ObjectiveLarge (≥20 mm) sessile serrated lesions (L-SSL) are premalignant lesions that require endoscopic removal. Endoscopic mucosal resection (EMR) is the existing standard of care but carries some risk of adverse events including clinically significant post-EMR bleeding and deep mural injury (DMI). The respective risk-effectiveness ratio of piecemeal cold snare polypectomy (p-CSP) in L-SSL management is not fully known.DesignConsecutive patients referred for L-SSL management were treated by p-CSP from April 2016 to January 2020 or by conventional EMR in the preceding period between July 2008 and March 2016 at four Australian tertiary centres. Surveillance colonoscopies were conducted at 6 months (SC1) and 18 months (SC2). Outcomes on technical success, adverse events and recurrence were documented prospectively and then compared retrospectively between the subsequent time periods.ResultsA total of 562 L-SSL in 474 patients were evaluated of which 156 L-SSL in 121 patients were treated by p-CSP and 406 L-SSL in 353 patients by EMR. Technical success was equal in both periods (100.0% (n=156) vs 99.0% (n=402)). No adverse events occurred in p-CSP, whereas delayed bleeding and DMI were encountered in 5.1% (n=18) and 3.4% (n=12) of L-SSL treated by EMR, respectively. Recurrence rates following p-CSP were similar to EMR at 4.3% (n=4) versus 4.6% (n=14) and 2.0% (n=1) versus 1.2% (n=3) for surveillance colonoscopy (SC)1 and SC2, respectively.ConclusionsIn a historical comparison on the endoscopic management of L-SSL, p-CSP is technically equally efficacious to EMR but virtually eliminates the risk of delayed bleeding and perforation. p-CSP should therefore be considered as the new standard of care for L-SSL treatment.

Hepatitis B virus (HBV) is a small DNA virus responsible for significant morbidity and mortality worldwide. The liver, which is the main target organ for HBV infection, provides the virus with the machinery necessary for persistent infection and propagation, a process that might ultimately lead to severe liver pathologies such as chronic hepatitis, cirrhosis and liver cancer. HBV gene expression is regulated mainly at the transcriptional level by recruitment of a whole set of cellular transcription factors (TFs) and coactivators to support transcription. Over the years, many of these TFs were identified and interestingly enough most are associated with the body's nutritional state. These include the hepatocyte nuclear factors, forkhead Box O1, Farnesoid X receptor, cyclic-AMP response element-binding (CREB), CCAAT/enhancer-binding protein (C/EBP) and glucocorticoid receptor TFs and the transcription coactivator PPARg coactivator-1a. Consequently, HBV gene expression is linked to hepatic metabolic processes such as glucose and fat production and utilization as well as bile acids' production and secretion. Furthermore, recent evidence indicates that HBV actively interferes with some of these hepatic metabolic processes by manipulating key TFs, such as CREB and C/EBP, to meet its requirements. The discovery of the mechanisms by which HBV is controlled by the hepatic metabolic milieu may broaden our understanding of the unique regulation of HBV expression and may also explain the mechanisms by which HBV induces liver pathologies. The emerging principle of the intimate link between HBV and liver metabolism can be further exploited for host-targeted therapeutic strategies.Hepatitis B virus (HBV) is a major global health burden, with approximately 350 million people chronically infected worldwide. HBV infection results in an acute infection that may evolve into a chronic disease, a medical state that carries a significant risk for serious liver pathologies including cirrhosis and hepatocellular carcinoma. About 1.2 million deaths a year are attributed to chronic HBV infection and its complications (1, 2).Hepatitis B virus has an extremely compact, partially double-stranded DNA genome approximately 3.2 kb in length, encoding four main gene products. Viral gene expression is controlled mainly at the transcriptional level, via four promoters and two enhancers (2-7) (Fig. 1). The Enhancer I element is located upstream to the Hepatitis B X (HBx) open reading frame and is activated by ubiquitous transcription factors (TFs) such as CCAAT/enhancer-binding protein (C/EBP), cyclic-AMP (cAMP) response element-binding (CREB), Ap-1, cAbl and RFX1 as well as by hepatocyte nuclear factor (HNF) 3 (FoxA) and the liver-enriched nuclear receptor (NR) .Enhancer II activation is liver-specific, owing to the large number of liver-enriched TFs and NRs recruited: C/ EBP, forkhead Box O1 (FoxO1), HNF3/FoxA, HNF4a, oestrogen-related receptors, Farnesoid X receptor (FXR) and peroxisome proliferator-activated receptors (PPARs) (4,(11)(12)...

a b s t r a c tHepatitis B virus (HBV) infects the liver and uses its cell host for gene expression and propagation. Therefore, targeting host factors essential for HBV gene expression is a potential anti-viral strategy. Here we show that treating HBV expressing cells with the natural phenolic compound curcumin inhibits HBV gene expression and replication. This inhibition is mediated via down-regulation of PGC-1a, a starvation-induced protein that initiates the gluconeogenesis cascade and that has been shown to robustly coactivate HBV transcription. We suggest curcumin as a host targeted therapy for HBV infection that may complement current virus-specific therapies.

ErratumErratum to ''Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1a" [FEBS Lett. 584 (2010) In the last stages of the production process of the printed version, after the authors' proof had been returned, an unfortunate error was made in the list of the names of authors. The correct names and affiliations are given above.