Certain Dietary Habits Contribute to the Functional Dyspepsia in South China Rural Area.

BACKGROUND Functional dyspepsia (FD) refers to a group of upper gastrointestinal syndromes, subdivided into two types: postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). The etiology of FD remains unclear; however, unhealthy dietary habit is one potential underlying cause. We aim to explore the association of poor dietary habits with FD and its subtypes. MATERIAL AND METHODS A validated epidemiological questionnaire was designed to investigate dietary habits and gastrointestinal syndromes. Citizens in the Baotun community of Dongguan were invited to complete the study questionnaire. All participants were asked to undergo a physical examination and a blinded physician interview. The study was conducted from June 2015 to June 2016. FD was diagnosed using ROME III criteria. The association between investigated dietary habits and dyspeptic symptoms were explored. RESULTS There were 1,304 adult residents recruited for the study survey; 165 residents had existing organic dyspepsia (OD), 203 residents were diagnosed with FD, and the other 936 participants, who were without dyspeptic symptoms or functional gastrointestinal diseases, were regarded as the control group. Subtype diagnosis indicated 61 participants had EPS, 66 participants had PDS, and 76 participants had coexisting EPS and PDS. Unhealthy dietary habits were more prevalent in the FD group than in the control groups (75.86% versus 37.50%; p<0.001). FD was found to be associated with irregular mealtime, dining out, fatty food, sweet food, and coffee (p<0.05). The impact of each dietary factor varied with FD subtypes. CONCLUSIONS Certain types of dietary habits were positively correlated with the prevalence of FD. FD subtypes showed relatively different associations with dietary factors.

The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.

The human genome contains thousands of long intergenic noncoding RNAs (lincRNAs). However, the functional roles of these transcripts and the mechanisms responsible for their deregulation in colorectal cancer (CRC) remain elusive. A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes' stage, and patient outcomes. In SW480 and SW620 cells, knockdown of UCC inhibited proliferation, invasion, and cell cycle progression and induced apoptosis in vitro. Xenograft tumors grown from UCC-silenced SW620 cells had smaller mean volumes and formed more slowly than xenograft tumors grown from control cells. Inversely, overexpression of UCC in HCT116 promoted cell growth and invasion in vitro. Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. Our results suggest that UCC and miR-143 may be promising molecular targets for CRC therapy.

MiR-143 Targeting TAK1 Attenuates Pancreatic Ductal Adenocarcinoma Progression via MAPK and NF-κB Pathway In Vitro.

BACKGROUND: Transforming growth factor (TGF)-ß-activated kinase 1 (TAK1) is one of the major regulators of inflammation-induced cancer cell growth and progression. MiR-143 dysregulation is a common event in a variety of human diseases including pancreatic ductal adenocarcinoma (PDA). AIMS: To identify the interaction between TAK1 and miR-143 in PDA. METHODS: Data mining of TAK1 expression in PDA patient gene profiling was conducted. QRT-PCR and western blot were performed to detect the expression of TAK1 in PDA tissues and cell lines. Ectopic miR-143 and TAK1 were introduced to PDA cells. Cell growth, apoptosis and migration were examined. Xenograft models were used to examine the function of TAK1 in vivo. Western blot and luciferase assay were carried out to investigate the direct target of miR-143. RESULTS: PDA patient gene profiling data (GSE15471 and GSE16515) showed that TAK1 mRNA was aberrantly up-regulated in PDA tissues. TAK1 protein levels were overexpressed in PDA tissues and cell lines. Overexpression of TAK1 was strongly associated with positive lymph node metastasis. Inhibition of TAK1 suppressed cell growth, migration, and induced cell apoptosis in vitro and in vivo. Further studies demonstrated that TAK1 was a direct target gene of miR-143. MiR-143 also inhibited PDA cells proliferation and migration, induced apoptosis and G1/S arrest. Moreover, TAK1 depletion inactivated MAPK and NF-κB pathway, mimicking the function of miR-143. CONCLUSIONS: The study highlights that miR-143 acts as a tumor suppressor in PDA through directly targeting TAK1, and their functional regulation may provide potential therapeutic strategies in clinics.

Somatostatin administration prior to ERCP is effective in reducing the risk of post-ERCP pancreatitis in high-risk patients.

Somatostatin has been extensively studied for the prophylaxis of pancreatitis following endoscopic retrograde cholangiopancreatography (ERCP). However, the results remain controversial. The present retrospective cohort study aimed to investigate the efficacy of pre- and post-ERCP somatostatin administration in the prevention of post-ERCP pancreatitis (PEP). All ERCP procedures performed at one hospital between January 2009 and December 2012 were reviewed. They were divided into three groups based on somatostatin administration: pre-ERCP som group (somatostatin administration: 0.25 mg/h for 24 h, starting 1 h prior to ERCP), post-ERCP som group (somatostatin administration: 0.25 mg/h for 24 h, starting immediately following ERCP), and control group (no somatostatin administration). Out of a total of 304 cases, 81 received pre-ERCP somatostatin; 126 received post-ERCP somatostatin and 97 were not administered somatostatin. Pre-ERCP somatostatin was effective in reducing the incidence of PEP compared with that in the control group (4.9 vs. 16.5%; P=0.017). This benefit was significant in high-risk patients (8.9 vs. 26.0%; P=0.035), but not in low-risk patients (0 vs. 6.4%; P=0.254). Post-ERCP somatostatin was not effective in preventing PEP in high- or low-risk patients. In conclusion, pre-ERCP somatostatin may be effective in reducing the risk of PEP in high-risk patients, but not in low-risk patients. Post-ERCP somatostatin did not reveal a benefit in high- or low-risk patients. However, large randomized controlled trials are required to further confirm these findings.

[Endoscopic, clinicopathologic and immunohistochemical features of gastric stromal tumor].

BACKGROUND & OBJECTIVE: For gastric stromal tumor (GST), the low incidence and high diversity in endoscopic and pathologic manifestations lead to misdiagnosis. This study was to explore the features of GST in endoscopy and clinicopathology. METHODS: Clinical data of 42 GST patients, treated at the Second Affiliated Hospital of Sun Yat-sen University from Jan. 1996 to Jan. 2006, were analyzed for their clinicopathologic and endoscopic features. The expression of CD117, CD34, smooth muscle actin (SMA), Desmin and S-100 were detected by immunohistochemistry. Their correlations to clinicopathologic features of GST were analyzed. RESULTS: Of the 42 cases of GST, 21 (50.0%) were at the fundus, 14 (33.3%) at the body, and 7 (16.7%) at the antrum; 17 (40.5%) were benign, 14 (33.3%) borderline, 11 (26.2%) malignant. Endoscopically, GST presented submucosal hemispheroid or polypoid protuberant lesions with clear border. While the positive rate of gastroendoscopic biopsy was low. Of the 42 cases, 29 were spindle cell type, 5 were epithelial cell type, and 8 were mixed type. The positive rates of CD34 and CD117 were 92.86% and 78.57%. CONCLUSIONS: GST has unique morphologic features. Combined detection of CD117 and CD34 benefits the diagnosis of GST.

[A meta-analysis of clinical efficiency of two methodologies of cholangiopancreatography].

OBJECTIVE: To compare the efficiency of endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance cholangiopancreatography (MRCP) in patients with suspected biliary tract or pancreatic diseases. METHODS: Find those prospective comparison trials about the efficiency of ERCP and MRCP in patients with suspected biliary tract or pancreatic diseases from many kinds of database, such as MEDLINE, EMBASE and so on. According to inclusion criteria, two operant choose suitable papers for this study. Collect corresponding original data and make a meta-analysis to compare the sensitivity and specificity of ERCP and MRCP in choledocholithiasis, strictures and malignant tumor. RESULTS: Finally we get 6 articles from 302 ones. To diagnose choledocholithiasis, strictures and malignant tumor, the difference of sensitive between ERCP's and MRCP's is not significant. When it comes to the specificity of ERCP and MRCP in those diseases, ERCP is better than MRCP only in strictures, OR is 6.17 (95% CI 1.35-20.24), P = 0.02. However, we find ERCP is better than MRCP not only in total sensitivity but specificity of biliary tract or pancreatic diseases, OR is 1.72 (95% CI 1.04-2.85) and 4.05 (95% CI 1.32-12.42) respectively, P = 0.04, 0.01. CONCLUSIONS: ERCP is better than MRCP, to biliary tract or pancreatic diseases, in not only sensitivity but specificity. Doctors should think much about patients' situation, tolerance and cost-effectiveness, when they make a decision which examination should patients take.