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Titanium has been widely used in prosthetic valves, but they are associated with serious defects in titanium‐based prosthetic valves, such as thrombosis, calcification, and decay. Therefore, it is very important to biofunctionalize titanium‐based valves to reduce inflammation and accelerate endothelialization of stents and antithrombosis. The titanium dioxide nanotubes were prepared from pure titanium (Ti) by anodic oxidation method in this study. The effects of titanium dioxide nanotubes on the metabolism of macrophages and the inflammatory reaction as implants were studied in vitro. The polarization state of macrophages and the ability to accelerate endothelialization were analyzed. The results demonstrated that titanium nanotubes promote M2 polarization of macrophages by inhibiting glycolysis and activating the Adenosine monophosphate‐activated protein kinase (AMPK) signaling pathway. In general, biofunctionalization titanium with nanotube could inhibit macrophage glycolysis, reduce inflammatory factor release and promote M2 polarization by activating the AMPK signaling pathway. And endothelialization was accelerated in vitro. Our result demonstrated that titanium nanotube could act as a potential approach to biofunctionlize titanium‐based prosthetic valves for endothelialization., Biofunctionalization titanium with nanotube could inhibit macrophage glycolysis, reduce inflammatory factor release and promote M2 polarization by activating the adenosine monophosphate‐activated protein kinase (AMPK) signaling pathway. And endothelialization was accelerated in vitro. Our result demonstrated that titanium nanotube could act as a potential approach to biofunctionlize titanium‐based prosthetic valves for endothelialization

Concurrent with a phase-II trial of 4HPR in patients with various cancers, we studied the plasma pharmacokinetics of both 4HPR and its major metabolite 4MPR as well as the effect of 4HPR administration on plasma retinol concentrations using a simple, specific and sensitive HPLC procedure. Initial estimates of plasma pharmacokinetic parameters after oral administration of 4HPR (300 mg/day) [corrected] in 3 cancer patients were the following: 4HPR, t beta 1/2 = 13.7 hr, AUC = 3.49 micrograms.hr/ml, CL = 56.57 L/hr/m2; 4MPR, t beta 1/2 = 23.0 hr, AUC = 1.15 micrograms.hr/ml, CL = 239.29 L/hr/m2. We also found that oral administration of 4HPR resulted in a rapid, profound and significant reduction in plasma retinol concentrations. The mean plasma retinol concentrations for 9 patients decreased 60% from baseline to below 200 ng/ml within 1-2 weeks of 4HPR dosing initiation. In addition, there was a concurrent, significant reduction in plasma retinol-binding protein levels in these patients. The mechanism whereby 4HPR reduces plasma retinol levels in vivo has not been determined. The addition of 4HPR to pooled human plasma at 37 degrees C in vitro did not reduce endogenous retinol levels, suggesting no direct chemical interaction between these 2 retinoids.