Publications by authors named "Jinzhao Wei"

Within the prefrontal-cingulate cortex, abnormalities in coupling between neuronal networks can disturb the emotion-cognition interactions, contributing to the development of mental disorders such as depression. Despite this understanding, the neural circuit mechanisms underlying this phenomenon remain elusive. In this study, we present a biophysical computational model encompassing three crucial regions, including the dorsolateral prefrontal cortex, subgenual anterior cingulate cortex, and ventromedial prefrontal cortex.

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Infrared neural stimulation (INS), as a novel form of neuromodulation, allows modulating the activity of nerve cells through thermally induced capacitive currents and thermal sensitivity ion channels. However, fundamental questions remain about the exact mechanism of INS and how the photothermal effect influences the neural response. Computational neural modeling can provide a powerful methodology for understanding the law of action of INS.

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As a promising medical imaging modality, electrical impedance tomography (EIT) can image the electrical properties within a region of interest using electrical measurements applied at electrodes on the region boundary. This paper proposes to combine frequency and time difference imaging methods in EIT to simultaneously image bio- and non-conductive targets, where the image fusion is accomplished by applying a wavelet-based technique. To enable image fusion, both time and frequency difference imaging methods are investigated regarding the reconstruction of bio- or non-conductive inclusions in the target region at varied excitation frequencies, indicating that none of those two methods can tackle with the scenarios where both bio- and non-conductive inclusions exist.

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The goal of treatment of metabolic syndrome is the prevention of diabetes and cardiovascular events. A series of novel tetrahydrocoptisine quaternary ammonium compounds were prepared to evaluate their action of hypoglycemia and hypolipidemia for finding the therapeutic agents of metabolic syndrome. Starting from the coptisine hydrochloride (2), fifteen target compounds were synthesized by reduction and substitution of the 7-N position.

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