A recursive computation of the 2-D DCT : algorithm, architectures and FPGA implementation

The discrete cosine transform (DCT) is widely used in the area of signal and image processing. The 2-D DCT has been used in image compression and become part of image and video standards. The 2-D DCT computation involves a large amount of data. Many applications require the systems to be in small volume and operate in real-time. Designing such a system for 2-D DCT is a challenging task. In this thesis, a new recursive algorithm and two types of circuit architectures are presented for the computation of the 2-D DCT. The new algorithm permits to compute the 2-D DCT by a simple procedure of the 1-D recursive calculations involving only cosine coefficients. A recursive kernel for the proposed algorithm contains a small number of operations. Also, it requires a smaller number of pre-computed data compared to many of existing algorithms in the same category. The kernel can be easily implemented in a simple circuit block with a short critical delay path. In order to evaluate the performance improvement resulting from the new algorithm, an architecture for the 2-D DCT designed by direct mapping from the computation structure of the proposed algorithm has been implemented on an FPGA board. The results show that the reduction of the hardware consumption can easily reach 25% and the clock frequency can increase 17% compared to a system implementing a recently reported 2-D DCT recursive algorithm. For a further reduction of the hardware, another architecture has been proposed for the same 2-D DCT computation. Using one recursive computation block to perform different functions in each clock cycle, this architecture needs only approximately one half of the hardware that is required in the first architecture, which has been confirmed by an FPGA implementatio

Recursive algorithm, architectures and FPGA implementation of the two-dimensional discrete cosine transform

In this paper, a new recursive algorithm and two types of circuit architectures are presented for the computation of the two dimensional discrete cosine transform (2-D DCT). The new algorithm permits to compute the 2-D DCT by a simple procedure of the 1-D recursive calculations involving only cosine coefficients. The recursive kernel for the proposed algorithm contains a small number of operations. Also, it requires a smaller number of pre-computed data compared to many of existing algorithms in the same category. The kernel can be easily implemented in a simple circuit block with a short critical delay path. In order to evaluate the performance improvement resulting from the new algorithm, an architecture for the 2-D DCT designed by direct mapping from the computation structure of the proposed algorithm has been implemented in a FPGA board. The results show that the reduction of the hardware consumption can easily reach 25% and the clock frequency can increase 17% compared to a system implementing a recently reported 2-D DCT recursive algorithm. For a further reduction of the hardware, another architecture has been proposed for the same 2-D DCT computation. Using one recursive computation block to perform different functions, this architecture needs only approximately one half of the hardware that is required in the first architecture, which has been confirmed by a FPGA implementation

Refining the accuracy of validated target identification through coding variant fine-mapping in type 2 diabetes.

We aggregated coding variant data for 81,412 type 2 diabetes cases and 370,832 controls of diverse ancestry, identifying 40 coding variant association signals (P < 2.2 × 10-7); of these, 16 map outside known risk-associated loci. We make two important observations. First, only five of these signals are driven by low-frequency variants: even for these, effect sizes are modest (odds ratio ≤1.29). Second, when we used large-scale genome-wide association data to fine-map the associated variants in their regional context, accounting for the global enrichment of complex trait associations in coding sequence, compelling evidence for coding variant causality was obtained for only 16 signals. At 13 others, the associated coding variants clearly represent 'false leads' with potential to generate erroneous mechanistic inference. Coding variant associations offer a direct route to biological insight for complex diseases and identification of validated therapeutic targets; however, appropriate mechanistic inference requires careful specification of their causal contribution to disease predisposition

The trans-ancestral genomic architecture of glycemic traits

Glycemic traits are used to diagnose and monitor type 2 diabetes and cardiometabolic health. To date, most genetic studies of glycemic traits have focused on individuals of European ancestry. Here we aggregated genome-wide association studies comprising up to 281,416 individuals without diabetes (30% non-European ancestry) for whom fasting glucose, 2-h glucose after an oral glucose challenge, glycated hemoglobin and fasting insulin data were available. Trans-ancestry and single-ancestry meta-analyses identified 242 loci (99 novel; P < 5 x 10(-8)), 80% of which had no significant evidence of between-ancestry heterogeneity. Analyses restricted to individuals of European ancestry with equivalent sample size would have led to 24 fewer new loci. Compared with single-ancestry analyses, equivalent-sized trans-ancestry fine-mapping reduced the number of estimated variants in 99% credible sets by a median of 37.5%. Genomic-feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways. Our results increase our understanding of diabetes pathophysiology by using trans-ancestry studies for improved power and resolution. A trans-ancestry meta-analysis of GWAS of glycemic traits in up to 281,416 individuals identifies 99 novel loci, of which one quarter was found due to the multi-ancestry approach, which also improves fine-mapping of credible variant sets.Peer reviewe

Precision Higgs physics at the CEPC

The discovery of the Higgs boson with its mass around 125 GeV by the ATLAS and CMS Collaborations marked the beginning of a new era in high energy physics. The Higgs boson will be the subject of extensive studies of the ongoing LHC program. At the same time, lepton collider based Higgs factories have been proposed as a possible next step beyond the LHC, with its main goal to precisely measure the properties of the Higgs boson and probe potential new physics associated with the Higgs boson. The Circular Electron Positron Collider~(CEPC) is one of such proposed Higgs factories. The CEPC is an $e^+e^-$ circular collider proposed by and to be hosted in China. Located in a tunnel of approximately 100~km in circumference, it will operate at a center-of-mass energy of 240~GeV as the Higgs factory. In this paper, we present the first estimates on the precision of the Higgs boson property measurements achievable at the CEPC and discuss implications of these measurements.Comment: 46 pages, 37 figure

FGF-2 induces the proliferation of human periodontal ligament cells and modulates their osteoblastic phenotype by affecting Runx2 expression in the presence and absence of osteogenic inducers

The exact phenotype of human periodontal ligament cells (hPDLCs) remains a controversial area. Basic fibroblast growth factor (FGF‑2) exhibits various functions and its effect on hPDLCs is also controversial. Therefore, the present study examined the effect of FGF‑2 on the growth and osteoblastic phenotype of hPDLCs with or without osteogenic inducers (dexamethasone and β‑glycerophosphate). FGF‑2 was added to defined growth culture medium and osteogenic inductive culture medium. Cell proliferation, osteogenic differentiation and mineralization were measured. The selected differentiation markers, Runx2, collagen type Ⅰ, α1 (Col1a1), osteocalcin (OCN) and epidermal growth factor receptor (EGFR), were investigated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Runx2 and OCN protein expression was measured by western blotting. FGF‑2 significantly increased the proliferation of hPDLCs, but did not affect alkaline phosphatase activity. RT‑qPCR analysis revealed enhanced mRNA expression of Runx2, OCN and EGFR, but suppressed Col1a1 gene expression in the absence of osteogenic inducers, whereas all these gene levels had no clear trend in their presence. The Runx2 protein expression was clearly increased, but the OCN protein level showed no evident trend. The mineralization assay demonstrated that FGF‑2 inhibited mineralized matrix deposition with osteogenic inducers. These results suggested that FGF‑2 induces the growth of immature hPDLCs, which is a competitive inhibitor of epithelial downgrowth, and suppresses their differentiation into mineralized tissue by affecting Runx2 expression. Therefore, this may lead to the acceleration of periodontal regeneration

A comparative study of the proliferation and osteogenic differentiation of human periodontal ligament cells cultured on beta-TCP ceramics and demineralized bone matrix with or without osteogenic inducers in vitro

The repair of bone defects that result from periodontal diseases remains a clinical challenge for periodontal therapy. β-tricalcium phosphate (β-TCP) ceramics are biodegradable inorganic bone substitutes with inorganic components that are similar to those of bone. Demineralized bone matrix (DBM) is an acid-extracted organic matrix derived from bone sources that consists of the collagen and matrix proteins of bone. A few studies have documented the effects of DBM on the proliferation and osteogenic differentiation of human periodontal ligament cells (hPDLCs). The aim of the present study was to investigate the effects of inorganic and organic elements of bone on the proliferation and osteogenic differentiation of hPDLCs using three-dimensional porous β-TCP ceramics and DBM with or without osteogenic inducers. Primary hPDLCs were isolated from human periodontal ligaments. The proliferation of the hPDLCs on the scaffolds in the growth culture medium was examined using a Cell‑Counting kit‑8 (CCK-8) and scanning electron microscopy (SEM). Alkaline phosphatase (ALP) activity and the osteogenic differentiation of the hPDLCs cultured on the β-TCP ceramics and DBM were examined in both the growth culture medium and osteogenic culture medium. Specific osteogenic differentiation markers were examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). SEM images revealed that the cells on the β-TCP were spindle-shaped and much more spread out compared with the cells on the DBM surfaces. There were no significant differences observed in cell proliferation between the β-TCP ceramics and the DBM scaffolds. Compared with the cells that were cultured on β-TCP ceramics, the ALP activity, as well as the Runx2 and osteocalcin (OCN) mRNA levels in the hPDLCs cultured on DBM were significantly enhanced both in the growth culture medium and the osteogenic culture medium. The organic elements of bone may exhibit greater osteogenic differentiation effects on hPDLCs than the inorganic elements

Protection of electroactive biofilms against hypersaline shock by quorum sensing

Quorum sensing (QS) is an ideal strategy for boosting the operating performance of electroactive biofilms (EABs), but its potential effects on the protection of electroactive biofilms against environmental shocks (e.g., hypersaline shock) have been rarely revealed. In this study, a QS signaling molecule, the N-(3-oxo-dodecanoyl)-L-homoserine lactone, was employed to promote the anti-shock property of the EABs against extreme saline shock. The maximum current density of the QS-regulated biofilm recovered to 0.17 mA/cm2 after 10% salinity exposure, which was much higher than those of its counterparts. The laser scanning confocal microscope confirmed a thicker and more compact biofilm with the presence of the QS signaling molecule. The extracellular polymeric substances (EPS) might play a crucial role in the anti-shocking behaviors, as the polysaccharides in EPS of QS-biofilm had doubled compared to the groups with acylase (the QS quencher). The microbial community analysis indicated that the QS molecule enriched the relative abundance of key species including Pseudomonas sp. and Geobacter sp., which were both beneficial to the stability and electroactivity of the biofilms. The functional genes related to the bacterial community were also up-regulated with the presence of the QS molecule. These results highlight the importance of QS effects in protecting electroactive biofilm under extreme environmental shock, which provides effective and feasible strategies for the future development of microbial electrochemical technologies