Lambertball4431

The aim of this study was to measure the occupational exposure using active personal dosimeters (APD) in the PET/CT department at different stages of the operation chain i.e. radiopharmaceutical arrival, activity preparation, dispensing, injection, patient positioning, discharge and compare the radiation exposure doses received using two automatic injection/infusion systems. This paper also reflects optimization processes that were performed to reduce occupational exposure.

Measured APD data were analysed for medical physicists, radiology technologists and administrative staff from 2014 till 2018. For dispensing and injecting

F-FDG, the automatic infusion/injection system IRIDE (Comecer, Italy) or the automatic fractionator ALTHEA (Comecer, Italy) with wireless injection system WIS (Comecer, Italy) were used. Radiation exposure optimization methods were applied during the data collection period (installation of the transport port, patient management, APD alarm threshold and etc.).

Radiology technologists who perform injection procedures, regardless of the automatic infusion system, received the highest radiation exposure dose. The average doses to the radiology technologists per one study were 1.72±0.33 μSv and 1.16±0.11 μSv with ALTHEA/WIS and IRIDE system, respectively. The average dose for accompanying the patient to the PET/CT scanner and scan procedure was 0.52±0.07 μSv. For the medical physicists, the average dose was 0.29±0.09 µSv. The measured dose for administrative staff was 0.30±0.15 μSv.

Occupational exposure can be effectively optimized by different means including staff monitoring with APD, implementation of radiation safety culture and the usage of automatic infusion systems.

Occupational exposure can be effectively optimized by different means including staff monitoring with APD, implementation of radiation safety culture and the usage of automatic infusion systems.

To test the performances of a volumetric arc technique named ViTAT (Virtual Tangential-fields Arc Therapy) mimicking tangential field irradiation for whole breast radiotherapy.

ViTAT plans consisted in 4 arcs whose starting/ending position were established based on gantry angle distribution of clinical plans for right and left-breast. MEK activation The arcs were completely blocked excluding the first and last 20°. Different virtual bolus densities and thicknesses were preliminarily evaluated to obtain the best plan performances. For 40 patients with tumor laterality equally divided between right and left sides, ViTAT plans were optimized considering the clinical DVHs for OARs (resulting from tangential field manual planning) to constrain them ViTAT plans were compared with the clinical tangential-fields in terms of DVH parameters for both PTV and OARs.

Distal angle values were suggested in the ranges [220°,240°] for the right-breast and [115°,135°] for the left-breast cases; medial angles were [60°,40°] for the right side and [295°,315°] for the left side, limiting the risk of collision. The optimal virtual bolus had -500 HU density and 1.5cm thickness. ViTAT plans generated dose distributions very similar to the tangential-field plans, with significantly improved PTV homogeneity. The mean doses of ipsilateral OARs were comparable between the two techniques with minor increase of the low-dose spread in the range 2-15Gy (few % volume); contralateral OARs were slightly better spared with ViTAT.

ViTAT dose distributions were similar to tangential-fields. ViTAT should allow automatic plan optimization by developing knowledge-based DVH prediction models of patients treated with tangential-fields.

ViTAT dose distributions were similar to tangential-fields. ViTAT should allow automatic plan optimization by developing knowledge-based DVH prediction models of patients treated with tangential-fields.The DNA damage response (DDR) is necessary to maintain genome integrity and prevent the accumulation of oncogenic mutations. Consequently, proteins involved in the DDR often serve as tumor suppressors, carrying out the crucial task of keeping DNA fidelity intact. Mediator of DNA damage checkpoint 1 (MDC1) is a scaffold protein involved in the early steps of the DDR. MDC1 interacts directly with γ-H2AX, the phosphorylated form of H2AX, a commonly used marker for DNA damage. It then propagates the phosphorylation of H2AX by recruiting ATM kinase. While the function of MDC1 in the DDR has been reviewed previously, its role in cancer has not been reviewed, and numerous studies have recently identified a link between MDC1 and carcinogenesis. This includes MDC1 functioning as a tumor suppressor, with its loss serving as a biomarker for cancer and contributor to drug sensitivity. Studies also indicate that MDC1 operates outside of its traditional role in DDR, and functions as a co-regulator of nuclear receptor transcriptional activity, and that mutations in MDC1 are present in tumors and can also cause germline predisposition to cancer. This review will discuss reports that link MDC1 to cancer and identify MDC1 as an important player in tumor formation, progression, and treatment. We also discuss mechanisms by which MDC1 levels are regulated and how this contributes to tumor formation.Unrepaired, or misrepaired, DNA damage can contribute to the pathogenesis of a number of conditions, or disease states; thus, DNA damage repair pathways, and the proteins within them, are required for the safeguarding of the genome. Human SNM1A is a 5'-to-3' exonuclease that plays a role in multiple DNA damage repair processes. To date, most data suggest a role of SNM1A in primarily ICL repair SNM1A deficient cells exhibit hypersensitivity to ICL-inducing agents (e.g. mitomycin C and cisplatin); and both in vivo and in vitro experiments demonstrate SNM1A and XPF-ERCC1 can function together in the 'unhooking' step of ICL repair. SNM1A further interacts with a number of other proteins that contribute to genome integrity outside canonical ICL repair (e.g. PCNA and CSB), and these may play a role in regulating SNM1As function, subcellular localisation, and post-translational modification state. These data also provide further insight into other DNA repair pathways to which SNM1A may contribute. This review aims to discuss all aspects of the exonuclease, SNM1A, and its contribution to DNA damage tolerance.