectively suppress the expression levels of E6AP mRNA, corresponding with a proliferation inhibition and an enhanced apoptosis of HeLa cells.

Cell Line, Tumor ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic ; genetics ; Gene Silencing ; HeLa Cells ; Humans ; RNA Interference ; RNA, Small Interfering ; genetics ; pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; Ubiquitin-Protein Ligases ; antagonists & inhibitors ; metabolism ; Uterine Cervical Neoplasms ; genetics ; metabolism