Whether or not esophagogastric varices (EGV) could determine the outcomes of patients with hepatocellular carcinoma (HCC) is still unclear. A total of 990 treatment-naive HCC patients who received an esophagogastroduodenoscopy at the time of HCC diagnosis were retrospectively enrolled. The factors in terms of prognosis were analyzed by Cox proportional hazards model and propensity score matching analysis. Among the enrolled patients, 480 (48.5%) patients had EGV. Patients with EGV had a significantly lower cumulative 5-year survival rate than those without EGV (24.9% versus 46.4%, p < 0.001). It was confirmed by a multivariate analysis and propensity score matching analysis. Stratified by tumor stage, the patients with EGV had lower survival rates than the patients without EGVs in all Barcelona Clinic Liver Cancer stages except stage D. Moreover, the patients with EGV had lower survival rates than those without EGV, both by curative or non-curative treatment modalities. In conclusion, EGV was an independent risk factor predicting poor prognosis for the patients with HCC by multivariate analysis, propensity score matching analysis, and subgroup analysis.

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Surfactant proteins (SPs)-A and -D are C-type lectins of the collectin family and function in the clearance of infectious particles in the lungs. Some polymorphisms of SPs that give rise to amino acid changes have been found to affect their function. Several SP-A gene polymorphisms have been reported to be associated with respiratory infection diseases, such as tuberculosis (TB). However, the relationship between surfactant proteins D (SP-D) polymorphisms and TB is still unclear. To study the associations between SP-D polymorphisms and TB, the correlations of SP-D polymorphisms with TB were examined in a case–control study, which included 364 patients with TB and 177 control subjects. In addition, we cloned two major SP-D exonic polymorphism C92T (rs721917) and A538G (rs2243639) constructs and used these for in vitro assays. The effects of SP-D polymorphisms on agglutination and other interactions with Mycobacterium bovis bacillus Calmette–Guérin (M. bovis BCG) were evaluated. In comparison with SP-D 92C (amino acid residue 16, Threonine), our results showed that SP-D 92T (amino acid residue 16, Methionine) had a lower binding ability to M. bovis BCG, a lower capacity to inhibit phagocytosis, lesser aggregation, poorer survival of bacillus Calmette–Guérin (BCG)-infected MH-S cells, and less inhibition of intracellular growth of M. bovis BCG. The case–control association study showed that the 92T homozygous genotype was a risk factor for TB. However, a lesser effect was seen for polymorphism A538G. In conclusion, the results of functional and genetic analyses of SP-D variants consistently showed that the SP-D 92T variant increased susceptibility to TB, which further confirmed the role of SP-D in pulmonary innate immunity against mycobacterial infection.

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Question: A 67-year-old woman, who is a hepatitis C virus carrier, suffered from early satiety, indigestion, and occasional abdominal fullness since 2013. Physical examination and laboratory tests were unremarkable. Esophagogastroduodenoscopy disclosed a polypoid nodule at anterior wall of duodenal bulb (Figure A). Biopsy showed inflammatory changes. Abdominal computed tomography revealed a 1.4-cm protruding, heterogeneously hypodense nodule at the duodenal bulb (Figure B, C; black arrow). Endoscopic ultrasonography with 12-MHz miniprobe showed an 18.6 Â 10.8-mm isoechoic tumor with cystic change arising from the submucosal layer (Figure D). The patient underwent endoscopic resection of the tumor. What is your diagnosis of this duodenal tumor? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

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piRNAs altered by AsIII (a biologically-relevant form of arsenic), evidencing their role in arsenic-related carcinogenic mechanisms. Conclusion: Arsenic induces persistent alterations in the lung sncRNA transcriptome, particularly piRNAs, impacting pathways linked to epigenetic regulation. Together, these results provide insights into sncRNA-related mechanisms in arsenic-induced lung carcinogenesis. Moreover, different arsenic species induce distinct alteration patterns, highlighting the relevance of the source of exposure. piRNAs, as with other sncRNAs, are stable in biofluids, circulating tumour cells, and archival clinical materials. Therefore, piRNAs hold great promise as potential exposure and monitoring biomarkers for arsenic-related health effects.