The pollution of surface water and ground water caused by pharmaceuticals and personal care products(PPCPs) can directly affect the quality of drinking water.The sources of PPCPs and the routes to the drinking water were introduced briefly in the present paper.The removal efficiency of PPCPs in different unit processes applied in drinking water treatment was discussed in detail,including clarify,oxidization-disinfection,advanced treatment and so on.The performances of drinking water treatment unit processes for PPCPs removal were evaluated simply.

AIM:To construct the recombinant eukaryotic expression plasmid pEGFP-C1-SR-A I for the high expression in 293T cells in order to identify functions of savenger receptor-A I(SR-A).METHODS:The primer was designed according to MSR1 cDNA and pEGFP-C1-SR-A I was constructed by standard molecular cloning technique and enzyme digestion.After sequencing,the plasmid was transfected into 293T cells by lipidosome method.The expression of scavenger receptor-A I was identified by RT-PCR and Western blotting.The foam cells were evaluated by the formation of lipid granules in the cells with oil red staining.Cell adhesion was analyzed by cell adhesion assay.RESULTS:24 h after transfection,SR-A I mRNA was highly expressed and the high level of the protein was detected.The ratio of foam cell formation was doubled,the efficacy of cell adhesion was enhanced two times compared to the control group and the empty vector group.CONCLUSION:The recombinant eukaryotic expression plasmid has been constructed successfully with enhancing the function of uptake ox-LDL and adhesion in 293T cells by overexpression of SR-A I.

Objective To observe the abnormity of heart function in rats with pressure overload-induced left ventricular hypertrophy and the changes of NCX,SERCA2a expression in myocardial tissues. Methods Cardiac hypertrophy was induced by clipping the abdominal aorta in rats. The cardiac hypertrophy was evaluated by Left ventricular weight index(LVWI,left ventricular weight/body weight). NCX, SERCA2a mRNA and protein expressions in left ventricular tissues were determined by half-quantitative RT-PCR and Western blot normalized to abundance of GAPDH mRNA and protein,respectively. Results LVSP and LVEDP were obviously enhanced(P

Objective To investigate the effect of adenosine A2A receptor on pituitary-adrenal axis response in acute phase of moderate craniocerebral trauma.Methods Eighteen adenosine A2A receptor knock-out mice in a C57BL/6 background and another eighteen their wild-type littermates were divided into normal control group and craniocerebral trauma for 4 hours group,and craniocerebral trauma for 24 hours group according to random number table,with siμ mice per group.Plasma levels of adrenocorticotropic-hormone (ACTH) and corticosterone at hours 4 and 24 postinjury were determined using ELISA method.Results At 4 and 24 hours,brain water content in wild-type mice [(80.950 ± 0.184) ％,(82.178 ± 0.255)％ respectively] was higher than that in gene knock-out mice [(80.006 ± 0.199)％,(81.091 ± 0.295)％ respectively,P ＜ 0.01].Besides,brain water content in both wild-type and gene knock-out mice increased after injury (P ＜ 0.01).Plasma levels of ACTH and corticosterone were higher in geneknock-out sham mice than in wild-type sham mice [(120.214 ± 2.472) ng/L vs (91.767 ±7.395) ng/L,(27.814 ±0.888) μg/L vs (11.430 ±0.644) μg/L respectively,P ＜0.0l].At 4 and 24 hours,plasma levels of ACTH [(174.776-± 5.040) ng/L,(189.613 ± 4.802) ng/L respectively] in geneknock-out mice showed a higher increase than those in wild-type mice [(119.594 ± 6.945) ng/L,(124.93-± 11.001 7) ng/L respectively,P ＜ 0.05].Moreover,plasma levels of corticosterone [(40.138 ±-0.805) μg/L] at 4 hours and [(37.440-0.485)μg/L] at 24 hours in gene knock-out mice showed a same result as compared with that in wild-type mice [(19.702 ± 0.804) μg/L,(17.602 ± 0.743) μg/L respectively,P ＜ 0.05].Conclusions Knock-out of adenosine A2A receptor increases the release of ACTH and corticosterone in acute stage of moderate craniocerebral trauma and promotes pituitary-adrenal stress response.This may provide a novel explanation for the neuroprotective effect of A2A receptor deficiency.