Remodeling and failure to normalize even after infusion of bevacizumab. On the other hand, the observed mean stO2 levels of figure 5B at different time points in responding tumors fluctuated depending on the patient, but they apparently trended higher than those of the adjacent normal tissues during the observation time window. For example, the No. 2 patient had a responding tumor that showed a gradual increase in stO2 on days 1 and 3 despite attenuation of tHb. This result may explain the effect of bevacizumab, which contributes to normalization of the tumor vasculature and enhances oxygenation. In fact, the No. 2 patient had a better pathological outcome with minimally invasive components at surgery. In the other patients defined as responders, the tumor stO2 levels also varied greatly in response to bevacizumab but remained high during the observation time window. However, these tumors substantially improved stO2 after paclitaxel and then achieved favorable pathological results. Thus, the concomitant change in tumor stO2 may indicate how efficiently tumor oxygenation has recovered following vascular remodeling due to VEGF blockage. In a retrospective study that examined 41 breast cancer patients who underwent neoadjuvant chemotherapy, Ueda et al. reported that elevated baseline levels of tumor stO2 significantly Ergosterol correlated with pCR. In addition, the investigators claimed that tumor reoxygenation exhibited by elevation of tumor O2Hb as early as day 1 after the 14alpha-hydroxy-Sprengerinin-C initiation of cytotoxic chemotherapy, which is called O2Hb flare, was adequate to discriminate nonresponding tumors from both partial and complete responders. These findings were consistent with the current result that showed the significance of tumor oxygenation to improve chemotherapy response. In essence, vascular normalization is considered to occur only in regions of the tumor where the abnormal and immature vasculature of the tumor microenvironment has been corrected by proper dosing and timing of bevacizumab, which would result in sufficient oxygen delivery. In other words, our experience suggests that if vascular remodeling fails, bevacizumab-induced vessel regression may cause more severe hypoxia in the tumor microenvironment. However, a limitation of this preliminary study is that the number of patients was too limited to confirm this speculation. A larger number of patients is needed to verify our findings and provide sufficient evidence to support our speculation concerning the possible effect of bevacizumab in patients with failure of vascular remodeling. In conclusion, this noninvasive optical imaging technique for visualizing vascularity and oxygenation could be useful for tracking the vascular normalization window. Although our findings are not definitive, the initial results suggest that a further study to identify a particular subset of patients who would benefit from bevacizumab may be beneficial. Cirrhosis, live failure, and/or hepatocellular carcinomaare expected to develop in 15%�C40% of patients with CHB without appropriate treatment, and approximately 1 million patients die annually of cirrhosis, liver failure, and HCC as a result of chronic HBV infection. Therefore, the main goal of treatment of chronic infection is to effectively suppress viral replication, preventing liver disease, progression to cirrhosis, liver failure, and HCC. 
Effective antiviral therapy via sustained HBV DNA suppression has become a priority research focus for chronic infection.