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Termites are eusocial insects with functionally specialized workers and soldiers, both sharing the same genotype. Additionally, lower termites host flagellates in their hindguts that assist in wood digestion. However, worker-biased and soldier-biased gene expression patterns of the host–flagellate symbiotic system remain underexplored in most taxonomic groups. In this study, we sequenced high-depth transcriptomes from the workers and soldiers of a lower termite, Neotermes binovatus (Kalotermitidae), to investigate the differentially expressed termite transcripts, flagellate transcript abundance, and co-expression patterns of the host–flagellate transcript pairs in both castes. The worker-biased transcripts were enriched in functions related to cuticle development, nervous system regulation, pheromone biosynthesis, and metabolism, whereas the soldier-biased transcripts were predominantly involved in muscle development and kinesis, body morphogenesis, protein modification, and aggression. Flagellate transcripts from the orders Cristamonadida, Trichomonadida, Tritrichomonadida, and Oxymonadida were identified in both workers and soldiers, with the abundance of most flagellate transcripts tending to be higher in workers than in soldiers. Furthermore, we observed a much larger number of strong co-expression correlations between the termite and flagellate transcripts in workers than in soldiers, suggesting the possibility that soldiers depend more on food processed by worker holobionts than on their own symbiotic system. This research provides insights into the functional specialization of the host–flagellate symbiotic system in the worker and soldier castes of termites, supporting the workers’ roles in nest maintenance, preliminary food processing, and communication, while emphasizing the defensive role of soldiers. Additionally, it offers new perspectives on the potential termite-flagellate interactions and underscores the need for whole-genome data of termite flagellates in further studies.

With the great development of sequencing technologies and systematic methods, our understanding of evolutionary relationships at deeper levels within the tree of life has greatly improved over the last decade. However, the current taxonomic methodology is insufficient to describe the growing levels of diversity in both a standardised and general way due to the limitations of using only morphological traits to describe clades. Herein, we propose the idea of a molecular classification based on hierarchical and discrete amino acid characters. Clades are classified based on the results of phylogenetic analyses and described using amino acids with group specificity in phylograms. Practices based on the recently published phylogenomic datasets of insects together with 15 de novo sequenced transcriptomes in this study demonstrate that such a methodology can accommodate various higher ranks of taxonomy. Such an approach has the advantage of describing organisms in a standard and discrete way within a phylogenetic framework, thereby facilitating the recognition of clades from the view of the whole lineage, as indicated by PhyloCode. By combining identification keys and phylogenies, the molecular classification based on hierarchical and discrete characters may greatly boost the progress of integrative taxonomy.

Aim： To investigate the protective effect and the possible mechanism of curcumin on anti-atherosclerosis. Methods： Morphological changes of atherosclerotic lesions taken from apoE knockout （apoE^-/-） mice were determined by hematoxylineosin staining. Intracellular lipid droplets and lipid levels were assayed by oil red O staining and HPLC. The protein expression of caveolin- 1 was quantified by Western blotting. Translocation and the expression of sterol response element-binding protein-1 （SREBP-1） were indirectly detected by an immunofluorescence analysis. Results： The administration of 20 mg.kg^-1.d^-1 curcumin to apoE^-/- mice for 4 months induced a 50% reduction of atherosclerotic lesions and yielded a 5- fold increase in the caveolin-1 expression level as compared to the model group. Rat vascular smooth muscle cells （VSMC） pretreated with 50 mg.L^-1 ox-lipid density lipoprotein（ox-LDL） for 48 h increased cellular lipid contents, and stimulated SREBP-1 translocation, but decreased the caveolin-1 expression level. Lipid-loaded cells exposed to curcumin at various concentrations （12.5, 25, and 50 μmol.L^-1） for different durations （0, 6, 12, 24, and 48 h） significantly diminished the number and area of cellular lipid droplets, total cholesterol, cholesterol ester, and free choles- terol accompanying the elevation of the caveolin- 1 expression level （approximately 3-fold）; the translocation of SREBP-1 from the cytoplasm to the nucleus was inhibited compared with the models. Lipid-loaded VSMC exposed to N-acetylLeu-Leu-norleucinal, a SREBP- 1 protease inhibitor, showed increased nuclear trans- location of SREBP-1, reduced caveolin-1 expression level, and upregulated cellu- lar lipid levels. Condusion： Curcumin inhibits ox-LDL-induced cholesterol accu- mulation in cultured VSMC through increasing the caveolin-1 expression via the inhibition of nuclear translocation of SREBP- 1.

With the development of artificial intelligence(AI) in computer science and statistics, it has been further applied to the medical field. These applications include the management of infectious diseases, in which machine learning has created inroads in clinical microbiology, radiology, genomics, and the analysis of electronic health record data. Especially, the role of machine learning in microbiology has gradually become prominent, and it is used in etiological diagnosis, prediction of antibiotic resistance, association between human microbiome characteristics and complex host diseases, prognosis judgment, and prevention and control of infectious diseases. Machine learning in the field of microbiology mainly adopts supervised learning and unsupervised learning, involving algorithms from classification and regression to clustering and dimensionality reduction. This Review explains crucial concepts in machine learning for unfamiliar readers, describes machine learning’s current applications in clinical microbiology and infectious diseases, and summarizes important approaches clinicians must be aware of when evaluating research using machine learning.

1,8-Cineole (eucalyptol), a monoterpene, has been widely reported for the anti-inflammatory effects. Our previous data confirmed that 1,8-cineole ameliorated the inflammatory phenotype of human umbilical vein endothelial cells (HUVECs) by mediating NF-κB expression . At present, we investigated the protection effects of 1,8-cineole on vascular endothelium in lipopolysaccharide (LPS)-induced acute inflammatory injury mice and the potential mechanisms involved in the protection in HUVECs. Results from enzyme linked immunosorbent assays revealed that 1,8-cineole suppressed the secretion of interleukin (IL)-6 and IL-8 and increased the expression of IL-10 in the serum of LPS-induced mice. 1,8-Cineole reduced the inflammatory infiltration and the expression of vascular cell adhesion molecular 1 (VCAM-1) in the sections of thoracic aorta in LPS-induced acute inflammatory mice. Western blotting indicated that 1,8-cineole significantly decreased the phosphorylation of NF-κB p65 and increased the expression of PPAR-γ in the thoracic aorta tissue. 1,8-Cineole increased the expression of PPAR-γ in LPS-induced HUVECs. 1,8-Cineole and rosiglitazone reduced the protein and mRNA levels of VCAM-1, E-selectin, IL-6, and IL-8 in LPS-induced HUVECs, which could be reversed by the action of GW9662 (inhibitor of PPAR-γ). 1,8-Cineole and rosiglitazone blocked the LPS-induced IκBα degradation and NF-κB p65 nucleus translocation, which could be reversed by the pretreatment of GW9662 or silence of PPAR-γ gene. In conclusion, 1,8-cineole attenuated LPS-induced vascular endothelial cells injury via PPAR-γ dependent modulation of NF-κB.

Drug-induced acute kidney damage (DI-AKI) is a clinical phenomenon of rapid loss of kidney function over a brief period of time as a consequence of the using of medicines. The lack of a specialized treatment and the instability of traditional kidney injury markers to detect DI-AKI frequently result in the development of chronic kidney disease. Thus, it is crucial to continue screening for DI-AKI hub genes and specific biomarkers. Differentially expressed genes (DEGs) of group iohexol, cisplatin, and vancomycin's were analyzed using Limma package, and the intersection was calculated. DEGs were then put into String database to create a network of protein-protein interactions (PPI). Ten algorithms are used in the Cytohubba plugin to find the common hub genes. Three DI-AKI models' hub gene expression was verified and using PCR and western blot. To investigate the hub gene's potential as a biomarker, protein levels of mouse serum and urine were measured by ELISA kits. The UUO, IRI and aristolochic acid I-induced nephrotoxicity (AAN) datasets in the GEO database were utilized for external data verification by WGCNA and Limma package. Finally, the Elisa kit was used to identify DI-AKI patient samples. 95 up-regulated common DEGs and 32 down-regulated common DEGs were obtained using Limma package. A PPI network with 84 nodes and 24 edges was built with confidence >0.4. Four hub genes were obtained by Algorithms of Cytohubba plugin, including TLR4, AOC3, IRF4 and TNFAIP6. Then, we discovered that the protein and mRNA levels of four hub genes were significantly changed in the DI-AKI model and . External data validation revealed that only the AAN model, which also belonged to DI-AKI model, had significant difference in these hub genes, whereas IRI and UUO did not. Finally, we found that plasma TLR4 levels were higher in patients with DI-AKI, especially in vancomycin-induced AKI. The immune system and inflammation are key factors in DI-AKI. We discovered the immunological and inflammatory-related genes TLR4, AOC3, IRF4, and TNFAIP6, which may be promising specific biomarkers and essential hub genes for the prevention and identification of DI-AKI.

Aim To determine the effect of osteopontin (OPN) on autophagy and autophagy‐apoptosis interactions after SAH. Methods The endovascular perforation model of SAH or sham surgery was performed in a total of 86 Sprague‐Dawley male rats. The temporal expressions of endogenous OPN and autophagy‐related proteins (Beclin 1, ATG5, LC3 II to I ratio) were measured in sham and SAH rats at different time points (3, 6, 12, 24, and 72 hours). Rats were randomly divided into three groups: Sham, SAH + Vehicle (PBS, phosphate‐buffered saline), and SAH + rOPN (5 μg/rat recombinant OPN). Neurobehavioral tests were performed 24 hours after SAH, followed by the collection of brain samples for assessment of autophagy and apoptosis proteins. These tests assessed whether an autophagy‐apoptosis relationship existed on the histological level in the brain. Results Endogenous OPN and autophagy‐related proteins all increased after SAH. rOPN administration improved neurological dysfunction, increased the expression of autophagy‐related proteins (Beclin 1, ATG5, LC3 II to I ratio) and antiapoptotic protein Bcl‐2, while decreasing the expression of proapoptotic proteins (cleaved Caspase‐3 and Bax). rOPN also regulated autophagy‐apoptosis interactions 24 hours after SAH. Conclusion rOPN attenuates early brain injury and inhibits neuronal apoptosis by activating autophagy and regulating autophagy‐apoptosis interactions.

Pterygium is a prevalent ocular disease characterized by abnormal conjunctival tissue proliferation, significantly impacting patients’ quality of life. However, the underlying molecular mechanisms driving pterygium pathogenesis remain inadequately understood. This study aimed to investigate gene expression changes following pterygium excision and their association with immune cell infiltration. Clinical samples of pterygium and adjacent relaxed conjunctival tissue were collected for transcriptomic analysis using RNA sequencing combined with bioinformatics approaches. Machine learning algorithms, including LASSO, SVM-RFE, and Random Forest, were employed to identify potential diagnostic biomarkers. GO, KEGG, GSEA, and GSVA were utilized for enrichment analysis. Single-sample GSEA was employed to analyze immune infiltration. The GSE2513 and GSE51995 datasets from the GEO database, along with clinical samples, were selected for validation analysis. Differentially expressed genes (DEGs) were identified from the PRJNA1147595 and GSE2513 datasets, revealing 2437 DEGs and 172 differentially regulated genes (DRGs), respectively. There were 52 co-DEGs shared by both datasets, and four candidate biomarkers ( FN1 , SPRR1B , SERPINB13 , EGR2 ) with potential diagnostic value were identified through machine learning algorithms. Single-sample GSEA demonstrated increased Th2 cell infiltration and decreased CD8 + T cell presence in pterygium tissues, suggesting a crucial role of the immune microenvironment in pterygium pathogenesis. Analysis of the GSE51995 dataset and qPCR results revealed significantly higher expression levels of FN1 and SPRR1B in pterygium tissues compared to conjunctival tissues, but SERPINB13 and EGR2 expression levels were not statistically significant. Furthermore, we identified four candidate drugs targeting the two feature genes FN1 and SPRR1B . This study provides valuable insights into the molecular characteristics and immune microenvironment of pterygium. The identification of potential biomarkers FN1 and SPRR1B highlights their significance in pterygium pathogenesis and lays a foundation for further exploration aimed at integrating these findings into clinical practice.

Cognitive impairment is a common finding in patients with chronic obstructive pulmonary disease (COPD), but little attention has been focused on therapeutic intervention for this complication. Chronic intermittent hypoxia hypercapnia (CIHH) exposure is considered to be responsible for the pathogenesis of COPD. Dl-3n-Butylphthalide (NBP), extracted from Apium graveolens Linn, has displayed a broad spectrum of neuroprotective properties. Our study aimed to investigate the potential of NBP on CIHH-induced cognitive deficits. The cognitive function of rats after CIHH exposure was evaluated by the Morris water maze, which showed that the NBP treated group performed better in the navigation test. NBP activated BDNF and phosphorylated CREB, the both are responsible for neuroprotection. Additionally, NBP decreased CIHH induced apoptosis. Moreover, NBP further induced the expression of HIF-1α, accompanied by the up-regulation of the autophagy proteins Bnip3, Beclin-1 and LC3-II. Finally, NBP also reversed the decreased expression of SIRT1 and PGC-1α, but the expression of Tfam, Cox II and mtDNA remained unchanged. These results suggested that the neuroprotective effects of NBP under CIHH condition possibly occurred through the inhibition of apoptosis, promotion of hypoxia-induced autophagy and activation of the SIRT1/PGC-1α signalling pathway, while stimulation of mitochondrial biogenesis may not be a characteristic response.

Flap endonuclease-1 (FEN1), a structure-specific nuclease participating in DNA replication and repair processes, has been confirmed to promote the proliferation and drug resistance of tumor cells. However, the biological functions of FEN1 in cancer cell migration and invasion have not been defined. In the present study, using online database analysis and immunohistochemistry of the specimens, it was found that FEN1 expression was associated with a highly invasive triple-negative breast cancer (TNBC) subtype in both breast cancer samples from the Oncomine database and from patients recruited into the study. Furthermore, FEN1 was an important biomarker of lymph node metastasis and poor prognosis in patients with TNBC. FEN1 promoted migration of TNBC cell lines and FEN1 knockdown reduced the number of spontaneous lung metastasis in vivo. Ingenuity Pathway Analysis of FEN1-related transcripts in 198 patients with TNBC demonstrated that the polo-like kinase family may be the downstream target of FEN1. PLK4 was further identified as a critical target of FEN1 mediating TNBC cell migration, by regulating actin cytoskeleton rearrangement. The results of the present study validate FEN1 as a therapeutic target in patients with TNBC and revealed a new role for FEN1 in regulating TNBC invasion and metastasis.