A self-reconstructed bifunctional electrocatalyst of pseudo-amorphous nickel carbide @ iron oxide network for seawater splitting.

Here, a sol-gel method is used to prepare a Prussian blue analogue (NiFe-PBA) precursor with a 2D network, which is further annealed to an Fe3 O4 /NiCx composite (NiFe-PBA-gel-cal), inheriting the ultrahigh specific surface area of the parent structure. When the composite is used as both anode and cathode catalyst for overall water splitting, it requires low voltages of 1.57 and 1.66 V to provide a current density of 100 mA cm-2 in alkaline freshwater and simulated seawater, respectively, exhibiting no obvious attenuation over a 50 h test. Operando Raman spectroscopy and X-ray photoelectron spectroscopy indicate that NiOOH2-x active species containing high-valence Ni3+ /Ni4+ are in situ generated from NiCx during the water oxidation. Density functional theory calculations combined with ligand field theory reveal that the role of high valence states of Ni is to trigger the production of localized O 2p electron holes, acting as electrophilic centers for the activation of redox reactions for oxygen evolution reaction. After hydrogen evolution reaction, a series of ex situ and in situ investigations indicate the reduction from Fe3+ to Fe2+ and the evolution of Ni(OH)2 are the origin of the high activity

Tuning the Double Layer of Graphene Oxide through Phosphorus Doping for Enhanced Supercapacitance

The electrochemical double layer plays a fundamental role in energy storage applications. Control of the distribution of ions in the double layer at the atomistic scale offers routes to enhanced material functionality and device performance. Here we demonstrate how the addition of an element from the third row of the periodic table, phosphorus, to graphene oxide increases the measured capacitance and present density functional theory calculations that relate the enhanced charge storage to structural changes of the electrochemical double layer. Our results point to how rational design of materials at the atomistic scale can lead to improvements in their performance for energy storage

The association of cytoplasmic overexpression of cyclin d1 and tumor metastasis in Hepatocellular Carcinoma

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Heterostructured core-Shell Ni-Co@Fe-Co nanoboxes of prussian blue analogues for efficient electrocatalytic hydrogen evolution from alkaline seawater.

The rational construction of efficient and low-cost electrocatalysts for the hydrogen evolution reaction (HER) is critical to seawater electrolysis. Herein, trimetallic heterostructured core-shell nanoboxes based on Prussian blue analogues (Ni-Co@Fe-Co PBA) were synthesized using an iterative coprecipitation strategy. The same coprecipitation procedure was used for the preparation of the PBA core and shell, with the synthesis of the shell involving chemical etching during the introduction of ferrous ions. Due to its unique structure and composition, the optimized trimetallic Ni-Co@Fe-Co PBA possesses more active interfacial sites and a high specific surface area. As a result, the developed Ni-Co@Fe-Co PBA electrocatalyst exhibits remarkable electrocatalytic HER performance with small overpotentials of 43 and 183 mV to drive a current density of 10 mA cm-2 in alkaline freshwater and simulated seawater, respectively. Operando Raman spectroscopy demonstrates the evolution of Co2+ from Co3+ in the catalyst during HER. Density functional theory simulations reveal that the H*-N adsorption sites lower the barrier energy of the rate-limiting step, and the introduced Fe species improve the electron mobility of Ni-Co@Fe-Co PBA. The charge transfer at the core-shell interface leads to the generation of H* intermediates, thereby enhancing the HER activity. By pairing this HER catalyst (Ni-Co@Fe-Co PBA) with another core-shell PBA OER catalyst (NiCo@A-NiCo-PBA-AA) reported by our group, the fabricated two-electrode electrolyzer was found to achieve high output current densities of 44 and 30 mA cm-2 at a low voltage of 1.6 V in alkaline freshwater and simulated seawater, respectively, exhibiting remarkable durability over a 100 h test

Explanation of the Colour Change in Alexandrites.

Alexandrites are remarkable and rare gemstones. They display an extraordinary colour change according to the ambient lighting, from emerald green in daylight to ruby red in incandescent light from tungsten lamps or candles. While this colour change has been correctly attributed to chromium impurities and their absorption band in the yellow region of the visible light spectrum, no adequate explanation of the mechanism has been given. Here, the alexandrite effect is fully explained by considering the von Kries model of the human colour constancy mechanism. This implies that our colour constancy mechanism is real (objective) and primarily attuned to correct for the colour temperature of black-body illuminants

Activation of Human Stearoyl-Coenzyme A Desaturase 1 Contributes to the Lipogenic Effect of PXR in HepG2 Cells

The pregnane X receptor (PXR) was previously known as a xenobiotic receptor. Several recent studies suggested that PXR also played an important role in lipid homeostasis but the underlying mechanism remains to be clearly defined. In this study, we found that rifampicin, an agonist of human PXR, induced lipid accumulation in HepG2 cells. Lipid analysis showed the total cholesterol level increased. However, the free cholesterol and triglyceride levels were not changed. Treatment of HepG2 cells with rifampicin induced the expression of the free fatty acid transporter CD36 and ABCG1, as well as several lipogenic enzymes, including stearoyl-CoA desaturase-1 (SCD1), long chain free fatty acid elongase (FAE), and lecithin-cholesterol acyltransferase (LCAT), while the expression of acyl:cholesterol acetyltransferase(ACAT1) was not affected. Moreover, in PXR over-expressing HepG2 cells (HepG2-PXR), the SCD1 expression was significantly higher than in HepG2-Vector cells, even in the absence of rifampicin. Down-regulation of PXR by shRNA abolished the rifampicin-induced SCD1 gene expression in HepG2 cells. Promoter analysis showed that the human SCD1 gene promoter is activated by PXR and a novel DR-7 type PXR response element (PXRE) response element was located at -338 bp of the SCD1 gene promoter. Taken together, these results indicated that PXR activation promoted lipid synthesis in HepG2 cells and SCD1 is a novel PXR target gene. © 2013 Zhang et al

Pd ion-exchange and ammonia etching of a Prussian blue analogue to produce a high-performance water-splitting catalyst

The authors report an ammonia‐assisted in situ cation‐exchange method for the synthesis of dodecagon N‐doped PdCoNi carbon‐based nanosheets (Pd‐e‐NiCo‐PBA‐C) and explore the catalytic performance. Pd‐e‐NiCo‐PBA‐C exerts extremely low overpotential and Tafel slope for hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) both in acidic and alkaline media, only 47 mV, 55 mV dec−1 (pH = 0, HER) and 147 mV, 67 mV dec−1 (pH = 14, HER), and 309 mV, 67 mV dec−1 (pH = 14, OER), outperforming commercial IrO2‐based and Pt‐based catalysts. In addition, after 5000 cycles, the linear sweep voltammetry curve shows a negligible shift, indicating excellent stability performance. To test its overall water‐splitting performance, Pd‐e‐NiCo‐PBA‐C is applied as both cathode and anode materials. A high current density of 33 mA cm−2 at a battery voltage of 1.6 V is obtained, with the catalytic activity maintained at 97.3% after over 50 h. To get a further insight into the superior OER and HER performance, theoretical calculations are carried out, the better performance originates from the affinity difference of Pd and Ni atoms for gas atoms, and the replacement of inert atoms can decrease the binding energy and enhance the electrocatalytic activity

A genetically-encoded crosslinker screen identifies SERBP1 as a PKCε substrate influencing translation and cell division

The PKCε-regulated genome protective pathway provides transformed cells a failsafe to successfully complete mitosis. Despite the necessary role for Aurora B in this programme, it is unclear whether its requirement is sufficient or if other PKCε cell cycle targets are involved. To address this, we developed a trapping strategy using UV-photocrosslinkable amino acids encoded in the PKCε kinase domain. The validation of the mRNA binding protein SERBP1 as a PKCε substrate revealed a series of mitotic events controlled by the catalytic form of PKCε. PKCε represses protein translation, altering SERBP1 binding to the 40 S ribosomal subunit and promoting the assembly of ribonucleoprotein granules containing SERBP1, termed M-bodies. Independent of Aurora B, SERBP1 is shown to be necessary for chromosome segregation and successful cell division, correlating with M-body formation. This requirement for SERBP1 demonstrates that Aurora B acts in concert with translational regulation in the PKCε-controlled pathway exerting genome protection

PARP Inhibitors Display Differential Efficacy in Models of BRCA Mutant High-Grade Serous Ovarian Cancer

Several poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitors are now in clinical use for tumours with defects in BReast CAncer genes BRCA1 or BRCA2 that result in deficient homologous recombination repair (HRR). Use of olaparib, niraparib or rucaparib for the treatment of high-grade serous ovarian cancer, including in the maintenance setting, has extended both progression free and overall survival for women with this malignancy. While different PARP inhibitors (PARPis) are mechanistically similar, differences are apparent in their chemical structures, toxicity profiles, PARP trapping abilities and polypharmacological landscapes. We have treated ovarian cancer cell line models of known BRCA status, including the paired cell lines PEO1 and PEO4, and UWB1.289 and UWB1.289+BRCA1, with five PARPis (olaparib, niraparib, rucaparib, talazoparib and veliparib) and observed differences between PARPis in both cell viability and cell survival. A cell line model of acquired resistance to veliparib showed increased resistance to the other four PARPis tested, suggesting that acquired resistance to one PARPi may not be able to be rescued by another. Lastly, as a proof of principle, HRR proficient ovarian cancer cells were sensitised to PARPis by depletion of BRCA1. In the future, guidelines will need to emerge to assist clinicians in matching specific PARPis to specific patients and tumours.</jats:p