Solar flares and Kelvin-Helmholtz instabilities: A parameter survey

Hard X-ray (HXR) sources are frequently observed near the top of solar flare loops, and the emission is widely ascribed to bremsstrahlung. We here revisit an alternative scenario which stresses the importance of inverse Compton processes and the Kelvin- Helmholtz instability (KHI) proposed by Fang et al. (2016). This scenario adds a novel ingredient to the standard flare model, where evaporation flows from flare-impacted chromospheric foot-points interact with each other near the loop top and produce turbulence via KHI. The turbulence can act as a trapping region and as an efficient accelerator to provide energetic electrons, which scatter soft X-ray (SXR) photons to HXR photons via the inverse Compton mechanism. This paper focuses on the trigger of the KHI and the resulting turbulence in this new scenario. We perform a parameter survey to investigate the necessary ingredients to obtain KHI through interaction of chromospheric evaporation flows. When turbulence is produced in the loop apex, an index of -5/3 can be found in the spectra of velocity and magnetic field fluctuations. The KHI development and the generation of turbulence are controlled by the amount of energy deposited in the chromospheric foot-points and the time scale of its energy deposition, but typical values for M class flares show the KHI development routinely. Asymmetry of energy deposition determines the location where the turbulence is produced, and the synthesized SXR light curve shows a clear periodic signal related to the sloshing motion of the vortex pattern created by the KHI.Comment: 12 pages, 14 figure

Stimulatory Effect of 5-Hydroxytryptamine (5-HT) on Rat Capsaicin-Sensitive Lung Vagal Sensory Neurons via Activation of 5-HT\u3csub\u3e3\u3c/sub\u3e Receptors

5-hydroxytryptamine (5-HT) is an inflammatory mediator known to be released in lung. Capsaicin-sensitive lung vagal (CSLV) afferents function as a primary sensor for detecting chemical stimuli and produce consequent reflexes during lung inflammation. To characterize the effect of 5-HT on CSLV afferents, responses of cardiorespiratory reflexes and single-unit C-fiber afferents to right-atrial injections of 5-HT were investigated in anesthetized Sprague-Dawley rats. Bolus injection of 5-HT (8 μg/kg) caused an immediate augmented breath and apnea, accompanied by hypotension and bradycardia. These initial responses were then followed by a brief pressor response and a more sustained depressor response. After a perineural treatment of both cervical vagi with capsaicin to block the conduction of C fibers, 5-HT still triggered the augmented breath, but no longer evoked the apnea, bradycardia and hypotension, indicating an involvement of C-fiber activation. The remaining augmented breath induced by 5-HT after perineural capsaicin treatment was totally eliminated by vagotomy. To further study the effect of 5-HT on CSLV afferents, activities arising from these afferents were determined using the single-fiber recording technique. Right-atrial injection of 5-HT evoked an intense discharge in CSLV afferents in a dose-dependent manner. The highest dose of 5-HT (16 μg/kg) activated 79% (19/24) of CSLV afferents which were also sensitive to capsaicin (0.8 μg/kg). The pretreatment of tropisetron, a selective antagonist of the 5-HT3 receptor, completely blocked CSLV-afferents stimulation induced by 5-HT but did not affect that by capsaicin. Furthermore, a similar afferent response of CSLV afferents was mimicked by phenylbiguanide, a selective agonist of the 5-HT3 receptor. In isolated rat lung vagal C neurons, 5-HT induced intense calcium transients in a dose-dependent manner. The highest concentration (3 μM) of 5-HT activated 67% (18/27) of the CSLV neurons. The 5-HT-induced response was totally abolished by pretreatment of tropisetron. In conclusion, 5-HT exerts an intense stimulatory effect on lung C-fiber terminals mediated through an activation of the 5-HT3 receptor, which may contribute to the airway hypersensitivity under lung inflammation

Delegatable access control for fine-grained XML

The access control mechanisms are critical to ensure security in XML (eXtensible Markup Language). Several such mechanisms have been used or proposed; however, the notion of delegation in XML has not been studied in the literature. In this paper, we propose an access control model encapsuling delegation authorization rules for XML documents that allow flexible data granularity and limited inference protection. Our access control policy specification is basically DTD-based. It can also be considered to be document-based

Transition region adaptive conduction (TRAC) in multidimensional magnetohydrodynamic simulations

In solar physics, a severe numerical challenge for modern simulations is properly representing a transition region between the million-degree hot corona and a much cooler plasma of about 10000 K (e.g., the upper chromosphere or a prominence). In previous 1D hydrodynamic simulations, the transition region adaptive conduction (TRAC) method has been proven to capture aspects better that are related to mass evaporation and energy exchange. We aim to extend this method to fully multidimensional magnetohydrodynamic (MHD) settings, as required for any realistic application in the solar atmosphere. Because modern MHD simulation tools efficiently exploit parallel supercomputers and can handle automated grid refinement, we design strategies for any-dimensional block grid-adaptive MHD simulations. We propose two different strategies and demonstrate their working with our open-source MPI-AMRVAC code. We benchmark both strategies on 2D prominence formation based on the evaporation--condensation scenario, where chromospheric plasma is evaporated through the transition region and then is collected and ultimately condenses in the corona. A field-line-based TRACL method and a block-based TRACB method are introduced and compared in block grid-adaptive 2D MHD simulations. Both methods yield similar results and are shown to satisfactorily correct the underestimated chromospheric evaporation, which comes from a poor spatial resolution in the transition region. Because fully resolving the transition region in multidimensional MHD settings is virtually impossible, TRACB or TRACL methods will be needed in any 2D or 3D simulations involving transition region physics.Comment: Accepted by A&

Exploring the heterogeneity of effects of corticosteroids on acute respiratory distress syndrome: a systematic review and meta-analysis

INTRODUCTION: The effectiveness of corticosteroid therapy on the mortality of acute respiratory distress syndrome (ARDS) remains under debate. We aimed to explore the grounds for the inconsistent results in previous studies and update the evidence. METHODS: We searched MEDLINE, Cochrane Central Register of Controlled Trials and Web of Science up to December 2013. Eligible studies included randomized clinical trials (RCTs) and cohort studies that reported mortality and that had corticosteroid nonusers for comparison. The effect of corticosteroids on ARDS mortality was assessed by relative risk (RR) and risk difference (RD) for ICU, hospital, and 60-day mortality using a random-effects model. RESULTS: Eight RCTs and 10 cohort studies were included for analysis. In RCTs, corticosteroids had a possible but statistically insignificant effect on ICU mortality (RD, −0.28; 95% confidence interval (CI), −0.53 to −0.03 and RR, 0.55; 95% CI, 0.24 to 1.25) but no effect on 60-day mortality (RD, −0.01; 95% CI, −0.12 to 0.10 and RR, 0.97; 95% CI, 0.75 to 1.26). In cohort studies, corticosteroids had no effect on ICU mortality (RR, 1.05; 95% CI, 0.74 to 1.49) but non-significantly increased 60-day mortality (RR, 1.30; 95% CI, 0.96 to 1.78). In the subgroup analysis by ARDS etiology, corticosteroids significantly increased mortality in influenza-related ARDS (three cohort studies, RR, 2.45, 95% CI, 1.40 to 4.27). CONCLUSIONS: The effects of corticosteroids on the mortality of ARDS differed by duration of outcome measures and etiologies. Corticosteroids did not improve longer-term outcomes and may cause harm in certain subgroups. Current data do not support routine use of corticosteroids in ARDS. More clinical trials are needed to specify the favorable and unfavorable subgroups for corticosteroid therapy

Evidence of Decreased Activity in Intermediate-Conductance Calcium-Activated Potassium Channels During Retinoic Acid–Induced Differentiation in Motor Neuron–Like NSC-34 Cells

Background/Aims: Intermediate-conductance Ca2+-activated K+ (IKCa; KCa3.1 or KCNN4) channels affect the behaviors of central neurons including motor neurons. The mechanism through which neuronal differentiation is related to the activity of these channels remains largely unclear. Methods: By using various molecular biology tools and electrophysiological measurements, we investigated possible changes in the activity of IKCa channels in a retinoic acid (RA)-induced differentiation process in motor neuron-like NSC-34 cells. Results: The protein and messenger RNA expression of KCa3.1 substantially diminished as NSC-34 cells were differentiated with low serum (1%) and 1 µM RA. In whole-cell current recordings, the density of delayed-rectifier K+ currents obtained from differentiated cells was elevated. However, the density of a ramp pulse-elicited K+ current that was sensitive to blockage by 1-((2-chlorophenyl) (diphenyl)methyl)-1H-pyrazole (TRAM-34)—an inhibitor of IKCa channels—was significantly higher in undifferentiated NSC-34 cells than in differentiated cells. In undifferentiated cells, the activity of IKCa channels was readily detected and the probability of channel openings was resistant to stimulation by diazoxide or suppression by verruculogen. Furthermore, this probability was increased by 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one or 9-phenanthrol and reduced by TRAM-34. The channel-opening probability decreased in RA-induced differentiated cells, whereas the single-channel conductance of IKCa channels did not differ between undifferentiated and differentiated cells. Moreover, the slow component of the mean closed time in these channels was significantly shorter in undifferentiated cells than in differentiated cells; however, the mean open time in the channel remained unchanged as cells were differentiated. Conclusion: RA-induced differentiation in neurons could exert a suppressive effect on the activity of IKCa channels

Neuroprotection of Catalpol for Experimental Acute Focal Ischemic Stroke: Preclinical Evidence and Possible Mechanisms of Antioxidation, Anti-Inflammation, and Antiapoptosis

Neuroprotection is defined as using a therapy that affects the brain tissue in the still-viable ischemic penumbra to salvage or delay the infarction. Catalpol, the main active principle of the root of Radix Rehmanniae, was reported to have pleiotropic neuroprotective effects in neurodegenerative diseases including ischemic stroke. Here, we evaluated the neuroprotective effects of catalpol in experimental acute ischemic stroke. Studies on catalpol in animal models of acute ischemic stroke were identified from 6 databases. Twenty-five studies involving 805 animals were included. Twelve comparisons showed significant effects of catalpol on decreasing infarct size according to 2,3,5-triphenyltetrazolium chloride staining compared with the control (P<0.05). One study reported significant effect of catalpol on reducing infarct size according to magnetic resonance imaging scan compared with the control (P<0.05). Meta-analysis of these studies indicated that catalpol significantly improved the neurological function score according to Zea Longa score, Bederson score, balance beam-walking test, adhesive removal test, bar-grasping score, and corner test compared with the control (P<0.05). In conclusion, catalpol exerted neuroprotective effects for experimental acute focal ischemic stroke, largely through reducing oxidative reactions, inhibiting apoptosis, and repressing inflammatory reactions and autophagy. However, these apparently positive findings should be interpreted with caution because of the methodological flaws