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UNLABELLED: Motility promotes biofilm initiation during the early steps of this process: microbial surface association and attachment. Motility is controlled in part by chemotaxis signaling, so it seems reasonable that chemotaxis may also affect biofilm formation. There is a gap, however, in our understanding of the interactions between chemotaxis and biofilm formation, partly because most studies analyzed the phenotype of only a single chemotaxis signaling mutant, e.g., cheA. Here, we addressed the role of chemotaxis in biofilm formation using a full set of chemotaxis signaling mutants in Helicobacter pylori, a class I carcinogen that infects more than half the worlds population and forms biofilms. Using mutants that lack each chemotaxis signaling protein, we found that chemotaxis signaling affected the biofilm initiation stage, but not mature biofilm formation. Surprisingly, some chemotaxis mutants elevated biofilm initiation, while others inhibited it in a manner that was not tied to chemotaxis ability or ligand input. Instead, the biofilm phenotype correlated with flagellar rotational bias. Specifically, mutants with a counterclockwise bias promoted biofilm initiation, e.g., ∆cheA, ∆cheW, or ∆cheV1; in contrast, those with a clockwise bias inhibited it, e.g., ∆cheZ, ∆chePep, or ∆cheV3. We tested this correlation using a counterclockwise bias-locked flagellum, which induced biofilm formation independent of the chemotaxis system. These CCW flagella, however, were not sufficient to induce biofilm formation, suggesting there are downstream players. Overall, our work highlights the new finding that flagellar rotational direction promotes biofilm initiation, with the chemotaxis signaling system operating as one mechanism to control flagellar rotation. IMPORTANCE: Chemotaxis signaling systems have been reported to contribute to biofilm formation in many bacteria; however, how they regulate biofilm formation remains largely unknown. Chemotaxis systems are composed of many distinct kinds of proteins, but most previous work analyzed the biofilm effect of loss of only a few. Here, we explored chemotaxis role during biofilm formation in the human-associated pathogenic bacterium Helicobacter pylori. We found that chemotaxis proteins are involved in biofilm initiation in a manner that correlated with how they affected flagellar rotation. Biofilm initiation was high in mutants with counterclockwise (CCW) flagellar bias and low in those with clockwise bias. We supported the idea that a major driver of biofilm formation is flagellar rotational direction using a CCW-locked flagellar mutant, which stays CCW independent of chemotaxis input and showed elevated biofilm initiation. Our data suggest that CCW-rotating flagella, independent of chemotaxis inputs, are a biofilm-promoting signal.

Gastric cancer remains a significant global health challenge, with Helicobacter pylori (H. pylori) recognized as a major etiological agent, affecting an estimated 50% of the world's population. There has been a rapidly expanding knowledge of the molecular and pathogenetic mechanisms of H. pylori over the decades. This review summarizes the latest research advances to elucidate the molecular mechanisms underlying the H. pylori infection in gastric carcinogenesis. Our investigation of the molecular mechanisms reveals a complex network involving STAT3, NF-κB, Hippo, and Wnt/β-catenin pathways, which are dysregulated in gastric cancer caused by H. pylori. Furthermore, we highlight the role of H. pylori in inducing oxidative stress, DNA damage, chronic inflammation, and cell apoptosis—key cellular events that pave the way for carcinogenesis. Emerging evidence also suggests the effect of H. pylori on the tumor microenvironment and its possible implications for cancer immunotherapy. This review synthesizes the current knowledge and identifies gaps that warrant further investigation. Despite the progress in our previous knowledge of the development in H. pylori-induced gastric cancer, a comprehensive investigation of H. pylori's role in gastric cancer is crucial for the advancement of prevention and treatment strategies. By elucidating these mechanisms, we aim to provide a more in-depth insights for the study and prevention of H. pylori-related gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori (H. pylori), a specific bacterium capable of surviving in the acidic environment of the stomach, has been recognized as a group of causative agents of gastric cancer. Therefore, the development of mucosal vaccines against H. pylori is expected to provide an important direction for the treatment of chronic gastritis and the prevention of gastric cancer. Methods and results: In this study, we used bacteria-like particles (BLPs) obtained by treating Lactic acid bacteria (L. lactis) with hot acid, and successfully displayed the M cell-targeted H. pylori multi-epitope purified antigen SAM-FAdE, with 90% display efficiency. In addition, BLPs-SAM-FAdE can effectively target M ​​cell models and M cells of mouse Peyer's patches (PPs) through oral immunization, promote the transport of particulate vaccines to dendritic cells (BMDCs) and stimulate their maturation, significantly increased proportion of plasma cells and germinal centers B cells. This indicates that the vaccination can induce notable antigen-specific mucosal immune responses (production of sIgA), CD4+ T cell responses (Th1/Th2/Th17) and humoral immune responses (production of serum IgG). Furthermore, oral BLPs-SAM-FAdE dramatically reduced the H. pylori adhesion and specific 16S rRNA expression of H. pylori in gastric mucosal tissue, protecting gastric tissue from damage. Conclusion: BLPs-SAM-FAdE can significantly reduce the adhesion of H. pylori in gastric mucosal tissue and inhibit gastritis and gastric damage caused by H. pylori infection. [ABSTRACT FROM AUTHOR]

Patients with gastric cancer experience symptoms that impact adequate nutritional intake. Delayed diagnosis may result in advanced disease. Surgery, chemotherapy, biologic therapy, and radiotherapy comprise interventions. This article discusses gastric cancer incidence and risks, treatment approaches, and nursing management of patients with gastric cancer, including advanced care planning for patients with terminal diagnoses. This article discusses gastric cancer incidence and risks, treatment approaches, and nursing management of patients with gastric cancer, including advanced care planning for patients with terminal diagnoses. [ABSTRACT FROM AUTHOR]

Coconut oil is eatable oil with many nutritional and cosmetic applications. In this investigation coconut oil was subjected to 0 to 5 L/min of ozone for 3 h and the chemical composition of both crude and ozonized oil was valued via Gas Chromatography-Mass Spectrometry (GC–MS). Some biological tests were done including antibacterial action versus Helicobacter pylori, anti-biofilm activity versus H. pylori, anti-hemolytic activity in the existence of H. pylori, anti-Alzheimer action, and cytotoxic effect towards A-413 cancer cell line to determine the activity of coconut oil and upon exposure to ozone. Fifteen compounds were detected in the coconut oil crude and ozonized oils where the fatty acid esters were the most common molecules in crude coconut oil, whereas alkenes were the most predominant compounds in ozonized coconut oil. A slight elevation of antibacterial action towards H. pylori from 23.0 ± 0.1 to 28.2 ± 0.5 mm was displayed upon exposure of the coconut oil to ozone. Both crude and ozonized coconut oil showed a bactericidal effect with MICs = 62.5 ± 0.1, 125.0 ± 0.2 µg/mL and MBCs = 15.62 ± 0.2, 31.25 0.2 µg/mL for crude and ozonized oil, respectively. A significant elevation in anti-biofilm activity was found upon using 25% of MBCs of ozonized oil relative to crude oil. A dramatic rise was observed in anti-hemolytic activity upon using 25 and 75% of MICs of ozonized oil relative to crude one. A notable elevation of anti-Alzheimer impact was evident upon exposing coconut oil to ozone. Besides, the cytotoxic impact towards A-431 cells was slightly increased after exposing the oil to ozone. The current results suggest a new technique to expose coconut oil to ozone to improve some of its in vitro pharmaceutical applications. [ABSTRACT FROM AUTHOR]

Background: Gastrointestinal infections caused by intestinal parasites and Helicobacter pylori are significant public health issues in Africa, where poor sanitation and limited access to healthcare contribute to high disease burden. Since there was no previous pooled data regarding the intestinal parasites and Helicobacter pylori co-infections among gastrointestinal symptomatic patients in the African context, this review aimed to determine the overall prevalence of intestinal parasites and Helicobacter pylori co-infection in people with gastrointestinal symptoms in Africa. Methods: The current review followed the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) standards and registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD42024598993). A comprehensive search was conducted across electronic databases: PubMed, Medline, EMBASE, Google Scholar, Web of Science, Science Direct, and African Journals Online. The data was extracted using Microsoft Excel 2010 and analyzed using STATA version 11.0 Software. A random-effects model was used to calculate the pooled effect size of outcome variables across studies, with a 95% confidence interval. The I2 statistic was employed to assess heterogeneity. A funnel plot and Egger's test were used to identify publication bias. A p-value < 0.05 indicated statistically significant publication bias. Results: The combined prevalence of intestinal parasites and H. pylori co-infections was 31.03% (95% CI: 18.66–43.39) with significant heterogeneity (I2 = 98.9%, p = 0.000). The Subgroup analysis revealed that Egypt and Ethiopia had the highest and lowest rates of intestinal parasites and H. pylori co-infection respectively at 39.84% (95% CI: 27.79–51.88%), and 5.86% (95% CI: 4.10–7.62). Moreover, the adjusted Egger's regression test did not reveal any publication bias (p = 0.116). Conclusion: This meta-analysis shows a significant prevalence of intestinal parasites and H. pylori co-infection in Africans with gastrointestinal symptoms. The coexistence of these diseases creates diagnostic and therapeutic problems. Thus, the findings underscore need for targeted interventions and further research is needed to develop effective control strategies to reduce the impact of these illnesses on public health in Africa. [ABSTRACT FROM AUTHOR]

The role of microbiota in human health and disease is becoming increasingly clear as a result of modern microbiome studies in recent decades. The gastrointestinal tract is the major habitat for microbiota in the human body. This microbiota comprises several trillion microorganisms, which is equivalent to almost ten times the total number of cells of the human host. Helicobacter pylori is a known pathogen that colonizes the gastric mucosa of almost half of the world population. H. pylori is associated with several gastric diseases, including gastric cancer (GC) development. However, the impact of the gastric microbiota in the colonization, chronic infection, and pathogenesis is still not fully understood. Several studies have documented qualitative and quantitative changes in the microbiota's composition in the presence or absence of this pathogen. Among the diverse microflora in the stomach, the Firmicutes represent the most notable. Bacteria such as Prevotella sp., Clostridium sp., Lactobacillus sp., and Veillonella sp. were frequently found in the healthy human stomach. In contrast, H.pylori is very dominant during chronic gastritis, increasing the proportion of Proteobacteria in the total microbiota to almost 80%, with decreasing relative proportions of Firmicutes. Likewise, H. pylori and Streptococcus are the most abundant bacteria during peptic ulcer disease. While the development of H. pylori-associated intestinal metaplasia is accompanied by an increase in Bacteroides, the stomachs of GC patients are dominated by Firmicutes such as Lactobacillus and Veillonella, constituting up to 40% of the total microbiota, and by Bacteroidetes such as Prevotella, whereas the numbers of H. pylori are decreasing. This review focuses on some of the consequences of changes in the gastric microbiota and the function of probiotics to modulate H. pylori infection and dysbiosis in general. [ABSTRACT FROM AUTHOR]

Background and Aim: Only a few studies have investigated the efficacy and safety of different durations of vonoprazan and amoxicillin (VA) high‐dose dual therapy for the eradication of Helicobacter pylori. We aimed to compare the efficacy and safety of 10 days versus 14 days of VA high‐dose dual therapy for H. pylori eradication. Methods: This study was conducted in 14 centers in China. A total of 250 patients infected with H. pylori were randomly assigned to Group VA‐10 or VA‐14. Both groups received the VA dual therapy (vonoprazan 20 mg twice daily + amoxicillin 1000 mg three times daily). The primary endpoint was the H. pylori eradication rate. Secondary endpoints included adverse events and patient compliance. Results: Group VA‐10 achieved eradication rates of 89.60%, 91.06%, and 91.67% as determined by the intention‐to‐treat (ITT), modified intention‐to‐treat (MITT), and per‐protocol (PP) analysis, respectively. The eradication rates were similar to those in Group VA‐14: 91.20%, 93.44%, and 93.39%. The difference and 90% confidence interval boundary −1.60% (−7.73% to 4.53%) in the ITT analysis, −2.39% (−8.00% to 3.23%) in the MITT analysis, and −1.72% (−7.29% to 3.85%) in the PP analysis were greater than the predefined noninferiority margin of −10%, establishing a noninferiority of Group VA‐10 versus Group VA‐14 (noninferiority P = 0.001 in ITT analysis, P < 0.001 in MITT analysis, and P < 0.001 in PP analysis, respectively). No significant differences were observed in adverse events between the two groups. Conclusions: Ten‐day VA dual therapy achieves comparable efficacy and safety to the 14‐day regimen in Chinese population, providing patients with greater convenience and economic benefits. [ABSTRACT FROM AUTHOR]

Background and Aim: Helicobacter pylori infection is one of the most common bacterial infections affecting humans, causing gastroduodenal and extraintestinal diseases. Treatment of the infection remains challenging for the clinicians, and different factors are involved in the failure of the therapeutic approach. The importance of the intensity of acid secretion inhibition remains an unclear issue. The aim of this study is to assess whether 80 mg/day esomeprazole‐based 10‐day sequential therapy (esomeprazole‐ST) achieved different eradication rates when compared to 80 mg/day pantoprazole‐based analogous regimen (pantoprazole‐ST). Methods: This was a retrospective observational study where data of consecutive patients referred by their physicians to our unit to perform an upper gastrointestinal endoscopy were analyzed. Results: Overall, 1,327 patients were available for the analysis: 599 and 728 patients received pantoprazole‐ST and esomeprazole‐ST, respectively. Eradication rate was significantly higher in patients receiving esomeprazole‐ST (92.6%, 95% CI: 91–94.5) than pantoprazole‐ST (89.3%, 95% CI: 86.7–91.7; difference: 3.3%; 95% CI: 0.2–6.5; P = 0.037). Even after a multivariate analysis, the esomeprazole‐ST achieved a significantly higher eradiation (OR: 1.44; 95% CI: 1.1–2.17). Conclusions: This study showed that esomeprazole‐ST achieved significantly higher H. pylori cure rates than pantoprazole‐ST. Prospective and well‐designed trials are demander to confirm this prelaminar finding. [ABSTRACT FROM AUTHOR]

Electrochemical biosensors offer a cost-effective way to identify Helicobacter pylori (H. pylori) (Hsp 60), responsible for stomach infections. The conductivity and surface area of the electrode were enhanced using Hap-Ag-ZnO composites on glassy carbon electrode (GCE) along with polythiophene (PP), as a conductive polymer to improve proficiency. The Hap-Ag-ZnO-PP composites have multiple functional group sites that facilitate aptamer immobilization on the GCE. This increases the sensitivity, stability, and dynamic range of the developed aptasensor. Electrochemical impedance spectroscopy, cyclic voltammetry, and square wave voltammetry were employed to examine the performance of the aptasensor. A linear behavior was observed for the modified electrode against the concentration of Hsp 60, showing a detection limit of 0.429 nM and a wide dynamic range of 0.05–300 nM. Moreover, the Hap-Ag-ZnO-PP-based aptasensor exhibits exceptional reproducibility, repeatability, fast response time (20 min), good selectivity, and excellent stability (electrochemical and storage). Therefore, the prepared sensitive aptasensor provides a promising platform for clinical diagnostics and H. pylori detection in real-world applications. [ABSTRACT FROM AUTHOR]

Objective: We aim to show whether endoscopic, histopathological and precancerous findings in childhood Helicobacter pylori (H. pylori) infection are associated with some changes in the host immune system and some virulence factors of the bacteria. For this purpose, we interpreted the changes in endoscopic and histopathological findings of TLR-4 and TLR-9 gene polymorphisms in the innate immune system of the host and cytotoxin associated gene A (Cag-A) and vacuolating cytotoxin A (Vac-A) positivity, the main virulence factors of the bacteria. Method: Between April 2009 and October 2010, 100 H. pylori-positive and 100 H. pylori-negative cases were cross-sectionally selected by retrospectively reviewing the files of patients admitted to a tertiary hospital with dyspepsia. After obtaining informed consent, blood samples from these patients were analysed for TLR-4 [Asp 299 Gly (rs4986790)] and TLR-9 [1237 TC (rs5743836)] gene polymorphisms and for the presence of Cag-A and Vac-A in isolates obtained from pathological specimens. Results: Poor socio-economic conditions were an important risk factor for H. pylori. The presence of Cag-A increased the likelihood of duodenal ulcer. There was no significant difference between TLR-4 [Asp 299 Gly (rs4986790)] gene polymorphism and endoscopic and histopathological findings. However, TLR-9 [-1237TC (rs5743836)] polymorphism increased precancerous intestinal metaplasia and atrophy. Conclusion: The presence of Cag-A increases the risk of duodenal ulceration due to H. pylori infection. The TLR-9 [-1237TC (rs5743836)] polymorphism is associated with gastric atrophy and intestinal metaplasia in the pathogenesis of H. pylori infection. Studies in large groups of patients are needed. [ABSTRACT FROM AUTHOR]

Background & Aims: Bacterial resistance toward the most used antibiotics is increasing in Helicobacter pylori (H. pylori) strains worldwide. The emergence of multidrug resistance significantly affects the efficacy of standard therapy regimens. Therefore, this prospective study has updated the prevalence rates of primary antibiotic resistance in H. pylori strains isolated in routine practice. Methods: H. pylori isolates obtained from patients consecutively observed in a single center were tested for primary resistance by using the E-test method. The minimum inhibitory concentration (MIC) breakpoints to define resistance to clarithromycin, metronidazole, and levofloxacin were, respectively, greater than 0. 25 mg/L, 8 mg/L, and 1 mg/L, according to updated EUCAST recommendations. The trend of antibiotic prevalence, either single or combined, during 2020-2023 was assessed. Results: A total of 789 patients meeting inclusion criteria were diagnosed with H. pylori infection, but bacterial strains were overall recovered in 632 (80.1%) cases. At bacterial culture, primary resistance rate was 36.7% for clarithromycin, 32.8% for metronidazole, and 22.1% for levofloxacin, whilst dual clarithromycin-metronidazole resistance rate was detected in 17.4%, and triple resistance in 9%. Conclusions: Our data found that primary resistance towards both clarithromycin and metronidazole, as well as dual resistance, is substantially stable in Italy whilst the prevalence of levofloxacin resistance seems to be decreasing in our geographic area. [ABSTRACT FROM AUTHOR]

Epidemiological and eradication trial evidence indicates that Helicobacter pylori, a major causative factor in peptic ulcer and gastric cancer, is a driver of the hypokinesia of Parkinson's disease (PD). Psychological (cognitive impairment, depression and anxiety) and gastrointestinal (peptic ulceration and constipation) PD features can precede the symptomatic onset of motor features by decades. We hypothesise that the non-H. pylori Helicobacters (NHPH), which have farm, companion and wild animals as their main hosts, can have a role in PD aetiopathogenesis. In those occupationally at risk of NHPH infection, we address whether there is increased mortality with PD, or depression or suicide. Our systematic review gave evidence that occupational exposure to animals/their products is associated with excess mortality with PD. Indeed, whilst livestock farming increased the risk, crop farming decreased it. Moreover, excess mortality from non-Hodgkin lymphoma in livestock farmers is compatible with NHPH being causal. Our scoping review showed that farmers, veterinarians and abattoir workers have an increased risk of depression and suicide; whether their depression is associated with being down the pathway to PD and/or the presence of Helicobacter infection needs investigation. Regarding Helicobacter species specificity, the link between the presence of NHPH in gastric biopsy and PD was described using a ureA polymerase chain reaction (PCR) assay, targeting the most-commonly named NHPH, H. suis. We describe its redesign and optimisation as a probe-based PCR, confirming the exclusion of H. pylori but not H. suis specificity (additionally identifying 6 species of a 22-NHPH-species panel). The exploration of the zoonotic hypothesis requires a non-invasive pan-Helicobacter PCR screen, allowing the detection and molecular grouping of Helicobacter species. [ABSTRACT FROM AUTHOR]

Objective: To study the interobserver agreement for diagnosing Helicobacter pylori gastritis using narrow band imaging (NBI) with magnification. Methods: This prospective study recruited patients who underwent gastroscopy for dyspepsia in the Department of Gastroenterology, Aster MIMS Hospital, Kannur.361 patients were included in the study. The gastroscopy was performed using high‐definition white light endoscopy (WLE) and NBI with magnification. Histopathology and rapid urease test were used to detect HP infection. Endoscopy videos were analyzed by three trained endoscopists who were blinded to each other. NBI patterns were classified into four types (Types 1, 2A, 2B, and 3). Interobserver variability was examined using Kappa Statistics. Results: 164 of 361 patients had HP infection (45.42%). Of 361 people, 199 had Type 1 (55.12%), 54 Type 2a (14.95%), 65 Type 2b (18%), and 43 Type 3 cases (11.91%). There was good interobserver agreement with a kappa value of 0.730 (95% confidence interval (CI) 0.693–0.768). 87% of HP‐negative patients had Type 1 NBI pattern. 79.5% of type 2A and 89.2% of Type 2b pattern were HP positive. The Type 1 pattern identified normal gastric mucosa with 84.75% sensitivity, 88.32% specificity and 87.4% negative predictive value. Type 2 and Type 3 NBI patterns had high positive predictive value and specificity for HP infection. Conclusions: This study demonstrates excellent interobserver agreement among experienced endoscopists in using NBI to identify gastric mucosal patterns associated with HP infection. While biopsies remain essential for comprehensive evaluation of gastric pathologies, our findings suggest that NBI, with appropriate training and validation, may have the potential to reduce the need for biopsies in specific cases where the primary concern is HP infection. The good level of interobserver agreement seen in our study is encouraging and suggests that NBI has the potential to be a reliable tool for diagnosing HP infection. [ABSTRACT FROM AUTHOR]

Helicobacterpylori colonizes the human gastric mucosa of more than half of the human population and has a unique lipopolysaccharide (LPS) structure. LPS is the most dominant and suitable pathogen-associated molecular pattern that is detected via pattern recognition receptors. Although the priming effect of H. pylori LPS on reactive oxygen species (ROS) production of PMNs is lower than that of Escherichia coli O111:B4 LPS, LPS released from H. pylori associated with antibiotics eradication therapy may activate PMNs and increase ROS production. In addition, we describe the effects of H. pylori and E. coli O111:B4 LPSs on gene expression and the anti-inflammatory effect of lansoprazole (LPZ) in human polymorphonuclear leukocytes. LPS isolated from H. pylori and E. coli O111:B4 alters toll-like receptor 2 (TLR) and TLR4 expressions similarly. However, LPS from E. coli O111:B4 and H. pylori caused a 1.8-fold and 1.5-fold increase, respectively, in CD14 expression. All LPS subtypes upregulated TNFα and IL6 expression in a concentration-dependent manner. Although E. coli O111:B4 LPS upregulated IL8R mRNA levels, H. pylori LPS did not (≦ 100 ng/mL). Gene expression levels of ITGAM demonstrated no significant change on using both LPSs. These different effects on the gene expression in PMNs may depend on variations in LPS structural modifications related to the acquired immunomodulatory properties of H. pylori LPS. Proton pump inhibitors, i.e., LPZ, are used in combination with antibiotics for the eradication therapy of H. pylori. LPZ and its acid-activated sulphenamide form AG-2000 suppress ROS production of PMNs in a dose-dependent manner. These results suggest that LPZ combination with antibiotics for H. pylori eradication reduces gastric inflammation by suppressing ROS release from PMNs. [ABSTRACT FROM AUTHOR]

Abstract Background Children are among the most vulnerable groups for Helicobacter pylori (H. pylori) infection, which was linked with an increased risk of anemia. H. pylori infection may cause the development of anemia through affecting the absorption of different micronutrients and increasing hepcidin production from hepatocytes. This study aimed to assess the effect of H. pylori infection on the occurrence of anemia in children. Methodology Previously published articles were systematically searched on major databases including Science Direct, PubMed, Embase, Scopus, Cochrane Library, and Science Citation Index using search terms. The search results were imported into EndNote X9 to organize and remove duplicates. Then, relevant data was extracted and analyzed using STATA version 16.0. The pooled odds ratio (OR) was calculated to evaluate the associations of H. pylori infection with Anemia. Moreover, pooled standardized mean difference (SMD) of Hemoglobin (Hgb) and Serum ferritin (SF) levels between cases and controls were calculated for group comparisons. Results A total of nine published articles were included in this study. The result showed that H. pylori-infected children had 2.68 times more risk of developing anemia compared to H. pylori-negative children (OR: 2.68:95% CI:1.44–4.99, p = 0.002). Subgroup analyses based on study design showed an increased significant association between H. pylori infection and anemia among case-control studies (OR:3.792:95%CI;1.767, 8.142, p = 0.001). Subgroup analyses based on the H. pylori detection method indicated an increased significant association between H. pylori infection and anemia when the stool antigen test method was used (OR:3.801;95%CI:1.090,13.250, p = 0.036). Moreover, there was a significant decrement of Hgb and SF levels in the H. pylori positive group compared to the negative group with SMD of -0.54(95%CI: -0.65, -0.42, p

Abstract Background Macrophages play a crucial role in chronic gastritis induced by the pathogenic Helicobacter pylori (H. pylori) infection. NLRP3 inflammasome has emerged as an important component of inflammatory processes. However, the molecular mechanism by which H. pylori infection drives NLRP3 inflammasome and macrophages activation remains unclear. Methods Human gastritis tissues were collected for clinical significance of NLRP3. Infection with H. pylori was performed using in vitro and in vivo models. Bone marrow-derived macrophages (BMDMs) from wild-type (WT), Nlrp3-knockout (KO) and Tnfr1-KO mice were infected with H. pylori. Western blotting, qRT-PCR, immunofluorescence, immunohistochemistry and ELISA were utilized for functional and mechanistic studies. Results Single-cell RNA sequencing (ScRNA-seq) analysis of human gastric tissues, followed by validation, indicated that NLRP3 was primarily expressed in myeloid cells and was significantly increased in H. pylori-positive gastritis compared to H. pylori-negative gastritis. Infection with PMSS1 and NCTC11637 H. pylori strains induced NLRP3 inflammasome activation in vitro (THP1 cells) and in the insulin-gastrin (INS-GAS) transgenic mouse model. Deletion of NLRP3 in BMDMs showed marked inhibition of H. pylori-induced M1 macrophage polarization. Furthermore, NLRP3 inflammasome activation upon TNFα, or H. pylori stimulation, was partially blocked by TNFα/TNFR1 signaling inhibitors. Deletion of TNFR1 in BMDMs significantly impaired NLRP3 inflammasome activation and M1 macrophages induced by H. pylori. Conclusion This study revealed that the activation of NLRP3 inflammasome, regulated by the TNF/TNFR1 signaling axis, is a key regulator of H. pylori-induced M1 macrophage activation and gastritis.

Background: Helicobacter pylori infection was mainly the factor that causes both gastric tumors and lymphomas. Objectives: This study aimed to detect H. pylori infection and investigate any relationship between the infection of H. pylori and the disease of diabetes, to find out if there is an association with certain human leukocyte antigen (HLA), and to study the frequency of H. pylori infection among type l diabetic and nondiabetic patients. Materials and Methods: Several 140 patients diagnosed with type 1 diabetes mellitus (T1DM), as well as 60 healthy individuals (nondiabetic) were enrolled in this study. The oligonucleotide technique of sequence-specific was performed for genotyping of HLAs using a polymerase chain reaction machine. A specific screening (H. pylori antibodies combo rapid test) is used to diagnose H. pylori infection by detection of specific antibodies in the samples. Results: This study revealed that people who are diagnosed T1DM are more predisposed to be infected by H. pylori (61%) compared with healthier people, and the pathogen infects significantly females compared with males. Results also revealed a great frequency of DQB1*0101 allele within diabetics (30%) in comparison with healthy (control) group, whereas HLA-A*3301,*1122 B*0826,*3948, DRB1*0701,*1101, and HLA-DQB1-*0604,*630,*730 alleles were recorded noteworthy low frequency according to the results after statistical analysis of P value (P < 0.05) in patients compared with healthy control groups. Conclusion: Diabetic women of the same age are more susceptible to the infection compared with males. The great frequencies of HLA-DQB1*0101 alleles could be a risk factor for T1DM patients.

Prophages can have major clinical implications through their ability to change pathogenic bacterial traits. There is limited understanding of the prophage role in ecological, evolutionary, adaptive processes and pathogenicity of Helicobacter pylori, a widespread bacterium causally associated with gastric cancer. Inferring the exact prophage genomic location and completeness requires complete genomes. The international Helicobacter pylori Genome Project (HpGP) dataset comprises 1011 H. pylori complete clinical genomes enriched with epigenetic data. We thoroughly evaluated the H. pylori prophage genomic content in the HpGP dataset. We investigated population evolutionary dynamics through phylogenetic and pangenome analyses. Additionally, we identified genome rearrangements and assessed the impact of prophage presence on bacterial gene disruption and methylome. We found that 29.5% (298) of the HpGP genomes contain prophages, of which only 32.2% (96) were complete, minimizing the burden of prophage carriage. The prevalence of H. pylori prophage sequences was variable by geography and ancestry, but not by disease status of the human host. Prophage insertion occasionally results in gene disruption that can change the global bacterial epigenome. Gene function prediction allowed the development of the first model for lysogenic-lytic cycle regulation in H. pylori. We have disclosed new prophage inactivation mechanisms that appear to occur by genome rearrangement, merger with other mobile elements, and pseudogene accumulation. Our analysis provides a comprehensive framework for H. pylori prophage biological and genomics, offering insights into lysogeny regulation and bacterial adaptation to prophages.

Abstract The immune cellular landscape from the gastric mucosa remains largely unknown despite its relevance in several inflammatory conditions. Human gastric biopsies were obtained from the antrum, body and incisura from 10 individuals to obtain lamina propria mononuclear cells that were further characterized by spectral cytometry. Phenotypic hierarchical analyses identified a total of 52 different immune cell subsets within the human gastric mucosa revealing that T-cells (> 60%) and NK cells (> 20%) were the main populations. Within T-cells, CD4+ and CD8+ were equally represented with both subsets displaying mainly a memory and effector phenotype. NK cells, on the contrary, were largely of the early phenotype. No regional differences were observed for any subsets among the 3 locations. Following unsupervised analysis, a total of 82 clusters were found. Again, no differences were observed amongst locations although a great degree of inter-individual variability was found, largely influenced by the presence of H. pylori infection and dyspepsia. We have unraveled the human gastric immune cellular subset composition and a unique interindividual immune fingerprint with no inter-regional variations.

Abstract Background The prevalence of Helicobacter pylori (H. pylori) infection and its potential relationship to various diseases is currently a focus of attention. The aim of this study is to investigate the association between current and past H. pylori infections and elevated levels of microalbuminuria in type 2 diabetic patients. Methods Two hundred patients with type 2 diabetes mellitus were tested for the presence of H. pylori infection. They were divided into three groups: 52 had a current H. pylori infection, 38 had a past H. pylori infection, and 110 had no H. pylori infection. All study participants underwent assessments of plasma glucose levels, glycated hemoglobin (HbA1c), albuminuria levels, inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), as well as other relevant investigations. Results The prevalence of H. pylori infection (current and past) was detected in 90 out of 200 diabetic patients (45%). There was no statistically significant difference between the three groups in terms of age, diabetes duration, family history of DM, family history of hypertension, residence, or dyspeptic symptoms, indicating that current or past infection with H. pylori has no association with these variables. The current H. pylori infection group showed the highest levels of inflammatory markers, ESR and CRP, which were significantly different from those in the non-infected group (p = 0.013 and p

Aim: to optimize outcomes of the treatment and prevention of gastrointestinal diseases in adults and children. Key points. The Methodological Guidelines contain sections on the terminology, classification, mechanisms of action, requirements for sale in the Russian Federation, requirements for proving the efficacy and safety of probiotics, prebiotics, synbiotics and metabiotics, as well as functional foods enriched with them. An overview of relevant data allowing to include these drugs and products in the treatment an d prevention of gastrointestinal diseases in adults and children is presented. Conclusion. The clinical efficacy of probiotics, prebiotics, synbiotics and metabiotics depends on the specificity and quantity of their components, the dosage form, the regimen and duration of treatment. Products and functional foods with proven efficacy and safety are recommended for the treatment and prevention of gastrointestinal diseases in adults and children.

Purpose: The purpose of this study was to assess the association between some clinical and epidemiological factors and the prevalence of Helicobacter Pylori (H. pylori) infection in children visited a paediatrics ambulatory care at University Hospital - Pleven for various symptoms pointing to gastritis and peptic ulcer. Materials and methods: an epidemiological study was conducted for the period June-September 2023. In total, 133 children aged from 2 to 18 years were evaluated. All visited a paediatrics ambulatory care at University Hospital - Pleven for various complaints pointing to gastritis and peptic ulcer. Results: During the study period, we recruited a total of 133 children and adolescents (age range 2-18 years, mean age 9.36 ± 4.08 years). More patients were males (54.14%) than females (45.86%). The most frequent symptoms were abdominal pain (51.88%), nausea and vomiting (21.80%), and losing weight (10.53%). The social status of the families is good - parents with a university education predominate (49.62%). There are risk factors for the presence of infection and the development of gastritis and ulcers in children: family history of H. pylori infection (47.37%) and use of unsuitable foods (48.87%). A high positivity is found for H. pylori (40.43%). Conclusions: Early diagnosis and etiological treatment of H. pylori infection reduces the risk of developing gastric complications like chronic gastritis, ulcer diseases and gastric cancer.

Background: Gastritis is the inflammation of gastric mucosa characterized by morphological and histopathological changes. This study was undertaken mainly to study the histo- morphological features of gastritis patients. Material and Methods: A cross sectional study was conducted in 100 cases of gastric biopsies in a tertiary care hospital in North Karnataka. The biopsies were fixed and sections were made from paraffin blocks. Two slides with three levels in each slide were examined under light microscope stained with Haematoxylin& Eosin and Giemsa. The slides were examined by two pathologists and findings were documented, compiled and analysed using statistical software. Results: This study had shown that 43.0% of the cases had gastric ulcer, 42.0% had chronic gastritis and acute gastritis in 15.0% of the cases. H. Pylori was found in 36.0% of the cases. The histological features included mild, moderate and severe inflammation, neutrophilic activity, mild mucosal atrophy, eosinophilic infiltration, lymphoid follicles and dysplasia. Conclusion: This study had shown morphological changes and histopathological changes along with H Pylori infection in cases with gastritis.

Abstract Objective The aim of this study was to evaluate the effectiveness and safety of the nine most widely studied Vonoprazan (VPZ)-based treatment regimens along with traditional Proton pump inhibitor (PPI)-based treatment regimens in eradicating Helicobacter pylori (H. pylori) infection. Design Through searching PubMed, Embase, Cochrane Library, Web of Science, we exclusively included randomized controlled trials (RCTs) to investigate the efficacy of VPZ-based and PPI-based therapies for H. pylori infection. The included studies were evaluated for methodological quality using the Cochrane bias risk assessment tool, and the data analysis software was used to analyze the data accordingly. Results The RCTs were collected from the earliest available date up to August 2023. Twenty-one RCTs were included, with a total sample size of 5481. The results of the network meta-analysis showed that the eradication rate of the VPZ-based quadruple 14-day (VPZ-Q14) treatment regimen in Intention-to-treat (ITT) analysis was the highest (SUCRA: 0.874); The eradication rate of the VPZ-based quadruple 10-day (VPZ-Q10) treatment plan in Per-protocol (PP) analysis was the highest (SUCRA: 0.849). All regimens were well tolerated without significant differences. According to the probability ranking of safety, high-dose VPZ-based dual 14-day therapy (H-VPZ-D14) ranked first in SUCRA, reaching 0.952. This indicates that H-VPZ-D14 treatment is the safest with a relatively low incidence of adverse effect. Therefore, VPZ-based therapies not only have a higher eradication rate, but also possess satisfactory safety. Conclusion Compared with traditional PPI-based therapies, VPZ-based therapies have shown superior eradication effects. Based on the Ranking Plot of the Network, the VPZ-Q14 or VPZ-Q10 treatment regimen for H. pylori has a higher eradication rate and acceptable differences compared to other treatment regimens. In addition, for regions with high antibiotic resistance rates, we recommend a 14-day quadruple therapy with bismuth based on VPZ.

The increased prevalence of Helicobacter pylori infection and inadequate genetic research on the same, demands a genetic study among Tamil population of South India to unravel the association of NLRP3 (NLR family pyrin domain containing 3) variants with persistent H. pylori infection. This research was aimed to study the correlation between persistent H. pylori infection and influence of such genetic variants in the development of disease progression. In this study, 200 healthy volunteers and 120 H. pylori-positive cases were screened for two NLRP3 variants, rs74163773 and rs10754558, using allele-specific PCR and TaqManTM SNP genotyping assay, respectively. Based on our genotype and allelic distribution, rs74163773 variant did not associate with the risk of developing the persistent infection. However, a significant association of heterozygous CG variant of rs10754558 with patient showing clinical symptoms of gastritis, PUD and persistent infection in the over-dominant, co-dominant and recessive models was found. Our findings suggest that persistent H. pylori infection susceptibility was influenced by genetic variant rs10754558 and its heterozygous CG variant can serve as an independent risk factor in the manifestation of chronic gastritis and PUD in the South Indian Tamils.

Helicobacter pylori is a human pathogen bacterium associated with gastritis, peptic ulcer, and gastric cancer. It can be identified through the 16S rRNA gene and characterized through cagA and vacA virulence genes. Clinical cultures of H. pylori were isolated and identified from human stomach biopsies. The isolates were characterized according to their colonial and microscopic morphology, and molecular genotyping was conducted to determine the bacterial virulence. A phylogenetic analysis of the 16S rRNA gene sequencing was performed. In addition, multilocus sequence typing analysis was performed to determine the phylogeographic nature of the isolated strains. Three bacterial isolates were selected from 22 gastric biopsies, identified as H. pylori through colonial morphology, Gram staining, urease, catalase, and oxidase tests and identification of the ureC gene through end-point PCR. Amplification of 16S rRNA, urea, and tonB genes was performed, as well. Differences between the cagA and vacA genotypes were determined among the isolates. The phylogenetic analysis confirmed the identity of the three isolates as the specie Helicobacter pylori. Different genotypes were obtained for each H. pylori strain, and all the clinical isolates showed the vacA s2/m2 genotype, indicating an absence of the VacA cytotoxin. Only HCGDL-MR01 is a cagA gene carrier with a greater risk to develop a serious disease, such as stomach cancer and peptic ulcer. The multilocus sequence typing placed all the strains within the hpEurope population structure.

This study aims to investigate the clinical, endoscopic, biologic and histopathological differences between Helicobacter pylori-associated and autoimmune gastric atrophy.

Background: To search for H. pylori infection and gastric precancerous lesions in cirrhotic patients is worthwhile when considering the high incidence of peptic ulcers and gastric cancer in these patients. We tested if gastric juice analysis allows to avoid unrewarding gastric biopsies. Methods: This prospective study enrolled consecutive patients with liver cirrhosis who underwent upper endoscopy with standard gastric biopsies. Real-time gastric juice analysis was performed with a specific device (EndoFaster®) that test ammonium concentration for H. pylori diagnosis, and pH values to suspect extensive atrophy/metaplasia involving gastric body mucosa. Sensitivity, specificity, positive predictive value, negative predictive value (NPV), the overall accuracy, and the likelihood ratio were calculated for both H. pylori infection and extensive precancerous lesions on gastric mucosa. Results: A total of 78 cirrhotic patients (males: 55; mean age: 66 ± 12 years) were enrolled. When considering as positive EndoFaster® results when at least one of two (ammonium and pH levels) tests were positive, the NPVs were as high as 89% and 86%, respectively, to rule out H. pylori and extensive precancerous lesions on gastric mucosa, with an overall accuracy of 83% and 74%. Conclusions: This study supports the evidence that real-time gastric juice analysis allows to avoid clinically unrewarding and potentially unsafe gastric biopsies in a definite portion of cirrhotic patients, but more data are needed.

The study of the extraesophageal reflux effect on the middle ear structures in adults is of considerable interest. The mechanism of formation of gastroesophageal reflux disease associated otitis media is closely related to such concepts as nasopharyngeal reflux and laryngopharyngeal reflux. The article presents an analysis of the medical literature focusing on the mechanisms of development of inflammation mechanisms in the middle ear cavity affected by the gastric contents. The article uses publications in such scientific databases as PubMed, eLIBRARY, Science Direct, Research Gate, dated from 1990 to 2024. A detailed understanding of pathophysiological mechanisms affecting formation of the middle ear cavity inflammation under the influence of extraesophageal reflux has been obtained. Major scientific studies confirm that gastroesophageal reflux disease acts as a risk factor for the middle ear cavity inflammation formation.

Background: Gastric intestinal metaplasia is a common pathological feature in patients with Helicobacter pylori (H. pylori) infection. Rabeprazole was widely used as the first-line regimen for H. pylori infectious treatment. The objective of this study is to explore the mechanism of rabeprazole in gastric intestinal metaplasia treatment. Methods: Real-time PCR, Western blotting (WB) and ROS analysis were conducted to confirm that rabeprazole could induce ferroptosis to suppress gastric intestinal metaplasia. Cellular fraction, luciferase and chromatin immunoprecipitation (ChIP) were used to identify the mechanism underlying rabeprazole modulated ferroptosis. Results: Herein, we found rabeprazole treatment led to inhibit CDX2 and MUC2 expression, alleviating gastric intestinal metaplasia, which was attributed to enhanced ferroptosis characterized by decreased GPX4 expression. Inhibition of ferroptosis by ferrostatin-1 (Fer-1) could reverse decreased CDX2 and MUC2 expression caused by rabeprazole. Mechanically, Rabeprazole could inhibit CREB phosphorylation and nuclear translocation, which further decreased the binding of CREB to GPX4 promoter, reducing GPX4 transactivity. Moreover, endogenous PKA interacted with CREB, and this interaction was drastically destroyed in response to rabeprazole treatment. Most importantly, enhanced ferroptosis was observed in H. pylori- infected gastric intestinal metaplasia in comparison to HC control. Conclusion: These findings suggested that rabeprazole induced ferroptosis to reduce CDX2 expression in gastric epithelial cells through PKA/CREB cascade signaling, implying that targeting ferroptosis could be a promising strategy in improving gastric intestinal metaplasia during H. pylori -infected patients. [ABSTRACT FROM AUTHOR]

Background: Inflammatory bowel diseases (IBD) are chronic inflammation conditions affecting the gastrointestinal tract. Studies point out an association between Helicobacter pylori (H. pylori) infection and IBD. This study aims to visually assess the research trends and hotspots in the field of H. pylori infection and IBD, review mainstream perspectives in this field, and provide a foundation for future research and treatment. Methods: We searched the Web of Science Core Collection Database for literature related to H. pylori and IBD, using VOS viewer to generate visual charts. Results: A total of 246 publications were included, with articles being the predominant type of document. A significant increase in the number of publications was observed after 2011. China contributed the most of researches. Keyword clusters revealed that the researches primarily focused on immune mechanism, gut microbiome, diagnosis and treatment of IBD. Time trend results indicated that current researches centered on gut microbiota and immune mechanisms. Conclusion: H. pylori infection may have a protective effect on IBD. The exact mechanisms remain unclear and may involve immunomodulation and changes of gut microbiota. Further researches are necessary for better understanding this relationship and its implications for clinical practice. Further researches and clinical practice should pay attention to this topic. [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]

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Background: Helicobacter pylori (H. pylori) is a known gastro-intestinal pathogen but implicated in extra-gastric diseases. The relationship between H. pylori infection and type 2 diabetes (T2DM) remains insufficiently elucidated, particularly in terms of molecular mediators such as microRNAs (miRNAs) and messenger RNAs (mRNAs). Objective: We aimed to characterize expression pattern of insulin signalling mRNAs and targeted miRNAs in T2DM patients exposed to H. pylori infection. Methods: We conducted a cross-sectional study among patients diagnosed with type 2 diabetes mellitus and were aged 18 to 60 years. Overnight fasting blood samples were collected and processed for plasma and serum. The plasma samples were used for glucose estimation and the serum used for H. pylori IgG screening. Total RNA was extracted from the serum with commercial kit, and mRNAs and miRNAs quantified by RT-qPCR with specific primers and under predetermined amplification conditions. Clinical data were obtained from medical records of patients. Results: Among 351 patients enrolled, 267 (76.1%) were females, 224 (63.8%) were married, and 79 (22.5%) had tertiary education. Expression level of insulin receptor mRNA was significantly lower in H. pylori positive T2DM patients compared to H. pylori negative (P <.05). There was no evidence of a difference in insulin receptor substrate 1 mRNA level (P >.05). Although not statistically significant, the expression levels of miRNA-222 and miRNA-155 in the patients exposed to H. pylori were higher than that of the unexposed group (P >.05). Conclusions: We found a significantly reduced serum insulin receptor messenger RNA level and higher levels of miRNA-222 and miRNA-155 in H. pylori exposed T2DM patients. The findings suggest a possible role of the infection in insulin signalling alteration in the patients. [ABSTRACT FROM AUTHOR]

Background and Aim: Periodic endoscopic screening for gastric cancer (GC) is widely performed in East Asia; however, the optimal screening strategy remains unclear. This study aimed to determine the most cost‐effective endoscopic screening strategy for the detection and treatment of GC in a cohort with a low Helicobacter pylori prevalence. Methods: The following data were retrospectively extracted from participants who received screening endoscopy between April 2019 and March 2023: age, H. pylori infection status, presence of intestinal metaplasia, pathological diagnosis of GC, and the interval between the most recent endoscopies. A Markov state transition model was constructed based on the cohort data. The cost‐effectiveness of 15 strategies with different starting ages (40/50/60 years) and screening intervals (1/2/3/4/5 years) was compared. The net monetary benefit (NMB) and incremental cost‐effectiveness ratio (ICER) of quality‐adjusted life‐years gained by treatment were used as outcomes. Results: A simulation model was constructed based on the cohort data of 94 137 participants (mean age 54.5 years, males 57.9%; 74.4% H. pylori‐naïve, 94.2% intestinal metaplasia‐negative). The results of the base‐case analysis showed that the screening strategy of 4‐year intervals starting at the age of 40 years had the highest NMB (97 401 578 yen). In both the Monte Carlo simulation and one‐way sensitivity analysis with a varying probability of H. pylori infection status transition, the ICER was superior in the screening strategy every 4 years, starting at age 40 years. Conclusions: Our simulation showed that endoscopic screening at 4‐year intervals starting at the age of 40 years was the most cost‐effective method. [ABSTRACT FROM AUTHOR]

Background: Celiac disease (CD) is an inflammatory small intestine autoimmune disease. The study aims to investigate the association and the detection of ATG5 polymorphism between celiac disease (CD) and H. pylori infection, and the association with Interleukin-33 (IL-33). Methods: The study groups included patients from Iraq, ages 4 to 35. Two primary patient groups were created: sixteen had positive H. pylori and celiac disease, and thirty had positive CD and negative H. pylori disease. The levels of tissue transglutaminase IgA (TTG IgA), H. pylori IgG, and IL-33 were measured using the ELISA method. The primers were amplified using PCR. Results: With celiac disease, the patient group's TTG IgA levels increased dramatically. The test also showed significant variations (P=0.054) in the H. pylori IgG levels between the patient and control groups. The H. pylori seropositivity test showed a statistically significant difference (p ≤0.033) between seropositive and seronegative individuals, while the patient group's IL-33 levels did not significantly differ (P ≤0.299) from the control group. Conclusions: Our results showed that CD is more common in women and occurs in the age range of 24-35 years. It also showed that the mutant variant of ATG5 is associated with CD, and the significance of H. pylori IgG serum levels in the patient group may indicate that the bacteria involved in CD. Furthermore, H. pylori infection is more strongly linked to serum IL-33 levels than CD. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori is one of the most prevalent infections in humans, it can cause gastrointestinal (GI) problems such as simple gastritis, gastric ulcers, and gastric cancer. It may pose an issue as opportunistic infections in specific situations, such as immunodeficiency and underlying illnesses. One of the underlying disorders caused by H. pylori is diabetes mellitus. Treating the H. pylori infection is essential since diabetic people have GI issues. There are conflicting and erratic reports on Helicobacter pylori infection in diabetics. We aimed to reveal the severity of complications of H. pylori among diabetic and nondiabetic patients and to identify the potential risk factors of H. pylori among diabetic. Methods: This case control study was carried out at Internal Medicine Department and Pathology Department, Faculty of Medicine, Zagazig University. Subjects were divided into group (1): 27 patients with DM and group (2): 27 non-diabetic individual's age and sex matched as control. Results: The severity of H. pylori gastritis was insignificantly different between the studied groups. Conclusion: Our results do not support an association between severity of H. pylori infection and diabetes mellitus. This is confirmed by the lack of difference between diabetics and nondiabetics regarding the severity of H.pylori infection. [ABSTRACT FROM AUTHOR]

This study investigates organotin (IV) complexes derived from the recently synthesized quinazoline Schiff base ligand (L). The research involves synthesizing and characterizing these complexes, including elemental analysis, UV–visible, FT‐IR, mass spectra, and conductometric measurements. Advanced studies such as density functional theory (DFT) are employed to gain insights into the stable electronic configuration. Specifically, the study explores the proposed geometry, revealing a distorted octahedral structure for the complexes. The findings contribute as critical molecular characteristics of these newly synthesized complexes, paving the way for potential applications in diverse fields, including medicinal chemistry. Through an investigation into the antimicrobial properties, the efficacy of the synthesized compounds was assessed against a diverse range of bacterial and fungal strains. Remarkably, the complexes demonstrated significant antimicrobial activities, showing potential applications in combating various microbial infections. In an extended exploration of their medical utility, the compounds were examined for their antibiotic properties against Helicobacter pylori. The Schiff base and its metal complexes emerged as promising antibiotics with notable efficacy against H. pylori, suggesting their potential in addressing infections associated with this bacterium. Furthermore, the antitumor potential of the synthesized complexes was investigated, focusing on their impact on MCF‐7 (Breast carcinoma) cells. The organotin (IV) Schiff base complexes in this research showed remarkable efficacy, evidenced by their notably low IC50 values (9, 10, 11 μg/mL) in comparison with cisplatin. In addition to their potent antitumor effects, these complexes exhibited reduced cytotoxicity toward normal cells (VERO cells) compared with cisplatin. The investigation extends to molecular docking, where this approach aims to elucidate their interactions with specific protein structures, including (2JFZ, 1SC7, and 6W41). The primary objective is to clarify the potential properties of these compounds, focusing on their antibiotic efficacy, anti‐H. pylori activity, antitumor potential, and anti‐COVID‐19 properties. [ABSTRACT FROM AUTHOR]