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Methylation of Cytidine 1407 Increases the Lifetimes of the A-Site Ground and Excited States of <i>E. coli</i> 16S Ribosomal RNA
Cell-type specific effects of the long non-coding RNA HIF1A-AS3 on HIF1A expression in kidney cells
Abstract The hypoxia-inducible factor 1α (Hif1α) represents the master transcription factor coordinating cellular responses to oxygen depletion. With hundreds of target genes it plays a key role in numerous bio-medical conditions as well as neoplastic and non-cancerous diseases, which in turn requires a strict regulation. Long non-coding RNAs have the potential to virtually control every step of gene expression. We aimed to investigate the expression and role of HIF1A antisense lncRNAs HIF1A-AS1, AS2, and AS3 under hyperglycemic, hypoxic, or both conditions in three non-cancerous human renal cell types: HK-2 cells, primary RPTECs, and mesangial cells. We observed that HIF1A-AS2 and AS3 expression was upregulated under oxygen deprivation. Furthermore, knockdown (KD) of HIF1A-AS3 resulted in a significant reduction of HIF1A-AS2 and even more important of Hif1α in HK-2 cells but not mesangial cells. While KD of HIF1A also had a diminishing effect on HIF1A-AS2 and AS3 RNA levels, KD of HIF1A-AS2 only affected HIF1A-AS3 but not HIF1A. Treating HK-2 cells with Actinomycin D revealed a high HIF1A-AS3 RNA stability. In conclusion, our data reveal a cell-type specific effect of HIF1A-AS3 on HIF1A RNA and protein expression which might allow the development of a cell-type specific HIF1A antagonist based on lncRNAs.
Disordered Ru–O<sub>6</sub> Octahedrons for Efficient and Selective Electro-oxidation of Sulfide to Sulfoxide via Boosted Surface Oxygen Kinetics
Quality of antenatal care and associated factors in public and private facilities of Western Hararghe Zone Ethiopia using WHO framework
Correlated Reaction Coordinate Motion Produces Nonadditive Rate Enhancement for Electron and Energy Transfer in Multiacceptor Structures
Development of a granular bioformulation of Achromobacter xylosoxidans AX77 16S for sustainable onion white rot management and growth enhancement
Abstract Onion white rot, caused by Stromatinia cepivora, is a major soil-borne fungal disease that severely affects onion production. This study introduces a novel endophytic bacterium, Achromobacter xylosoxidans AX77 16S, isolated from healthy onion seeds, as a potential biocontrol agent and growth promoter. Out of 78 bacterial isolates screened, AX77 16S showed the strongest antifungal activity, inhibiting pathogen growth by 50% in dual culture assays. Its application significantly enhanced seed germination (up to 82%) and improved shoot and root development, increasing vigor indices by over 100% compared to untreated controls. The strain was identified by biochemical and molecular techniques and registered in GenBank (ON679518). GC–MS analysis revealed ten bioactive compounds in the bacterial filtrate, while scanning electron microscopy confirmed its damaging effects on fungal structures. Additionally, AX77 16S was formulated into a granular product that remained viable for up to one year. This study presents a promising, sustainable, and cost-effective alternative to chemical fungicides for managing onion white rot and promoting crop growth.
Engineering the Coordination Environment of Metal Centers for Selective and High-Current CO<sub>2</sub> Electromethanation
Ultrasound derived deep learning features for predicting axillary lymph node metastasis in breast cancer using graph convolutional networks in a multicenter study
Abstract The purpose of this study was to create and validate an ultrasound-based graph convolutional network (US-based GCN) model for the prediction of axillary lymph node metastasis (ALNM) in patients with breast cancer. A total of 820 eligible patients with breast cancer who underwent preoperative breast ultrasonography (US) between April 2016 and June 2022 were retrospectively enrolled. The training cohort consisted of 621 patients, whereas validation cohort 1 included 112 patients, and validation cohort 2 included 87 patients. A US-based GCN model was built using US deep learning features. In validation cohort 1, the US-based GCN model performed satisfactorily, with an AUC of 0.88 and an accuracy of 0.76. In validation cohort 2, the US-based GCN model performed satisfactorily, with an AUC of 0.84 and an accuracy of 0.75. This approach has the potential to help guide optimal ALNM management in breast cancer patients, particularly by preventing overtreatment. In conclusion, we developed a US-based GCN model to assess the ALN status of breast cancer patients prior to surgery. The US-based GCN model can provide a possible noninvasive method for detecting ALNM and aid in clinical decision-making. High-level evidence for clinical use in later studies is anticipated to be obtained through prospective studies.
Total Synthesis of (+)-Herpotrichones A–C
Caerin 1.1/1.9 interfere KHDRBS1-DDX5 regulatory axis to induce IL-18 mediated pyroptosis in a HeLa cell tumour model
Abstract Cervical cancer remains a significant global health challenge, particularly in developing countries where access to HPV vaccination is limited. We previously demonstrated that caerin 1.1/1.9 (F1F3) peptides inhibit tumour growth in vitro and in vivo by inducing pyroptosis, followed by apoptosis and immune activation. In this study, we elucidate the molecular mechanisms underlying F1F3-induced pyroptosis in HeLa cells. Our results show that F1F3 triggers pyroptosis independently of GSDME, as evidenced by comparable IL-18 and LDH release in both wild type and GSDME knockout cells. Cross-linking mass spectrometry identified the interaction of F1 to KHDRBS1 and F3 to DDX5, respectively. Knockout of either KHDRBS1 or DDX5 enhanced HeLa cell sensitivity to F1F3 and significantly elevated IL-18 secretion. Notably, KHDRBS1-deficint tumours displayed accelerated growth yet responded more robustly to F1F3 treatment, suggesting a context-dependent tumour-suppressive role of KHDRBS1. These findings uncover a previously uncharacterised pathway regulated by KHDRBS1-DDX5 and demonstrate that F1F3 can effectively interfere with this axis to induce anti-tumour immune responses, highlighting their potential as novel therapeutic agents for cervical cancer.