Solvent effects on the π-dimerization of cation radicals of conjugated oligomers

π-Dimerization of cation radicals of conjugated oligomers has been investigated in various solvents to assess the effect of the polarity of the medium on the dimerization enthalpy. It is found that π-dimerization is favored in less polar solvents, unless solubilizing substituents are present

Synthesis and and characterisation of novel regioregular polythiophenes - Tuning the redox properties

The synthesis and full characterisation of three novel regioregular polythiophenes 8, 9, and 15 is presented. By varying the nature of the substituents on the polythiophene backbone in these materials it is possible to increase their first oxidation potential by almost 0.5 V. Because the first reduction potential follows the same trend, the electrochemical band gap of these polymers is essentially constant. The constant band gap inferred from the electrochemical data is confirmed by the onset of the optical absorption spectrum of the polythiophenes, which shows only small changes

Synthesis and characterization of novel regioregular polythiophenes

Three novel regioregular polythiophenes with side chain substituents resulting in increased oxidation potentials relative to poly(3-dodecylthiophene) have been synthesized using the McCullough polymerization protocol. All polymers have >95% head-to-tail couplings as evidenced from 1H-NMR and are furthermore characterized by SEC, solution and solid-state UV-vis spectroscopy, and cyclic voltammetry. By varying the nature of the side chains the redox properties could be altered: the first oxidation potentials vary between 0.75 V and 1.25 V and the first reduction potentials between -1.40 V and -1.85 V. The optical properties of the polymers in solution and as thin solid films were much less affected by the different substituents

The antiproteinuric effects of blood pressure-lowering agents:differences between nondiabetics and diabetics

The mechanism of the antiproteinuric effect of angiotensin-converting enzyme (ACE) inhibitors in diabetic and nondiabetic renal disease is as yet unknown. A meta-analysis of studies on the effects of ACE inhibitors and other antihypertensive drugs on proteinuria, blood pressure, and renal hemodynamics in nondiabetic renal disease revealed that ACE inhibitors lower proteinuria more than other antihypertensives. Moreover, a close correlation (p <0.01) between changes in urinary protein loss and in filtration fraction was found, whereas such a correlation could not be detected between changes in proteinuria and in blood pressure. This suggests that, at least in nondiabetic renal disease, the fall in proteinuria during ACE inhibition is the consequence of the intrarenal effect of the drug more than the systemic effect. Data on the mechanism of action of ACE inhibitors in diabetic microalbuminuria and in diabetic overt proteinuria are less consistent. A fall in proteinuria on antihypertensive drugs in these patients can be observed also without a significant fall in blood pressure, and without any change in filtration fraction. We therefore conclude that one should be cautious in extrapolating the data from studies in diabetic renal disease to patients with nondiabetic nephropathies. Moreover, we argue also that nonhemodynamic effects of ACE inhibitors also could be involved in the antiproteinuric effect of these drugs

The antiproteinuric effects of blood pressure-lowering agents:differences between nondiabetics and diabetics

The mechanism of the antiproteinuric effect of angiotensin-converting enzyme (ACE) inhibitors in diabetic and nondiabetic renal disease is as yet unknown. A meta-analysis of studies on the effects of ACE inhibitors and other antihypertensive drugs on proteinuria, blood pressure, and renal hemodynamics in nondiabetic renal disease revealed that ACE inhibitors lower proteinuria more than other antihypertensives. Moreover, a close correlation (p <0.01) between changes in urinary protein loss and in filtration fraction was found, whereas such a correlation could not be detected between changes in proteinuria and in blood pressure. This suggests that, at least in nondiabetic renal disease, the fall in proteinuria during ACE inhibition is the consequence of the intrarenal effect of the drug more than the systemic effect. Data on the mechanism of action of ACE inhibitors in diabetic microalbuminuria and in diabetic overt proteinuria are less consistent. A fall in proteinuria on antihypertensive drugs in these patients can be observed also without a significant fall in blood pressure, and without any change in filtration fraction. We therefore conclude that one should be cautious in extrapolating the data from studies in diabetic renal disease to patients with nondiabetic nephropathies. Moreover, we argue also that nonhemodynamic effects of ACE inhibitors also could be involved in the antiproteinuric effect of these drugs