Holographic recording mechanisms of gratings in indium oxide films using 325nm Helium-Cadmium laser irradiation

UV (325 nm) holographic recording of gratings in indium oxide films fabricated by reactive pulsed laser deposition has been investigated as a function of growth temperature, oxygen pressure and angle of incidence of the plasma plume on the substrate. The influence of the ambient environment (air or vacuum) and the film temperature during recording has also been studied. Large steady state refractive index changes up to 6×10-3 were observed in layers grown at an oblique angle of 75°. About 77% of the magnitude of these changes residues after thermal annealing and is attributed to UV-induced permanent structural rearrangements. In contrast, refractive index changes in films grown at normal incidence were smaller in magnitude and completely reversible

The Temozolomide–Doxorubicin paradox in Glioblastoma in vitro–in silico preclinical drug-screening

Abstract Adjuvant Temozolomide is considered the front-line Glioblastoma chemotherapeutic treatment; yet not all patients respond. Latest trends in clinical trials usually refer to Doxorubicin; yet it can lead to severe side-effects if administered in high doses. While Glioblastoma prognosis remains poor, little is known about the combination of the two chemotherapeutics. Patient-derived spheroids were generated and treated with a range of Temozolomide/Doxorubicin concentrations either as monotherapy or in combination. Optical microscopy was used to monitor the growth pattern and cell death. Based on the monotherapy experiments, we developed a probabilistic mathematical framework in order to describe the drug-induced effect at the single-cell level and simulate drug doses in combination assuming probabilistic independence. Doxorubicin was found to be effective in doses even four orders of magnitude less than Temozolomide in monotherapy. The combination therapy doses tested in vitro were able to lead to irreversible growth inhibition at doses where monotherapy resulted in relapse. In our simulations, we assumed both drugs are anti-mitotic; Temozolomide has a growth-arrest effect, while Doxorubicin is able to cumulatively cause necrosis. Interestingly, under no mechanistic synergy assumption, the in silico predictions underestimate the in vitro results. In silico models allow the exploration of a variety of potential underlying hypotheses. The simulated-biological discrepancy at certain doses indicates a supra-additive response when both drugs are combined. Our results suggest a Temozolomide–Doxorubicin dual chemotherapeutic scheme to both disable proliferation and increase cytotoxicity against Glioblastoma