ESR and TL dosimetry systems: comparative measurements for human phantom.

Mixtures of small fragments of tooth enamel as well as thermoluminescence (TL) dosimeters were placed into the tissue-equivalent phantom of the human head with skeleton (approximately at the level of the jaws) and irradiated using 137Cs low dose-rate gamma therapeutic sources ('SELEKTRON' LDR 137Cs). Phantom, samples of teeth and TL detectors were irradiated behind water tank to produce scattered irradiation. The same irradiation with the same geometry was performed in air too. For gamma-spectrometry 137Cs sources with very low activity were used but with the same geometry as therapeutic sources. The absorbed dose in enamel was estimated with the help of ESR spectrometer 'ESP-300 E' (Brucker). The samples of tooth enamel were partially used for preliminary dose evaluation by ESR signal before starting of experiment. TL dosimetry was performed by TL reader model 8800 (HARSHAW) using TL dosimeters calibrated with 137Cs. The paper presents data obtained in comparative aspects.

The state of actin assembly regulates actin and vinculin expression by a feedback loop.

Actin filaments are major determinants of cell shape, motility and adhesion, which control important biological processes including embryonic development and wound healing. These processes are associated with changes in actin assembly, which is regulated by controlling the balance between polymerized and non-polymerized actin. To maintain a significant pool of non-polymerized actin, mechanism(s) linking actin synthesis to its state of polymerization were proposed. We have studied this relationship between actin synthesis and organization by modulating actin assembly using different drugs. Unassembled actin was increased in 3T3 cells using either the Clostridium botulinum C2 toxin, which ADP-ribosylates actin, or by latrunculin A, a Red Sea sponge product, which binds monomeric actin. The synthesis of actin was dramatically reduced in these cells owing to a concomitant decrease in actin RNA level. Similar results were obtained with HeLa cells grown in both monolayer and in suspension, suggesting that cell shape changes associated with drug treatment are not the primary cause for the effect on actin synthesis. In contrast, the scrape-loading of 3T3 cells with phalloidin, a stabilizer of polymerized actin that increased the level of assembled actin, resulted in elevated actin synthesis and RNA content. The expression of vinculin, a major component of adhesion plaques and cell-cell junctions, which is involved in actin-membrane associations, was altered in parallel with that of actin in cells treated with these drugs. The decrease in actin RNA resulted from destabilization of actin mRNA in cells where unassembled actin level was elevated. This is suggested by the unchanged transcription of actin in isolated nuclei from drug-treated cells, and by demonstrating that actin mRNA was degraded faster in cells after C2 toxin treatment than in control cells. This feedback control mechanism is mainly confined to the cytoplasm, as it remained active in enucleated cells. The results suggest the existence of an autoregulatory pathway for the expression of actin and other microfilament-associated proteins which is linked to the state of actin polymerization in the cell.