Б.Саруулжавхлан
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Товч нэр
Б.Саруулжавхлан
Бүтэн нэр
Батсайхан Саруулжавхлан
Латин нэр
Batsaikhan Saruuljavkhlan
Албан тушаал
Гэрээт багш
ORCID
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4 results
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Item type:Publication, Species-level dynamics of gastric microbiome after Helicobacter pylori eradication in high-risk Mongolian population(2026-02); ; Luvsandagva, BayasgalanBACKGROUND: Species-level resolution is essential to understand gastric microbiome recovery after Helicobacter pylori eradication, yet short-read 16 S rRNA approaches often obscure clinically relevant changes. METHODS: Gastric biopsies from 121 adults in Bayan-Ölgii, Mongolia (71 H. pylori-positive, 50 H. pylori-negative) were analyzed, including nine paired pre- and post-eradication gastric biopsy samples collected six months apart, enabling exploratory longitudinal analysis. Full-length 16 S rRNA (V1-V9) sequencing was performed using the Oxford Nanopore platform with EMU taxonomic assignment (SILVA v138.1/NCBI RefSeq). Ecological changes were evaluated using diversity indices, principal coordinates analysis (PCoA) with PERMANOVA, and differential abundance testing (DESeq2, FDR < 0.05). Eradication therapy (esomeprazole-bismuth-doxycycline-levofloxacin) achieved success in 54 of 57 H. pylori-positive patients (94.7%). RESULTS: H. pylori-positive microbiomes were dominated by H. pylori (91.8% ± 3.9%) and exhibited markedly reduced diversity (Shannon = 0.44 ± 0.11) compared with H. pylori-negative samples (2.08 ± 0.25; p < 0.001). Six months after eradication, diversity increased significantly (2.17 ± 0.20; p = 0.0001), with enrichment of oral commensals including Streptococcus mitis (↑ 11.9×), Neisseria elongata (↑ 13.7×), and Prevotella melaninogenica (↑ 13.0×). However, post-eradication profiles at six months remained distinct from H. pylori-negative communities (PERMANOVA R² = 0.12; p = 0.02). In total, 174 amplicon sequence variants changed significantly, including persistence of Fusobacterium nucleatum. CONCLUSIONS: Nanopore full-length 16 S sequencing reveals fine-scale, clinically relevant shifts that are masked by partial-gene assays. Eradication rapidly restores microbial diversity, but at six months, is associated with a novel ecological equilibrium rather than complete normalization. This species-resolved approach offers a practical framework for post-eradication microbiome monitoring and may inform strategies to reduce residual gastric cancer risk in high-burden populations. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Utilization of an Automated Latex Agglutination Turbidity Assay for Assessing Gastric Mucosal Alteration during Helicobacter pylori Infection(The Editorial Office of Gut and Liver, 2024-01); ; Azzaya, DashdorjBACKGROUND/AIMS: : A latex agglutination turbidity (LA) assay to test for serum antibodies has been approved in Japan and Korea for mass screening of Helicobacter pylori infection. In this study, we evaluated the LA assay for diagnosing H. pylori infection and predicting gastric mucosal changes in a Mongolian population. METHODS: : In total, 484 individuals were classified into H. pylori-positive (n=356) and H. pylori-negative (n=128) groups, as determined by histology and H. pylori culture. RESULTS: : The best cutoff, sensitivity, and specificity values for the LA assay were 18.35 U/mL, 74.2%, and 65.6%, respectively. The LA values in the atrophic gastritis group were statistically higher than those in the other groups (healthy, chronic gastritis, intestinal metaplasia, and gastric cancer, p<0.0001). The cutoff value to distinguish the atrophic gastritis group from the other four groups was 32.0 U/mL, and its area under the curve was 0.673, which was the highest among the E-plate, pepsinogen (PG) I, PG II, and PG I/II ratio tests in our data. The odds ratios for atrophic gastritis determined by the LA assay and PG I test in multiple logistic regression were 2.5 and 1.9, respectively, which were significantly higher than for the other tests. CONCLUSIONS: : The LA assay can determine the risk of atrophic gastritis, which in turn is a considerable risk factor for gastric cancer. We propose using this assay in combination with the PG I/II ratio to avoid missing gastric cancer patients who have a low LA value (less than 32.0 U/mL). - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Study of Helicobacter pylori Isolated from a High-Gastric-Cancer-Risk Population: Unveiling the Comprehensive Analysis of Virulence-Associated Genes including Secretion Systems, and Genome-Wide Association Study(MDPI AG, 2023-09); ; Khangai, AyushBACKGROUND: The prevalence of gastric cancer in Mongolia, in East Asia, remains the highest in the world. However, most Helicobacter pylori strains in Mongolia have a less virulent Western-type CagA. We aimed to determine how H. pylori genomic variation affected gastric diseases, especially gastric cancer, based on comprehensive genome analysis. METHODS: We identified a set of 274 virulence-associated genes in H. pylori, including virulence factor and outer membrane protein (OMP) genes, the type four secretion system gene cluster, and 13 well-known virulence gene genotypes in 223 H. pylori strains and their associations with gastric cancer and other gastric diseases. We conducted a genome-wide association study on 158 H. pylori strains (15 gastric cancer and 143 non-gastric cancer strains). RESULTS: Out of 274 genes, we found 13 genes were variable depending on disease outcome, especially iron regulating OMP genes. H. pylori strains from Mongolia were divided into two main subgroups: subgroup (Sg1) with high risk and Sg2 with low risk for gastric cancer. The general characteristics of Sg1 strains are that they possess more virulence genotype genes. We found nine non-synonymous single nucleotide polymorphisms in seven genes that are linked with gastric cancer strains. CONCLUSIONS: Highly virulent H. pylori strains may adapt through host-influenced genomic variations, potentially impacting gastric carcinogenesis. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Exploring Alternative Treatment Choices for Multidrug-Resistant Clinical Strains of Helicobacter pylori in Mongolia(MDPI AG, 2023-11); ; Oyuntsetseg, KhasagHelicobacter pylori is a pathogen related to severe diseases such as gastric cancer; because of rising antimicrobial-resistant strains, failure to eradicate H. pylori with antibiotics has increased worldwide. Multidrug-resistant H. pylori and gastric cancer is common in Mongolia; therefore, we aimed to explore alternative antimicrobial treatments and the genomes of resistant strains in this country. A total of 361 H. pylori strains isolated from patients in Mongolia were considered. Minimal inhibitory concentrations for two fluoroquinolones (ciprofloxacin and moxifloxacin), rifabutin, and furazolidone were determined via two-fold agar dilution. Genomic mutations in antibiotic-resistant strains were identified by next-generation sequencing using the Illumina Miseq platform and compared with genes from a reference H. pylori strain (26695). The resistance rate of H. pylori strains to quinolones was high (44% to ciprofloxacin and 42% to moxifloxacin), and resistance to rifabutin was low (0.5%); none were resistant to furazolidone. Most quinolone-resistant strains possessed gyrA gene mutations causing amino acid changes (e.g., N87K, A88P, and D91G/Y/N). While one rifabutin-resistant strain had amino acid-substituting mutations in rpoB (D530N and R701C), the other had three novel rpoB mutations; both rifabutin-resistant strains were sensitive to furazolidone. Overall, our findings suggest that rifabutin and/or furazolidone may be an alternative, effective H. pylori treatment in patients who have failed to respond to other treatment regimens.