No abstract

M-doped ZnO (M: Cd, Mg) powders obtained by mechanical milling were analyzed by X-ray diffraction (XRD), scanning electron microscopy (SEM) and positron lifetime annihilation spectroscopy (PALS). The mixing of the oxides is followed by means of XRD and SEM. As milling proceeds, a clear reduction of grain size and homogenization are observed. The evolution of annihilation parameters with milling time and cation content were analyzed and related with the kind of mechanical induced defect involved. Ternary oxides Zn 1−x M x O were efficiency obtained for certain compositions. The results showed that positrons constitute a well suited probe to characterize the cation substitution in the ZnO oxide lattice.

On this paper the first Building Integrated Hybrid Photovoltaic (BIHPV) cell obtained on a commercial tile is presented. The experimental techniques used allow a future low cost development of these cells for its massive use on facades for buildings. The basic concept includes a metal projected layer as back contact with an electron injection layer of electrodeposited ZnO, an organic PBCBM/P3HT photovoltaic cell with a closing TCO thin film on top. Integration with the substrate problems have been solved and allow further work on cell performance and durability.

Zn 1-x Mg x O powders at various compositions were obtained by mechanical milling from the binary oxides. The progressive incorporation of Mg atoms into the ZnO lattice was monitored by X-ray diffraction (XRD). The evolution of annihilation parameters with milling time and composition were analyzed and related to the possible types of mechanical and substitutional induced defect present. It was concluded that the average lifetime constitute a useful parameter to sense the complete cation substitution in the wurtzite structure.

Ischemic heart disease (IHD) is the leading cause of sudden cardiac death (SCD) and often non-thrombosed severe coronary stenoses with or without myocardial scars are detected. Left dominant arrhythmogenic cardiomyopathy (LDAC) is a life-threating rare disease which has been more thoroughly studied in the last 10 years. The macroscopic study of an SCD victim was conducted and re-evaluated 9 years later. The cardiological work-up in his first-degree relatives initially comprised an electrocardiogram (ECG) and an echocardiogram. When they were re-evaluted 9 years later, a cardiac magnetic resonance, an ECG-monitoring, an exercise testing and a genetic study were performed and the pedigree was extended accordingly. In 2008, an IHD was suspected in the sports-triggered SCD of a 37-year-old man upon the postmortem (75% stenosis of the left main and circumflex coronary arteries; the subepicardial left ventricular fibrofatty infiltration with mild myocardial degeneration was assumed to be a past myocardial infarction). No cardiomyopathy was identified in any of the two proband’s sisters. Nine years thereafter, distant relatives were diagnosed with LDAC due to a pathogenic desmoplakin mutation. The reanalysis of the two sisters showed ventricular arrhythmias in one of them without structural heart involvement and the reviewed postmortem of the proband was reclassified as LDAC based on the fibrofatty infiltration; both were mutation carriers. The completion of the family study on 19 family members yielded one SCD due to LDAC (the proband), three living patients diagnosed with LDAC (two with a defibrillator), one mutation carrier without structural ventricular involvement, and 14 healthy relatives (who were discharged) with a very good co-segregation of the mutation. Although rare, LDAC exists and sometimes its differential diagnosis with IHD has to be faced. Modifying previous postmortem misdiagnoses can help family screening to further prevent SCDs.