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Profil bibliographique

Nobuyuki Ara

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

83Publications signalées
1190Citations signalées
2Affiliations récentes

Les institutions déclarées

Les domaines associés

Helicobacter pylori-related gastroenterology studiesEsophageal Cancer Research and TreatmentGastric Cancer Management and OutcomesGastroesophageal reflux and treatmentsEsophageal and GI Pathology

Les publications récentes

Accès ouvert 2024 article OpenAlex

Prevalence and Distribution of Gastric Endoscopy Findings in Non-eosinophilic Esophagitis Eosinophilic Gastrointestinal Diseases: Influence of Atrophic Gastritis

Naoko Mizumoto, Yasuhiko Abe, Yu Sasaki, Makoto Yagi et autres

Objective The impact of Helicobacter pylori infection on gastric endoscopic findings in non-eosinophilic esophagitis eosinophilic gastrointestinal diseases (non-EoE EGIDs) remains unclear. This study investigated the influence of H. pylori infection on the prevalence and distribution of gastric lesions. Methods The details of …

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2 citations Internal Medicine
Accès ouvert 2024 article OpenAlex

Endoscopic and histological risk stratification for gastric cancer using gastric intestinal metaplasia

Masashi Kawamura, Noriya Uedo, Kenshi Yao, Tomoyuki Koike et autres

BACKGROUND AND AIM: Intestinal metaplasia (IM) of the gastric mucosa is strongly associated with the risk of gastric cancer (GC). This study was performed to investigate the usefulness of endoscopic and histological risk stratification for GC using IM. METHODS: This was a …

jp (code pays fourni par la source)

11 citations Journal of Gastroenterology and Hepatology
Accès ouvert 2023 other OpenAlex

Data from Cdx2 Expression and Intestinal Metaplasia Induced by H. pylori Infection of Gastric Cells Is Regulated by NOD1-Mediated Innate Immune Responses

Naoki Asano, Akira Imatani, Tomohiro Watanabe, Jun Fushiya et autres

Abstract Chronic infection with the bacterial Helicobacter pylori is a major cause of gastric and duodenal ulcer disease, gastric mucosal atrophy, and cancer. H. pylori–induced expression of the intestinal epithelial–specific transcription factor caudal-related homeobox 2 (Cdx2) contributes to intestinal metaplasia, a precursor …

0 citations
Accès ouvert 2023 other OpenAlex

Data from Cdx2 Expression and Intestinal Metaplasia Induced by H. pylori Infection of Gastric Cells Is Regulated by NOD1-Mediated Innate Immune Responses

Naoki Asano, Akira Imatani, Tomohiro Watanabe, Jun Fushiya et autres

Abstract Chronic infection with the bacterial Helicobacter pylori is a major cause of gastric and duodenal ulcer disease, gastric mucosal atrophy, and cancer. H. pylori–induced expression of the intestinal epithelial–specific transcription factor caudal-related homeobox 2 (Cdx2) contributes to intestinal metaplasia, a precursor …

0 citations
Accès ouvert 2023 supplementary-materials OpenAlex

Supplementary Figures 1-10 from Cdx2 Expression and Intestinal Metaplasia Induced by H. pylori Infection of Gastric Cells Is Regulated by NOD1-Mediated Innate Immune Responses

Naoki Asano, Akira Imatani, Tomohiro Watanabe, Jun Fushiya et autres

Supplementary Figure 1. Cdx2 expression in human gastric epithelial cell lines. Supplementary Figure 2. The expression of Cdx2 was enhanced by H. pylori infection in gastric epithelial cell. Supplementary Figure 3. Scheme of the Cdx2 prmoter-luciferase reporter plasmids used in this study. …

0 citations
Accès ouvert 2023 supplementary-materials OpenAlex

Supplementary Figures 1-10 from Cdx2 Expression and Intestinal Metaplasia Induced by H. pylori Infection of Gastric Cells Is Regulated by NOD1-Mediated Innate Immune Responses

Naoki Asano, Akira Imatani, Tomohiro Watanabe, Jun Fushiya et autres

Supplementary Figure 1. Cdx2 expression in human gastric epithelial cell lines. Supplementary Figure 2. The expression of Cdx2 was enhanced by H. pylori infection in gastric epithelial cell. Supplementary Figure 3. Scheme of the Cdx2 prmoter-luciferase reporter plasmids used in this study. …

0 citations

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