Without effective medical interventions for complete reverse of NAFLD, it needs to urgently explore the underlying molecular mechanisms of non-alcoholic fatty liver disease (NAFLD) to offer a novel therapeutic strategy for people suffering from NAFLD. Sprague-Dawley (SD) rats were used to establish the NAFLD animal model. Lipofectamine 2000 was used to silence or over-express NEAT1. The expression of NEAT1 and the mRNA levels of ACC and FAS were determined by qRT-PCR. Western blot assays were performed to detect the expression of ACC and FAS at protein levels and the related protein levels of mTOR/S6K1 signaling pathway. The levels of liver triglyceride (TG), serum total cholesterol (TC), ALT, and AST were assessed by an automatic biochemistry analyzer. The levels of liver TG and serum cholesterol were obviously up-regulated in NAFLD rat model. The level of NEAT1 expression and the mRNA levels of ACC and FAS were obviously enhanced in NAFLD model both in vivo and in vitro. Knockdown of NEAT1 could also reduce the elevation of ACC and FAS induced by FFA in liver cells. Moreover, inhibition of mTOR/S6K1 pathway presented with the same effect with knockdown of NEAT1 on the expression of ACC and FAS mRNA levels. The injection of si-NEAT1 lentivirus was performed to treat NAFLD of rats and the obvious efficacy for NAFLD rats was achieved. In a word, the down-regulated level of NEAT1 could remit the non-alcoholic fatty liver disease through mTOR/S6K1 signaling pathway in rats.
Background: Since December 2019, a new strain of coronavirus named 2019 novel coronavirus (2019-nCoV) has been discovered in Wuhan. The prevalence of diabetes mellitus, which is a great public health issue leading to immunity inhibition and an increased incidence of infections, has been increasing over the past ten years. The aim of this research was to systematically assess the prevalence of diabetes mellitus among 2019-nCoV. Methods: We searched PubMed, Embase, Web of Science and Medline for observational studies up to February 25, 2020. A random effects model or fixed-effects model was applied to evaluate the pooled prevalence of diabetes mellitus and odds ratio (OR) with 95% confidence interval (CI). Findings: In total, nine papers met the eligibility criteria. The pooled prevalence of DM was 9% (95% CI 6%-12%). There was obvious heterogeneity (I 2 65%, p = 0.004) in the prevalence of DM in these studies. The prevalence of DM in moderate patients with 2019-nCoV was 7% (95% CI 4%-10%). The prevalence of DM in severe patients with 2019-nCoV was 17% (95% CI 13%-21%). The prevalence of DM in severe patients with 2019-nCoV was significantly higher than that in moderate patients with 2019-nCoV (OR 2.49, 95% CI 1.70 to 3.64).
Recently emerging SARS-CoV-2 virus has caused a global pandemic, with millions of infections and over 200, 000 deaths1. However, development of effective anti-coronavirus treatments has lagged behind. Competitive co-evolution between microbes and viruses has led to the diversification of microbe’s CRISPR/Cas defense systems against infectious viruses2,3. Among class-2 single effector systems, Cas13 is effective in combating RNA phages4. Previous studies have discovered novel Cas9 and Cas12 systems from metagenomic sequence of natural microbes5-7. Here we report the identification of two additional compact Cas13 families from natural microbes that are effective in degrading RNA viruses in mammalian cells. Using metagenomic terabase data sets, we searched for previously uncharacterized Cas13 genes proximal to the CRISPR array with a customized computational pipeline, and identified two most compact families (775 to 803 amino acids) of CRISPR-Cas ribonucleases, named hereafter as CRISPR/Cas type VI-E and VI-F. Out of seven Cas13 proteins, we found that Cas13e.1 was the smallest and could be engineered for efficient RNA interference and base editing in cultured mammalian cell lines. Moreover, Cas13e.1 has a high activity for degrading SARS-CoV-2 sequences and the genome of live influenza A virus (IAV). Together with a minimal pool of 10 crRNAs, Cas13e.1 could target over 99% of all known 3,137 coronavirus genomes for achieving antiviral defense. Overall, our results demonstrated there exist untapped bacterial defense systems in natural microbes that can function efficiently in mammalian cells, thus potentially useful for preventing viral infection in humans such as COVID-19.
This study was carried out to investigate the effects of mild heat, lactic acid, benzalkonium chloride and nisin treatments on the inactivation, sublethal injury, and subsequent growth of Listeria monocytogenes. Results showed that the Bigelow model successfully described the thermal inactivation kinetics, while the Log-linear model with tail consistently offered the most accurate fit to LA, BC, and nisin inactivation curves of cells. Differential plating indicated that percentage of sublethal injury for nisin treated cells was significantly higher than that for the other three treatments. Compared to non-treated cells, significant extension of lag time was observed for all treated cells. The longer exposures to heat treatment contributed to the extended lag time of the survivors. While for LA, BC and nisin treated cells, the longest lag time was not observed at the most severe treatment conditions. The correlation analysis of sublethal injury percentage on the duration of lag time revealed that only heat treatment showed the significant correlation. Overall, the lag time analysis could evaluate a wide range of bacterial injury. Lag time of treated cells was significantly influenced by stress treatments and temperatures of recovery, however, there were not any significant changes in the maximum specific growth rate between treated and non-treated cells under isothermal recovery conditions. The information generated from this study is valuable for utilizing intervention strategies in the elimination or growth inhibition of L. monocytogenes.
SARS-CoV-2 has challenged global healthcare systems in part because its clinical manifestations are heterogeneous. Variable symptoms of SARS-CoV-2 could be attributed to the virus’ ability to mildly induce an innate immune response, as prior transcriptomic data has suggested. Mitochondrial dynamics might partially mediate the effect of SARS-CoV-2 on innate immunity. Many proteins encoded by SARS-CoV have been shown to localize to mitochondria and inhibit Mitochondrial Antiviral Signaling protein (MAVS). We analyzed multiple publicly available RNASeq data in order to unravel the metabolic and mitochondrial transcriptome signature of SARS-CoV-2 in primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report here that SARS-CoV-2 does not dramatically regulate (1) mitochondrial-gene expression or (2) MAVS expression, but (3) downregulates nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex 1 assembly. We also report cell-specific and tissue-specific effects of SARS-CoV-2 on the mitochondrial-encoded and NEM transcriptome that could inform future experimental paradigm selection.
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