Visible light communication is a present technology which allows data to be transmitted by modulating information onto a light source. It has many advantages over traditional radio frequency communication and up to 10,000 times larger bandwidth. Many existing research in visible light communication assumes a synchronized channel, however, this is not always easily achieved. This paper proposes a novel synchronized VLC system with the potential to ensure reliable communication in both intra- and inter-vehicle communication. The protocol achieves synchronization at the symbol level using the transistor-transistor logic protocol and achieves frame synchronizations with markers. Consequently, the deployment of the system in both intra- and inter-vehicle communication may present numerous advantages over existing data transmission processes. A practical application where visible light communication is used for media streaming is also previewed. In addition, various regions of possible data transmission are determined to infer forward error correction schemes to ensure reliable communication.

Lipopolysaccharide exerts many effects on many cell lines, including cytokine secretion, and cell apoptosis and necrosis. We investigated the in vitro effects of lipopolysaccharide on apoptosis of cultured human dental pulp cells and the expression of Bcl-2 and Bax. Dental pulp cells showed morphologies typical of apoptosis after exposure to lipopolysaccharide. Flow cytometry showed that the rate of apoptosis of human dental pulp cells increased with increasing lipopolysaccharide concentration. Compared with controls, lipopolysaccharide promoted pulp cell apoptosis (P < 0.05) from 0.1 to 100 μg/mL but not at 0.01 μg/mL. Cell apoptosis was statistically higher after exposure to lipopolysaccharide for 3 days compared with 1 day, but no difference was observed between 3 and 5 days. Immunohistochemistry showed that expression of Bax and Bcl-2 was enhanced by lipopolysaccharide at high concentrations, but no evident expression was observed at low concentrations (0.01 and 0.1 μg/mL) or in the control groups. In conclusion, lipopolysaccharide induced dental pulp cell apoptosis in a dose-dependent manner, but apoptosis did not increase with treatment duration. The expression of the apoptosis regulatory proteins Bax and Bcl-2 was also up-regulated in pulp cells after exposure to a high concentration of lipopolysaccharide.