Background The aortic valve (AV) is the most commonly affected valve in valvular heart diseases (VHDs). The objective of the study is to identify microRNA (miRNA) molecules expressed in VHDs and the differential expression patterns of miRNA in AVs with either calcification or rheumatism etiologies. Methods Human AVs were collected during valve replacement surgery. RNA was extracted and miRNA containing libraries were prepared and sequenced using the next generation sequencing (NGS) approach. miRNAs identified as differentially expressed between the two etiologies were validated by quantitative real-time polymerase chain reaction (qPCR). The receiver operating characteristic (ROC) curve analysis was performed to examine the ability of relevant miRNA to differentiate between calcification and rheumatism etiologies. Results Rheumatic and calcified AV samples were prepared for the NGS and were successfully sequenced. The expression was validated by the qPCR approach in 46 AVs, 13 rheumatic, and 33 calcified AVs, confirming that miR-145-5p, miR-199a-5p, and miR-5701 were significantly higher in rheumatic AVs as compared with calcified AVs. ROC curve analysis revealed that miR-145-5p had a sensitivity of 76.92% and a specificity of 94.12%, area under the curve (AUC) = 0.88 (P = .0001), and miR-5701 had a sensitivity of 84.62% and a specificity of 76.47%, AUC = 0.78 (P = .0001), whereas miR-199a-5p had a sensitivity of 84.62%, and a specificity of 57.58%, AUC = 0.73 (P = .0083). Conclusion We documented differential miRNA expression between AV disease etiologies. The miRNAs identified in this study advance our understanding of the mechanisms underlining AV disease.Potassium (K) cations are spontaneously formed upon thermal deposition of low-coverage K onto an ultrathin CuO monolayer grown on Cu(110) and explored by low-temperature scanning tunneling microscopy (STM) and X-ray photoemission spectroscopy. The formed K cations are highly immobile and thermally stable. The local work function around an individual K cation decreases by 1.5 ± 0.3 eV, and a charging zone underneath it establishes within ~ 1.0 nm. https://www.selleckchem.com/products/bb-94.html The cationic and neutral states of the K atom are switchable upon application of an STM bias voltage pulse, which is simultaneously accompanied by an adsorption site relocation.Although the production of extranuptial nectar is a common strategy of indirect defence against herbivores among tropical plants, the presence of extranuptial nectaries in reproductive structures is rare, especially in ant-plants. This is because the presence of ants in reproductive organs can generate conflicts between the partners, as ants can inhibit the activity of pollinators or even castrate their host plants. Here we evaluate the hypothesis that the ant-plant Miconia tococa produces nectar in its petals which attracts ants and affects fruit set. Floral buds were analysed using anatomical and histochemical techniques. The frequency and behaviour of floral visitors were recorded in field observations. Finally, an ant exclusion experiment was conducted to evaluate the effect of ant presence on fruit production. The petals of M. tococa have a secretory epidermis that produces sugary compounds. Nectar production occurred during the floral bud stage and attracted 17 species of non-obligate ants (i.e. have a facultative association with ant-plants). Ants foraged only on floral buds, and thus did not affect the activity of pollinators in the neighbouring open flowers. The presence of ants in the inflorescences increased fruit production by 15%. To our knowledge, the production of extranuptial nectar in the reproductive structures of a myrmecophyte is very rare, with few records in the literature. Although studies show conflicts between the partners in the ant-plant interaction, ants that forage on M. tococa floral buds protect the plant against floral herbivores without affecting bee pollination.Prostate cancer is the most common malignancy in urinary system and brings heavy burdens in men. We downloaded gene expression profile of mRNA and related clinical data of GSE70768 data set from public database. Weighted gene co-expression network analysis (WGCNA) was used to identify the relationships between gene modules and clinical features, as well as the candidate genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were developed to investigate the potential functions of related hub genes. Importantly, basic experiments were performed to verify the relationship between hub genes and the phenotype previously identified. Lastly, copy number variation (CNV) analysis was conducted to explore the genetical alteration. WGCNA identified that black module was the most relevant module which was tightly related to castration-resistant prostate cancer (CRPC) phenotype. KEGG and GO analysis results revealed genes in black module were mainly related to RNA splicing. Additionally, 9 genes were chosen as hub genes and heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1), golgin A8 family member B (GOLGA8B) and mitogen-activated protein kinase 8 interacting protein 3 (MAPK8IP3) were identified to be associated with PCa progression and prognosis. Moreover, all above three genes were highly expressed in CRPC-like cells and their suppression led to hindered cell proliferation in vitro. Finally, CNV analysis found that amplification was the main type of alteration of the 3 hub genes. Our study found that HNRNPA2B1, GOLGA8B and MAPK8IP3 were identified to be tightly associated with tumour progression and prognosis, and further researches are needed before clinical application.Eukaryotic initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) binds eIF4E and represses protein translation by displacing it from the mRNA. In this study, we investigated the influence of 4E-BP1 translational apparatus on the regulation of transforming growth factor-beta 1 (TGF-β1)-induced anabolic signaling in chondrocytes. The level of 4E-BP1 expression was significantly higher in human OA cartilage than normal cartilage. TGF-β1 increased total protein synthesis, including aggrecan (ACAN) and collagen type II (Col II), together with activation of Akt/mTOR signaling pathway. mTOR silencing significantly suppressed ACAN and Col II expressions through decreasing TGF-β1-induced phosphorylation of 4E-BP1. On the contrary, 4E-BP1 knockdown promoted total protein synthesis but suppressed Col II and ACAN expressions with decreased expression of Smad2/3 and Smad4 and increased expression of inhibitory Smad6 and Smad7. TGF-β1 suppressed the interaction of 4E-BP1 and eIF4E and subsequently enhanced protein synthesis.