Dosimetric properties of radiophotoluminescent glass detector in low-energy photon beams.

PURPOSE: A radiophotoluminescent glass rod dosimeter (RGD) has recently become commercially available. It is being increasingly used for dosimetry in radiotherapy to measure the absorbed dose including scattered low-energy photons on the body surface of a patient and for postal dosimetry audit. In this article, the dosimetric properties of the RGD, including energy dependence of the dose response, reproducibly, variation in data obtained by the RGD for each energy, and angular dependence in low-energy photons, are discussed. METHODS: An RGD (GD-301, Asahi Techno Glass Corporation, Shizuoka, Japan) was irradiated with monochromatic low-energy photon beams generated by synchrotron radiation at Photon Factory, High Energy Accelerator Research Organization (KEK). The size of GD-301 was 1.5 mm in diameter and 8.5 mm in length and the active dose readout volume being 1 mm diameter and 0.6 mm depth located 0.7 mm from the end of the detector. The energy dependence of the dose response and reproducibility and variation were investigated for RGDs irradiated with a plastic holder and those irradiated without the plastic holder. Response of the RGD was obtained by not only conventional single field irradiation but also bilateral irradiation. Angular dependence of the RGD was measured in the range of 0°-90° for 13, 17, 40, and 80 keV photon beams by conventional single field irradiation. RESULTS: The dose responses had a peak at around 40 keV. For the energy range of less than 25 keV, all dose response curves steeply decreased in comparison with the ratio of mass energy absorption coefficient of the RGD to that of air. As for the reproducibility and variation in data obtained by the RGD, the coefficient of variance increased with decrease in photon energy. Furthermore, the variation for bilateral irradiation was less than that for single field irradiation. Regarding angular dependence of the RGD, for energies of 13 and 17 keV, the response decreased with increase in the irradiation angle, and the minimum values were 93.5% and 86%, respectively. CONCLUSIONS: Our results showed the dosimetric properties of the RGD, including the energy dependence of the dose response, reproducibly, variation, and angular dependence in low-energy photons and suggest that the accuracy of the absorbed dose in low-energy photons is affected by the readout method and the distribution of radiophotoluminescence centers in the RGD.

Distribution of dolichol in the serum and relationships between serum dolichol levels and various laboratory test values.

We examined the correlations between serum dolichol levels and laboratory test parameters in patients affected by disease, as well as the distribution of dolichol in sera from patients with hyperbetalipoproteinemia and hyperalphalipoproteinemia. Serum dolichol was evaluated by a reverse-phase HPLC method. After centrifugation, the serum dolichol found in healthy controls was mainly associated with medium-sized particles of the high-density lipoprotein (HDL) fraction. For patients with hyperbetalipoproteinemia, serum dolichol was also associated with the medium HDL fractions. However, for hyperalphalipoproteinemia patients the levels of large HDL and serum dolichol were increased, and serum dolichol was mainly associated with the large HDL fraction. On laboratory tests of components, the dolichol level was not correlated with the values for markers of the liver and biliary system, with the values of renal function markers, with creatine kinase activity, amylase activity or uric acid concentration, but was correlated with total cholesterol, HDL-cholesterol and apoA-I concentrations, and with lactate dehydrogenase (LDH) activity. These results suggest that serum dolichol exclusively localized in HDL, and in subpopulation, that in normocholesterolemia or hyperbeta-cholesterolemia is associated with HDL(3), which is small sized and high density HDL, however, that in hyperalphacholesterolemia is associated with HDL(2), which is large sized and lower density HDL.

Inhibition of putrescine aminopropyltransferase influences rat liver regeneration.

A close relationship between rat liver regeneration and the concentration ratio of spermidine to spermine (spd:spm) was demonstrated by the oral administration of trans-4-methylcyclohexylamine (MCHA), a specific inhibitor of putrescine aminopropyltransferase. A decrease in recovery rate of remnant liver with MCHA, as a percentage index of remnant liver weight to body weight, correlated well with a decrease of the spd:spm value, with a correlation coefficient of 0.952 for the remnant livers on day 3 after partial hepatectomy. The decrease in recovery rate could be explained by a prolonged cell cycle based on the data of the proliferating cell nuclear antigen labelling index and mitotic cell index in both livers of day 2 and day 3 after partial hepatectomy. The results presented here will give a new aspect in the field of polyamine regulation to control cell growth in vivo.

Effects of peroxisome proliferators gemfibrozil and clofibrate on syntheses of dolichol and cholesterol in rat liver.

The effects of two peroxisome proliferators, gemfibrozil and clofibrate, on syntheses of dolichol and cholesterol in rat liver were investigated. Gemfibrozil did not affect the overall content of dolichyl phosphate, but it changed the chain-length distribution of dolichyl phosphate, increasing the levels of species with shorter isoprene units. Gemfibrozil suppressed synthesis of dolichyl phosphate from [(3)H]mevalonate and [(3)H]farnesyl pyrophosphate in rat liver. In contrast, clofibrate increased the content of dolichol (free and acyl ester forms). It remarkably enhanced dolichol synthesis from mevalonate, but did not affect dolichol synthesis from farnesyl pyrophosphate. Gemfibrozil elevated cholesterol synthesis from [(14)C]acetate, but did not affect the synthesis from mevalonate. Clofibrate suppressed cholesterol synthesis from acetate, but did not affect cholesterol synthesis from mevalonate. These results suggest that gemfibrozil suppresses synthesis of dolichyl phosphate by inhibiting, at the least, the pathway from farnesyl pyrophosphate to dolichyl phosphate. As a result, the chain-length pattern of dolichyl phosphate may show an increase in shorter isoprene units. Clofibrate may increase the content of dolichol by enhancing dolichol synthesis from mevalonate. Gemfibrozil may increase cholesterol synthesis by activating the pathway from acetate to mevalonate. Unlike gemfibrozil, clofibrate may decrease cholesterol synthesis by inhibiting the pathway from acetate to mevalonate.