GRB 091208B: First Detection of the Optical Polarization in Early Forward Shock Emission of a Gamma-Ray Burst Afterglow

We report that the optical polarization in the afterglow of GRB 091208B is measured at t = 149 - 706 s after the burst trigger, and the polarization degree is P = 10.4% +/- 2.5%. The optical light curve at this time shows a power-law decay with index -0.75 +/- 0.02, which is interpreted as the forward shock synchrotron emission, and thus this is the first detection of the early-time optical polarization in the forward shock (rather than that in the reverse shock reported by Steele et al. (2009). This detection disfavors the afterglow model in which the magnetic fields in the emission region are random on the plasma skin depth scales, such as amplified by the plasma instabilities, e.g., Weibel instability. We suggest that the fields are amplified by the magnetohydrodynamic instabilities, which would be tested by future observations of the temporal changes of the polarization degrees and angles for other bursts.Comment: 12 pages, 4 figures, accepted for publication in ApJ Letter

Early phase observations of extremely luminous Type Ia Supernova 2009dc

We present early phase observations in optical and near-infrared wavelengths for the extremely luminous Type Ia supernova (SN Ia) 2009dc. The decline rate of the light curve is $\Delta m_{15}(B)=0.65\pm 0.03$, which is one of the slowest among SNe Ia. The peak $V$-band absolute magnitude is $M_{V}=-19.90\pm 0.15$ mag even if the host extinction is $A_{V}=0$ mag. It reaches $M_{V}=-20.19\pm 0.19$ mag for the host extinction of $A_{V}=0.29$ mag as inferred from the observed Na {\sc i} D line absorption in the host. Our $JHK_{s}$-band photometry shows that the SN is one of the most luminous SNe Ia also in near-infrared wavelengths. These results indicate that SN 2009dc belongs to the most luminous class of SNe Ia, like SN 2003fg and SN 2006gz. We estimate the ejected $^{56}$Ni mass of $1.2\pm 0.3$ \Msun for no host extinction case (or 1.6$\pm$ 0.4 M$_{\odot}$ for the host extinction of $A_{V}=0.29$ mag). The C {\sc ii} $\lambda$6580 absorption line keeps visible until a week after maximum, which diminished in SN 2006gz before its maximum brightness. The line velocity of Si {\sc ii} $\lambda$6355 is about 8000 km s$^{-1}$ around the maximum, being considerably slower than that of SN 2006gz, while comparable to that of SN 2003fg. The velocity of the C {\sc ii} line is almost comparable to that of the Si {\sc ii}. The presence of the carbon line suggests that thick unburned C+O layers remain after the explosion. SN 2009dc is a plausible candidate of the super-Chandrasekhar mass SNe Ia

Functional roles of cardiac and vascular ATP-sensitive potassium channels clarified by Kir6.2-knockout mice

ATP-sensitive potassium (K ATP) channels were discovered in ventricular cells, but their roles in the heart remain mysterious. K ATP channels have also been found in numerous other tissues, including vascular smooth muscle. Two pore-forming subunits, Kir6.1 and Kir6.2, contribute to the diversity of K ATP channels. To determine which subunits are operative in the cardiovascular system and their functional roles, we characterized the effects of pharmacological K + channel openers (KCOs, ie, pinacidil, P-1075, and diazoxide) in Kir6.2-deficient mice. Sarcolemmal K ATP channels could be recorded electrophysiologically in ventricular cells from Kir6.2 +/+ (wild-type [WT]) but not from Kir6.2 -/- (knockout [KO]) mice. In WT ventricular cells, pinacidil induced an outward current and action potential shortening, effects that were blocked by glibenclamide, a K ATP channel blocker. KO ventricular cells exhibited no response to KCOs, but gene transfer of Kir6.2 into neonatal ventricular cells rescued the electrophysiological response to P-1075. In terms of contractile function, pinacidil decreased force generation in WT but not KO hearts. Pinacidil and diazoxide produced concentration-dependent relaxation in both WT and KO aortas precontracted with norepinephrine. In addition, pinacidil induced a glibenclamide-sensitive current of similar magnitude in WT and KO aortic smooth muscle cells and comparable levels of hypotension in anesthetized WT and KO mice. In both WT and KO aortas, only Kir6.1 mRNA was expressed. These findings indicate that the Kir6.2 subunit mediates the depression of cardiac excitability and contractility induced by KCOs; in contrast, Kir6.2 plays no discernible role in the arterial tree.link_to_subscribed_fulltex

The ryanodine receptor channel as a molecular motif in atrial fibrillation: pathophysiological and therapeutic implications

Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with substantial morbidity and mortality. It causes profound changes in sarcoplasmic reticulum (SR) Ca2+ homeostasis, including ryanodine receptor channel dysfunction and diastolic SR Ca2+ leak, which might contribute to both decreased contractile function and increased propensity to atrial arrhythmias. In this review, we will focus on the molecular basis of ryanodine receptor channel dysfunction and enhanced diastolic SR Ca2+ leak in AF. The potential relevance of increased incidence of spontaneous SR Ca2+ release for both AF induction and/or maintenance and the development of novel mechanism-based therapeutic approaches will be discussed