Biomedical subjects

Jiachang Yue

Publications and source records attributed to Jiachang Yue.

3 recordsLinked to original sources

PubMed2006

Constructing a novel Nanodevice powered by delta-free FoF1-ATPase.

A Nanodevice was constructed by delta-free F(o)F(1)-ATPase within chromatophores and actin filaments through biotinlipid-streptavidin-biotin-(AC(5))(2)Sulfo-OSu system. One actin filament linking with many chromatophores functions as the Nanodevice body and many delta-free F(o)F(1)-ATPase as the Nanodevice motors. Movement of the Nanodevice was observed directly by fluorescence microscopy with CCD camera after illumination. The moving speed was about 2.17-24.43mum/s for various length Nanodevices and most of them were stopped by adding CCCP. This means that the Nanodevice was driven by PMF (proton-motive force) in the cooperating delta-free F(o)F(1)-ATPase. From bioengineering point of view, the cooperation of F(o)F(1)-ATPase is a very important research field in the future.

Actins↗

PubMed2006

F0F1-ATPase as biosensor to detect single virus.

F(0)F(1)-ATPase within chromatophore was constructed as a biosensor (immuno-rotary biosensor) for the purpose of capturing single virus. Capture of virus was based on antibody-antigen reaction. The detection of virus based on proton flux change driven by ATP-synthesis of F(0)F(1)-ATPase, which was indicated by F1300, was directly observed by a fluorescence microscope. The results demonstrate that the biosensor loading of virus particles has remarkable signal-to-noise ratio (3.8:1) compared to its control at single molecular level, and will be convenient, quick, and even super-sensitive for detecting virus particles.

Biosensing Techniques↗

PubMed2002

Association of the phosphatidylinositol signal pathway with prolonged myocardial ischemia.

OBJECTIVE: To study the changes in activity of phosphatidylinositol 4 kinase (PI 4 kinase), phosphatidylinositol 4 phosphate 5 kinase (PIP 5 kinase) and protein kinase C (PKC) during myocardial ischemia and elucidate the relationship between phosphatidylinositol signal pathways and prolonged myocardial ischemia. METHODS: In vivo an ischemic rat model was used. Activity of PI 4 kinase, PIP 5 kinase and PKC were measured at different times in postischemic heart cells using isotope analysis. RESULTS: The activity of PI kinase, PIP kinase and PKC in the myocardium increased to peak at 1 hour postischemia, with activities 6.1, 3.0 and 4.0 fold over control levels, respectively. Their activities declined to normal levels with time. CONCLUSION: The phosphatidylinositol signal pathway is involved in prolonged myocardial ischemia, but its mechanism needs further study.

1-Phosphatidylinositol 4-Kinase↗