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.

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 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.

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 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.

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.

Rhizobium leguminosarum biov.trifolii H954 has been fermented for eight days on the GMS medium.Culture supernatant is extracted by ethanol precipitation,sample is purified by Sephadex G\|50,Sephadex G\|10 and DEAE\|Cellulose chromatoraphy.Gas chromatography(GC), 13 C nuclear magnetic resonance spectroscopy(NMR)and mass spectrometry(MS) analysis indicated that the sample is cyclic,neutral glucan,and composes of glucose linked solely by 1→2 glucosidic bonds.Cyclic glucan has degrees of polymerization ranging form 17 to 22,with a degree of ploymerization of 19 as the major glucan cycles.

Objective:To investigate the expression of Survivin and it's relationship with the expression of Bcl-2 in sinonasal inverted papilloma (SNIP).Method:Immunohistochemical method was used to determine the expression of Survivin and Bcl-2 in 30 cases of SNIP,10 cases of sinonasal squamous cell carcinoma(SCC) and 10 cases of normal inferior concha tissues.Result:Survivin was expressed in 22 of 30(73.3%)cases of SNIP,8 of 10(80.0%)cases of SCC and not expressed in 10(0%)cases of normal inferior concha tissues.Expression of Survivin was significantly higher in SNIP and SCC than in normal tissues.Bcl-2 was expressed in 9 of 10(90.0%)cases of SCC and 2 of 10(20.0%)cases of normal inferior concha tissues.Expression of Bcl-2 was significantly higher in SCC than in normal tissues.Bcl-2 was expressed in 14 of 30(46.7%)cases of SNIP,higher than normal tissues.Expression of Bcl-2 was positively related to expression of Survivin.Conclusion:Survivin may play an important role in the pathway of progression of SNIP and SCC.It may be identified as a new therapeutic target.Bcl-2 may play a synergic role with Survivin in progression of SNIP.