MicroRNAs (miRNAs) have been shown to be important regulators of TLR signaling pathway at the post-transcriptional level. In this study, the potential role of miR-149 was explored in murine alveolar macrophage RAW264.7 cells. Our results demonstrated a dynamic change of the expressions of miR-149 expression and MyD88 in macrophage RAW264.7 upon Mycobacterium bovis Bacillus Calmette-Guerlin (BCG) infection or lipopolysaccharide (LPS) stimulation. The presence of BCG or LPS dynamically reduced the miR-149 expression, along with a substantially striking increase of MyD88 expression in these cells. More importantly, overexpression of miR-149 in RAW264.7 cells was associated with a significant decrease of MyD88 protein expression, as well as a reduced production of inflammatory mediator NF-κB 1, TNF-α and IL-6 in response to BCG infection or LPS stimulation. Further studies using immunoblotting assay against anti-MyD88 antibody and microRNA targeting luciferase reporter assay revealed that miR-149 was able to directly target the 3'-UTR of MyD88 mRNA and post-transcriptionally regulated MyD88 protein expression. These data suggested that miR-149 might be a key player of immune modulator for TLR/MyD88 signaling pathway in macrophages, which may through a mechanism of negatively regulating MyD88-dependent Toll-like receptors signaling pathway.

The COVID-19 pandemic is increasing the need for personal protective equipment (PPE) worldwide, including the demand for facial masks used by healthcare workers. Disinfecting and reusing these masks may offer benefits in the short term to meet urgent demand. Germicidal ultraviolet light provides a nonchemical, easily deployable technology capable of achieving inactivation of H1N1 virus on masks. Working with N95-rated masks and nonrated surgical masks, we demonstrated that neither 254 nor 265 nm UV-C irradiation at 1 and 10 J/cm 2 had adverse effects on the masks' ability to remove aerosolized virus-sized particles. Additional testing showed no change in polymer structure, morphology, or surface hydrophobicity for multiple layers in the masks and no change in pressure drop or tensile strength of the mask materials. Results were similar when applying 254 nm low-pressure UV lamps and 265 nm lightemitting diodes. On the basis of the input from healthcare workers and our findings, a treatment system and operational manual were prepared to enable treatment and reuse of N95 facial masks. Knowledge gained during this study can inform techno-economic analyses for treating and reusing masks or lifecycle assessments of options to reduce the enormous waste production of single-use PPE used in the healthcare system, especially during pandemics.

BackgroundmicroRNA 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.MethodsThe 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.ResultsBy 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.ConclusionsThese 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.

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Functional fault diagnosis at board-level is desirable for high-volume production since it improves product yield. However, to ensure diagnosis accuracy and effective board repair, a large number of syndromes must be used. Therefore, the diagnosis cost can be prohibitively high due to the increase in diagnosis time and the complexity of syndrome collection/analysis. We propose an adaptive diagnosis method based on decision trees (DTs). Faulty components are classified according to the discriminative ability of the syndromes in DT training. The diagnosis procedure is constructed as a binary tree, with the most discriminative syndrome as the root and final repair suggestions are available as the leaf nodes of the tree. The syndrome to be collected in the next step is determined based on the observations of syndromes collected thus far in the diagnosis procedure. The number of syndromes required for diagnosis can also be significantly reduced compared to the number of syndromes used for system training. Diagnosis results for two complex boards from industry, currently in volume production, and additional synthetic data highlight the effectiveness of the proposed approach.

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Mangiferin is a xanthone glucoside, which possesses antioxidant, antiviral, antitumor and anti-inflammatory functions, and is associated with gene regulation. However, it remains unknown whether mangiferin protects osteoblasts, such as the MC3T3-E1 cell line, against glucocorticoid-induced damage. In the present study, MC3T3-E1 cells were treated with dexamethasone (Dex), which is a well-known synthetic glucocorticoid, in order to establish a glucocorticoid-induced cell injury model. After Dex and/or mangiferin treatment, cell viability, apoptosis and reactive oxygen species (ROS) production was measured by Cell Counting kit-8 (CCK-8) and flow cytometry, respectively, and the concentration of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and macrophage colony-stimulating factor (M-CSF) was measured by ELISA. The expression of bone morphogenetic protein 2 (BMP2), phosphorylated-SMAD family member 1 (p-Smad-1), t-Smad-1, osterix (OSX), osteocalcin (OCN), osteoprotegerin (OPG), receptor activator of nuclear factor-κB (RANK), RANK ligand (RANKL), B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) was measured by real-time PCR and/or western blot analysis. The results indicated that pretreatment of MC3T3-E1 cells with mangiferin for 3 h prior to exposure to Dex for 48 h significantly attenuated Dex-induced injury and inflammation, as demonstrated by increased cell viability, and decreases in apoptosis, ROS generation, and the secretion of TNF-α, IL-6 and M-CSF. In addition, pretreatment with mangiferin markedly reduced Dex-induced BMP2 and p-Smad-1 downregulation, and corrected the expression of differentiation- and apoptosis-associated markers, including alkaline phosphatase, OSX, OCN, OPG, RANK, RANKL, Bcl-2 and Bax, which were altered by Dex treatment. Similar to the protective effects of mangiferin, overexpression of BMP2 suppressed not only Dex-induced cytotoxicity, but also ROS generation, and the secretion of TNF-α, IL-6 and M-CSF. In conclusion, the results of the present study are the first, to the best of our knowledge, to demonstrate that mangiferin protects MC3T3-E1 cells against Dex-induced apoptosis and oxidative stress by activating the BMP2/Smad-1 signaling pathway.