Anisotropic diffusion of Fe ions in Fricke-XO-Pluronic F-127 and Fricke-XO-gelatine 3D radiotherapy dosimeters.

A new radiochromic dosimeter was examined with Raman spectroscopy and an optical approach for assessment of 3D dose distribution integrity. The acronym of the dosimeter is Fricke-XO-Pluronic F-127, where XO denotes xylenol orange; Pluronic F-127 is a copolymer matrix of poly(ethylene oxide)-block-poly(propylene oxide)-block-poly(ethylene oxide), and the dosimeter contains the components of a Fricke dosimetric solution. Two dosimeter samples in cuvettes were partially irradiated such that a radiation dose was absorbed at the bottom of the cuvettes. After irradiation, one sample was stored upside down such that the irradiated part was at the top and another one was stored with the irradiated part at the bottom. Two diffusion coefficients of ferric ion complexes with XO ([XO-Fe]+3) were calculated. They were compared with those for similar dosimeter, however with gelatine matrix instead of Pluronic F-127. The results obtained indicate an impact of the gravitational force on the diffusion of [XO-Fe]+3ions over time after irradiation and thus a possibility of severely undermining the integrity of a dose distribution in irradiated dosimeter. The conclusions drawn suggest the necessity of examination of different 3D Fricke dosimeter compositions for anisotropic diffusion of ferric ions.

Lactoferrin stimulates killing and clearance of bacteria but does not prevent mortality of diabetic mice.

We have previously shown that bovine lactoferrin (BLF) given intravenously (i.v.) protected mice against a lethal dose of Escherichia coli and strongly stimulated both the clearing and killing activities in liver, lungs, spleen and kidney. Since some studies indicated a reduction of the manifestation of experimental pancreatitis with lactoferrin (LF), we decided to examine the protective activity of BLF against lethal E. coli infection in animals with alloxan (Alx)-induced diabetes. It appeared that 48 h diabetes substantially lowered the killing activity in all four organs as well as the clearing rate of E. coli from the circulation. BLF given i.v. reduced this undesirable effect of diabetes. However, in 10- and 20-day diabetic animals, the diabetes alone stimulated the killing activity in the organs investigated, and upregulated the clearing rate of E. coli from the circulation. Lactoferrin significantly increased both the killing and the clearing activity in these long-term diabetic animals. In some cases the stimulating effect of BLF was very high, suggesting a concerted action of BLF and diabetes in that category of mice. Despite these beneficial effects of BLF and diabetes on the killing process in the investigated organs, the survival time of animals from all the diabetic groups (48 h, 10 and 20 days) was not prolonged by BLF. The protective properties of BLF did not depend on the blood glucose levels in the diabetic animals. BLF partly delayed the development of experimental Alx-induced diabetes, measured by the glucose level, but only if administered shortly after Alx injection. In conclusion, we demonstrated that the state of diabetes alone could increase killing of bacteria in the investigated organs and LF enhanced this process. However, LF had no protective effect against the mortality of diabetic mice infected with a lethal dose of E. coli.