Bright 22 μ\mum Excess Candidates from WISE All-Sky Catalog and Hipparcos Main Catalog

In this paper we present a catalog which includes 141 bright candidates ($\leq10.27$ mag, V band) showing the infrared (IR) excess at 22 $\mu$m. Of which, 38 stars are known IR excess stars or disk, 23 stars are double or multiple stars and 4 are Be stars. While the remaining more than 70 stars are identified as the 22 $\mu$m excess candidates in our work. The criterion of selecting candidates is $K_s-[22]_{\mu m}$. All these candidates are selected from \emph{WISE} All-sky data cross-correlated with \emph{Hipparcos} Main Catalog and the likelihood-ratio technique is employed. Considering the effect of background, we introduce the \emph{IRAS} 100 $\mu$m level to exclude the high background. We also estimated the coincidence probability of these sources. In addition, we presented the optical to mid-infrared SEDs and optical images of all the candidates, and gave the observed optical spectra of 6 stars with NAOC's 2.16-m telescope. To measure for the dust amount around each star, the fractional luminosity is also provided. We also test whether our method of selecting IR excess stars can be used to search for extra-solar planets, we cross-matched our catalog with known IR-excess stars having planets but none is matched. Finally, we give the fraction of stars showing IR-excess for different spectral type of main-sequence stars.Comment: 45 pages, 16 figures, 4 tables. Accepted for publication in ApJ

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Purpose: To investigate the protective role of tectorigenin in myocardial ischaemia/reperfusion. Methods: Myocardial cells (H9c2) were treated with different concentrations of tectorigenin and exposed to hypoxia/reoxygenation. Cell viability and apoptosis were determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining, respectively. Oxidative stress and inflammation were evaluated using enzyme-linked immunosorbent assay (ELISA), while autophagy and the underlying mechanisms of action were evaluated by Western blot. Results: Tectorigenin enhanced the proliferative activity of H9c2 under hypoxia/reoxygenation conditions, and significantly reduced the apoptotic activity (p < 0.001) through decrease in Bax and increase in Bcl-2. Tectorigenin also significantly up-regulated SOD (superoxide dismutase) and GSH (glutathione) levels (p < 0.01), and down-regulated MDA (malondialdehyde) and MPO (myeloperoxidase) in hypoxia/reoxygenation-induced H9c2. TNF-α (tumor necrosis factor-α), IL(interleukin)-1β, and IL-6 levels were also inhibited by tectorigenin by down-regulating p-p65. Hypoxia/reoxygenation-induced increase in p62 and decrease in Beclin-1 and LC3-II/LC3-I were reversed by tectorigenin. Protein expressions of p-mTOR, p-AKT, and p-PI3K in hypoxia/reoxygenation-induced H9c2 were elevated by tectorigenin. Conclusion: Tectorigenin exerts anti-oxidant, anti-inflammatory, and anti-autophagic effects on hypoxia/reoxygenation-induced H9c2 through the activation of PI3K/AKT/mTOR pathway, thus suggesting that it is a potential agent for the management of myocardial ischaemia/reperfusion