Enhanced Electrokinetic Transport of Sulfate in Saline Soil

The electrokinetic transport of sulfate was investigated as a means of treating and restoring a sulfate-accumulating saline soil. The electrokinetic treatment decreased the electrical conductivity of the soil, an indicator of soil salinity, to 58.6%, 73.1%, and 83.5% for 7, 14 and 21 days, respectively. More than 96% of the chloride and nitrate were removed within 7 days. However, the removal of sulfate was highly influenced by the anode material. An iron anode removed sulfate effectively, whereas, sulfate was hyper-accumulated in the anodic region when an inert anode was used. The iron anode was oxidized in a sacrificial anodic reaction, which competed with the electrolysis reaction of water at the anode, and finally the reaction prevented the severe acidification of the soil in the anodic region. However, the competing reactions produced hydrogen ions at the anode, and the ions were transported toward the cathode, which, in turn, acidified the soil, especially, in the anodic region. The acidification switched the surface charge of the soil from negative to positive, increasing the interaction between the soil surface and sulfate, and thus inhibiting the transport of sulfate under the electric field. The zeta potential analysis of the soil provided an explanation. The results indicate that preventing severe acidification is an important factor which influences the transport of anions and iron anode for the enhanced removal of anionic pollutants by electrokinetic remediation

Substantial improvements of long-term stability in encapsulation-free WS2 using highly interacting graphene substrate

We report the novel role of graphene substrates in obstructing the aging propagation in both the basal planes and edges of two-dimensitional sheets of transition metal dichalcogenides (TMDs). Even after 300 d in ambient air conditions, the epitaxially grown WS2/graphene samples have a clean, uniform surface without any encapsulation. We show that high crystallinity is an effective factor that determines the excellent air stability of WS2/graphene, and we present impressive experimental evidence of the relation between defects and the aging phenomena. Moreover, we reveal the strong interlayer charge interaction as an additional factor for the enhanced air stability as a result of charge transfer-induced doping. This work not only proposes a simple method to create highly stable TMDs by the selection of a suitable substrate but also paves the way for the realization of practical TMDs-based applications.clos

Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage

Mature microRNA-binding protein QKI promotes microRNA-mediated gene silencing

ABSTRACTAlthough Argonaute (AGO) proteins have been the focus of microRNA (miRNA) studies, we observed AGO-free mature miRNAs directly interacting with RNA-binding proteins, implying the sophisticated nature of fine-tuning gene regulation by miRNAs. To investigate microRNA-binding proteins (miRBPs) globally, we analyzed PAR-CLIP data sets to identify RBP quaking (QKI) as a novel miRBP for let-7b. Potential existence of AGO-free miRNAs were further verified by measuring miRNA levels in genetically engineered AGO-depleted human and mouse cells. We have shown that QKI regulates miRNA-mediated gene silencing at multiple steps, and collectively serves as an auxiliary factor empowering AGO2/let-7b-mediated gene silencing. Depletion of QKI decreases interaction of AGO2 with let-7b and target mRNA, consequently controlling target mRNA decay. This finding indicates that QKI is a complementary factor in miRNA-mediated mRNA decay. QKI, however, also suppresses the dissociation of let-7b from AGO2, and slows the assembly of AGO2/miRNA/target mRNA complexes at the single-molecule level. We also revealed that QKI overexpression suppresses cMYC expression at post-transcriptional level, and decreases proliferation and migration of HeLa cells, demonstrating that QKI is a tumour suppressor gene by in part augmenting let-7b activity. Our data show that QKI is a new type of RBP implicated in the versatile regulation of miRNA-mediated gene silencing

Mature microRNA-binding protein QKI promotes microRNA-mediated gene silencing

Although Argonaute (AGO) proteins have been the focus of microRNA (miRNA) studies, we observed AGO-free mature miRNAs directly interacting with RNA-binding proteins, implying the sophisticated nature of fine-tuning gene regulation by miRNAs. To investigate microRNA-binding proteins (miRBPs) globally, we analyzed PAR-CLIP data sets to identify RBP quaking (QKI) as a novel miRBP for let-7b. Potential existence of AGO-free miRNAs were further verified by measuring miRNA levels in genetically engineered AGO-depleted human and mouse cells. We have shown that QKI regulates miRNA-mediated gene silencing at multiple steps, and collectively serves as an auxiliary factor empowering AGO2/let-7b-mediated gene silencing. Depletion of QKI decreases interaction of AGO2 with let-7b and target mRNA, consequently controlling target mRNA decay. This finding indicates that QKI is a complementary factor in miRNA-mediated mRNA decay. QKI, however, also suppresses the dissociation of let-7b from AGO2, and slows the assembly of AGO2/miRNA/target mRNA complexes at the single-molecule level. We also revealed that QKI overexpression suppresses cMYC expression at post-transcriptional level, and decreases proliferation and migration of HeLa cells, demonstrating that QKI is a tumour suppressor gene by in part augmenting let-7b activity. Our data show that QKI is a new type of RBP implicated in the versatile regulation of miRNA-mediated gene silencing.</p