Our core generated several types of transgenic micea stable humanized ACE2 mice using a combi-CRISPR genetic engineering technique. We hope these mouse models can help to dissect COVID-19 pathogenic mechanismthe interaction(s) between spike proteinACE2 K353.

We have developed the device recorded the neuronal action potential of multiple mouse brainstheir cerebellum with high sampling rate (30 kHz)multiple channels to accelerate the study of the pathogenesis of neurodegenerative diseases. The team hopes to extend the multi-channel BCI devicebrainwave technology to more neurodegenerative disease biomarker analysis to help pharmaceutical companies to explore the pathogenesis of neurodegenerative diseaseshelp in new drug developmentclinical diagnosis.

Our inter-institutional research team developed RS-D7, a novel NMDAR modulator/DAO inhibitor as a drug candidate for the treatment of ataxia/MSA. Based upon the core symptoms, we designedapplied preclinical mouse behavioral phenotyping techniquesclinical motor assessments to demonstrate the effectiveness of RS-D7our functional assays. RS-D7 offers multi-symptomatic relief.

Our previous studies suggested that increase Cisd2 levels may attenuate the pathogenesis of NAFLD/NASH. Accordingly, potent Cisd2 activators with the capacity to enhance Cisd2 levels were identified through the screening of skeletally diverse collections and structural optimization. So far BPRCD0001S0 is the most potent Cisd2 activator obtained, which has been studied extensively. Data obtained revealed that BPRCD0001S0 has no detectable toxicity in vivo, can activate Cisd2 in liver and ameliorate obese-related and fructose-induced NAFLD/NASH.