Search

In this paper, a high efficient decoding algorithm is developed here in order to correct both erasures and errors for Reed-Solomon (RS) codes based on the Euclidean algorithm together with the Berlekamp-Massey (BM) algorithm. The new decoding algorithm computes the errata locator polynomial and the errata evaluator polynomial simultaneously without performing polynomial divisions, and there is no need for the computation of the discrepancies and the field element inversions. Also, the separate computation of the Forney syndrome needed in the decoder is completely avoided. As a consequence, the complexity of this new decoding algorithm is dramatically reduced. Finally, the new algorithm has been verified through a software simulation using [C.sup.++] language. An illustrative example of (255,239) RS code using this program shows that the speed of the decoding process is approximately three times faster than that of the inverse-free Berlekamp-Massey algorithm. Index Terms--Berlekamp-Massey (BM), erasure, errata, Forney, Euclidean, Reed-Solomon (RS) code.

The central problem in the implementation of a Reed-Solomon code is finding the roots of the error locator polynomial. In 1967, Berlekamp et al. found an algorithm for finding the roots of an affine polynomial in GF([2.sup.m]) that can be used to solve this problem. In this paper, it is shown that this Berlekamp-Rumsey-Solomon algorithm, together with the Chien-search method, makes possible a fast decoding algorithm in the standard-basis representation that is naturally suitable in a software implementation. Finally, simulation results for this fast algorithm are given. Index Terms--Berlekamp-Rumsey-Solomon algorithm, Chien search, error locator polynomial, p-polynomial, Reed-Solomon code.

Chang MC, Chen YJ, Lee MY, Lin LD, Wang TM, Chan CP, Tsai YL, Wang CY, Lin BR, Jeng JH. Prostaglandin F2α stimulates MEK-ERK signalling but decreases the expression of alkaline phosphatase in dental pulp cells. International Endodontic Journal, 43, 461–468, 2010. Aim To study prostaglandin F2α (PGF2α) receptor expression and downstream signalling in cultured human dental pulp cells and the effect of PGF2α on the alkaline phosphatase (ALP) activity of dental pulp cells. Methodology Human dental pulp cells were cultured and exposed to PGF2α. The expression of PGF2α (FP) receptors was analysed by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. The activation of extracellular regulated kinase (ERK) and cAMP responsive element binding protein/activating transcription factor-1 (CREB/ATF-1) signalling was determined by Western blotting. The expression of ALP in pulp cells after exposure to PGF2α was evaluated by ALP staining and PCR. Results Dental pulp cells expressed FP receptor mRNA and protein. Exposure to PGF2α revealed little cytotoxicity to pulp cells. PGF2α induced both ERK and CREB/ATF-1 phosphorylation in pulp cells. Exposure to PGF2α (>1 μmol L−1) further decreased the ALP activity and mRNA expression. However, U0126 (an inhibitor of MEK1) showed little preventive effect on the decline of ALP activity in dental pulp cells by PGF2α. Conclusion PGF2α may potentially activate FP receptors leading to ERK/CREB-ATF-1 activation during its production in inflamed dental pulp. PGF2α attenuated the ALP activity of pulp cells possibly via pathways not solely by MEK/ERK activation. PGF2α is a contributing factor of pulpal inflammation by regulating the activities of pulp cells. [ABSTRACT FROM AUTHOR]

Aim To determine whether (i) proinflammatory cytokines stimulate prostaglandin E2 (PGE2) production and cyclooxygenase (COX) gene expression in dental pulp cells, and (ii) pulp cells that express different prostaglandin E2 receptor (EP) isoforms and their activation by PGE2 leads to downstream Ca2+ signalling. Methodology Cultured human dental pulp cells were exposed to interleukin (IL)-1 β and tumour necrotic factor-alpha (TNF- α). The expression of COX-1 and COX-2 was measured with reverse transcriptase-polymerase chain reaction (RT-PCR). The production of PGE2 was measured using an enzyme-linked immunosorbent assay. Expression of prostaglandin EP receptor isoforms was studied by RT-PCR, whereas fura-2 fluorescence was used to measure calcium mobilization. The Kruskal–Wallis test and Wilcoxon sum rank test with Bonferroni correction were used for statistical analysis. Results Interleukin-1 β and TNF- α stimulate PGE2 production of human dental pulp cells ( P < 0.05). IL-1 β stimulated the COX-2 but not COX-1 mRNA expression. Pulp cells express mainly EP2, EP3 and EP1 receptors as analysed by RT-PCR. PGE2 (0.25–2 μmol L−1) stimulated the Ca2+ mobilization as indicated by increase in fura-2 fluorescence. Conclusions Interleukin-1 β and TNF- α may stimulate PGE2 production in dental pulp cells. Activation of prostaglandin EP receptors in dental pulp cells by PGE2 may induce Ca2+ signalling to regulate cellular biological activity during inflammation. [ABSTRACT FROM AUTHOR]

Various glass ionomer cements (GICs) and resin-modified GICs are widely used as tooth-colored restorative materials. However, their potential effects on pulp tissues are not fully understood. In this study, the authors compared the toxicity of nine types of GICs on cultured human dental pulp cells. Exposure of pulp cells to GICs for five days led to differential growth inhibition as analyzed by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. Exposure of pulp cells to ProTec CEM, Fuji II LC, Compoglass and GC Lining cement for five days decreased the cell numbers to 11%, 12%, 19% and 25%, respectively. By contrast, Hy-Bond and Fuji I showed only mild suppression on the growth of pulp cells, with 12% and 16% decreased cell numbers. Morphologically, marked retraction and rounding of pulp cells were noted following exposure to GC Lining cement; in addition, cell surface blebbing was noted following exposure to Compoglass, Fuji II LC and ProTec CEM. Exposure of the pulp cells to Fuji II SC and Fuji IX, however, led to decreases in the cell density, with no obvious morphological changes. These results indicate that resin-modified GICs, such as Compoglass, Fuji II LC, ProTec CEM and GC Lining cements, are more toxic to pulp cells than conventional GICs. It is not recommended that resin-modified GICs be directly applied onto dental pulp cells. However, additional in vivo studies are needed to evaluate the potential toxicities of these resin-modified GICs during clinical operative procedures. [ABSTRACT FROM AUTHOR]

Various dentin-bonding agents (DBAs) have been widely used to improve the bonding strength of dental resins and to prevent microleakage at the resin-dentin interface, although DBA may exert potentially detrimental effects upon dental pulp. In this study, a DBA (Scotchbond Multi-purpose) cured at different light intensities (100, 200 and 300-mW/cm²) for 10 seconds was extracted with Dulbecco's modified Eagle's medium (DMEM) for 24 hours. Thereafter, pulp cells (1 x 104 cells/well) were exposed to DMEM with or without DBA extract for 12 hours, 24 hours and five days. Pulp-cell cytotoxicity was measured with a modified 3-(4,5-dimethyl-thiazol -2-yl) -2,5-diphenyl-tetrazolium bromide (MTT) assay. No significant cytotoxicity of DBA eluents on pulp cells was found for the 12-hour exposure group. Following 24-hour exposure of cells to DBA cured at 100-mW/cm², pulp cells became rounder, more retracted and lost some cellular processes as compared to controls. Five-day exposure of pulp cells to DBA extract cured by light at levels of 100, 200 and 300 mW/cm², respectively, led to a growth retardation of 26%, 48% and 70% as analyzed by the inhibition of mitochondrial dehydrogenase activity. These results indicate that DBA may exert some cytotoxic effects upon dental pulp, especially when DBA-curing is insufficiently complete, as may occur at a low light intensity. [ABSTRACT FROM AUTHOR]

Betel quid (BQ) chewing has a strong correlation with oral leukoplakia, submucous fibrosis and oral cancer. For elucidation of its pathogenesis, we investigated the effects of areca nut (AN) and inflorescence piper betle (IPB) extracts and arecoline on the growth, total DNA synthesis (TDS) and unscheduled DNA synthesis (UDS) of cultured human gingival keratinocytes (GK). Arecoline and AN extract suppressed the growth of GK over 5 days of incubation in a dose-dependent fashion. At concentrations of 100, 200 and 400 microg/ml, AN extract suppressed the growth of GK by 31%, 46% and 90%, respectively. The IPB extracts exerted less inhibitory effect on the growth of GK. IPB extract (200-400 microg/ml) decreased cell numbers by 20-40% over 5 days of incubation. Moreover, at a concentration of 0.1, 0.2 and 0.4 mM, arecoline suppressed cell growth by 44%, 77% and 96%, respectively. However, only AN extract induced TDS and UDS in cultured GK within 6 h of exposure. Induction of UDS by AN extract was concomitant with the presence of apparent intracellular vacuolization. Arecoline was also toxic to GK, but did not induce intracellular vacuolization. At a concentration range of 200-1600 microg/ml, AN extract induced TDS by 2.1- to 6.5-fold. Furthermore, at a concentration of 400-1600 microg/ml, AN extract elevated the UDS by 2.4- to 5.5-fold more than that of untreated control. On the contrary, IPB extract (200-1600 microg/ml) and arecoline (0.2-1.6 mM) inhibited the TDS and UDS of GK to a different extent. Simultaneous exposure of confluent GK to AN extract, IPB extract and arecoline for 1 to 5 days led to different degrees of cytotoxicity that was dose- and time-dependent. These results indicate that AN, IPB and arecoline take part in the pathogenesis of BQ chewing-related oral mucosal lesions, possibly through both genotoxic and non-genotoxic mechanisms. [ABSTRACT FROM AUTHOR]

Proposes an inverse-free Berlekamp-Massey (BM) algorithm to simplify the Reed-Solomon (RS) codes. Uses/applications of a RC code; Time-domain decoders for the codes; Computation time of an algorithm for decoding codewords corrupted by errors and erasure patterns.

Because betel quid (BQ) chewing has been linked to a higher prevalence of periodontal diseases, the pathobiological effects of arecoline, a main alkaloid found in areca nut, were investigated in cultured human gingival fibroblasts. At concentrations higher than 0.4 mM, arecoline inhibits cell attachment, cell spreading and cell migration in a dose-dependent manner. These inhibitory effects were associated with intracellular depletion of glutathione (GSH). At concentrations of 0.4 mM and 1 mM, arecoline depleted about 26% and 45% of GSH after 2 h incubation. Exposure of cells to arecoline at concentrations lower than 0.4 mM for 2 h showed no significant decrease in either cell viability or intracellular GSH. However, incubation of cells for 24 h in 1 mM are colined decreased the cell numbers to only 35% of those in the untreated control. Arecoline also decreased cell growth and collagen synthesis in a dose-dependent manner. Because of repeated and long-term exposure to arecoline, BQ chewers could be more susceptible to periodontal damage and less responsive to new attachment procedures. [ABSTRACT FROM AUTHOR]

To understand the role of betel quid (BQ) in the pathogenesis of oral submucous fibrosis (OSF) and oral cancer, we used DNA damage, cytotoxicity, and cell proliferation assays to study the pathobiological effects of aqueous extracts of three BQ constituents [betel nut (Areca catechu, BN), inflorescence of Piper betle (IPB), and lime], one BN alkaloid (arecoline), and one BN polyphenol [(+)-catechinl on cultured oral mucosal fibroblasts. Extracts of BN and IPB induced DNA strand break formation in a dose-dependent manner. Extracts of BN and IPB, (+)-catechin, and arecoline decreased cell survival and proliferation in a dose-dependent manner. However, aqueous extract of lime (50-800 µg/mL) increased cell proliferation by 20-40%. These results indicate that BQ contains not only genotoxic and cytotoxic agents, but also compounds which stimulate cell proliferation. These compounds may act synergistically in the pathogenesis of OSF and oral cancer in BQ chewers. In addition, five anti-oxidants [glutathione (GSH), cysteine, mannitol, catalase, and superoxide dismutase (SOD)] were tested for their protective effects against the cytotoxicity of BQ constituents. GSH (1.95 and 2.6 mmol/L) and cysteine (4 and 8 mmol/L) prevented the arecoline-induced cytotoxicity. In contrast, mannitol, catalase, and SOD did not decrease the arecoline-induced cytotoxicity. These results indicate that thiol depletion, but not the attack of oxygen free radicals, could be the mechanism for arecoline cytotoxicity. GSH could also protect cells from the cytotoxicity of IPB extract. Increasing dietary intake of GSH-rich foods or dietary supplements of GSH may have chemopreventive potential to reduce BQ-associated oral lesions. [ABSTRACT FROM AUTHOR]

Pathobiological effects of eugenol (4-allyl-2-methoxyphenol), a major constituent of betel quid (BQ), were studied on oral mucosal fibroblasts. At a concentration higher than 3 mmol/L, eugenol was cytotoxic to oral mucosal fibroblasts in a concentration-and time-dependent manner. Cell death was associated with intracellular depletion of glutathione (GSH). Most of the GSH was depleted prior to the onset of cell death. At concentrations of 3 mmol/L and 4 mmol/L, eugenol depleted about 45% and 77% of GSH after one-hour incubation. In addition, eugenol decreased cellular ATP level in a concentration- and time-dependent manner. Eugenol also inhibited lipid peroxidation. Inhibition of lipid peroxidation was partially explained by its dose-dependent inhibition of xanthine oxidase activity. The IC50 of eugenol on xanthine oxidase activity was about 0.3 mmol/L. No DNA strand break activity for eugenol was found at concentrations between 0.5 and 3 mmol/L. Taken together, frequent exposure of oral mucosa to a high concentration of eugenol during the chewing of BQ might be involved in the pathogenesis of oral submucous fibrosis and oral cancer via its cytotoxicity. In contrast, eugenol at a concentration less than 1 mmol/L might protect cells from the genetic attack of reactive oxygen species via inhibition of xanthine oxidase activity and lipid peroxidation. [ABSTRACT FROM AUTHOR]