Enhanced oxidation resistance of active nanostructures via dynamic size effect.

A major challenge limiting the practical applications of nanomaterials is that the activities of nanostructures (NSs) increase with reduced size, often sacrificing their stability in the chemical environment. Under oxidative conditions, NSs with smaller sizes and higher defect densities are commonly expected to oxidize more easily, since high-concentration defects can facilitate oxidation by enhancing the reactivity with O2 and providing a fast channel for oxygen incorporation. Here, using FeO NSs as an example, we show to the contrary, that reducing the size of active NSs can drastically increase their oxidation resistance. A maximum oxidation resistance is found for FeO NSs with dimensions below 3.2 nm. Rather than being determined by the structure or electronic properties of active sites, the enhanced oxidation resistance originates from the size-dependent structural dynamics of FeO NSs in O2. We find this dynamic size effect to govern the chemical properties of active NSs

Orientin Ameliorates LPS-Induced Inflammatory Responses through the Inhibitory of the NF- κ

Inflammation is a complex response to diverse pathological conditions, resulting in negative rather than protective effects when uncontrolled. Orientin (Ori), a flavonoid component isolated from natural plants, possesses abundant properties. Thus, we aimed to discover the potential therapeutic effects of orientin on lipopolysaccharide- (LPS-) induced inflammation in RAW 264.7 cells and the underlying mechanisms. In our studies, we evaluated the effects of Ori on proinflammatory mediator production stimulated by LPS, including tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, IL-18, and IL-1β, along with prostaglandin E2 (PGE2) and NO. Our data indicated that orientin dramatically inhibited the levels of these mediators. Consistent with these results, the expression levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were also reduced. Further study demonstrated that such inhibitory effects of Ori were due to suppression of the nuclear factor-kappa B (NF-κB) pathway and nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3) inflammasome activation, which may contribute to its anti-inflammatory effects. Together, these findings show that Ori may be an effective candidate for ameliorating LPS-induced inflammatory responses

Identification of TRIM14 as a Type I IFN-Stimulated Gene Controlling Hepatitis B Virus Replication by Targeting HBx

Hepatitis B virus (HBV) remains a major cause of hepatic disease that threatens human health worldwide. Type I IFN (IFN-I) therapy is an important therapeutic option for HBV patients. The antiviral effect of IFN is mainly mediated via upregulation of the expressions of the downstream IFN-stimulated genes. However, the mechanisms by which IFN induces ISG production and inhibits HBV replication are yet to be clarified. TRIM14 was recently reported as a key molecule in the IFN-signaling pathway that regulates IFN production in response to viral infection. In this study, we sought to understand the mechanisms by which IFN restricts HBV replication. We confirmed that TRIM14 is an ISG in the hepatic cells, and that the pattern-recognition receptor ligands polyI:C and polydAdT induce TRIM14 dependent on IFN-I production. In addition, IFN-I-activated STAT1 (but not STAT3) directly bound to the TRIM14 promoter and mediated the induction of TRIM14. Interestingly, TRIM14 played an important role in IFN-I-mediated inhibition of HBV, and the TRIM14 SPRY domain interacted with the C-terminal of HBx, which might block the role of HBx in facilitating HBV replication by inhibiting the formation of the Smc-HBx–DDB1 complex. Thus, our study clearly demonstrates that TRIM14 is a STAT1-dependent ISG, and that the IFN-I–TRIM14–HBx axis shows an alternative way to understand the mechanism by which IFN-I inhibits virus replication

Buffering of pulp pH and its influence on process water chemistry during iron ore flotation

It is inevitable for the occurrences of pulp pH buffering during pH control in flotation as the minerals with acidic/alkali properties tend to interact with pH modifiers and restore the pulp pH. This could result in some disturbing ions and alter the water/pulp chemistry. The purpose of this study was to identify the influences of pulp pH buffering on process water chemistry through a series of pH buffering tests, bench flotation experiments, ore dissolution tests, zeta potential measurement, and Xray diffraction (XRD) analysis. The built-up and distribution of the dominant cations in the process water from different locations in an industrial flotation system of the iron ore were analyzed and recorded by Inductively Coupled Plasma-Optical Emission (ICP-OES) at a period of about six months when the operations were stable. The data showed that a near five-minute buffer of pulp pH at a range from near 7.9 to 8.9 occurred before it reached a stable value. At this period, the dissolution of Ca/Mg from the iron ore was dominant. And, the pulp pH at a lower value tended to induce more dissolved $Ca^{2+}$ and $Mg^{2+}$ ions. These divalent cations seem to have different influences on the flotation properties of iron oxides at the same concentrations, indicating a positive effect on the recovery of iron oxides with the presence of $Mg^{2+}$ ions but an opposite effect if $Ca^{2+}$ ions occurred. The presence of sulfate, however, tended to restore the floatability of silicate depressed by $Ca^{2+}$ ions

The temporal order of word presentation modulates the amplitudes of P2 and N400 during recognition of causal relations

The processing of causal relations has been constantly found to be asymmetrical once the roles of cause and effect are assigned to objects in interactions. We used a relationship recognition paradigm and recorded electroencephalographic (EEG) signals to explore the neural mechanism underlying the asymmetrical representations of causal relations in semantic memory. The results revealed that the verification of causal relations is faster if two words appear in cause–effect order (e.g., virus-epidemic) than if they appear in effect–cause order (e.g., epidemic-virus), whereas no such asymmetrical representation was found for the verification of hierarchical relations with reverse orders (e.g., bird-sparrow v. sparrow-bird) in Experiment 1. Furthermore, the P2 amplitude elicited by superordinate-subordinate order was larger than that when in reverse order, whereas the N400 effect elicited by cause-effect order was smaller (more positive) than when in reverse order. However, no such asymmetry, as well as P2 and N400 components, were observed when verifying the existence of a general associative relation in Experiment 2. We suggested that the smaller N400 in cause-effect order indicates their increased salience in semantic memory relative to the effect-cause order. These results provide evidence for dissociable neural processes, which are related to role binding, contributing to the generation of causal asymmetry

Decreased expression of transforming growth factor-β1 and α-smooth muscle actin contributes to the protection of lotensin against chronic renal failure in rats

Background: Lotensin has been shown to have a protective function in the early stage of chronic renal failure. However, its role in the intermediate and late stages of chronic renal failure remains largely unknown. The present study aimed to investigate the role and underlying mechanism of lotensin in advanced chronic kidney disease. Methods: Female Wistar rats were randomly divided into three groups (n = 10): sham group, 5/6 nephrectomy (5/6 Nx) group, and lotensin group (oral administration of lotensin for 9 weeks following 5/6 Nx). Rats were sacrificed and pathological parameters were measured. Western blot assay and immunohistochemical staining were performed to detect the expression of transforming growth factor-β1 (TGF-β1) and α-smooth muscle actin (α-SMA) in kidney tissues. Results: Compared to the 5/6 Nx group, lotensin administration significantly decreased 5/6 Nx-induced elevation in blood urea nitrogen, serum creatinine and 24-h urinary protein excretion (UPE) rates, but markedly increased red blood cell count, plasma albumin and hemoglobin levels, along with improved renal morphology. Mechanistically, lotensin dramatically downregulated the renal expression of TGF-β1 and α-SMA induced by 5/6 Nx. Conclusions: Lotensin protects against advanced chronic kidney disease in rats with 5/6 Nx through the downregulation of TGF-β1 and α-SMA

Licochalcone A Upregulates Nrf2 Antioxidant Pathway and Thereby Alleviates Acetaminophen-Induced Hepatotoxicity

Acetaminophen (APAP) overdose-induced fatal hepatotoxicity is majorly characterized by overwhelmingly increased oxidative stress while enhanced nuclear factor-erythroid 2-related factor 2 (Nrf2) is involved in prevention of hepatotoxicity. Although Licochalcone A (Lico A) upregulates Nrf2 signaling pathway against oxidative stress-triggered cell injury, whether it could protect from APAP-induced hepatotoxicity by directly inducing Nrf2 activation is still poorly elucidated. This study aims to explore the protective effect of Lico A against APAP-induced hepatotoxicity and its underlying molecular mechanisms. Our findings indicated that Lico A effectively decreased tert-butyl hydroperoxide (t-BHP)- and APAP-stimulated cell apoptosis, mitochondrial dysfunction and reactive oxygen species generation and increased various anti-oxidative enzymes expression, which is largely dependent on upregulating Nrf2 nuclear translocation, reducing the Keap1 protein expression, and strengthening the antioxidant response element promoter activity. Meanwhile, Lico A dramatically protected against APAP-induced acute liver failure by lessening the lethality; alleviating histopathological liver changes; decreasing the alanine transaminase and aspartate aminotransferase levels, malondialdehyde formation, myeloperoxidase level and superoxide dismutase depletion, and increasing the GSH-to-GSSG ratio. Furthermore, Lico A not only significantly modulated apoptosis-related protein by increasing Bcl-2 expression, and decreasing Bax and caspase-3 cleavage expression, but also efficiently alleviated mitochondrial dysfunction by reducing c-jun N-terminal kinase phosphorylation and translocation, inhibiting Bax mitochondrial translocation, apoptosis-inducing factor and cytochrome c release. However, Lico A-inhibited APAP-induced the lethality, histopathological changes, hepatic apoptosis, and mitochondrial dysfunction in WT mice were evidently abrogated in Nrf2-/- mice. These investigations firstly implicated that Lico A has protective potential against APAP-induced hepatotoxicity which may be strongly associated with the Nrf2-mediated defense mechanisms

Additional file 1 of Shenkang protects renal function in diabetic rats by preserving nephrin expression

Additional file 1: Supplementary fig.