Magnetic flux supplement to coronal bright points

Coronal bright points (BPs) are associated with magnetic bipolar features (MBFs) and magnetic cancellation. Here, we investigate how BP-associated MBFs form and how the consequent magnetic cancellation occurs. We analyse longitudinal magnetograms from the Helioseismic and Magnetic Imager to investigate the photospheric magnetic flux evolution of 70 BPs. From images taken in the 193 A passband of the Atmospheric Imaging Assembly (AIA) we dermine that the BPs' lifetimes vary from 2.7 to 58.8 hours. The formation of the BP MBFs is found to involve three processes, namely emergence, convergence and local coalescence of the magnetic fluxes. The formation of a MBF can involve more than one of these processes. Out of the 70 cases, flux emergence is the main process of a MBF buildup of 52 BPs, mainly convergence is seen in 28, and 14 cases are associated with local coalescence. For MBFs formed by bipolar emergence, the time difference between the flux emergence and the BP appearance in the AIA 193 \AA\ passband varies from 0.1 to 3.2 hours with an average of 1.3 hours. While magnetic cancellation is found in all 70 BPs, it can occur in three different ways: (I) between a MBF and small weak magnetic features (in 33 BPs); (II) within a MBF with the two polarities moving towards each other from a large distance (34 BPs); (III) within a MBF whose two main polarities emerge in the same place simultaneously (3 BPs). While a MBF builds up the skeleton of a BP, we find that the magnetic activities responsible for the BP heating may involve small weak fields.Comment: 20 pages, 16 figures, accepted for publication in Ap

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies

Global Slim Accretion Disk Solutions Revisited

We show that there exists a maximal possible accretion rate, beyond which global slim disk solutions cannot be constructed because in the vertical direction the gravitational force would be unable to balance the pressure force to gather the accreted matter. The principle for this restriction is the same as that for the Eddington luminosity and the corresponding critical accretion rate, which were derived for spherical accretion by considering the same force balance in the radial direction. If the assumption of hydrostatic equilibrium is waived and vertical motion is included, this restriction may become even more serious as the value of the maximal possible accretion rate becomes smaller. Previous understanding in the literature that global slim disk solutions could stand for any large accretion rates is due to the overestimation of the vertical gravitational force by using an approximate potential. For accretion flows with large accretion rates at large radii, outflows seem unavoidable in order for the accretion flow to reduce the accretion rate and follow a global solution till the central black hole.Comment: Accepted by Ap