Notes

Drugs repurposed with regard to COVID-19 by electronic screening process of 6,218 medicines and also cell-based assay.
Lung cancer leads to the highest mortality among all cancer types in the world, and non-small-cell lung cancer (NSCLC) occupies over 80% of the lung cancer cases. Numerous studies have demonstrated that long non-coding RNA (lncRNA) is involved in various human diseases including cancer. LncRNA FTX was firstly identified in Xist gene locus and was dysregulated in many human cancers. read more However, the function of FTX in NSCLC is still unclear. Here, we report that long non-coding RNA FTX expression level is down-regulated in NSCLC clinical tissue samples and cell lines. Ectopic expression of FTX inhibits proliferation and metastasis of lung cancer cells in vitro and in vivo. Furthermore, we find that FTX overexpression activates the expression of transcription factor FOXA2, an important regulator in lung cancer progression, and we reveal a novel FTX/miR-200a-3p/FOXA2 competing endogenous RNA regulatory axis in lung cancer cells. Our results provide new insights and directions for exploring the function of FTX in lung cancer progression. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.Nucleic acid tests have been widely used for diagnosis of diseases by detecting the relevant genetic markers that are usually amplified using polymerase chain reaction (PCR). This work reports the use of a plasmonic device as an efficient and low-cost PCR thermocycler to facilitate nucleic acid-based diagnosis. The thermoplasmonic device, consisting of a one-dimensional metal grating, exploited the strong light absorption of plasmonic resonance modes to heat up PCR reagents using a near-infrared laser source. The plasmonic device also integrated a thin-film thermocouple on the metal grating to monitor the sample temperature. The plasmonic thermocycler is capable of performing a PCR amplification cycle in ~2.5 minutes. We successfully demonstrated the multiplex and real-time PCR amplifications of the antibiotic resistance genes using the genomic DNAs extracted from Acinetobacter baumannii, Klebsiella pneumonia, Escherichia coli and Campylobacter. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Cytokines produced by immune cells have been demonstrated to act on muscle stem cells (MuSCs) and direct their fate and behavior during muscle repair and regeneration. Nevertheless, it is unclear whether and how MuSCs can also in turn modulate the properties of immune cells. Here, we showed that in vitro expanded MuSCs exhibited a potent anti-inflammatory effect when infused into mice suffering from inflammatory bowel disease (IBD). Supernatant conditioned by MuSCs similarly ameliorated IBD. This beneficial effect of MuSCs was not observed when macrophages were depleted. The MuSC supernatant was found to greatly attenuate the expression of inflammatory cytokines but increase the expression of programmed death-ligand 1 in macrophages treated with lipopolysaccharide and interferon gamma. Further analysis revealed that MuSCs produce a large amount of insulin-like growth factor-2 (IGF-2) that instructs maturing macrophages to undergo oxidative phosphorylation and thus acquire anti-inflammatory properties. Interestingly, the IGF-2 production by MuSCs is much higher than by mesenchymal stem cells. Knockdown or neutralization of IGF-2 abrogated the anti-inflammatory effects of MuSCs and their therapeutic efficacy on IBD. Our study demonstrated that MuSCs possess a strong anti-inflammatory property and the bidirectional interactions between immune cells and MuSCs have important implications in muscle-related physiological and pathological conditions. © 2020 The Authors. STEM CELLS TRANSLATIONAL MEDICINE published by Wiley Periodicals, Inc. on behalf of AlphaMed Press.Acetylcholine (ACh) has been reported to play various physiological roles, including wound healing in the cornea. Here, we study the role of ACh in the transition of corneal fibroblasts into myofibroblasts, and in consequence its role in the onset of fibrosis, in an in vitro human corneal fibrosis model. Primary human keratocytes were obtained from healthy corneas. Vitamin C (VitC) and transforming growth factor-β1 (TGF-β1) were used to induce fibrosis in corneal fibroblasts. qRT-PCR and ELISA analyses showed that gene expression and production of collagen I, collagen III, collagen V, lumican, fibronectin (FN) and alpha-smooth muscle actin (α-SMA) were reduced by ACh in quiescent keratocytes. ACh treatment furthermore decreased gene expression and production of collagen I, collagen III, collagen V, lumican, FN and α-SMA during the transition of corneal fibroblasts into myofibroblasts, after induction of fibrotic process. ACh inhibited corneal fibroblasts from developing contractile activity during the process of fibrosis, as assessed with collagen gel contraction assay. Moreover, the effect of ACh was dependent on activation of muscarinic ACh receptors. These results show that ACh has an anti-fibrotic effect in an in vitro human corneal fibrosis model, as it negatively affects the transition of corneal fibroblasts into myofibroblasts. Therefore, ACh might play a role in the onset of fibrosis in the corneal stroma. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.Mitochondria are essential organelles involved in energy supply and calcium homeostasis. The regulated distribution of mitochondria in polarized cells, particularly neurons, is thought to be essential to these roles. Altered mitochondrial function and impairment of mitochondrial distribution and dynamics is implicated in a number of neurologic disorders. Several recent reports have described mechanisms regulating the activity-dependent distribution of mitochondria within astrocyte processes and the functional consequences of altered mitochondrial transport. Here we provide an ex vivo method for monitoring the transport of mitochondria within the processes of astrocytes using organotypic "slice" cultures. These methods can be easily adapted to investigate a wide range of mitochondrial behaviors, including fission and fusion dynamics, mitophagy, and calcium signaling in astrocytes and other cell types of the central nervous system. © 2020 by John Wiley & Sons, Inc. Basic Protocol 1 Preparation of brain slices Basic Protocol 2 Preparation of gene gun bullets Basic Protocol 3 Gene gun transfection of slices Basic Protocol 4 Visualization and tracking of mitochondrial movement Alternate Protocol Transduction of EGFP-mito via viral injection of the neonatal mouse brain.
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