55 research outputs found

    A Piezoelectric Immunosensor Using Hybrid Self-Assembled Monolayers for Detection of Schistosoma japonicum

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    BACKGROUND: The parasite Schistosoma japonicum causes schistosomiasis disease, which threatens human life and hampers economic and social development in some Asian countries. An important lesson learned from efforts to reduce the occurrence of schistosomiasis is that the diagnostic approach must be altered as further progress is made towards the control and ultimate elimination of the disease. METHODOLOGY/PRINCIPAL FINDINGS: Using mixed self-assembled monolayer membrane (mixed SAM) technology, a mixture of mercaptopropionic acid (MPA) and mercaptoethanol (ME) was self-assembled on the surface of quartz crystals by gold-sulphur-bonds. Soluble egg antigens (SEA) of S. japonicum were then cross-linked to the quartz crystal using a special coupling agent. As compared with the traditional single self-assembled monolayer immobilization method, S. japonicum antigen (SjAg) immobilization using mixed self-assembled monolayers exhibits much greater immunoreactivity. Under optimal experimental conditions, the detection range is 1:1500 to 1:60 (infected rabbit serum dilution ratios). We measured several infected rabbit serum samples with varying S. japonicum antibody (SjAb) concentrations using both immunosensor and ELISA techniques and then produced a correlation analysis. The correlation coefficients reached 0.973. CONCLUSIONS/SIGNIFICANCE: We have developed a new, simple, sensitive, and reusable piezoelectric immunosensor that directly detects SjAb in the serum. This method may represent an alternative to the current diagnostic methods for S. japonicum infection in the clinical laboratory or for analysis outside the laboratory

    Synthesis, Structures, and Optical Properties of Ruthenium(II) Complexes of the Tris(1-pyrazolyl)methane Ligand

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    Four new complex salts [Ru^(II)Cl(Tpm)(L^A)_2][PF_6]_n [Tpm = tris(1-pyrazolyl)methane; n = 1, L^A = pyridine (py) 1 or ethyl isonicotinate (EIN) 2; n = 3, L^A = N-methyl-4,4′-bipyridinium (MeQ^+) 3 or N-phenyl-4,4′-bipyridinium (PhQ^+) 4] have been prepared and characterized. Electronic absorption spectra show intense d → π^* metal-to-ligand charge-transfer (MLCT) absorption bands, while cyclic voltammetry reveals a reversible Ru^(III/II) wave, accompanied by quasireversible or irreversible L^A-based reductions for all except 1. Single crystal X-ray structures have been obtained for 1•Me_2CO, 2, and 3•Me_2CO. For 2–4, molecular first hyperpolarizabilities β have been measured in acetonitrile solutions via the hyper-Rayleigh scattering (HRS) technique at 800 nm. Stark (electroabsorption) spectroscopic studies on the MLCT bands in frozen butyronitrile allow the indirect estimation of static first hyperpolarizabilities β_0. The various physical data obtained for 3 and 4 are compared with those reported previously for related cis-{Ru^(II)(NH_3)_4}^(2+) species [Coe, B. J. et al. J. Am. Chem. Soc. 2005, 127, 4845]. TD-DFT calculations on the complexes in 1–4 confirm that their lowest energy absorption bands are primarily Ru^(II) → L^A MLCT in character, while Ru^(II) → Tpm MLCT transitions are predicted at higher energies. DFT agrees with the Stark, but not the HRS measurements, in showing that β_0 increases with the electron-accepting strength of L^A. The 2D nature of the chromophores is evidenced by dominant β_(xxy) tensor components

    Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage

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    This study was aimed at investigating the effects of subchronic administration of doxorubicin (DOX) on brain mitochondrial bioenergetics and oxidative status. Rats were treated with seven weekly injections of vehicle (sc, saline solution) or DOX (sc, 2 mg kg−1), and 1 week after the last administration of the drug the animals were sacrificed and brain mitochondrial fractions were obtained. Several parameters were analyzed: respiratory chain, phosphorylation system, induction of the permeability transition pore (PTP), mitochondrial aconitase activity, lipid peroxidation markers, and nonenzymatic antioxidant defenses. DOX treatment induced an increase in thiobarbituric acid-reactive substances and vitamin E levels and a decrease in reduced glutathione content and aconitase activity. Furthermore, DOX potentiated PTP induced by Ca2+. No statistical differences were observed in the other parameters analyzed. Altogether our results show that DOX treatment increases the susceptibility of brain mitochondria to Ca2+-induced PTP opening and oxidative stress, predisposing brain cells to degeneration and deathThe work was funded by the Portuguese Foundation for Science and Technology (PTDC-SAU-OSM-64084-2006). Referenceshttp://www.sciencedirect.com/science/article/B6T38-4T7087K-3/2/399a0c99d1e73842d49f885883fb79d

    Metformin promotes isolated rat liver mitochondria impairment

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    Abstract Metformin, a drug widely used in the treatment of type 2 diabetes, has recently received attention due to the new and contrasting findings regarding its effects on mitochondrial function. In the present study, we evaluated the effect of metformin in isolated rat liver mitochondria status. We observed that metformin concentrations =8 mM induce an impairment of the respiratory chain characterized by a decrease in RCR and state 3 respiration. However, only metformin concentrations =10 mM affect the oxidative phosphorylation system by decreasing the mitochondrial transmembrane potential and increasing the repolarization lag phase. Moreover, our results show that metformin does not prevent H2O2 production, neither protects against lipid peroxidation induced by the pro-oxidant pair ADP/Fe2+. In addition, we observed that metformin exacerbates Ca2+-induced permeability transition pore opening by decreasing the capacity of mitochondria to accumulate Ca2+ and increasing the oxidation of thiol groups. Taken together, our results show that metformin can promote liver mitochondria injury predisposing to cell death
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