The energy distribution of relativistic electrons in the kilo-parsec scale jet of M87 with Chandra

The X-ray emission from the jets in Active Galactic Nuclei (AGN) carries important information on the distributions of relativistic electrons and magnetic fields on large scales. We reanalyze archival Chandra observations on the jet of M87 from 2000 to 2016 with a total exposure of 1460 kiloseconds to explore the X-ray emission characteristics along the jet. We investigate the variability behaviours of the nucleus and the inner jet component HST-1, and confirm indications for day-scale X-ray variability in the nucleus contemporaneous to the 2010 high TeV gamma-ray state. HST-1 shows a general decline in X-ray flux over the last few years consistent with its synchrotron interpretation. We extract the X-ray spectra for the nucleus and all knots in the jet, showing that they are compatible with a single power-law within the X-ray band. There are indications of the resultant X-ray photon index to exhibit a trend, with slight but significant index variations ranging from $\simeq 2.2$ (e.g. in knot D) to $\simeq 2.4-2.6$ (in the outer knots F, A, and B). When viewed in a multi-wavelength context, a more complex situation is arising. Fitting the radio to X-ray spectral energy distributions (SEDs) assuming a synchrotron origin, we show that a broken power-law electron spectrum with break energy $E_b$ around $1~(300\mu G/B)^{1/2}$ TeV allows a satisfactorily description of the multi-band SEDs for most of the knots. However, in the case of knots B, C and D we find indications that an additional high energy component is needed to adequately reproduce the broadband SEDs. We discuss the implications and suggest that a stratified jet model may account for the differences.Comment: accepted for publication in A&

Ponicidin Inhibits Monocytic Leukemia Cell Growth by Induction of Apoptosis

In this study two monocytic leukemia cell lines, U937 and THP-1 cells, were used to investigate the anti-proliferation effects caused by ponicidin. Cell viability was measured by an MTT assay. Cell apoptosis was assessed by flow cytometry as well as DNA fragmentation analysis. Cell morphology was observed using an inverted microscope and Hoechst 33258 staining. RT-PCR and Western blot analysis were used to detect survivin as well as Bax and Bcl-2 expressions after the cells were treated with different concentrations of ponicidin. The results revealed that ponicidin could inhibit the growth of U937 and THP-1 cells significantly by induction of apoptosis. The suppression was in both time- and dose-dependent manner. Marked morphological changes of cell apoptosis were observed clearly after the cells were treated with ponicidin for 48∼72 h. RT-PCR and Western blot analysis demonstrated that both survivin and Bcl-2 expressions were down-regulated remarkably while Bax expression remained constant before and after apoptosis occurred. We therefore conclude that ponicidin has significant anti-proliferation effects by inducing apoptosis on leukemia cells in vitro, downregulation of survivin as well as Bcl-2 expressions may be the important apoptosis inducing mechanisms. The results suggest that ponicidin may serve as potential therapeutic agent for leukemia