X-ray Observation and Analysis of The Composite Supernova Remnant G327.1-1.1

Based on the data from the observation of the SNR G327.1-1.1 by ASCA and ROSAT, we find that G327.1-1.1 is a composite remnant with both a nonthermal emission component and a diffuse thermal emission component. The nonthermal component is well fitted by a power-law model with photon index about 2.2. This component is attributed to the emission from the synchrotron nebula powered by an undiscovered central pulsar. The thermal component has a temperature of about 0.4 keV. We attribute it to the emission from the shock-heat swept-up ISM. Its age, explosion energy and density of ambient medium are derived from the observed thermal component. Some charactistics about the synchrotron nebula are also derived. We search for the pulsed signal, but has not found it. The soft X-ray(0.4 - 2 keV) and hard X-ray(2 - 10 keV) images are different, but they both elongate in the SE-NW direction. And this X-ray SE-NW elongation is in positional coincidence with the radio ridge in MOST 843MHz radio map. We present a possibility that the X-ray nonthermal emission mainly come from the trail produced by a quickly moving undiscoverd pulsar, and the long radio ridge is formed when the pulsar is moving out of the boundary of the plerionic structure.Comment: 20 pages, 4 Postscript figures, aasms4.sty and psfig.sty, to be published in Astrophysical Journal, January 20, 1999, Vol. 51

Increased Expression of Foxj1 after Traumatic Brain Injury

Foxj1 is a member of the Forkhead/winged-helix (Fox) family of transcription factors, which is required for postnatal differentiation of ependymal cells and a subset of astrocytes in the subventricular zone. The subpopulation of astrocytes has the ability of self-renew and neurogenic potential differentiated into astrocytes, oligodendrocytes, and neurons. However, its expression and function in the central nervous system lesion are not well understood. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the changed expression of Foxj1 in the brain cortex. Western blot and immunohistochemistry analysis showed that the expression of Foxj1 gradually increased, reached a peak at day 3 after TBI, and declined during the following days. Double immunofluorescence staining revealed that Foxj1 was co-expressed with MAP-2 and GFAP. In addition, we detected that Ki67 had the co-localization with NeuN, GFAP, and Foxj1. All our findings suggested that Foxj1 may be involved in the pathophysiology of brain after TBI