The Lactulose Breath Test Can Predict Refractory Gastroesophageal Reflux Disease by Measuring Bacterial Overgrowth in the Small Intestine.

OBJECTIVE: The diagnosis of RGERD in patients typically involves 24-hour esophageal pH monitoring, but due to its invasiveness and low patient compliance, new screening methods are needed. In this study, a lactulose breath test (LBT) was conducted to detect the growth of small intestine bacteria (SIBO) and explore the potential relationship between LBT and RGERD to identify a new treatment method for RGERD. METHODS: A total of 178 patients with gastroesophageal reflux were enrolled from June 2020 to December 2022 in the Gastroenterology Department, Building 3, the First Affiliated Hospital of Kunming Medical University; these patients included 96 patients with nonrefractory GERD (NRGERD) and 82 patients with RGERD. The Gerd Q score, reflux symptom index (RSI) score, gastroscopy results, clinical symptoms, and other related indicators were collected. Statistical methods were used to analyze the gathered data. RESULTS: The incidence of acid reflux and heartburn in patients with RGERD was significantly greater than that in patients with NRGERD (67.10% vs. 42.70%, P<0.01 and 65.00% vs. 34.40%, P<0.01). The CH4 values of patients with RGERD were significantly greater than those of patients with NRGERD at each time point, and there was a correlation between the CH4 values at 60 min and RGERD (P<0.05). For patients with RGERD, the incidence of abdominal pain, acid regurgitation, and heartburn was greater in the CH4-positive group than in the CH4-negative group (61.90% vs. 57.50%, 69.05% vs. 65.00%, 69.05% vs. 57.50%, P>0.05). The incidence of nausea was also greater in the CH4-positive group than in the CH4-negative group (61.90% vs. 35.00%, P<0.05). CONCLUSION: Increased CH4 levels are correlated with RGERD. In addition, patients with RGERD may develop SIBO after long-term use of PPIs, and interventions involving SIBO could provide new ideas for the treatment of RGERD.

Two new monoterpenoid indole alkaloids from the leaves and twigs of Ochrosia borbonica.

Two new monoterpenoid indole alkaloids, ochrobonines A (1) and B (2), together with five known compounds (3-7), were isolated from the leaves and twigs of Ochrosia borbonica. Their structures were determined by spectroscopic method, and the absolute configuration of compound 3 was first established by single-crystal X-ray diffraction. Compounds 1 and 2 represent a rare class of monoterpenoid indole alkaloids that with a 2-[1-(3-ethylpiperidin-4-yl)vinyl]-3-methyl-1H-indole skeleton.

Long non­coding RNA RP11­400N13.3 promotes the progression of colorectal cancer by regulating the miR­4722­3p/P2RY8 axis.

Accumulating evidence has shown that long non­coding RNAs (lncRNAs) play significant roles in the development and progression of many types of cancer including colorectal cancer. RP11­400N13.3 is a novel lncRNA discovered recently and its biological function and underlying mechanism in colorectal cancer remain elusive. This study aimed to reveal the relationship between RP11­400N13.3 and colorectal cancer. Our results demonstrated that the expression of RP11­400N13.3 was significantly upregulated in both colorectal cancer tissues and cell lines as compared to normal adjacent tissues and normal colonic epithelial cells by RT­qPCR, respectively. Upregulation of RP11­400N13.3 was found to be correlated with a poor overall survival rate. Functional studies revealed that RP11­400N13.3 facilitated the proliferation, migration, invasion and tumor growth of colorectal cancer cells while inhibiting the apoptosis of cancer cells in vitro and in vivo. We also observed that RP11­400N13.3 serves as a sponge for miR­4722­3p, and that P2Y receptor family member 8 (P2RY8) was predicted to be a target of miR­4722­3p by bioinformatics analysis. Western blot assay indicated that the expression of P2RY8 was negatively or positively regulated by miR­4722­3p or RP11­400N13.3. In addition, rescue experiments revealed that RP11­400N13.3 promoted proliferation, migration and invasion by directly regulating the expression of miR­4722­3p and P2RY8. In conclusion, our results revealed that RP11­400N13.3 promoted colorectal cancer progression via modulating the miR­4722­3p/P2RY8 axis, thus suggesting RP11­400N13.3 as a potential therapeutic target for the treatment of colorectal cancer.