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Various ionizing radiations, such as electrons and alpha particles, transfer their energy to media by produced secondary electrons and induce double- or single-strand break of DNA, which result in variable effects. To understand how the ionizing radiations interact with DNA and break it, several models have been developed, most of them consider the water as a vapor state. Actually, the ionizing particles interact with DNA which is solved in liquid water. To compare the difference of vapor and liquid water models, we calculate the stopping power, continuous slowing down approximation (CSDA) range and S value of electrons and alpha particles at cellular scale in liquid and vapor by Monte Carlo simulations, respectively. Our data show that the stopping power and CSDA range are different in liquid and vapor water in a special energy range. For many S values, the liquid model is better than the vapor model when the energy of the electrons is higher than 100 keV and the vapor model is higher than the liquid model for the 1 MeV alpha particles. [ABSTRACT FROM AUTHOR]

To reveal the saddle-type dose effect relationship, we propose a radiation mutagenesis model based on maize nutrition difference resulting from heavy ion 7Li radiation. Through irradiation mutagenesis, apparent trait selection, amino acids and fatty acids content determination, and modeling, dynamic evolution from microscopic damage and repair initiation to the final macroscopic biological effects are considered simultaneously. The results show that the steady state nature is independent of evolution time and only relates to different radiation doses. Heavy ion 7Li radiation could effectively cause maize phenotypic variation and could improve nutritional quality. This model not only gives a good fit to the experimental results on most types of amino acids and fatty acids, but also offers an adequate explanation of the experimental phenomenon underlying the saddle-type bimodal dose effect. By combining experimental results with theoretical analyses, we suggest that the synergy of the stimulus effect and momentum transfer is the main cause of the saddle-type dose effect bimodal curve. This provides an effective strategy for conducting maize germplasm innovation. [ABSTRACT FROM AUTHOR]

We computationally study the possible effects of thermosensitive transient receptor potential (TRP) channels on the spontaneous calcium oscillations in astrocytes at various temperatures. Based on the previous model and the result of thermosensitive TRP channels’ open probabilities, some meaningful conclusions are obtained. It is shown that the occurrence of calcium oscillations depends on temperature and the molar heat capacity difference between the closed and open channels (). The data indicate that calcium oscillations in astrocytes occurred in the ranges of 7 °C–11 °C and 27 °C–30 °C whenis, and calcium oscillations only occur in the range of 27 °C–30 °C whenis. In this study, the frequency decreases rapidly at temperatures ranging from 7 °C to 11 °C, and there is a contrary result in the range of 27 °C–30 °C. [ABSTRACT FROM AUTHOR]

As a member of the inwardly rectifying channel (Kir) family, Kir2.1 allows to influx the cell more easily than to efflux, a biophysical phenomenon named inward rectification. The function of Kir2.1 is to set the resting membrane potential and modulate membrane excitability. It has been reported that residue E224 plays a key role in regulating inward rectification. The mutant Kir2.1 (E224G) displays weaker inward rectification than the WT channel. Gating of Kir2.1 depends on the membrane lipid, PIP2, such that the channel gates are closed in the absence of PIP2. Here we perform electrophysiological and computational approaches, and demonstrate that E224 also plays an important role in the PIP2-dependent activation of Kir2.1 in addition to its influence on inward rectification. The E224G mutant takes 4.5 times longer to be activated by PIP2. To probe the mechanism by which E224G slows the channel opening kinetics, we perform targeted molecular dynamics simulations and find that the mutant weakens the interactions between CD-loop and C-linker (H221-R189) and the adjacent G-loops (R312-E303) which are thought to stabilize the open state of the channel in our previous work. These data provide new insights into the regulation of Kir2.1 channel activity and suggest that a common mechanism may be involved in the distinct biophysical processes, such as inward rectification and PIP2-induced gating. [ABSTRACT FROM AUTHOR]