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Introduction: The consumption of large amounts of ethanol can directly lead to acute gastric mucosal bleeding, edema, and erosion, while long-term drinking has been associated with gastric ulcers. Previous research has demonstrated that Har Gabur, a traditional Mongolian medicine, alleviates gastric ulcers through the physical adsorption of its carbon components. It is well known that the immune response has an important role in gastric ulceration. Methods: In the present study, we used an ethanol-induced injury cell and mice model to investigate whether Har Gabur can inhibit the immune response stimulated by ethanol and identify the active constituents of Har Gabur involved in this process. Results: We found that Har Gabur significantly repressed the activated Fas/FasL signal pathway and endogenous Bax/Bcl-2 apoptosis pathway. The molecular mechanism of the protective effect most likely involved the transcription or mRNA stability, as Har Gabur remarkably reversed the change in mRNA level of apoptosis-related genes induced by ethanol. Conclusion: Har Gabur operated in a cell-state-specific manner in vivo without inducing adverse effects in normal mice. Importantly, GO was identified as the main active ingredient of Har Gabur for gastric ulcers.

INTRODUCTION AND AIM Helicobacter pylori (H. pylori) is known to be capable of causing chronic inflammation of the gastric mucosa that slowly progresses through the premalignant stages, reaching localized gastric adenocarcinoma (GAC). Its outcome is closely related to the stage at which diagnosis is made. The aim of the present study was to determine cost-benefit by comparing esophagogastroduodenoscopy, serum pepsinogen detection, and no screening at all. MATERIAL AND METHODS Utilizing Markov chains and Monte Carlo simulation, the costs and effects of various detection modalities were simulated to analyze the cost-benefit of each strategy. For our population, we used the published data of patients with gastric cancer, applicable to the Mexican population. RESULTS The results were reported as incremental cost-effectiveness ratios. The best strategy was serum pepsinogen determination, followed by the strategy of endoscopic examination with continued monitoring every 3 years. CONCLUSIONS The performance of serum pepsinogen serology and directed endoscopic examination (and continued monitoring, if necessary) for GAC screening could be a cost-effective intervention in Mexico, despite the low-to-moderate general prevalence of the disease.

Background Exposed endoscopic full-thickness resection (Eo-EFTR) is emerging as a promising minimally invasive alternative to surgery for the treatment of deep gastric submucosal tumors (G-SMTs). However, literature concerning this subject is heterogeneous and data mostly come from relatively small retrospective studies. Aims We aimed to perform a pooled analysis of published data with regard to gastric Eo-EFTR, providing a pooled estimate of technical and clinical outcomes. Methods The protocol was registered in PROSPERO. MEDLINE and EMBASE databases were searched for studies published from 1998 to 2020. The primary outcomes were complete resection and surgical conversion rates. The secondary outcomes were overall and selected major adverse events rates. The Forest plots on primary and secondary endpoints were produced based on fixed and random effect models. Results Nineteen studies including 952 Eo-EFTR-treated G-SMTs were included. The pooled estimate of the complete resection rate and surgical conversion rates was 99.3% and 0.09%, respectively. The pooled estimate of overall major adverse events, delayed bleeding, delayed perforation and peritonitis, abdominal abscess and/or abdominal infection was 0.29%, 0.14%, 0.14%, and 0.12%, respectively. Conclusion Gastric Eo-EFTR has a high rate of complete resection with a low surgical conversion rate. It appears to be relatively safe and might represent a non-inferior minimally invasive alternative to surgery in selected cases.

Background: Despite the fact that Helicobacter spp. has been detected in equine gastric mucosa, no evidence exists about this infection in Colombian horses affected by equine ulcerative gastric syndrome (EGUS), nor in dental tartar. Objective: To detect Helicobacter spp. DNA in equine gastric mucosa and dental tartar and determine the relationship between the presence of Helicobacter spp. and gastric lesions. Methods: Samples of glandular gastric mucosa and dental tartar were collected from 30 equine slaughterhouses. Macroscopic lesions of the stomachs were classified and the total DNA in all samples was extracted using a commercial extraction kit. A final-point PCR was performed using primers for amplification of a segment of 251 bp of the gene encoding the 16s rRNA region; the amplified fragments were subjected to a second PCR to determine the presence of H. pylori, the VacA gene was typified. The resulting amplicons were sequenced. Results: It was possible to amplify 16s rRNA in several samples but there was no amplification of VacA. Fragments of the sequences were compatible with H. heilmannii. The 23.3 and 10% of gastric and tartar samples were positive for 16s rRNA of Helicobacter spp., respectively. Conclusion: Although genetic material of Helicobacter spp. was found in some animals, there was no relationship with gastric lesions. It is possible that helicobacteriosis has no bearing in EGUS etiology.

Microgravity is an ecological factor that affects the environment of the body. In this study, quantitative isobaric labeling (tandem mass tag) method was used to study the changes in human gastric mucosal cells under simulated microgravity for the first time. Comparative proteomic analysis identified 394 (202 upregulated and 192 downregulated) and 542 (286 upregulated and 256 downregulated) proteins differentially regulated by simulated microgravity after 3 and 7 days, respectively. Then the identified proteins were subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses for further exploration. The results of the analysis showed that the ribosomes of gastric mucosal cells were significantly impacted after exposure to simulated microgravity for 3 days, and the cells appeared to be in a state of stress and inflammation. Exposure to simulated microgravity for 7 days significantly affected the mitochondria of the cells, oxidative stress became more evident, while inflammation and weakened connections were observed in the cells. The results of this study highlighted the temporal response trend of gastric mucosal cells to the stressor of microgravity at the two time points of 3 and 7 days. These findings will provide insights into the development of methods to protect the gastric mucosa during space flight.

The mucosa of the body of the stomach (ie, the gastric corpus) uses 2 overlapping, depth-dependent mechanisms to respond to injury. Superficial injury heals via surface cells with histopathologic changes like foveolar hyperplasia. Deeper, usually chronic, injury/inflammation, most frequently induced by the carcinogenic bacteria Helicobacter pylori, elicits glandular histopathologic alterations, initially manifesting as pyloric (also known as pseudopyloric) metaplasia. In this pyloric metaplasia, corpus glands become antrum (pylorus)-like with loss of acid-secreting parietal cells (atrophic gastritis), expansion of foveolar cells, and reprogramming of digestive enzyme-secreting chief cells into deep antral gland-like mucous cells. After acute parietal cell loss, chief cells can reprogram through an orderly stepwise progression (paligenosis) initiated by interleukin-13-secreting innate lymphoid cells (ILC2s). First, massive lysosomal activation helps mitigate reactive oxygen species and remove damaged organelles. Second, mucus and wound-healing proteins (eg, TFF2) and other transcriptional alterations are induced, at which point the reprogrammed chief cells are recognized as mucus-secreting spasmolytic polypeptide-expressing metaplasia cells. In chronic severe injury, glands with pyloric metaplasia can harbor both actively proliferating spasmolytic polypeptide-expressing metaplasia cells and eventually intestine-like cells. Gastric glands with such lineage confusion (mixed incomplete intestinal metaplasia and proliferative spasmolytic polypeptide-expressing metaplasia) may be at particular risk for progression to dysplasia and cancer. A pyloric-like pattern of metaplasia after injury also occurs in other gastrointestinal organs including esophagus, pancreas, and intestines, and the paligenosis program itself seems broadly conserved across tissues and species. Here we discuss aspects of metaplasia in stomach, incorporating data derived from animal models and work on human cells and tissues in correlation with diagnostic and clinical implications.

Eradication of Helicobacter pylori is the first-line treatment for gastric mucosa-associated lymphoid tissue (MALT) lymphomas; however, lesions may persist in 20% of patients after initial treatment, thereby necessitating the use of an additional therapeutic approach. Other treatment options include radiation therapy, chemotherapy, endoscopic resection, rituximab therapy, or watchful waiting. We present a case of localized gastric MALT lymphoma that did not respond to H. pylori eradication therapy. The patient waited for 12 months but the tumor showed no signs of regression endoscopically. Histologic examination revealed residual MALT lymphoma. The tumor was then successfully treated using endoscopic submucosal dissection and the patient remained disease-free for 4 years. To our knowledge, this is the first case in which a gastric MALT lymphoma was treated with endoscopic submucosal dissection. In conclusion, endoscopic resection may be recommended as second-line therapy for properly selected patients with gastric MALT lymphoma as it is effective and minimally invasive.

У статті наведені результати порівняльної характеристики даних стандартного ендоскопічного дослідження слизової оболонки шлунка у дітей, хворих на хронічний гастрит, асоційований з Helicobacter pylori-інфекцією, з урахуванням цитотоксичності штаму Helicobacter pylori. Визначені характерні ендоскопічні особливості патологічних змін слизової оболонки шлунка при хронічних гастритах, асоційованих з цитотоксичними штамами Helicobacter pylori, у дітей.

Posttreatment evaluation of gastric mucosa-associated lymphoid tissue (MALT) lymphoma currently relies on esophagogastroduodenoscopy with histological assessment of biopsies. Overexpression of the G protein–coupled C-X-C chemokine receptor type 4 (CXCR4) has been previously observed in MALT lymphoma. The aim of this prospective study was to evaluate positron emission tomography (PET) with the novel CXCR4 tracer [68Ga]Pentixafor as a potential alternative to follow up biopsies for assessment of residual disease (noncomplete remission [CR]) after first-line Helicobacter pylori eradication. Forty-six post–H pylori eradication [68Ga]Pentixafor–PET/magnetic resonance imaging (MRI) examinations of 26 gastric MALT lymphoma patients, and 20 [68Ga]Pentixafor–PET/MRI examinations of 20 control group patients without lymphoma, were analyzed. In the MALT lymphoma group, time-matched gastric biopsies were used as reference standard and showed CR in 6 cases. Pooled examination-based accuracy, sensitivity, specificity, and positive and negative predictive values of [68Ga]Pentixafor–PET for detection of residual gastric MALT lymphoma at follow-up were 97.0%, 95.0%, 100.0%, 100.0%, and 92.9%, respectively. Maximum and mean PET standardized uptake values showed moderate correlation with immunohistochemistry-based CXCR4+ cell counts, with correlation coefficients of r = 0.51 and r = 0.52 (P = .008 and P = .006). In summary, CXCR4 imaging with [68Ga]Pentixafor–PET may represent a promising test for assessment of residual gastric MALT lymphomas after H pylori eradication.

Background Although almost all cases of gastric cancer are caused by Helicobacter pylori (HP) infection, there are some rare exceptions. Furthermore, the clinicopathological characteristics of gastric cancer may differ depending on HP infection status. This study aimed to determine the clinicopathological characteristics of undifferentiated-type gastric cancer (UD-GC) according to HP status. Methods The study involved 83 patients with UD-GC who were selected from 1559 patients with gastric cancer who underwent endoscopic resection at our hospital and whose HP infection status was confirmed. Clinicopathological characteristics were evaluated according to HP status (eradicated, n = 28; infected, n = 32; not infected, n = 23). Results In patients without HP infection, UD-GCs were Conclusion The clinicopathological characteristics of UD-GC were similar between HP-infected patients and HP-eradicated patients. Three of four patients with eradicated HP whose UD-GC developed ≥ 10 years after eradication were not eligible for endoscopic treatment and required additional surgery resection. In contrast, UD-GC was curable by endoscopic resection in all patients without HP infection.

Gastrointestinal bleeding is the most frequent major complication of antiplatelet therapy. In patients at low bleeding risk, however, clinically overt gastrointestinal bleeding is relatively uncommon.The authors sought to assess the effects of different antiplatelet regimens on gastrointestinal mucosal injury by means of a novel magnetically controlled capsule endoscopy system in patients at low bleeding risk.Patients (n = 505) undergoing percutaneous coronary intervention in whom capsule endoscopy demonstrated no ulcerations or bleeding (although erosions were permitted) after 6 months of dual antiplatelet therapy (DAPT) were randomly assigned to aspirin plus placebo (n = 168), clopidogrel plus placebo (n = 169), or aspirin plus clopidogrel (n = 168) for an additional 6 months. The primary endpoint was the incidence of gastrointestinal mucosal injury (erosions, ulceration, or bleeding) at 6-month or 12-month capsule endoscopy.Gastrointestinal mucosal injury through 12 months was less with single antiplatelet therapy (SAPT) than with DAPT (94.3% vs 99.2%; P = 0.02). Aspirin and clopidogrel monotherapy had similar effects. Among 68 patients without any gastrointestinal injury at randomization (including no erosions), SAPT compared with DAPT caused less gastrointestinal injury (68.1% vs 95.2%; P = 0.006), including fewer new ulcers (8.5% vs 38.1%; P = 0.009). Clinical gastrointestinal bleeding from 6 to 12 months was less with SAPT than with DAPT (0.6% vs 5.4%; P = 0.001).Despite being at low risk of bleeding, nearly all patients receiving antiplatelet therapy developed gastrointestinal injury, although overt bleeding was infrequent. DAPT for 6 months followed by SAPT with aspirin or clopidogrel from 6 to 12 months resulted in less gastrointestinal mucosal injury and clinical bleeding compared with DAPT through 12 months. (OPT-PEACE [Optimal Antiplatelet Therapy for Prevention of Gastrointestinal Injury Evaluated by Ankon Magnetically Controlled Capsule Endoscopy]; NCT03198741).

MSI-78A (Pexiganan A) is one of the few antimicrobial peptides (AMPs) able to kill Helicobacter pylori, a pathogenic bacterium that colonizes the gastric mucosa of half of the world's population. Antibiotics fail in 20–40% of H. pylori-infected patients, reinforcing the need for alternative treatments. Herein, a bioengineered approach was developed. MSI-78A with a C-terminal cysteine was grafted onto chitosan microspheres (AMP-ChMic) by thiol-maleimide (Michael-addition) chemistry using a long heterobifunctional spacer (NHS-PEG113-MAL). Microspheres with ∼4 µm diameter (near H. pylori length) and stable at low pH were produced by spray drying using a chitosan solution with an incomplete genipin crosslinking. A 3 × 10−5 µg AMP/microsphere grafting was estimated/confirmed by UV/Vis and FTIR spectroscopies. AMP-ChMic were bactericidal against H. pylori J99 (highly pathogenic human strain) at lower concentrations than the free peptide (∼277 µg grafted MSI-78A-SH/mL vs 512 µg free MSI-78A-SH/mL), even after pre-incubation in simulated gastric conditions with pepsin. AMP-ChMic killed H. pylori by membrane destabilization and cytoplasm release in a ratio of ∼10 bacteria/microsphere. This can be attributed to H. pylori attraction to chitosan, facilitating the interaction of grafted AMP with bacterium membrane. Overall, it was demonstrated that the peptide-microsphere conjugation chemistry did not compromise the MSI-78A antimicrobial activity, instead it boosted its bactericidal performance against H. pylori. Statement of significance Half of the world's population is infected with Helicobacter pylori, a gastric bacterium that is responsible for 90% of non-cardia gastric cancers. Therefore, H. pylori eradication is now advocated in all infected individuals. However, available antibiotic therapies fail in up to 40% patients. Antimicrobial peptides (AMPs) are appealing alternatives to antibiotics, but their high susceptibility in vivo limits their clinical translation. AMP immobilization onto biomaterials surface will overcome this problem. Herein, we demonstrate that immobilization of MSI-78A (one of the few AMPs with activity against H. pylori) onto chitosan microspheres (AMP-ChMic) enhances its anti-H. pylori activity even at acidic pH (gastric settings). These results highlight the strong potential of AMP-ChMic as an antibiotic alternative for H. pylori eradication.

Background: With growing incidence of early gastric cancer (EGC), endoscopic submucosal dissection (ESD) is widely performed as a standard treatment for mucosal cancer. Due to the increasing application of ESD, the number of non-curative resection after ESD is also growing, leading to escalating number of patients who require additional gastrectomy with lymph node dissection after non-curative ESD. However, effects of ESD prior to surgery on technical difficulties during operation for EGC remain unclear. Therefore, this study aimed to determine the effect of non-curative ESD on short-term surgical outcomes in patients who underwent additional surgical treatment using propensity score matching method. Methods: To evaluate the effect of ESD on short-term surgical outcomes in patients who underwent additional surgical treatment after a non-curative ESD procedure, patients were divided into two groups: (1) those who underwent additional gastrectomy after non-curative resection of ESD [ESD + Surgery (ES) Group], and (2) those who underwent gastrectomy as the initial treatment [Surgery Only (SO) Group]. To minimize differences in baseline demographic features that could potentially be associated with short-term outcomes, propensity-scored matching analysis was performed. Results: After propensity-scored matching (1:1 matching), 140 patients altogether were selected and analyzed in this study. Complications were experienced by 18 (25.7%) patients in the ES group and 13 (18.6%) patients in the SO group, showing no significant (p

Background & Aims: Dysbiosis is associated with gastric cancer (GC) development. However, no longitudinal study was carried out to identify key bacteria that could predict for GC progression. Here, we aimed to investigate changes in bacterial metagenome prior to GC and develop a microbiome-based predictive model to accurately classify patients at risk of GC. Methods: Bacterial 16S rDNA was sequenced from 89 gastric antral biopsies obtained from 43 participants. This study was nested in a prospective, longitudinal study, whereby study participants underwent screening gastroscopy, with further 1-2 yearly surveillance gastroscopies for at least 5 years. Putative bacterial taxonomic and functional features associated with GC carcinogenesis were identified by comparing between controls, patients with gastric intestinal metaplasia (IM) and patients with early gastric neoplasia (EGN). Results: Patients with EGN had enrichment of Proteobacteria (in particular Proteus genus) and depletion of Bacteroidetes (in particular S24-7 family) in their gastric mucosa. Sequencing identified more patients with Helicobacter pylori compared to histopathological assessment, while H. pylori was also significantly enriched in EGN. Furthermore, a total of 261 functional features, attributing to 97 KEGG pathways were differentially abundant at baseline between patients who subsequent developed EGN (n = 13/39) and those who did not. At the same time, a constellation of six microbial taxonomic features present at baseline, provided the highest classifying power for subsequent EGN (AUC = 0.82). Conclusion: Our study highlights early microbial changes associated with GC carcinogenesis, suggesting a potential role for prospective microbiome surveillance for GC.

Iron deficiency anaemia is a known complication of a large hiatal hernia in adults. It occurs as a result of erosions on the gastric mucosa secondary to traction at the hiatus during respiration and/or gastric acid-related injuries to the mucosa. Even though anaemia occurs as a result of chronic gastrointestinal blood loss, testing for faecal occult blood is often negative and upper gastrointestinal endoscopy normal as the bleeding is intermittent. In children, a hiatus hernia as a rare cause of iron deficiency anaemia and has been described only in case reports. Here, we describe a 5-year-old boy who presented with severe transfusion-dependent iron deficiency anaemia caused by a paraoesophageal hernia. Surgical repair of the hiatus hernia led to complete resolution of anaemia. One should consider a hiatus hernia as a diagnostic possibility when evaluating a child with refractory iron deficiency anaemia.

OBJECTIVE We sought to investigate the clinical efficacy and safety of a novel endoscopic closure technique in repairing gastric wall defects after endoscopic full-thickness resection (EFTR) of gastric submucosal tumors (SMTs) originating from the muscularis propria layer. METHODS From December 2016 to December 2019, patients with gastric submucosal tumors were enrolled and clinicopathological data were collected. All SMTs were resected by EFTR and gastric wall defects were closed using a novel endoscopic closure technique. The feasibility, efficacy, and safety were evaluated. RESULTS A total of 21 patients with gastric SMTs were included in this study. Among the included SMTs, 15 tumors were located in the fundus of the stomach, and 6 were located in the upper body of the stomach. The average size of the lesions was 2.3 cm (range: 1.9-2.5 cm). All patients underwent EFTR and the gastric wall defect was closed by endoscopic closure. The average endoscopic closure time was 9 min (range: 7-15 min) and the average hospitalization stay length was five days (range: 4-6 days). One patient developed abdominal pain on the first day after the procedure and their body temperature increased; he received treatments such as anti-infection, antacid, and gastrointestinal decompression and was cured and discharged after 4 days. No instance of delayed bleeding, postoperative gastrointestinal fistula, or abdominal infection occurred. No case was transferred to surgery. The postoperative pathology profile included 18 stromal tumors and 3 leiomyomas. During the follow-up period (6-24 months), no case of residual or recurrence was recorded. CONCLUSION The described endoscopic loop ligation technique is feasible, effective, and safe for repairing gastric wall defects after EFTR for gastric submucosal tumors originating from the muscularis propria layer.

Introduction Currently, embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) can be induced to differentiate at the cellular level but not to form mature tissues or organs suitable for transplantation. ESCs/iPSCs form immature teratomas after injection into immunodeficient mice. In humans, immature teratomas often transform into fully differentiated mature teratomas after administration of anticancer agents. Methods We first investigated the ability of cisplatin to induce changes in mouse ESCs/iPSCs in vitro. Next, we designed experiments to analyze ESC/iPSC-derived immature teratoma tissue in vivo after treatment of cisplatin. Groups of six mice carrying ESC- or iPSC-derived teratomas were given either low or high dose intraperitoneal injection of cisplatin, while the control group received saline for 4 weeks. Results Treatment of ESC/iPSC cultures with cisplatin for 3 days caused a dose-related decrease in cell numbers without inducing any morphological changes to the cells. ESC/iPSC-derived teratomas showed lower growth rates with a significantly higher mature components ratio in a concentration dependent manner after cisplatin treatment (P, Highlights • Transformation of immature to mature teratoma after chemotherapy was verified. • Mice bearing ESC/iPSC-derived immature teratomas were used. • Mice were treated with intraperitoneal injection of cisplatin for 4 weeks. • Newly differentiated structures were found only in the tumors of treated mice. • Cisplatin can induce differentiation in ESC/iPSC-derived immature teratomas.

Background Since 2006, surgery combined with perioperative chemotherapy is the standard of care for resectable gastric adenocarcinoma in Europe. Specific effects of neoadjuvant chemotherapy remain unknown. The aim was to evaluate the rate of tumor downstaging and its impact on survival in patients undergoing curative resection after neoadjuvant chemotherapy (NeoCT) for gastric adenocarcinoma. Material and Methods All patients treated in a curative intent for gastric or esophagogastric junction adenocarcinomas between 1996 and 2016 in our high-volume center were retrospectively included. Tumor downstaging after NeoCT was defined as ypTN inferior to cTN. The accuracy of clinical staging was evaluated in patients treated by upfront surgery before 2006. Results During the study period, 491 patients were operated for gastric adenocarcinoma, and 449 patients were finally analyzed. Among the 163 (36.3%) patients who received NeoCT, 61 (37.4%) had tumor downstaging. Overall survival and disease-free survival were longer in patients with tumor downstaging compared to patients without it (5-year survival: 84.8% vs 49.7%; P = .002 and 61.7% vs 43.4%; P = .054). In multivariate analysis tumor downstaging was an independent prognosis factor for better overall survival (HR = 5.258; P = .002) and disease-free survival (HR = 2.286; P = .028). Moreover, 45.5% of patients staged cT1-T2N0, in whom upfront surgery was performed, were understaged and ultimately had a more advanced tumor on pathological analysis. Conclusion Response to neoadjuvant chemotherapy constitutes a major prognostic factor for overall and disease-free survival. In the absence of predictive factors for tumor downstaging, the indication for perioperative chemotherapy should remain broad, in particular because of the low accuracy of pretherapeutic staging and therefore the high risk of understaging tumors.

The gastric mucosa is an important endocrine organ, most of which is resected in sleeve gastrectomy (SG). The effect of removing most of the gastric mucosa has not been studied.To assess the effect of ablating the gastric mucosa (an area proportional to that in SG), on obesity and diabetes in a rat model.The Affiliated Hospital of Xuzhou Medical University in Xuzhou Jiangsu, P. R. China.Among 34 fatty Sprague-Dawley rats, 26 randomly received low-dose streptozotocin (STZ) to induce diabetes and then were randomly assigned to gastric mucosa ablation (GMA, n = 10), sleeve gastrectomy (SG, n = 8), and sham (n = 8) groups. The remaining normal fatty rats were assigned to the non-diabetic gastric mucosa ablation (nGMA, n = 8) group. In the GMA groups, the gastric mucosa was thermally ablated using electrocautery. Rats were followed for 8 weeks postoperatively. Preoperative oral glucose tolerance test (OGTT), insulin tolerance test (ITT), and mixed meal tolerance test (MMTT) were repeated at designated time points postoperatively. Changes in body weight, food intake, and fasting blood glucose were also recorded.Fasting ghrelin concentration and area under curve (AUC) decreased significantly (P.05) in the GMA groups and the SG group after surgery. Gastrin concentration remained unchanged in SG but decreased significantly in the GMA groups after surgery. Significantly increased GLP-1 AUC was found in the GMA groups and the SG group postoperatively. The decrease in fasting blood glucose did not differ significantly between the diabetic GMA and SG groups after surgery. Glucose AUC during OGTT in both SG and diabetic GMA groups was decreased significantly from the preoperative level, but the decreased glucose AUC in the SG group was significantly greater (P.05). The decrease in body weight and food intake in the SG group was significantly greater than in the GMA groups.Ablation of most of the gastric mucosa along the greater curvature is effective in weight loss and glycemic control in a rodent model.

We aimed to explore the correlation between P27 expression and Helicobacter pylori (H. pylori) infection in gastric cancer, so as to provide evidence for understanding the pathogenesis of gastric cancer caused by H. pylori infection. A total of 82 samples of gastric cancer tissues and 56 samples of tumor-adjacent normal tissues collected from the gastrectomy were enrolled in this study. Then, 14C-urease breathing test was carried out to evaluate the infection of H. pylori in gastric cancer tissues, the expression of P27 in the tissue samples was detected by the immunohistochemistry staining, and the correlation between the H. pylori infection and P27 expression in gastric cancer was analyzed. Of 82 gastric cancer patients, there were 53 patients with H. pylori infection (64.63%). Among the patients with highly or moderately differentiated gastric cancer, the expression of P27 was much higher than that of patients with poorly differentiated gastric cancer (p 0.01). Besides, comparison of the P27 expression between males and females, among different age groups, tumor sizes, TNM stages, tumor infiltration degrees, or lymph node metastasis, showed no significant differences (p 0.05). Analysis of the correlation revealed that P27 expression was negatively correlated with the infection of H. pylori (p 0.01). Multifactorial logistics regression analysis indicated that tumor differentiation was a risk factor of P27-positive expression in gastric cancer tissues (p 0.01). In addition, P27 expression in the gastric cancer tissues was lower than that in the tumor-adjacent normal tissues (p 0.01). In gastric cancer patients, expression of P27 is correlated with H. pylori infection which, via downregulating P27, can cause the cancerization of gastric mucosa, and P27, for its role in the development and progression of gastric cancer, is a potential auxiliary indicator for clinical diagnosis whether gastric cancer is complicated with H. pylori infection. So, P27 is a key indicator for diagnosis, treatment, and prognostic evaluation of disease in the advanced stage.

Objectives The Kyoto classification of gastritis was established for diagnosing Helicobacter pylori (H. pylori) infection via endoscopic findings. We investigated the role of the Kyoto classification of gastritis in the diagnosis of H. pylori infection and histological gastritis in Japanese individuals. Moreover, the histological findings of gastritis in H. pylori infection were examined based on age and sex differences. Methods We selected 561 patients aged 20-79 years who underwent gastroduodenal endoscopy at our hospital between 2010 and 2018. Endoscopic biopsy specimens from the antrum and corpus were used to investigate H. pylori infection and histology. Endoscopic findings were based on the Kyoto classification of gastritis, and histological findings were based on the updated Sydney System. Results Endoscopic findings based on the Kyoto classification of gastritis (H. pylori positive, 303 patients; H. pylori negative, 258 patients, based on endoscopic findings) had 98.7% sensitivity and 98.4% specificity for histological gastritis. In addition, endoscopic findings in the three age groups (20-39, 40-59, and 60-79 years) had high sensitivity and specificity. Atrophy and intestinal metaplasia were found only in the H. pylori-positive group and progressed with age. Histological inflammation of pyloric mucosa in the younger age group of H. pylori-positive patients was significantly higher than that in the elderly group. Significant inflammation was observed in young women. Conclusions The Kyoto classification of gastritis can not only diagnose H. pylori infection but also detect histological gastritis. Histological gastritis has varying characteristics of inflammation, atrophy, and intestinal metaplasia, depending on age and sex.

Objective: to determine the specifi c number and expression intensity of gelatinase B-positive cells in the gastric surface epithelium and lamina propria (cell component) in the area of the ulcerous defect in rats with experimental acetate ulcer of the stomach.Materials and methods: 18 white Wistar rats were divided into three groups: initial (intact), experimental (modeling of an acetate ulcer) and control (falsely operated) in the experiment. Tissues were obtained from the ulceration zone or the presumed ulceration zone (in the initial and control groups) to asses morphological changes and also indicators, characterizing the activity of gelatinase B 7 days after the simulation of the experiment.Results and Discussion. It was revealed some increase in the specifi c number of gelatinase B-positive cells against the background of moderate accumulation of lymphocytes in the integument epithelium of the gastric mucosa. A signifi cant increase in the specifi c number of gelatinase B-positive cells at the maximum intensity of its expression and a moderate accumulation of eff ector cells of tissue alterations was determined in the cellular component of the lamina propria of the gastric mucosa at the same time.

PURPOSE: Gastric cancers are classified as diffuse-type (DTGC) or intestinal-type (ITGC). DTGCs have distinct clinical and histopathologic features, and carry a worse overall prognosis compared to ITGCs. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known precursors to ITGC. It is unknown if AG and IM increase risk for DTGC. METHODS: We performed a systematic review to identify studies reporting on the association of AG/IM and DTGC. We extracted the odds ratio (OR) of the association from studies, and performed pool analysis. Subgroup analysis was performed on studies reporting histologic severity (using operative link systems) to assess if histologic severity of AG/IM was associated with higher risk. RESULTS: We identified six case-control and eight cohort studies for inclusion. Both AG (pooled OR=1.9, 95% CI 1.5 to 2.4, p

The aim of the present study was to investigate the ability of fish collagen peptides (FCP) from the skin of great hammerhead shark (Sphyrna mokarran) to avert the occurrence of gastric ulcer in experimental rats. FCP treatment prevented the formation of ulcerative lesions on gastric tissues with 86% of inhibition. The histopathology analysis of gastric tissue revealed that the FCP intake prevented the occurrence of hemorrhage and erosion in gastric tissue with formation of mild edema and necrosis, as well as normalized the pH and volume of gastric juice. It also downregulated the expression of pro-inflammatory marker interferon-ɤ (IFN-ɤ) and upregulated the anti-inflammatory marker interleukin-4 (IL-4) in gastric tissue. FCP is capable to modulate the oxidative stress by enhancing the activity of antioxidant defense enzymes superoxide dismutase (SOD) and catalase and by lowering the levels of membrane lipid peroxidation.

The incidence of gastrointestinal (GI) mucosal diseases, including various types of gastritis, ulcers, inflammatory bowel disease and GI cancer, is increasing. Therefore, it is necessary to identify new therapeutic targets. Ion channels/transporters are located on cell membranes, and tight junctions (TJs) affect acid–base balance, the mucus layer, permeability, the microbiota and mucosal blood flow, which are essential for maintaining GI mucosal integrity. As ion channel/transporter dysfunction results in various GI mucosal diseases, this review focuses on understanding the contribution of ion channels/transporters to protecting the GI mucosal barrier and the relationship between GI mucosal disease and ion channels/transporters, including Cl−/HCO3− exchangers, Cl− channels, aquaporins, Na+/H+ exchangers, and K+ channels. Here, we provide novel prospects for the treatment of GI mucosal diseases.

Gastric cancer is a malignant tumor that originates from the epithelium of the gastric mucosa. It is the result of a combination of multiple factors, but the current research has not yet clarified its pathogenesis, so further research and exploration are needed. This article is mainly based on the meta-analysis of the improvement of gastrointestinal tumor-related symptoms and prognosis based on medical care and exercise intervention. The control group followed routine care after enrollment. In addition to routine care, patients in the intervention group exercised through assessment, formulation of exercise prescriptions, implementation of supervision, and adjustment. By viewing the subjects' physical examination reports, determine their blood routine, urine routine, blood lipids, blood sugar, liver and kidney function, and electrocardiogram examination. In this experiment, dual-contrast ultrasound in each T staging was greater than 0.8, indicating that the diagnostic method is very accurate in the preoperative diagnosis of gastric cancer T staging. The results show that exercise intervention can improve the pain of patients with gastrointestinal tumors after chemotherapy, relieve cancer-induced fatigue, and improve the quality of life.

Introduction. The aim of the study was to detect the dependence of the composition of the parietal microflora of the colon on the activity of Helicobacter pylori-associated chronic gastritis and the degree of Helicobacter pylori contamination of the gastric mucosa. Materials and methods. The study was carried out on 50 patients aged 24 to 72 years, who were diagnosed with HP-associated chronic gastritis in the phase of exacerbation based on the results of FEGDS and histological examination of biopsies of the mucous membrane of the antrum of the stomach in combination with a rapid urease test. A series of dilutions 10¹-10⁹ was prepared from a homogenized biopsy specimen of the mucous membrane of the sigmoid colon in 0.1 ml of isotonic sodium chloride solution, and 0.1 ml of a solution of the corresponding dilution was inoculated onto the surface of the nutrient medium. The study of mucosal microflora was carried out by means of bacteriological examination of biopsies of the mucous membrane of the sigmoid and cecum. The degree of H. pylori contamination of the gastric mucosa was assessed in the course of histological examination by a semi-quantitative method: low degree of contamination — up to 20 microbial bodies, average — 20-50 microbial bodies, strong — over 50 microbial bodies in the field of view. Results. The study demonstrated that the indicators of the average concentrations of bifidobacteria, lactobacilli and typical strains of E. coli progressively decreased with the transition to a higher degree of HP infection. This tendency was maximum in relation to bifidobacteria — 6.1-1.57-1.09 x 10⁸ CFU/g, with a difference between the maximum (I degree) and minimum (III degree) 5.59 times. A similar relationship, but much less pronounced, was observed for Lactobacterium spp. and E. coli. As the severity of HP infiltration of the gastric mucosa increases, there is a decrease in the concentration of the above microorganisms in the parietal mucin - the correlation coefficient is r = -0.74. Discussion. Since the mucous microflora is more stable and functionally significant than the cavity microflora, the data obtained allow us to consider Helicobacter pylori as an etiological factor of colonic dysbiosis. Conclusion. The probability of excessive growth of conditionally pathogenic fraction of intestinal parietal microflora has a direct dependence on the severity of Helicobacter pylori infestation, being maximum at degree III contamination. Content of bifidobacteria, lactobacilli and typical E. coli strains in the intestinal biotope of the large intestine is inversely related to the degree of histological activity of HP-associated gastritis.

We examined the relationship between zonulin and gastric motility in critical care patients and a translational mouse model of systemic inflammation. Gastric motility and haptoglobin (HP) 2 isoform quantification, proxy for zonulin, were examined in patients. Inflammation was triggered by lipopolysaccharide (LPS) injection inC57Bl/6zonulin transgenic mouse (Ztm) and wildtype (WT) mice as controls, and gastro-duodenal transit was examined by fluorescein-isothiocyanate, 6 and 12 h after LPS-injection. Serum cytokines and zonulin protein levels, and zonulin gastric-duodenal mRNA expression were examined. Eight of 20 patients [14 years, IQR (12.25, 18)] developed gastric dysmotility and were HP2 isoform-producing. HP2 correlated with gastric dysmotility (r = − 0.51, CI − 0.81 to 0.003, p = 0.048). LPS injection induced a time-dependent increase in IL-6 and KC-Gro levels in all mice (p

Background The progression to gastric cancer has been linked to chronic infection with Helicobacter pylori (H. pylori). Immune checkpoint inhibitors (programmed cell death -1, PD-1; programmed cell death –ligand 1, PD-L1) have a role in cancer immune escape. The relationship between H. pylori virulence factors with PD-1, PD-L1 T helper 1 (Th1), T helper 17 (Th17), and regulatory T cell (Treg) response genes, has not been thoroughly investigated in the development of gastric cancer. Therefore, we evaluated how H. pylori virulence factors influence the expression levels of immune-related genes in the development of gastric immunopathology. Methods A total of 92 gastric tissues of normal controls and patients with gastritis, gastric ulcer, and gastric cancer were examined for the expression of immune-checkpoint inhibitor genes (PD-1 PD-L1), Th1 (interferon- γ, IFN-γ), Th17 (interleukin- 17, IL-17, Retinoic-acid-receptor- related orphan nuclear receptor gamma t, RORγ-t), and Treg (Forkhead box P3, FOXP3) response genes with quantitative real-time PCR (qRT-PCR). Furthermore, correlation of H. pylori virulence factors’ (cytotoxin-associated gene A, cagA; vacuolating cytotoxin gene A, vacA (s1,s2,m1,m2); blood group antigen-binding adhesin gene A, babA, duodenal ulcer promoting gene A, dupA; the putative neuraminyllactose-binding hemagglutinin homolog, hpaA; neutrophil-activating protein A napA; outer inflammatory protein A, oipA; urease A, ureA; and urease B, ureB) genotypes with a degree of inflammation and density of H. pylori were investigated. Next, the relationship between H. pylori virulence factors and immune-checkpoint inhibitor genes, and T-cell response genes was evaluated. Eventually, a decision tree model was developed to determine the clinical outcome of patients using expression data. Results The intensity of PD-1 and PD-L1 mRNA expression was increased significantly in gastric tissue of patients with gastric ulcer (PD-1: 2.3 fold, p=0.01; PD-L1: 2.1 fold, p=0.004), and gastric cancer (PD-1: 2 fold, p= 0.04; PD-L1: 1.8 fold, p=0.05) compared with control subjects. Also, PD-1: PD-L1 expression was significantly higher in patients with gastritis, who were infected with a marked density of H. pylori compared with its mildly infected counterparts. Furthermore, a novel negative correlation was found between PD-1 (r= -0.43) and PD-L1 (r= -0.42) with FOXP3 in patients with gastritis. CagA-positive H. pylori strain's negative association with PD-L1 expression (r=-0.34) was detected in patients with gastritis. Interestingly, PD-1 mRNA expression correlated positively with vacA s2/m2, in gastritis (r=0.43) and ulcer (r=0.43) patients. Furthermore, PD-1: PDL1 expression negatively correlated with vacA m1/m2 (r=-0.43 for PD-1; r=-0.38 for PD-L1) in gastritis patients. Moreover, an inverse correlation of PDL1 was present with vacA m1 (r=0.52) and vacA s1/m1 (r=0.46) versus vacA m2 (r=-0.44) and vacA m1 (r=0.52) and vacA s1/m2 (r=-0.14) in ulcer patients, respectively. Also, a correlation of vacA m2 (r=-0.47) and vacA s1/s2 (r= 0.45) with PD-1 was detected in ulcer patients. In addition, a novel negative correlation between FOXP3 mRNA levels and napA was shown in patients with gastritis and ulcer (r=-0.59). Finally, a computer-based model that was developed showed that knowing the expression levels of PD-L1, RORγ-t, and vacA s1/m2 would be useful to detect the clinical outcome of a patient. Conclusion Our results suggested that PD-1:PD-L1 immune checkpoint inhibitors were increased in gastric pre-cancerous lesions that progress to gastric cancer. Herein, we report the relationship between H. pylori virulence factors and expression of host immune checkpoint inhibitors for diagnostic prediction of gastric malignancies using computer-based models.

Introduction: Sonneratia apetala Buch-Ham is a true mangrove inhabitant in Indian Sunderban and it is used in folk medicine for digestive disorders. Method: Hydro-methanolic (20:80) extract of Sonneratia apetala leaves (SA) was chemically standardized by HPTLC and evaluated for its antiradical and gastro-protective properties. Phenolics and flavonoids present in SA were determined and antiradical activities were assessed by in vitro methods like, DPPH (1,1-diphenyl-2-picrylhydrazyl), nitric oxides, superoxides, hydroxyl and ABTS (2,2/-azino-bis-3-ethyl benzthiazoline-6-sulphonic acid). Further, gastro-protective efficacy of SA was assessed in alcohol (50% v/v, 5 ml/kg) induced oxidative ulceration in rats. Results: Chemically standardized SA exhibited presence of polyphenolic compounds. It also showed strong antiradical properties. Oral administrations of SA (125 mg/kg and 250 mg/kg) significantly protected gastric mucosal membrane from ulcerative damage caused by alcohol, similar to Omeprazole (20 mg/kg) in rats. Moreover, SA treatment significantly reduced the elevation of lipid peroxides; while enhanced the concentration of glutathione and catalase in gastric mucosa in respect to ethanol induced untreated control rats. Conclusions The results obtained from this study suggest Sonneratia apetala leaf has antioxidant properties and has capabilities to protect gastric mucosal injury caused by alcohol ingestion.

Marta Szandruk-Bender,1 Anna Merwid-Ląd,1 Benita Wiatrak,1 Maciej Danielewski,1 Stanisław Dzimira,2 Danuta Szkudlarek,3 Łukasz Szczukowski,4 Piotr Świątek,4 Adam Szeląg1 1Department of Pharmacology, Wroclaw Medical University, Wrocław, Poland; 2Department of Pathology, Wroclaw University of Environmental and Life Sciences, Wrocław, Poland; 3Foundation of the Wroclaw Medical University, Wroclaw Medical University, Wrocław, Poland; 4Department of Chemistry of Drugs, Wroclaw Medical University, Wrocław, PolandCorrespondence: Marta Szandruk-BenderDepartment of Pharmacology, Wroclaw Medical University, Mikulicza-Radeckiego 2, Wrocław, 50-345, PolandTel +48717841438Fax +48717840094Email marta.szandruk@umed.wroc.plBackground and Purpose: Due to the risk of gastrointestinal damage and various tissue toxicity associated with non-steroidal anti-inflammatory drugs (NSAIDs) use, investigating new anti-inflammatory agents with efficacy comparable to that of NSAIDs but reduced toxicity is still a major challenge and a clinical need. Based on our previous study, new 1,3,4-oxadiazole derivatives of pyrrolo[3,4-d]pyridazinone, especially 6-butyl-3,5,7-trimethyl-1-[[4-[[4-(4-nitrophenyl)piperazin-1-yl]methyl]-5-thioxo-1,3,4-oxadiazol-2-yl]methoxy]pyrrolo[3,4-d]pyridazin-4-one and 6-butyl-1-[[4-[[4-(4-chlorophenyl)-4-hydroxy-1-piperidyl]methyl]-2-thioxo-1,3,4-oxadiazol-5-yl]methoxy]-3,5,7-trimethyl-pyrrolo[3,4-d]pyridazin-4-one (hereafter referred to as the compounds 10b and 13b, respectively) seem to be promising anti-inflammatory agents. This study aimed to elucidate the effects of these two new derivatives on the course of experimental rat inflammation, liver and kidney function, and gastric mucosa.Methods: The anti-inflammatory effect of compounds 10b and 13b was evaluated using the carrageenan-induced paw edema test in rats. The increase in paw volume (paw edema), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α) and myeloperoxidase (MPO) levels, histological alterations, and inflammatory cell infiltration in paw tissue were determined. Serum alanine transaminase (ALT) and aspartate transaminase (AST) activities, serum urea and creatinine levels, as well as changes in gastric mucosa, were measured as indicators of hepatic, renal, and gastric toxicity.Results: Pretreatment with both novel derivatives at 10 mg/kg and 20 mg/kg doses reduced paw edema, counteracted the increased PGE2 and TNF-α levels, reduced the influx of inflammatory cells, and decreased histopathological alterations in paw tissue. Compound 13b at a dose of 20 mg/kg was more effective than indomethacin in reversing the increased TNF-α levels and reducing the influx of inflammatory cells. Only compound 13b at all studied doses (5, 10, or 20 mg/kg) counteracted the increased MPO level in paw tissue. Both compounds neither caused alterations in ALT, AST, urea, creatinine parameters nor gastric mucosal lesions.Conclusion: New compounds exert an anti-inflammatory effect, presumably via inhibiting inflammatory mediators release and inflammatory cell infiltration. Moreover, both possess a more favorable benefit–risk profile than indomethacin, especially compound 13b.Keywords: carrageenan, anti-inflammatory agents, pyrrolo[3,4-d]pyridazinone, 1,3,4-oxadiazole, inflammatory mediators, toxicity

Background:. With the wide application of endoscopic submucosal dissection (ESD) for early gastric neoplasms, metachronous gastric neoplasms (MGN) have gradually become a concern. This study aimed to analyze the characteristics of MGN and evaluate the treatment and follow-up outcomes of MGN patients. Methods:. A total of 814 patients were retrospectively enrolled. All these patients were treated by ESD for early gastric cancer or gastric dysplasia between November 2006 and September 2019 at The First Medical Center of Chinese People's Liberation Army General Hospital. The risk factors for MGN were analyzed using Cox hazard proportional model. Moreover, the cumulative incidence, the correlation of initial lesions and MGN lesions, and the treatment and follow-up outcomes of MGN patients were analyzed. Results:. A total of 4.5% (37/814) of patients had MGN after curative ESD. The 3-, 5-, and 7-year cumulative incidences of MGN were 3.5%, 5.1%, and 6.9%, respectively, and ultimately reaching a plateau of 11.3% at 99 months after ESD. There was no significant correlation between initial lesions and MGN lesions in terms of gross type (P = 0.178), location (long axis: P = 0.470; short axis: P = 0.125), and histological type (P = 0.832). Cox multivariable analysis found that initial multiplicity was the only independent risk factor of MGN (hazard ratio: 4.3, 95% confidence interval: 2.0–9.4, P < 0.001). Seventy-three percent of patients with MGN were treated by endoscopic resection. During follow-up, two patients with MGN died of gastric cancer with lymph node metastasis. The disease-specific survival rate was significantly lower in patients with MGN than that in patients without MGN (94.6% vs. 99.6%, P = 0.006). Conclusions:. The MGN rate gradually increased with follow-up time within 99 months after curative gastric ESD. Thus, regular and long-term surveillance endoscopy may be helpful, especially for patients with initial multiple neoplasms.