Use of optically stimulated luminescence dosimeter and radiophotoliminescent glass dosimeter for dose measurement in dual-source dual-energy computed tomography.

We aimed to evaluate properties of optically stimulated luminescence dosimeters (OSLDs) and radiophotoluminescent glass dosimeters (RPLDs) used in dual-source dual-energy (DE) computed tomography (DECT) dosimetry. Energy dependence was evaluated in single-energy (SE) and DE modes, and their relative dose responses differed by 3.8% and 6.6% under equivalent effective energy with OSLD and RPLD, respectively. Dose variation was evaluated using coefficients of variation of dose values from 10 dosimeters, and dose variation of OSLD and RPLD in SE mode ranged from 2.1 to 3.0% and from 2.1 to 2.8%, and those in the DE mode were 1.8 and 2.6%, respectively. Dose linearity was evaluated from 1 to 150 mGy, and linear relationships of dose response were observed between the dosimeters and the ionization chamber (correlation coefficients ≥ 0.9991). Angular dependence was evaluated from - 90° to + 90°, and it was smaller in DE mode than in SE mode for OSLD. The normalized response of RPLD was higher at ± 30° and ± 60° and lower at - 90° in SE and DE modes. This study demonstrated both OSLD and RPLD can perform dosimetry in dual-source DECT with small influence of the properties of the dosimeters compared with that in SECT.

Administered chrysanthemum flower oil attenuates hyperuricemia: mechanism of action as revealed by DNA microarray analysis.

We applied Chrysanthemum flower oil (CFO) to a hyperuricemia model by feeding rats a hyperuricemia-inducing diet (HID) and investigated its effect on serum uric acid (SUA) levels and its mode of action. CFO is the oily fraction that contains polyphenols derived from chrysanthemum flowers. Oral administration of CFO to HID-fed rats significantly decreased their SUA levels. It also inhibited xanthine oxidase activities in the liver and increased urine uric acid levels. The effects of CFO on the renal gene expressions that accompanied the induction of hyperuricemia were comprehensively confirmed by DNA microarray analysis. The analysis showed up-regulation of those genes for uric acid excretion by CFO administration. These results suggest that CFO suppresses the increase in SUA levels via two mechanisms: suppression of uric acid production by inhibition of xanthine oxidase in the liver and acceleration of its excretion by up-regulation of uric acid transporter genes in the kidney.