The goals of this study
1. Explore association between psychological factors and Hpylori associated gastritis.
2. Assess prevalence and severity of psychology symptoms among patients with H pylori associated gastritis and their effects on their life.
3. Examine relation between demographic and clinical variables .
4. Effect of eradication of H pylori on psychological status of patients.

Start Date22 Oct 2024

Sponsor / Collaborator

Assiut University

CTR20242803 / RecruitingNot Applicable

评估受试制剂奥美拉唑肠溶片（规格：20 mg）与参比制剂奥美拉唑肠溶片（Omepral®，规格：20 mg）在健康成年参与者空腹及餐后状态下的生物等效性临床研究

[Translation] A clinical study to evaluate the bioequivalence of the test preparation, omeprazole enteric-coated tablets (strength: 20 mg), and the reference preparation, omeprazole enteric-coated tablets (Omepral®, strength: 20 mg), in healthy adult participants under fasting and fed conditions

主要目的：研究空腹及餐后状态下单次口服受试制剂奥美拉唑肠溶片（规格：20 mg，浙江京新药业股份有限公司生产）与参比制剂奥美拉唑肠溶片（Omepral®，规格：20 mg，太陽ファルマ株式会社持证）在健康成年参与者体内的药代动力学，评价两种制剂是否具有生物等效性。次要目的：研究受试制剂奥美拉唑肠溶片（规格：20 mg）和参比制剂奥美拉唑肠溶片（Omepral®，规格：20 mg）在健康成年参与者中的安全性。

[Translation]

Main purpose: To study the single oral administration of the test preparation omeprazole enteric-coated tablets (specification: 20 mg, produced by Zhejiang Jingxin Pharmaceutical Co., Ltd.) and the reference preparation omeprazole enteric-coated tablets in the fasting and postprandial state. (Omepral®, strength: 20 mg, licensed by Taiyo Fantasia Co., Ltd.) Pharmacokinetics in healthy adult participants to evaluate whether the two preparations are bioequivalent. Secondary purpose: To study the safety of the test preparation omeprazole enteric-coated tablets (strength: 20 mg) and the reference preparation omeprazole enteric-coated tablets (Omepral®, strength: 20 mg) in healthy adult participants .

Start Date02 Aug 2024

Sponsor / Collaborator

Zhejiang Jingxin Pharmaceutical Co., Ltd.

ChiCTR2400085283 / SuspendedPhase 4IIT

A randomized, controlled clinical study of Bifidobacterium triple live bacteria enteric coated tablets (Bifid) combined with quadruple therapy for the treatment of Helicobacter pylori positive chronic gastritis.

Start Date10 Jun 2024

Sponsor / Collaborator

The First Affiliated Hospital of Nanchang University

100 Clinical Results associated with Helicobacter-associated gastritis

100 Translational Medicine associated with Helicobacter-associated gastritis

0 Patents (Medical) associated with Helicobacter-associated gastritis

3,060

Literatures (Medical) associated with Helicobacter-associated gastritis

01 Apr 2025·DEN Open

Iron deposition in gastric black spots: Clinicopathological insights and NanoSuit‐correlative light and electron microscopy analysis

Article

Author: Sugiura, Kiichi ; Hamaya, Yasushi ; Kaneko, Masanao ; Ishida, Natsuki ; Kawasaki, Hideya ; Baba, Satoshi ; Takeuchi, Hiroya ; Iwaizumi, Moriya ; Egami, Takatoshi ; Osawa, Satoshi ; Tani, Shinya ; Yamade, Mihoko ; Sugimoto, Ken ; Tamura, Satoshi

AbstractObjectivesBlack spots (BSs) are lentiginous findings observed in the gastric body and fundus during upper gastrointestinal endoscopy and are predominantly seen in patients undergoing Helicobacter pylori eradication treatment. However, the detailed patient background and exact composition are poorly understood. This study aims to clarify the clinicopathological features of BSs, examine patient demographics, and use the NanoSuit‐correlative light and electron microscopy (CLEM) method combined with scanning electron microscopy‐energy dispersive X‐ray spectroscopy for elemental analysis.MethodsPatients who underwent upper gastrointestinal endoscopy between 2017 and 2022 were included. Data on age, medications, blood tests, and H. pylori infection status were retrospectively gathered from medical records. Univariate analysis was conducted to examine BS presence, with results then used in a multivariate model to identify associated risk factors. Additionally, pathological specimens from patients with BSs were analyzed for elemental composition using the NanoSuit‐CLEM method combined with scanning electronmicroscopy‐energy dispersive X‐ray spectroscopy.ResultsAn analysis of 6778 cases identified risk factors for BSs, including older age and using proton pump inhibitors, statins, corticosteroids, and antithrombotic drugs. Endoscopically, BSs correlated with higher gastric atrophy and lower active H. pylori infection. Iron deposition at BS sites was specifically identified using NanoSuit‐CLEM.ConclusionsBSs on gastrointestinal endoscopy may indicate an absence of active H. pylori inflammation. The discovery of iron deposition within BSs using the NanoSuit‐CLEM method has offered new insights into the possible causative factors and advances our understanding of the etiology of BSs, bringing us closer to unraveling the underlying mechanisms of their formation.

31 Dec 2024·Gut Microbes

AUF1-mediated inhibition of autophagic lysosomal degradation contributes to CagA stability and Helicobacter pylori -induced inflammation

Article

Author: Zhang, Jing ; Zhang, Ting ; Wei, Guochao ; Zheng, Huiling ; Fu, Weiwei ; Chen, Xiangmei ; Shi, Yanyan ; Ding, Shigang ; Wang, Ye ; Ning, Jing

CagA, a virulence factor of Helicobacter pylori (H. pylori), is known to drive inflammation in gastric epithelial cells and is typically degraded through autophagy. However, the molecular mechanism by which CagA evades autophagy-mediated degradation remains elusive. This study found that H. pylori inhibits autophagic flux by upregulating the expression of AU-rich element RNA-binding factor 1 (AUF1). We confirmed that AUF1 does not affect autophagy initiation but instead hampers lysosomal clearance, as evidenced by treatments with 3-MA, CQ and BafA1. Upregulated AUF1 stabilizes CagA protein levels by inhibiting the autolysosomal degradation of intracellular CagA in H. pylori-infected gastric epithelial cells. Knocking down AUF1 promotes CagA degradation, an effect that can be reversed by the lysosome inhibitor BafA1 and CQ. Transcriptome analysis of AUF1-knockdown gastric epithelial cells infected with H. pylori indicated that AUF1 regulates the expression of lysosomal-associated hydrolase genes, specifically CTSD, to inhibit autolysosomal degradation. Moreover, we observed that knockdown of AUF1 enhanced the stability of CTSD mRNA and identified AUF1 binding to the 3'UTR region of CTSD mRNA. AUF1-mediated downregulation of CTSD expression contributes to CagA stability, and AUF1 overexpression leads to an increase in CagA levels in exosomes, thus promoting extracellular inflammation. In clinical gastric mucosa, the expression of AUF1 and its cytoplasmic translocation are associated with H. pylori-associated gastritis, with CagA being necessary for the translocation of AUF1 into the cytoplasm. Our findings suggest that AUF1 is a novel host-positive regulator of CagA, and dysregulation of AUF1 expression increases the risk of H. pylori-associated gastritis.

31 Dec 2024·Gut Microbes

Inflammation promotes stomach epithelial defense by stimulating the secretion of antimicrobial peptides in the mucus

Article

Author: D’Amore, Antonella ; Tosco, Alessandra ; Zagami, Claudia ; Lisle, Richard ; Woelffling, Sara ; Voli, Antonia ; Link, Alexander ; Licursi, Valerio ; Traulsen, Jan ; Schmid, Monika ; Meyer, Thomas F. ; Vllahu, Megi ; Crickley, Robbie ; Boccellato, Francesco

The mucus serves as a protective barrier in the gastrointestinal tract against microbial attacks. While its role extends beyond merely being a physical barrier, the extent of its active bactericidal properties remains unclear, and the mechanisms regulating these properties are not yet understood. We propose that inflammation induces epithelial cells to secrete antimicrobial peptides, transforming mucus into an active bactericidal agent. To investigate the properties of mucus, we previously developed mucosoid culture models that mimic the healthy human stomach epithelium. Similar to organoids, mucosoids are stem cell-driven cultures; however, the cells are cultivated on transwells at air-liquid interface. The epithelial cells of mucosoids form a polarized monolayer, allowing differentiation into all stomach lineages, including mucus-secreting cells. This setup facilitates the secretion and accumulation of mucus on the apical side of the mucosoids, enabling analysis of its bactericidal effects and protein composition, including antimicrobial peptides. Our findings show that TNFα, IL1β, and IFNγ induce the secretion of antimicrobials such as lactotransferrin, lipocalin2, complement component 3, and CXCL9 into the mucus. This antimicrobial-enriched mucus can partially eliminate Helicobacter pylori, a key stomach pathogen. The bactericidal activity depends on the concentration of each antimicrobial and their gene expression is higher in patients with inflammation and H.pylori-associated chronic gastritis. However, we also find that H. pylori infection can reduce the expression of antimicrobial encoding genes promoted by inflammation. These findings suggest that controlling antimicrobial secretion in the mucus is a critical component of epithelial immunity. However, pathogens like H. pylori can overcome these defenses and survive in the mucosa.

News (Medical) associated with Helicobacter-associated gastritis

30 Aug 2024

·www.prnewswire.com

Debbie's Dream Foundation Celebrates Groundbreaking Research by Dr. Valerie O'Brien on H. pylori and Gastric Cancer

Pioneering Scientist Honored for Advancing Understanding of the Bacterial Origins of Stomach Cancer FORT LAUDERDALE, Fla., Aug. 30, 2024 /PRNewswire/ -- Debbie's Dream Foundation: Curing Stomach Cancer (DDF) proudly recognizes Dr. Valerie O'Brien for her groundbreaking research into the link between Helicobacter pylori (H. pylori) and gastric cancer. Dr. O'Brien's work, supported by Debbie's Dream Foundation-AACR Gastric Cancer Research Fellowship in memory of Sally Mandel, represents a significant advancement in understanding how H. pylori contributes to the development of gastric cancer, particularly in vulnerable populations. Continue Reading Dr. Valerie O'Brien discusses her groundbreaking research on the link between H. pylori and gastric cancer, supported by Debbie's Dream Foundation-AACR Gastric Cancer Research Fellowship in memory of Sally Mandel. Dr. O'Brien's work is paving the way for new treatments and early detection strategies in the fight against stomach cancer. Credit: Screenshot from video courtesy of the American Association for Cancer Research (AACR). Dr. O'Brien, who now serves as an Assistant Professor at Purdue University, has utilized her expertise in microbiology to explore the molecular mechanisms by which H. pylori infection leads to gastric cancer. Her research has identified critical changes at the cellular level that may inform future treatments and early detection strategies for this deadly disease. "We are incredibly proud of Dr. O'Brien's achievements and the impact of her research on the global fight against gastric cancer," said Andrea Eidelman, Chief Executive Officer of DDF. "Her work exemplifies the power of research funded by organizations like ours, and we are committed to continuing our support for innovative studies that can change the lives of those affected by this disease." Dr. O'Brien's research has garnered significant attention, including a recent publication in Cancer Research Communications. Her studies have shown that H. pylori-driven inflammation can cause harmful changes in stomach cells, a discovery that could lead to better diagnostic markers and therapeutic options. In addition to celebrating Dr. O'Brien's accomplishments, DDF has taken further steps to combat the global impact of H. pylori. The foundation has successfully drafted language to the Senate to advocate for vital H. pylori testing in the U.S. Armed Forces, a move that could prevent gastric cancer in thousands of service members. Dr. O'Brien will be honored as a Luminary at the upcoming Gastric Cancer Awareness Illuminations Ceremony & Celebration Dinner, hosted by DDF on November 9, 2024. This event will celebrate individuals who have contributed to advancing the mission to cure stomach cancer. About Debbie's Dream Foundation: Curing Stomach Cancer DDF is a 501(c)(3) non-profit organization dedicated to raising awareness about gastric cancer, advancing research funding, and providing international education and support to patients, families, and caregivers. DDF's ultimate goal is to make the cure for stomach cancer a reality. DDF was founded in 2009 by Debbie Zelman after she was diagnosed with stage IV incurable gastric cancer in 2008 and given only weeks to live. Debbie is considered a pioneer by many for bringing awareness to the plight of stomach cancer patients worldwide, as well as to the lack of federal funding for stomach cancer research. She did all of this while receiving hundreds of rounds of chemo and daily oral treatments. Debbie passed away on December 23, 2017, at 50, almost a decade later. As a result of her leadership, DDF now has a Scientific and Medical Advisory Board of world-renowned doctors and chapters throughout the United States, and in Canada, Germany, and Japan. DDF strives to continue Debbie's mission to make her dream a reality. To learn more, visit . Media Contact: Brittnay Starks, Communications Director Debbie's Dream Foundation: Curing Stomach Cancer (954) 475-1200 [email protected] SOURCE Debbie's Dream Foundation: Curing Stomach Cancer

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