13 research outputs found
Accreting Millisecond X-Ray Pulsars
Accreting Millisecond X-Ray Pulsars (AMXPs) are astrophysical laboratories
without parallel in the study of extreme physics. In this chapter we review the
past fifteen years of discoveries in the field. We summarize the observations
of the fifteen known AMXPs, with a particular emphasis on the multi-wavelength
observations that have been carried out since the discovery of the first AMXP
in 1998. We review accretion torque theory, the pulse formation process, and
how AMXP observations have changed our view on the interaction of plasma and
magnetic fields in strong gravity. We also explain how the AMXPs have deepened
our understanding of the thermonuclear burst process, in particular the
phenomenon of burst oscillations. We conclude with a discussion of the open
problems that remain to be addressed in the future.Comment: Review to appear in "Timing neutron stars: pulsations, oscillations
and explosions", T. Belloni, M. Mendez, C.M. Zhang Eds., ASSL, Springer;
[revision with literature updated, several typos removed, 1 new AMXP added
Disease proteomics
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62680/1/nature01514.pd
NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder
NGFI-B/Nur77/TR3, originally identified as an immediate-early gene rapidly induced by serum and growth factors, is a member of the steroid hormone nuclear receptor superfamily with no identified endogenous ligand. NGFI-B induces apoptosis in a number of cell lineages exposed to proapoptotic stimuli by directly targeting the mitochondria, inducing cytochrome c release. The present study was designed to determine the role of NGFI-B in cardiomyocytes of restraint-stressed rats. The NGFI-B content was increased in mitochondria and reduced in plasma as apoptosis increased. Analysis showed that NGFI-B induces cardiomyocyte apoptosis in restraint-stressed rats by mediating mitochondrial energy metabolism disorder. Several novel mitochondrial proteins, which correlate with NGFI-B, were reported in cardiomyocyte apoptosis of restraint-stressed rats. Five proteins associated with NGFI-B participate directly in mitochondrial energy metabolism. Studies of mitochondrial respiratory efficiency and ATP synthase activity strongly support the findings. These results provide significant information for comprehensively understanding the cellular mechanism of cardiovascular diseases