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Introduction: Interventional procedures are associated with potentially high radiation doses to the skin. º Monte Carlo codes of radiation transport are considered to be one of the most reliable tools available to assess doses. However, they are usually too time consuming for use in clinical practice. This work presents the validation of the fast Monte Carlo code MC-GPU for application in interventional radiology. Methodologies: MC-GPU calculations were compared against the well-validated Monte Carlo simulation code PENELOPE/penEasy by simulating the organ dose distribution in a voxelized anthropomorphic phantom. In a second phase, the code was compared against thermoluminescent measurements performed on slab phantoms, both in a calibration laboratory and at a hospital. Results: The results obtained from the two simulation codes show very good agreement, differences in the output were within 1%, whereas the calculation time on the MC-GPU was 2500 times shorter. Comparison with measurements is of the order of 10%, within the associated uncertainty. Conclusions: It has been verified that MC-GPU provides good estimates of the dose when compared to PENELOPE program. It is also shown that it presents very good performance when assessing organ doses in very short times, less than one minute, in real clinical set-ups. Future steps would be to simulate complex procedures with several projections.

Cyclin-dependent kinase (Cdk) stimulates resection of DNA double-strand breaks ends to generate single-stranded DNA (ssDNA) needed for recombinational DNA repair. Here we show in Saccharomyces cerevisiae that lack of the Cdk-counteracting phosphatase Cdc14 produces abnormally extended resected tracts at the DNA break ends, involving the phosphatase in the inhibition of resection. Over-resection in the absence of Cdc14 activity is bypassed when the exonuclease Dna2 is inactivated or when its Cdk consensus sites are mutated, indicating that the phosphatase restrains resection by acting through this nuclease. Accordingly, mitotically activated Cdc14 promotes Dna2 dephosphorylation to exclude it from the DNA lesion. Cdc14-dependent resection inhibition is essential to sustain DNA re-synthesis, thus ensuring the appropriate length, frequency, and distribution of the gene conversion tracts. These results establish a role for Cdc14 in controlling the extent of resection through Dna2 regulation and demonstrate that the accumulation of excessively long ssDNA affects the accurate repair of the broken DNA by homologous recombination.

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