Oral squamous cell carcinoma (OSCC) is one of the most common malignancies worldwide. Emerging evidence has suggested that long noncoding RNAs (lncRNAs) play vital roles in various biological processes of cancers, such as cell proliferation, migration, invasion, and apoptosis. As reported previously, long intergenic non-protein coding RNA 284 (LINC00284) is an important regulator in multiple cancers.  https://www.selleckchem.com/products/pf429242.html  However, the biological role, as well as regulatory mechanism of LINC00284 in OSCC, has not been investigated. In our study, RT-qPCR results indicated that LINC00284 was significantly upregulated in OSCC tissues and cells. Moreover, loss-of-function experiments demonstrated that LINC00284 downregulation suppressed cell proliferation and migration and facilitated cell apoptosis. Mechanistically, we found that LINC00284 sponged microRNA 211-3p (miR-211-3p) to upregulate MAF bZIP transcription factor G (MAFG) expression in OSCC cells. Additionally, LINC00284 interacted with FUS protein to increase KAZN mRNA stability. Functional assays showed that either MAFG or KAZN overexpression promoted the malignant behaviors of OSCC cells. Through a series of rescue assays, we found that the inhibitory effect of silencing LINC00284 on OSCC cells can be reversed by upregulated MAFG and KAZN. Overall, silencing LINC00284 inhibits the malignant characteristics of OSCC cells by downregulating MAFG and inhibiting the binding of FUS to KAZN mRNA.Human innate cellular defence pathways have evolved to sense and eliminate pathogens, of which, viruses are considered one of the most dangerous. Their relatively simple structure makes the identification of viral invasion a difficult task for cells. In the course of evolution, viral nucleic acids have become one of the strongest and most reliable early identifiers of infection. When considering RNA virus recognition, RNA sensing is the central mechanism in human innate immunity, and effectiveness of this sensing is crucial for triggering an appropriate antiviral response. Although human cells are armed with a variety of highly specialized receptors designed to respond only to pathogenic viral RNA, RNA viruses have developed an array of mechanisms to avoid being recognized by human interferon-mediated cellular defence systems. The repertoire of viral evasion strategies is extremely wide, ranging from masking pathogenic RNA through end modification, to utilizing sophisticated techniques to deceive host cellular RNA degrading enzymes, and hijacking the most basic metabolic pathways in host cells. In this review, we aim to dissect human RNA sensing mechanisms crucial for antiviral immune defences, as well as the strategies adopted by RNA viruses to avoid detection and degradation by host cells. We believe that understanding the fate of viral RNA upon infection, and detailing the molecular mechanisms behind virus-host interactions, may be helpful for developing more effective antiviral strategies; which are urgently needed to prevent the far-reaching consequences of widespread, highly pathogenic viral infections.Inappropriate antimicrobial use is a key problem causing antimicrobial resistance and increased health care costs. Although global point prevalence surveys on antimicrobial prescribing in hospitals were described, there is lack of data from Turkish hospitals. Here, we aimed to perform systematic review and meta-analysis for the point prevalence surveys on antimicrobial prescribing in Turkish hospitals. The Preferred Reporting Items for Systematic reviews and Meta-Analyses guideline was used to identify studies for the review. Articles published between January 2004 and September 2020 by Turkish investigators were included if they used the point prevalence survey method. The Joanna Briggs Institute's critical appraisal tool and the World Health Organization's point prevalence survey tool were used to the evaluate studies. Results were combined using random effects meta-analysis. The pooled point prevalence of antimicrobial use in Turkish hospitals was 48% (95% confidence interval 43-54). There was considerable heterogeneity in prevalence among the studies (I2= 98.75 %, 95 % CI 98.49-98-97). The most commonly prescribed antimicrobial and indication for antimicrobial use were third generation cephalosporins (36%) and respiratory tract infections (88%), respectively. More than two thirds of the antimicrobials were prescribed empirically (median 71% [interquartile range 56-80]) in hospitals. The point prevalence and inappropriateness of antimicrobial use are high in Turkish hospitals. Turkey is one of the biggest consumers of antimicrobials. There is an urgent need for antimicrobial stewardship programmes at Turkish hospitals to improve antimicrobial prescribing. Our study findings can contribute to improving antimicrobial prescribing, and thereby control antimicrobial resistance.Hereditary spastic paraplegia (HSP) denotes genetically heterogeneous disorders characterized by leg spasticity due to degeneration of corticospinal axons. SPG11 and SPG15 have a similar clinical course and together are the most prevalent autosomal recessive HSP entity. The respective proteins play a role for macroautophagy/autophagy and autophagic lysosome reformation (ALR). Here, we report that spg11 and zfyve26 KO mice developed motor impairments within the same course of time. This correlated with enhanced accumulation of autofluorescent material in neurons and progressive neuron loss. In agreement with defective ALR, tubulation events were diminished in starved KO mouse embryonic fibroblasts (MEFs) and lysosomes decreased in neurons of KO brain sections. Confirming that both proteins act in the same molecular pathway, the pathologies were not aggravated upon simultaneous disruption of both. We further show that PI4K2A (phosphatidylinositol 4-kinase type 2 alpha), which phosphorylates phosphatidylinositoltein; HSP hereditary spastic paraplegia; KO knockout; LAMP1 lysosomal-associated membrane protein 1; MAP1LC3B/LC3 microtubule-associated protein 1 light chain 3 beta; MEF mouse embryonic fibroblast; SQSTM1/p62 sequestosome 1; PI4K2A phosphatidylinositol 4-kinase type 2 alpha; PtdIns3P phosphatidylinositol-3-phosphate; PtdIns4P phosphatidylinositol-4-phosphate; RFP red fluorescent protein; SPG spastic paraplegia gene; TGN trans-Golgi network; WT wild type.