Positron Annihilation in Chloropolystyrenes

Results of angular correlation of annihilation radiation and positron annihilation lifetime measurements are presented for atactic polystyrene and chloropolystyrenes. The inhibition of positronium formation follows the chlorine introduction as the decrease in intensities of the narrow component in angular correlation of annihilation radiation curves and of the longest-lived component in positron annihilation lifetime spectra prove. In general, the chlorine "activity" towards positrons seems to depend on its position in the polymer structure. The annihilation rate distribution as well as the radius and volume distributions of free-volume sites where positronium is assumed to be formed obtained with the use of CONTIN program for the raw sample in the 2nd series are given additionally

Positronium inhibition and free volume in chloropolystyrenes studied by positron annihilation

Positron annihilation phenomenon has been studied in chloropolystyrenes. PAL and ACAR measurements have been performed in air and at room temperature for amorphous samples of different chlorine content. The increase in the latter is followed by the decrease in both the intensity of the narrow component of ACAR curves and the intensity of the longest-lived component (I3) in PAL spectra. The latter one, related to the ortho-positronium intensity in polystyrene I03', changes according to the formula : I3/I03=[1+(19.93*C)0.56]-1 where C denotes the number of Cl atoms per unit of the polymer. The inductive effect produced by the chlorine in chloropolystyrenes is assumed to be the reason of the inhibition of the positronium formation in them. In general the chlorine reactivity towards positrons seems to depend on its position in the polymer structure. The numerical Laplace inversion technique /1/ has been applied to PAL data to recover the radius distribution of free volumes for each sample of the second series. A tendency towards decrease in mean radius of free volumes is seen when chlorine content increases in studied samples. The only exception is the sample in which the highest amount of chlorine atoms has been substituted at α-carbons in the aliphatic chain

Retinopathy in type 2 diabetes mellitus is associated with increased intima-media thickness and endothelial dysfunction

Background  Microangioathy and macroangiopathy in type 2 diabetes mellitus (T2DM) frequently coexist. Both types of vascular complications share traditional risk factors. It is not clear whether the presence of microangiopathy, such as diabetic retinopathy (DR), constitutes a predictor of atherosclerosis in T2DM. Here we described the search for the association between DR and intima-media thickness (IMT) in T2DM. We also compared endothelial function in subjects with and without DR. Material and methods  We examined 182 consecutive patients with T2DM for at least 5 years (mean age at examination 56·3 ± 6·52 years). We assessed (i) IMT of carotid artery by ultrasound and (ii) endothelial function by flow-mediated dilatation (FMD) method as well as by measurement of concentrations of von Willebrand factor (vWF) and s-ICAM-1. All patients underwent ophthalmological examination. Statistical analysis included Student's, Mann–Whitney, chi-square, Fisher tests and multiple regression. Results  DR was found in 71 (39·0%) subjects. IMT was higher in patients with DR than those without DR (0·87 mm vs. 0·79 mm, respectively, P = 0·0001). FMD was lower in the complication group than in subjects without DR (8·38% vs. 10·45%, respectively, P = 0·0023). Concentrations of s-ICAM-1 and vWF were not different between the groups. In multiple regression analysis, DR was among the predictors of increased IMT (P = 0·016) and decreased FMD (P = 0·002). We did not find a significant association of DR with vWF and s-ICAM-1 (P = 0·09 and P = 0·11, respectively). Conclusions  DR is associated with increased IMT and endothelial dysfunction in T2DM. Impaired endothelial function may be a common denominator of pathogenesis of microvascular complications and atherosclerosis in T2DM