More and more attentions have been paid to the harm of environmental arsenic pollution to human health.The mechanism of arsenic metabolism in human body was described,the interaction mechanism and research advance were reviewed in the present paper,including the damages to skin,digestive system,urinary system,immune function,nervous system,cardiovascular system,respiratory system and inheritance system.It is useful not only to enhance understanding for the relation between arsenic pollution and health damage,but also to provide the basic theory to control the arsenic pollution.The present paper also made suggestions in the future research in this field.

Objective To investigate the efficacy of sequential add-on of pegylated interferon α-2a (PEGIFN-α-2a) for 48 weeks in chronic hepatitis B (CHB) patients with low serum hepatitis B e antigen (HBeAg) titer after long term adefovir dipivoxil (ADV) monotherapy.Methods This was a randomized,open and prospective clinical trial.Patients who had been treated with ADV for 72 to 144 weeks,with undetectable serum hepatitis B virus (HBV) DNA level,low HBeAg titer (5 S/CO＜ HBeAg＜50 S/CO) and serum hepatitis B surface antigen (HBsAg) ＜5000 IU/mL were included.The patients were categorized into ADV monotherapy group and ADV plus PEGIFN-a-2a combination therapy group by random number table.Patients in ADV group continued ADV monotherapy and patients in combination therapy group added PEGIFN-α-2a to ADV for 48 weeks.After the treatment,efficacy of the two therapies were assessed by comparing the reduction of serum HBeAg reduction,HBeAg loss rate,HBeAg seroconversion rate,and reduction of intrahepatic HBV DNA and HBV covalently closed circular DNA (cccDNA).Pre-and post-treatment results were compared by paired samples t test.Comparison between groups was performed using indepedent samples t test.Comparison of rates between groups was performed using x2 test.Results The trial enrolled 55 CHB patients,and there were 27 patients in ADV monotherapy group,28 patients in combination therapy group.Baseline characteristics including age distribution,sex ratio,alanine aminotransferase (ALT),aspartate aminotransferase (AST),total bilirubin (TBil),serum HBeAg and HBsAg,hepatic HBV DNA and HBV cccDNA were all comparable (all P＞0.05).Twenty-five patients in ADV monotherapy group and 26 patients in combination therapy group completed 48 weeks treatment.HBeAg loss rates and seroconversion rates of combination therapy group were higher than those of ADV monotherapy group (x2 =5.38 and 4.69,respectively,both P＜0.05).HBeAg titers of both groups were significantly lower than those of baseline (t=8.43 and 8.50,respectively,both P＜0.05).The HBeAg titer of combination therapy group was lower than that of monotherapy group (t=5.60,P＜ 0.01).HBV DNA and HBV cccDNA in liver tissue of combination therapy group was (6.934±0.52) lg IU/mg and (5.63±0.54) lg IU/mg post-treatment,respectively,which were both lower than baseline (t＝7.12.6.67,respectively,both P＜0.01).HBV DNA in liver tissue of monotherapy group was (7.09＝0.43) lg IU/mg post-treatment,which was lower than baseline (t=2.67,P=0.02).After treatment,HBV cccDNA in liver tissue of combination therapy group was lower than that of monotherapy group (t =2.87,P=0.00).Conclusions Compared with ADV monotherapy,sequential add-on of PEGIFN-a-2a in combination with ADV can achieve higher serum HBeAg loss rate and seroconversion rate and facilitate the clearance of hepatic HBV DNA and HBV cccDNA in CHB patients with low HBeAg titer after long-term ADV monotherapy.

Objective The aim to assess the methodology and feasibility of ultrasound guided percutaneous thrombin injection(UGTI) for the treatment of Iarogenic Femoral Arterial Complexity Pseudoaneurysms(IFACP).Methods Thirty two iarogenic femoral arterial complexity pseudoaneurysms patients following femoral arerial puncture for arterial angiography were treated with UGTI.Twenty-three IFACP with 2 lobes,8 IFACP with 3 lobes,1 IFACP with 4 lobes.Under local anesthesia the lobe was pene trated by artery needle successively and thrombin jection was performed slowely into distal lobe with US guide precise localization.Dynamical observation was performed for the status of thrombogenesis and cavity plugging.US follow-up examination were performed after 24 h and 7 d.Results Reperfusion occurred in IFACP with 3 lobes after 24 h and UGTI failure.IFACPs with 4 lobes failure.Nothromboembolic,infectious,allergic complication soccurred.Conclusion UGTI is the first mothed for the treatment of IFACP.Precise localization and percutaneous can enhance the ratio of treatment of IFACPs and avoid the severe complications.

Objective To observe the effect of curcumin on the expression of smad7 and TGF-β1 in rats renal tubular cells of with Ang II, and discuss the mechanism of curcumin to improve renal interstitial fibrosis.Methods Cultured rat renal tubular epithelial cells were divided into the blank group, the Ang II control group and the low, medium and high dose curcumin group. The rest of the groups were intervened by 10-8 mol/L Ang II except the blank group; the low, medium and high dose groups of curcumin were intervened by 2.5, 5.0, 10.0μmol/L curcumin. Then Western blot was used to detect the expression of TGF-β1 and smad7 protein, RT-PCR was used to detect the TGF-β1 and smad7 mRNA expression.Results Compared with the blank group, the expression of TGF-β1 protein (0.23 ± 0.03vs. 0.16 ± 0.01), and TGF-β1 mRNA (1.89 ± 0.20vs. 1.00 ± 0.00) significantly increasedin AngⅡ control group (P<0.05), and the expression of smad7 protein (0.19 ± 0.03vs. 0.24 ± 0.02), and smad7 mRNA (0.48 ± 0.05vs. 1.00 ± 0.00) significantly reduced in AngⅡcontrol group (P<0.05). Compared with the AngⅡ control group, the expression of TGF-β1 protein in low, medium and high dose curcumingroup (0.18 ± 0.02, 0.17 ± 0.02, 0.16 ± 0.03vs. 0.23 ± 0.03) and TGF-β1 mRNA (1.58 ± 0.11, 1.34 ± 0.16, 0.97 ± 0.19vs. 1.89 ± 0.20) significantly decreased (P<0.05), and the expression of smad7 protein (0.28 ± 0.04, 0.31 ± 0.03, 0.34 ± 0.04vs. 0.19 ± 0.03) and smad7 mRNA (0.68 ± 0.07, 0.80 ± 0.06, 0.98 ± 0.09vs.0.48 ± 0.05) increased significantly (P<0.05).Conclusions Curcumin can thus play its role in renal protection by counteract the AngⅡ mediated renal interstitial fibrosis. Its mechanism may be related to the reduction of TGF-β1 protein and its mRNA expression, up regulation of smad7 protein and its mRNA expression.

ObjectiveTo investigate the early diagnosis and treatment of pleuropulmonary blastoma in children. Meth-ods The progress of pleuropulmonary blastoma from type 1 to type 3 was retrospectively analyzed.Results The male infant had no obvious abnormality in chest X-ray at 18 days. At one year old, X-ray iflm of the chest showed cystic lesions near hilum of the left lung (about 5 cm × 4 cm × 4 cm). The congenital cystic adenomatoid malformation was considered and an operation resection was suggested. However, it had been rejected by his parents. At 3 years and 2 months old, chest X-ray and CT showed left lung had a solid cystic lesion, the volume was signiifcantly enlarged, the back side was solid and the upper part had a large gas cavity. Two months later, the patient had asthmatic suffocation. The chest CT showed the tumor was completely solid. Pleuropulmonary blastoma type 3 was considered. The patient received the conventional chemotherapy after operation excision, and was followed up for 1 year. No recurrence was observed after the treatment.Conclusions Type 1 pleuropulmonary blastoma and congenital cystic adenomatoid malformation are hard to be differentially diagnosed. Early diagnosis and treatment of type 1 pleuropulmo-nary blastoma can improve the prognosis.

Objective To investigate the relationship between high-glucose-induced fibronectin(FN) expression and up-regulation of integrin-linked kinase(ILK) in human kidney tubular epithelial cells (HKC) and kidney of CD-1 mice. Methods Cultured human kidney tubular epithelial cells and streptozotocin (STZ)-indueed diabetic model of CD-1 mice were enrolled in this study.Western blot was used to detect the expression of FN and ILK.The kinase dead ILK plasmid (pCMV-kdlLK) were transferred to HKC. Results Four weeks after injection of STZ,CD-1 mice had higher blood glucose level as compared to the control [(20.3±2.7) mmol/L vs (6.1±1.4) mmol/L,P＜0.01].Meanwhile,expression of FN and ILK was significantly increased in diabetic mice as compared to the control (P＜0.01).There was positive correlation between the expression of FN and ILK (r=0.899,P＜0.01).High-glucose could up-regulate FN and ILK expression in cultured HKC in a time- and dose-dependent manner.Blockage of ILK activation by pCMV-kdILK abrogated high-glucose-incuced FN expression in HKC. Conclusions Highglucose can induce FN expression through up-regulating ILK expression.Blockage of ILK activation abrogates this effect.

Objective To investigate the effect of high glucose on renal tubular epithelial-mesenchymal transition,and to analyze the relationship between high glucose and transforming growth factor β1(TGF-β1)and the mechanism of renal interstitial fibrosis. Methods HKC and Smad7-overexpression HKC cells were grown in DMEM/F12 medium containing 5%～10%newborn calf serum.They were cultured for 16 h in free serum medium after 80%cells were adhered onto the surface of the flask.Afterwards,they were stimulated by high glucose(glucose concentration:25 mmol/L and 50 mmol/L).The expression of α-SMA,E-cadherin and fibronectin was detected by Western blot while the supernatant level of TGF-β1 was detected by ELISA.Cell motility and migration was evaluated using Boyden chamber motogenicity assay. Results In HKC induced by high glucose,the expression of α-SMA and fibronectin protein was highly upregulated while the expression of E-cadhefin protein was down-regulated.The expression of TGF-β1was up-regulated in a dose-dependent manner.These above-mentioned effects could be obviously inhibited by anti-TGF-β1 antibody.The protein expression of α-SMA,fibronectin and E-cadherin had no obvious change in Smad7-overexpression HKC induced by high glucose.HKC exhibited enhanced motility and invasive capacity in high glucose groups,compared to that in control group.Migrated cell counting was(12.4±3.7)and(18.6±4.4)cell/HP in 25 and 50 mmol/L glucose groups respectively. Conclusion High glucose may induce renal tubular epithelialmesenchymal transition through TGF-β1 pathway,which can be inhibited by blocking the Smad signal pathway.

OBJECTIVE To evaluate the anti-tumor activities of WX-127-07,a new microtubule-tar-geting agent invitroand probe its molecular mechanism. METHODS The well-known microtubule-targe-ting anti-tumor drugs taxol,vincristine and anti-gout drug colchicine were used as positive controls. The anti-proliferation activity was examined in five different cell lines after treatment with WX-127-07(0.3 -300 nmol·L-1 )for 72 h by SRB assay. The cell cycle arrest profile was assayed by flow cytometry. The multiparameters of cytotoxicity,cell morphology,apoptosis and different signaling pathways related to tumorigenesis and inflammation were analyzed using the high content analysis platform. Tubulin tryptic digestion and competition inhibition assay for colchicine or vinblastine site were used to confirm the bind-ing site in microtubules at a molecular level. RESULTS All the tested compounds obviously inhibited the growth of A549,HepG2,HeLa,HLF and HUVEC cells. The lC50 values of WX-127-07 were 4.47±0.05, 5.18±0.08,4.90±0.19,4.10±0.16 and(5.04±0.08)nmol·L-1 respectively,lower than those of colchicine〔the lC50 values were 21. 17 ± 1. 22,14. 19 ± 0. 53,43. 80 ± 1. 64,145. 89 ± 10. 97 and( 27. 67 ± 1.79)nmol·L-1 ,respectively〕and those of vincristine〔the lC50 values were 16.51±0.36,16.76±0.33, 27.80±2.75,43.80±1.48 and(9.15±0.78)nmol·L-1 ,respectively〕,but were similar to or lower than those of taxol〔the lC50 values were 10. 68 ± 0. 61,12. 86 ± 0. 25,4. 81 ± 0. 61,102. 07 ± 15. 17 and( 3. 04 ± 0.12)nmol·L-1 ,respectively〕. High content multi-parameter analysis revealed that WX-127-07 induced a concentration-dependent microtubular depolymerization(P=0.0075)with the same pattern as colchicine and vincristine,but at a lower concentration. Both WX-127-07 and positive drugs could induce cell cycle arrest in A549 cells,increase nuclear membrane permeability and early signs of apoptosis in HepG2 cells,but neither cancer related pathways nor inflammation related pathways were affected. Microtubular competition inhibition assay showed that WX-127-07 inhibited the binding of colchicine with tubulin(P =0.0259). Tryptic digestion of tubulin-WX-127-07 premixture showed a similar electrophoretic band to that of tubulin-colchicine premixture. CONCLUSION WX-127-07 is a novel microtubule-depolymerizing agent with anti-proliferation activity and acting on the colchicine binding site.

Objective To explore the association of galactose-deifcient IgA1 levels with clinical features, and further to provide guidance for individualized treatment of HSP. Methods According to the clinical symptoms and curative effect, 57 children with HSP were divided into four groups:non-HSPN group (n=26), HSPN group (n=7), refractory HSP group (n=7) and remission group (n=17). In non-HSPN group, 12 cases received glucorticoid therapy and 14 cases did not. Serum galactose-de-ifcient IgA1 (Gd-IgA1) concentrations were detected using a Helix aspersa-lectin-based enzyme-linked immunosorbent assay (ELISA), and the total IgA1 levels were measured by ELISA. Results The serum Gd-IgA1 level was signiifcantly higher in 40 HSP children who were not cured than that in remission group and control group (P<0.05). However, there was no difference in Gd-IgA1 level between remission group and control group (P>0.05). Compared with the control group, the serum Gd-IgA1 level was signiifcantly higher in HSPN group, non-HSPN group and refractory HSP, and children with refractory HSP had signiifcantly higher Gd-IgA1 level than children in non-HSPN group (P<0.05). No signiifcant difference in Gd-IgA1 level was found either between HSPN group and refractory HSP group or between HSPN group and non-HSPN group (P>0.05). Furthermore, in non-HSPN group, the serum Gd-IgA1 level in HSP children who were not treated with glucorticoid was signiifcantly higher than that in HSP children treated with glucorticoid (P<0.05). Conclusions The serum Gd-IgA1 level is associated with the disease activ-ity and curative effect of HSP, especially in children with refractory HSP, and it is thus likely to be a new non-invasive disease activity marker for guiding the proper usage of glucocorticoid and immunosuppressants in HSP children.

Objective To investigate the plasma vitamin D3 level and its association with B cell subsets of patients with primary Sj(o)gren's syndrome (pSS).The role of vitamin D3 levels in the pathogenesis of pSS was explored.Methods The expression of plasma vitamin D3 levels of 55 patients with pSS and 32 controls were analyzed by ELISA.Frequencies of peripheral blood CD19+CD27-na(i)ve B cells,CD19+CD27+ memory B cells and CD19+CD27high plasma cells were analyzed by flow cytometry in 34 pSS patients without therapy and 22 controls.The relationship between the vitamin D3 levels and B cell subsets,SSDAI,tear flow rate,saliva flow rate,rheumatoid factor,immunoglobulin was analyzed in pSS patients.Non-parametric test,t test,one-way ANOVA,x2test,Pearman's and Spearman's correlation analysis were used for statistical analysis.Results ① There was significant difference in the levels of plasma 1,25 (OH)2D3 between the pSS patients group and normal control group,1,25 (OH)2D3 was significantly lower in pSS patients than that in the normal control group [24.17(22.20,28.41) pg/ml and 41.25(23.38,62.18) pg/ml,P＜0.05],and that was also obviously lower in the active group [22.64(20.74,24.90) pg/ml] than that in the normal control group (P＜0.05),and that was also obviously lower in the active disease group than that in the inactive disease group [25.39 (23.16,33.09) pg/ml,P＜0.05],but there was no difference between the inactive group and the normal control group (P＞0.05).② The percentage of peripheral blood of CD19+CD27high plasma cells and CD19+CD27+ memory B cells in CD19+ cells was reduced in patients in the pSS group compared with the control group [(0.89±0.30)％ and (1.72±0.43)％,(24±8)％ and (34±5)％; P＜0.05],and that was also significantly lower in the active group [(1.03±0.59) ％ ; (26± 10)％] and inactive group [(1.00±0.16)％,(26± 3)％] than that in the normal controls (P＜0.05).However,there was no difference between the active group and the inactive group (P＞0.05),but the frequency of peripheral blood of CD19+ CD27-naive B cells in CD19+ B cells was increased in patients with pSS compared with normal control group [(75.4±7.5)％ and (63.9±5.2)％,P＜0.05],and that was also significantly higher in the active group [(73.4±9.7)％] and inactive group [(73.3±2.9)％] than that in the normal control (P＜0.05),there was no difference between the active group and the inactive group.③ Significant negative correlation was observed between 1,25 (OH)2D3 and the percentage of peripheral blood CD19+CD27+ memory B cells in CD19+ cells as well as immunoglobulin G(r=-0.627,P=0.039; r=-0.657,P＜0.01) level.Conclusions These results demonstrate that abnormality of vitamin D levels may play an important role in the pathogenesis of pSS.