Optimal Folding of Data Flow Graphs based on Finite Projective Geometry using Lattice Embedding

A number of computations exist, especially in area of error-control coding and matrix computations, whose underlying data flow graphs are based on finite projective-geometry(PG) based balanced bipartite graphs. Many of these applications are actively being researched upon. Almost all these applications need bipartite graphs of the order of tens of thousands in practice, whose nodes represent parallel computations. To reduce its implementation cost, reducing amount of system/hardware resources during design is an important engineering objective. In this context, we present a scheme to reduce resource utilization when performing computations derived from PG-based graphs. In a fully parallel design based on PG concepts, the number of processing units is equal to the number of vertices, each performing an atomic computation. To reduce the number of processing units used for implementation, we present an easy way of partitioning the vertex set. Each block of partition is then assigned to a processing unit. A processing unit performs the computations corresponding to the vertices in the block assigned to it in a sequential fashion, thus creating the effect of folding the overall computation. These blocks have certain symmetric properties that enable us to develop a conflict-free schedule. The scheme achieves the best possible throughput, in lack of any overhead of shuffling data across memories while scheduling another computation on the same processing unit. This paper reports two folding schemes, which are based on same lattice embedding approach, based on partitioning. We first provide a scheme for a projective space of dimension five, and the corresponding schedules. Both the folding schemes that we present have been verified by both simulation and hardware prototyping for different applications. We later generalize this scheme to arbitrary projective spaces.Comment: 31 pages, to be submitted to some discrete mathematics journa

Establishment of Adult Reference Values For Some Biochemical Analytes in A Rwandan Population

Objectives: To establish the reference values for some routinely performed biochemical analytes in CHUK.Design: Cross-sectional descriptive study.Settings: National Center for Blood Transfusion, Rwanda and Kigali University Teaching Hospital,  Laboratory Department. This study was conducted during the period between 15th September 2014 and 23rd February in 2015.Subjects: Blood donors donating blood at National Center for Blood Donation, and recruited by mobile teams across the country.Results: Median (Reference values:2.5th and 97.5th percentiles) for male and female respectively: Bilirubin Direct,3.9(2-6.9) and 3.9(2.6-6.5) μmol/L; Bilirubin Total,10.3(4.8-21.6) and 10.4(5.9-17.3) μmol/L; Aspartate Aminotransferase, 27.8(16.1-49.2) and 26.7(16.8-45.1) U/L;Urea,3.2(1.3-5.8) and 3.1(1.4-5.2)mmol/L; Glucose, 5.0(3.2-7.7) and 4.6(3.1-6.7) mmol/L; Total Proteins, 76.8(68.2-87.7) and 76.9(66.6-85.7)g/L; Albumin, 46.4(39.7-55.5) and 46.7(40-54.5) g/L; Alanine Aminotransferase,  17.1(7.2-36.2) and 16.0(7.3-33.9) U/L; Gamma Glutamyltransferase, 20.3(8-75.6) and 21.1(7.1-63.3) U/L; Alkaline Phosphatase, 74.3(43.8-145.7) and 73.5(50.3-135.4) U/L; Creatinine, 84.4(65.2- 107.1) and 81.1(62.5-98.6) μmol/L; Sodium, 139.0(134.5-145.5) and 141.0(134.5-146.5) mmol/L; Potassium, .4.4(3.7-5) and 4.3(3.5-5.0) mmol/L; Chloride, 95.7(89.9-104.2) and 99.3(90.6-103.1) mmol/L;  Magnesium, 0.9(0.7-1.0) and 0.9(0.7-1) mmol/L; Phosphate, 1.1(0.8-1.5) and 1.2(0.7-1.6) mmol/L.Conclusion: The results of our study on Clinical Chemistry parameters are similar to those published in other African countries, with variations due to the diet and geographical location. This study has shown that a strict adherence to reference ranges developed from industrialised countries could qualify many healthy Rwandans as pathological cases, and also exclude them from participating in clinical trials. Compared to other reference ranges established, reference values in our study presented remarkably low levels of urea which may be due to the diet low in proteins generally in Rwandan population

Down-regulation of miR-15a/b accelerates fibrotic remodelling in the Type 2 diabetic human and mouse heart

Correspondence: Rajesh Katare ([email protected]) Aim: Myocardial fibrosis is a well-established cause of increased myocardial stiffness and subsequent diastolic dysfunction in the diabetic heart. The molecular regulators that drive the process of fibrotic events in the diabetic heart are still unknown. We determined the role of the microRNA (miR)-15 family in fibrotic remodelling of the diabetic heart. Methods and results: Right atrial appendage (RAA) and left ventricular (LV) biopsy tissues collected from diabetic and non-diabetic (ND) patients undergoing coronary artery bypass graft surgery showed significant down-regulation of miR-15a and -15b. This was associated with marked up-regulation of pro-fibrotic transforming growth factor-β receptor-1 (TGFβR1) and connective tissue growth factor (CTGF), direct targets for miR-15a/b and pro-senescence p53 protein. Interestingly, down-regulation of miR-15a/b preceded the development of diastolic dysfunction and fibrosis in Type 2 diabetic mouse heart. Therapeutic restoration of miR-15a and -15b in HL-1 cardiomyocytes reduced the activation of pro-fibrotic TGFβR1 and CTGF, and the pro-senescence p53 protein expression, confirming a causal regulation of these fibrotic and senescence mediators by miR-15a/b. Moreover, conditioned medium (CM) collected from cardiomyocytes treated with miR-15a/b markedly diminished the differentiation of diabetic human cardiac fibroblasts. Conclusion: Our results provide first evidence that early down-regulation of miR-15a/b activates fibrotic signalling in diabetic heart, and hence could be a potential target for the treatment/prevention of diabetes-induced fibrotic remodelling of the heart

Biochemical systems identification by a random drift particle swarm optimization approach

BACKGROUND: Finding an efficient method to solve the parameter estimation problem (inverse problem) for nonlinear biochemical dynamical systems could help promote the functional understanding at the system level for signalling pathways. The problem is stated as a data-driven nonlinear regression problem, which is converted into a nonlinear programming problem with many nonlinear differential and algebraic constraints. Due to the typical ill conditioning and multimodality nature of the problem, it is in general difficult for gradient-based local optimization methods to obtain satisfactory solutions. To surmount this limitation, many stochastic optimization methods have been employed to find the global solution of the problem. RESULTS: This paper presents an effective search strategy for a particle swarm optimization (PSO) algorithm that enhances the ability of the algorithm for estimating the parameters of complex dynamic biochemical pathways. The proposed algorithm is a new variant of random drift particle swarm optimization (RDPSO), which is used to solve the above mentioned inverse problem and compared with other well known stochastic optimization methods. Two case studies on estimating the parameters of two nonlinear biochemical dynamic models have been taken as benchmarks, under both the noise-free and noisy simulation data scenarios. CONCLUSIONS: The experimental results show that the novel variant of RDPSO algorithm is able to successfully solve the problem and obtain solutions of better quality than other global optimization methods used for finding the solution to the inverse problems in this study

Glutaredoxin-1 Overexpression Enhances Neovascularization and Diminishes Ventricular Remodeling in Chronic Myocardial Infarction

Oxidative stress plays a critical role in the pathophysiology of cardiac failure, including the modulation of neovascularization following myocardial infarction (MI). Redox molecules thioredoxin (Trx) and glutaredoxin (Grx) superfamilies actively maintain intracellular thiol-redox homeostasis by scavenging reactive oxygen species. Among these two superfamilies, the pro-angiogenic function of Trx-1 has been reported in chronic MI model whereas similar role of Grx-1 remains uncertain. The present study attempts to establish the role of Grx-1 in neovascularization and ventricular remodeling following MI. Wild-type (WT) and Grx-1 transgenic (Grx-1Tg/+) mice were randomized into wild-type sham (WTS), Grx-1Tg/+ Sham (Grx-1Tg/+S), WTMI, Grx-1Tg/+MI. MI was induced by permanent occlusion of the LAD coronary artery. Sham groups underwent identical time-matched surgical procedures without LAD ligation. Significant increase in arteriolar density was observed 7 days (d) after surgical intervention in the Grx-1Tg/+MI group as compared to the WTMI animals. Further, improvement in myocardial functional parameters 30 d after MI was observed including decreased LVIDs, LVIDd, increased ejection fraction and, fractional shortening was also observed in the Grx-1Tg/+MI group as compared to the WTMI animals. Moreover, attenuation of oxidative stress and apoptotic cardiomyocytes was observed in the Grx-1Tg/+MI group as compared to the WTMI animals. Increased expression of p-Akt, VEGF, Ang-1, Bcl-2, survivin and DNA binding activity of NF-κB were observed in the Grx-1Tg/+MI group when compared to WTMI animals as revealed by Western blot analysis and Gel-shift analysis, respectively. These results are the first to demonstrate that Grx-1 induces angiogenesis and diminishes ventricular remodeling apparently through neovascularization mediated by Akt, VEGF, Ang-1 and NF-κB as well as Bcl-2 and survivin-mediated anti-apoptotic pathway in the infarcted myocardium

Increased Expression of Fatty-Acid and Calcium Metabolism Genes in Failing Human Heart

Heart failure (HF) involves alterations in metabolism, but little is known about cardiomyopathy-(CM)-specific or diabetes-independent alterations in gene expression of proteins involved in fatty-acid (FA) uptake and oxidation or in calcium-(Ca(2+))-handling in the human heart.RT-qPCR was used to quantify mRNA expression and immunoblotting to confirm protein expression in left-ventricular myocardium from patients with HF (n = 36) without diabetes mellitus of ischaemic (ICM, n = 16) or dilated (DCM, n = 20) cardiomyopathy aetiology, and non-diseased donors (CTL, n = 6).Significant increases in mRNA of genes regulating FA uptake (CD36) and intracellular transport (Heart-FA-Binding Protein (HFABP)) were observed in HF patients vs CTL. Significance was maintained in DCM and confirmed at protein level, but not in ICM. mRNA was higher in DCM than ICM for peroxisome-proliferator-activated-receptor-alpha (PPARA), PPAR-gamma coactivator-1-alpha (PGC1A) and CD36, and confirmed at the protein level for PPARA and CD36. Transcript and protein expression of Ca(2+)-handling genes (Two-Pore-Channel 1 (TPCN1), Two-Pore-Channel 2 (TPCN2), and Inositol 1,4,5-triphosphate Receptor type-1 (IP3R1)) increased in HF patients relative to CTL. Increases remained significant for TPCN2 in all groups but for TPCN1 only in DCM. There were correlations between FA metabolism and Ca(2+)-handling genes expression. In ICM there were six correlations, all distinct from those found in CTL. In DCM there were also six (all also different from those found in CTL): three were common to and three distinct from ICM.DCM-specific increases were found in expression of several genes that regulate FA metabolism, which might help in the design of aetiology-specific metabolic therapies in HF. Ca(2+)-handling genes TPCN1 and TPCN2 also showed increased expression in HF, while HF- and CM-specific positive correlations were found among several FA and Ca(2+)-handling genes