Double transition metal-containing M₂TiAlC₂ <i>o</i>-MAX phases as Li-ion batteries anodes: a theoretical screening

Here, thermodynamic stability and lithium storage properties of double transition metal M2TiAlC2 o-MAX phases (M = Cr, V, Mo, Nb, Ta, Hf, Zr, Sc, Y, La) are theoretically investigated by density functional theory (DFT) calculation. M2TiAlC2 with a larger M atomic radius shows larger interlayer space that may benefit the Li-ion intercalation. A promising theoretical capacity of 276.87 mAh g-1 is predicted for Sc2TiAlC2. The low Li-ion diffusion barriers (0.57–0.64 eV) for M2TiAlC2 indicate the possibility to achieve fast Li-ion diffusion that is crucial for designing high-power batteries. This work provides opportunities to explore MAX phases as promising Li-ion storage materials. This work investigates the thermostability and lithium storage properties of double transition metal o-MAX phases by DFT calculation and provides a guideline for exploring MAX phases for lithium storage applications.</p

Protein-Induced Gold Nanoparticle Assembly for Improving the Photothermal Effect in Cancer Therapy

Gold nanoparticles (AuNPs) are promising photothermal agents for cancer therapy. However, the absorption of spherical AuNPs is weak in the desired tissue-penetrating near-infrared (NIR) window, resulting in low photothermal efficiency within this window. Here, we show that fibrous nanostructures assembled from spherical AuNPs since the templating effect of silk fibroin (SF) could red-shift the optical absorption to NIR and thus present improved photothermal efficiency within the NIR window. Specifically, negatively charged SF, a protein derived from Bombyx mori, was assembled into nanofibers due to the interaction with the positively charged AuNPs and concomitantly templated the AuNPs into fibrous nanostructures. The resultant AuNPs/SF nanofibers presented higher NIR light absorption at 808 nm and higher photothermal efficiency under 808 nm NIR irradiation than nonassembled AuNPs. In vitro and in vivo analyses proved that AuNPs/SF nanofibers could efficiently kill breast cancer cells and destruct breast cancer tumor tissues under one-time NIR irradiation for 6 min by photothermal therapy (PTT) but nonassembled AuNPs could not. This work suggests that the self-assembled AuNPs/SF nanofibers are effective photosensitizers for PTT, and biotemplated assembly of photothermal agents into highly ordered nanostructures is a promising approach to increasing the PTT efficiency

MTOR-siRNA reduced the formation of Raptor/mTOR complex and inhibited the phosphorylation of p70S6K.

(A) mTOR-siRNA significantly down-regulated p70S6K mRNA expression at 48 hours of transfection, and this effect was enlarged at 72 hours of transfection. The values of p70S6K mRNA were normalized to Actin mRNA and then normalized to control relative value. (B) The phosphorylation of p70S6K was reduced by mTOR-siRNA after 72 hours of transfection. (C) The interaction of Raptor and mTOR were assessed using co-immunoprecipitation assay. In the anti-mTOR antibody precipitates, the levels of Raptor were drastically reduced by mTOR-siRNA. (Data = Mean ± SEM, **p<0.01, compared with the non-silencing siRNA).</p

The inhibition of cell migration by mTOR-siRNA.

<p>(<b>A</b>) Representative images were taken from Scratch assay. (<b>B</b>) TGF-β-induced cell migration was blocked by mTOR-siRNA. The Gap closure was reduced by mTOR-siRNA. (<b>C</b>) Cell migration was assessed using the Byoden chamber in the absence of TGF-β. The mTOR-siRNA transfected HLE B3 cells were seeded into the Boyden chamber and incubated for 48 hours. The cell migration was significantly reduced by mTOR-siRNA at 48 hours. (Data = Mean ± SEM, *<i>p</i> < 0.05).</p

MTOR-siRNA eliminated the protein interaction of Rictor and mTOR protein and inhibited the phosphorylation of AKT.

<p>(<b>A</b>) HLE B3 cells were treated with mTOR-siRNA, non-silencing siRNA or control and harvested after 24, 48 and 72 hours of transfection. The levels of mRNA were determined by quantitative real-time PCR. The values of AKT mRNA were normalized to Actin mRNA and then normalized to the control value. (<b>B</b>) The phosphorylation of AKT was reduced by mTOR-siRNA after 72 hours of transfection. (<b>C</b>) The interaction of Rictor and mTOR proteins was assessed by co-immunoprecipitation using an anti-mTOR antibody. The precipitates were examined by western blot with anti-Rictor antibody. In the mTOR antibody precipitates, Rictor was undetectable in the samples treated with mTOR-siRNA. (Data = Mean ± SEM, **<i>p</i><0.01, compared with the non-silencing siRNA).</p

Primer sequences employed for real-time PCR.

<p>Primer sequences employed for real-time PCR.</p

The effect of mTOR-siRNA on the levels of mTOR mRNA and protein.

<p>HLE B3 cells were treated with mTOR-siRNA, non-silencing siRNA or control (transfection reagent only), and harvested after 24 h, 48 h and 72 h of transfection. (<b>A</b>) MTOR mRNA was quantified by real-time PCR. The values of mTOR were normalized to Actin and then normalized to control relative value. (<b>B</b>) Representative agarose gel images of the real-time PCR products. (<b>C</b>) MTOR protein levels were examined by Western blot. (Data = Mean ± SEM, *<i>p</i><0.05, **<i>p</i><0.01, compared with the control groups).</p

MTOR-siRNA blocked EMT induced by TGF-β.

<p>HLE B3 cells were transfected with mTOR-siRNA and 24 hours later cells were treated with TGF-β for 48 hours. Cells were then lysed and subjected to Western blot.</p

The effect of mTOR-siRNA on HLE B3 proliferation.

<p>CCK8 assay was used to determine HLE B3 proliferation. MTOR-siRNA significantly reduced cell proliferation at 48 hours of transfection and this effect was enhanced at 72 hours of transfection. (Data = Mean ± SEM, *<i>p</i><0.05, compared with the control groups).</p

The HLE B3 cells growth curve in the presence of mTOR-siRNA and rapamycin.

<p>mTOR-siRNA inhibited cell growth at 48 hours of transfection and this effect was dramatically enlarged at 72 hours of transfection. Rapamycin significantly reduced cell growth at 72 hours of transfection. (Data = Mean ± SEM, *<i>p</i> < 0.05).</p