Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1075029 | ENA |
REPOSITORIES: ENA
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Project description:The spread of carbapenemase-producing Enterobacterales (CPE) is emerging as a significant clinical concern in tertiary hospitals and in particular, long-term care facilities with deficiencies in infection control. This study aims to evaluate an advanced matrix-assisted laser desorption/ionization mass spectrometry (A-MALDI) method for the identification of carbapenemases and further discrimination of their subtypes in clinical isolates. The A-MALDI method was employed to detect CPE target proteins. Enhancements were made to improve detectability and mass accuracy through the optimization of MALDI-TOF settings and internal mass calibration. A total of 581 clinical isolates were analyzed, including 469 CPE isolates (388 KPC, 51 NDM, 40 OXA, and 2 GES) and 112 carbapenemase-negative isolates. Clinical evaluation of the A-MALDI demonstrated 100% accuracy and precision in identifying all the collected CPE isolates. Additionally, A-MALDI successfully discriminated individual carbapenemase subtypes (KPC-2 or KPC-3/4; OXA-48 or OXA-181 or OXA-232; GES-5 or GES-24) and also differentiated co-producing carbapenemase strains (KPC & NDM; KPC & OXA; KPC & GES; NDM & OXA), attributed to its high mass accuracy and simultaneous detection capability. A-MALDI is considered a valuable diagnostic tool for accurately identifying CPE and carbapenemase’s subtypes in clinical isolates. It may also aid in selecting appropriate antibiotics for each carbapenemase subtype. Ultimately, we expect that the A-MALDI method will contribute to preventing the spread of antibiotic resistance and improving human public health.
2024-11-26 | PXD058284 | Pride
Project description:OXA-23-producing in Enterobacterales
| PRJEB80458 | ENA
Project description:OXA-48-producing Enterobacterales in dogs feaces
| PRJNA793783 | ENA
Project description:Liver fibrosis is a common pathological process of various chronic liver diseases that can develop into liver cancer. MicroRNAs (miRNAs) are a king of non-coding RNA which are closely related to liver diseases. Thus, this research hope to explore the effect of miR-484 on liver fibrosis and reveal its mechanism. The miRNAs profiles were screened by microRNA sequencing and the location of miR-484 was identified by fluorescence in situ hybridization (FISH) in human liver fibrotic tissues. MiR-484 expression was detected by qRT-PCR in rat primary hepatic stellate cells (HSCs). Bioinformatics analysis and dual-luciferase reporter assay were performed to determine the target gene of miR-484. Liver fibrosis specific signatures were analyzed by qRT-PCR and western blot after miR-484 mimic/inhibitor transfection. The cell apoptosis was detected by Annexin V-FITC/PI double staining. The effect of miR-484 silencing on fibrosis in vivo was investigated in thioacetamide (TAA) induced mice model using the adeno-associated virus carrying miR-484 inhibitor. Enrichment of miR-484 was observed in human liver fibrosis tissues and activated rat primary HSCs. FISH showed that miR-484 was prominently located at fibrotic region and the cytoplasm of HSCs in human liver tissues. Dual-luciferase reporter assay verified that the homeodomain-interacting protein kinases 1 (HIPK1) was the direct target of miR-484. After transfecting miR-484 inhibitor into HSC-T6, HIPK1 were significantly up-regulated, and α-SMA, col1a1, Wnt-3a, Wnt-5a, β-catenin and p-β-catenin were down-regulated, suggesting the restrain effect of miR-484 knockdown on HSCs activation. Conversely, the results were opposite with miR-484 mimic transfection. In addition, the apoptosis of HSC-T6 altered significantly after miR-484 modulation. Moreover, adeno-associated virus carrying miR-484 inhibitor alleviated mice liver fibrosis induced by TAA. In conclusion, miR-484 knockdown ameliorates liver fibrosis by promoting the apoptosis and suppressing HSCs activation via blocking Wnt/β-catenin signaling pathway. MiR-484 and its downstream gene HIPK1 might be selected as novel therapeutic targets of liver fibrosis.
2021-12-09 | GSE190366 | GEO
Project description:Clinical Enterobacterales producing novel OXA-163-like in Argentina
| PRJNA413168 | ENA
Project description:Purpose: Pancreatic ductal adenocarcinoma (PDAC) remains a lethal malignancy with limited treatment options. While oxaliplatin-based (Oxa) therapy, such as FOLFIRINOX, has improved outcomes in select patients, Oxa resistance significantly limits its efficacy. This study investigates cell cycle mechanisms driving Oxa resistance and explores targeting these pathways as a therapeutic strategy. Experimental Design: Murine KPC and human Panc1 oxaliplatin-resistant (Oxa-R) cell lines were established. RNA sequencing, Western blotting, and flow cytometry were used to analyze DNA damage and cell cycle regulators. Viability assays and a murine orthotopic PDAC model were employed to evaluate the therapeutic potential of CDK4/6 inhibition with Oxa. Results: Oxa-R cell lines exhibited slower proliferation rates, reduced response to Oxa treatment, and significant upregulation of G2/M and E2F1 signaling pathways, findings that correlated with poor survival outcomes in human clinical datasets. In Oxa-sensitive PDAC cells, Oxa treatment activated the ATR-Chk1 pathway, leading to cyclin D1 suppression and apoptosis. In contrast, Oxa resistance was characterized by compensatory upregulation of CDK4/6 signaling, which enabled cells to bypass DNA damage-induced cell cycle arrest. Notably, the addition of CDK4/6 inhibitors restored Oxa sensitivity in resistant cell lines, resulting in enhanced apoptosis in vitro and significantly reduced tumor growth in vivo. Conclusion: Oxa resistance in PDAC is mediated by cell cycle dysregulation involving cyclin D1 and CDK4/6. Targeting CDK4/6 with Abemaciclib reverses resistance and enhances Oxa efficacy, offering a promising therapeutic strategy for resistant PDAC.
2025-06-30 | GSE300379 | GEO
Project description:Characterisation of OXA-484, an OXA-48-type carbapenemhydrolysing class D beta-lactamase from E. coli
| PRJNA644256 | ENA