The present paper has two main objectives: (1) to create a digital twin of an onshore wind turbine to provide to the owner of the wind farm a tool for continuous tracking of accumulated fatigue damage and evaluation of alternative operation strategies; (2) to perform the first tasks for the creation a reliable numerical of a floating wind turbine to simulate experimental data for the testing of monitoring tools on this type of wind turbines. A numerical model of an onshore wind turbine was created with FAST software developed by the US National Renewable Energy Laboratory (NREL). The structural and mechanical properties of the structure were calculated from the geometric properties of the tower and blades. The aerodynamic properties of different sections of the blades were computed with 2D models created with ANSYS Fluent. Having the wind turbine fully characterised, the control mechanisms were calibrated using data from the manufacturer catalogues. Numerous time series of wind excitation for different operation conditions were generated, and the structural response computed. Additionally, the Supervisory Control and Data Acquisition (SCADA) operating in parallel with a series of extensometers and accelerometers located in strategic points along a real wind turbine tower and blades provided a full description of the internal forces in both locations and the estimation of the modal properties for different operating conditions. Both measured and simulated response allowed the identification and validation of structural dynamic properties and static and dynamic internal loads. In spite of several approximations and simplifications, the results obtained with the numerical model were in good agreement with the ones measured in the field.

Repairing damage and errors that occur in the DNA molecule is essential to maintain the integrity of the genome and cell viability. Deficits in DNA repair mechanisms lead to an increased risk of genetic instability and contribute to neoplastic transformation. Poly (ADP-ribose) polymerases (PARP) are a group of enzymes that play a key role in signalling and repairing DNA errors. The inhibition of its activity is a therapeutic strategy that takes advantage of the mechanism of synthetic lethality and that can be used in the treatment of tumours with specific defects in DNA repair pathways, namely in tumours with mutations in the tumour suppressor genes BRCA1 and BRCA2. There are several PARP inhibitors (iPARP), already approved by the USA Food and Drug Administration and the European Medicines Agency used in the treatment of breast, ovarian, pancreatic and prostate cancer. However, as with other target therapies, despite being well tolerated and widely used in the clinical practice, iPARP resistance is common and can be developed through various molecular mechanisms. In this article, we intend to make an updated review on iPARP and its main role in tumour cells, highlighting the several resistance mechanisms that have been recently revealed, as well as the current clinical applications and toxicity associated with this target therapy.