To date, the number of studies reporting use of NUC for prevention of HCC recurrence is limited to four studies, each with small case numbers (10–43) and short treatment duration (12–43 months), so that the results of each study are inconclusive (Table 1). As viral hepatocarcinogenesis progresses through multiple stages and is a multifactorial process, its progression takes years, often decades. Although the efficacy of LAM, ADV and ETV in the tertiary prevention of HCC recurrence is still unsatisfactory, more effective long-term HBV DNA suppression is likely to increase the survival

rate and Alectinib chemical structure probably will significantly reduce the HCC recurrence. In addition, long-term studies will undoubtedly confirm that the effects of ETV or tenofovir in reducing HCC recurrence are similar to or better than those of LAM because of their superior potency, which ensures both lower levels of residual HBV DNA (in serum and liver) and correspondingly

much lower risk of drug resistance. Hence, we await with interest the results of long-term large-scale prospective surveys of clinical outcomes involving these better antiviral regimens. It is also expected that such observations will prove that tertiary prevention of HCC recurrence is possible in patients receiving curative physical treatments (surgical resection or ablation) for HCC. “
“We read with great interest the article by Kamo et al.[1] in which the authors showed that after hepatic ischemia-reperfusion learn more (I/R) injury, inflammasome activation mediated by apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) leads to interleukin-1β (IL-1β) production and subsequently promotes high mobility group box 1(HMGB1) induction, which triggers a Toll-like receptor 4 (TLR4)-driven inflammatory response. Carnitine palmitoyltransferase II Consistent with their findings, we recently showed that ASC-mediated inflammasome activation plays an essential role in the initial inflammatory response after myocardial I/R injury.[2] Recently, it has been shown that inflammasome components such as ASC and NLR family pyrin domain containing 3 (NLRP3) can function independently of inflammasomes. Shigeoka et al.[3]

showed that mice deficient in NLRP3 but not ASC or caspase-1 had reduced renal I/R. Because the inflammasome is defined as a molecular platform that induces caspase-1 activation, they concluded that an NLRP3-dependent and inflammasome-independent pathway contributed to the development of I/R injury in the kidney. Similar to their findings, we observed that hepatic I/R injury was significantly ameliorated in mice deficient for NLRP3 but not ASC. This was inconsistent with the finding of Kamo et al.[1] Although the reason for this discrepancy is unclear, the differences between our study and Kamo et al.’s study are the hepatic I/R protocol used and the extent of injury. We subjected C57BL/6 wild-type mice to hepatic I/R with 60 minutes ischemia of the left lateral and median lobes (i.e.