Ten-Day Vonoprazan-Amoxicillin Dual Therapy vs Standard 14-Day Bismuth-Based Quadruple Therapy for First-Line Helicobacter pylori Eradication: A Multicenter Randomized Clinical Trial.

INTRODUCTION: Whether 10-day short-course vonoprazan-amoxicillin dual therapy (VA-dual) is noninferior to the standard 14-day bismuth-based quadruple therapy (B-quadruple) against Helicobacter pylori eradication has not been determined. This trial aimed to compare the eradication rate, adverse events, and compliance of 10-day VA-dual regimen with standard 14-day B-quadruple regimen as first-line H. pylori treatment. METHODS: This prospective randomized clinical trial was performed at 3 institutions in eastern China. A total of 314 treatment-naive, H. pylori -infected patients were randomly assigned in a 1:1 ratio to either 10-day VA-dual group or 14-day B-quadruple group. Eradication success was determined by 13 C-urea breath test at least 4 weeks after treatment. Eradication rates, adverse events, and compliance were compared between groups. RESULTS: Eradication rates of VA-dual and B-quadruple groups were 86.0% and 89.2% ( P = 0.389), respectively, by intention-to-treat (ITT) analysis; 88.2% and 91.5% ( P = 0.338), respectively, by modified ITT analysis; and 90.8% and 91.3% ( P = 0.884), respectively, by per-protocol (PP) analysis. The efficacy of the VA-dual remained noninferior to B-quadruple therapy in all ITT, modified ITT, and PP analyses. The incidence of adverse events in the VA-dual group was significantly lower compared with that in the B-quadruple group ( P < 0.001). Poor compliance contributed to eradication failure in the VA-dual group ( P < 0.001), while not in the B-quadruple group ( P = 0.110). DISCUSSION: The 10-day VA-dual therapy provided satisfactory eradication rates of >90% (PP analysis) and lower rates of adverse events compared with standard 14-day B-quadruple therapy as first-line H. pylori therapy. TRAIL REGISTRATION NUMBER: ChiCTR2300070100.

Fatty liver is associated with significant liver inflammation and increases the burden of advanced fibrosis in chronic HBV infection.

BACKGROUND: Concurrent non-alcoholic fatty liver disease (NAFLD) is common in patients with chronic HBV infection. But the impact of fatty liver on the histologic progression of HBV infection remains controversial. METHODS: Consecutive HBV-infected patients who underwent liver biopsy between 2016 and 2021 were included. Alcohol consumption and other types of viral hepatitis were excluded. All biopsies were scored for grading and staging by Scheuer's score, and the steatosis was scored as an estimate of the percentage of liver parenchyma replaced by fat. Logistic regression analyses were applied to assess the associated factors for significant liver inflammation (G ≥ 2), significant fibrosis (S ≥ 2) and advanced fibrosis (S ≥ 3). RESULTS: Among the 871 HBV-infected patients, hepatic steatosis was prevalent in 255 patients (29.28%). Significant liver inflammation was present in 461 patients (52.93%). Significant fibrosis was observed in 527 patients (60.51%), while advanced liver fibrosis was observed in 171 patients (19.63%). Patients with concomitant NAFLD were more likely to have significant liver inflammation and advanced fibrosis. Fatty liver was an independent risk factor for significant liver inflammation (OR: 2.117, 95% CI: 1.500-2.988), but it could not predict the development of fibrosis. Especially, in HBV-infected patients with persistent normal ALT (immune tolerant and inactive carrier phase), the presence of significant liver inflammation was higher in NAFLD than those without NAFLD. The prevalence of advanced liver fibrosis was higher in NAFLD than non-NAFLD only in the immune tolerant phase, while NAFLD did not increase fibrosis burden in other stages of HBV infection. We developed a predictive model for significant liver inflammation with the area under receiver operating characteristic curve (AUROC) of 0.825, and a model for significant fibrosis with the AUROC of 0.760. CONCLUSIONS: NAFLD is independently associated with significant liver inflammation, and increases the burden of advanced liver fibrosis in HBV-infected patients. The influence of NAFLD on the degree of liver inflammation and fibrosis is different in distinct clinical phases of chronic HBV infection.

Synthesis of allenes via gold-catalyzed intermolecular reaction of propargylic alcohols and aromatic compounds.

Functionalized allenes are efficiently synthesized in moderate to high yield from gold-catalyzed intermolecular reaction of propargylic alcohols and aromatic compounds. The user-friendly process could be conducted under mild reaction conditions with easily accessible starting materials.

MicroRNA-376b-3p ameliorates nonalcoholic fatty liver disease by targeting FGFR1 and regulating lipid oxidation in hepatocytes.

AIMS: Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease whose molecular mechanisms remain unclear. This study aimed to explore the role and mechanisms of microRNA-376b-3p in NAFLD. MATERIALS AND METHODS: We used a microarray to reveal hepatic microRNA expression profiles and validated their expression in cellular and mouse models via qRT-PCR. In vitro, the expression of microRNA-376b-3p was increased by a microRNA-376b-3p mimic and decreased by a microRNA-376b-3p inhibitor. The role and potential mechanisms of microRNA-376b-3p in NAFLD were investigated in mice injected with lentiviral vectors before high-fat diet (HFD) feeding, and the direct target gene was explored using a dual-luciferase reporter gene assay and confirmed by Western blotting. KEY FINDINGS: Microarray analysis and subsequent validation showed that the expression of microRNA-376b-3p was downregulated by nearly 90 % in the livers of HFD-fed mice and by >50 % in free fatty acid-stimulated hepatocytes. Overexpression of microRNA-376b-3p markedly ameliorated hepatic lipid accumulation, which was attributable to an increase in fatty acid oxidation. Conversely, inhibition of miR-376b-3p exhibited the opposite effects. The luciferase reporter assay indicated that Fgfr1 is a direct target gene of miR-376b-3p. Fgfr1 intervention eliminated the effect of miR-376b-3p on the lipid oxidation pathway and hepatocyte steatosis, which suggests that miR-376b-3p regulates fatty acid oxidation by targeting Fgfr1 to influence NAFLD development. SIGNIFICANCE: miR-376b-3p was downregulated in NAFLD and has a novel regulatory role in lipid oxidation through a miR-376b-3p-Fgfr1-dependent mechanism. Thus, miR-376b-3p may serve as a potential diagnostic marker or therapeutic target for NAFLD.

Metabolic dysfunction is associated with steatosis but no other histologic features in nonalcoholic fatty liver disease.

BACKGROUND: Recently, nonalcoholic fatty liver disease (NAFLD) has been renamed metabolic-associated fatty liver disease (MAFLD). Based on the definition for MAFLD, a group of non-obese and metabolically healthy individuals with fatty liver are excluded from the newly proposed nomenclature. AIM: To analyze the histologic features in the MAFLD and non-MAFLD subgroups of NAFLD. METHODS: Eighty-three patients with biopsy-proven NAFLD were separated into MAFLD and non-MAFLD groups. The diagnosis of MAFLD was established as hepatic steatosis along with obesity/diabetes or evidence of metabolic dysfunction. The histologic features were compared according to different metabolic disorders and liver enzyme levels. RESULTS: MAFLD individuals had a higher NAFLD activity score (P = 0.002) and higher severity of hepatic steatosis (42.6% Grade 1, 42.6% Grade 2, and 14.8% Grade 3 in MAFLD; 81.8% Grade 1, 13.6% Grade 2, and 4.5% Grade 3 in non-MAFLD; P = 0.007) than the non-MAFLD group. Lobular and portal inflammation, hepatic ballooning, fibrosis grade, and the presence of nonalcoholic steatohepatitis (NASH) and significant fibrosis were comparable between the two groups. The higher the liver enzyme levels, the more severe the grades of hepatic steatosis (75.0% Grade 1 and 25.0% Grade 2 in normal liver function; 56.6% Grade 1, 39.6% Grade 2, and 3.8% Grade 3 in increased liver enzyme levels; 27.8% Grade 1, 27.8% Grade 2, and 44.4% Grade 3 in liver injury; P < 0.001). Patients with liver injury (alanine aminotransferase > 3 × upper limit of normal) presented a higher severity of hepatocellular ballooning (P = 0.021). Moreover, the grade of steatosis correlated significantly with hepatocellular ballooning degree (r = 0.338, P = 0.002) and the presence of NASH (r = 0.466, P < 0.001). CONCLUSION: Metabolic dysfunction is associated with hepatic steatosis but no other histologic features in NAFLD. Further research is needed to assess the dynamic histologic characteristics in NAFLD based on the presence or absence of metabolic disorders.

A novel model for predicting fatty liver disease by means of an artificial neural network.

BACKGROUND: The artificial neural network (ANN) emerged recently as a potent diagnostic tool, especially for complicated systemic diseases. This study aimed to establish a diagnostic model for the recognition of fatty liver disease (FLD) by virtue of the ANN. METHODS: A total of 7,396 pairs of gender- and age-matched subjects who underwent health check-ups at the First Affiliated Hospital, College of Medicine, Zhejiang University (Hangzhou, China) were enrolled to establish the ANN model. Indices available in health check-up reports were utilized as potential input variables. The performance of our model was evaluated through a receiver-operating characteristic (ROC) curve analysis. Other outcome measures included diagnostic accuracy, sensitivity, specificity, Cohen's k coefficient, Brier score, and Hosmer-Lemeshow test. The Fatty Liver Index (FLI) and the Hepatic Steatosis Index (HSI), retrained using our training-group data with its original designated input variables, were used as comparisons in the capability of FLD diagnosis. RESULTS: Eight variables (age, gender, body mass index, alanine aminotransferase, aspartate aminotransferase, uric acid, total triglyceride, and fasting plasma glucose) were eventually adopted as input nodes of the ANN model. By applying a cut-off point of 0.51, the area under ROC curves of our ANN model in predicting FLD in the testing group was 0.908 [95% confidence interval (CI), 0.901-0.915]-significantly higher (P < 0.05) than that of the FLI model (0.881, 95% CI, 0.872-0.891) and that of the HSI model (0.885; 95% CI, 0.877-0.893). Our ANN model exhibited higher diagnostic accuracy, better concordance with ultrasonography results, and superior capability of calibration than the FLI model and the HSI model. CONCLUSIONS: Our ANN system showed good capability in the diagnosis of FLD. It is anticipated that our ANN model will be of both clinical and epidemiological use in the future.

Anti-cancer activity of anti-p185HER-2 ricin A chain immunotoxin on gastric cancer cells.

BACKGROUND AND AIM: Overexpression of the human epidermal growth factor receptor 2 (HER-2) protein has been detected in gastric cancer and has been associated with an unfavorable prognosis. We investigated the anti-cancer effects of anti-p185(HER-2) ricin A chain (RTA) immunotoxin, alone or in combination with 5-flurouracil on SGC7901-HER-2+ cells. METHODS: SGC7901-HER-2+ cells were obtained by transfecting SGC7901 cells with HER-2-pcDNA3.1. Anti-p185(HER-2)-RTA was prepared by chemical conjugation of anti-HER-2 monoclonal antibody (mAb) and RTA. The SGC7901-HER-2+ cells were incubated with RTA, anti-p185(HER-2)-RTA, and/or 5-flurouracil. The effects of drugs on cells were evaluated by MTT assay and Annexin V-fluorescein isothiocyanate and propidium iodide double staining flow cytometry. The expression of caspase-3, caspase-9, cyclooxygenase-2, and nuclear factor-kappaB/p65 were assayed by western blot. SGC7901-HER-2+ cells were transplanted into BALB/c nude mice to produce solid tumors in an attempt to study the immunotoxin activity in vivo. RESULTS: In vitro, anti-p185(HER-2)-RTA inhibited cell growth and induced apoptosis in SGC7901-HER-2+ cells. Anti-p185(HER-2)-RTA enhanced caspase-3 and caspase-9 activity, while downregulating the expression of cyclooxygenase-2 and nuclear factor-kappaB/p65. Its combination with 5-flurouracil further inhibited the growth of SGC7901-HER-2+ cells. In vivo, our data showed that anti-p185(HER-2)-RTA significantly inhibited the growth of SGC7901-HER-2+ cells-transplanted tumors. CONCLUSIONS: Anti-p185(HER-2)-RTA inhibits the growth of SGC7901-HER-2+ cells. The effect may be related to the activation of caspase-3 and caspase-9 and inhibition of cyclooxygenase-2 and nuclear factor-kappaB/p65. Anti-p185(HER-2)-RTA plus 5-FU enhance anti-cancer activity, suggesting useful clues for further study for the treatment of HER-2 positive gastric cancers.

Association between Serum Uric Acid to HDL-Cholesterol Ratio and Nonalcoholic Fatty Liver Disease in Lean Chinese Adults.

METHODS: A cross-sectional study was performed among 6285 lean Chinese adults (body mass index < 24 kg/m2) who took their annual health checkups. NAFLD was diagnosed based on hepatic ultrasound examination, with exclusion of other etiologies. RESULTS: Of 6285 lean participants enrolled, 654 NAFLD cases were diagnosed. The overall NAFLD prevalence was 10.41%, and the prevalence was 15.45% and 7.16% in men and women, respectively. UHR was significantly higher in NAFLD patients than in controls (14.25 ± 5.33% versus 10.09 ± 4.23%, P < 0.001). UHR quintiles were positively associated with NAFLD prevalence, which was 1.91% in the first UHR quintile and increased to 3.58%, 7.81%, 14.17%, and 24.54% in the second, third, fourth, and fifth quintile groups, respectively (P < 0.001 for trend). Multivariate logistic regression analysis showed that UHR was independently associated with an increased risk of NAFLD (odds ratio: 1.105; 95% CI: 1.076-1.134; P < 0.001). Sensitivity analysis showed that UHR remained significantly associated with NAFLD in lean participants with normal range of serum uric acid and HDL-cholesterol levels. CONCLUSIONS: UHR was significantly associated with NAFLD and may serve as a novel and reliable marker for NAFLD in lean adults.

Current status of Helicobacter pylori eradication and risk factors for eradication failure.

BACKGROUND: The Helicobacter pylori (H. pylori) eradication rate is decreasing in the general population of China. AIM: To evaluate the H. pylori eradication status in real-world clinical practice and to explore factors related to eradication failure. METHODS: Patients with H. pylori infection who were treated with standard 14-d quadruple therapy and received a test of cure at a provincial medical institution between June 2018 and May 2019 were enrolled. Demographic and clinical data were recorded. Eradication rates were calculated and compared between regimens and subgroups. Multivariate analysis was performed to identify predictors of eradication failure. RESULTS: Of 2610 patients enrolled, eradication was successful in 1999 (76.6%) patients. Amoxicillin-containing quadruple regimens showed a higher eradication rate than other quadruple therapy regimens (83.0% vs 69.0%, P < 0.001). The quadruple therapy containing amoxicillin plus clarithromycin achieved the highest eradication rate (83.5%). Primary therapy had a higher eradication rate than rescue therapy (78.3% vs 66.5%, P < 0.001). In rescue therapy, the amoxicillin- and furazolidone-containing regimens achieved the highest eradication rate (80.8%). Esomeprazole-containing regimens showed a higher eradication rate than those containing other proton pump inhibitors (81.8% vs 74.9%, P = 0.001). Multivariate regression analysis found that older age, prior therapy, and use of omeprazole or pantoprazole were associated with an increased risk of eradication failure. CONCLUSION: The total eradication rate is 76.6%. Amoxicillin-containing regimens are superior to other regimens. Age, prior therapy, and use of omeprazole or pantoprazole are independent risk factors for eradication failure.

Construction of a convolutional neural network classifier developed by computed tomography images for pancreatic cancer diagnosis.

BACKGROUND: Efforts should be made to develop a deep-learning diagnosis system to distinguish pancreatic cancer from benign tissue due to the high morbidity of pancreatic cancer. AIM: To identify pancreatic cancer in computed tomography (CT) images automatically by constructing a convolutional neural network (CNN) classifier. METHODS: A CNN model was constructed using a dataset of 3494 CT images obtained from 222 patients with pathologically confirmed pancreatic cancer and 3751 CT images from 190 patients with normal pancreas from June 2017 to June 2018. We established three datasets from these images according to the image phases, evaluated the approach in terms of binary classification (i.e., cancer or not) and ternary classification (i.e., no cancer, cancer at tail/body, cancer at head/neck of the pancreas) using 10-fold cross validation, and measured the effectiveness of the model with regard to the accuracy, sensitivity, and specificity. RESULTS: The overall diagnostic accuracy of the trained binary classifier was 95.47%, 95.76%, 95.15% on the plain scan, arterial phase, and venous phase, respectively. The sensitivity was 91.58%, 94.08%, 92.28% on three phases, with no significant differences (χ 2 = 0.914, P = 0.633). Considering that the plain phase had same sensitivity, easier access, and lower radiation compared with arterial phase and venous phase , it is more sufficient for the binary classifier. Its accuracy on plain scans was 95.47%, sensitivity was 91.58%, and specificity was 98.27%. The CNN and board-certified gastroenterologists achieved higher accuracies than trainees on plain scan diagnosis (χ 2 = 21.534, P < 0.001; χ 2 = 9.524, P < 0.05; respectively). However, the difference between CNN and gastroenterologists was not significant (χ 2 = 0.759, P = 0.384). In the trained ternary classifier, the overall diagnostic accuracy of the ternary classifier CNN was 82.06%, 79.06%, and 78.80% on plain phase, arterial phase, and venous phase, respectively. The sensitivity scores for detecting cancers in the tail were 52.51%, 41.10% and, 36.03%, while sensitivity for cancers in the head was 46.21%, 85.24% and 72.87% on three phases, respectively. Difference in sensitivity for cancers in the head among the three phases was significant (χ 2 = 16.651, P < 0.001), with arterial phase having the highest sensitivity. CONCLUSION: We proposed a deep learning-based pancreatic cancer classifier trained on medium-sized datasets of CT images. It was suitable for screening purposes in pancreatic cancer detection.

Association of MicroRNA-223 expression with hepatic ischemia/reperfusion injury in mice.

MicroRNAs are a group of small non-coding RNAs with modulator activity of gene expression. Recent studies have uncovered a profound role of microRNAs in liver diseases. This study aimed to investigate a potential relationship between microRNA-223 (miR-223) expression and hepatic ischemia/reperfusion injury in mice. Quantitative RT-PCR analysis showed that miR-223 expression levels were greatly up-regulated in the livers after 75 min ischemia followed by 120 min reperfusion when compared to sham controls (2.59 +/- 0.23 vs. 0.83 +/- 0.15; P < 0.01). Correlation analysis also revealed that hepatic miR-223 expression level was significantly positively correlated with serum markers of ischemic injury. By prediction assay of miRNA targets mRNA, acyl-CoA synthetase long-chain family member 3, ephrin A1, and ras homolog gene family member B were predicted to be downstream targets of miR-223. Thus, we conclude that hepatic ischemia/reperfusion injury might be another form of liver disease that is associated with alteration in miR-223 expression.

Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways.

BACKGROUND: Allyl isothiocyanate (AITC), a classic anti-inflammatory and antitumorigenic agent, was recently identified as a potential treatment for obesity and insulin resistance. However, little is known about its direct impact on the liver. AIM: To investigate the effect and underlying mechanism of AITC in nonalcoholic fatty liver disease (commonly referred to as NAFLD). METHODS: To establish a mouse and cellular model of NAFLD, C57BL/6 mice were fed a high fat diet (HFD) for 8 wk, and AML-12 cells were treated with 200 µM palmitate acid for 24 h. For AITC treatment, mice were administered AITC (100 mg/kg/d) orally and AML-12 cells were treated with AITC (20 µmol/L). RESULTS: AITC significantly ameliorated HFD-induced weight gain, hepatic lipid accumulation and inflammation in vivo. Furthermore, serum alanine aminotransferase and aspartate aminotransferase levels were markedly reduced in AITC-treated mice. Mechanistically, AITC significantly downregulated the protein levels of sterol regulatory element-binding protein 1 (SREBP1) and its lipogenesis target genes and upregulated the levels of proteins involved in fatty acid ß-oxidation, as well as the upstream mediators Sirtuin 1 (Sirt1) and AMP-activated protein kinase α (AMPKα), in the livers of HFD-fed mice. AITC also attenuated the nuclear factor kappa B (NF-κB) signaling pathway. Consistently, AITC relieved palmitate acid-induced lipid accumulation and inflammation in AML-12 cells in vitro through the Sirt1/AMPK and NF-κB signaling pathways. Importantly, further studies showed that the curative effect of AITC on lipid accumulation was abolished by siRNA-mediated knockdown of either Sirt1 or AMPKα in AML-12 cells. CONCLUSION: AITC significantly ameliorates hepatic steatosis and inflammation by activating the Sirt1/AMPK pathway and inhibiting the NF-κB pathway. Therefore, AITC is a potential therapeutic agent for NAFLD.

Risk factors for alcohol-related liver injury in the island population of China: a population-based case-control study.

AIM: To investigate the association of alcohol dose, duration of drinking and obesity with abnormal alcohol-related liver injury indicators, the prevalence of alcohol-related liver injury in the island population of China. METHODS: Randomized multistage stratified cluster sampling from the island population of China was used in the population-based case-control study. Then interview, physical examination, laboratory assessments and ultrasonography were done. RESULTS: Daily alcohol intake > or = 20 g, duration of drinking > or = 5 years and obesity were closely related to alcohol-related liver injury (P < 0.05). The odds-ratio (OR) (95% CI) was 1.965 (1.122-3.442), 3.412 (1.789-6.507) and 1.887 (1.261-2.824), respectively. The prevalence rate of alcohol-related liver injury in > or = 20 g daily alcohol intake group and < 20 g daily alcohol intake group was 37.14% and 12.06%, respectively. The prevalence rate of alcohol-related liver injury in > or = 5 years drinking group and < 5 years drinking group was 34.44% and 8.53%, respectively. No significant dose-response relation was found between daily alcohol intake and abnormal alcohol-related liver injury indicators as well as between duration of drinking and abnormal alcohol-related liver injury indicators. There was no significant difference in the prevalence of alcohol-related liver injury between beer drinking group and yellow rice wine drinking group, hard liquor drinking group, multiple drinking group. CONCLUSION: The risk threshold of daily alcohol intake is 20 g and duration of drinking inducing alcohol-related liver injury 5 years in the island population of China. Liver injury induced by obesity should be concerned.

Application of Machine Learning Techniques for Clinical Predictive Modeling: A Cross-Sectional Study on Nonalcoholic Fatty Liver Disease in China.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases. Machine learning techniques were introduced to evaluate the optimal predictive clinical model of NAFLD. METHODS: A cross-sectional study was performed with subjects who attended a health examination at the First Affiliated Hospital, Zhejiang University. Questionnaires, laboratory tests, physical examinations, and liver ultrasonography were employed. Machine learning techniques were then implemented using the open source software Weka. The tasks included feature selection and classification. Feature selection techniques built a screening model by removing the redundant features. Classification was used to build a prediction model, which was evaluated by the F-measure. 11 state-of-the-art machine learning techniques were investigated. RESULTS: Among the 10,508 enrolled subjects, 2,522 (24%) met the diagnostic criteria of NAFLD. By leveraging a set of statistical testing techniques, BMI, triglycerides, gamma-glutamyl transpeptidase (γGT), the serum alanine aminotransferase (ALT), and uric acid were the top 5 features contributing to NAFLD. A 10-fold cross-validation was used in the classification. According to the results, the Bayesian network model demonstrated the best performance from among the 11 different techniques. It achieved accuracy, specificity, sensitivity, and F-measure scores of up to 83%, 0.878, 0.675, and 0.655, respectively. Compared with logistic regression, the Bayesian network model improves the F-measure score by 9.17%. CONCLUSION: Novel machine learning techniques may have screening and predictive value for NAFLD.

Olfactomedin-4 in digestive diseases: A mini-review.

Olfactomedin-4 (OLFM4, GW112, hGC-1) is a glycoprotein belonging to the olfactomedin family. The expression of OLFM4 is strong in the small intestine, colon and prostate, and moderate in the stomach and bone marrow. Previous studies have revealed that OLFM4 is closely associated with many digestive diseases. Up-regulation of OLFM4 has been detected in the Helicobacter pylori (H. pylori)-infected gastric mucosa, inflammatory bowel disease tissue and gastrointestinal malignancies, including gastric cancer, colorectal cancer, pancreatic cancer and gallbladder cancer. Down-regulation of OLFM4 has also been detected in some cases, such as in poorly differentiated, advanced-stage and metastatic tumors. Studies using OLFM4-deficient mouse models have revealed that OLFM4 acts as a negative regulator of H. pylori-specific immune responses and plays an important role in mucosal defense in inflammatory bowel disease. Patients with OLFM4-positive gastric cancer or colorectal cancer have a better survival rate than OLFM4-negative patients. However, the prognosis is worse in pancreatic cancer patients with high levels of expression of OLFM4. The NF-κB, Notch and Wnt signaling pathways are involved in the regulation of OLFM4 expression in digestive diseases, and its role in pathogenesis is associated with anti-inflammation, apoptosis, cell adhesion and proliferation. OLFM4 may serve as a potential specific diagnostic marker and a therapeutic target in digestive diseases. Further studies are required to explore the clinical value of OLFM4.

Association of the frequency of peripheral natural killer T cells with nonalcoholic fatty liver disease.

AIM: To investigate whether changes in the frequency of peripheral natural killer T (NKT) cells were correlated with liver disease in patients who had metabolic predispositions to nonalcoholic fatty liver disease (NAFLD). METHODS: Peripheral blood samples were obtained from 60 Chinese NAFLD patients and 60 age and gender matched healthy controls. The frequency of peripheral NKT cells was detected by flow cytometry. Clinical and laboratory data were collected for further analysis. RESULTS: NAFLD patients had a lower frequency of peripheral NKT cells than healthy controls (1.21% +/- 0.06% vs 1.62% +/- 0.07%, P < 0.001). Further analysis revealed that the frequency of peripheral NKT cells was negatively correlated with body mass index, waist circumference and serum levels of alanine aminotransferase. Logistic regression analysis revealed that elevated body mass index [hazard ratio (HR): 2.991], aspartate aminotransferase levels (HR: 1.148) and fasting blood sugar (HR: 3.133) increased the risk of NAFLD, whereas an elevated frequency of peripheral NKT cells (HR: 0.107) decreased the risk. CONCLUSION: Changes in the frequency of peripheral NKT cells were correlated with NAFLD and a decreased frequency of peripheral NKT cells was a risk factor for NAFLD.

Endoscopic Ultrasonography in the Diagnosis and Treatment Strategy Choice of Esophageal Leiomyoma.

OBJECTIVES:: Esophageal leiomyoma is the most common benign tumor of the esophagus, and it originates from mesenchymal tissue. This study analyzed the clinicopathological characteristics of esophageal leiomyoma and aimed to evaluate the role of endoscopic ultrasonography in the diagnosis and treatment selection for these lesions. METHODS:: Two hundred and twenty-five patients who had suspected esophageal leiomyomas in endoscopic ultrasonography were enrolled at the Endoscopy Center of The First Affiliated Hospital, Zhejiang University from January 1st, 2009 to May 31th, 2015. The main outcomes included the demographic and morphological characteristics, symptoms, comparisons of diagnosis and treatment methods, adverse events, and prognosis. RESULTS:: One hundred and sixty-seven patients were diagnosed as having an esophageal leiomyoma by pathological examination. The mean patient age was 50.57±9.983 years. In total, 62.9% of the lesions originated from the muscularis mucosa, and the others originated from the muscularis propria. The median distance to the incisors was 30±12 cm. The median diameter was 0.72±0.99 cm. As determined by endoscopic ultrasonography, most existing leiomyomas were homogeneous, endophytic, and spherical. The leiomyomas from the muscularis mucosa were smaller than those from the muscularis propria and much closer to the incisors (p<0.05). SMA (smooth muscle antibody) (97.2%) and desmin (94.5%) were positive in the majority of patients. In terms of treatments, patients preferred endoscopic therapies, which led to less adverse events (e.g., intraoperative bleeding, local infection, pleural effusion) than surgical operations (p<0.05). The superficial leiomyomas presented less adverse events and better recovery (p<0.05) than deep leiomyomas. CONCLUSION:: Endoscopic ultrasonography has demonstrated high accuracy in the diagnosis of esophageal leiomyomas and provides great support in selecting treatments; however, EUS cannot completely avoid misdiagnosis, so combining it with other examinations may be a good strategy to solve this problem.