Reaction mechanism and detecting properties of a novel molecularly imprinted electrochemical sensor for microcystin based on three-dimensional AuNPs@MWCNTs/GQDs.

Microcystins with leucine arginine (MC-LR) is a virulent hepatotoxin, which is commonly present in polluted water with its demethylated derivatives [Dha7] MC-LR. This study reported a low-cost molecularly imprinted polymer network-based electrochemical sensor for detecting MC-LR. The sensor was based on a three-dimensional conductive network composed of multi-walled carbon nanotubes (MWCNTs), graphene quantum dots (GQDs), and gold nanoparticles (AuNPs). The molecularly imprinted polymer was engineered by quantum chemical computation utilizing p-aminothiophenol (p-ATP) and methacrylic acid (MAA) as dual functional monomers and L-arginine as a segment template. The electrochemical reaction mechanism of MC-LR on the sensor was studied for the first time, which is an irreversible electrochemical oxidation reaction involving an electron and two protons, and is controlled by a mixed adsorption-diffusion mechanism. The sensor exhibited a great detection response to MC-LR in the linear range of 0.08-2 µg/L, and the limit of detection (LOD) is 0.0027 µg/L (S/N = 3). In addition, the recoveries of the total amount of MC-LR and [Dha7] MC-LR in the actual sample by the obtained sensor were in the range from 91.4 to 116.7%, which indicated its great potential for environmental detection.

Evolutionary analysis of replicator dynamics about anti-cancer combination therapy.

The emergence and growth of drug-resistant cancer cell subpopulations during anti-cancer treatment is a major challenge for cancer therapies. Combination therapies are usually applied for overcoming drug resistance. In the present paper, we explored the evolution outcome of tumor cell populations under different combination schedules of chemotherapy and p53 vaccine, by construction of replicator dynamical model for sensitive cells, chemotherapy-resistant cells and p53 vaccine-resistant cells. The local asymptotic stability analysis of the evolutionary stable points revealed that cancer population could evolve to the population with single subpopulation, or coexistence of sensitive cells and p53 vaccine-resistant cells, or coexistence of chemotherapy-resistant cells and p53 vaccine-resistant cells under different monotherapy or combination schedules. The design of adaptive therapy schedules that maintain the subpopulations under control is also demonstrated by sequential and periodic application of combination treatment strategies based on the evolutionary velocity and evolutionary absorbing regions. Applying a new replicator dynamical model, we further explored the supportive effects of sensitive cancer cells on targeted therapy-resistant cells revealed in mice experiments. It was shown that the supportive effects of sensitive cells could drive the evolution of cell population from sensitive cells to coexistence of sensitive cells and one type of targeted therapy-resistant cells.