As a kind of heavy metal, cadmium has the toxicity to multiple organs and tissues. Much progress has been made in the toxicological research, especially in the toxicity to the reproductive system. The recent researches on the toxicity on Cd, the toxicological mechanism and the preventive methods of cadmium poisoning were reviewed in the present paper.

Although tumor immunotherapy has been proposed for many years,the consensus denoting it as an essential approach for fighting against cancer is reached only in recent years. Tumor immunotherapy can be categorized as active and passive ones. In order to successfully cure cancer,safe and efficient active immunotherapy is required. Dendritic cells (DCs)are not only the bridge linking innate and adaptive immunity,but also the key determinants of the quality of adaptive immunity:immunity versus immune tolerance. Therefore,the safe and efficient DC-based tumor-specific and broad-spectral tumor vaccine has an irreplaceable important position in tumor immunotherapy. Because of the high heterogeneity of DCs, the research on DC-based tumor vaccine has encountered a bottleneck. Here,we reviewed the progress in research on DC-based tumor vaccine and related problems needed to be resolved with the incorporation of our experiences.

Objective To investigate the effect of pigment epithelium- derived factor (PEDF) on p38MAPK-CREB pathway and the expression of fibronectin (FN) in human mesangial cells (HMCs) cultured with high glucose. Methods HMCs were treated with different concentrations of glucose and the osmotic control respectively in the presence or absence of PEDF for 24 h:normal glucose (5.6 mmol/L),24.4 mmol/L mannitol,high glucose (30 mmol/L),high glucose+PEDF(30 mmol/L glucose with 10 nmol/L PEDF,40 nmol/L PEDF or 100 nmol/L PEDF).After samples were collected,the expression of phospho-p38MAPK (p-p38) and p-CREB was assessed by Western blotting,while FN mRNA and protein expression was assessed with RT-PCR and ELISA respectively. Results In contrast to normal glucose and mannitol treatments,the expression of p-p38MAPK,p-CREB and FN increased significantly in high glucose group (all P＜ 0.01).However,PEDF abolished the up-regulation of p-p38MAPK,p-CREB and FN induced by high glucose (all P＜0.05). Conclusion PEDF may inhibit fibrosis through P38MAPK-CREB pathway in diabetic nephropathy.

ObjectiveTo investigate the expression of urotensin Ⅱ(UⅡ) in the lung cancer tissue from surgical resection of lung cancer patients,and to detect the relationship between UⅡ expression and pathologie types and the clinical stages of lung cancer.MethodsThe expression rates of UⅡof 45 lung cancer tissues and 20 inflammatory pseudotumor were measured by immunohistochemical assay,and the relationship between UⅡ expression and the pathologic types and clinical stages of lung cancer was analyzed.ResultsUⅡwas mainly distributed in lung cancer cell cytoplasm,which was tan-yellow particles.The positive expression rate of UⅡin nonsmall cell lung cancer was 61.3％ (19/31),which was higher than that in small cell lung cancer(7.1％,1/14)and pulmonary inflammatory pseudotumor( 15.0％,3/20) (P ＜ 0.01 ).The positive expression rate of UⅡ was 100％ in adenocareinoma.The positive expression rate of UⅡin staging Ⅲ non-small cell lung cancer( 85.7％ )was higher than that of staging Ⅰ ( 16.7％ ) ( P ＜ 0.05).ConclusionUⅡ cxists in the cytoplasm of lung cancer cells,and the expression of UⅡis correlated with the pathological type and TNM staging of lung cancer.

Objective To investigate the effect of dysadherin gene silencing on metastasis and invasion in pancreatic cancer cell line PANC1,BxPC3 in vitro.Methods PANC1 and BxPC3 cells were divided into dysa group,negative siRNA control group(HK),liposomes control group(control),dysa group and HK group were tranfected by dysadherin siRNA and Negative siRNA,respectively.The expression of dysadherin mRNA and protein were detected by RT-PCR and immunohistochemical method.Transwell test was used to evaluate the invasion ability of pancreatic cancer cells.Results After transfected by dysadherin siRNA,the dysadherin mRNA levels in PANC1 and Bxpc3 cells were decreased by 95.4% and 52.1%.The expression of dysadherin protein was also down-regulated by 91.2% and 83.6%,respectively,when compared with HK groups (P＜0.05 ).The numbers of invasive cells migrated in Transwell in PANC1 cells control group,HK group and dysa group were 163.2±15.5,154.4±17.3 and 53.6±7.9;the numbers of invasive cells in BxPC cells control group,HK group and dysa group were 30.7±3.2,27.5±2.8 and 4.7±2.4,respectively.The numbers in dysa group were significantly lower than those of HK group and control group (P＜0.01 ).Conclusions Silencing the dysadherin gene of PANC1,BxPC3 by RNA interference could significantly inhibit the invasive and migratory ability of canceroas cells.

Objective To explore the effect of araloside on the proliferation and apoptosis of HeLa cells.Methods Human cervical cancer cell line HeLa was cultured in vitro,the experiment was divided into 4 groups as follows:blank group,araloside trea-ted groups(50,100,200 μg/mL).Normal saline and araloside (50,100,200 μg/mL)were gave,respectively.24,48 and 72 hours lat-er,the cells were collected.Cell proliferation was detected by MTT,cell apoptosis was determined by flow cytometry,the expression of pAkt1,pIкBα,NF-κB (p65),Bcl-2 and Caspase-3 were evaluated by western blot.Results Araloside obviously inhibited the pro-liferation and increased the apoptosis level of HeLa cells in a time-dose dependent manner.Moreover,Araloside significantly de-creased the phosphorylation of Akt1 and IκBα,reduced the expression of NF-κB(p65)and Bcl-2,whereas obviously increased Caspase-3 content.Conclusion Araloside could inhibit the proliferation and promote the apoptosis of HeLa cells via suppressing Akt/NF-кB signaling pathway.

Objective To explore the inhibition role of araloside on cervical cancer HeLa cell proliferation and migration to reveal the molecular mechanism of NF-κB in HeLa cell in the process of tumor suppression.Methods The in vitro cultured cervical cancer HeLa cell line served as the research object.The experiment was divided into the control group and araloside(200 μg/mL) treatment group(observation group).The change of proliferation and migration ability after 48 h were observed in the two groups.Western blot was used to detect the expression of NF-κB molecule and change of autophagy involved protein Beclin 1 and LC3B.Results Araloside could significantly inhibit the proliferation and migration of HeLa cells and the NF-κB signaling pathway,and promoted the expression of autophagy related molecule Beclin 1,Atg 5 and LC3B.Conclusion Araloside could inhibit the NF-κB signaling pathways,thus induces autophagy occurrence and influences the proliferation and migration of cervical cancer HeLa cells.

AIM: To investigate the inhibitory effect of L-carnitine on high glucose-induced apoptosis of human aortic endothelial cells (HAECs) and the molecular mechanisms.METHODS: The apoptosis of HAECs was induced by high-glucose incubation.HAECs were treated with L-carnitine at different concentrations (50, 100 and 200 μmol/L).The cell viability was measured by MTT assay.The cell apoptosis was assessed by Hoechst 33258 staining and flow cytometry.Colorimetric method was employed to detect the caspase-3 activity in the HAECs.The protein expression and phosphorylation levels were determined by Western blot.RESULTS: High-glucose incubation dramatically decreased the cell viability and induced apoptosis.The protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme-1 (IRE1) and activating transcription factor 6 (ATF6) signaling pathways of endoplasmic reticulum stress were activated to induce cell apoptosis via down-stream caspase-4/3 cascade.However, L-carnitine treatment significantly attenuated the cell apoptosis and increased the cell viability in a concentration-dependent manner.L-carnitine also significantly suppressed endoplasmic reticulum stress and ATF6 signaling in high glucose-incubated HAECs without attenuating PERK and IRE1 signaling.The expression of site-1 protease (S1P) and site-2 protease (S2P) was inhibited by L-carnitine treatment, thus decreasing pro-apoptotic factor ATF6 p50 produced by ATF6 cleavage.CONCLUSION: L-carnitine inhibits high glucose-induced apoptosis of HAECs by inhibiting ATF6 signaling.

Objective To assess the effects of health management on high-risk diabetic populations.Methods A total of 307 diabetic high-risk adults from 6 communities of Tianjin were recruited by using diabetes risk screening technology.Three-month intensive health management and nine-month follow-up were conducted in this participants.Paired t test for continuous variables and paired contingency table x2 test were used for data analysis.Results Energy intake (1989.8 vs.1766.4 kcal,t =6.84,P ＜0.05),effective exercises (120.4 vs.157.5 kcal,t =-5.00,P ＜ 0.05),body weight (73.0 vs.71.5 kg,t =6.92,P ＜0.05),systolic blood pressure (130.4 vs.124.6 mm Hg (1 mm Hg =0.133 kPa),t =8.36,P ＜0.05),diastolic blood pressure (81.8 vs.78.4 mm Hg,t =7.40,P ＜ 0.05),serum total cholesterol (5.21 vs.5.08 mmol/L,t =2.73,P ＜ 0.05),fasting plasma glucose (6.4 vs.5.8 mmol/L,t =16.37,P ＜ 0.05)and 2 h postprandial blood glucose (7.7 vs.6.9 mmol/L,t =9.67,P ＜ 0.05) were significantly improved after the intervention.Conclusions Community-based health management may provide an effective way to prevent and control the risk factors of diabetes.

Objective To explore the effect of ectopic overexpression of Smac/DIABLO on the proliferation of pancreatic cancer cell line SW1990,and the sensitization to TRAIL and Gemcitabine induced apoptosis.Methods The Smac/DIABLO gene was transfected into the pancreatic cancer cell line SW1990 with the participation of Lipofectamine 2000 (SW1990/Smac).The cell line transfected with empty vector served as controls (SW1990/neo).The SW1990/neo and SW1990/Smac cells were assigned into the following treatment groups:TRAIL group,Gemcitabine group,TRAIL plus Gemcitabine group,and the control group.The SW1990 cells were treated with TRAIL and Gemcitabine in different concentrations and time.The cell growth inhibition rate (CGIR) was detected by MTT,the rate of apoptosis was measured by flow eytometry,the apoptosis morphous was observed by Heochst 33342 staining.The expressions of apoptosis-associated proteins such as Smas/DIABLO,XIAP,cytochrome C and caspase-3 were detected by Western blot.Results The cell growth of SW1990/Smac was significantly lower than growth of SW1990/ neo.The concentration of TRAIL were 200,500,1000 and 2500 ng/ml respectively.After 24 hours,the CGIR of SW1990/neo and SW1990/Smac were 11.11％,46.03％,67.08％,76.19％ and 22.11％,42.67％,56.63％,67.6％ respectively (P ＜ 0.05).The concentration of Gemcitabine were 10,20,40 and 60 μmol/L respectively.After 24 hours,the CGIR of SW1990/neo and SW1990/Smac were 15.2％,34.6％,55.16％,76.4％ and 22.65％,36.85％,55.11％,79.99％ respectively (P＜0.05).The cells of SW1990/neo and SW1990/Smac were treated by TRAIL(500 ng/ml),Gemcitabine (20 μmol/L) and combination group.The apoptosis rate were 5.64％,15.30％,27.27％ and 20.37％,23.27％,67.30％ (P ＜ 0.05) respectively.In combination group,the expressions of activators of caspase such as Smas/DIABLO,cytochrome C and caspase-3 increased significantly,while the expressions of inhibitor of apoptosis protein XIAP decreased.Conclusions Ectopic expression of Smac/DIABLO could induce the apoptosis of SW1990 cell,inhibit the cell proliferation,and enhence the sensitivity of SW1990 cell to TRAIL and Gemcitabine.The mechanism of apoptosis sensitization effect by Smac/DIABLO was associated with significant up-regulation of Smac/DIABLO,cytochrome C,down-regulation of XIAP,and the activation of caspase-3.