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We have been trying to find a miRNA that can specifically regulate the function of mycobacterial host cells to achieve the purpose of eliminating Mycobacterium tuberculosis. The purpose of this study is to investigate the regulation of mmu-let-7a-5p on macrophages apoptosis and its effect on intracellular BCG clearance. After a series of in vitro experiments, we found that mmu-let-7a-5p could negatively regulate the apoptosis of macrophages by targeting Caspase-3. The extrinsic apoptosis signal axis TNFR1/FADD/Caspase-8/Caspase-3 was inhibited after BCG infection. Up-regulated the expression level of mmu-let-7a-5p increase the cell proliferation viability and inhibit apoptosis rate of macrophages, but down-regulated its level could apparently reduce the bacterial load of intracellular Mycobacteria and accelerate the clearance of residual Mycobacteria effectively. Mmu-let-7a-5p has great potential to be utilized as an optimal candidate exosomal loaded miRNA for anti-tuberculosis immunotherapy in our subsequent research. [ABSTRACT FROM AUTHOR]

[Purpose / significance] China Asset Management Co., Ltd. (ChinaAMC) is one of the leading enterprises in the public fund industry. Guided by the innovative knowledge management concept and based on the advanced system technology, it fully collects all kinds of knowledge generated in the operation process of the company and applies it to customer service, operation management, investment operation and other businesses. It drives production with knowledge and creates value for customers, employees, shareholders and even the society Value. [Method / process]Taking customer service as an example, this paper introduced in detail the establishment of service knowledge system, system evolution, research and development of intelligent application in the past 12 years. [Result / conclusion] While explaining the construction and application of intelligent services, this paper expands to other knowledge applications from childhood, and provides reference solutions to some common problems in the development of enterprises.

Background: microRNA 21 (miR-21) has been demonstrated to be significantly elevated in many types of cancers, including the hepatocellular carcinoma (HCC). In the present study, we investigated the role of miR-21 in HCC by identifying its novel targets, as well as its underlying molecular mechanism.Methods: The expression of mitogen-activated protein kinase-kinase 3 (MAP2K3) in human HCC tumor tissues and adjacent non-tumor tissues was determined by immunohistochemistry staining (IHC) analysis. The 3'-untranslated region (3'-UTR) of MAP2K3 combined with miR-21 was experimentally verified by a miRNA luciferase reporter approach. Moreover, the role of miR-21 in regulating HCC cell proliferation was analyzed by an MTT assay infected with miR-21mimics/sponge inhibitor Adenoviral viral vectors.Results: By immunohistochemistry staining analysis, we found that mitogen-activated protein kinase-kinase 3 (MAP2K3) was strikingly repressed in the human HCC tumor tissues, in comparison with the adjacent non-tumor tissues in clinical settings. More importantly, the repression of MAP2K3 was inversely correlated with the expression of miR-21 in HCC. Further study demonstrated that the MAP2K3 was a novel direct target of miR-21, which was experimentally validated by a miRNA luciferase reporter approach. In HepG2 cells, inhibition of miR-21 expression with an adenoviral miR-21 sponge vector profoundly suppressed cell proliferation by up-regulating MAP2K3 expression at both mRNA and protein levels.Conclusions: These results provide a clinical evidence that MAP2K3 may be a tumor repressor gene, and it is a direct target of miR-21 in HCC, indicating an underlying mechanism by which miR-21 is able to directly target MAP2K3 and inhibit its expression during the carcinogenesis of HCC, at both transcriptional and post-translational levels. This study also suggests that targeting miR-21-MAP2K3 pathway may be a promising strategy in the prevention and treatment of HCC. [ABSTRACT FROM AUTHOR]

Pharmacokinetic characters of rhynchophylline (RIN), gastrodin (GAS), and gastrodigenin (p-hydroxybenzyl alcohol, HBA) were investigated after oral administration of different prescriptions of Yizhi: Yizhi tablets or effective parts of tianma (total saponins from Gastrodiae, EPT) and gouteng (rhynchophylla alkaloids, EPG). At different predetermined time points after administration, the concentrations of GAS, HBA, and RIN in rat plasma were determined by an HPLC-ESI/MS method, and the main pharmacokinetic parameters were investigated. The results showed that the pharmacokinetic parameters C max and AUC0-∞ (P < 0.05) were dramatically different after oral administration of different prescriptions of Yizhi. The data indicated that the pharmacokinetic processes of GAS, HBA, and RIN in rats would interact with each other or be affected by other components in Yizhi. The rationality of the compatibility of Uncaria and Gastrodia elata as a classic "herb pair" has been verified from the pharmacokinetic viewpoint.

A new thin layer plate, the RP-C18 sintered plate, is described. The electroosmotic flow can be produced without any buffer salts by the carefully controlled bonding degree. It is very convenient and saves a lot of time. Some new development modes and skills can be derived. Based on the firmness of the new plate the operator can brush the mobile phase on the plate directly, which is very simple and fast for wetting the plate and saves much reagent. If the plate becomes dry during the process of planar electrochromatography, the operator can re-wet the plate on the local and then develop it again. Such operation can be repeated many times until the spots are separated completely, so it is called multiple-electro-development. The buffer salt in the mobile phase is abolished, which makes the process of multiple-electro-development possible. As the bonding degree descends, the effect of the plate is not as good as before, but the total separation efficiency and the potential increase due to the multiple-electro-development.