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003). CONCLUSION The minor allele G at position rs1946518 might serve as a marker for the risk of WDEIA. Breast cancer is one of the most common tumors in women. Current data indicate that the overexpression of some microRNAs (miRNAs) is associated with breast cancer, in relation to stage, tumor size and potential for metastasis. Some studies have reported that miRNAs have critical roles in cellular processes implicated in breast cancer cell growth, migration and metastasis by targeting the PI3K/AKT oncogenic signaling pathway. Therefore, identifying novel regulatory miRNAs for this oncogenic pathway and discovery of their related target genes may represent a promising therapeutic approach for breast cancer therapy. This review highlights the recent findings about the potential role of PI3K/AKT signaling regulatory miRNAs in breast cancer tumorigenesis. V.MicroRNA390 (miR390), an ancient and highly conserved miRNA family in land plants, plays multiple roles in plant growth, development and stress responses. In this study, we isolated and identified MIR390, miR390, TAS3a/b/c, tasiARF-1/2/3 (trans-acting small interfering RNAs influencing Auxin Response Factors) and ARF2/3/4 in Jerusalem artichoke (Helianthus tuberosus L.). Treatment with 100 mM NaCl induced expression of miR390, increased cleavage of TAS3, produced high levels of tasiARFs, and subsequently enhanced cleavage of ARF3/4, which was most likely associated with salt tolerance of the plants. In contrast, treatment with 300 mM NaCl inhibited expression of miR390, attenuated cleavage of TAS3, produced a small amount of tasiARFs, and reduced cleavage of ARF3/4. We proposed that ARF2, one of the targets of tasiARFs, induced under salinity was likely to play an active role in salt tolerance of Jerusalem artichoke. The study of the miR390-TAS3-ARF model in Jerusalem artichoke may broaden our understanding of salt tolerance mechanisms, and provides a theoretical support for further genetic identification and breeding crops with increased tolerance to salt stress. Hepatocellular carcinoma (HCC) is the most common type of liver tumors. There is only one chemodrug for treatment called sorafenib that is an effective multikinase inhibitor. However, most of the patients gain resistance to sorafenib treatment in six months. Thus, there is a limitation for treatment of HCC. Apigenin is a natural flavonoid that has been used for many years as an antioxidant and anti-inflammatory agent. The aim of this study is to investigate the combined therapeutic effects of sorafenib and apigenin upon apoptosis and cell cycle on HepG2 cell line. Cytotoxic effects of sorafenib and apigenin on HepG2 cells were determined by XTT assay. Effects of single and combined treatment on cell migration, invasion and colony formation were analysed by wound healing, transwell matrigel invasion assay and colony formation assay, respectively. TUNEL assay was performed for analyse apoptosis rates. Expression changes of genes related with apoptosis and cell cycle were analysed by quantitative real-time PCR. Combined treatment of sorafenib and apigenin has more decreasing effects on cell viability than single treatment groups. selleck kinase inhibitor Also, combination group caused significant increase of apoptotic cells. Migration and invasion capability of cells in combined treatment group are decreased. Lastly, quantitative real-time PCR results showed that combination of both drugs arrested cell cycle and increased apoptotic gene expressions more than single treatment groups. This is the first study that investigating the combined treatment of sorafenib and apigenin on HCC in vitro. By combined treatment, apigenin potentiates sorafenib cytotoxicity on HepG2 cells. Effects of combined treatment on migration, invasion, apoptosis and gene expressions showed that may sorafenib and apigenin have synergistic effect. The erythroblastic island (EBI) is a multicellular structure forming an erythropoietic niche consisting of a central macrophage surrounded by a rosette of maturing erythroblasts. Since their discovery more than 60 years ago, simultaneous quantification and visualization of EBIs remain difficult. Although flow cytometry enables high-throughput quantification of cell aggregates co-expressing macrophage and erythroblast markers, it cannot visually confirm whether the aggregates are genuine EBIs. While immunofluorescence microscopy allows visualization of EBIs, its low throughput limits its use for quantification. In the current study we employed nine-channel imaging flow cytometry (IFC) to develop a method to directly visualize and quantify EBIs in the mouse bone marrow. We found that EBI central macrophages do express F4/80, VCAM-1, and CD169, but not CD11b or Ly6G, and that CD11b+Ly6G+F4/80- granulocytes are found associated at the periphery of 40%-60% EBIs. Furthermore, we show for the first time using IFC that in vivo treatment with the hematopoietic stem cell-mobilizing cytokine granulocyte colony-stimulating factor (G-CSF) reduced EBI frequency in the bone marrow by more than 100-fold. These results indicate that mobilizing doses of G-CSF cause a collapse of EBIs in the bone marrow. The gut microbiota has been recently interpreted in terms of a metabolic organ that influences the host through reciprocal interactions, encompassing metabolic and immune pathways, genetic and epigenetic programming in host mammal tissues in a diet-depended manner, that shape virtually all aspects of host physiology. In this scenario, dietary nitrate, a major component of leafy green vegetables known for their health benefits, might fuel microbiota metabolism with ensued consequences for microbiota-host interaction. Cumulating evidence support that nitrate shapes oral microbiome communities with impact on the kinetics and systemic levels of both nitrate and nitrite. However, the impact of nitrate, which is steadily delivered into the lower gastrointestinal tract after a vegetable-rich meal, in the intestinal microbiome communities and their functional capacity remains largely elusive. Several mechanisms reinforce the notion that nitrate may be a nutrient for the lower microbiome and might participate in local redox interactions with relevance for bacteria-host interactions, among these nitric oxide-dependent mechanisms along the nitrate-nitrite-nitric oxide pathway.