Ultra-Processed Food Consumption and Long-Term Risk of Irritable Bowel Syndrome: A Large-Scale Prospective Cohort Study.

BACKGROUND & AIMS: The considerable disease burden of irritable bowel syndrome (IBS) has coincided with the increase of ultraprocessed food (UPF) consumption over the past few decades. However, epidemiologic evidence for an association is lacking. We aimed to examine the long-term risk of IBS associated with UPF consumption in a large-scale prospective cohort. METHODS: Participants who completed 24-hour dietary recalls during 2009 to 2012 from the UK Biobank, and free of IBS, celiac disease, inflammatory bowel disease, and any cancer at baseline, were included (N = 178,711; 53.1% female). UPF consumption was defined according to the NOVA food classification system, expressed as a percentage of UPF content in the total diet intake (as grams per day). The primary outcome was incident IBS. A Cox proportional hazard model was performed to estimate associated risk. RESULTS: The mean UPF consumption was 21.0% (SD, 11.0%) of the total diet. During a median of 11.3 years of follow-up, 2690 incident IBS cases were identified. An 8% higher risk of IBS (hazard ratio, 1.08; 95% CI, 1.04-1.12) was associated with every 10% increment of UPF consumption. Compared with the lowest quartile of UPF consumption, the highest quartile was associated with a significantly increased risk of incident IBS (hazard ratio, 1.19; 95% CI, 1.07-1.33; Ptrend < .001). Subgroup analyses by age, sex, body mass index, smoking, and alcohol drinking status also showed similar results, except for the never/previous drinking subgroup. Further sensitivity analyses confirmed the positive association with a higher UPF consumption. CONCLUSIONS: Our findings provide evidence that a higher UPF consumption is associated with an increased risk of incident IBS, with a significant dose-response relationship.

Lysophosphatidic acid promotes ESCC progression by increasing the level of CCL2 secreted by esophageal epithelial cells.

BACKGROUND: Lysophosphatidic acid (LPA) is a small bioactive lipid which acts as a potent regulator in various tumor progressions through six G-protein-coupled receptors (LPA1-LPA6). Our previous study demonstrated that the LPA-producing enzyme, autotaxin (ATX), was upregulated in esophageal squamous cell carcinoma (ESCC) and ATX high expression levels indicated a poor prognosis. Esophageal squamous cell carcinoma is a type of malignant tumor which originates from epithelial cells. Its progression can be affected by the interaction between cancer cells and normal cells. However, the impact of LPA on the interaction between esophageal epithelial cells and cancer cells in the development of ESCC remains uncertain. METHODS: MTS and Edu assays were performed to determine ESCC cell proliferation in culture medium (CM) derived from LPA-stimulated esophageal epithelial cells (Het-1a). A wound healing assay, transwell migration and an invasion assay were performed to assess the metastatic ability of ESCC cells. Cytokine array analysis was conducted to detect the differentially secreted cytokines in CM. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were utilized to uncover the pathways and cytokines that are influenced by LPA in ESCC. Immunohistochemical staining was employed to measure the expression of ATX and CCL2 in early-stage ESCC. Quantitative real-time PCR, western blot, enzyme-linked immunosorbent assay and an antibody neutralization assay were employed to measure the mechanism of LPA-mediated communication between epithelial cells and cancer cells. RESULTS: Functional experiments showed that exposing ESCC cancer cells to CM from LPA-treated Het-1a results in promoting proliferation, migration, invasion and epithelial-mesenchymal transition processes. Using cytokine array analysis, we discovered that LPA triggers the release of multiple cytokines from epithelial cells. After screening of the TCGA and GEO databases, CCL2 was identified and found to be correlated with ATX expression in ESCC. Furthermore, CCL2 levels in both mRNA expression and secretion were observed to be upregulated in epithelial cells upon stimulation with LPA. Blocking CCL2 effectively reduced the pro-migration influence of CM derived from LPA-treated Het-1a. Mechanism studies have demonstrated that LPA activated the NF-κB signaling pathway through LPA1/3, ultimately causing an increase in CCL2 expression and secretion in Het-1a. CONCLUSIONS: Our findings, taken together, demonstrate that CM from LPA-treated esophageal epithelial cells plays a significant role in promoting the progression of ESCC, with CCL2 acting as the primary regulator.

Improved Adenoma Detection Rate Using a Novel Colonoscopic Distal Attachment: A Multicenter Randomized Controlled Trial.

INTRODUCTION: To evaluate the effect of Embrella, a novel-designed colonoscopic distal attachment, on adenoma detection rate (ADR) and adenoma per colonoscopy (APC), compared with standard colonoscopy in routine practice. METHODS: All consecutive participants who underwent routine colonoscopic examinations at 3 endoscopy centers in China were enrolled. Participants were randomly assigned in a 1:1 ratio to the Embrella-assisted colonoscopy (EAC) or standard colonoscopy (SC) groups. ADR, APC, inspection time, pain scores, and adverse events were recorded. RESULTS: Overall, 1,179 participants were randomized into the EAC (n = 593) and SC groups (n = 586). EAC increased the overall ADR from 24.6% to 34.2% ( P < 0.001) and improved APC from 0.44 to 0.64 ( P = 0.002). Subgroup analyses indicated that EAC significantly improved ADR for adenomas < 10 mm (13.8% vs 8.5%, P = 0.004 for 5-9 mm and 27.0% vs 17.2%, P < 0.001 for < 5 mm), nonpedunculated adenomas (26.6% vs 18.8%, P < 0.001), and adenomas in the transverse (10.8% vs 6.1%, P = 0.004) and left colon (21.6% vs 13.7%, P < 0.001). APC in the subgroup analyses was consistent with ADR. The mean inspection time was shorter with EAC (6.52 vs 6.68 minutes, P = 0.046), with no significant impact on participants' pain scores ( P = 0.377). Moreover, no EAC-related adverse events occurred. DISCUSSION: EAC significantly increased ADR and APC compared with SC, particularly for adenomas <10 mm, nonpedunculated adenomas, and adenomas in the transverse and left colon.

Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice.

BACKGROUND: Sympathoexcitation contributes to myocardial remodeling in heart failure (HF). Increased circulating pro-inflammatory mediators directly act on the Subfornical organ (SFO), the cardiovascular autonomic center, to increase sympathetic outflow. Circulating mitochondria (C-Mito) are the novel discovered mediators for inter-organ communication. Cyclic GMP-AMP synthase (cGAS) is the pro-inflammatory sensor of damaged mitochondria. OBJECTIVES: This study aimed to assess the sympathoexcitation effect of C-Mito in HF mice via promoting endothelial cGAS-derived neuroinflammation in the SFO. METHODS: C-Mito were isolated from HF mice established by isoprenaline (0.0125 mg/kg) infusion via osmotic mini-pumps for 2 weeks. Structural and functional analyses of C-Mito were conducted. Pre-stained C-Mito were intravenously injected every day for 2 weeks. Specific cGAS knockdown (cGAS KD) in the SFO endothelial cells (ECs) was achieved via the administration of AAV9-TIE-shRNA (cGAS) into the SFO. The activation of cGAS in the SFO ECs was assessed. The expression of the mitochondrial redox regulator Dihydroorotate dehydrogenase (DHODH) and its interaction with cGAS were also explored. Neuroinflammation and neuronal activation in the SFO were evaluated. Sympathetic activity, myocardial remodeling, and cardiac systolic dysfunction were measured. RESULTS: C-Mito were successfully isolated, which showed typical structural characteristics of mitochondria with double-membrane and inner crista. Further analysis showed impaired respiratory complexes activities of C-Mito from HF mice (C-MitoHF) accompanied by oxidative damage. C-Mito entered ECs, instead of glial cells and neurons in the SFO of HF mice. C-MitoHF increased the level of ROS and cytosolic free double-strand DNA (dsDNA), and activated cGAS in cultured brain endothelial cells. Furthermore, C-MitoHF highly expressed DHODH, which interacted with cGAS to facilitate endothelial cGAS activation. C-MitoHF aggravated endothelial inflammation, microglial/astroglial activation, and neuronal sensitization in the SFO of HF mice, which could be ameliorated by cGAS KD in the ECs of the SFO. Further analysis showed C-MitoHF failed to exacerbate sympathoexcitation and myocardial sympathetic hyperinnervation in cGAS KD HF mice. C-MitoHF promoted myocardial fibrosis and hypertrophy, and cardiac systolic dysfunction in HF mice, which could be ameliorated by cGAS KD. CONCLUSION: Collectively, we demonstrated that damaged C-MitoHF highly expressed DHODH, which promoted endothelial cGAS activation in the SFO, hence aggravating the sympathoexcitation and myocardial injury in HF mice, suggesting that C-Mito might be the novel therapeutic target for sympathoexcitation in HF.

Helicobacter pylori disrupts gastric mucosal homeostasis by stimulating macrophages to secrete CCL3.

BACKGROUND: Helicobacter pylori (H. pylori) is the predominant etiological agent of gastritis and disrupts the integrity of the gastric mucosal barrier through various pathogenic mechanisms. After H. pylori invades the gastric mucosa, it interacts with immune cells in the lamina propria. Macrophages are central players in the inflammatory response, and H. pylori stimulates them to secrete a variety of inflammatory factors, leading to the chronic damage of the gastric mucosa. Therefore, the study aims to explore the mechanism of gastric mucosal injury caused by inflammatory factors secreted by macrophages, which may provide a new mechanism for the development of H. pylori-related gastritis. METHODS: The expression and secretion of CCL3 from H. pylori infected macrophages were detected by RT-qPCR, Western blot and ELISA. The effect of H. pylori-infected macrophage culture medium and CCL3 on gastric epithelial cells tight junctions were analyzed by Western blot, immunofluorescence and transepithelial electrical resistance. EdU and apoptotic flow cytometry assays were used to detect cell proliferation and apoptosis levels. Dual-luciferase reporter assays and chromatin immunoprecipitation assays were used to study CCL3 transcription factors. Finally, gastric mucosal tissue inflammation and CCL3 expression were analyzed by hematoxylin and eosin staining and immunohistochemistry. RESULTS: After H. pylori infection, CCL3 expressed and secreted from macrophages were increased. H. pylori-infected macrophage culture medium and CCL3 disrupted gastric epithelial cells tight junctions, while CCL3 neutralizing antibody and receptor inhibitor of CCL3 improved the disruption of tight junctions between cells. In addition, H. pylori-infected macrophage culture medium and CCL3 recombinant proteins stimulated P38 phosphorylation, and P38 phosphorylation inhibitor improved the disruption of tight junctions between cells. Besides, it was identified that STAT1 was a transcription factor of CCL3 and H. pylori stimulated macrophage to secret CCL3 through the JAK1-STAT1 pathway. Finally, after mice were injected with murine CCL3 recombinant protein, the gastric mucosal injury and inflammation were aggravated, and the phosphorylation level of P38 was increased. CONCLUSIONS: In summary, our findings demonstrate that H. pylori infection stimulates macrophages to secrete CCL3 via the JAK1-STAT1 pathway. Subsequently, CCL3 damages gastric epithelial tight junctions through the phosphorylation of P38. This may be a novel mechanism of gastric mucosal injury in H. pylori-associated gastritis.

Long-term risk of cardiovascular disease associated with MASLD and different cardiometabolic risk factors in IBD patients: A prospective cohort study.

BACKGROUND: To examine the cardiovascular disease (CVD) risks associated with metabolic dysfunction-associated steatotic liver disease (MASLD) and different numbers of cardiometabolic risk factors (CMRFs) in patients with inflammatory bowel disease (IBD) based on a long-term prospective cohort. METHODS: Prevalent IBD patients at baseline who were free of CVD, cancer, alcoholic liver disease, cancer and hepatitis B/C virus seropositive were included (N = 4204). MASLD, MASLD subtypes [pure MASLD, MASLD with increased alcohol intake (MetALD)], lean/non-lean MASLD and CMRFs at baseline were defined according to the latest criteria proposed by AASLD and EASL. The primary outcome was incident CVD, including ischaemic heart disease (IHD), heart failure (HF) and stroke. Multivariable Cox proportional hazard models were used to estimate the relationship. RESULTS: Overall, 1528 (36.4%) were diagnosed with MASLD at baseline. During a median of 13.1-year follow-up, 503 incident CVDs were identified. Compared with IBD-only, IBD-MASLD patients had an increased risk of CVD (HR = 1.77, 95%CI: 1.26-2.49), especially in those with MetALD (HR = 2.34, 1.34-4.11) and lean MASLD (HR = 2.30, 1.13-4.66). As the number of CMRFs increased, the risks of CVD were significantly increased (ptrend <0.001), with a 116% and 92% excess risk in MASLD with 3 CMRFs (HR = 2.16, 1.48-3.15) and ≥4 CMRFs (HR = 1.92, 1.27-2.91). Similar excess risk of incident IHD and HF was observed in IBD-MASLD, either pure MASLD or MetALD, as well as lean/non-lean MASLD. CONCLUSIONS: MASLD is associated with increased CVD risk in IBD patients, with greater risk as number of CMRFs increased and evidently higher risk in MetALD and lean MASLD patients.

Current research on the interaction between Helicobacter pylori and macrophages.

Helicobacter pylori (H. pylori) is a gram-negative bacteria with a worldwide infection rate of 50%, known to induce gastritis, ulcers and gastric cancer. The interplay between H. pylori and immune cells within the gastric mucosa is pivotal in the pathogenesis of H. pylori-related disease. Following H. pylori infection, there is an observed increase in gastric mucosal macrophages, which are associated with the progression of gastritis. H. pylori elicits macrophage polarization, releases cytokines, reactive oxygen species (ROS) and nitric oxide (NO) to promote inflammatory response and eliminate H. pylori. Meanwhile, H. pylori has developed mechanisms to evade the host immune response in order to maintain the persistent infection, including interference with macrophage phagocytosis and antigen presentation, as well as induction of macrophage apoptosis. Consequently, the interaction between H. pylori and macrophages can significantly impact the progression, pathogenesis, and resolution of H. pylori infection. Moreover, macrophages are emerging as potential therapeutic targets for H. pylori-associated gastritis. Therefore, elucidating the involvement of macrophages in H. pylori infection may provide novel insights into the pathogenesis, progression, and management of H. pylori-related disease.

Endoscopic application of magnetic compression anastomosis: a review.

Magnetic compression anastomosis (MCA) is a new method that provides sutureless passage construction for tubular organs. Due to the high recurrence rate of conventional endoscopic treatment and the high morbidity and mortality of surgical procedures, the MCA technique shows promise. The aim of this review is to comprehensively examine the literature related to the use of MCA in different gastrointestinal diseases over the past few years, categorizing them according to the anastomotic site and describing in detail the various methods of magnet delivery and the clinical outcomes of MCA. MCA is an innovative technique, and its use represents an advancement in the field of minimally invasive interventions. Comparison studies have shown that the anastomosis formed by MCA is comparable to or better than surgical sutures in terms of general appearance and histology. Although most of the current research has involved animal studies or studies with small populations, the safety and feasibility of MCA have been preliminarily demonstrated. Large prospective studies involving populations are still needed to guarantee the security of MCA. For technologies that have been initially used in clinical settings, effective measures should also be implemented to identify, even prevent, complications. Furthermore, specific commercial magnets must be created and optimized in this emerging area.

Activation of NOTCH signaling via DLL1 is mediated by APE1-redox-dependent NF-κB activation in oesophageal adenocarcinoma.

OBJECTIVE: Oesophageal adenocarcinoma (EAC) arises in the setting of Barrett's oesophagus, an intestinal metaplastic precursor lesion that can develop in patients with chronic GERD. Here, we investigated the role of acidic bile salts, the mimicry of reflux, in activation of NOTCH signaling in EAC. DESIGN: This study used public databases, EAC cell line models, L2-IL1ß transgenic mouse model and human EAC tissue samples to identify mechanisms of NOTCH activation under reflux conditions. RESULTS: Analysis of public databases demonstrated significant upregulation of NOTCH signaling components in EAC. In vitro studies demonstrated nuclear accumulation of active NOTCH1 cleaved fragment (NOTCH intracellular domain) and upregulation of NOTCH targets in EAC cells in response to reflux conditions. Additional investigations identified DLL1 as the predominant ligand contributing to NOTCH1 activation under reflux conditions. We discovered a novel crosstalk between APE1 redox function, reflux-induced inflammation and DLL1 upregulation where NF-κB can directly bind to and induce the expression of DLL1. The APE1 redox function was crucial for activation of the APE1-NF-κB-NOTCH axis and promoting cancer cell stem-like properties in response to reflux conditions. Overexpression of APE1 and DLL1 was detected in gastro-oesophageal junctions of the L2-IL1ß transgenic mouse model and human EAC tissue microarrays. DLL1 high levels were associated with poor overall survival in patients with EAC. CONCLUSION: These findings underscore a unique mechanism that links redox balance, inflammation and embryonic development (NOTCH) into a common pro-tumorigenic pathway that is intrinsic to EAC cells.

Effect of 3-Dimensional Imaging Device on Polyp and Adenoma Detection During Colonoscopy: A Randomized Controlled Trial.

INTRODUCTION: To evaluate the effect of 3-dimensional (3D) imaging device on polyp and adenoma detection during colonoscopy. METHODS: In a single-blind, randomized controlled trial, participants aged 18-70 years who underwent diagnostic or screening colonoscopy were consecutively enrolled between August 2019 and May 2022. Each participant was randomized in a 1:1 ratio to undergo either 2-dimensional (2D-3D) colonoscopy or 3D-2D colonoscopy through computer-generated random numbers. Primary outcome included polyp detection rate (PDR) and adenoma detection rate (ADR), defined as the proportion of individuals with at least 1 polyp or adenoma detected during colonoscopy. The primary analysis was intention-to-treat. RESULTS: Of 1,196 participants recruited, 571 in 2D-3D group and 583 in 3D-2D group were finally included after excluding those who met the exclusion criteria. The PDR between 2D and 3D groups was separately 39.6% and 40.5% during phase 1 (odds ratio [OR] = 0.96, 95% confidence interval [CI]: 0.76-1.22, P = 0.801), whereas PDR was significantly higher in 3D group (27.7%) than that of 2D group (19.9%) during phase 2, with a 1.54-fold increase (1.17-2.02, P = 0.002). Similarly, the ADR during phase 1 between 2D (24.7%) and 3D (23.8%) groups was not significant (OR = 1.05, 0.80-1.37, P = 0.788), while ADR was significantly higher in 3D group (13.8%) than that of 2D group (9.9%) during phase 2, with a 1.45-fold increase (1.01-2.08, P = 0.041). Further subgroup analysis confirmed significantly higher PDR and ADR of 3D group during phase 2, particularly in midlevel and junior endoscopists. DISCUSSION: The 3D imaging device could improve overall PDR and ADR during colonoscopy, particularly in midlevel and junior endoscopists. Trial number: ChiCTR1900025000.

Circulating Tumor Cells as Diagnostic Markers of Early Gastric Cancer and Gastric Precancerous Lesions.

INTRODUCTION: Circulating tumor cells (CTCs) may be potential diagnostic biomarkers of various malignancies including gastric cancer. This study aimed to evaluate whether CTCs could be used to facilitate the diagnosis of early gastric cancer (EGC) or precancerous gastric lesions. METHODS: The diagnostic study included consecutive patients with EGC, gastric precancerous lesions, or fundic gland polyps admitted to the Gastroenterology Department, Beijing Friendship Hospital Affiliated to Capital Medical University (National Center for Digestive Diseases) between October 2016 and January 2018. RESULTS: A total of 92 patients were enrolled, including 57 patients with EGC, 14 patients with gastric precancerous lesions, and 21 patients with fundic gland polyps (control group). CTCs were detected in 47.89% (34/71) of patients with EGC/gastric precancerous lesions and 4.76% (1/21) of patients with fundic gland polyps (p < 0.001). CTC detection distinguished EGC/precancerous lesions from fundic gland polyps with an area under the receiver operating characteristic curve of 0.740 (95% confidence interval, 0.640-0.840; p = 0.001), a sensitivity of 49.10%, a specificity of 95.00%, a positive predictive value of 97.00%, and a negative predictive value of 64.90%. CONCLUSIONS: Peripheral blood CTCs are more common in patients with EGC or gastric precancerous lesions than in patients with fundic gland polyps. Measurement of CTCs may be a useful tool to aid in the diagnosis of EGC and precancerous lesions.

A nomogram and risk classification system predicting esophageal stricture after endoscopic submucosal dissection of a large area for early esophageal cancer.

BACKGROUND AND OBJECTIVES: Esophageal stricture is a troublesome adverse effect of endoscopic submucosal dissection (ESD) for early esophageal cancer. However, risk factors of post-ESD esophageal stricture formation are incomprehensive. This study aimed to conduct a comprehensive analysis of independent risk factors and provide predictive tools. METHODS: Patients who underwent ESD for early esophageal cancer between 2014 and 2021 at the Beijing Friendship Hospital, Capital Medical University, were recruited. A nomogram and risk classification system was established based on Cox proportional hazards analyses and validated using the concordance index (C-index), calibration curves, decision curve analysis (DCA), and Kaplan-Meier (K-M) curves. RESULTS: Stricture formed in 36 patients, while stricture was not observed in the remaining 112 patients. Operative time (odds ratio [OR]: 1.01; 95% confidence interval [CI]: 1.00-1.01; p < 0.01); lesions >3/4 circumferential range of esophagus (OR: 3.82; 95% CI: 1.90-7.66; p < 0.01), and tumor infiltration to the mucosal lamina propria (m2) or deeper (OR: 2.40; 95% CI: 1.24-4.66; p = 0.01) were independent predictive factors for post-ESD esophageal stricture. The nomogram and risk classification system was developed and validated with 0.79 C-index, good calibration curves, good DCA results, and good K-M curves. CONCLUSIONS: We developed a nomogram and risk stratification system to predict post-ESD esophageal stricture using three independent risk factors.

Role of BMI in the relationship between dietary inflammatory index and non-alcoholic fatty liver disease: an intermediary analysis.

OBJECTIVE: Previous studies have indicated that a pro-inflammatory diet is associated with non-alcoholic fatty liver disease (NAFLD), but the role of BMI remains ambiguous. We aim to study the intermediary effect of BMI on the relationship between dietary inflammatory properties and NAFLD. METHODS: A total of 19536 adult participants from the National Health and Nutrition Examination Surveys (NHANES) were included. Dietary inflammatory index (DII) was used to evaluate the dietary inflammatory properties and NAFLD was diagnosed by non-invasive biomarkers. Weighted multivariable logistic regression models estimated ORs and 95% CIs between DII and incidence of NAFLD. Interaction effect between DII and BMI on NAFLD was tested and the mediation analysis of BMI was performed. RESULTS: Higher DII scores, representing higher inflammatory potential of diet, were positively associated with a higher risk of NAFLD. Compared with the first quartile of DII, people from the second quartile (OR: 1.23 [95% CI: 1.04, 1.46]) to the fourth quartile (OR: 1.59 [95% CI: 1.31, 1.94]) have a higher risk of NAFLD before adjustment for BMI. The overall association was completely mediated by BMI (89.19%). CONCLUSIONS: Our findings suggested that a higher pro-inflammatory potential diet was associated with a higher prevalence of NAFLD, and this association might be mediated by BMI.

The usefulness of fecal hemoglobin and calprotectin tests in diagnosing significant bowel diseases: a prospective study.

OBJECTIVES: Although colonoscopy remains the gold standard for determining bowel diseases, it's invasive and expensive. New non-invasive diagnostic methods are urgently needed as an initial screening modality. We aimed to investigate the value of fecal calprotectin (FC) and fecal immunochemical test (FIT) in differentiation of significant and non- significant bowel diseases. METHODS: In this prospective study, consecutive individuals were included if they underwent colonoscopy for symptoms of lower gastrointestinal (GI) tract, positive fecal occult blood test, surveillance for IBD or colorectal cancer (CRC) screening. Diagnostic value of FC and FIT in discriminating significant bowel diseases (advanced neoplasia, active inflammatory bowel diseases or bowel inflammation due to other causes) and non-significant bowel diseases (normal, asymptomatic diverticulum, non-adenomatous polyp, or non-advanced neoplasia) were evaluated. RESULTS: Among 201 individuals included, 107 patients had significant bowel diseases. FC and FIT had an area under the curve (AUC) of 0.722 (95% confidence interval [CI] 0.653-0.792) and 0.797 (95%CI 0.734-0.860), respectively, for determining significant bowel diseases. Combination of FC and FIT predicted significant bowel diseases with an AUC, sensitivity, specificity, and accuracy of 0.832 (95% CI 0.775-0.890), 77.6%, 74.5%, and 76.1%, respectively. Moreover, combination of FC and FIT was more sensitive among patients with lower GI symptoms than asymptomatic individuals (80.8% vs. 74.1%) to identify significant bowel diseases. CONCLUSIONS: A single measurement of FC or FIT is not sufficiently accurate to identify patients with significant bowel disease. However, combination of FC and FIT can help increase the sensitivity, especially in patients with lower GI symptoms.

Comparison of endoscopic submucosal dissection outcomes between early gastric cardiac and non-cardiac cancers: a retrospective single-center study.

OBJECTIVES: This study aims to compare the efficacy of endoscopic submucosal dissection (ESD) between early gastric cardiac cancer (EGCC) and early gastric non-cardiac cancer (EGNCC), and investigate associated risk factors for non-curative resection. METHODS: Early gastric cancer (EGC) patients who underwent ESD from January 2015 to September 2020 in Beijing Friendship Hospital were consecutively enrolled. The clinical, histopathological and endoscopic data were retrospectively analyzed. The study was registered in Chinese Clinical Trial Registry (ChiCTR1800017117). RESULTS: Among 500 patients with 534 EGC lesions, 117 patients with 118 lesions were allocated to the EGCC group, and 383 patients with 416 lesions to the EGNCC group. The rates of en bloc resection, complete resection and curative resection in the EGCC group were 97.5%, 78.8% and 71.2%, respectively, significantly lower than those in the EGNCC group (99.8%, 94.5% and 90.4%, p = .010, <.001 and <.001). Among non-curative resected lesions, EGCC had more cases in both endoscopic curability (eCura) C-1 and C-2 groups than EGNCC (10.2% and 18.6% vs. 2.4% and 7.2%, p < .001). Multivariate analysis showed that tumor size (OR 2.393, 95% CI 1.388-4.126) and submucosal invasion (OR 11.498, 95% CI 3.759-35.175) were risk factors for non-curative resection in the EGCC group. For EGCC larger than 3 cm, none achieved curative resection, 86.7% were classified as eCura C-2 and 46.7% exhibited deep submucosal infiltration. CONCLUSIONS: The curative resection rate of ESD for EGCC was lower than that for EGNCC. ESD for EGCC larger than 3 cm should be cautiously considered.

Potential intestinal infection and faecal-oral transmission of human coronaviruses.

Human coronaviruses (HCoVs) were first described in 1960s for patients experiencing common cold. Since then, increasing number of HCoVs have been discovered, including those causing severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and the circulating coronavirus disease 2019 (COVID-19), which can cause fatal respiratory disease in humans on infection. HCoVs are believed to spread mainly through respiratory droplets and close contact. However, studies have shown that a large proportion of patients with HCoV infection develop gastrointestinal (GI) symptoms, and many patients with confirmed HCoV infection have shown detectable viral RNA in their faecal samples. Furthermore, multiple in vitro and in vivo animal studies have provided direct evidence of intestinal HCoV infection. These data highlight the nature of HCoV GI infection and its potential faecal-oral transmission. Here, we summarise the current findings on GI manifestations of HCoVs. We also discuss how HCoV GI infection might occur and the current evidence to establish the occurrence of faecal-oral transmission.

Changes in the gut microbiome can predict and decrease Epstein-Barr virus infection risk in children after liver transplantation.

OBJECTIVE: Primary Epstein-Barr virus (EBV) infection is observed in 60% of children during the first year after liver transplantation as usage of imm-unosuppressant. Finding predictive indicators of EBV infection is important to reduce the morbidity and mortality of EBV infection-related diseases by suggesting a dose reduction of immunosuppressant. METHODS: We compared and analysed the gut microbiome of EBV-infected children with an asymptomatic virus-carrying status and EBV-uninfected children after liver transplantation using high-throughput sequencing. RESULTS: Significant differences in gut microbiome composition in two groups were detected. In detail, Firmicutes and Lactobacillus were increased in EBV-infected group, while Clostridium was increased in EBV-uninfected group. Furthermore, CD4 percentage in T cells of blood showed a significant positive correlation with the content of Clostridium sp. CAG: 127 in EBV-uninfected group. CONCLUSION: Changes in the gut microbiome could predict and decrease the EBV infection risk of children after liver transplantation.

The efficacy and safety of cold snare polypectomy with submucosal injection for the removal of polyps less than 20 mm in size: a systematic review and meta-analysis.

BACKGROUND AND AIM: Neoplastic polyp removal is important for colorectal cancer prevention. Endoscopists have proposed cold snare endoscopic mucosal resection (CS-EMR) as a solution to solve positive cutting edges and postoperative bleeding. However, many controversies regarding its specific performance in practice have been reported. The aim of this pooled analysis was to report the efficacy and safety of CS-EMR. METHODS: PubMed/Medline, Embase, Google Scholar, and the Cochrane Library searched up to January 2022 to identify studies in which CS-EMR was performed for the removal of colorectal polyps measuring less than 20 mm. The primary outcome was the complete resection rate (CRR), and the secondary outcome was the rate of adverse events. RESULTS: Eleven studies were included in the final analysis, which included 861 colorectal polyps. The overall CRR with CS-EMR was 96.3% (95% CI, 93.9-98.2%). The early and delayed bleeding rates of CS-EMR were 3.1% (95% CI, 1.2-5.5%) and 1.4% (95% CI, 0.6-2.4%), respectively. There were no statistical significances between CS-EMR and cold snare polypectomy (CSP) in terms of the CRR and adverse events, as well as CS-EMR and hot snare endoscopic mucosal resection (HS-EMR). CONCLUSIONS: For resecting colorectal polyps measuring ≤20 mm, CS-EMR is an effective attempt. However, compared with CSP and HS-EMR, CS-EMR did not improve the efficiency and safety of polypectomy as expected. Multicenter randomized controlled trials are needed to compare CSP with CS-EMR in the resection of <10 mm polyps and HSP with CS-EMR in the resection of ≥10 mm polyps.

Recovery of driving skills after endoscopy under propofol sedation: a prospective pilot study to assess the driving skills after endoscopic sedation using driving simulation.

BACKGROUND: Patients are recommended not to drive for at least the first 24 h after endoscopy with propofol sedation. However, the evidence underlying these recommendations is scarce. We hypothesized that after endoscopic procedures performed under propofol sedation, the subject's driving ability was restored in less than 24 h. METHODS: We prospectively enrolled thirty patients between 20 and 70 years possessing a legitimate driver's license scheduled for endoscopy at our hospital. The sample chosen was a convenience sample. Gastroscopy or colonoscopy was performed with propofol sedation. Before and after endoscopy, the investigator drove the subjects to the laboratory to assess their driving skills using a driving simulation system, which employs 3 driving scenarios designed by professional transportation researchers. The blood propofol concentration was estimated before endoscopy, and 2 and 4 h after endoscopy. The primary outcome was the time required for subjects to recover their driving ability after propofol sedation. The secondary outcome was the blood propofol concentration before and after endoscopic procedures under propofol anesthesia. RESULTS: Thirty volunteers participated in the study and 18 of them completed all the interventions. In the low-risk S-curve scene, the mean acceleration, lane deviation, and number of deviations from the path at baseline (0.016 cm/s2, 42.50 cm, and 0.83, respectively) were significantly less than that at post-2 h (0.029 cm/s2, P = 0.001; 53.80 cm, P = 0.014; 2.06, P = 0.022). In the moderate-(overtaking) and high-risk (emergency collision avoidance) scenes, the tested parameters at baseline and post-2 h were statistically comparable. In the low-, moderate-, and high-risk scenes the tested parameters at baseline and post-4 h were statistically comparable. The total range of propofol was 120-280 mg.The mean blood concentration of propofol at post-2 h was 0.81 ± 0.40 µg/mL, and at post-4 h was below the limit of detection. CONCLUSION: After endoscopy performed under propofol sedation, subjects' driving abilities were completely restored at 4 h when tested on a simulator.

Endoscopic ultrasound-guided gallbladder endoscopic mucosal resection: a pilot porcine study.

INTRODUCTION: Endoscopic ultrasound (EUS)-guided natural orifice transluminal gallbladder polypectomy provides a minimally invasive alternative to cholecystectomy. The study aimed to investigate the feasibility and safety of protocol for gallbladder endoscopic mucosal resection (gEMR) under EUS guidance using a porcine model. MATERIAL AND METHODS: Fifteen Bama mini pigs were randomly divided into the control (CG, n = 3) and experimental (EG, n = 12) groups. EUS-guided fine needle aspiration was performed in the CG and used to establish a gallbladder pathway for polyp resection under EUS guidance in the EG. Procedural safety was evaluated using routine blood and biochemical tests, microbial bile cultures, histopathological tests, and enzyme-linked immunosorbent assays for inflammatory adhesion factors. RESULTS: EUS-guided metal stents were successfully deployed in all 12 pigs. Two cases of stent displacement occurred postoperatively, and one pig died of infectious peritonitis on the first day after stent implantation. In 11 surviving experimental animals, mature gallbladder paths were formed at 7-14 days after gastro-cholecystostomy, through which gEMR of gallbladder polyps was successfully performed. There were no significant changes in levels of inflammatory and adhesion factors during the postoperative process. CONCLUSIONS: EUS-gEMR may be a safe and effective minimally invasive treatment approach for gallbladder polyps.