The positions and widths of the J=0 energy levels of the tdμ molecular ion have been computed including the effects of strong nuclear interaction on the tdμ wave function. The applied formalism incorporates the strong force into the nonadiabatic treatment of tdμ by means of a nuclear surface boundary condition derived from the latest R-matrix parametrization of nuclear scattering data. Accurate basis-set expansions of the tdμ wave functions have been used, including basis functions containing inverse powers of the t-d distance. Relative to the results of adiabatic calculations employing the same nuclear input, the computed energy shifts and widths are reduced by 4% and 8% for the ground and excited states, respectively. Our results are qualitatively consistent with the results of recent nonadiabatic optical potential calculations. The fusion rates derived from our calculations, 1.25×${10}^{12}$ and 1.05×${10}^{12}$ ${\mathrm{s}}^{\mathrm{-}1}$ for the ground and excited states, respectively, are about 15% larger than those given by the standard formula that factorizes the nuclear and molecular effects.

The solution utilized to design a compact transverse electromagnetic mode (TEM)-CPT (circular polarized TE11) mode converter with high power handling capability and high efficiency, especially at high frequency bands is proposed in this paper. The analysis shows that increasing the quantity of the arms of the converter could make the converter work under overmoded state. The problem that the power capability of the converter working at high frequency bands is low will be addressed. To verify the feasibility of this solution, simulations and experiments on a 20 arms converter are carried out, and the results show that the converter would convert the TEM mode into CPT mode efficiently in a 2-3 free wavelengths longitudinal size and that the power capability is in gigawatt (GW) class. Moreover, this kind of converter can also be utilized in the design of GW TEM phase shifter, whether at low or high frequency bands, which plays a key role in the power combining technology.

With the wide application of microwave technology, concerns about its health impact have arisen. The signal transmission mode of the central nervous system and neurons make it particularly sensitive to electromagnetic exposure. It has been reported that abnormal release of amino acid neurotransmitters is mediated by alteration of p-SYN1 after microwave exposure, which results in cognitive dysfunction. As the phosphorylation of SYN1 is regulated by different kinases, in this study we explored the regulatory mechanisms of SYN1 fluctuations following microwave exposure and its subsequent effect on GABA release, aiming to provide clues on the mechanism of cognitive impairment caused by microwave exposure. In vivo studies with Timm and H&E staining were adopted and the results showed abnormality in synapse formation and neuronal structure, explaining the previously-described deficiency in cognitive ability caused by microwave exposure. The observed alterations in SYN1 level, combined with the results of earlier studies, indicate that SYN1 and its phosphorylation status (ser-553 and ser62/67) may play a role in the abnormal release of neurotransmitters. Thus, the role of Cdk5, the upstream kinase regulating the formation of p-SYN1 (ser-553), as well as that of MEK, the regulator of p-SYN1 (ser-62/67), were investigated both in vivo and in vitro. The results showed that Cdk5 was a negative regulator of p-SYN1 (ser-553) and that its up-regulation caused a decrease in GABA release by reducing p-SYN1 (ser-553). While further exploration still needed to elaborate the role of p-SYN1 (ser-62/67) for neurotransmitter release, MEK inhibition had was no impact on p-Erk or p-SYN1 (ser-62/67) after microwave exposure. In conclusion, the decrease of p-SYN1 (ser-553) may result in abnormalities in vesicular anchoring and GABA release, which is caused by increased Cdk5 regulated through Calpain-p25 pathway after 30 mW/cm² microwave exposure. This study provided a potential new strategy for the prevention and treatment of microwave-induced cognitive dysfunction.

A real-time RF exposure setup for studying the mechanism of RF biological effects based on microelectrode array (MEA) is proposed in this letter. The reflection simulation and measurement of the exposure setup show that the exposure setup has a wide working bandwidth in the frequency range of dc-3.0 GHz. The specific adsorption rate (SAR) measurement and simulation results at some frequencies show that the SAR distributions in the electrode region are relatively uniform. The test of the real-time effects on neuron activities at the SAR of 2.2 W/kg with a continuous 2.45-GHz RF signal injection was carried out. The results show that most of the electrodes can work normally and will not be affected by electromagnetic field noise. Additionally, the setup is compact and the system with MEA platform is almost covered by metal, which would significantly improve the ability to isolate the internal and external electromagnetic waves.

In recent years, high-power microwave (HPM) technology has developed rapidly. However, the current research mainly focuses on how to improve its performance and its impact on electronic devices, and there has been relatively little research on its effects on organisms. In particular, the research on the biological effects of HPMs in the X-band is even more limited. The purpose of this paper is to conduct a study on the effects of HPMs in the X-band with a frequency of 9.375 GHz on mood, learning, and cognitive abilities, as well as the antioxidant defense system. Upon observation, it was noted that the mice in the exposed groups, when compared to the control group, did not display significant signs of depression or anxiety. Furthermore, their learning capabilities, memory retention, and cognitive functions remained intact and were not adversely affected. The results of oxidative-stress-related indicators in serum and brain tissue showed increased levels of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), reduced levels of protein carbonyl (PCO) and malondialdehyde (MDA), and no significant changes in reactive oxygen species (ROS). In summary, acute exposure to 9.375 GHz HPM did not cause significant damage to the organisms, and the body could defend against the acute stress caused by HPMs through its own antioxidant system. This investigation provides substantial theoretical foundations and robust experimental evidence for establishing safety parameters and potential biomedical applications of microwave radiation within defined exposure limits.