Water-soluble cupric oxide nanoparticles are fabricated via a quick-precipitation method and used as peroxidase mimetics for ultrasensitive detection of hydrogen peroxide and glucose. The water-soluble CuO nanoparticles show much higher catalytic activity than that of commercial CuO nanoparticles due to their higher affinity to hydrogen peroxide. In addition, the as-prepared CuO nanoparticles are stable over a wide range of pH and temperature. This excellent stability in the form of aqueous colloidal suspensions makes the application of the water-soluble CuO nanoparticles easier in aqueous systems. A colorimetric assay for hydrogen peroxide and glucose has been established based on the catalytic oxidation of phenol coupled with 4-amino-atipyrine by the action of hydrogen peroxide. This analytical platform not only confirms the intrinsic peroxidase-like activity of the water-soluble cupric oxide nanoparticles, but also shows its great potential applications in environmental chemistry, biotechnology and medicine.

Multiple studies demonstrated that early growth response factor 1 (EGR1) induces myocardial damage after acute myocardial infarction (AMI). Recent evidence indicates that microRNAs (miRNA) play an important role in exosome-mediated cardioprotection after AMI. Bioinformatics analysis has shown that miR-146a can regulate the expression of EGR1, so the aim of this study was to determine if miR-146a plays a role in exosome-mediated cardioprotection by regulation of EGR1 after AMI. Exosomes were isolated from wild-or miR-146a-modified adipose-derived stem cells (ADSCs), and the therapeutic effect of exosomes was assessed in an AMI model in rats and hypoxic-induced H9c2 model cells. The results showed that miR-146a containing exosomes had more effect than the exosome treatment group on the suppression of AMI-induced apoptosis, inflammatory response, and fibrosis in an AMI rat model. Both in vivo and in vitro experiments found that miR-146a interacted with the 3′-untranslated region of EGR1 and suppressed posttranscriptional EGR1 expression, which was confirmed by the luciferase reporter assay. We also found that suppressed EGR1 expression reversed AMI or hypoxia-induced TLR4/NFκB signal activation, which played an important role in the promotion of myocardial cell apoptosis, inflammatory response, and fibrosis. Taken together, these findings suggested that exosomes derived from miR-146a-modified ADSCs attenuated AMI-induced myocardial damage via downregulation of EGR1. K E Y W O R D Sacute myocardial infarction (AMI), adipose-derived stem cells (ADSCs), early growth response factor 1 (EGR1), exosomes, miR-146a

Myeloid differentiation primary response protein 88 (MyD88), which can be induced by alpha interferon (IFN-␣), has an antiviral activity against the hepatitis B virus (HBV). The mechanism of this antiviral activity remains poorly understood. Here, we report that MyD88 inhibited HBV replication in HepG2.2.15 cells and in a mouse model. The knockdown of MyD88 expression weakened the IFN-␣-induced inhibition of HBV replication. Furthermore, MyD88 posttranscriptionally reduced the levels of viral RNA. Remarkably, MyD88 accelerated the decay of viral pregenomic RNA in the cytoplasm. Mapping analysis showed that the RNA sequence located in the 5-proximal region of the pregenomic RNA was critical for the decay. In addition, MyD88 inhibited the nuclear export of pre-S/S RNAs via the posttranscriptional regulatory element (PRE). The retained pre-S/S RNAs were shown to degrade in the nucleus. Finally, we found that MyD88 inhibited the expression of polypyrimidine tract-binding protein (PTB), a key nuclear export factor for PRE-containing RNA. Taken together, our results define a novel antiviral mechanism against HBV mediated by MyD88.Hepatitis B virus (HBV) is a noncytopathic, enveloped virus with a circular, double-stranded DNA genome. It causes both acute and chronic infection of the human liver. Although a highly effective preventive vaccine is now available, HBV infection remains a major health problem worldwide. It is estimated that chronic HBV infection affects 350 to 400 million people globally, about a quarter of whom will eventually develop severe liver diseases, including liver cirrhosis, liver failure, and hepatocellular carcinoma (HCC) (4).Current antiviral therapies involve the use of nucleoside analogs and alpha interferon (IFN-␣) (28). IFN-␣, a type I interferon, engages the IFN-␣ receptor complex to activate the Jak/Stat pathway and trigger the transcription of a diverse set of genes, referred to as IFN-stimulated genes (ISGs) (2, 40). In total, the gene products of ISGs establish an antiviral response in target cells (2, 40). IFN-␣ inhibits HBV replication through a variety of mechanisms. It was reported previously that IFN-␣ can suppress viral gene expression, prevent the formation of viral RNA-containing core particles, and reduce the accumulation of viral replicative intermediates (11,35,37,(46)(47)(48). Importantly, the precise antiviral mechanism of IFN-␣ and the biological functions of many ISGs have not been fully elucidated.Myeloid differentiation primary response protein 88 (MyD88) is a key adaptor in the signaling cascade of the innate immune response (22). We and others have shown that MyD88 expression can be induced by IFN-␣ and that MyD88 has an antiviral activity against HBV in hepatoma cells that is mediated by nuclear factor B (NF-B) activation (12, 25, 51, 52). To counteract its inhibition, the HBV polymerase dampens the activation of the MyD88 promoter by blocking the nuclear translocation of Stat1, thereby reducing IFN-␣-inducible MyD88 expression (50), further suggesting a critical rol...

A multiplexed fiber Bragg grating sensor for simultaneous salinity and temperature measurement

No abstract

Purpose: This study aimed to describe the use of a novel 4-lncRNA signature to predict prognosis in patients with laryngeal cancer and to explore its possible mechanisms. Methods: We identified lncRNAs that were differentially expressed between 111 tumor tissue samples and 12 matched normal tissue samples from The Cancer Genome Atlas Database (TCGA). We used Cox regression analysis to identify lncRNAs that were correlated with prognosis. A 4-lncRNA signature was developed to predict the prognosis of patients with laryngeal cancer. The receiver operating characteristic (ROC) curves and area under the curve (AUC) were used to verify the validity of this Cox regression model, and an independent prognosis analysis was used to confirm that the 4-lncRNA signature was an independent prognostic factor. Furthermore, the function of these lncRNAs was inferred using related gene prediction and Gene ontology (GO) enrichment analysis in order to clarify the possible mechanisms underlying their predictive ability. Results: In total, 214 differentially expressed lncRNAs were identified, and a 4-lncRNA signature was constructed using Cox survival analysis. The risk coefficients in the multivariate Cox analysis revealed that LINC02154 and MNX1-AS1 are risk factors for laryngeal cancer, whereas MYHAS and LINC01281 appear to be protective factors. The results of a functional annotation analysis suggested that the mechanisms by which these lncRNAs influence prognosis in laryngeal cancer may involve the extracellular exosome, the Notch signaling pathway, voltage-gated calcium channels, and the Wnt signaling pathway. Conclusion: We identified a novel 4-lncRNA signature that can predict the prognosis of patients with laryngeal cancer and that may influence the prognosis of laryngeal cancer by regulating immunity, tumor apoptosis, metastasis, invasion, and other characteristics through the Notch signaling pathway, voltage-gated calcium channels, and the Wnt signaling pathway.

Mitochondrial dynamic imbalance associates with several cardiovascular diseases. However, the role of mitochondrial dynamics in TLR4 activation-mediated dilated cardiomyopathy (DCM) progress remains unknown. A model of experimental autoimmune myocarditis (EAM) was established in BALB/c mice on which TLR4 activation by LPS-EB or TLR4 inhibition by LPS-RS was performed to induce chronic inflammation for 5 weeks. TLR4 activation promoted the transition of EAM to DCM as demonstrated by increased cardiomyocyte apoptosis, myocardial fibrosis, ventricular dilatation, and declined heart function. TLR4 inhibition mitigated the above DCM changes. Transmission electron microscope study showed that mitochondria became fragmented, also with damaged crista in ultrastructure in EAM mice. TLR4 activation aggravated the above mitochondrial aberration, and TLR4 inhibition alleviated it. The mitochondrial dynamic imbalance and damage in DCM development were mainly associated with OPA1 downregulation, which may be caused by elevated TNF-α level and ROS stress after TLR4 activation. Furthermore, OMA1/YME1L abnormal degradation was involved in the OPA1 dysfunction, and intervening OMA1/YME1L in H9C2 significantly alleviated mitochondrial fission, ultrastructure damage, and cell apoptosis induced by TNF-α and ROS. These data indicate that TLR4 activation resulted in OPA1 dysfunction, promoting mitochondrial dynamic imbalance and damage, which may involve in the progress of EAM to DCM.

A significantly enhanced, ultrafast third-order optical nonlinearity at the wavelengths of 1150-1600 nm was demonstrated with cross-linked C60-containing polyurethane films using the Z-scan technique. Good-quality polymer films with a high loading of C60 derivative were obtained by cross-linking of the hydroxyl-containing C60 derivative and a triisocyanate. The positive Kerr coefficient with nonresonant nonlinear refractive index n2 falls in the range of (3.7 +/- 0.80) x 10-4 to (2.0 +/- 0.6) x 10-3 cm2/GW, and the calculated chi(3) and gamma values are up to 9.7 x 10-11 and 9.6 x 10-32 esu at 1550 nm, which are several orders of enhancement in third-order optical nonlinearity over pristine C60 in solution and 1-2 orders of enhancement over recently reported C60 derivatives and conjugated polymers.