Search

BACKGROUND/AIMS: While DNA methylation and gastric microbiome are each associated with gastric cancer (GC), their combined role in predicting GC remains unclear. This study investigated the potential of a combined DNA methylation and gastric microbiome signature to predict Helicobacter pylori-negative GC. METHODS: In this case-control study, we conducted quantitative methylation-specific polymerase chain reaction to measure the methylation levels of DKK3, SFRP1, EMX1, NKX6-1, MIR124-3, and TWIST1 in the gastric mucosa from 75 H. pylori-negative patients, including chronic gastritis (CG), intestinal metaplasia (IM), and GC. A combined analysis of DNA methylation and gastric microbiome, using 16S rRNA gene sequencing, was performed in 30 of 75 patients. RESULTS: The methylation levels of DKK3, SFRP1, EMX1, MIR124-3, and TWIST1 were significantly higher in patients with GC than in controls (all q

Helicobacter pylori (H. pylori)-induced inflammation increases the risk of developing various upper gastrointestinal conditions which may progress to gastric cancer (CA). Early prediction and detection of infection are crucial for reducing cancer-induced mortality rates. The present case-control study aimed to investigate the combination of serum and molecular markers and H. pylori-associated gastroduodenal conditions as risk factors for predicting CA development in dyspeptic patients. Consecutive gastric biopsies and blood samples were collected from 100 adult dyspeptic patients. Serum IgG antibody levels against H. pylori were determined, and receiver operating characteristic (ROC) analysis was performed. The expression of the virulence genes cagA and vacA was evaluated by polymerase chain reaction (PCR). A significant association was reported between the disease condition and the status of several risk factors, such as family history, serum IgG antibody concentration, and the virulence genes cagA and vacA. Among the 71 H. pylori-positive patients, 35.2% (25/71) had CA. Both cagA and vacA genes were found in 46 out of 71 (64.7%) patients, and 92% (23/25) of CA patients carried the cagA+vacA s1 gene. ROC analysis of the serum IgG concentrations revealed AUC values of 0.81 and 0.78 for differentiating patients with non-ulcer dyspepsia from those with ulceration/inflammation and CA, respectively. The concordance between the IgG-positive and PCR-positive patients was 84% (k value=0.41). Patients who had a family history of CA with an increased serum IgG concentration and the presence of H. pylori cagA-vacA s1 genotypes may be considered strong predictors of future development of gastric pathologies, including CA. [ABSTRACT FROM AUTHOR]

Background: Heterotopic gastric mucosa in the upper esophagus (HGMUE) is considered to be accompanied by pharyngolaryngeal symptoms, whereas the association strength between HGMUE and pharyngolaryngeal symptoms remains controversial. This study assessed the strength of the association between HGMUE and pharyngolaryngeal symptoms using a meta-analytic approach. Methods: PubMed, Embase, Web of Science, and CNKI databases were searched for relevant articles published between January 2010 and January 2024. The pharyngolaryngeal symptoms of chronic cough, dysphagia, hoarseness, and globus in patients with HGMUE were summarized. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using a random-effects model. The exploratory analyses were also performed, including sensitivity and subgroup analyses. Results: A total of 17 observational studies (1 cohort study and 16 cross-sectional studies) with 626,369 patients (2414 HGMUE patients and 623,955 non-HGMUE patients) were included in the meta-analysis. HGMUE was significantly associated with an elevated incidence of chronic cough (OR: 3.36; 95% CI 1.25–9.01; P = 0.02), dysphagia (OR: 1.58; 95% CI 1.12–2.25; P = 0.01), hoarseness (OR: 4.13; 95% CI 1.47–11.56; P = 0.007), and globus (OR: 2.41; 95% CI: 1.43–4.04, P < 0.001). The association between HGMUE and the risk of dysphagia was found to be potentially influenced by study design, sample size, country, and diagnostic method, whereas the association between HGMUE with the risk of globus was potentially affected by the study design and country. Conclusion: HGMUE was significantly associated with chronic cough, dysphagia, hoarseness, and globus. HGMUE should be taken into consideration for patients with pharyngolaryngeal symptoms. [ABSTRACT FROM AUTHOR]

Sometimes non-neoplastic changes of the gastric mucosa mimic diffuse-type gastric carcinoma, specifically signet-ring cell adenocarcinoma. In fact, gastric epithelial cells undergoing signet-ring cell change have a cellular morphology that is almost identical to signet-ring cell adenocarcinoma, often leading to misdiagnosis. Accurate recognition of signet-ring cell change is essential to avoid overdiagnosis and overtreatment of signet-ring cell adenocarcinoma. Research on this topic is limited and clinicians lack formal diagnostic tools when signet-ring cells are detected in biopsy specimens. The aims of this study are 3-fold. Firstly, to increase the awareness of both clinicians and pathologists of this rare but highly significant entity. Secondly, to report 4 additional examples of signet-ring cell change and analyze them alongside signet-ring cell adenocarcinoma to compare their morphological and phenotypic features and their evolution over time. Finally, to highlight the potential utility of endoscopic resection to confirm the diagnosis. Cells in signet-ring cell change strongly express E-cadherin, show a wild-type p53 expression, and have a low Ki67 index. In contrast, cells in signet-ring cell adenocarcinoma strongly express p53, have high proliferation rates, and show either no or weak E-cadherin staining. Genetic analysis may be useful in identifying patients at risk of hereditary early diffuse gastric adenocarcinoma, which can mimic signet-ring cell change. [ABSTRACT FROM AUTHOR]

The article discusses a rare case of emphysematous gastritis (EG) in a patient with gastric malperfusion due to congenital absence of the celiac axis and previous splenectomy. The patient presented with chest and lower extremity pain, and was managed with conservative treatment including IV antibiotics, fluid resuscitation, and surgical intervention. The patient underwent a superior mesenteric artery to gastric artery bypass to improve perfusion to the stomach and prevent further complications. The article emphasizes the importance of recognizing and treating ischemic gastropathy to ensure patient survival. [Extracted from the article]

Enterococcus faecalis is a newly emerged fish pathogen affecting many cultured fish species. The present work aimed to determine the cause of mortalities affecting the cultured Meagre farm and study the infectious agent virulence, disease pathology. Also, to determine the influence of infection on complement 3, cyclooxygenase, and lysozyme gene expression and concentrations in fish serum. The internal organs of diseased fish were severely congested with the presence of petechial haemorrhages on the liver, gonads, and all over the elementary tract. Thirty-one bacterial isolates were recovered from naturally infected fish; seventeen were identified biochemically as E. faecalis. Random E. faecalis isolate was verified for pathogenicity in meager fingerlings and was indeed pathogenic with lethal dose-fifty (LD50) estimated by 4.6 × 106 colony forming unit (CFU) fish−1. The posterior kidney and hepatopancreas of experimentally infected fish showed severe inflammation, necrosis, degeneration, and haemorrhage. Detachment of mucosa lining the stomach and intestine (intestinal villi and gastric glands) was prominent. The examined gastric tissues exhibited inflammation, leucocytic infiltration, and congestion. The expression of C3, Cox2, and Lyz was upregulated 24-h post-infection and then decreased near the baseline at 96 h. Serum C 3 and Lyz concentrations peaked at 24 h and 48 h after that decreased. IgM level gradually increased with time and peaked at 96 h. In conclusion, E. faecalis is assumed pathogenic for cultured meager, experimental infection stimulated immune systems and upregulated the expression of some immune-related genes. [ABSTRACT FROM AUTHOR]

Gastric ulcer disease remains one of the common medical burdens affecting millions worldwide due to its prevalent risk factors with the chronic usage of non-steroidal anti-inflammatory drugs at the top, reportedly through the stimulation of oxidative stress and triggering of inflammatory and apoptotic cascades in the gastric mucosa. Astaxanthin, a dietary keto-carotenoid derived from marine organisms is gaining a wide interest as a nutraceutical for its pronounced antioxidant properties. Here, we aim to examine the potential modulatory role of astaxanthin on indomethacin-induced gastric ulceration in experimental mice. Twenty-four Swiss albino mice were randomly distributed into four groups: a control group, an indomethacin group, and two groups pre-treated with either omeprazole or astaxanthin. The gastric tissues were assessed using gross morphology, ulcer scoring, gastric juice acidity, as well as reduced glutathione (GSH) and malondialdehyde (MDA) levels. Histopathological examination and immunostaining for nuclear factor-kappa B (NF-κB) and caspase-3 levels were also employed. Indomethacin group tended to show a higher number of mucosal ulcerations relative to control and pre-treated groups. The indomethacin group also showed significantly lower GSH levels and higher MDA levels relative to control. Immunostaining of gastric tissue sections showed a higher reactivity to NF-κB and caspase-3 in indomethacin group. Astaxanthin pre-treatment significantly elevated gastric juice pH, normalized GSH levels, and lowered the indomethacin-induced elevations in MDA, NF-κB, and caspase-3 levels. These results indicate that astaxanthin exhibits a comparable protective effect to omeprazole, against indomethacin-induced gastric ulceration. This anti-ulcerogenic effect could be mediated through its antioxidant, anti-inflammatory, and anti-apoptotic modulatory activities. [ABSTRACT FROM AUTHOR]

Background: Detection of gastric cancer (GC) at early stages is an effective strategy for decreasing mortality. This study aimed to construct a prediction nomogram based on a questionnaire to assess the risk of developing GC. Methods: Our study comprised a total of 4379 participants (2326 participants from outpatient at Fengqing People's Hospital were considered for model development and internal validation, and 2053 participants from outpatients at the endoscopy center at the Seventh Affiliated Hospital of Sun Yat-Sen University were considered for independent external validation) and gastric mucosa status was determined by endoscopy and biopsies. The eligible participants in development cohort from Fengqing people's Hospital were randomly separated into a training cohort (n=1629, 70.0%) and an internal validation cohort (n=697, 30.0%). The relevant features were selected by a least absolute shrinkage and selection operator (LASSO), and the ensuing features were evaluated through multivariable logistic regression analysis. Subsequently, the variables were selected to construct a prediction nomogram. The discriminative ability and predictive accuracy of the nomogram were evaluated by the C-index and calibration plot, respectively. Decision curve analysis (DCA) curves were used for the assessment of clinical benefit of the model. This model was developed to estimate the risk of developing neoplastic lesions according to the "transparent reporting of a multivariable prediction model for individual prognosis or diagnosis" (TRIPOD) statement. Results: Six variables, including age, sex, alcohol consumption, cigarette smoking, education level, and Hp infection status, were independent risk factors for the development of neoplastic lesions. Thus, these variables were incorporated into the final nomogram. The AUC of the nomogram were 0.701, 0.657 and 0.699 in the training, internal validation, and external validation cohorts, respectively. The calibration curve showed that the nomogram was in good agreement with the observed outcomes. Compared to treatment of all patients or none, our nomogram showed a notably higher clinical benefit. Conclusion: This nomogram proved to be a convenient, cost-effective tool to effectively predict an individual's risk of developing neoplastic lesions, and it can act as a prescreening tool before gastroscopy. [ABSTRACT FROM AUTHOR]

Background: Several surveys conducted at slaughter sites have highlighted that gastric lesions are a widespread issue in fattening pigs, mainly due to feeding regimes. Diets with small particle sizes and low fibre contents guarantee high digestibility and performance but generate more rapid stomach emptying with a negative effect on gastric mucosa integrity. Providing fattening pigs with fibrous materials (e.g., straw provided in racks) or coarse fibrous ingredients (e.g., coarse silages) reduced the presence of gastric ulcers. The present research compares a traditional corn-soy-based diet with an experimental diet where bran and a portion of corn meal was substituted with whole ear and whole plant corn silages at the maximum dosages permitted by new Protected Designation of Origin for Italian dry-cured ham (20 and 10% of DM, respectively). This study aimed to examine the impact of the inclusion of corn silages in the diet on the productive performance of heavy Italian pigs and their ability to mitigate gastric mucosa damage. Results: The growth performances were satisfactory (750–800 g/d) given the advanced interval of growth of animals (from 120 to 180 kg). However, the inclusion of corn silages tended to reduce the growth rate by 5–6% due to the reduction of organic matter digestibility, without compromising the slaughter traits or the back-fat fatty acid profile. The experimental diet substantially affected both stomach development and mucosal integrity. The first consequence was an increase in stomach weight of approximately 6% (P < 0.01) but the most notable advantage of coarse feeding was a reduction in stomach damage severity, with a low number of cases with higher scores in animals fed coarse materials (P < 0.01). Conclusions: The dietary inclusion of corn silages (30% of diet DM) decrease effectivelly the severity of stomach damage in finishing heavy pigs. Based on the feeding trial performances, the perspective of feeding heavy pigs corn silage should consider specific agronomic and harvesting techniques to improve digestibility and not reduce the growth rate. [ABSTRACT FROM AUTHOR]

Helicobacter pylori is a highly prevalent pathogen in human gastric mucosa epithelial cells with strong colonization ability. Weizmannia coagulans is a kind of active microorganism that is beneficial to the improvement of host gut microbiota balance and can prevent and treat intestinal diseases. We investigated the beneficial effects of W. coagulans BC99 in H. pylori infected mice and measured inflammation response, oxidative stress, and gut microbiota. Results showed that BC99 could alleviate the gastric inflammation, inhibit the increasing of inflammation parameters endotoxin, interleukin‐10, transforming growth factor‐β, and interferon‐γ and oxidative stress myeloperoxidase and malondialdehyde, promote the levels of superoxide dismutase and catalase. Furthermore, 16S rRNA gene sequencing analysis revealed that BC99 reversed the change of gut microbiota by reducing the abundance of Olsenella, Candidatus_Saccharimonas, Monoglobus, and increasing the abundance of Tyzzerella. Meanwhile, BC99 caused elevated levels of Ligilactobacillus and Lactobacillus. In view of the beneficial effect of BC99 on the content of short‐chain fatty acid, valeric acid with sodium valerate interfered with H. pylori infection in mice found that valeric acid had a good restorative effect of H. pylori infection relating inflammation and oxidative stress responses. These results suggest that W. coagulans BC99 can be used as a potential probiotic to prevent and treat H. pylori infection by regulating the inflammation, oxidative stress, and gut microbiota. [ABSTRACT FROM AUTHOR]

Simple Summary: Gastric polyps (GPs) are frequent gastric lesions, usually diagnosed incidentally. As upper gastrointestinal endoscopy becomes more frequent, the prevalence of GPs increases, with implications in clinical practice, as some of them can present different grades of malignant risk. The more common polyps are the epithelial ones, with a predominance of fundic gland polyps (FGPs) and gastric hyperplastic polyps (GHPs), in which prevalence varies according to local epidemiology. Up to now, the general recommendation is that all GPs should have histological evaluation by biopsy. However, novel advances in endoscopic techniques could allow for a more expectant management based on histopathological prediction by optical diagnosis. Further research and refinement of these techniques are necessary before their application in the clinical management of GPs. Gastric polyps (GPs) are common luminal lesions of the gastrointestinal tract, frequently detected incidentally in 1–6% of all upper gastrointestinal endoscopy. With the increasing use of endoscopy, the diagnosis of GPs has risen, highlighting the need for a thorough understanding of their pathophysiology and associated cancer risks. This review focuses on epithelial GPs, particularly fundic gland polyps (FGPs), hyperplastic polyps (GHPs) and gastric adenomas (GAs), discussing their classification, epidemiology, histopathology, endoscopic diagnosis, and current management. FGPs are predominantly associated with proton pump inhibitor (PPI) use and are common in regions with low Helicobacter pylori (Hp) prevalence, whereas GHPs are linked with Hp infection and chronic gastritis. GAs, although less common, have a significant risk of malignant transformation, especially in larger lesions. Management strategies vary according to polyp type, size, and dysplastic features, with resection recommended for high-risk lesions. Advances in endoscopic techniques, particularly narrow-band imaging (NBI), offer promising tools for differentiating between polyp types, potentially reducing the need for routine biopsies in the low-risk GPs. This review underscores the role of advanced imaging endoscopic techniques for the accurate classification and individualized management of GPs to mitigate the risk of gastric cancer. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (H. pylori) infection is widely acknowledged as the primary risk factor for gastric cancer, facilitating its progression via the Correa cascade. Concurrently, Hexokinase Domain Containing 1 (HKDC1) has been implicated in the mediation of aerobic glycolysis, contributing to tumorigenesis across various cancers. However, the precise role of HKDC1 in the inflammatory transformation associated with H. pylori-induced gastric cancer remains elusive. In this study, transcriptome sequencing revealed a significant correlation between HKDC1 and H. pylori-induced gastric cancer. Subsequent validation using qRT-PCR, immunohistochemistry, and Western blot analysis confirmed elevated HKDC1 expression in both human and murine gastritis and gastric tumors. Moreover, in vitro and in vivo experiments demonstrated that H. pylori infection up-regulates TGF-β1 and p-Smad2, thereby activating the epithelial-mesenchymal transition (EMT) pathway, with HKDC1 playing a pivotal role. Suppression of HKDC1 expression or pharmacological inhibition of TGF-β1 reversed EMT activation, consequently reducing gastric cancer cell proliferation and metastasis. These results underscore HKDC1's essential contribution to H. pylori-induced gastric cancer progression via EMT activation. [ABSTRACT FROM AUTHOR]

ABSTRACT Copper (Cu) is an effective additive in feed for promoting growth. Growth dan axis comprising growth hormone (GH), somatostatin (SS) and GH‐releasing hormone (GHRH), with ghrelin regulating their release. The growth‐promoting effects of Cu are closely related to ghrelin, but the specific mechanism behind the relationship remains unknown. We investigated the adjustment of ghrelin synthesis and secretion by Cu. Sprague–Dawley rats were fed basal diets with an addition of 0, 120 or 240 mg/kg Cu sulfate for 28 day to establish a growth‐promoting model. Signalling molecules relevant to ghrelin synthesis and secretion were detected and mechanistically explored using enzyme‐linked immunosorbent assay, quantitative reverse‐transcription polymerase chain reaction and Western blot analysis. The 120 mg/kg supplement improved growth performance; significantly increased the serum levels of ghrelin, ghrelin O‐acyltransferase (GOAT), acylated ghrelin (AG), GH, and reactive oxygen species (ROS) and decreased those of SS; significantly increased the mRNA and protein expression of ghrelin, GOAT, ghrelin receptor (GHS‐R1α), and activator protein 1 (AP‐1); increased the phosphorylation ratio of JNK and p38 MAPK; and inhibited the mRNA and protein expression of SS and SS receptor subtype 2 (SSTR2) in gastric fundic gland tissues. Thus, Cu may affect gastric ghrelin synthesis at the transcriptional level by activating the JNK/p38 MAPK pathway through increased ROS levels and regulating the activation of the downstream redox‐sensitive transcription factor AP‐1. SS plays a crucial determinant role in ghrelin regulation via intragastric Cu. Cu promotes GOAT activity and ghrelin secretion by inhibiting SS secretion, affecting AG levels, and promoting ghrelin acylation through ghrelin/GOAT/GHS‐R1α system, modulating ghrelin secretion. [ABSTRACT FROM AUTHOR]

Background: Chronic infection by Helicobacter pylori strains expressing cytotoxin-associated gene A (CagA) are the strongest risk factor for gastric cancer. CagA can be classified into East Asian-type and Western-type (CagAE and CagAW), with CagAE being more closely associated with gastric cancer. This study aimed to investigate the impact of CagAE on intracellular signaling pathways to explain its high oncogenicity. Results: Mutant H. pylori strains expressing either CagAE or CagAW were generated by transforming CagAE/W-expression plasmid into CagA-deleted G27 strain (G27ΔCagA). In human gastric epithelial cells (GES-1) infection, CagAE induced more severe cytopathic changes, including higher interleukin-8 (IL-8) secretion, reduced cell viability, more pronounced "hummingbird phenotype" alterations, and increased cell migration and invasion compared to CagAW. Transcriptome analysis revealed that CagAE had a stronger effect on the up-regulation of key intracellular processes, including tumor necrosis factor-ɑ (TNF-ɑ) signal pathway via nuclear factor kappa-B (NF-κB), inflammatory response, interferon-γ (IFN-γ) response, hypoxia, ultraviolet (UV) response, and Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) signaling. A significant upregulation of hypoxia-related genes was a notable feature of CagAE. GES-1 cells infected with CagAE exhibited more severe intracellular hypoxia and higher levels of reactive oxygen species (ROS) than those infected with CagAW. Inhibition of hypoxia-inducible factor-1α (HIF-1α), which blocks hypoxia signaling, mitigated CagAE-induced cell migration, emphasizing the role of hypoxia in mediating CagAE effects. Conclusions: The study provides transcriptome evidence of CagA-associated intracellular regulation during H. pylori infection, demonstrating that CagAE exerts stronger effects on intracellular signaling than CagAW. These findings offer insights into the heightened carcinogenic potential of CagAE in H. pylori-induced gastric cancer. [ABSTRACT FROM AUTHOR]

Helicobacter pylori, invades the gastric mucosa and is one of the causative agents of stomach cancer and peptic ulcers. Origanum vulgare, is a flavouring herb used worldwide. But little is known about the effects of extracts prepared by maceration in cold PBS. This study was aimed at determining the superoxide dismutase (SOD)- and peroxidase (Px)-like antioxidant activities as well as the immunomodulatory activity (anti-inflammatory/pro-inflammatory) of an aqueous extract of O. vulgare by evaluating the production of nitric oxide (NO) in macrophages stimulated with H. pylori derivatives. The cold extract presented SOD-like and Px-like activities with effective concentration 50 (EC50) values of Px = 489.7 ± 48 µg/ml and SOD= 384.7 ± 30 µg/ml. The extract was also capable of modulating the production of NO in macrophages stimulated by H. pylori derivatives by exerting a pro-inflammatory activity at high concentrations and an anti-inflammatory activity at low concentrations. [ABSTRACT FROM AUTHOR]

Copyright of Baghdad Science Journal is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Arsenic exposure is associated with numerous morbidities due to dysfunction of various organ systems including the gastrointestinal tract. We investigated the protective effect of grape seed oil (GSO) against sodium arsenite (NaAsO2)-induced gastric, hepatic and colonic injuries in rats. Twenty-four male Wistar rats were divided into four groups of six as follows: Group A (control) received saline; group B received NaAsO2 (2.5 mg/kg) orally for 7 days; group C were treated concurrently with NaAsO2 and GSO (2 ml/kg), while group D received only GSO. Administration of NaAsO2 induced significant (p < 0.05) increases in alanine aminotransferase (ALT) and aspartate aminotransferase (AST); increased periodic acid Schiff (PAS) staining for mucus and increased goblet cell numbers in the stomach and colon; inflammatory cell infiltration and vascular congestion and alterations in the fecal bacterial flora. GSO supplementation generally promoted a reversal of changes induced by NaAsO2 towards control levels. Additionally, there was increased immunohistochemically detected expression of colonic B-cell lymphoma-1 (Bcl-2) and cytokeratins AE1/AE3, but reduced expression of mucin 1 (MUC1) and carcinoembryonic antigen (CEA) in NaAsO2 + GSO and GSO treated rats when compared with the NaAsO2 group. These results suggest that GSO promoted anti-inflammatory processes in the liver, stomach and colon, as well as opposing apoptosis in the colon, resulting in significant attenuation of damage to these tissues. [ABSTRACT FROM AUTHOR]

Background: Eupatilin, a flavone isolated from Artemisia species, exerts anti-inflammatory, anti-oxidative, and anti-neoplastic activities. However, the effects of eupatilin on H. pylori-associated gastritis remain unclear. Thus, this study aimed to investigate the anti-inflammatory effects of eupatilin on gastric epithelial cells infected with cytotoxin-associated gene A (CagA)-positive Helicobacter pylori. Materials and methods: AGS human gastric carcinoma cells were infected with a CagA-positive H. pylori strain and then treated with 10, 50, or 100 ng of eupatilin. After 24 h, the expression levels of CagA, phosphoinositide 3-kinase 1 (PI3K), nuclear factor (NF)-κB, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α in the cell lysates were measured using western blotting, and the mRNA levels of IL-6, IL-8, and monocyte chemoattractant protein (MCP)-1 were measured using real-time polymerase chain reaction. Results: CagA translocation into AGS cells resulted in an elongated cell morphology, which was significantly suppressed by eupatilin treatment in a dose-dependent manner. Immunofluorescence staining for anti-CagA showed that eupatilin treatment dose-dependently inhibited CagA expression in the H. pylori-infected AGS cells. H. pylori infection increased the levels of pro-inflammatory cytokines including IL-1β, TNF-α, IL-6, IL-8, and MCP-1, and eupatilin treatment significantly reduced the levels of these cytokines in a dose-dependent manner. Additionally, eupatilin treatment dose-dependently suppressed the expression of PI3K and NF-κB. Conclusions: Eupatilin treatment demonstrated anti-inflammatory effects on CagA-positive H. pylori-infected gastric epithelial cells by inhibiting CagA translocation, thereby suppressing the NF-κB signaling pathway. These results suggest that eupatilin plays a protective role against CagA-positive H. pylori-induced gastritis. [ABSTRACT FROM AUTHOR]

Background: This study investigated clinicopathological factors associated with the visibility of early gastric cancer and the efficacy of linked color imaging. Methods: Patients with early gastric cancer who underwent endoscopic treatment between April 2021 and July 2022 were enrolled. All cases underwent white light imaging and linked color imaging. Three experts evaluated lesion visibility using a visual analog scale. A mean score ≥3 on white light imaging was defined as "good visibility", and <3 as "poor visibility". We extracted patient information and endoscopic and pathological data for the lesion and background mucosa, analyzed factors associated with the visibility of early gastric cancer, and compared visibility between white light imaging and linked color imaging. Results: Ninety-seven lesions were analyzed, with good visibility in 49 and poor visibility in 48. Multivariate analysis revealed small lesion size (odds ratio 1.89) and presence of endoscopic intestinal metaplasia (odds ratio 0.49) as significantly associated with the poor visibility of early gastric cancer. Mean visibility score was significantly higher for linked color imaging (P<0.001). Mean score for linked color imaging was significantly higher in the poor visibility group (P<0.001), but not significantly different in the good visibility group (P = 0.292). Mean score was significantly higher with linked color imaging in cases with endoscopic intestinal metaplasia (P = 0.0496) and lesions <20 mm in diameter (<10 mm, P = 0.002; 10–20 mm, P = 0.004). Conclusions: Lesion size and endoscopic intestinal metaplasia are associated with the visibility of early gastric cancer in white light imaging. Linked color imaging improves visibility of gastric cancer with these factors. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Vigilant intraoperative inspection is crucial during gallbladder surgery to detect any abnormal tissue including the rare pyloric gland adenomas, which can be easily missed. Thorough examination and removal of unusual lymph nodes or thickened tissues are essential to prevent the risk of malignant transformation and ensure comprehensive patient care. Pyloric gland adenomas are uncommon tumors that can be discovered in various organs such as the stomach, gallbladder, and pancreas. Typically lacking noticeable symptoms, these tumors are categorized into subtypes, with the pyloric variant being the most frequent. The term "intracholecystic papillary‐tubular neoplasms (ICPN)" is used to emphasize growth patterns and associated risks. In a discussed case, a detached pyloric gland adenoma was identified incidentally during a cholecystectomy procedure. A 58‐year‐old obese male presented with upper abdominal pain, nausea, and vomiting. He was diagnosed with early cholecystitis caused by gallstones. Subsequently, during a laparoscopic cholecystectomy, a detached adenoma was discovered. Vigilant screening is crucial, as the identification of gallbladder pyloric gland adenomas is a rare occurrence that might be missed during gallbladder surgery. Any unusual lymph nodes or thickened tissues found in association with the gallbladder ought to be carefully removed, as they could potentially indicate detached gallbladder adenomas with a significant risk of becoming malignant. Failing to consider this possibility may subject the patient to prolonged risks if not meticulously examined. [ABSTRACT FROM AUTHOR]

Background: Limited information is available on gastric diseases in neonatal foals as compared with extensive studies in young, adult, and geriatric horses. Reports on fetuses are scarce. Objectives: Assess at necropsy stomachs of horse, donkey and mule fetuses in the third trimester of gestation to characterize lesions present during intrauterine life. Animals: Forty‐six fetal stomachs from both sexes (21 horses, 21 donkeys, and 4 mules) in the third trimester of gestation were collected from a processing plant immediately after slaughter. Methods: Measurements of longitudinal and transverse axes, weight and volume and gastric fluid pH were taken, and glandular and squamous mucosae were inspected. All findings of the gastric mucosa and measurements of the stomachs were presented descriptively. Groups were compared statistically, with significance level set at P <.05 for all evaluations. Results: All gastric contents had pH >5.8, and mules had larger stomachs and higher weights compared with horses (P <.05). Macroscopic lesions were classified as hyperemic, punctate, and erosive. Histopathologically, lesions were consistent with a chronic inflammatory process. Conclusions and Clinical Importance: Our study provides evidence of macroscopic and histopathological lesions in the gastric mucosae of equid fetuses in the last trimester of gestation. Relevant information for perinatology and neonatology is provided regarding the prevalence and classification of preulcerous lesions in equids before birth. [ABSTRACT FROM AUTHOR]

Background: To analyze the diagnostic efficiency of the four absolute endoscopic submucosal dissection (ESD) indications for lymph node metastasis (LNM) of Chinese patients with early gastric cancer (EGC). Methods: We retrospectively analyzed EGC patients who underwent radical D2 gastrectomy from January 2019 to December 2022. We evaluated the rate of LNM, false-negative rate, and negative predictive value of the four ESD indications. Results: Of enrolled 2722 EGC patients, 388 (14.3%) patients presented LNM. Tumor size > 2 cm, ulceration, submucosal invasion, undifferentiated type, and lymphovascular invasion were independent risk factors of LNM in patients with EGC. 1062 (39%) cases of EGC conformed to the four EDS indications; however, 4% of them had LNM. 451 cases were fully in accord with the fourth ESD indication (undifferentiated intramucosal carcinoma without ulceration and a maximum lesion diameter of ≤ 2 cm), and 35 of them had LNM, with a false-negative rate (FNR) of 9.02% and a negative predictive value (NPV) of 92.24%. There was significant difference among the four indications in terms of the rate of LNM (1.0% vs 1.5% vs 1.3% vs 7.8%, P < 0.001), FNR (1.03% vs 0.52% vs 0.26% vs 9.02%, P < 0.001), and NPV (98.99% vs 98.53% vs 98.75% vs 92.24%, P < 0.001). Conclusion: Overall, the fourth ESD indication was associated with a high rate of LNM compared to the other three indications. Thus, it might not be safe to classify it as an absolute indication in Chinese patients with EGC. [ABSTRACT FROM AUTHOR]

Gastric and duodenal ulcers are increasingly becoming global health burdens. The side effects of conventional treatments such as non-steroid anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), antibiotics, and cytoprotective agents have necessitated the search for new medications. Plants are a rich source of active metabolites and herbal medicines have been used in the treatment of ulcers and cancers. In this study, we used in silico methods like molecular docking and MM-GBSA calculations to evaluate the effects of some anti-ulcer and anti-inflammatory phytochemicals on some key enzymes, cyclooxygenase (COX), and lipoxygenase (LOX), which are implicated in the protection and destruction of the gastric mucosa. The phytochemicals were retrieved from the literature and docked toward the binding sites of the three enzymes (COX-1, COX-2, and 5-LOX). Five compounds, rhamnetin, kaempferol, rutin, rosmarinic acid, and chlorogenic acid were observed to putatively bind to cyclooxygenase 2 (COX-2) and 5-lipoxygenase (5-LOX) but not to cyclooxygenase 1 (COX-1). The interaction mechanisms between these phytochemicals and the target proteins are discussed. The compounds' drug metabolism, pharmacokinetics, and toxicity have been evaluated to assess their suitability as potential next-generation anti-ulcer and anti-inflammatory drugs. [ABSTRACT FROM AUTHOR]

Objective(s): Some species of Prunus L. are popularly used to treat gastric ulcers. However, the possible healing mechanisms of the anti-ulcer activity of P. spinosa, which has proven antioxidant, anti-inflammatory, and wound-healing properties, are unclear. Materials and Methods: Ethanol extracts of P. spinosa fruits were administered orally at 100 mg/ kg and 200 mg/kg to Wistar albino rats, with an indomethacin-induced gastric ulcer model. The ulcerous areas on the stomach surface were examined macroscopically. Tissues were examined histopathologically and biochemically. LC-HRMS revealed the phytochemical content. Results: TNF-α, IL-6, IL-1β, IL-8, and NF-kB levels were higher in the gastric ulcer group than in the extract groups. The VEGF values did not differ in each group. A significant difference was found between the lansoprazole group and the high-dose P. spinosa group regarding PGE2 levels. A histopathologically significant difference was observed between the healthy group and the indomethacin-applied groups in terms of neutrophilic infiltration of the gastric mucosa. Ascorbic acid (1547.521 µg/g), homoprotocatechuic acid (1268.217 µg/g), and genistein (1014.462 µg/g) were found as the main compounds in the P. spinosa extract by LC-HRMS. Conclusion: Our results demonstrated that P. spinosa protected the gastric mucosa from inflammation and also modulated the PGE2 pathway. When considered in terms of TNF-α, IL-1 β, IL-8, IL-6, PGE2, and NF-kB values, it can be concluded that it has a similar or even more positive effect than the reference substance. P. spinosa showed its effects in a dose-dependent manner. [ABSTRACT FROM AUTHOR]

Background: In familial adenomatous polyposis (FAP) patients, fundic gland polyps (FGPs) have been considered a risk factor for gastric neoplasms. We speculated that FGPs in FAP patients spread directionally from the greater to the lesser curvature of the gastric body and investigated the relationship between the distribution of FGPs and gastric neoplasm development. Methods: We extracted 195 FAP patients from two institutions and reviewed their medical records. Gastric polyposis was classified based on the FGP distribution (P0, no FGPs; P1, localized in the fundus or greater curvature of the gastric body; P2, spreading to the anterior or posterior wall; P3, involving the proximal half of the lesser curvature; and P4, spreading from P3 to the anal side of the lesser curvature). Results: The 195 eligible patients were divided into the neoplasm group (n = 54, 28%) and the non-neoplasm group (n = 141, 72%). Overall, 24% of the patients were Helicobacter pylori (H. pylori)-positive. In the FGP distribution, the rate of patients with gastric neoplasm tended to increase significantly with each step towards an increasingly wide distribution from P0 to P4 in H. pylori-negative patients, but not in H. pylori-positive ones. In addition, in H. pylori-negative patients, the likelihood of neoplasm increased consistently from P0 to P4, with the highest odds ratio (95% confidence interval) at P4 of 14.1 (2.5–154.4). Furthermore, multivariate analysis showed P4 and Spigelman stage ≥III were significantly associated with gastric neoplasm development. Conclusion: FGP distribution was correlated with gastric neoplasm development in FAP patients. [ABSTRACT FROM AUTHOR]

Background: Between food and medicine, nutraceuticals are widely used in human health for the prevention and treatment of various diseases. This study aims to determine the cytoprotective effects of Anethum gravelons fruit extract (AGFAE) on castor oil‐induced diarrhea in rats due to its phytochemical and antioxidant properties. Methods: Male rats were divided into six groups of six animals each: Control (C), Castor oil (CO), CO + different doses of AGFAE (50, 100, and 200 mg/kg, b.w., p.o.), and the CO + loperamide group (LOP, 10 mg/kg, b.w., p.o.). Key Results: In vitro, the chemical composition of aqueous Dill fruit extract showed strong antioxidant activity, with a high content of total polyphenols, flavonoids, and tannins. In our in vivo studies, pre‐treatment with AGFAE reduced malondialdehyde and hydrogen peroxide levels and maintained normal activity of enzymatic and non‐enzymatic antioxidants in the gastric and intestinal mucosa. In addition, we found that AGFAE prophylaxis improved the stability of many plasma biochemical parameters altered by castor oil intoxication, such as C‐reactive protein concentrations and alkaline phosphatase activities. Conclusions & Inferences: We suggest that AGFAE phenolic compounds had significant protection against diarrhea involving several mechanisms such as reducing hypersecretion, peristaltic, inflammation, and preserving the endogenous antioxidant levels. [ABSTRACT FROM AUTHOR]

BACKGROUND: Dendrobium officinale flos (DOF), a novel food raw material, is used in Chinese folk medicine to nourish the stomach. However, there is still no available study to evaluate the effects of DOF on animal models of acute gastric injury and its mechanism by modern pharmacological research. RESULTS: Herein, we characterized the major components of an aqueous extract of DOF and assessed its potential ameliorative effects in a rat model of acute gastric mucosal injury. The DOF water extract showed significant protective effects on the gastric mucosa and exhibited excellent antioxidant and anti‐inflammatory activities. Acute gastric injury rat models induced by ethanol (6 mL kg−1) were pretreated with different doses of DOF water extract (50–100 mg kg−1 day−1), and the biological effects of DOF extract in gastric tissues were evaluated. DOF extract alleviated the symptoms of ethanol‐stimulated acute gastric mucosal injury, as evidenced by a significant reduction in gastric injury index and the degree of gastric pathological changes. Additionally, treatment with DOF extract upregulated mucin expression in the gastric mucosa, attenuated oxidative stress, decreased the release of inflammatory mediators (TNF‐α, IL‐6), suppressed the expression of key proinflammatory enzymes (COX‐2 and iNOS), reduced the phosphorylation of p38 MAPK and p65 NF‐κB and increased the level of PGE2 in gastric tissues. CONCLUSION: DOF exerts protective effects against ethanol‐induced acute gastric mucosal injury, mainly by inhibiting inflammation and oxidative stress. © 2024 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Grapes, recognized as a nutritionally rich fruit, have been found through extensive research to contain various bioactive components. However, the roles of polysaccharides and their bioactive properties remain unclear. Based on this, in our research, four different grape polysaccharides were obtained using an enzymatic-assisted extraction method. We investigated and compared their physicochemical properties, antioxidant activities, and protective effects on gastric mucosa in mice. The results indicated that the monosaccharide compositions of these specific grape polysaccharides were similar; however, their molar ratios, molecular weights, and morphological characteristics varied. The results of radical scavenging tests revealed that red-fleshed grape polysaccharide (RFP) exhibited superior antioxidant properties. In vivo assessments demonstrated that RFP protects against gastric mucosal injury in mice by inhibiting inflammation and radical generation. Therefore, the polysaccharide from red-fleshed grape holds potential application value in the pharmaceutical and food industries. [ABSTRACT FROM AUTHOR]

Gastric ulcer disease is associated with significant morbidity and mortality rates. The most two common causes of the ulcer are Helicobacter pylori infection and non-steroidal anti-inflammatory drugs. In the past few decades, a significant decrease in the morbidity and mortality rate has been observed probably due to the discovery of proton pump inhibitors. However, the medications used to treat gastric ulcers impose several nauseous side effects. Therefore, recent studies focus on the use of natural products to treat gastric ulcers. In the current study, gastric ulcer was effectively induced using indomethacin, and the protective effect of apigenin, a potent antioxidant flavonoid, was assessed in comparison to omeprazole. The administration of a single oral indomethacin (50 mg/kg) induced gastric ulcer as manifested by hemorrhagic lesions in the gastric mucosa, increased ulcer index, and histopathological alterations. Indomethacin also increased lipid peroxidation, decreased the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase, increased the immunoreactivity of the inflammatory markers cyclo-oxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-κB), increased the transcription of the apoptotic marker, Bax, and decreased that of the antiapoptotic Bcl-2. Indomethacin also decreased the immunoreactivity of transforming growth factor-beta 1 (TGF-β1). On the other hand, pretreatment with apigenin (10 and 20 mg/kg) resulted in a dose-dependent improvement in the macroscopic and microscopic features of the gastric mucosa in a manner comparable to that of omeprazole. The gastroprotective effects of apigenin may be attributed to its anti-inflammatory, anti-antioxidant, and anti-apoptotic activities as well as enhancing the expression of TGF-β1. Further experimental and clinical research is required to confirm activity of apigenin as anti-ulcer agent. [ABSTRACT FROM AUTHOR]

Copyright of Microbes & Infectious Diseases is the property of Microbes & Infectious Diseases and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tumor microenvironment (TME) immune cells and gastric mucosal microbiome constitute two vital elements of tumor tissue. Increasing evidence has elucidated their clinicopathological significance in predicting outcomes and therapeutic efficacy. However, comprehensive characterization of immune cell-associated microbiome signatures in the TME is still in the early stages of development. Here, we characterized the gastric mucosa microbiome and its associations with immune-activated related transcripts (IATs) in 170 GC tumor tissues and matched non-tumor tissues using 16s rRNA gene sequencing and quantitative reverse transcription-PCR. Microbial diversity and richness were significantly higher in GC tumor tissues than in non-tumor tissues. Differences in microbial composition between the groups were evident, with Firmicutes, Proteobacteria, Bacteroidota, Campilobacterota, Actinobacteria, Fusobacteriota, Verrucomicrobiota, Acidobacteriota, and Cyanobacteria being the dominant phyla in the gastric mucosal microbiota. Microbial interaction network analysis revealed distinctive centralities of oral bacteria (such as Fusobacterium, Porphyromonas, Prevotella, etc.) in both tumor and normal mucosae networks, suggesting their significant influence on GC microbial ecology. Furthermore, we analyzed the expression of IATs (CXCL9, CXCL10, GZMA, GZMB, PRF1, CD8A, IFNG, TBX2, and TNF) and characterized IAT-relevant gastric microbiome signatures in GC patients. Our results showed that the expression of CXCL9, CXCL10, GZMA, GZMB, PRF1 and IFNG was significantly higher in tumor tissues than in adjacent normal tissues in GC patients. Notably, high expression of IATs in tumor tissues was associated with improved survival in GC patients and could serve as a powerful predictor for disease-free survival. Additionally, analysis of IAT levels and mucosal microbiota diversity revealed a correlation between higher IAT expression and increased microbiota richness and evenness in the IATs high group, suggesting potential interactions between mucosal microbiota and tumor immunopathology. Spearman correlation analysis showed positive associations between IAT expression and specific mucosal bacterial species. Notably, Akkermansia muciniphila demonstrated potential involvement in modulating GZMB expression in the GC mucosal microenvironment. These findings underscore the importance of mucosal microbiota alterations in GC and suggest potential therapeutic targets focusing on modulating the tumor microbiota for improved clinical outcomes. The detailed characterization of these elements has profound implications for both treatment and survival prediction in GC. We observed that microbial diversity and richness were significantly higher in GC tumor tissues compared to non-tumor tissues. These differences highlight the unique microbial landscape of GC tumors and suggest that the microbiome could influence tumor development and progression. Importantly, our study demonstrated that high expression levels of IATs in GC tumor tissues were associated with improved patient survival. This suggests that IATs not only reflect immune activation but also serve as valuable biomarkers for predicting disease-free survival. The potential of IATs as predictive markers underscores their utility in guiding therapeutic strategies and personalizing treatment approaches. Moreover, the correlation between higher IAT expression and increased microbiota richness and evenness suggests that a diverse and balanced microbiome may enhance immune responses and contribute to better clinical outcomes. These findings highlight the critical need to consider mucosal microbiota alterations in GC management. Targeting the tumor microbiota could emerge as a promising therapeutic strategy, potentially leading to more effective treatments and improved patient outcomes. Understanding and modulating the microbiome’s role in GC opens new avenues for innovative therapeutic interventions and personalized medicine. [ABSTRACT FROM AUTHOR]

Purpose: In the Zhejiang region, research on Helicobacter pylori is lacking. The purpose of this study was to assess the extent of antibiotic resistance in H. pylori in this region, explore alternative methods for predicting the resistance patterns of H. pylori, and investigate the colonization of native gastric mucosa by other clades of H. pylori in the structure population of this bacterium. Methods: Strains were cultured under microaerobic conditions, and antimicrobial susceptibility testing (AST) was performed via agar dilution. Whole-genome sequencing (WGS) was performed via next-generation sequencing (NGS) technology. Epidemiological data including data from this study and reported articles from Zhejiang, China, were included. Further analyses based on AST, WGS, and epidemiological date include virulence genes, antibiotic resistance-related mutations, and phylogenetic trees based on 7 housekeeping genes and core-genome single nucleotide polymorphisms (SNPs). Results: The bacterial isolates in this study presented higher antibiotic resistance rates than previously reported, especially against levofloxacin and clarithromycin. The point mutation A2147G in 23 S rRNA is specific to clarithromycin resistance. Mutations at position/s 87 and/or 91 of the gyrA gene amino acid sequence are highly consistent with levofloxacin resistance highly. The point mutations C1707T in 23 S rRNA and E463K in the gyrB gene have not been previously documented in China. All the bacterial isolates belong to Asian branches in the structure population. The resistance rate to clarithromycin of isolates from hosts born after January 1, 1977 is statistically higher than that of hosts born before 1977. Conclusion: Eradication therapy based on AST results is urgently needed in Zhejiang. The point mutation A2147G in 23 S rRNA and point mutations in the gyrA gene at amino acid/s 87 and/or 91 are sufficient for predicting resistance to clarithromycin and levofloxacin, respectively. The isolate with the mutation E463K in the gyrB gene represents a significant contribution to the field. Mutations in 23 S rRNA may offer valuable insights into the dynamics of H. pylori transmission among hosts. [ABSTRACT FROM AUTHOR]

Simple Summary: Intestinal microbiota (the gut microbiome) are important for normal gut function, especially in horses which rely on gut bacteria to break down plant material in the hindgut. Understanding normal microbiota is essential to be able to assess changes that occur during disease or in response to treatments. Post-mortem studies and biopsies have found different populations in the stomach mucosa (lining) compared to feces, but the gastric fluid has not been evaluated. The objective of this study was to describe the gastric fluid microbiome of healthy horses over time, under two housing conditions, and to compare the gastric fluid to fecal microbiome of paired samples. We found that while there were fewer bacteria (taxa) identified in the gastric juice compared to feces, there was a stable population of gastric microbiota which did not vary from week-to-week under either housing condition. There was a significant difference in compositional diversity (the relatedness of taxa present) between housing conditions, with changes in the relative proportions of a few key groups when horses moved from pasture to stable. These findings are important to inform future investigations of the gastric fluid microbiota in horses. Equine gastrointestinal microbial communities vary across the gastrointestinal tract and in response to diet or disease. Understanding the composition and stability of gastric fluid microbiota in healthy horses is a prerequisite to understanding changes associated with the development of disease. The objective of this study was to describe microbial communities in the gastric fluid and feces of healthy horses longitudinally. Horses were maintained on pasture (6 weeks), stabled (5 weeks), then returned to pasture. A consistent forage diet was provided throughout. Native gastric fluid and feces were collected weekly for full-length 16S ribosomal DNA sequencing and microbial profiling analysis. Fewer taxa were identified in the gastric fluid (770) than in the feces (5284). Species richness and diversity were significantly different between sample types (p < 0.001), but not between housing locations (p = 0.3). There was a significant effect of housing and horse on the Bray–Curtis compositional diversity of gastric (p = 0.005; p = 0.009) and fecal (p = 0.001; p = 0.001) microbiota. When horses moved from pasture to stable, the relative proportions of gastric fluid Lactobacillaceae increased and Streptococcaceae decreased, while fecal Firmicutes increased and Bacteriodota decreased. Within each housing condition, there was no significant week-to-week variation in gastric (p = 0.9) or fecal (p = 0.09) microbiota. Overall, these findings support the maintenance of stable gastric and fecal microbial populations under each management condition, providing a basis for further investigation of gastric fluid microbiota in diseases of the foregut. [ABSTRACT FROM AUTHOR]

Relevance to Clinical Practice Nasogastric tubes (NGTs) are commonly used in the intensive care unit (ICU) and are often inserted blindly at the bedside. Previous studies have highlighted various complications associated with NGT misplacement, including epistaxis, pneumothorax and even fatal perforations. To reduce the incidence of complications, guidelines recommend confirming the correct position of the NGT through radiography, pH testing, end‐expiratory carbon dioxide monitoring, ultrasonography, etc. Herein, we present the case of a 78‐year‐old man who experienced sudden dyspnoea, was brought to the ICU and subsequently developed gastrointestinal bleeding following improper NGT placement. In this patient, air was rapidly injected down the NGT while auscultating for a ‘whooshing sound’ over the epigastrium. However, the correct position of the NGT was eventually confirmed by X‐ray. Urgent upper gastrointestinal endoscopy revealed an oesophagogastric submucosal tunnelling of the NGT. This case emphasizes that auscultation may be unreliable and no longer encouraged. Additionally, various verification methods may not detect such rare complications related to NGT placement, making it necessary to focus on the emerging clinical manifestations following NGT insertion. Moreover, gaining further insight into the history of gastrointestinal diseases in patients may be beneficial.This case underscores the importance of noting resistance during a blind nasogastric tube (NGT) insertion in the intensive care unit (ICU). Additionally, the ‘whooshing testing’ for tube placement verification is not recommended. Although radiographic confirmation remains the gold standard, it may not effectively identify rare complications. Furthermore, emerging clinical signs (such as the abnormal nature of the gastrointestinal decompression drainage fluid, hypotension and anaemia) after insertion may suggest NGT misalignment. Finally, in urgent ICU settings, the patient's history of gastrointestinal disease should not be overlooked, as it can lead to complications such as gastrointestinal bleeding. [ABSTRACT FROM AUTHOR]

Chronic gastritis (CG) is a common inflammatory disease of chronic inflammatory lesion of gastric mucosa and in the diagnosis of gastritis in traditional Chinese medicine (TCM), CG can be classified into Cold ZHENG (syndrome in TCM) and Hot ZHENG. However, the molecular features of Cold/Hot ZHENG in CG and the mechanism of Cold/Hot herbs in formulae for CG remained unclear. In this study, we collected a transcriptomics data including 35 patients of Cold/Hot ZHENG CG and 3 scRNA-seq CG samples. And 25 formulae for CG and 89 herbs recorded in these formulae were also collected. We conduct a comprehensive analysis based on the combination of transcriptomics datasets and machine learning algorithms, to discover biomarkers for Cold/Hot ZHENG CG. Then the target profiles of the collected formulae and Cold/Hot herbs were predicted to uncover the features and biomarkers of them against Cold/Hot ZHENG CG. These biomarkers suggest that Hot ZHENG CG might be characterized by over-inflammation and exuberant metabolism, and Cold ZHENG CG showed a trend of suppression in immune regulation and energy metabolism. Biomarkers and specific pathways of Hot herbs tend to regulate immune responses and energy metabolism, while those of Cold herbs are more likely to participate in anti-inflammatory effects. Finally, the findings were verified based on public transcriptomics datasets, as well as transcriptomics and ELISA detection, taking Jin Hong tablets as a case study. Biomarkers like leptin and IL-6 together with proportions of immune cells showed significant changes after the intervention. These findings might reflect the mechanism and build a bridge between macro and micro views of Cold/Hot ZHENG as well as Cold/Hot herbs. [ABSTRACT FROM AUTHOR]

Background: Gastritis, a significant public health concern worldwide, involves inflammation or irritation of the gastric mucosa. This condition is influenced by various factors such as health behaviors, socioeconomic status, lifestyle, living conditions, and habits. It can be acute, chronic, or severe and is often associated with Helicobacter pylori (H. pylori) infection. Contributing factors to gastritis include smoking, alcohol consumption, spicy foods, medications, stress, and infections. In India, the prevalence of gastritis is notable, with recent studies indicating a high incidence of H. pylori infection. This study aims to investigate the prevalence and contributing factors of gastritis among patients in a tertiary care hospital. Methodology: A descriptive, observational, noninterventional study was conducted with 150 subjects aged 14-65 years diagnosed with gastritis at MKCG Medical College and Hospital, Berhampur. Data were collected using a structured questionnaire covering socio-demographic details, dietary habits, economic status, family history, stress levels, drug use, and medical history. Ethical approval was obtained, and written consent was provided by each participant. Results: Out of 150 subjects, 73% were male and 27% female, indicating a male predominance. The age groups 14-25 and 36-45 years had the highest prevalence. A significant proportion (75%) had a mixed diet, and 54% were alcoholics, predominantly males. Urban residents (68%) exhibited a higher incidence of gastritis. Blood group A Rh+ was predominant (46%), and 6% were hypertensive. Spicy food consumption (73%) and frequent NSAID use (61%) were notable risk factors. High stress levels were reported by 47% of the participants. Associations were found between gastritis and psychological stress, menstrual history, sleeping patterns, and educational levels. Discussion: Gastritis prevalence is influenced by male gender, urban residence, alcohol consumption, spicy food intake, and frequent NSAID use. The findings highlight the importance of targeted interventions to address these risk factors. Physical labor, particularly among males, and stress are significant contributors. The study underscores the need for preventive strategies focusing on lifestyle modifications and stress management to reduce gastritis incidence. Conclusion: This study provides a comprehensive overview of the prevalence and contributing factors of gastritis in the hospital. Males, urban residents, and individuals consuming spicy food and alcohol are at higher risk. The findings call for public health initiatives to address these risk factors through education, lifestyle changes, and stress reduction programs. Future research should explore tailored preventive strategies to mitigate the burden of gastritis in this population. [ABSTRACT FROM AUTHOR]

Objective: This study explored the distributions of gastric mucosal status and their links to gastric cancer within urban high‐risk individuals in China. Methods: From 2014 to 2015, a questionnaire survey was administered among individuals aged 40 to 69 years, residing for over 3 years in seven selected cities across China. Utilizing the questionnaire data, high‐risk individuals for gastric cancer were screened. These identified high‐risk individuals were invited to undergo endoscopy, followed by pathological examinations conducted for those with suspicious lesions. Prior cancer patients and those newly diagnosed with gastric cancer were excluded, and the remaining endoscopic participants were prospectively followed up until December 2021. Results: The prospective study followed 8911 individuals at high risk of gastric cancer for a median duration of 6.77 years. The incidence density of gastric cancer was 58.55 per 100,000 person‐years. At baseline, the distributions of subjects across normal gastric mucosa, gastritis/ulcer/polyp, atrophic gastritis/intestinal metaplasia, and intraepithelial neoplasia groups were 47.09%, 36.27%, 9.57%, and 7.07%, respectively. Compared with normal gastric mucosa, the hazard ratios (HRs) for gastric cancer in the other groups were 0.89 [95% confidence interval (95%CI): 0.38–2.08], 1.52 (95%CI: 0.50–4.66), and 4.63 (95%CI: 1.98–10.82). When using the 40–54 age group as the reference, the HR for 55–69 age group was 3.49 (95%CI: 1.52–7.98). Conclusion: Among high‐risk individuals with gastric cancer, the proportions of individuals exhibiting different gastric mucosal status inversely correlated with the severity of mucosal lesions, whereas the risk of gastric cancer progressively escalated with the increasing severity of mucosal lesions and advancing age. [ABSTRACT FROM AUTHOR]

Simple Summary: Channa striatus (striped murrel) is a valuable freshwater fish known for its taste and medicinal properties. Despite the advances in breeding technology, larval rearing remains a major challenge for producing high-quality seeds for commercial production. A key issue is the lack of a scientifically validated weaning protocol, resulting in high mortality during early developmental stages. After feeding different early weaning diets over 29 days, we have found that larvae fed with Artemia nauplii increased the overall larval performance during the initial exogenous feeding phase. However, constraints due to feeding solely with Artemia nauplii necessitate weaning with an artificial micro diet. By 12 dph, the performance of larvae fed with Artemia nauplii and co-feed diet (Artemia nauplii and formulated diet) showed comparable results, and by 20 dph, the larvae fed with protease supplemented formulated micro diet showed better performance compared to other treatments. Therefore, this study gives an insight for standardizing weaning protocol for C. striatus larvae based on the effects of different early weaning diets, which positively enhances survival and growth of the Channa striatus larvae. The present study was carried out to evaluate the survival, growth, and digestive ontogeny of C. striatus larvae fed with different experimental diets from 4 days post-hatch (dph) to 32 dph at three-day intervals. A total of 24,000 larvae, with 1600 larvae per tank in triplicate and an initial mean weight of 0.64 ± 0.01 mg at 4 days post hatch (dph) were subjected to five different early weaning diets, namely Artemia nauplii (T1), co-feed diet comprising Artemia nauplii and formulated micro diet (T2), formulated micro diet (T3), formulated micro diet with protease supplementation (T4), and a commercial diet (T5). All the early weaning diets significantly affected the survival, growth, and ontogeny of the digestive system. Initially at 8 dph, C. striatus fed with T1 showed better survival and growth performance compared to other treatments. By 12 dph, the larvae fed with T1 and T2 showed similar results in terms of survival and growth performance, outperforming other treatments. However, the larvae fed with T2 and T4 outperformed T1 in survival and growth performance at 16 dph. By 24–32 dph, the larvae fed with all treatments met the basic nutritional needs for survival, with T4 fed larvae showing better growth compared to other treatments. At the end of the trial, cumulative mortality was lowest in larvae fed with T1 and highest in the larvae fed with T3 and T5. Similarly, the larvae fed with T4 showed significantly higher weight gain, specific growth rate (SGR), and average daily growth (ADG), while T1 fed larvae exhibited better feed conversion ratio (FCR) and protein efficiency ratio (PER). The enzyme activity fluctuated throughout the experimental duration. Lavae fed with T1 and T2 showed higher enzyme activities initially. However, T4 fed larvae showed higher trypsin and chymotrypsin specific activity at 16 dph along with well-developed intestinal folds with dense microvilli, higher pepsin-specific activity at 20 dph onwards with fully developed gastric glands and thicker gastric mucosal epithelium, and higher amylase and lipase activity at 16 dph with large and prominent zymogen granules in the exocrine pancreas. Peaking at 4 dph, the activity of protein metabolic enzymes (AST and ALT) sharply declined at 8 dph and increased until 32 dph. Larvae fed with T1 showed higher AST and ALT activity along with increased lipid deposits, followed by those fed with T2 and the larvae fed with T4 showing higher activity without fat accumulation but significantly lower than those fed T1 and T2. From the present research findings, it is recommended to initiate weaning for Channa striatus larvae with Artemia nauplii (from 4 dph to 8 dph) followed by a co-feeding regime (Artemia nauplii and formulated diet) between 9 and 16 dph and transition to protease-supplemented micro diet (T4) from 17 dph onwards. [ABSTRACT FROM AUTHOR]

This article discusses the misdiagnosis of synaptophysin-expressing gastric glomus tumors as gastric neuroendocrine tumors. The authors present two cases of patients with gastric glomus tumors that were initially misdiagnosed due to the expression of synaptophysin. The article emphasizes the importance of using a comprehensive panel of immunomarkers, including chromogranin, CD56, and keratin, to differentiate between neuroendocrine tumors and glomus tumors. The authors also highlight the potential diagnostic pitfalls and implications of synaptophysin expression in visceral glomus tumors. [Extracted from the article]

Human sialic acid-binding immunoglobulin-like lectins (Siglecs) are expressed on subsets of immune cells. Siglec-8 is an immune inhibitory Siglec on eosinophils and mast cells, which are effectors in allergic disorders including eosinophilic esophagitis. Inhibition occurs when Siglec-8 is crosslinked by multivalent Siglec ligands in target tissues. Previously we discovered a high-affinity Siglec-8 sialoglycan ligand on human airways composed of terminally sialylated keratan sulfate chains carried on a single protein, DMBT1. Here we extend that approach to another allergic inflammatory target tissue, human esophagus. Lectin overlay histochemistry revealed that Siglec-8 ligands are expressed predominantly by esophageal submucosal glands, and are densely packed in submucosal ducts leading to the lumen. Expression is tissue-specific; esophageal glands express Siglec-8 ligand whereas nearby gastric glands do not. Extraction and resolution by gel electrophoresis revealed a single predominant human esophageal Siglec-8 ligand migrating at >2 MDa. Purification by size exclusion and affinity chromatography, followed by proteomic mass spectrometry, revealed the protein carrier to be MUC5B. Whereas all human esophageal submucosal cells express MUC5B, only a portion convert it to Siglec-8 ligand by adding terminally sialylated keratan sulfate chains. We refer to this as MUC5B S8L. Material from the esophageal lumen of live subjects revealed MUC5B S8L species ranging from ~1–4 MDa. We conclude that MUC5B in the human esophagus is a protein canvas on which Siglec-8 binding sialylated keratan sulfate chains are post-translationally added. These data expand understanding of Siglec-8 ligands and may help us understand their roles in allergic immune regulation. [ABSTRACT FROM AUTHOR]

The misuse of antibiotics has led to high levels of drug-resistance in specific pathogens, promoting the search of molecules from different natural sources or the design of novel drug candidates. Medicinal and edible plants are a rich source of bioactive compounds, in particular those of polyphenol class. In the present work, we screen the antimicrobial properties of an aqueous extract prepared from the leaves of Ugni molinae (Turz) against a panel of pathogenic bacteria strains formed by Helicobacter pylori (ATCC 43504), Listeria monocytogenes (ATCC 7644), Staphylococcus aureus (ATCC 9144), Escherichia coli (ATCC 11775), and Salmonella enterica (ATCC 13076). Preliminary fast HPLC-micro fractionation allows the identification of potential urease inhibitors using high throughput urea-phenol microplate assay. Afterwards, preparative fractionation by Centrifugal Partition Chromatography (CPC) allow to select the specific bioactive fractions. A combination of antimicrobial tests, enzyme assays and molecular docking resulted in the identification by HPLC-MS/MS of two quercetin-O-(6"-O-galloyl)-hexosides as the most dominant compounds in the active CPC-fractions. These bioactive compounds were quercetin-3-O-(6"-O-galloyl)-8-galactopyranoside (hyperin 6"-gallate) and quercetin-3-O-ß-D-(6"-O-galloyl)- ß-glucopyranoside (tellimoside). The molecular docking evaluation revealed that hyperin-6"-gallate enter the binding site of urease and bind in through pi-cation, pi-pi, and H-bond interactions. In concordance with the in-silico assay, the CPC fraction containing this compound has the lowest values of IC50 for Jack bean (0.41 ± 0.08 µg/mL) and Helicobacter pylori (0.28 ± 0.08 µg/mL) ureases, respectively. Moreover, Label-Free Microscale Thermophoresis (MST) analysis suggest that this flavonoid forms a complex with urease, even inducing protein aggregation. In conclusion, Ugni molinae leaves has potent anti-urease flavonoids that can contribute to significantly reduce the acclimation of H. pylori in the acidic environmental of gastric mucosa. [ABSTRACT FROM AUTHOR]

Copyright of Revista Foco (Interdisciplinary Studies Journal) is the property of Revista Foco and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The metabolism of abnormal bile acids (BAs) is implicated in the initiation and development of gastrointestinal (GI) cancer. However, there was a lack of research on the molecular mechanisms of BAs metabolism in GI. Methods: Genes involved in BAs metabolism were excavated from public databases of The Cancer Genome Atlas (TCGA) database, Gene Expression Omnibus (GEO) database, and Molecular Signatures Database (MSigDB). ConsensusClusterPlus was used to classify molecular subtypes for GI. To develop a RiskScore model for predicting GI prognosis, univariate Cox analysis was performed on the genes in protein–protein interaction (PPI) network, followed by using Lasso regression and stepwise regression to refine the model and to determine the key prognostic genes. Tumor immune microenvironment in GI patients from different risk groups was assessed using the ESTIMATE algorithm and enrichment analysis. Reverse transcription–quantitative real‐time PCR (RT‐qPCR), Transwell assay, and wound healing assay were carried out to validate the expression and functions of the model genes. Results: This study defined three molecular subtypes (C1, C2, and C3). Specifically, C1 had the best prognosis, while C3 had the worst prognosis with high immune checkpoint gene expression levels and TIDE scores. We selected nine key genes (AXIN2, ATOH1, CHST13, PNMA2, GYG2, MAGEA3, SNCG, HEYL, and RASSF10) that significantly affected the prognosis of GI and used them to develop a RiskScore model accordingly. Combining the verification results from a nomogram, the prediction of the model was proven to be accurate. The high RiskScore group was significantly enriched in tumor and immune‐related pathways. Compared with normal gastric mucosal epithelial cells, the mRNA levels of the nine genes were differential in the gastric cancer cells. Inhibition of PNMA2 suppressed migration and invasion of the cancer cells. Conclusion: We distinguished three GI molecular subtypes with different prognosis based on the genes related to BAs metabolism and developed a RiskScore model, contributing to the diagnosis and treatment of patients with GI. [ABSTRACT FROM AUTHOR]

Growth factor receptor bound protein 7 (GRB7) is reportedly upregulated in human gastric cancer (GC), which is closely associated with tumor progression and prognosis. However, the mechanism underlying its dysregulation in GC remains poorly understood. In this study, we found that GRB7 overexpression was associated with Helicobacter pylori (H. pylori) infection. GC cells (AGS and MGC-803) infection assays revealed that this upregulation was mediated by the transcription factor STAT3, and activation of STAT3 by H. pylori promoted GRB7 expression in infected GC cells. Moreover, CagA, the key virulence factor of H. pylori, was found involved in STAT3-mediated GRB7 overexpression. The overexpressed GRB7 further promoted GC cell proliferation, migration, and invasion by activating ERK signaling. Mice infection was further used to investigate the action of GRB7. In H. pylori infection, GRB7 expression in mice gastric mucosa was elevated, and higher STAT3 and ERK activation were also detected. These results revealed GRB7-mediated pathogenesis in H. pylori infection, in which H. pylori activates STAT3, leading to increased GRB7 expression, then promotes activation of the ERK signal, and finally enhances malignant properties of infected cells. Our findings elucidate the role of GRB7 in H. pylori-induced gastric disorders, offering new prospects for the treatment and prevention of H. pylori-associated gastric carcinogenesis by targeting GRB7. [ABSTRACT FROM AUTHOR]

Crohn's disease (CD) is a chronic inflammatory bowel condition with increasing global incidence. Diagnosing CD is challenging and requires close collaboration between clinicians and pathologists due to the lack of specific diagnostic criteria. Histologically, CD is characterized by transmural inflammation, crypt distortion, metaplasia, and granulomas, although granulomas are not always present. Schaumann bodies (SB), initially described in sarcoidosis, are rare in CD but have been reported in about 10% of cases. This case report presents a 4-year-old female with chronic hemorrhagic diarrhea, severe anemia, and elevated inflammatory markers. Endoscopic and histological evaluations suggested CD, with the presence of SB in the gastric mucosa. Further investigations ruled out sarcoidosis, confirming a diagnosis of multi-segmental, very early onset CD with atypical histological features. SB are inclusions composed of calcium carbonate crystals and conchoid bodies, typically found within giant cells. The presence of SB in the mucosa is rare, limiting their diagnostic significance in endoscopic biopsies. Differential diagnosis should exclude other granulomatous diseases such as intestinal tuberculosis and sarcoidosis. This case highlights the importance of considering SB in the diagnosis of CD, particularly in pediatric patients. [ABSTRACT FROM AUTHOR]

This document discusses a new database that contains 520 studies on the carcinogenicity data of 238 pharmaceuticals across 14 ATC classifications. The database includes non-clinical animal studies and human information for approved drugs, and can be used for correlation and concordance analyses. It provides insights into the tumorigenic potential of structural analogues and includes information on species, strain sensitivities, and affected organs/tissues. The authors emphasize the importance of repeat-dose toxicity studies in identifying potential concerns regarding tumorigenic potential. The database also includes information on the incidence and severity of effects observed in these studies, such as hyperplasia and neoplastic changes, which are relevant in assessing the carcinogenicity of pharmaceuticals. [Extracted from the article]

Helicobacter pylori (H. pylori) is a bacterial pathogen that exclusively colonizes the human gastric mucosa and can cause persistent infection. In this process, H. pylori employs various strategies to avoid recognition by the human immune system. These range from passive defense strategies (e.g., altered LPS or flagellin structures) that prevent recognition by pattern recognition receptors (PRRs) to more active approaches, such as inhibition of IL-2 secretion and proliferation of T cells via VacA. Despite the growing evidence that H. pylori actively manipulates the human immune system for its own benefit, the direct interaction of H. pylori with immune cells in situ is poorly studied. Here, we present a novel intravital imaging model of the murine stomach gastric mucosa and show for the first time the in situ recruitment of neutrophils during infection and a direct H. pylori-macrophage interaction. For this purpose, we applied multiphoton intravital microscopy adapted with live drift correction software (VivoFollow) on LysM-eGFP and CX3CR1-eGFP reporter mice strains in which specific subsets of leukocytes are fluorescently labeled. Multiphoton microscopy is proving to be an excellent tool for characterizing interactions between immune cells and pathogens in vivo. Author summary: This study focuses on the dynamics of H. pylori infection and its interaction with myeloid immune cells, using an innovative in vivo multiphoton imaging approach to observe real-time events in the infected gastric mucosa. In contrast to conventional methods, this novel technique allows us to dynamically investigate the host immune response. Our results show the spatio-temporal distribution of neutrophils and the internalization of H. pylori by macrophages over time. Using intravital multiphoton microscopy enhanced with live drift correction software and utilizing LysM-eGFP and CX3CR1-eGFP reporter mice, we established an intravital imaging model for the gastric mucosa of mice. Notably, we observe a significant increase in neutrophil infiltration into the gastric submucosa during early infection, indicating a rapid response of the innate immune system within the gastric crypts. However, in the chronic infection phase, a contrasting decrease in neutrophil influx is seen, indicating an adaptive innate immune response with fewer neutrophils infiltrating the tissue at an increased rate. Importantly, our data suggest that H. pylori is dependent on macrophages to proliferate and colonize the gastric mucosa during chronic infection. [ABSTRACT FROM AUTHOR]

Objective: Unusual clinical course. Background: The finding of pneumoperitoneum frequently leads to operative management for diagnosis and treatment. The etiology of pneumoperitoneum includes perforated viscus, such as perforated peptic ulcers, small or large intestinal perforations, appendicitis, and complicated sigmoid diverticulitis. We describe the preoperative, intraoperative, and postoperative course of a patient with perforated Meckel's diverticulitis presenting with pneumoperitoneum. This unusual presenting finding highlights that Meckel's diverticulum should be included in the differential diagnosis in adolescents and young adults presenting with pneumoperitoneum. Case Report: We describe a case of an 18-year-old male who presented with 1 day of abdominal pain, found to have pneumoperitoneum during workup, attributed to perforated Meckel's diverticulum. CT scans of the abdomen and pelvis were performed, confirming pneumoperitoneum, an inflamed segment of distal ileum, and a non-visualized appendix, which made the diagnosis difficult. Perforated Meckel's diverticulum, likely due to infection, was confirmed by diagnostic laparoscopy. The Meckel's diverticulum was then exteriorized and removed by segmental small bowel resection with primary anastomosis. The final pathology report confirmed perforated Meckel's diverticulum with gastric oxyntic-type mucosa. Conclusions: This case illustrates an uncommon presentation of Meckel's diverticulum in an adolescent with pneumoperitoneum. Pneumoperitoneum requires broadening the diagnosis to include other causes, including Meckel's diverticulum, especially in the setting of an acute abdomen. This case highlights that a high index of suspicion should be kept for Meckel's diverticulum, even in adolescents and young adults with pneumoperitoneum. [ABSTRACT FROM AUTHOR]

Background: Recent studies have suggested an association between H. pylori and metabolic-disfunction associated fatty liver disease (MASLD). However, epidemiologic studies have yielded inconsistent results. We aim to evaluate the association of H. pylori and G-allele PNPLA3 in MASLD diagnosis, and markers of severity. Methods: A multi-center cross-sectional study was conducted. A total 224 functional dyspepsia (FD) patients cohort who underwent gastroscopy was selected. Biochemical, clinical parameters, ultrasound, FIB-4 score, LSM by VCTE, gastric biopsies, H. pylori status, and rs738409 PNPLA3 were evaluated. A second retrospective cohort of 86 patients with biopsy-proven MASLD who underwent gastroscopy with gastric biopsies was analyzed. Results: In the FD cohort MASLD was observed in 52%, and H. pylori-positive in 51%. H. pylori infection was associated with MASLD prevalence, but in multivariate analyses adjusted for G-allele PNPLA3, it became not significant. Then in MASLD-only dyspeptic cohort, H. pylori infection was significantly linked to elevated serum AST levels and increased liver stiffness measurements, suggesting a potential role in liver injury and fibrosis. Histopathological analysis in biopsy-proven MASLD patients further supported these findings, showing a significant association between H. pylori infection and increased NAS score, fibrosis stage, and prevalence of MASH. Notably, the combination of H. pylori infection and G-allele PNPLA3 appeared to exacerbate MASLD severity beyond individual effects. Conclusions: Our results suggest that H. pylori infection may play a role in the progression of liver injury and fibrosis in patients with MASLD, especially in those with specific genetic predispositions. [ABSTRACT FROM AUTHOR]

Helicobacter pylori is one of the most common bacterial pathogens worldwide and the main etiological agent of numerous gastric diseases. The frequency of multidrug resistance of H. pylori is growing and the leading factor related to this phenomenon is its ability to form biofilm. Therefore, the establishment of a proper model to study this structure is of critical need. In response to this, the aim of this original article is to validate conditions of the optimal biofilm development of H. pylori in monoculture and co-culture with a gastric cell line in media simulating human fluids. Using a set of culture-based and microscopic techniques, we proved that simulated transcellular fluid and simulated gastric fluid, when applied in appropriate concentrations, stimulate autoaggregation and biofilm formation of H. pylori. Additionally, using a co-culture system on semi-permeable membranes in media imitating the stomach environment, we were able to obtain a monolayer of a gastric cell line with H. pylori biofilm on its surface. We believe that the current model for H. pylori biofilm formation in monoculture and co-culture with gastric cells in media containing host-mimicking fluids will constitute a platform for the intensification of research on H. pylori biofilms in in vitro conditions that simulate the human body. [ABSTRACT FROM AUTHOR]