Computer aided synthesis and optimisation of electronic logic circuits

In this thesis, a variety of algorithms for synthesis and optimisation of combinational and sequential logic circuits are developed. These algorithms could be part of new commercial EGAD package for future VLSI digital designs. The results show that considerable saving in components can be achieved resulting in simpler designs that are smaller, cheaper, consume less power and easier to test. The purpose of generating different sets of coefficients related to Reed Muller (RM) is that they contain different number of terms; therefore the minimum one can be selected to design the circuits with reduced gate count. To widen the search space and achieve better synthesis tools, representations of Mixed Polarity Reed Muller (MPRM), Mixed Polarity Dual Reed Muller (MPDRM), and Pseduo Kronecker Reed Muller (PKRO RM) expansions are investigated. Efficient and fast combinatorial techniques and algorithms are developed for the following: â Bidirectional conversion between MPRM/ MPDRM form and Fixed Polarity Reed Muller forms (FPRM)/Fixed Polarity Dual Reed Muller forms (FPDRM) form respectively. The main advantages for these techniques are their simplicity and suitability for single and multi output Boolean functions. â Computing the coefficients of any polarity related to PKRO_RM class starting from FPRM coefficients or Canonical Sum of Products (CSOP). â Computing the coefficients of any polarity related to MPRM/or MPDRM directly from standard form of CSOP/Canonical Product of sums (CPOS) Boolean functions, respectively. The proposed algorithms are efficient in terms of CPU time and can be used for large functions. For optimisation of combinational circuits, new techniques and algorithms based on algebraic techniques are developed which can be used to generate reduced RM expressions to design circuits in RM/DRM domain starting from FPRM/FPDRM, respectively. The outcome for these techniques is expansion in Reed Muller domain with minimal terms. The search space is 3`" Exclusive OR Sum of Product (ESOP)/or Exclusive NOR Product of Sums (ENPOS) expansions. Genetic Algorithms (GAs) are also developed to optimise combinational circuits to find optimal MPRM/MPDRM among 3° different polarities without the need to do exhaustive search. These algorithms are developed for completely and incompletely specified Boolean functions. The experimental results show that GA can find optimum solutions in a short time compared with long time required running exhaustive search in all the benchmarks tested. Multi Objective Genetic Algorithm (MOGA) is developed and implemented to determine the optimal state assignment which results in less area and power dissipation for completely and incompletely specified sequential circuits. The goal is to find the best assignments which reduce the component count and switching activity simultaneously. The experimental results show that saving in components and switching activity are achieved in most of the benchmarks tested compared with recently published research. All algorithms are implemented in C++.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Field-Effect Sensors

This Special Issue focuses on fundamental and applied research on different types of field-effect chemical sensors and biosensors. The topics include device concepts for field-effect sensors, their modeling, and theory as well as fabrication strategies. Field-effect sensors for biomedical analysis, food control, environmental monitoring, and the recording of neuronal and cell-based signals are discussed, among other factors

T-plastin, a cytoskeletal protein with important function in axonal growth, acts as a modifier of spinal muscular atrophy

Spinal muscular atrophy (SMA) is a common inherited disorder characterized by neurodegeneration of α-motor neurons. SMA is caused by mutation and/or deletion of the SMN1 gene that encodes the survival of motor neuron protein (SMN). Homozygous SMN1 deletion in unaffected persons is a rare event suggesting that the SMA phenotype is modified by other factors. The microarray expression analysis of the SMA discordant families revealed for the first time, a transcript that encodes for a cytoskeletal protein, namely T-plastin, to be the most up-regulated gene in asymptomatic vs. symptomatic SMN1-deleted sibs. A closer look to a possible involvement of T-plastin in SMA pathophysiology revealed exciting observations. First, T-plastin was found to be expressed at high levels in spinal cord and muscle of fetal and adult tissues by semi-quantitative PCR, an observation that provides a strong evidence for T-plastin implication in neuronal differentiation and neuromuscular maturation. Moreover, T-plastin associates with SMN as shown by Co-IP experiments, but this interaction, as demonstrated by in vitro binding assay, is mediated by another so far unknown protein. Second, T-plastin and SMN were found by immunofluorescence to co-localize along the axons, at branch points and at the growth cones in neurite-like extensions in differentiated PC12 cells. Interestingly, the T-plastin protein amount was found to be up-regulated in differentiated PC12 cells under NGF stimulation, an observation that might propose a possible function for T-plastin as substrate for signalling molecules. Moreover, under NGF stimulation, the affinity of T-plastin for SMN increased up to 50% suggesting that a transient complex might occur during neuronal differentiation that contributes to a specific role during this biological process. Third, the effect of T-plastin loss/overexpression in differentiated PC12 cells (cells presenting either shorter neurites when T-plastin was depleted or longer neurites when T-plastin was overexpressed) hints to a perturbation in the axon growth, guidance (and perhaps branching) due to the involvement of T-plastin in F-actin filament formation and stabilization. Interestingly, by in vitro experiments it has been observed that in differentiated PC12 cells expressing low amount of SMN protein, but overexpressing T-plastin, the length of the neurites was rescued at least in part by higher T-plastin levels. This suggests that a higher amount of T-plastin protein might help the growth cone structures to reach their target (the muscle in case of motor neurons). While all analyzed unaffected SMN1-deleted sibs expressed T-plastin in both peripheral blood and EBV-transformed lymphoblastoid cell lines, only 6.5% of the control population expressed T-plastin. In classical SMA patients, T-plastin was highly expressed in 5.9%, medium in 7.4% and very weak in 13.4%. Finally, 8% patients without SMN1 mutations expressed T-plastin. These data suggest that T-plastin expression in leukocytes happens as a rare event in humans and its expression in blood significantly correlates with an SMA protection. Nevertheless, not all blood-T-plastin-expressing SMN1-deleted individuals are SMA protected, which suggest a potential differential regulation in the spinal cord.The answer to the question by which mechanism T-plastin is expressed in unaffected sibs with homozygous absence of SMN1 gene or in control population and classical SMA patients, was not found. No correlation between the T-plastin expression and any mutation or DNA variation in the T-plastin coding region, promoter, 3'UTR or intron 1 was observed. Moreover, epigenetic analysis of the T-plastin regulatory region (promoter-first exon-first intron) revealed no differences in DNA modification level. These observations together with the haplotype analysis of two blocks described within the T-plastin genomic region in both SMA discordant families and control population, strongly suggest that likely a trans- rather than a cis-acting factor is responsible for the differential expression between SMA discordant sibs or between SMA discordant families and control population. In hope to find additional modifying genes or factors that are able to regulate T-plastin expression, a genome-wide scan analysis was performed in 42 SMA discordant families. Regions on chromosomes 3q, 7p, 16p and 22q, respectively, are suggestive for linkage and require further investigations, however, none of these reached a significant LOD score. Taken together, the discovery of the T-plastin protein as a modulator of the SMA phenotype provides the opportunity to identify novel regulatory mechanisms that may act specifically in motor neurons from asymptomatic sibs with SMN1 homozygous deletion