Deep-PowerX: A Deep Learning-Based Framework for Low-Power Approximate Logic Synthesis

This paper aims at integrating three powerful techniques namely Deep Learning, Approximate Computing, and Low Power Design into a strategy to optimize logic at the synthesis level. We utilize advances in deep learning to guide an approximate logic synthesis engine to minimize the dynamic power consumption of a given digital CMOS circuit, subject to a predetermined error rate at the primary outputs. Our framework, Deep-PowerX, focuses on replacing or removing gates on a technology-mapped network and uses a Deep Neural Network (DNN) to predict error rates at primary outputs of the circuit when a specific part of the netlist is approximated. The primary goal of Deep-PowerX is to reduce the dynamic power whereas area reduction serves as a secondary objective. Using the said DNN, Deep-PowerX is able to reduce the exponential time complexity of standard approximate logic synthesis to linear time. Experiments are done on numerous open source benchmark circuits. Results show significant reduction in power and area by up to 1.47 times and 1.43 times compared to exact solutions and by up to 22% and 27% compared to state-of-the-art approximate logic synthesis tools while having orders of magnitudes lower run-time

Genomic Runs of Homozygosity Record Population History and Consanguinity

The human genome is characterised by many runs of homozygous genotypes, where identical haplotypes were inherited from each parent. The length of each run is determined partly by the number of generations since the common ancestor: offspring of cousin marriages have long runs of homozygosity (ROH), while the numerous shorter tracts relate to shared ancestry tens and hundreds of generations ago. Human populations have experienced a wide range of demographic histories and hold diverse cultural attitudes to consanguinity. In a global population dataset, genome-wide analysis of long and shorter ROH allows categorisation of the mainly indigenous populations sampled here into four major groups in which the majority of the population are inferred to have: (a) recent parental relatedness (south and west Asians); (b) shared parental ancestry arising hundreds to thousands of years ago through long term isolation and restricted effective population size (N(e)), but little recent inbreeding (Oceanians); (c) both ancient and recent parental relatedness (Native Americans); and (d) only the background level of shared ancestry relating to continental N(e) (predominantly urban Europeans and East Asians; lowest of all in sub-Saharan African agriculturalists), and the occasional cryptically inbred individual. Moreover, individuals can be positioned along axes representing this demographic historic space. Long runs of homozygosity are therefore a globally widespread and under-appreciated characteristic of our genomes, which record past consanguinity and population isolation and provide a distinctive record of the demographic history of an individual's ancestors. Individual ROH measures will also allow quantification of the disease risk arising from polygenic recessive effects

Argininosuccinate synthetase activity in cultured human lymphocytes

The activity of argininosuccinate synthetase (E.C. 6.3.4.5), a urea cycle enzyme, was measured in cultured human lymphocytes using a new radioactive assay. Control cells had a maximum specific activity of 15.7±8.7 nmoles per hour per milligram of protein and an apparent K m for citrulline of 2 × 10 −4 m , whereas cells derived from a patient with citrullinemia had no detectable activity. A nutritional variant, selected out of the citrullinemic lymphocyte population by ability to grow in citrulline, had a maximum specific activity of 10.7±3.8 nmoles/hr/mg and an apparent K m for citrulline of 2 × 10 −2 m . These measurements confirm the observation that citrullinemia is associated with a defect in argininosuccinate synthetase activity and provide further evidence that citrullinemia is expressed in cultured lymphocytes. The emergence of a nutritional variant with a partial defect in argininosuccinate synthetase enzyme suggests that this citrullinemic patient has a heterogeneous population of cells, some totally defective and others only partially defective in argininosuccinate synthetase. The new activity assay is described in detail.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44125/1/10528_2004_Article_BF00484469.pd

Citrulline metabolism in normal and citrullinemic human lymphocyte lines

Citrullinemia is one of the five aminoacidurias associated with the Krebs-Henseleit urea cycle. A long-term lymphocyte line (UM-21) derived from a patient with this disease and nine of ten clones of this line were found to have no activity for the enzyme argininosuccinate synthetase (AS), as demonstrated by their inability to grow in medium in which citrulline had been substituted for arginine, by their inability to incorporate arginine-C 14 derived from citrulline-C 14 into cellular protein, and by direct enzyme assay. One clone had normal or nearly normal argininosuccinate synthetase activity, as demonstrated by the same criteria. Nutritional “variants” able to grow logarithmically in medium containing citrulline were isolated from UM-21 and three clones. The apparent K m s of AS for citrulline in UM-21, the ten clones, the variant lines, and a normal line were measured and fell into three groups: AS in UM-21 and nine clones had no measurable apparent K m for citrulline; AS in the variant cells had apparent K m s for citrulline of approximately 20 m m ; and AS in the normal cell line and one clone had apparent K m s for citrulline of 0.2 m m . The data suggest that the defect in the citrullinemic cell lines is due to a mutation in the structural gene coding for argininosuccinate synthetase.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44122/1/10528_2004_Article_BF00485789.pd

Role of epithelial architecture and intracellular metabolism in proline uptake and transtubular reclamation in PRO/re mouse kidney.

The homozygous PRO/Re mouse has less than 1 percent of the very high proline oxidase activity that characterizes normal kidney cortex. In PRO/Re mouse the endogenous proline concentration is eight times normal in plasma and four times normal in kidney cortex cell, but 50 times normal in urine. The integrity of the membrane transport systems for proline uptake at the antiluminal surface of absorbing epithelium is retained in PRO/Re kidney, as determined by the slice method. Clearance studies in vivo under steady-state conditions indicate that the integrity of the luminal uptake system shared by glycine and proline, and serving proline absorption, is also intact. The exaggerated renal clearance of proline in PRO/Re mice (50 times normal) is explained when its raised intracellular concentration, caused by impaired proline oxidation, is considered. Backflux into urine flowing down the nephron will occur under these conditions, thus impairing net reclamation of proline in PRO/Re kidney. The findings reveal that membrane transport and intracellular metabolism of a substrate are, indeed, independent functions, but that metabolism of a substance can influence its transcellular transport

Localization of the membrane defect in transepithelial transport of taurine by parallel studies in vivo and in vitro in hypertaurinuric mice.

We investigated the mechanism of taurinuria in three inbred strains of mice: A/J, a normal taurine excretor (taut+); and two hypertaurinuric (taut-) strains, C57BL/6J and PRO/Re. Plasma taurine is comparable in the three strains (approximately 0.5 mM), but taurinuria is 10-fold greater in taut- animals. Fractional reabsorption of taurine is 0.967 +/- 0.013 (mean +/- SD) in A/J); and 0.839 +/- 0.08 and 0.787 +/- 0.05 in C57BL/6J and PRO/Re, respectively. Taurine concentration in renal cortex intracellular fluid (free of urine contamination) is similar in the three strains. Taurine reabsorption is inhibited by beta-alanine, in taut+ and taut- strains. These in vivo findings reveal residual taurine transport activity in the taut- phenotype and no evidence for impaired efflux at basilar membranes as the cause of impaired taurine reabsorption. Cortex slices provide information about uptake of amino acids at the antiluminal membrane. Taurine behaves as an inert metabolite in mouse kidney cortex slices. Taurine uptake by slices is active and, at less than 1 mM, is greater than normal in taut- slices. Concentration-dependent uptake studies reveal more than one taurine carrier in taut+ and taut- strains. The apparent Km values for uptake below 1 mM are different in taut- and taut+ slices (approximately 0.2 mM and approximately 0.7 mM, respectively); the apparent Km values above 1 mM taurine are similar in taut+ and taut- slices. Efflux from slices in all strains in the same (0.0105-0.0113 mumol-min-1-g-1 wet wt), but taut- tissue retains about 10% more radioactivity over the period of efflux. beta-Alanine is actively metabolized in mouse kidney. Its uptake in the presence of blocked transamination, is greater; its intracellular oxidation is attenuated; and its exchange with intracellular taurine is diminished in taut- slices. These findings indicate impaired beta-amino acid permeation on a low-Km uptake system at the luminal membrane in the taut- phenotype. beta-Amino acids are not reclaimed efficiently either from the innermost luminal pool in cortex slices or from the ultrafiltrate in the tubule lumen in vivo. The former leads to high uptake ratios in vitro, the latter to high clearance rates in vivo. In vitro and in vivo data are thus concordant. This is the first time that a hereditary defect in amino acid transport has been assigned to a specific membrane surface in mammalian kidney