Electronic waste management is one of the key challenges for the green revolution without affecting the environment. The wide use of printer devices has brought a horde of discarded waste toner, which release ∼6000 tons of processed carbon powder into the atmosphere every year that would essentially pollute the atmosphere. Here, we propose a one-step thermal conversion of waste toner powder into carbon/Fe3O4 nanocomposites for energy storage applications. Recovered toner carbon (RTC) and toner carbon calcined at 300 °C (RTC-300) were characterized using various analytical tools. From the FE-SEM analysis, the presence of carbon particles with uniformly decorated Fe3O4 nanoparticles was confirmed. RTC-300 carbon was used as an electrode material for supercapacitors, and it exhibited a high specific capacitance of 536 F/g at a current density of 3 A/g, which is almost six times higher than that of the commercial mesoporous graphitized carbon black. RTC-300 showed excellent electrochemical stability of 97% over 5000 cycles at a high current density of 20 A/g. The fabricated symmetric cell using RTC-300 electrode materials in an aqueous electrolyte with a cell voltage of 1.8 V delivered a high energy and high-power density of 42 W h/kg and 14.5 kW/kg, respectively. The fabricated device is stable up to 20,000 cycles at a high current density of 20 A/g with a loss of 23% capacitance.

BackgroundB-cell translocation gene 2 (BTG2) belongs to antiproliferative (ARPO) gene family and the expression of BTG2, human ortholog of rat PC3 and mouse TIS21 gene, has been shown to render cancer cells more sensitive to doxorubicin treatment by upregulating MnSOD expression without regulating any other reactive oxygen species (ROS) scavenging enzymes.ResultsIn the present study, by employing exogenous and endogenous BTG2/TIS21/Pc3 expression by transfection and transduction analyses, and by knockdown of gene expression using RNA interference or using gene knockout cells, we observed that BTG2 increased the binding of activated NF-κB (p65/RelA) to the enhancer element of MnSOD gene in the 2nd intron, which was regulated by p-Akt1, and the induction of MnSOD by BTG2 was accompanied with subsequent downregulation of ROS level and cyclin B1 biosynthesis along with the increase of p21WAF1, resulting in the G2/M arrest independent of p53.ConclusionsThese results show for the first time that BTG2 mediates crosstalk between PI3K-Akt1 and NF-κB pathways, which regulates p53-independent induction of G2/M phase arrest both in normal and cancer cells.

Herein, we report the syntheses, structure, Na-ion conductivity, and theoretical investigation of two moisture stable quaternary compounds, Na3ZnGaQ 4 (Q = S, Se). These compounds are synthesized using high-temperature solid-state synthesis routes employing polychalcogenide flux or by metathesis reactions. The crystal structure of these compounds is built up of a three-dimensional (3-D) network of corner-shared supertetrahedral (T2) units, where two such 3-D networks are interlocked. The d-block metal and the main group metal, Ga, occupy the same crystallographic site with a 1:1 ratio, making it a rare form of building unit. Band structure calculations show that both the compounds are wide band gap semiconductors with band gaps of 2.25 and 1.61 eV, respectively, for Na3ZnGaS4 (I) and Na3ZnGaSe4 (II), which are slightly underestimated compared to experimentally determined band gaps of 3.0 and 1.90 eV, respectively. I and II possess ionic conductivities of 3.74 × 10–4 and 0.12 mS/cm with activation energies of 0.42 and 0.38 eV, respectively, at 30 °C. Interestingly, I shows a significantly high ionic conductivity of 0.13 mS/cm at 30 °C upon exposure to air, which could be due to water adsorption on the surface or occlusion in the grain boundaries. Assuming the vacancy-assisted diffusion mechanism for ionic conductance, this difference is consistent with the difference on vacancy formation energies in these compounds, as predicted by DFT calculations. The bond valence sum map indicates that in both structures, the lowest energy diffusion path is one dimensional and it is along the c axis of the unit cell.

Twist1, a key transcription factor regulating epithelial–mesenchymal transition and cancer metastasis, is highly expressed in invasive cancers in contrast to the loss of BTG2 /TIS21 expression. Based on our observation that forced expression of BTG2 /TIS21 downregulated Twist1 protein expression without altering mRNA level, we investigated molecular mechanisms of the BTG2 /TIS21 -inhibited Twist1 translation in the triple negative breast cancer (TNBC) cells and in vivo BTG2 /TIS21 -knockout (KO) mice and human breast cancer tissues. (1) C-terminal domain of Twist1 and Box B of BTG2 /TIS21 interacted with each other, which abrogated Twist1 activity. (2) BTG2 /TIS21 inhibited translational initiation by depleting eIF4E availability via inhibiting 4EBP1 phosphorylation. (3) Expression of BTG2 /TIS21 maintained p-eIF2α that downregulates initiation of protein translation, confirmed by eIF2α-AA mutant expression and BTG2 /TIS21 knockdown in MEF cells. (4) cDNA microarray analysis revealed significantly higher expression of initiation factors-eIF2A, eIF3A, and eIF4G2-in the BTG2 /TIS21 -KO mouse than that in the wild type. (5) BTG2 /TIS21 -inhibited translation initiation lead to the collapse of polysome formation and the huge peak of 80s monomer in the BTG2 /TIS21 expresser, but not in the control. (6) mRNAs and protein expressions of elongation factors were also downregulated by BTG2 /TIS21 expression in TNBC cells, but much higher in both TIS21-KO mice and lymph node-positive human breast cancers. (7) BTG2 /TIS21 -mediated Twist1 loss was not due to the protein degradation by ubiquitination and autophagy activation. (8) Twist1 protein level was significantly higher in various organs of TIS21-KO mice compared with that in the control, indicating the in vivo role of BTG2 /TIS21 gene in the regulation of Twist1 protein level. Altogether, the present study support our hypothesis that BTG2 /TIS21 is a promising target to combat with metastatic cancers with high level of Twist1 without BTG2 /TIS21 expression.

A missing member of well-known ternary chalcometallates, a sodium selenogallate, NaGaSe2, has been synthesized by employing a polyselenide flux and stoichiometric reaction. Crystal structure analysis using X-ray diffraction techniques reveals that it contains supertetrahedral adamantane-type Ga4Se10 secondary building units. These Ga4Se10 secondary building units are further connected via corners to form two-dimensional (2D) [GaSe2]∞ – layers stacked along the c-axis of the unit cell, and the Na ions reside in the interlayer space. The compound has an unusual ability to absorb water molecules from the atmosphere or a nonanhydrous solvent to form distinct hydrated phases, NaGaSe2·xH2O (where x can be 1 and 2), with an expanded interlayer space, as verified by X-ray diffraction (XRD), thermogravimetric–differential scanning calorimetry (TG-DSC), desorption, and Fourier transform infrared spectroscopy (FT-IR) studies. The in situ thermodiffractogram indicates the emergence of an anhydrous phase before 300 °C with the decrease of interlayer spacings and reverting to the hydrated phase within a minute of re-exposure to the environment, supporting the reversibility of such a process. Structural transformation induced through water absorption results in an increase of Na ionic conductivity by 2 orders of magnitude compared to that of the pristine anhydrous phase, as verified by impedance spectroscopy. Na ions from NaGaSe2 can be exchanged in the solid-state route with other alkali and alkaline earth metals in a topotactic or nontopotactic way, leading to 2D isostructural and three-dimensional networks, respectively. Optical band gap measurements show a band gap of ∼3 eV for the hydrated phase, NaGaSe2·xH2O, which is in good agreement with the calculated band gap using a density functional theory (DFT)-based method. Sorption studies further confirm the selective absorption of water over MeOH, EtOH, and CH3CN with a maximum water uptake of 6 molecules/formula unit at a relative pressure, P/P 0, of 0.9.

TIS21 significantly lost in the infiltrating ductal carcinoma, but it can inhibit cancer growth via the TIS21-tsc1/2-mTORc1-p70S6K axis and downregulate cancer progression via the TIS21-mTORc2-AKT1-NFAT1-PHLPP2 pathway.

To understand the regulation of Helicobacter pylori (H. pylori)-associated gastric carcinogenesis, we examined the effect of B-cell translocation gene 2 (BTG2) expression on the biological activity of Tipα, an oncoprotein secreted from H. pylori. BTG2, the human ortholog of mouse TIS21 (BTG2/TIS21), has been reported to be a primary response gene that is transiently expressed in response to various stimulations. Here, we report that BTG2 is constitutively expressed in the mucous epithelium and parietal cells of the gastric gland in the stomach. Expression was increased in the mucous epithelium following H. pylori infection in contrast to its loss in human gastric adenocarcinoma. Indeed, adenoviral transduction of BTG2/TIS21 significantly inhibited Tipα activity in MKN-1 and MGT-40, human and mouse gastric cancer cells, respectively, thereby downregulating tumor necrosis factor-α (TNFα) expression and Erk1/2 phosphorylation by reducing expression of nucleolin, a Tipα receptor. Chromatin immunoprecipitation proved that BTG2/TIS21 inhibited Sp1 expression and its binding to the promoter of the nucleolin gene. In addition, BTG2/TIS21 expression significantly reduced membrane-localized nucleolin expression in cancer cells, and the loss of BTG2/TIS21 expression induced cytoplasmic nucleolin availability in gastric cancer tissues, as evidenced by immunoblotting and immunohistochemistry. Higher expression of BTG2 and lower expression of nucleolin were accompanied with better overall survival of poorly differentiated gastric cancer patients. This is the first report showing that BTG2/TIS21 inhibits nucleolin expression via Sp1 binding, which might be associated with the inhibition of H. pylori-induced carcinogenesis. We suggest that BTG2/TIS21 is a potential inhibitor of nucleolin in the cytoplasm, leading to inhibition of carcinogenesis after H. pylori infection.

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