Elucidation of Active Sites on S, N Codoped Carbon Cubes Embedding Co-Fe Carbides toward Reversible Oxygen Conversion in High-Performance Zinc-Air Batteries.

The development of high-performance but low-cost catalysts for the electrochemical oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) is of central importance for realizing the prevailing application of metal-air batteries. Herein a facile route is devised to synthesize S, N codoped carbon cubes embedding Co-Fe carbides by pyrolyzing the Co-Fe Prussian blue analogues (PBA) coated with methionine. Via the strong metal-sulfur interaction, the methionine coating provides a robust sheath to restrain the cubic morphology of PBA upon pyrolysis, which is proved highly beneficial for promoting the specific surface area and active sites exposure, leading to remarkable bifunctionality of ORR and OER comparable to the benchmarks of Pt/C and RuO2 . Further elaborative investigations on the activity origin and postelectrolytic composition unravel that for ORR the high activity is mainly contributed by the S, N codoped carbon shell with the inactive carbide phase converting into carbonate hydroxides. For OER, the embedded Co-Fe carbides transform in situ into layered (hydr)oxides, serving as the actual active sites for promoting water oxidation. Zn-air batteries employing the developed hollow structure as the air cathode catalyst demonstrate superb rechargeability, energy efficiency, as well as portability.

MicroRNA-183 functions as the tumor suppressor via inhibiting cellular invasion and metastasis by targeting MMP-9 in cervical cancer.

OBJECTIVE: MicroRNAs have been reported to play an important role in the invasion and metastasis of cervical cancer. miR-183 was found to inhibit or promote the invasion and metastasis of multiple solid tumors. However, the roles of miR-183 in cervical cancer are unclear. METHODS: In this study, miR-183 expression levels were measured in 53 cervical cancer and 13 normal cervical tissues by qRT-PCR. The effects of forced expression of miR-183 on cervical cancer cells invasion and metastasis were investigated using Transwell uncoated or coated with growth factor-reduced Matrigel for migration or invasion assays, respectively. RESULTS: We found that miR-183 expression levels were significantly down-regulated in cervical cancer tissues compared with normal tissues (0.15±0.011 to 0.86±0.049). Ectopic expression of miR-183 resulted in the suppression of invasion and migration of cervical cancer cell lines, siha and Hela cells (p<0.0001). Bioinformatics analysis revealed that MMP-9 was the potential target of miR-183 and it was found that MMP-9 was remarkably up-regulated in cervical cancer. Furthermore, a dual-luciferase reporter assay showed that MMP-9 as a target of miR-183 (p<0.0001). The invasion and metastasis ability of siha and Hela was suppressed when MMP-9 was down-regulated in vitro (p<0.0001). CONCLUSIONS: In conclusion, our study revealed that miR-183 might be a tumor suppressor via inhibiting the invasion and metastasis of cervical cancer cells through targeting MMP-9, indicating that miR-183 may be a novel potential therapeutic target for cervical cancer.

TGF-ß1 mediates estrogen receptor-induced epithelial-to-mesenchymal transition in some tumor lines.

More and more studies have reported that epithelial-mesenchymal transition (EMT) involved in the process of cancer development and progression occurs. The EMT also plays an important role in the movement and transfer of the tumors. Transforming growth factor-ß (TGF-ß) could induce the EMT in some cancer cell types. However, the mechanism underlying this transition process has also not been entirely clarified. In this study, the results indicated that TGF-ß1-mediated EMT in the tumor was associated with the estrogen receptor (ER). The decreased expression of vimentin and snail resulted in the decrease of the ER expression by small interfering RNA-mediated silencing and preventing the TGF-ß-induced EMT. In conclusion, our results indicated that TGF-ß1 is an estrogen receptor signaling and essential novel downstream targets and could act as an important factor in the TGF-ß-induced EMT.

Forkhead factor FOXQ1 promotes TGF-ß1 expression and induces epithelial-mesenchymal transition.

Epithelial-mesenchymal transition (EMT) promotes tumor invasion and metastasis, but the coordination and integration mechanisms of these processes are still not fully understood. In this study, we used a cross-species expression profiling strategy of Hela cells to determine an important genetic program transfers. In particular, we have discovered a new transfer function, which is not previously known about transcription factor forkhead box Q1 (FOXQ1). The shRNA anti-FOXQ1 gene was synthesized and transfected into the Hela and EpRas cells. RT-PCR assay was performed to detect the mRNA levels in cells. Cell adhesion and separation assay were used to examine the cell-cell adhesion and separation among cells. Wound healing assay was utilized to examine cell migration and invasion ability. Chromatin immunoprecipitation assay was used to investigate the interaction between E-cadherin and N-cadherin and FOXQ1 promoter region. The results indicated that ectopic expression of FOXQ1 increased cell migration and invasion in vitro, enhanced mammary epithelial cells in vivo lung metastasis, and triggered significant EMT. In contrast, the opposite effects in vitro and in vivo of FOXQ1 knockdown phenotypes were caused by these mechanisms. Notably, FOXQ1 repressed core EMT regulation of the expression of TGF-ß1. FOXQ1 protein directly interacts with E-cadherin and N-cadherin promoter region. And surveys show that FOXQ1 expression regulation by TGF-ß1 and blockade induced EMT both morphological and molecular levels. Our findings emphasize the feasibility of cross-species expression profiles, as a strategy to identify metastasis-related genes. The induction of EMT by FOXQ1 defines a new transfer function in promoting cancer behind possible mechanisms.

Revisiting the Grain and Valence Effect of Oxide-Derived Copper on Electrocatalytic CO2 Reduction Using Single Crystal Cu(111) Foils.

Oxide-derived Cu (OD-Cu) has been viewed as a highly active form for catalyzing the multielectron transfer of electrochemical CO2 reduction, but the underlying catalytic mechanism is still controversial. In the current study, the crystalline and valency factors that influence the CO2R activities of OD-Cu are revisited by employing single crystal Cu(111) foils that exclude convolutions from initial morphological and crystallographic heterogeneity. We observe that the overall CO2R performance, especially the C2H4 selectivity, correlates well with the initial oxidation level of the Cu(111) foil, of which the surface oxide layer is reduced into small fragments comprising rich grain boundaries and diversely orientated facets. Nonetheless, we find that the polycrystallinity and grain boundaries of OD-Cu, in this circumstance, are not the major causes of the observed activity enhancement. Instead, a transition state between the initial oxide and the finally reduced copper phases, as well as its longevity, dictates the catalytic property of OD-Cu in electrochemical CO2 reduction. Consequently, this work furnishes further evidence and in-depth understanding to help clarify the catalytic mechanism of OD-Cu in CO2R.

Wax-Transferred Hydrophobic CVD Graphene Enables Water-Resistant and Dendrite-Free Lithium Anode toward Long Cycle Li-Air Battery.

One of the key challenges in achieving practical lithium-air battery is the poor moisture tolerance of the lithium metal anode. Herein, guided by theoretical modeling, an effective tactic for realizing water-resistant Li anode by implementing a wax-assisted transfer protocol is reported to passivate the Li surface with an inert high-quality chemical vapor deposition (CVD) graphene layer. This electrically conductive and mechanically robust graphene coating enables serving as an artificial solid/electrolyte interphase (SEI), guiding homogeneous Li plating/stripping, suppressing dendrite and "dead" Li formation, as well as passivating the Li surface from moisture erosion and side reactions. Consequently, lithium-air batteries fabricated with the passivated Li anodes demonstrate a superb cycling performance up to 2300 h (230 cycles at 1000 mAh g-1 , 200 mA g-1 ). More strikingly, the anode recycled thereafter can be recoupled with a fresh cathode to continuously run for 400 extended hours. Comprehensive time-lapse and ex situ microscopic and spectroscopic investigations are further carried out for elucidating the fundamentals behind the extraordinary air and electrochemical stability.

Redox-Driven Lithium Perfusion to Fabricate Li@Ni-Foam Composites for High Lithium-Loading 3D Anodes.

As the hostless nature of the conventional Li anodes with planar surfaces inevitably causes volume expansion and parasitic dendrite growth, it is essential to develop a composite electrode structure with improved Li plating/stripping behaviors to mitigate such issues. Herein, a composite Li@NF anode was successfully fabricated through lithium perfusion into the commercial nickel foam (NF) decorated with lithiophilic NiO nanosheets, demonstrating an exceptionally high areal Li loading of 53.2 mg cm-2 with suppressed Li dendrite formation and volume expansion, improved Coulombic efficiency, as well as extended cycling stability in all half, symmetric, and full cell tests. More importantly, density functional theory calculations and control studies with Fe2O3@NF, pristine NF, and Cu2O@CF reveal a linear correlation between the thermodynamics of the surface reactions and the lithiophilicity of the reaction products, attesting to a redox-driven Li perfusion process. Further, through ex situ scanning electron and in situ optical microscopy, the enhanced performance of Li@NF is mainly attributed to the mediation of Li plating/stripping through homogenizing the Li+ flux, decentralizing local charge density, and accommodating multidirectional Li deposition by the conductive 3D scaffolds. Consequently, this study offers important insights into the driving of thermal Li perfusion through appropriate material and surface design for achieving safe and stable lithium metal anodes.

Carved nanoframes of cobalt-iron bimetal phosphide as a bifunctional electrocatalyst for efficient overall water splitting.

Water electrolysis for hydrogen production has long been regarded as an ideal tactic for renewable energy conversion and storage, but is impeded by the sluggish kinetics of both the hydrogen and oxygen evolution reactions, which are therefore in urgent need for high-performance but low-cost electrocatalysts. Herein, nanoframes of transition metal phosphides (TMPs) with the 3D framework carved open have been demonstrated as highly potent bifunctional catalysts for overall water splitting, reaching the benchmark performance of the Pt/C‖RuO2 couple, and are much superior to their nanocubic counterparts. This excellent water splitting behavior can be attributed to the enlarged active surface area, less obstructed electrolyte infiltration, promoted charge transfer, and facilitated gas release. Further through in-depth activity analysis and post-electrocatalysis characterization, special attention has been paid to the fate and role of phosphorus in the electrocatalytic process, suggesting that despite the chemical instability of the TMPs (especially under OER conditions), excellent electrocatalytic stability can still be achieved through the amorphous bimetallic hydroxides/oxides formed in situ.

Human mesenchymal stem cell homing induced by SKOV3 cells.

Human mesenchymal stem cell (hMSC) homing is the migration of endogenous and exogenous hMSCS to the target organs and the subsequent colonization under the action chemotaxic factors. This is an important process involved in the repair of damaged tissues. However, we know little about the mechanism of hMSC homing. Stromal cell derived factor-1 (SDF-1) is a cytokine secreted by stromal cells. Its only receptor CXCR4 is widely expressed in blood cells, immune cells and cells in the central nervous system. SDF-1/CXCR4 signaling pathway plays an important role in hMSC homing and tissue repair. Human cbll1 gene encodes E3 ubiquitin-protein ligase Hakai (also known as CBLL1) consisting of RING-finger domain that is involved in ubiquitination, endocytosis and degradation of epithelial cadherin (E-cadherin) as well as in the regulation of cell proliferation. We successfully constructed LV3-CXCR4 siRNA lentiviral vector, LV3-CBLL1 RNAi lentiviral vector and the corresponding cell systems which were used to induce hMSC homing in the presence of SKOV3 cells. Thus the mechanism of hMSC homing was studied.

Suppression of microRNA-135b-5p protects against myocardial ischemia/reperfusion injury by activating JAK2/STAT3 signaling pathway in mice during sevoflurane anesthesia.

The study aims to explore the effects of miR-135b-5p on myocardial ischemia/reperfusion (I/R) injuries by regulating Janus protein tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription (STAT) signaling pathway by mediating inhalation anesthesia with sevoflurane. A sum of 120 healthy Wistar male mice was assigned into six groups. Left ventricular ejection fraction (LVEF) and left ventricular shortening fraction (LVSF) were detected. Cardiomyocyte apoptosis was determined by terminal dexynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) assay. MiR-135b-5p expression, mRNA and protein expression of p-STAT3, p-JAK2, STAT3, JAK2, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein B (Bax) were detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Target relationship between miR-135b-5p and JAK2 was confirmed by dual-luciferase reporter assay. The other five groups exhibited increased cardiomyocyte necrosis, apoptosis, miR-135b-5p and Bax expression, mRNA expression of JAK2 and STAT3, and protein expression of p-STAT3 and p-JAK2 compared with the sham group, but showed decreased LVEF, LVFS, and Bcl-2 expression. Compared with the model and AG490 + Sevo groups, the Sevo, inhibitor + Sevo and inhibitor + AG490 + Sevo groups displayed reduced cardiomyocyte necrosis, apoptosis, miR-135b-5p and Bax expression, but displayed elevated mRNA expression of JAK2 and STAT3, protein expression of p-STAT3 and p-JAK2, LVEF, LVFS and Bcl-2 expression. Compared with the Sevo and inhibitor + AG490 + Sevo groups, the AG490 + Sevo group showed decreased LVEF, LVFS, Bcl-2 expression, mRNA expressions of JAK2 and STAT3, and protein expressions of p-STAT3 and p-JAK2, but increased cardiomyocyte necrosis, apoptosis, and Bax expressions. MiR-135b-5p negatively targetted JAK2. Inhibition of miR-135b-5p can protect against myocardial I/R injury by activating JAK2/STAT3 signaling pathway through mediation of inhalation anesthesia with sevoflurane.

Mechanistic Study on Triptorelin Action in Protecting From 5-FU-Induced Ovarian Damage in Rats.

Triptorelin, a kind of GnRH agonist, is widely used in the treatment of hormone-responsive cancers in the clinic. This study aimed to discover the underlying mechanism of triptorelin in protection from 5-fluorouracil (5-FU)-induced ovarian damage in Sprague-Dawley rats. In the present study, after using 5-FU to induce ovarian damage in rats, body weight and wet ovaries were weighed, the levels of estradiol (E2), follicle-stimulating hormone (FSH), and anti-Müllerian hormone (AMH) in blood were detected, and the expression of Bcl-2, Bax, and NF-κB was determined. It suggested that, compared to the control, body weight gain, the ratio of ovarian wet weight to body weight, primary follicle numbers, and the levels of AMH were significantly decreased, while the concentration of E2 and FSH was heavily increased following 5-FU administration. In contrast, after coadministration of triptorelin with 5-FU, the ratio of ovarian wet weight to body weight and the levels of AMH were significantly increased, whereas the level of E2 and FSH was decreased significantly when compared with the 5-FU group. Furthermore, at indicated times, 5-FU led to the reduced Bcl-2 and NF-κB expression and increased Bax expression while triptorelin plus 5-FU increased Bcl-2 and NF-κB expression and decreased Bax expression. It was indicated that triptorelin could protect rats from 5-FU-induced ovarian damage by modulation of hormones, Bcl-2, Bax, and NF-κB. These results might highlight the mechanism of triptorelin as a protective agent in clinical chemotherapy for ovarian damage.