Energetics of a solar flare and a coronal mass ejection generated by a hot channel eruption

Hot channels (HCs) are prevalent in the solar corona and play a critical role in driving flares and CMEs. In this paper, we estimate the energy contents of an X1.4 eruptive flare with a fast CME generated by a HC eruption on 2011 September 22. Originating from NOAA AR11302, the HC is the most dramatic feature in 131 and 94 {\AA} images observed by SDO/AIA. The flare is simultaneously observed by SDO/AIA, RHESSI, and STEREO-B/EUVI. The CME is simultaneously detected by the white-light coronagraphs of SOHO/LASCO and STEREO-B/COR1. Using multiwavelength and multiview observations of the eruption, various energy components of the HC, flare, and CME are calculated. The thermal and kinetic energies of the HC are (1.77$\pm$0.61)$\times10^{30}$ erg and (2.90$\pm$0.79)$\times10^{30}$ erg, respectively. The peak thermal energy of the flare and total radiative loss of SXR-emitting plasma are (1.63$\pm$0.04)$\times10^{31}$ erg and (1.03$-$1.31)$\times10^{31}$ erg, respectively. The ratio between the thermal energies of HC and flare is 0.11$\pm$0.03, suggesting that thermal energy of the HC is not negligible. The kinetic and potential energies of the CME are (3.43$\pm$0.94)$\times10^{31}$ erg and (2.66$\pm$0.49)$\times10^{30}$ erg, yielding a total energy of (3.69$\pm$0.98)$\times10^{31}$ erg for the CME. Continuous heating of the HC is required to balance the rapid cooling by heat conduction, which probably originate from intermittent magnetic reconnection at the flare current sheet. Our investigation may provide insight into the buildup, release, and conversion of energies in large-scale solar eruptions.Comment: 11 pages, 9 figures, accepted for publication by Ap

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

Intracerebral hemorrhage (ICH) is the second-largest stroke subtype and has a high mortality and disability rate. Secondary brain injury (SBI) is delayed after ICH. The main contributors to SBI are inflammation, oxidative stress, and excitotoxicity. Harmful substances from blood and hemolysis, such as hemoglobin, thrombin, and iron, induce SBI. When cells suffer stress, a critical protective mechanism called “autophagy” help to maintain the homeostasis of damaged cells, remove harmful substances or damaged organelles, and recycle them. Autophagy plays a critical role in the pathology of ICH, and its function remains controversial. Several lines of evidence demonstrate a pro-survival role for autophagy in ICH by facilitating the removal of damaged proteins and organelles. However, many studies have found that heme and iron can aggravate SBI by enhancing autophagy. Autophagy and inflammation are essential culprits in the progression of brain injury. It is a fascinating hypothesis that autophagy regulates inflammation in ICH-induced SBI. Autophagy could degrade and clear pro-IL-1β and apoptosis-associated speck-like protein containing a CARD (ASC) to antagonize NLRP3-mediated inflammation. In addition, mitophagy can remove endogenous activators of inflammasomes, such as reactive oxygen species (ROS), inflammatory components, and cytokines, in damaged mitochondria. However, many studies support the idea that autophagy activates microglia and aggravates microglial inflammation via the toll-like receptor 4 (TLR4) pathway. In addition, autophagy can promote ICH-induced SBI through inflammasome-dependent NLRP6-mediated inflammation. Moreover, some resident cells in the brain are involved in autophagy in regulating inflammation after ICH. Some compounds or therapeutic targets that regulate inflammation by autophagy may represent promising candidates for the treatment of ICH-induced SBI. In conclusion, the mutual regulation of autophagy and inflammation in ICH is worth exploring. The control of inflammation by autophagy will hopefully prove to be an essential treatment target for ICH

Induction of mitochondria-mediated apoptosis and suppression of tumor growth in zebrafish xenograft model by cyclic dipeptides identified from Exiguobacterium acetylicum

Abstract Colorectal cancer is the most common type of gastrointestinal cancers with poor survival and limited therapeutic options. In this study, four structurally different cyclic dipeptides (or diketopiperazine) were isolated and identified as cyclo (l-Pro-l-Leu), cyclo (l-Pro-l-Val), cyclo (l-Pro-l-Phe) and cyclo (l-Pro-l-Tyr) from the ethyl acetate extract in the cell-free filtrate of Exiguobacterium acetylicum S01. The anticancer potential of identified DKPs on colorectal cancer HT-29 cells in vitro and in vivo zebrafish xenograft model was evaluated. The MTT (3-(4, 5-dimethylthiazol-2yl)-2, 5-diphenyltetrazolium bromide)) assay showed that four DKPs exhibited significant inhibition of HT-29 cells viability in a dose-dependent manner whereas there were no cytotoxic effects on normal mouse fibroblast 3T3 cells. Also, we observed that all DKPs induce early and late apoptotic cell death in HT-29 cells. Moreover, the expression levels of apoptotic (cytochrome-c, caspase-3 and Bid) and anti-apoptotic (Bcl-2) markers were up- and down-regulated in HT-29 cells in response to DKPs treatments. Furthermore, these four DKPs remarkably inhibited the tumor progression in a zebrafish xenograft model within a nonlethal dose range. Overall, our findings suggest that cyclic dipeptides derived from E. acetylicum S01 could be promising chemopreventive/ therapeutic candidates against cancer