Optimum Design of a Pultruded FRP Bridge Deck.

In this paper, an optimum design of GFRP bridge deck having a pultruded cellular cross-section is presented. The optimization process utilizes a modified genetic algorithm with the index technique. Based on the optimum design, viable cross-sectional dimension, volumes of fibers and matrix, fiber orientation, and stacking sequence for GFRP decks suitable for the pultrusion process are proposed

MODULATORY EFFECT OF PERIOSTRACUM CICADAE AND BETULAE CORTEX EXTRACTS ON THE ACTIVATION OF ATOPIC DERMATITIS-RELATED ION CHANNELS ORAI1 AND TRPV3

Background: The cast-off shells of Cryptotympana pustulata (Periostracum Cicadae, PC) and the bark of Betula platyphylla (Betulae Cortex, BC) are used as traditional medicines for the treatment of skin diseases. This study was conducted to investigate the regulatory effects of PC and BC extracts on the activation of the ion channels, calcium release-activated calcium channel protein 1 (ORAI1) and transient receptor potential cation channel subfamily V member 3 (TRPV3). Materials and Methods: Human HEK293T cells, co-overexpressing ORAI1/stromal interaction molecule 1 (STIM1) or overexpressing TRPV3, were treated with PC or BC extracts at 0.1 mg/mL. The changes in ORAI1 and TRPV3 activities were measured using a conventional whole-cell patch-clamp technique. Results: PC and BC extracts significantly decreased ORAI1 activation in ORAI1-STIM1 co-overexpressing HEK293T cells and significantly increased TRPV3 activation in TRPV3 overexpressing cells, compared to that of 2- aminoethoxydiphenyl borate (2-APB, 100 μM), a known agonist of TRPV3. Conclusion: Our results suggest that PC and BC extracts have therapeutic potential to improve skin barrier abnormalities in atopic dermatitis via modulation of ORAI1 and TRPV3 activation

Antiproliferative effect of gold(I) compound auranofin through inhibition of STAT3 and telomerase activity in MDA-MB 231 human breast cancer cells

Signal transducer and activator of transcription 3 (STAT3) andtelomerase are considered attractive targets for anticancertherapy. The in vitro anticancer activity of the gold(I) compoundauranofin was investigated using MDA-MB 231 human breastcancer cells, in which STAT3 is constitutively active. In cellculture, auranofin inhibited growth in a dose-dependent manner,and N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygenspecies (ROS), markedly blocked the effect of auranofin.Incorporation of 5-bromo-2’-deoxyuridine into DNA andanchorage-independent cell growth on soft agar were decreasedby auranofin treatment. STAT3 phosphorylation and telomeraseactivity were also attenuated in cells exposed to auranofin, butNAC pretreatment restored STAT3 phosphorylation andtelomerase activity in these cells. These findings indicate thatauranofin exerts in vitro antitumor effects in MDA-MB 231 cellsand its activity involves inhibition of STAT3 and telomerase.Thus, auranofin shows potential as a novel anticancer drug thattargets STAT3 and telomerase. [BMB Reports 2013; 46(1): 59-64

Auxin response factor 2 (ARF2) plays a major role in regulating auxin-mediated leaf longevity

Auxin regulates a variety of physiological and developmental processes in plants. Although auxin acts as a suppressor of leaf senescence, its exact role in this respect has not been clearly defined, aside from circumstantial evidence. It was found here that ARF2 functions in the auxin-mediated control of Arabidopsis leaf longevity, as discovered by screening EMS mutant pools for a delayed leaf senescence phenotype. Two allelic mutations, ore14-1 and 14-2, caused a highly significant delay in all senescence parameters examined, including chlorophyll content, the photochemical efficiency of photosystem II, membrane ion leakage, and the expression of senescence-associated genes. A delay of senescence symptoms was also observed under various senescence-accelerating conditions, where detached leaves were treated with darkness, phytohormones, or oxidative stress. These results indicate that the gene defined by these mutations might be a key regulatory genetic component controlling functional leaf senescence. Map-based cloning of ORE14 revealed that it encodes ARF2, a member of the auxin response factor (ARF) protein family, which modulates early auxin-induced gene expression in plants. The ore14/arf2 mutation also conferred an increased sensitivity to exogenous auxin in hypocotyl growth inhibition, thereby demonstrating that ARF2 is a repressor of auxin signalling. Therefore, the ore14/arf2 lesion appears to cause reduced repression of auxin signalling with increased auxin sensitivity, leading to delayed senescence. Altogether, our data suggest that ARF2 positively regulates leaf senescence in Arabidopsis

Stochastic Particle Flow for Nonlinear High-Dimensional Filtering Problems

A series of novel filters for probabilistic inference that propose an alternative way of performing Bayesian updates, called particle flow filters, have been attracting recent interest. These filters provide approximate solutions to nonlinear filtering problems. They do so by defining a continuum of densities between the prior probability density and the posterior, i.e. the filtering density. Building on these methods' successes, we propose a novel filter. The new filter aims to address the shortcomings of sequential Monte Carlo methods when applied to important nonlinear high-dimensional filtering problems. The novel filter uses equally weighted samples, each of which is associated with a local solution of the Fokker-Planck equation. This hybrid of Monte Carlo and local parametric approximation gives rise to a global approximation of the filtering density of interest. We show that, when compared with state-of-the-art methods, the Gaussian-mixture implementation of the new filtering technique, which we call Stochastic Particle Flow, has utility in the context of benchmark nonlinear high-dimensional filtering problems. In addition, we extend the original particle flow filters for tackling multi-target multi-sensor tracking problems to enable a comparison with the new filter

Comparison of Endothelial Progenitor Cells in Parkinson's Disease Patients Treated with Levodopa and Levodopa/COMT Inhibitor

BACKGROUND: Levodopa treatment in Parkinson's disease (PD) increases in serum homocysteine levels due to its metabolism via catechol O-methyltransferase. Endothelial progenitor cells (EPCs) have the capacity to differentiate into mature endothelial cells and are markers for endothelial functions and cardiovascular risks. Along with traditional vascular risk factors, hyperhomocysteinemia is known to decrease the level of EPCs. In the present study, we hypothesized that that levodopa-induced hyperhomocysteinemia leads to a change in EPC levels. METHODOLOGY/PRINCIPAL FINDINGS: We prospectively enrolled PD patients who had been prescribed either levodopa/carbidopa (PD-L group, n = 28) or levodopa/carbidopa/COMT inhibitor (PD-LC group, n = 25) for more than 1 year. The number of circulating EPCs was measured by flow cytometry using dual staining of anti-CD34 and anti-KDR antibodies. The EPCs were divided into tertiles based on their distributions and a logistic regression analysis was used to estimate independent predictors of the highest tertile of EPCs. The number of endothelial progenitor cells was significantly decreased in PD-L patients (118±99/mL) compared with either PD-LC patients (269±258/mL, p = 0.007) or controls (206±204/mL, p = 0.012). The level of homocysteine was significantly increased in PD-L patients (14.9±5.3 µmol/L) compared with either PD-LC patients (11.9±3.0 µmol/L, p = 0.028) or controls (11.1±2.5 µmol/L, p = 0.012). The level of homocysteine was negatively correlated with endothelial progenitor cell levels (r = -0.252, p = 0.028) and was an independent predictor of the highest tertile of endothelial progenitor cell levels (OR; 0.749 [95% CI: 0.584-0.961]). CONCLUSIONS/SIGNIFICANCE: These data indicate that a higher consumption of EPC for restoration of endothelial damage may be associated with chronic levodopa treatment in PD patients