Multiple etiological factors are integrally involved in the development of hepatitis B virus (HBV)infection.Interleukin-10 (IL-10)is an essential cytokine of immune regulation,and IL-10 gene promoter polymorphism affects its mRNA transcription and serum level. IL-10 is related to the prognosis of HBV infection.This review briefly discusses the association of IL-10 gene polymorphism and its serum level with the prognosis of HBV infection,and summarizes the role of IL-10,as an anti-inflammatory cytokine,in host immune function, the prognosis and progression of HBV infection,and HBV-related complications.IL-10 gene polymorphism and its serum level are closely associated with inflammatory response after HBV infection,influence HBV clearance,and are related to the severity of HBV-related liver injury,liver cirrhosis,and hepatocellular carcinoma.The determination of IL-10 gene and serum levels may provide a predictive marker for the prognosis of HBV infection.

Gastric cancer is the fifth most common cancer and the third leading cause of death globally .Apart from the suc-cessful phase Ⅲclinical trial of trastuzumab and Ramucirumab , other targeted therapies in gastric cancer ( GC) have fallen short or still in early clinical development .In this review, we will summarize the most up to date information on many of the potential actionabledriver genesin gastric cancer and the importance of using the optimal diagnostic test to select for these molecularly defined patients . We focus on the following aspects:HER-2, EGFR, FGFR, MET, IGF-1R and VEGF.

Lymphoma is a malignancy of mature lymphocytes. Signalling through the B cell receptor ( BCR ) is central to the development and maintenance of B cells. In light of the numer-ous proliferative and survival pathways activated downstream of the BCR, it comes as no surprise that malignant B cells would co-opt this receptor to promote their own growth and survival. Compounds that inhibit various components of this pathway, in-cluding spleen tyrosine kinase(Syk), Bruton’s tyrosine kinase (Btk), and phosphoinositol-3 kinase(PI3K), have been devel-oped. In this paper,the B-cell receptor signaling and its targeted inhibitors of lymphoid malignancies are reviewed.

ObjectiveTo investigate the protective mechanism of emodin(大黄素) on intestinal mucosal injury induced by intestinal ischemia/reperfusion(I/R) in rats.Methods Thirty male Wistar rats were randomly divided into three groups,namely sham operation group(Group A),group of ischemia 45 minutes followed by reperfusion 6 hours(Group B),emodinpretreated group(Group C).The superior mesenteric artery was occluded and then released to produce the intestinal I/R model in rats.Group C was administrated emodin intravenously(2.5 mg/kg) before 30 minutes of the operation.In the sham operation group and model group,similar volume of normal saline was administered respectively.After 45 minutes of ischemia and 6 hours of reperfusion, the blood was collected from the inferior vena cava respectively in each group.Afterwards,the rats were sacrificed,and the mesenteric lymph node(MLN) and small intestinal tissues were taken for pathological analysis by light microscopy.The serum levels of intestinal fatty acid binding protein(IFABP),nitrogen monoxidum(NO),tumor necrosis factor-?(TNF-?),and the activities of malondialdehyde(MDA),superoxide dismutase(SOD),myeloperoxidase(MPO)in the small intestinal tissues were measured,and the rates of bacterial translocation(BT) in blood and MLN were examined at 6 hours after reperfusion in each group. Results The contents of IFABP,NO,TNF-?,MDA and MPO were significantly lower(all P

Anti-Bacterial Agents ; therapeutic use ; Antitubercular Agents ; therapeutic use ; Coal Mining ; Drug Therapy, Combination ; Follow-Up Studies ; Humans ; Male ; Ofloxacin ; therapeutic use ; Pneumoconiosis ; complications ; Silicotuberculosis ; drug therapy

OBJECTIVEThis study measures the glutaredoxin (Grx) gene and protein expression in umbilical vein endothelial cells upon exposure to Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). The involvement of the Akt-signaling pathway is also determined.

METHODSEA-hy926 cells were pretreated with 1,000 ng · mL⁻¹ P. gingivalis LPS for 4, 12, 18, and 24 h, and then real-time reverse transcription polymerase chain reaction was employed to detect Grx1 expression. The effect of Grx on Akt activity was investigated using Western blot for the control, LPS (1,000 ng · mL⁻¹ LPS), and carmus- tine (BCNU) groups (1,000 ng · mL⁻¹ LPS, and the EA-hy926 cells were pretreated with 25 μmol · ml⁻¹ BCNU for 30 min).

RESULTSGene expression of Grx1 significantly increased in LPS group compared with that in the control group. The Grx1 expression reached the peak level in 12 h, and the variation between the expression in 4 and 12 h was significant (P < 0.05). After 12 h, the protein levels of Grx and phosphorylated-Akt (p-Akt) significantly increased in the LPS group (P < 0.05), whereas the BCNU group showed a considerable decrease in both Grx and p-Akt expression levels (P < 0.05). Moreover, a slight difference was observed in the total Akt protein levels in the three groups (P > 0.05).

CONCLUSIONGrx expression increased upon exposure of EA-hy926 cells to the LPS. Akt activity could be inhibited by BCNU (a Grx inhibitor), which indicated that Akt might act as a downstream regulator of Grx.

Endothelial Cells ; Glutaredoxins ; genetics ; Humans ; Lipopolysaccharides ; pharmacology ; Oxidative Stress ; drug effects ; Phosphorylation ; Porphyromonas gingivalis ; pathogenicity ; Proto-Oncogene Proteins c-akt ; drug effects ; Signal Transduction ; drug effects ; Umbilical Veins

AIM:To investigate the myocardial protective effect of endometrial stem cell ( EnSC)-derived cyto-kine cocktail ( EdCC) on myocardial ischemic reperfusion injury and the MEK-ERK signaling pathway.METHODS: A mouse model of myocardial ischemic reperfusion injury was established.Infarct area, cell apoptosis, and expression of cleaved caspase-3 and phosphorylatied ERK1/2 were determined by TTC/Evans blue staining, TUNEL assay and Western blot, respectively.RESULTS:The mesenchymal characteristics were observed in the EnSCs with expressing CD90 and in absence of CD34 and CD45.EdCC contained (6 811 ±312) ng/g epidermal growth factor (EGF) protein.The phospho-rylation of ERK1/2 markedly increased after injection of EdCC, but was abolished by MEK1 inhibitor PD98059 ( 5 mg/kg) .EdCC decreased the infarct area and apoptotic cell number in the border zone and inhibited caspase-3 activation. However, the effects were abolished by MEK1 specific inhibitor PD98059.EGF did not decrease the infarct area, but the EGF receptor antagonist AG-1487 (6 mg/kg) partly abolished the myocardial protective effect of EdCC.CONCLUSION:EdCC protects the myocardium from ischemic reperfusion injury via activating MEK1-ERK signaling pathway, indicating an essential role in the transmission of stem cell therapy from the cell transplantation to cytokine based strategy.

Breast Neoplasms ; therapy ; Consensus ; Female ; Humans ; Neoadjuvant Therapy

Objective To examine the application value of reticulocyte hemoglobin content (CHr)for diagnosing iron deficiency in premenopausal women.Methods The levels of CHr,hemoglobin (Hb), mean cellular volume(MCV),red cell distribution width (RDW) were measured on the ADVIA 120 (Bayer Diagnostics) automated hematology analyzer.Transferrin saturation (TS) and ferritin (SF) were measured on chemistry analyzer.Results CHr in iron deficiency without anemia group were significantly lower than that in the healthy control group (P＜0.01)and significantly higher than that in iron deficiency anemia group(P＜0.01).CHr in anemia of chronic disease group were significantly higher than that in iron deficiency anemia group(P＜0.01).Receiver operator characteristic curve (ROC) analysis in diagnosis of iron dificiency without anemia demonstrated that the area under the curve for CHr,SF,RDW,MCV,Hb were 0.872,0.798,0.721,0.713,0.677,respectively (P＜0.01).So CHr has a better overall sensitivity than SF,Hb,MCV and RDW in the diagnosis of iron deficiency without anemia.ROC also showed that the area under the curve for Hb,RDW,CHr,SF and MCV was 1.000,0.969,0.958,0.953 and 0.926,respectively (P＜0.01) in iron deficiency anemia.Conclusion CHr is the early and sensitive predictor of iron deficiency in premenopausal women,especially for the diagnosis of iron deficiency without anemia.

Objective To test thyroid-stimulating hormone (TSH) suppress GLUT4 expression and translocation by stimulating TNF-α secretion in 3T3-L1 adipocytes via a cAMP-PKA pathway.Methods 3T3-L1 preadipocytes were induced to differentiate into adipocytes.The adipocytes were treated with bovine TSH,Forskolin,H89 and Rapamycin,respectively.The concentration of TNF-α in the cell culture medium was measured by ELISA.The level of GLUT4 mRNA in adipocytes was assessed by real time polymerase chain reaction.Protein levels of GLUT4 in total cell lysates and plasma membrane lysates were quantified by Western blotting.Results Incubating 3T3-L1 adipocytes with TSH markedly increased the concentration of TNF-α in medium in a time-and dosedependent manner (P ＜ 0.05); meanwhile,the levels of GLUT4 mRNA and total and plasma membrane GLUT4 protein were decreased in a dose-dependent manner (P＜0.05 or ＜0.01).H89 and rapamycin could block the above effects respectively (326.7±43.2 vs.341.9±12.0,P＞0.05).However,there was no statistical difference in the TNF-α levels between stimulation with 1 μmmol/L forskolin versus 0.04 μmmol/L bovine TSH (481.9± 28.4 vs.522.7± 36.2,P＞0.05).Conclusions TSH can down-regulate GLUT4 expression and translocation in 3T3-L1 adipocytes by stimulating TNF-α secretion through a cAMP-PKA pathway.