Shu-Ling Wang

Bioinformatic analysis suggests that UGT2B15 activates the Hippo‑YAP signaling pathway leading to the pathogenesis of gastric cancer

Gastric cancer (GC) is one of the most common malignancies that threatens human health. As the molecular mechanisms unerlying GC are not completely understood, identification of genes related to GC could provide new insights into gene function as well as potential treatment targets. We discovered that UGT2B15 may contribute to the pathogenesis and progression of GC using GEO data and bioinformatic analysis. Using TCGA data, UGT2B15 mRNA was found to be significantly overexpressed in GC tissues; patients with higher UGT2B15 had a poorer prognosis. It was further discovered that UGT2B15 and FOXA1 were both upregulated, and UGT2B15 and Foxa1 were positively correlated in GC. It is known that Foxa1 is a vital threshold to activate the Hippo-YAP signaling pathway. In addition, we suggest that a potential molecular mechanisms includes UGT2B15 which may upregulate Foxa1, activate the Hippo-YAP signaling pathway and contribute to the development of GC. Taken together, our findings demonstrate that UGT2B15 may be an oncogene in GC and is a promising therapeutic target for cancer treatment.

Impact of intraduodenal acetic acid infusion on pancreatic duct cannulation during endoscopic retrograde cholangiopancreatography: A double-blind, randomized controlled trial: Acetic acid for pancreatic cannulation

Endoscopic retrograde cholangiopancreatography (ERCP) is associated with risk of complications. Methods to facilitate ductal cannulation may reduce complications. Intraduodenal acid infusion is a physiological approach to stimulate secretin release in human body and may facilitate cannulation. The objective of this study was to investigate the effect of intraduodenal acid infusion on pancreatic duct cannulation during ERCP.

Diagnostic role of carbohydrate antigen 72-4 for gastrointestinal malignancy screening in Chinese patients: a prospective study: The diagnostic role of CA72-4

Over the past decades, carbohydrate antigen 72‐4 (CA72‐4) was thought to be a tumor marker that was elevated in healthy individuals and patients with malignancies, including gastrointestinal (GI), ovarian, endometrial and lung malignancies. Furthermore, studies found that elevated serum CA72‐4 might predict digestive tumors, especially gastric tumors, although there was still neither a sensitive nor specific tumor biomarker for gastric cancer (GC). This study aimed to evaluate the diagnostic accuracy of CA72‐4 in predicting malignancies, especially GC.

Deep learning–based endoscopic image recognition for detection of early gastric cancer: a Chinese perspective

I read with interest the study by Tomizawa and Ginsberg in Gastrointestinal Endoscopy in 2018. They identified that increasing adenoma size may be associated with increased risk of recurrence and postEMR bleeding. The results were very interesting; however, I am concerned about the statistical methods that estimated the effect of increasing adenoma size on the studied outcomes. First, I question why the authors did not consider adenoma size as a continuous variable, given that there are efficient statistical methods for analyzing continuous variables. Second, I am concerned why the authors did not attempt to estimate relative effect sizes such as odds ratio (OR) for the association between adenoma size and the studied outcomes. In fact, judgment about the presence of associations based only on P value does not provide information about magnitude and direction of association. I estimated OR (95% confidence interval [CI]) for the effect of each category of adenoma size compared with adenoma size of <15 as a reference group on the risk of recurrence with the penalization method. The ORs (95% CI) for 15 <20 mm, 20 <30 mm, and 30 mm were found to be 0.87 (95% CI, 0.18-4.10), 3.66 (95% CI, 0.95-14.14), and 7.19 (95% CI, 2.02-25.58), respectively. Therefore, only adenoma size >30 mm was associated with the risk of recurrence. Here, re-estimating the true association between the studied predictors and the studied outcomes is suggested for the authors.

Impact of Paneth Cell Autophagy on Inflammatory Bowel Disease

Intestinal mucosal barrier, mainly consisting of the mucus layer and epithelium, functions in absorbing nutrition as well as prevention of the invasion of pathogenic microorganisms. Paneth cell, an important component of mucosal barrier, plays a vital role in maintaining the intestinal homeostasis by producing antimicrobial materials and controlling the host-commensal balance. Current evidence shows that the dysfunction of intestinal mucosal barrier, especially Paneth cell, participates in the onset and progression of inflammatory bowel disease (IBD). Autophagy, a cellular stress response, involves various physiological processes, such as secretion of proteins, production of antimicrobial peptides, and degradation of aberrant organelles or proteins. In the recent years, the roles of autophagy in the pathogenesis of IBD have been increasingly studied. Here in this review, we mainly focus on describing the roles of Paneth cell autophagy in IBD as well as several popular autophagy-related genetic variants in Penath cell and the related therapeutic strategies against IBD.

Disconnected pancreatic duct syndrome - Wait! Why not try one more time?

A 42-year-old man with a history of necrotizing pancreatitis complicated by pancreatic fluid collections (PFCs) who underwent percutaneous drainage for 4 months but still had a persistent external fistula with high amylase activity in the drainage fluid was referred. A previous endoscopic retrograde cholangiopancreatography (ERCP) in another endoscopy center had suggested complete main pancreatic duct (MPD) disruption (▶Fig. 1). Contrast injection through the drainage catheter showed no opacification of the proximal MPD (▶Fig. 2 a). During a second ERCP, carried out in our endoscopy center, contrast injection through the major duodenal papilla also demonstrated complete cutoff of the proximal MPD and no opacification of the distal MPD (▶Fig. 2b). Therefore, the diagnosis of complete MPD disruption was made and normally surgical treatment would have been considered. Fortunately, in this case, after several attempts by the endoscopist, the disruption site was traversed with a guidewire, and the route from the MPD complete cutoff to the site of the PFCs was not opacified by any contrast. A pancreatic stent was placed to drain the PFCs (▶Fig. 2 c and ▶Fig. 3; ▶Video1) and immediately there was cessation of fluid drainage from the percutaneous drainage catheter. The patient had an uneventful recovery and was discharged 1 day later, with surgery having been avoided. The diagnosis of disconnected pancreatic duct syndrome (DPDS) is usually confirmed on ERCP if there is extravasation of injected contrast from the MPD without filling of the distal MPD [1]. Once the diagnosis of complete MPD disruption has been made, it is often treated by surgery [2], while endotherapy is effective for partial pancreatic ductal disruption [3]. However, we have shown in this case, where both percutaneous and endoscopic contrast injection had demonstrated complete cutoff of the pancreatic duct, that there is still a possibility that the guidewire may cross the site of the disruption and that a stent can be placed to drain the pancreatic juice or PFC. But only if we try!