Suzaku Observation of the Intermediate Polar V1223 Sagittarii

We report on the Suzaku observation of the intermediate polar V1223 Sagittarii. Using a multi-temperature plasma emission model with its reflection from a cold matter, we obtained the shock temperature to be 37.9^{+5.1}_{-4.6} keV. This constrains the mass and the radius of the white dwarf (WD) in the ranges 0.82^{+0.05}_{-0.06} solar masses and (6.9+/-0.4)x10^8 cm, respectively, with the aid of a WD mass-radius relation. The solid angle of the reflector viewed from the post-shock plasma was measured to be Omega/2pi = 0.91+/-0.26. A fluorescent iron Kalpha emission line is detected, whose central energy is discovered to be modulated with the WD rotation for the first time in magnetic-CVs. Detailed spectral analysis indicates that the line comprises of a stable 6.4 keV component and a red-shifted component, the latter of which appears only around the rotational intensity-minimum phase. The equivalent width (EW) of the former stable component ~80 eV together with the measured Omega indicates the major reflector is the WD surface, and the shock height is not more than 7% of the WD radius. Comparing this limitation to the height predicted by the Aizu model (1973), we estimated the fractional area onto which the accretion occurs to be < 7x10^{-3}$ of the WD radius, which is the most severe constraint in non-eclipsing IPs. The red-shifted iron line component, on the other hand, can be interpreted as emanating from the pre-shock accretion flow via fluorescence. Its EW (28^{+44}_{-13} eV) and the central energy (6.30_{-0.05}^{+0.07} keV) at the intensity-minimum phase are consistent with this interpretation.Comment: 25 pages, 13 figures, accepted for publication in PASJ (Suzaku & MAXI special issue

A case of hypoxic encephalopathy with delayed exacerbation

Most patients contract hypoxic encephalopathy after suffering a cardiac arrest. They usually endure severe neurological sequelae and the temporal profile of the disease progression remains unclear. This case study shows how the effects of hypoxic encephalopathy continue to progress for several years after the initial event. Up to eight years after the hypoxic insult, the patient’s intellect steadily deteriorated, and brain atrophy progressed. As the hypoxic insult on the brain is only transient, the neurological disability seems not to be exacerbated for years. However, our case indicates that this disorder may have a long progression