No abstract

The X-Ray Spectrometer (XRS) has been designed to provide the Suzaku Observatory with non-dispersive, high-resolution X-ray spectroscopy. As designed, the instrument covers the energy range 0.3 to 12 keV, which encompasses the most diagnostically rich part of the X-ray band. The sensor consists of a 32-channel array of X-ray microcalorimeters, each with an energy resolution of about 6 eV. The very low temperature required for operation of the array (60 mK) is provided by a four-stage cooling system containing a single-stage adiabatic demagnetization refrigerator, a superfluid-helium cryostat, a solid-neon dewar, and a single-stage, Stirling-cycle cooler. The Suzaku/XRS is the first orbiting X-ray microcalorimeter spectrometer and was designed to last more than three years in orbit. The early verification phase of the mission demonstrated that the instrument worked properly and that the cryogen consumption rate was low enough to ensure a mission lifetime exceeding 3 years. However, the liquid-He cryogen was completely vaporized two weeks after opening the dewar guard vacuum vent. The problem has been traced to inadequate venting of the dewar He and Ne gases out of the spacecraft and into space. In this paper we present the design and ground testing of the XRS instrument, and then describe the in-flight performance. An energy resolution of 6 eV was achieved during pre-launch tests and a resolution of 7 eV was obtained in orbit. The slight degradation is due to the effects of cosmic rays.

The effects of alpha-lipoic acid (ALA) on the growth, body composition, postmortem AMP-activated protein kinase (AMPK) activation, and 24-h muscle pH were investigated. Thirty male C57BL/6J mice were fed diets containing 0, 0.5, or 1.0% ALA (DM basis). At the end of the 3-wk feeding trial, carcass weights decreased (P < 0.05) 14 and 30% for mice fed 0.5 and 1.0% ALA, respectively, compared with the 0% group, with decreases in BW as the levels of dietary ALA increased. This change in carcass weight occurred because carcass fat content for mice receiving 0.5 and 1.0% ALA was 7.32 and 8.09% lower (P < 0.05), respectively, than for the 0% ALA treatment, and because gonadal fat decreased (P < 0.05) 85% in mice fed 1.0% ALA compared with those fed 0% ALA. Dietary ALA caused a slight increase (P < 0.05) in carcass moisture content, with no (P = 0.07) effect on protein and ash content. Furthermore, ALA supplement decreased (P < 0.05) ADFI (DM basis) from 4.3 g/d for 0% ALA-fed mice to 3.4 g/d for 1.0% ALA-fed mice. At 20 min postmortem, pH was greater (P < 0.05) in muscle of mice fed 1.0% ALA than in muscle of mice fed 0% ALA. Ultimate (24-h) pH values differed (P < 0.05) among treatments, and mean values were 5.83, 6.08, and 6.29 for 0, 0.5, and 1.0% ALA, respectively. Phosphorylation of AMPK alpha subunit at Thr172, an indicator of AMPK activation, was decreased (P < 0.05) in muscle of ALA-treated mice at 20 min postmortem. Because AMPK has a crucial role in the control of glycolysis, the reduction in AMPK activation decreases glycolysis, and thereby increases the ultimate pH of postmortem muscle. In summary, dietary ALA supplement can decrease fat accumulation in mice, and because ALA increased muscle pH at 20 min and 24 h postmortem, these results suggest that dietary ALA supplementation might decrease carcass fatness and prevent the development of PSE pork and poultry. However, further research is required to test the effects of ALA in swine and poultry.

SENCAR mice were used to determine the effects of the provitamin A compound beta-carotene on papilloma formation and the conversion of papillomas to carcinomas in a two-stage protocol with one application of the initiator 7,12-dimethylbenz[a]anthracene (DMBA, 20 micrograms) and 20 weekly applications of the promotor 12-O-tetradecanoylphorbol-13-acetate (TPA, 2 micrograms). A purified vitamin A-free diet was supplemented with beta-carotene at four levels (0.6, 6, 60 and 600 micrograms/g of diet) for female mice and two levels (60 and 600 micrograms/g) for male mice. Dietary supplementations of beta-carotene did not result in significant changes in body weight and survival of female and male mice. However, papillomas developed more rapidly and papilloma incidence (% mice with papillomas) reached its maximum (100%) sooner in male mice fed 600 micrograms of beta-carotene/g of diet than those fed 60 micrograms/g. There were smaller differences in papilloma incidence among the dietary groups in female mice, but the papilloma incidence again reached 100% sooner in mice fed 600 micrograms of beta-carotene/g of diet. Female and male mice fed 600 micrograms of beta-carotene/g of diet had significantly higher papilloma yields (average number of papillomas/mouse) than other dietary groups and a very low percentage of these papillomas converted to carcinomas in these mice. Thus, beta-carotene at 600 micrograms/g inhibited the conversion of papillomas to carcinomas in both sexes. In addition, papilloma yields were higher in female mice and these papillomas regressed more quickly than those in the corresponding groups of male mice. In conclusion, dietary beta-carotene caused differential effects on papilloma and carcinoma yields and sex-dependent differences in papilloma formation in female and male SENCAR mice treated with DMBA and TPA in a two-stage carcinogenesis protocol.

Previously we have shown that dietary retinoids are essential for papilloma formation induced by either an initiation-promotion or a complete skin carcinogenesis protocol. The present study was conducted to further determine the effect of dietary retinoic acid (RA) on papilloma formation and the conversion of papillomas to carcinomas. Skin tumors were induced in 3 week old female SENCAR mice by an initiation-promotion protocol with one application of 20 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA), followed by 20 weekly applications of 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). Mice were fed RA at one of the three doses: 0.3 (nutritionally marginal dose), 3 (near physiological) and 30 (pharmacological) micrograms/g of diet. Mice fed 30 micrograms of RA/g of diet had the same survival rate as the other two groups despite a lower body weight and all three groups had similar papilloma incidence, which reached 100% at age 18 weeks. Mice fed 3 micrograms of RA/g of diet had the highest papilloma yield (approximately 14 papillomas/mouse) of all groups and it peaked between weeks 18 and 38 of age. These papillomas later regressed such that mice from all three groups had about the same papilloma yield at week 44 of age. Mice fed 30 micrograms of RA/g of diet failed to develop any visible carcinoma, while mice fed 0.3 or 3 micrograms/g showed 1.9% conversion of papillomas to carcinomas. Therefore, dietary RA at 30 micrograms/g of diet inhibited the conversion of papillomas to carcinomas without affecting papilloma incidence. In addition, dietary RA at 30 and 0.3 micrograms/g of diet lowered papilloma yield.