Abstract: A method is provided for optimizing power consumption of a vehicle which may include sending data from a vehicle Electronic Control Unit and vehicle Global Positioning System receiver to a network cloud and/or server upon starting the vehicle, calculating a most probable final destination and most probable optimized route of the vehicle in the network cloud and/or server based on the sent vehicle data, and calculating a most probable driving mode map in the network cloud and/or server. The method may further include calculating an optimized power utilization of propulsion sources for the vehicle in the network cloud and/or server, returning the optimized power utilization of propulsion sources to the vehicle from the network cloud and/or server, and using the optimized power utilization of propulsion sources to control drive train modes and/or peripheral equipment of the vehicle during driving in order to optimize the power consumption of the vehicle.

Abstract: A method is provided for optimizing power consumption of a vehicle which may include sending data from a vehicle Electronic Control Unit and vehicle Global Positioning System receiver to a network cloud and/or server upon starting the vehicle, calculating a most probable final destination and most probable optimized route of the vehicle in the network cloud and/or server based on the sent vehicle data, and calculating a most probable driving mode map in the network cloud and/or server. The method may further include calculating an optimized power utilization of propulsion sources for the vehicle in the network cloud and/or server, returning the optimized power utilization of propulsion sources to the vehicle from the network cloud and/or server, and using the optimized power utilization of propulsion sources to control drive train modes and/or peripheral equipment of the vehicle during driving in order to optimize the power consumption of the vehicle.

Abstract: The mechanism of action of Ebselen differentiates between bacterial and mammalian thioredoxin reductase (TrxR). It displays fast oxidation of mammalian Trx and via the NADPH-TrxR catalyzed turnover of ebselen selenol with hydrogen peroxide, and therefore are mammalian antioxidants. Ebselen, and its diselenide, are strong competitive inhibitors of E. coli TrxR with Ki of 0.14 ?M and 0.46 ?M, respectively. E. coli mutants lacking glutathione reductase or glutathione were much more sensitive to inhibition by ebselen. Since either glutaredoxin or thioredoxin systems are electron donors to ribonucleotide reductase, ebselen targets primarily glutathione and glutaredoxin-negative bacteria, a class which includes major pathogens. Ebselen, and similar compounds are therefore useful as antibacterial agents, even for multiresistant strains.

Abstract: The mechanism of action of Ebselen differentiates between bacterial and mammalian thioredoxin reductase (TrxR). It displays fast oxidation of mammalian Trx and via the NADPH-TrxR catalyzed turnover of ebselen selenol with hydrogen peroxide, and therefore are mammalian antioxidants. Ebselen, and its diselenide, are strong competitive inhibitors of E. coli TrxR with Ki of 0.14 ?M and 0.46 ?M, respectively. E. coli mutants lacking glutathione reductase or glutathione were much more sensitive to inhibition by ebselen. Since either glutaredoxin or thioredoxin systems are electron donors to ribonucleotide reductase, ebselen targets primarily glutathione and glutaredoxin-negative bacteria, a class which includes major pathogens. Ebselen, and similar compounds are therefore useful as antibacterial agents, even for multiresistant strains.

Abstract: Compounds based on the following structures: wherein each of R1, R2, R3 and R4 is independently selected from: hydrogen, alkyl, and substituted alkyl; and each of R5, R6 and R7 is independently selected from: hydrogen, alkyl, substituted alkyl, alkoxy, substituted alkoxy, N,N-dialkylamino, substituted N,N-dialkylamino, N-monoalkylamino, substituted N-monoalkylamino, and electron-donating substituents are useful in the treatment of disorders or conditions caused by or involving free radical-mediated or oxidative tissue damage.

Abstract: The mechanism of action of Ebselen differentiates between bacterial and mammalian thioredoxin reductase (TrxR). It displays fast oxidation of mammalian Trx and via the NADPH-TrxR catalyzed turnover of ebselen selenol with hydrogen peroxide, and therefore are mammalian antioxidants. Ebselen, and its diselenide, are strong competitive inhibitors of E. coli TrxR with Ki of 0.14 ?M and 0.46 ?M, respectively. E. coli mutants lacking glutathione reductase or glutathione were much more sensitive to inhibition by ebselen. Since either glutaredoxin or thioredoxin systems are electron donors to ribonucleotide reductase, ebselen targets primarily glutathione and glutaredoxin-negative bacteria, a class which includes major pathogens. Ebselen, and similar compounds are therefore useful as antibacterial agents, even for multiresistant strains.

Abstract: The mechanism of action of Ebselen differentiates between bacterial and mammalian thioredoxin reductase (TrxR). It displays fast oxidation of mammalian Trx and via the NADPH-TrxR catalyzed turnover of ebselen selenol with hydrogen peroxide, and therefore are mammalian antioxidants. Ebselen, and its diselenide, are strong competitive inhibitors of E. coli TrxR with Ki of 0.14 ?M and 0.46 ?M, respectively. E. coli mutants lacking glutathione reductase or glutathione were much more sensitive to inhibition by ebselen. Since either glutaredoxin or thioredoxin systems are electron donors to ribonucleotide reductase, ebselen targets primarily glutathione and glutaredoxin-negative bacteria, a class which includes major pathogens. Ebselen, and similar compounds are therefore useful as antibacterial agents, even for multiresistant strains.