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Abstract Background In recent years, ophthalmology has emerged as a new frontier in medical artificial intelligence (AI) with multi-modal AI in ophthalmology garnering significant attention across interdisciplinary research. This integration of various types and data models holds paramount importance as it enables the provision of detailed and precise information for diagnosing eye and vision diseases. By leveraging multi-modal ophthalmology AI techniques, clinicians can enhance the accuracy and efficiency of diagnoses, and thus reduce the risks associated with misdiagnosis and oversight while also enabling more precise management of eye and vision health. However, the widespread adoption of multi-modal ophthalmology poses significant challenges. Main text In this review, we first summarize comprehensively the concept of modalities in the field of ophthalmology, the forms of fusion between modalities, and the progress of multi-modal ophthalmic AI technology. Finally, we discuss the challenges of current multi-modal AI technology applications in ophthalmology and future feasible research directions. Conclusion In the field of ophthalmic AI, evidence suggests that when utilizing multi-modal data, deep learning-based multi-modal AI technology exhibits excellent diagnostic efficacy in assisting the diagnosis of various ophthalmic diseases. Particularly, in the current era marked by the proliferation of large-scale models, multi-modal techniques represent the most promising and advantageous solution for addressing the diagnosis of various ophthalmic diseases from a comprehensive perspective. However, it must be acknowledged that there are still numerous challenges associated with the application of multi-modal techniques in ophthalmic AI before they can be effectively employed in the clinical setting.

Abstract This study aimed to evaluate the regulatory effect and molecular mechanism of long noncoding RNA small nucleolus RNA host gene 8 (LncRNA SNHG8) in the migration and angiogenesis of primary human umbilical vein endothelial cells (pHUVECs) under high-glucose (HG) conditions. The HG-induced endothelial injury model was established in vitro.The cell model of silencing SNHG8, overexpressing SNHG8, and silencing TRPM7 was established by transfecting SNHG8-siRNA, SNHG8 plasmid and TRPM7-siRNA into cells with liposomes.The SNHG8 level was determined through reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression levels of transient receptor potential melastatin 7 (TRPM7), endothelial nitric oxide synthase (eNOS), p-eNOS, extracellular signal-regulated kinase 1/2(ERK1/2), and p-ERK1/2 were assessed through western blot. Nitric oxide (NO) levels were measured with DAF-FM. pHUVEC migration was examined through wound healing and Transwell assay, and pHUVEC angiogenesis was observed through a tube formation assay. Results showed that HG promoted the expression of lncRNA SNHG8 and TRPM7 and decreased the ratio of p-eNOS/eNOS and p-ERK1/2/ERK1/2 in pHUVECs . NO production, migration , and angiogenesis were inhibited in pHUVECs under HG conditions. Silencing lncRNA SNHG8 and TRPM7 could significantly reverse the HG-induced decrease in eNOS activation, NO production , migration, and angiogenesis . SNHG8 and U0126 (ERK pathway inhibitor) overexpression enhanced the HG effects, whereas using U0126 did not affect the TRPM7 expression. In conclusion, lncRNA SNHG8 participates in HG-induced endothelial cell injury and likely regulates NO production, migration, and angiogenesis of pHUVECs via the TRPM7/ERK1/2 signaling axis.

Abstract Public metabolites such as vitamins play critical roles in maintaining the ecological functions of microbial community. However, the biochemical and physiological bases for fine-tuning of public metabolites in the microbiome remain poorly understood. Here, we examine the interactions between myxobacteria and Phytophthora sojae, an oomycete pathogen of soybean. We find that host plant and soil microbes complement P. sojae’s auxotrophy for thiamine. Whereas, myxobacteria inhibits Phytophthora growth by a thiaminase I CcThi1 secreted into extracellular environment via outer membrane vesicles (OMVs). CcThi1 scavenges the required thiamine and thus arrests the thiamine sharing behavior of P. sojae from the supplier, which interferes with amino acid metabolism and expression of pathogenic effectors, probably leading to impairment of P. sojae growth and pathogenicity. Moreover, myxobacteria and CcThi1 are highly effective in regulating the thiamine levels in soil, which is correlated with the incidence of soybean Phytophthora root rot. Our findings unravel a novel ecological tactic employed by myxobacteria to maintain the interspecific equilibrium in soil microbial community.

Abstract Background Pulmonary arterial hypertension (PAH) is a pathophysiological syndrome, characterized by pulmonary vascular remodeling. Immunity and inflammation are progressively recognized properties of PAH, which are crucial for the initiation and maintenance of pulmonary vascular remodeling. This study explored immune cell infiltration characteristics and potential biomarkers of PAH using comprehensive bioinformatics analysis. Methods Microarray data of GSE117261, GSE113439 and GSE53408 datasets were downloaded from Gene Expression Omnibus database. The differentially expressed genes (DEGs) were identified in GSE117261 dataset. The proportions of infiltrated immune cells were evaluated by CIBERSORT algorithm. Feature genes of PAH were selected by least absolute shrinkage and selection operator (LASSO) regression analysis and validated by fivefold cross-validation, random forest and logistic regression. The GSE113439 and GSE53408 datasets were used as validation sets and logistic regression and receiver operating characteristic (ROC) curve analysis were performed to evaluate the prediction value of PAH. The PAH-associated module was identified by weighted gene association network analysis (WGCNA). The intersection of genes in the modules screened and DEGs was used to construct protein–protein interaction (PPI) network and the core genes were selected. After the intersection of feature genes and core genes, the hub genes were identified. The correlation between hub genes and immune cell infiltration was analyzed by Pearson correlation analysis. The expression level of LTBP1 in the lungs of monocrotaline-induced PAH rats was determined by Western blotting. The localization of LTBP1 and CD4 in lungs of PAH was assayed by immunofluorescence. Results A total of 419 DEGs were identified, including 223 upregulated genes and 196 downregulated genes. Functional enrichment analysis revealed that a significant enrichment in inflammation, immune response, and transforming growth factor β (TGFβ) signaling pathway. CIBERSORT analysis showed that ten significantly different types of immune cells were identified between PAH and control. Resting memory CD4+ T cells, CD8+ T cells, γδ T cells, M1 macrophages, and resting mast cells in the lungs of PAH patients were significantly higher than control. Seventeen feature genes were identified by LASSO regression for PAH prediction. WGCNA identified 15 co-expression modules. PPI network was constructed and 100 core genes were obtained. Complement C3b/C4b receptor 1 (CR1), thioredoxin reductase 1 (TXNRD1), latent TGFβ binding protein 1 (LTBP1), and toll-like receptor 1 (TLR1) were identified as hub genes and LTBP1 has the highest diagnostic efficacy for PAH (AUC = 0.968). Pearson correlation analysis showed that LTBP1 was positively correlated with resting memory CD4+ T cells, but negatively correlated with monocytes and neutrophils. Western blotting showed that the protein level of LTBP1 was increased in the lungs of monocrotaline-induced PAH rats. Immunofluorescence of lung tissues from rats with PAH showed increased expression of LTBP1 in pulmonary arteries as compared to control and LTBP1 was partly colocalized with CD4+ cells in the lungs. Conclusion LTBP1 was correlated with immune cell infiltration and identified as the critical diagnostic maker for PAH.

Abstract MnSe and Co0.85Se embedded in nitrogen‐doped carbon nanofibers (MnSe/Co0.85Se/N‐CNFs) were synthesized by electrospinning and high‐temperature calcination, and evaluated for the first time as sodium/potassium‐ion battery anode material via constant current charge/discharge, cyclic voltammetry, electrochemical impedance spectroscopy.Ex‐situ XRD revealed the potassium storage mechanism of MnSe/Co0.85Se/N‐CNFs, indicating that its capacity was mainly provided by the conversion reaction. Compared with MnSe/N‐CNFs and Co0.85Se/N‐CNFs, the reversible capacity and cycling performance of MnSe/Co0.85Se/N‐CNFs were significantly improved due to the synergistic effect of bimetals. The MnSe/Co0.85Se/N‐CNFs electrode showed a charging capacity of 262.3 mAh g−1 after 700 cycles at 1 A g−1 in Na‐ion batteries and a discharge capacity of 183.4 mAh g−1 after 400 cycles at 0.1 A g−1 in K‐ion batteries, The results showed that binder‐free binary metal MnSe/Co0.85Se/N‐CNFs have a certain development prospect as anode for sodium/potassium‐ion batteries.