Adaptive partitioning of real-time tasks on multiple processors

This paper presents a new algorithm for scheduling real-time tasks on multiprocessor/multicore systems. This new algorithm is based on combining EDF scheduling with a migration strategy that moves tasks only when needed. It has been evaluated through an extensive set of simulations that showed good performance when compared with global or partitioned EDF: a worst-case utilisation bound similar to partitioned EDF for hard real-time tasks, and a tardiness bound similar to global EDF for soft real-time tasks. Therefore, the proposed scheduler is effective for dealing with both soft and hard real-time workloads

Idiosyncrasies in decoding mitochondrial genomes.

Mitochondria originate from the α-proteobacterial domain of life. Since this unique event occurred, mitochondrial genomes of protozoans, fungi, plants and metazoans have highly derived and diverged away from the common ancestral DNA. Present-day mitochondrial DNAs have a very reduced coding capacity. These genomes highly differ between them. Strikingly however, ATP production coupled to electron transport and translation of mitochondrial proteins are the two common functions retained in all mitochondrial DNAs. Paradoxically, most components essential for these two functions are now expressed from nuclear genes. Understanding how mitochondrial translation evolved in various eukaryotic models is essential to acquire new knowledge of mitochondrial genome expression. In this review, we provide a thorough analysis of the idiosyncrasies of mitochondrial translation as they occur between organisms. We address this by looking at mitochondrial codon usage and tRNA content. Then, we look at the aminoacyl-tRNA-forming enzymes in terms of peculiarities, dual origin, and alternate function(s). Finally we show examples of the atypical structural properties of mitochondrial tRNAs found in some organisms and the resulting adaptive tRNA-protein partnership

Missense mutation in sterile alpha motif of novel protein SamCystin is associated with polycystic kidney disease in (cy/+)rat

Autosomal dominant polycystic kidney disease (PKD) is the most common genetic disease that leads to kidney failure in humans. In addition to the known causative genes PKD1 and PKD2, there are mutations that result in cystic changes in the kidney, such as nephronophthisis, autosomal recessive polycystic kidney disease, or medullary cystic kidney disease. Recent efforts to improve the understanding of renal cystogenesis have been greatly enhanced by studies in rodent models of PKD. Genetic studies in the (cy/+) rat showed that PKD spontaneously develops as a consequence of a mutation in a gene different from the rat orthologs of PKD1 and PKD2 or other genes that are known to be involved in human cystic kidney diseases. This article reports the positional cloning and mutation analysis of the rat PKD gene, which revealed a C to T transition that replaces an arginine by a tryptophan at amino acid 823 in the protein sequence. It was determined that Pkdr1 is specifically expressed in renal proximal tubules and encodes a novel protein, SamCystin, that contains ankyrin repeats and a sterile {alpha} motif. The characterization of this protein, which does not share structural homologies with known polycystins, may give new insights into the pathophysiology of renal cyst development in patients