Suzaku observations of Jovian diffuse hard X-ray emission

We report on results of systematic analyses of the entire three X-ray data sets of Jupiter taken by Suzaku in 2006, 2012, and 2014. Jovian diffuse hard X-ray emission was discovered by Suzaku in 2006 when the solar activity went toward its minimum. The diffuse emission was spatially consistent with the Jovian inner magnetosphere and was spectrally fitted with a flat power-law function suggesting non-thermal emission. Thus, a scenario in which ultra-relativistic (tens of MeV) electrons in the Jovian inner magnetosphere inverse-Comptonize solar visible photons into X-ray bands has been hypothetically proposed. We focused on the dependence of the Jovian diffuse hard X-ray emission on the solar activity to verify this scenario. The solar activity in 2012 and 2014 was around the maximum of the 24th solar cycle. By combining the imaging and spectral analyses for the three data sets, we successfully separated the contribution of the diffuse emission from the emission of Jupiter’s body (i.e., the aurora and disk emission). The 1–5 keV luminosity of the diffuse emission has been stable and did not vary significantly, and did not simply depend on the solar activity, which is also known to affect the high-energy electron distribution in the Jovian inner magnetosphere scarcely. The luminosity of the body emission both in 0.2–1 and 1–5 keV, in contrast, probably depended on the solar activity and varied by a factor of 2–5. These results strongly supported the inverse-Compton scattering scenario by the ultra-relativistic electrons. In this paper, we estimate spatial and spectral distributions of the inverse-Compton scattering X-rays by Jovian magnetospheric high-energy electrons with reference to the Divine–Garrett model and found a possible agreement in an inner region (≲10 RJ) for the X-ray observations

Effect of the Charged Pressure on GM Cryocooler Performance.

Presented at the 16th International Cryocooler Conference, held May 17-20, 2008 in Atlanta, Georgia.This paper presents experimental results that show that the refrigeration efficiency of GM refrigerators can be improved by applying a charged pressure. Recently, there has been remarkable progress in superconducting systems, such as magnetic resonance imaging systems, silicon singlecrystal pull-up apparatus, and cryopumps. GM cryocoolers are used to cool these systems because of their high reliability. Thus, to improve the efficiency of superconducting systems, it is important to improve the efficiency of GM cryocoolers. If the compression ratio of a GM cryocooler is reduced, its coefficient of performance (COP) will approach the Carnot COP, since the cryocooler will operate with Simon expansion. Therefore, we investigated the effect of varying the charged pressure of a cryocooler and the cycle frequency on its refrigeration efficiency. We developed a GM cryocooler that can be operated at various charged pressures and we measured its efficiency at various charged pressures and operating frequencies. The optimum charged pressure and operating frequency were determined by comparing the experimental results with numerical simulation results

Gas selection for Xe-based LCP-GEM detectors onboard the CubeSat X-ray observatory NinjaSat

We present a gas selection for Xe-based gas electron multiplier (GEM) detectors, Gas Multiplier Counters (GMCs) onboard the CubeSat X-ray observatory NinjaSat. To achieve an energy bandpass of 2-50 keV, we decided to use a Xe-based gas mixture at a pressure of 1.2 atm that is sensitive to high-energy X-rays. In addition, an effective gain of over 300 is required for a single GEM so that the 2 keV X-ray signal can be sufficiently larger than the electrical noise. At first, we measured the effective gains of GEM in nine Xe-based gas mixtures (combinations of Xe, Ar, CO2, CH4, and dimethyl ether; DME) at 1.0 atm. The highest gains were obtained with Xe/Ar/DME mixtures, while relatively lower gains were obtained with Xe/Ar/CO2, Xe/Ar/CH4, and Xe+quencher mixtures. Based on these results, we selected the Xe/Ar/DME (75%/24%/1%) mixture at 1.2 atm as the sealed gas for GMC. Then we investigated the dependence of an effective gain on the electric fields in the drift and induction gaps ranging from 100-650 V cm$^{-1}$ and 500-5000 V cm$^{-1}$, respectively, in the selected gas mixture. The effective gain weakly depended on the drift field while it was almost linearly proportional to the induction field: 2.4 times higher at 5000 V cm$^{-1}$ than at 1000 V cm$^{-1}$. With the optimal induction and drift fields, the flight model GMC achieves an effective gain of 460 with an applied GEM voltage of 590 V.Comment: 7th international conference on Micro Pattern Gaseous Detectors 2022 - MPGD2022, 3 pages, 2 figure

Temperature Dependence of Gas X-Ray Detectors Onboard the 6U CubeSat X-Ray Observatory NinjaSat.

We report the temperature dependence of Gas Multiplier Counters (GMCs) onboard the 6U CubeSat X-ray observatory NinjaSat.The detector performance of GMC depends on the temperature. The temperature dependence of the gain was calibrated for the detector response function in orbit using data from the Crab Nebula. The fit results using the function created improved the ratio of the fit curve to the data from 12% to 4% before and after gain correction

Ion beam induced surface pattern formation and stable travelling wave solutions

This article was published in the Journal of Physics: Condensed Matter [© IOP Publishing Ltd.] and the definitive version is available at: http://dx.doi.org/10.1088/0953-8984/25/9/095003The formation of ripple structures on ion bombarded semiconductor surfaces is examined theoretically. Previous models are discussed and a new nonlinear model is formulated, based on the infinitesimal local atomic relocation induced by elastic nuclear collisions in the early stages of collision cascades and an associated density change in the near surface region. Within this framework ripple structures are shown to form without the necessity to invoke surface diffusion or large sputtering as important mechanisms. The model can also be extended to the case where sputtering is important, and it is shown that in this case certain 'magic' angles can occur at which the ripple patterns are most clearly defined. The results are in very good agreement with experimental observations

The Nrf1 CNC-bZIP Protein Is Regulated by the Proteasome and Activated by Hypoxia

BACKGROUND: Nrf1 (nuclear factor-erythroid 2 p45 subunit-related factor 1) is a transcription factor mediating cellular responses to xenobiotic and pro-oxidant stress. Nrf1 regulates the transcription of many stress-related genes through the electrophile response elements (EpREs) located in their promoter regions. Despite its potential importance in human health, the mechanisms controlling Nrf1 have not been addressed fully. PRINCIPAL FINDINGS: We found that proteasomal inhibitors MG-132 and clasto-lactacystin-β-lactone stabilized the protein expression of full-length Nrf1 in both COS7 and WFF2002 cells. Concomitantly, proteasomal inhibition decreased the expression of a smaller, N-terminal Nrf1 fragment, with an approximate molecular weight of 23 kDa. The EpRE-luciferase reporter assays revealed that proteasomal inhibition markedly inhibited the Nrf1 transactivational activity. These results support earlier hypotheses that the 26 S proteasome processes Nrf1 into its active form by removing its inhibitory N-terminal domain anchoring Nrf1 to the endoplasmic reticulum. Immunoprecipitation demonstrated that Nrf1 is ubiquitinated and that proteasomal inhibition increased the degree of Nrf1 ubiquitination. Furthermore, Nrf1 protein had a half-life of approximately 5 hours in COS7 cells. In contrast, hypoxia (1% O(2)) significantly increased the luciferase reporter activity of exogenous Nrf1 protein, while decreasing the protein expression of p65, a shorter form of Nrf1, known to act as a repressor of EpRE-controlled gene expression. Finally, the protein phosphatase inhibitor okadaic acid activated Nrf1 reporter activity, while the latter was repressed by the PKC inhibitor staurosporine. CONCLUSIONS: Collectively, our data suggests that Nrf1 is controlled by several post-translational mechanisms, including ubiquitination, proteolytic processing and proteasomal-mediated degradation as well as by its phosphorylation status

Expression of Transient Receptor Potential Ankyrin 1 (TRPA1) and Its Role in Insulin Release from Rat Pancreatic Beta Cells

<div><h3>Objective</h3><p>Several transient receptor potential (TRP) channels are expressed in pancreatic beta cells and have been proposed to be involved in insulin secretion. However, the endogenous ligands for these channels are far from clear. Here, we demonstrate the expression of the transient receptor potential ankyrin 1 (TRPA1) ion channel in the pancreatic beta cells and its role in insulin release. TRPA1 is an attractive candidate for inducing insulin release because it is calcium permeable and is activated by molecules that are produced during oxidative glycolysis.</p> <h3>Methods</h3><p>Immunohistochemistry, RT-PCR, and Western blot techniques were used to determine the expression of TRPA1 channel. Ca²⁺ fluorescence imaging and electrophysiology (voltage- and current-clamp) techniques were used to study the channel properties. TRPA1-mediated insulin release was determined using ELISA.</p> <h3>Results</h3><p>TRPA1 is abundantly expressed in a rat pancreatic beta cell line and freshly isolated rat pancreatic beta cells, but not in pancreatic alpha cells. Activation of TRPA1 by allyl isothiocyanate (AITC), hydrogen peroxide (H₂O₂), 4-hydroxynonenal (4-HNE), and cyclopentenone prostaglandins (PGJ₂) and a novel agonist methylglyoxal (MG) induces membrane current, depolarization, and Ca²⁺ influx leading to generation of action potentials in a pancreatic beta cell line and primary cultured pancreatic beta cells. Activation of TRPA1 by agonists stimulates insulin release in pancreatic beta cells that can be inhibited by TRPA1 antagonists such as HC030031 or AP-18 and by RNA interference. TRPA1-mediated insulin release is also observed in conditions of voltage-gated Na⁺ and Ca²⁺ channel blockade as well as ATP sensitive potassium (K_ATP) channel activation.</p> <h3>Conclusions</h3><p>We propose that endogenous and exogenous ligands of TRPA1 cause Ca²⁺ influx and induce basal insulin release and that TRPA1-mediated depolarization acts synergistically with K_ATP channel blockade to facilitate insulin release.</p> </div