Inhibitory Effect on the Tyrosinase Activity and Low Cytotoxicity of Monounsaturated Long-Chain Chelating Fatty Ester.

In the present study, 5-Hydroxy-2-(Oleoyloxymethyl) -4H-pyran-4-one (KMO 3), and their chelated with Cu(II) and Fe(III) ions were synthesized to explore their inhibitory activity against tyrosinase and cytotoxicity. To this end, the structures of the obtained compounds were confirmed by ATR/FT-IR, 13C and 1H-NMR, and UV-vis techniques. The results show that chelating fatty ester presents the bands at 1567m, 1511w cm-1 attributed to the coordinated carbonyl (Cu(II)←[O=C]2), and the bands at 1540m, 1519m cm-1 which were attributed to the coordinated carbonyl (Fe(III)←[O=C]3).

Durvalumab as consolidation therapy in patients who received chemoradiotherapy for unresectable stage III NSCLC: Real-world data from an expanded access program in Brazil (LACOG 0120).

Objective: The PACIFIC trial established standard therapy for patients with unresectable stage III NSCLC who did not progress after platinum-based concurrent chemoradiation therapy. However, real-world data, particularly from Latin America, remain limited. The LACOG 0120 study aimed to evaluate the efficacy and safety of consolidation therapy with durvalumab in a real-world setting in Brazil.

Modeling tumor dynamics and predicting response to chemo-, targeted-, and immune-therapies in a murine model of pancreatic cancer.

We seek to establish a parsimonious mathematical framework for understanding the interaction and dynamics of the response of pancreatic cancer to the NGC triple chemotherapy regimen (mNab-paclitaxel, gemcitabine, and cisplatin), stromal-targeting drugs (calcipotriol and losartan), and an immune checkpoint inhibitor (anti-PD-L1). We developed a set of ordinary differential equations describing changes in tumor size (growth and regression) under the influence of five cocktails of treatments. Model calibration relies on three tumor volume measurements obtained over a 14-day period in a genetically engineered pancreatic cancer model (KrasLSLG12D-Trp53LSLR172H-Pdx1-Cre).

Exploring the antivirulence potential of phenolic compounds to inhibit quorum sensing in Pseudomonas aeruginosa.

Bacteria coordinate gene expression in a cell density-dependent manner in a communication process called quorum sensing (QS). The expression of virulence factors, biofilm formation and enzyme production are QS-regulated phenotypes that can interfere in human health. Due to this importance, there is great interest in inhibiting QS, comprising an anti-virulence strategy.