Proton Irradiation Experiment for the X-ray Charge-Coupled Devices of the Monitor of All-sky X-ray Image mission onboard the International Space Station: I. Experimental Setup and Measurement of the Charge Transfer Inefficiency

We have investigated the radiation damage effects on a CCD to be employed in the Japanese X-ray astronomy mission including the Monitor of All-sky X-ray Image (MAXI) onboard the International Space Station (ISS). Since low energy protons release their energy mainly at the charge transfer channel, resulting a decrease of the charge transfer efficiency, we thus focused on the low energy protons in our experiments. A 171 keV to 3.91 MeV proton beam was irradiated to a given device. We measured the degradation of the charge transfer inefficiency (CTI) as a function of incremental fluence. A 292 keV proton beam degraded the CTI most seriously. Taking into account the proton energy dependence of the CTI, we confirmed that the transfer channel has the lowest radiation tolerance. We have also developed the different device architectures to reduce the radiation damage in orbit. Among them, the ``notch'' CCD, in which the buried channel implant concentration is increased, resulting in a deeper potential well than outside, has three times higher radiation tolerance than that of the normal CCD. We then estimated the charge transfer inefficiency of the CCD in the orbit of ISS, considering the proton energy spectrum. The CTI value is estimated to be 1.1e-5 per each transfer after two years of mission life in the worse case analysis if the highest radiation-tolerant device is employed. This value is well within the acceptable limit and we have confirmed the high radiation-tolerance of CCDs for the MAXI mission.Comment: 17 pages, 2 table, 12 figures. Accepted for publication of Japanese Journal of Applied Physics. High resolution file is available from http://wwwxray.ess.sci.osaka-u.ac.jp/~miyata/paper/proton_cti.pd

Identification of a Cytokine-induced Antiapoptotic Molecule Anamorsin Essential for Definitive Hematopoiesis

Many growth factors and cytokines prevent apoptosis. Using an expression cloning method, we identified a novel antiapoptotic molecule named Anamorsin, which does not show any homology to known apoptosis regulatory molecules such as Bcl-2 family, caspase family, or signal transduction molecules. The expression of Anamorsin was completely dependent on stimulation with growth factors such as interleukin 3, stem cell factor, and thrombopoietin in factor-dependent hematopoietic cell lines, and forced expression of Anamorsin conferred resistance to apoptosis caused by growth factor deprivation in vitro. Furthermore, Anamorsin was found to act as an antiapoptotic molecule in vivo because Anamorsin−/− mice die in late gestation due to defective definitive hematopoiesis in the fetal liver (FL). Although the number of hematopoietic stem/progenitor cells in the FL did not decrease in these mice, myeloid, and particularly erythroid colony formation in response to cytokines, was severely disrupted. Also, Anamorsin−/− erythroid cells initiated apoptosis during terminal maturation. As for the mechanism of Anamorsin-mediated cell survival, a microarray analysis revealed that the expression of Bcl-xL and Jak2 was severely impaired in the FL of Anamorsin−/− mice. Thus, Anamorsin is considered to be a necessary molecule for hematopoiesis that mediates antiapoptotic effects of various cytokines