Objective To establish a rapid specific quantitative assay for Bacillus anthracis detection. Methods According to the principle of complex probe quantitative assay, the primers and quantitative probes targeted at chromatosome DNA rpoB were designed and applied to detect Bacillus anthracis. The influence factor of quantitative PCR were determined. Results The optimal system of this method was aquired: the length of quenching probe is 15mer,the ratio of fluorescent probe to quenching probe is 1/2 and the concentrtion of Mg 2+ is 3 mmol/L.The sensitivity of this assay for Bacillus anthracis is 10 3 copies. It can distinguish Bacillus anthracis from other closely related Bacillus. Conclusion The method can rapidly quantitatively detect the Bacillus anthracis with high sensitivity and specificity, it can be applied to clinical diagnosis.

Objective To measure the expression of CD80 and CD86 in renal tissue of lupus nephritis (LN) and explore its mechanism in the development of LN.Methods Forty-nine patients with active LN and 9 patients with minor glomerular abnormalities tissues as controls were studied.The expression of CD80, and CD86 in renal tissues was detected by immunohistochemical methods.Results CD86 was expressed extensively in glomerulus, periglomerular area, tubular epithelial cells and peritubular interstitium, while CD80 was expressed only in tubular epithelial cells and peritubular interstitium.Moreover, the percentage of CD+80 and CD+86 cells in tubular epithelial cells and peritubular interstitium showed a tendency to increase with tubulointerstitial damage.The expression of CD80 and CD86 in renal tissue correlated with the systemic lupus erythematosus (SLE) disease activity index score, the degree of proteinuria, creatinine clearance and anti- dsDNA antibody.Conclusions This study shows that increased CD80 and CD86 expression with the progression of tubulointerstitial lesion might play an important role in the development of lupus nephropathy, and the tubulointerstitial expression of CD80 and CD86 could potentially serve as a surrogate marker of SLE disease activity.The co-stimulatory molecules CDg, and CD86 might play an important role in the pathogenesis of LN.

Objective: The present study was designed to evaluate the protective effects of oligomeric proanthocyanidins (OPC) in mice exposed to paraquat (PQ) , and to explore the molecular mechanism. Methods: Four experimental groups were designed. Control group: 10 BALB/c mice were intraperitoneally injected with normal saline) . PQ group: 10 BALB/c mice were intraperitoneally injected with PQ (100 mg/kg) . PQ+OPC group: 10 BALB/c mice were administered with OPC (100 mg/kg) for 1 h before PQ (100 mg/kg) expo-sure. OPC group: 10 BALB/c mice were intraperitoneally injected with OPC (100 mg/kg) . The peripheral blood samples or lung tissue samples were collected at the designed time points for measuring the levels of oxi-dative stress indicators, the related protein levels of nuclear factor-kappa B (NF-κB) pathway and nuclear fac-tor erythroid related factor-2 (Nrf2) pathway. Results: Compared with the control group, the level of reactive oxygen species (ROS) , the content of malondialdehyde (MDA) in the PQ group were significantly induced, and the activity of superoxide dismutase (SOD) in the PQ group was decreased in the peripheral blood. As com-pared with the PQ group, the level of ROS and the content of MDA in the PQ+OPC group were significantly re-duced, the activity SOD in the PQ+OPC group was increased in the peripheral blood; the level of ROS and the content of MDA were also reduced in lung tissues in the PQ+OPC group. Moreover, compared with the con-trol group, the phosphorylation of IκBα and the expression of NF-κB p65 were increased in lung tissues in the PQ group. The phosphorylation of IκBα and the expression of NF-κB p65 were decreased in lung tissues in the PQ+OPC group as compared with the PQ group. In addition, compared with the control group, the expressions of HO-1 and Nrf2 were increased in lung tissues in OPC group, and these were decreased in lung tissues in PQ groups. Furthermore, the expressions of HO-1 and Nrf2 were also increased in lung tissues in PQ+OPC as com-pared with the PQ group. Conclusion OPC could alleviate PQ-induced systemic toxicity in mice by regulating oxidative stress via NF-κB and Nrf2 pathway.