A Chandra Observation of Abell 13: Investigating the Origin of the Radio Relic

We present results from the Chandra X-ray observation of Abell 13, a galaxy cluster that contains an unusual noncentral radio source, also known as a radio relic. This is the first pointed X-ray observation of Abell 13, providing a more sensitive study of the properties of the X-ray gas. The X-ray emission from Abell 13 is extended to the northwest of the X-ray peak and shows substructure indicative of a recent merger event. The cluster X-ray emission is centered on the bright galaxy H of Slee et al. 2001. We find no evidence for a cooling flow in the cluster. A knot of excess X-ray emission is coincident with the other bright elliptical galaxy F. This knot of emission has properties similar to the enhanced emission associated with the large galaxies in the Coma cluster. With these Chandra data we are able to compare the properties of the hot X-ray gas with those of the radio relic from VLA data, to study the interaction of the X-ray gas with the radio emitting electrons. Our results suggest that the radio relic is associated with cooler gas in the cluster. We suggest two explanations for the coincidence of the cooler gas and radio source. First, the gas may have been uplifted by the radio relic from the cluster core. Alternatively, the relic and cool gas may have been displaced from the central galaxy during the cluster merger event.Comment: 11 pages, 9 figures, Accepted for Publication in the Astrophysical Journal, higher-resolution figures can be found at http://www.astro.virginia.edu/~amj3r/Abell13

Bcl-2 protein family: Implications in vascular apoptosis and atherosclerosis

Apoptosis has been recognized as a central component in the pathogenesis of atherosclerosis, in addition to the other human pathologies such as cancer and diabetes. The pathophysiology of atherosclerosis is complex, involving both apoptosis and proliferation at different phases of its progression. Oxidative modification of lipids and inflammation differentially regulate the apoptotic and proliferative responses of vascular cells during progression of the atherosclerotic lesion. Bcl-2 proteins act as the major regulators of extrinsic and intrinsic apoptosis signalling pathways and more recently it has become evident that they mediate the apoptotic response of vascular cells in response to oxidation and inflammation either in a provocative or an inhibitory mode of action. Here we address Bcl-2 proteins as major therapeutic targets for the treatment of atherosclerosis and underscore the need for the novel preventive and therapeutic interventions against atherosclerosis, which should be designed in the light of molecular mechanisms regulating apoptosis of vascular cells in atherosclerotic lesions