Hinode/Extreme-Ultraviolet Imaging Spectrometer Observations of the Temperature Structure of the Quiet Corona

We present a Differential Emission Measure (DEM) analysis of the quiet solar corona on disk using data obtained by the Extreme-ultraviolet Imaging Spectrometer (EIS) on {\it Hinode}. We show that the expected quiet Sun DEM distribution can be recovered from judiciously selected lines, and that their average intensities can be reproduced to within 30%. We present a subset of these selected lines spanning the temperature range $\log$ T = 5.6 to 6.4 K that can be used to derive the DEM distribution reliably. The subset can be used without the need for extensive measurements and the observed intensities can be reproduced to within the estimated uncertainty in the pre-launch calibration of EIS. Furthermore, using this subset, we also demonstrate that the quiet coronal DEM distribution can be recovered on size scales down to the spatial resolution of the instrument (1$"$ pixels). The subset will therefore be useful for studies of small-scale spatial inhomogeneities in the coronal temperature structure, for example, in addition to studies requiring multiple DEM derivations in space or time. We apply the subset to 45 quiet Sun datasets taken in the period 2007 January to April, and show that although the absolute magnitude of the coronal DEM may scale with the amount of released energy, the shape of the distribution is very similar up to at least $\log$ T $\sim$ 6.2 K in all cases. This result is consistent with the view that the {\it shape} of the quiet Sun DEM is mainly a function of the radiating and conducting properties of the plasma and is fairly insensitive to the location and rate of energy deposition. This {\it universal} DEM may be sensitive to other factors such as loop geometry, flows, and the heating mechanism, but if so they cannot vary significantly from quiet Sun region to region.Comment: Version accepted by ApJ and published in ApJ 705. Abridged abstrac

Quantum Effects in Small-Capacitance Single Josephson Junctions

We have measured the current-voltage (I-V) characteristics of small-capacitance single Josephson junctions at low temperatures (T=0.02-0.6 K), where the strength of the coupling between the single junction and the electromagnetic environment was controlled with one-dimensional arrays of dc SQUIDs. The single-junction I-V curve is sensitive to the impedance of the environment, which can be tuned IN SITU. We have observed Coulomb blockade of Cooper-pair tunneling and even a region of negative differential resistance, when the zero-bias resistance R_0' of the SQUID arrays is much higher than the quantum resistance R_K = h/e^2 = 26 kohm. The negative differential resistance is evidence of coherent single-Cooper-pair tunneling within the theory of current-biased single Josephson junctions. Based on the theory, we have calculated the I-V curves numerically in order to compare with the experimental ones at R_0' >> R_K. The numerical calculation agrees with the experiments qualitatively. We also discuss the R_0' dependence of the single-Josephson-junction I-V curve in terms of the superconductor-insulator transition driven by changing the coupling to the environment.Comment: 11 pages with 14 embedded figures, RevTeX4, final versio

Altering HIF-1α through 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure affects coronary vessel development.

Differential tissue hypoxia drives normal cardiogenic events including coronary vessel development. This requirement renders cardiogenic processes potentially susceptible to teratogens that activate a transcriptional pathway that intersects with the hypoxia-inducible factor (HIF-1) pathway. The potent toxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is known to cause cardiovascular defects by way of reduced myocardial hypoxia, inhibition of angiogenic stimuli, and alterations in responsiveness of endothelial cells to those stimuli. Our working hypothesis is that HIF-1 levels and thus HIF-1 signaling in the developing myocardium will be reduced by TCDD treatment in vivo during a critical stage and in particularly sensitive sites during heart morphogenesis. This inadequate HIF-1 signaling will subsequently result in outflow tract (OFT) and coronary vasculature defects. Our current data using the chicken embryo model showed a marked decrease in the intensity of immunostaining for HIF-1α nuclear expression in the OFT myocardium of TCDD-treated embryos. This area at the base of the OFT is particularly hypoxic during normal development; where endothelial cells initially form a concentrated anastomosing network known as the peritruncal ring; and where the left and right coronary arteries eventually connect to the aortic lumen. Consistent with this finding, anomalies of the proximal coronaries were detected after TCDD treatment and HIF-1α protein levels decreased in a TCDD dose-dependent manner