To improve the sensitivity of molecularly imprinted electrochemical sensors, a Pd nanoparticles-modified molecularly imprinted polymer (MIP) film for the determination of trimethoprim (TMP) was developed by thermal polymerization with N, N′-methylene diacrylamide as a functional monomer, Pd nanoparticle as a dopant and ethylene glycol maleic rosinate acrylate as a crosslinking agent.The morphologies and chemical structures of the Pd nano-materials and the imprinted films were characterized using Fourier transform infrared spectroscopy and scanning electron microscopy, respectively.The electrochemical properties of the nano-doped and undoped MIP sensors were investigated by cyclic voltammetry and electrochemical impedance spectroscopy.Results showed that the morphologies and chemical structures and the electrochemical properties of the doped molecularly imprinted sensor were remarkably different from those of the undoped imprinted sensor.Linear responses of the imprinted sensor to TMP were observed for concentrations ranging from 5.0×10-7 mol/L to 4.0×10-3 mol/L (R=0.9995), with a detection limit of 3.2×10-8 mol/L (S/N=3).The Pd nanoparticle doped MIP sensors exhibited high selectivity.The chronoamperometry showed that no interference from potential interfering species such as sulfamethoxazole, sulfadiazine, glucose, and urea were noted.The proposed electrochemical sensor was used to determine TMP in actual samples, with average recoveries of 96.8%-102.0%.

Objective To study the benzo(a)pyrene (B[a]P)-induced mRNA expression of aromatic hydrocarbon receptor (AHR) and cytochrome P4501A1 (CYP1A1) genes in rat liver. Methods Rats were injected intraperitoneally with 5, 10 and 15mg/kg of B[a]P. The total RNAs were extracted from rat livers by RNA purification kit, and the mRNA expression of AHR and CYP1A1 genes was determined by reverse transcription polymerase chain reaction (RT-PCR). β-actin was used as the internal control. The mRNA expression of both AHR and CYP1A1 genes was measured at indicated time points (24, 48 and 72h) after B[a]P treatment at three different concentrations (5, 10 and 15mg/kg). Results The mRNA expression of AHR gene increased in a time-dependent manner at the concentration of 10mg/kg but not at 5 and 15mg/kg of B[a]P. The mRNA expression of CYP1A1 gene differed significantly at 48h and 24h in rat livers treated with 10 and 15mg/kg dosage of B[a]P. The mRNA expression of AHR and CYP1A1 genes increased with B[a]P treatment in a concentration-dependent manner. The time-dependent increase in mRNA expression was shown by AHR but not by CYP1A1 gene with B[a]P (10mg/kg) treatment. Conclusion This study demonstrates that toxic B[a]P increases the mRNA expression of both AHR and CYP1A1 genes in vivo, suggesting that B[a]P may play a role in cancer genesis by this way.

Objective To estimate the relative risk for lung cancer associated with genetic polymorphism of T6235C mutation in 3' non-coding region (Msp Ⅰ) of cytochrome P450 1A1 (CYP1A1) and glntathione S-transferase M1 (GSTM1) in the Mongolian population in Inner Mongolian Region of China. Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and multiplex PCR methods were used to analyze blood samples obtained from 263 case subjects and 263 control subjects to determine their genotypes for CYP1A1 and GSTM1.Control subjects were matched with case subjects by ethnic background, age and gender. Results The frequencies of the variant CYP1A1 genotypes (CYP1A1C) and GSTM1-null in lung cancer groups were higher than those in control groups (38.4% vs. 28. 5% and 57.8% vs. 48.0%). The individuals who corried with CYP1A1C genotype had a significantly higher risk of lung cancer (OR=1.56, 95% CI=1.08 to 2.25, P=0.016) than those who carried with non-variation CYP1A1 genotype. The ones who carried with GSTM1-null genotype also had a significantly higher risk of lung cancer (OR=1.49, 95% CI=1.06 to 2.10, P=0.023) than these who carried with GSTM1-present genotype.When combination of polymorphisms of CYP1A1 and GSTM1 genotypes was analyzed, the risk of lung cancer for combination of CYP1A1C and GSTM1-null genotypes was increased significantly (OR=2.084, 95e CI=1.27 to 3.42, P=0.003). Susceptibility to lung cancer was related to smoking (OR=2.10, 95% CI=1.48 to 2.98, P=0.000). Considering smoking status, the risk of lung cancer for combination of smoking and CYP1A1C genotype was remarkably increased (OR=2.76, 950/0 CI=1.74 to 4. 37, P=0.000). It was the same case with combination of smoking and GSTM1-null genotype (OR=4. 38, 95% CI=2.35 to 8.15, P=0.000). Conclusion The polymorphisms of CYP1A1C genotype and GSTM1-null are the risk factors of lung cancer in the Mongolian population in Inner Mongolia Region of China. Smoking is also related to susceptibility to lung cancer. There may be a synergetic interaction between CYP1A1C and GSTM1-null in the elevated susceptibility of lung cancer. Smoking may have a synergetic interaction with CYP1A1C and GSTM1-null in the elevated susceptibility of lung cancer.

Toimprovethesensitivity,aCuOnanoparticledopedinmolecularlyimprintedpolymer(MIP)film for the determination of phenobarbital was prepared by using methacrylic acid as functional monomers, ethylene glycol maleic rosinate acrylate as a cross linking agent by thermal polymerization method. The electrochemical properties of the nano-doped sensor were investigated using cyclic voltammetry ( CV ) , differential pulse voltammetry ( DPV ) , electrochemical impedance spectroscopy ( EIS ) and chrono-amperometry ( CA) . The chemical structures and morphologies of the imprinted films were characterized using Fourier transform infrared spectroscopy and scanning electron microscopy. The results indicated that the sensors response value of peak current showed a linear dependence on the phenobarbital concentration in the ranges of 1. 2 × 10-7-1. 5 × 10-4 mol/L of phenobarbital. ( Linear regression coefficient=0. 9984 ) with the detection limit ( S/N=3 ) of 8. 2 × 10-9 mmol/L. The prepared sensor was successfully applied to the determination of phenobarbital in practical samples with recovery ranging from 96 . 5% to 103 . 0%.

Objective To investigate the protective effect of GuanXinShiWeiWan on ischemia reperfusion(I-R) injury rat.Methods 50 Wistar rats were randomly divided into normal group, model group, GuanXinShiWeiWan low ( 0.3 mg/kg ) and high ( 0.9 mg/kg ) dose group and positive group, each had 10 rats.Adopting the model of ischemia reperfusion injury of isolated rat hearts, the contents of SOD,MDA,LDH,CK and Ca2 +-ATP, Ca2 +-Mg2 +-ATP, Na +-K +-ATP in cardiac muscle tissue were tested and compared.Results Compared with model group, GuanXinShiWeiWan significantly improved the activities of SOD、Ca2 +-ATP,Ca2 +-Mg2 +-ATP and Na +-K +-ATP (P<0.05 or P<0.01) in cardiac muscle tissue which injured by ischemia reperfusion, while reducing markedly the contents of MDA,LDH,CK(P<0.05 or P<0.01).Conclusion GuanXinShiWeiWan can profect the cardiac muscle of ischemia reperfusion.