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This study is registered at ClinicalTrials.gov (NCT01267344). All patients gave written informed consent.

Hepatitis B virus (HBV) infection can cause a wide spectrum of sequelae, ranging from asymptomatic chronic infection to chronic active hepatitis. Three hundred million people around the world are chronically infected with HBV (38, 39). Clinically, it is estimated that 5 to 10% of HBV-infected adults will develop chronic hepatitis (CH) and will thus be at a higher (Ͼ100 times) risk of developing hepatocellular carcinoma (HCC) (1,12,41). Several viral and host factors have been suggested to be involved in the chronicity and diversity of HBV-associated disease (25, 43). The association, at the molecular level, between HBV infection and HBV-related diseases remains unclear.The small, 3.2-kb DNA genome of HBV contains four known open reading frames, called S, C, P, and X. The hepatitis B virus X (HBx) gene is the smallest, with a length of 465 nucleotides (10). HBx protein is 154 amino acids long, with a molecular weight (MW) of 17,000, and is conserved among all mammalian hepadnaviruses, but the deduced amino acid sequence of the HBx gene product does not correspond to any known viral proteins (26). Although the HBx protein has been shown to stimulate cell cycle progression of quiescent cells (18), it is mainly a pleiotropic transactivator, due to its ability to stimulate not only the HBV promoter and enhancer (28, 33) but also a wide range of other viral promoters (33,35,40). The necessity for HBx gene expression during the viral life cycle, in vitro and in vivo, has been suggested (3, 44). The HBx protein acts either through interaction with other cellular transcription factors or via a signal transduction pathway controlled by protein kinase C (15, 30, 31). As a consequence of its activity, the HBx protein appears capable of inducing transformation (32) and liver tumors in a selected strain of mice that express the HBx protein from a transgene (16,17).During the natural course of HBV infection, the HBx gene expresses a polypeptide, HBx, that is implicated in HBV-mediated HCC (4, 16). When liver tissue samples from HCC and CH patients were reacted with an anti-HBx antibody and evaluated by immunohistochemistry, reactive antigen was detected in 80% of HCC liver samples and 30% of CH liver samples (4). In another study, the sera of patients with acute hepatitis, CH, and cirrhosis were tested for HBx protein and anti-HBx antibodies by an enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody and recombinant HBx protein.The results indicated that 23% of patients' sera were HBx positive and 14% of patients' sera were anti-HBx positive (20). In another approach, using HBx oligopeptides as antigens to detect antibodies in the sera of HCC patients, 73% of HCC sera tested positive for anti-HBx antibodies (27). With similar approaches, data showed that 74% of sera from patients with cirrhosis and 54% of sera from patients with HCC were positive for anti-HBx antibodies and HBV surface antigen (HBs) (36). Therefore, the expression of HBx protein in infected patients did not correlate well with the occurrence of...

Ferroelectric photoelectrodes, other than conventional semiconductors, are alternative photo-absorbers in the process of water splitting. However, the capture of photons and efficient transfer of photo-excited carriers remain as two critical issues in ferroelectric photoelectrodes. In this work, we overcome the aforementioned issues by decorating the ferroelectric BiFeO3 (BFO) surface with Au nanocrystals, and thus improving the photoelectrochemical (PEC) performance of BFO film. We demonstrate that the internal field induced by the spontaneous polarization of BFO can (1) tune the efficiency of the photo-excited carriers' separation and charge transfer characteristics in bare BFO photoelectrodes, and (2) modulate an extra optical absorption within the visible light region, created by the surface plasmon resonance excitation of Au nanocrystals to capture more photons in the Au/BFO heterostructure. This study provides key insights for understanding the tunable features of PEC performance, composed of the heterostructure of noble metals and ferroelectric materials.

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BackgroundGossypiboma is a term used to describe a mass that forms around a cotton sponge or abdominal compress accidentally left in a patient during surgery. Transmural migration of an intra-abdominal gossypiboma has been reported to occur in the digestive tract, bladder, vagina and diaphragm. Open surgery is the most common approach in the treatment of gossypiboma. However, gossypibomas can be extracted by endoscopy while migrating into the digestive tract. We report a case of intractable duodenal ulcer caused by transmural migration of gossypiboma successfully treated by duodenorrhaphy. A systemic literature review is provided and a scheme of the therapeutic approach is proposed.Case presentationA 61-year-old Han Chinese man presented with intermittent epigastric pain for the last 10 months. He had undergone laparoscopic cholecystectomy conversion to open cholecystectomy for acute gangrenous cholecystitis 10 months ago at another hospital. Transmural migration of gossypiboma into the duodenum was found. Endoscopic intervention failed to remove the entire gauze, and duodenal ulcer caused by the gauze persisted. Surgical intervention was performed and the gauze was removed successfully. The penetrated ulcer was repaired with duodenorrhaphy. The postoperative period was uneventful.We systematically reviewed the literature on transmural migration of gossypiboma into duodenum and present an overview of published cases. Our PubMed search yielded seven reports of transmural migration of retained surgical sponge into the duodenum. Surgical interventions were necessary in two patients.ConclusionTransmural migration of gossypiboma into the duodenum is a rare surgical complication. The treatment strategies include endoscopic extraction and surgical intervention. Prompt surgical intervention should be considered for emergent conditions such as active bleeding, gastrointestinal obstruction, or intra-abdominal sepsis. For non-emergent conditions, surgical intervention could be considered for intractable cases in which endoscopic extraction failed.

Metabolic risk factors, such as obesity, fatty liver, high lipidemia, and diabetes mellitus are associated with increased risk for nonviral hepatocellular carcinoma (HCC); however, few nonviral HCC studies have stratified patients according to underlying etiologies. From 2005 to 2011, 3,843 patients with HCC were recruited into the Taiwan Liver Cancer Network. Of these patients, 411 (10.69%) who were negative for hepatitis B virus (HBV), surface antigen, HBV DNA, and anti‐hepatitis C virus (HCV) antibody were classified as non‐HBV non‐HCV (NBNC)‐HCC. Detailed clinical analyses of these patients were compared with age‐ and sex‐matched patients with HBV‐HCC or HCV‐HCC for the associated metabolic risk factors. For this comparison, 420 patients with HBV‐HCC and 420 patients with HCV‐HCC were selected from the 3,843 patients with HCC. Multivariate analyses showed fatty liver (by echography), high triglyceride levels (>160 mg/dL), and diabetes mellitus history to be significantly associated only with NBNC‐HCC and not with the matched patients with HBV‐ or HCV‐HCC. When the patients with HCC were further divided into four groups based on history of alcoholism and cirrhotic status, the group without alcoholism and without cirrhosis exhibited the strongest association with the metabolic risk factors. Based on trend analyses, patients with NBNC‐HCC with or without alcoholism were significantly different from the matched patients with HBV‐ or HCV‐HCC, except for patients with alcoholism and cirrhosis, in having more than two of the above three risk factors. Conclusion: Metabolic risk factors are significantly associated with nonviral HCC, especially for patients without alcoholism in Taiwan. Because the prevalence of viral HCC is decreasing due to the success of universal vaccination and antiviral therapy, strategies for cancer prevention, prediction, and surveillance for HCC will require modification. (Hepatology Communications 2018;2:747‐759)

AIM:Several epidemiological studies have demonstrated a close association between Helicobacter pylori (H Pylori) infection and non-cardiac carcinoma of the stomach. H pylori infection induces active inflammation with neutrophilic infiltrations as well as production of oxygen free radicals that can cause DNA damage. The DNA damage induced by oxygen free radicals could have very harmful consequences, leading to gene modifications that are potentially mutagenic and/or carcinogenic. The aims of the present study were to assess the effect of H pylori infection on the expression of inducible nitric oxidative synthase (iNOS) and the production of 8-hydroxy-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA injury in human gastric mucosa with and without tumor lesions, and to assess the possible factors affecting cell death signaling due to oxidative DNA damage. METHODS:In this study, 40 gastric carcinoma specimens and adjacent specimens were obtained from surgical resection. We determined the level of 8-OHdG formation by HPLC-ECD, and the expression of iNOS and mechanism of cell death signaling [including nuclear factor-κB(NFκB), MEKK-1, Caspase 3, B Cell lymphomal leukemia-2 (Bcl-2), inhibitor of apoptosis protein (IAP ) and myeloid cell leukemia-1 (Mcl-1)] by Western-blot assay. RESULTS:The concentrations of 8-OHdG, iNOS, NFκB, Mcl-1 and IAP were significantly higher in cancer tissues than in adjacent non-cancer tissues. In addition, significantly higher concentrations of 8-OHdG, iNOS, NFκB, Mcl-1 and IAP were detected in patients infected with H pylori compared with patients who were not infected with H pylori. Furthermore, 8-OHdG, iNOS, NFκB, Mcl-1 and IAP concentrations were significantly higher in stage 3 and 4 patients than in stage 1 and 2 patients. CONCLUSION:Chronic H pylori infection induces iNOS expression and subsequent DNA damage as well as enhances anti-apoptosis signal transduction. This sequence of events supports the hypothesis that oxygen-free radical-mediated damage due to H pylori plays a pivotal role in the development of gastric carcinoma in patients with chronic gastritis.Chang CS, Chen WN, Lin HH, Wu CC, Wang CJ. Increased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor κB expression and enhanced antiapoptosisrelated proteins in Helicobacter pylori-infected non-cardiac gastric adenocarcinoma. World J Gastroenterol 2004; 10 (15): 2232-2240