Masashi Fujii

This study uses multiomic analysis of skeletal muscle in obese and healthy mice to reveal differences in metabolic regulation by metabolites and genes after glucose administration.

The paper shows that omeprazole disrupts F-actin polarity in sea urchin embryos, leading to partial exogastrulation by affecting secondary invagination.

The paper identifies transcription termination defects at hypomethylated TTSs in Dnmt3a-deficient vertebrates using methylome and transcriptome data.

The paper develops a mathematical model to predict an optimal glucose ingestion pattern that minimizes peak blood glucose levels in humans, validated through experimental testing.

The paper analyzes trans-omic data from healthy and obese mice to reveal that glucose-responsive liver metabolism is regulated by rapid changes in metabolites and gene expression in the healthy state, and by slow transcriptional regulation in the obese state.

The paper shows that small intracellular and large intercellular variations enhance information transmission, enabling precise tissue function control.

The paper uses stochastic simulations to show that small, numerous dendritic spines enhance robustness and efficiency of information transfer by reducing noise impact and increasing parallel processing.

The paper develops a mathematical model to show that bidirectional changes in hepatic and peripheral insulin clearance explain abnormal serum insulin concentration patterns in diabetic subjects.

The paper develops a system identification method using compressed sensing to analyze signaling-decoding systems with different time scales, revealing gene expression responses to signaling activation.

The paper constructs a trans-omic network of insulin action using phosphoproteomic, transcriptomic, and metabolomic data to identify fed and fasting insulin signals.