Phase Structure of Compact Star in Modified Quark-Meson Coupling Model

The K$^-$ condensation and quark deconfinement phase transitions are investigated in the modified quark-meson coupling model. It is shown that K$^-$ condensation is suppressed because of the quark deconfinement when $B^{1/4}<$202.2MeV, where $B$ is the bag constant for unpaired quark matter. With the equation of state (EOS) solved self-consistently, we discuss the properties of compact stars. We find that the EOS of pure hadron matter with condensed K$^-$ phase should be ruled out by the redshift for star EXO0748-676, while EOS containing unpaired quark matter phase with $B^{1/4}$ being about 180MeV could be consistent with this observation and the best measured mass of star PSR 1913+16. We then probe into the change of the phase structures in possible compact stars with deconfinment phase as the central densities increase. But if the recent inferred massive star among Terzan 5 with M$>$1.68M$_{\odot}$ is confirmed, all the present EOSes with condensed phase and deconfined phase would be ruled out and therefore these exotic phases are unlikely to appear within neutron stars.Comment: 11 pages, 5 figure

Myricetin Increases Hepatic Peroxisome Proliferator-Activated Receptor α Protein Expression and Decreases Plasma Lipids and Adiposity in Rats

The aim of this study was to investigate the antiobesity and antihyperlipidaemic effects of myricetin. Myricetin exhibited a significant concentration-dependent decrease in the intracellular accumulation of triglyceride in 3T3-L1 adipocytes. The high-fat diet (HFD)-fed rats were dosed orally with myricetin or fenofibrate, once daily for eight weeks. Myricetin (300 mg kg−1 per day) displayed similar characteristics to fenofibrate (100 mg kg−1 per day) in reducing lowered body weight (BW) gain, visceral fat-pad weights and plasma lipid levels of HFD-fed rats. Myricetin also reduced the hepatic triglyceride and cholesterol contents, as well as lowered hepatic lipid droplets accumulation and epididymal adipocyte size in HFD-fed rats. Myricetin and fenofibrate reversed the HFD-induced down-regulation of the hepatic peroxisome proliferator activated receptor (PPAR)α. HFD-induced decreases of the hepatic protein level of acyl-CoA oxidase and cytochrome P450 isoform 4A1 were up-regulated by myricetin and fenofibrate. The elevated expressions of hepatic sterol regulatory element binding proteins (SREBPs) of HFD-fed rats were lowered by myricetin and fenofibrate. These results suggest that myricetin suppressed BW gain and body fat accumulation by increasing the fatty acid oxidation, which was likely mediated via up-regulation of PPARα and down-regulation of SREBP expressions in the liver of HFD-fed rats

P-type tin monoxide thin-film transistors on cellulose nanopaper substrates

Oxide-based thin-film transistors (TFTs) possess advantages such as relatively high mobility, low process temperature and good uniformity, which make them attractive for flexible electronics applications. Most flexible oxide-based TFTs reported today were made on plastic substrates. In this work, flexible inverted-staggered bottom-gate p-type tin monoxide (SnO) thin-film transistors (TFTs) were demonstrated on cellulose nanopaper substrates using a photolithography-compatible direct-fabrication approach. The paper substrate was formed by drop-casting suspension containing cellulose nanofibers and cellulose nanocrystals on a rigid carrier substrate. A buffer layer consisting of parylene, SiNx and SiO2 was then deposited to protect the paper substrate from processing gases and chemicals. The processing temperatures of the TFT were kept ≤ 200°C to ensure the paper substrate remained intact during the process. The channel, gate, source, and drain patterns were defined by using conventional photolithography techniques. Fig. 1(a) shows the micrograph of p-type SnO TFTs made on a cellulose nanopaper substrate. The channel width and length are 60 μm and 30 μm, respectively. Figs. 1(b), (c), and (d) illustrate the transfer characteristics, output characteristics and linear field-effect mobility as a function gate voltage of a p-type SnO TFT fabricated on a cellulose nanopaper substrate. The on-paper SnO TFT exhibits a field-effect mobility of 1.21 cm2V-1s-1, threshold voltage of 3.56 V, subthreshold swing of 2.36 V/dec and on/off current ratio of 2.06×103. Please click Download on the upper right corner to see the full abstract

Aciculatin inhibits lipopolysaccharide-mediated inducible nitric oxide synthase and cyclooxygenase-2 expression via suppressing NF-κB and JNK/p38 MAPK activation pathways

<p>Abstract</p> <p>Objectives</p> <p>Natural products have played a significant role in drug discovery and development. Inflammatory mediators such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) have been suggested to connect with various inflammatory diseases. In this study, we explored the anti-inflammatory potential of aciculatin (8-((2<it>R</it>,4<it>S</it>,5<it>S</it>,6<it>R</it>)-tetrahydro-4,5-dihydroxy-6-methyl-2<it>H</it>-pyran-2-yl)-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4<it>H</it>-chromen-4-one), one of main components of <it>Chrysopogon aciculatis</it>, by examining its effects on the expression and activity of iNOS and COX-2 in lipopolysaccharide (LPS)-activated macrophages.</p> <p>Methods</p> <p>We used nitrate and prostaglandin E₂(PGE₂) assays to examine inhibitory effect of aciculatin on nitric oxide (NO) and PGE₂levels in LPS-activated mouse RAW264.7 macrophages and further investigated the mechanisms of aciculatin suppressed LPS-mediated iNOS/COX-2 expression by western blot, RT-PCR, reporter gene assay and confocal microscope analysis.</p> <p>Results</p> <p>Aciculatin remarkably decreased the LPS (1 μg/mL)-induced mRNA and protein expression of iNOS and COX-2 as well as their downstream products, NO and PGE₂respectively, in a concentration-dependent manner (1-10 μM). Such inhibition was found, via immunoblot analyses, reporter gene assays, and confocal microscope observations that aciculatin not only acts through significant suppression of LPS-induced NF-κB activation, an effect highly correlated with its inhibitory effect on LPS-induced IκB kinase (IKK) activation, IκB degradation, NF-κB phosphorylation, nuclear translocation and binding of NF-κB to the κB motif of the iNOS and COX-2 promoters, but also suppressed phosphorylation of JNK/p38 mitogen-activated protein kinases (MAPKs).</p> <p>Conclusion</p> <p>Our results demonstrated that aciculatin exerts potent anti-inflammatory activity through its dual inhibitory effects on iNOS and COX-2 by regulating NF-κB and JNK/p38 MAPK pathways.</p

Significance of Coronary Calcification for Prediction of Coronary Artery Disease and Cardiac Events Based on 64-Slice Coronary Computed Tomography Angiography

This work aims to validate the clinical significance of coronary artery calcium score (CACS) in predicting coronary artery disease(CAD) and cardiac events in 100 symptomatic patients (aged 37–87 years, mean 62.5, 81 males) that were followed up for a mean of 5 years. Our results showed that patients with CAD and cardiac events had significantly higher CACS than those without CAD and cardiac events, respectively. The corresponding data were 1450.42 ± 3471.24 versus 130 ± 188.29 (P 1000. Increased CACS (>100)was also associated with an increased frequency of multi-vessel disease. Nonetheless, 3 (20%) out of 15 patients with zero CACS had single-vessel disease. Significant correlation (P < 0.001) was observed between CACS and CAD on a vessel-based analysis for coronary arteries. It is concluded that CACS is significantly correlated with CAD and cardiac events