Error Detection Enhancement in COTS Superscalar Processors with Performance Monitoring Features

Increasing use of commercial off-the-shelf (COTS) superscalar processors in industrial, embedded, and real-time systems necessitates the development of error detection mechanisms for such systems. This paper presents an error detection scheme called Committed Instructions Counting (CIC) to increase error detection in such systems. The scheme uses internal Performance Monitoring features and an external watchdog processor (WDP). The Performance Monitoring features enable counting the number of committed instructions in a program. The scheme is experimentally evaluated on a 32-bit Pentium® processor using software implemented fault injection (SWIFI). A total of 8181 errors were injected into the Pentium® processor. The results show that the error detection coverage varies between 90.92 and 98.41%, for different workloads. To verify the experimental results an analytical evaluation of the coverage is also performed.     

An efficient method for synthesis of some heterocyclic compounds containing 3-iminoisatin and 1,2,4-triazole using Fe3O4 magnetic nanoparticles

1,2,4-triazole derivatives were prepared by reaction of thiocarbohydrazide and some esters in 60% ethanol. Condensation of 1,2,4-triazole derivatives with isatin gave Schiff bases of 3-iminoisatin derivatives. Reaction of malonic or succinic acid dihydrazide with isatin lead to formation of N,N'-bis-(3-imino-1,3-dihydro-indolyl-2-one)-malonamide 8a and N,N'-bis-(3-imino-1,3-dihydro-indolyl-2-one)succinamide 8b in good yields under mild reaction conditions. These reactions are catalyzed by Fe₃O₄ MNPs. The chemical structures were confirmed by Fourier transform-infrared, ¹H-NMR, ¹³C-NMR, gas chromatography-mass spectrometry spectroscopy, and elemental analysis.     

Buccal Mucosa Cells as a Potential Diagnostic Tool to Study Onset and Progression of Arrhythmogenic Cardiomyopathy

In arrhythmogenic cardiomyopathy (ACM) pathogenic variants are found in genes encoding desmosomal proteins and in non-desmosomal genes, such as phospholamban (PLN, p.Arg14del variant). Previous research showed that plakoglobin protein levels and localization in the cardiac tissue of ACM patients, and PLN p.Arg14del patients diagnosed with an ACM phenotype, are disturbed. Moreover, the effects of pathogenic variants in desmosomal genes are reflected in non-cardiac tissues like buccal mucosa cells (BMC) which could serve as a promising new and non-invasive tool to support diagnosis. We collected the BMC of 33 ACM patients, 17 PLN p.Arg14del patients and 34 controls, labelled the BMC with anti-plakoglobin antibodies at different concentrations, and scored their membrane labelling. We found that plakoglobin protein levels were significantly reduced in BMC obtained from diagnosed ACM patients and preclinical variant carriers when compared to controls. This effect was independent from age and sex. Moderate to strong correlations were found with the revised 2010 Task Force Criteria score which is commonly used for ACM diagnosis (r_s = −0.67, n = 64, p < 0.0001 and r_s = −0.71, n = 64, p < 0.0001). In contrast, plakoglobin scores in PLN p.Arg14del patients were comparable to controls (p > 0.209), which suggests differences in underlying etiology. However, for the individual diagnosis of the ‘classical’ ACM patient, this method might not be discriminative enough to distinguish true patients from variant carriers and controls, because of the high interindividual variability.