Because of the popularity of smart electronics, multifunctional energy storage devices, especially electrochromic supercapacitors (SCs), have attracted tremendous research interest. Herein, a solid-state electrochromic asymmetric SC (ASC) window is designed and fabricated by introducing WO and polyaniline as the negative and positive electrodes, respectively. The two complementary materials contribute to the outstanding electrochemical and electrochromic performances of the fabricated device. With an operating voltage window of 1.4 V and an areal capacitance of 28.3 mF cm, the electrochromic devices show a high energy density of 7.7 × 10 mW h cm. Meanwhile, they exhibit an obvious and reversible color transition between light green (uncharged state) and dark blue (charged state), with an optical transmittance change between 55 and 12% at a wavelength of 633 nm. Hence, the energy storage level of the ASC is directly related to its color and can be determined by the naked eye, which means it can be incorporated with other energy cells to visual display their energy status. Particularly, a self-powered and color-indicated system is achieved by combining the smart windows with commercial solar cell panels. We believe that the novel electrochromic ASC windows will have great potential application for both smart electronics and smart buildings.

BackgroundSaikosaponin-a and -d, two naturally occurring compounds derived from Bupleurum radix, have been shown to exert anti-cancer activity in several cancer cell lines. However, the effect of combination of saikosaponins with chemotherapeutic drugs has never been addressed. Thus, we investigated whether these two saikosaponins have chemosensitization effect on cisplatin-induced cancer cell cytotoxicity.MethodsTwo cervical cancer cell lines, HeLa and Siha, an ovarian cancer cell line, SKOV3, and a non-small cell lung cancer cell line, A549, were treated with saikosaponins or cisplatin individually or in combination. Cell death was quantitatively detected by the release of lactate dehydrogenase (LDH) using a cytotoxicity detection kit. Cellular ROS was analyzed by flow cytometry. Apoptosis was evaluated by AO/EB staining, flow cytometry after Anexin V and PI staining, and Western blot for caspase activation. ROS scavengers and caspase inhibitor were used to determine the roles of ROS and apoptosis in the effects of saikosaponins on cisplatin-induced cell death.ResultsBoth saikosaponin-a and -d sensitized cancer cells to cisplatin-induced cell death in a dose-dependent manner, which was accompanied with induction of reactive oxygen species (ROS) accumulation. The dead cells showed typical apoptotic morphologies. Both early apoptotic and late apoptotic cells detected by flow cytometry were increased in saikosaponins and cisplatin cotreated cells, accompanied by activation of the caspase pathway. The pan-caspase inhibitor z-VAD and ROS scanvengers butylated hydroxyanisole (BHA) and N-acetyl-L-cysteine (NAC) dramatically suppressed the potentiated cytotoxicity achieved by combination of saikosaponin-a or -d and cisplatin.ConclusionsThese results suggest that saikosaponins sensitize cancer cells to cisplatin through ROS-mediated apoptosis, and the combination of saikosaponins with cisplatin could be an effective therapeutic strategy.

The radiation of an electric dipole emitter can be drastically enhanced if the emitter is placed in the nano-gap of a metallic dipole antenna. By assuming that only surface plasmon polaritons (SPPs) are excited on the antenna, we build up an intuitive pure-SPP model that is able to comprehensively predict the electromagnetic features of the antenna radiation, such as the total or radiative emission rate and the far-field radiation pattern. With the model we can distinguish the respective contributions from SPPs and from other surface waves to the antenna radiation. It is found that for antennas with long arms that support higher-order resonances, SPPs provide a dominant contribution to the antenna radiation, while for other cases, the contribution of surface waves other than SPPs should be considered. The model reveals an intuitive picture that the enhancement of the antenna radiation is due to surface waves that are resonantly excited on the two antenna arms and that are further coupled into the nano-gap or scattered into free space. From the model we can derive a phase-matching condition that predicts the antenna resonance and the resultant enhanced radiation. The model is helpful for a physical understanding and intuitive design of antenna devices. R esonant optical nano-antennas are intensively studied in recent years due to their superior properties of generating strong electromagnetic field under far-field illuminations 1-6 and reciprocally, enhancing the radiation of emitters such as molecules or quantum dots in the vicinity of antennas [7][8][9][10][11][12][13][14][15][16][17][18][19] . Plasmonic nanoantennas are widely used in enhanced Raman scattering spectroscopy [20][21][22][23] , nonlinear optical control [24][25][26][27] , and single-emitter fluorescence enhancement [9][10][11][15][16][17][18]28 . Much experimental and theoretical work has been devoted to achieve an understanding of the underlying physics of resonant nano-antennas for guiding the design of relevant devices. For a simple single-wire nano-antenna, it is described as a Fabry-Pérot resonator of surface plasmon polaritons (SPPs) 4,5,12,19 for predicting the resonance frequency. The single-wire nano-antenna is also treated as an equivalent circuit composed of resistors, inductors and capacitors [29][30][31] , and radiation or scattering features such as the resonance frequency and the extinction spectrum can be predicted. Resonant dipole antennas, which are made of two metallic nano-wires separated by a nano-gap 1 , can achieve a much stronger enhancement effect than the single-wire antenna. Concepts of impedance and resistance are proposed for dipole antennas [32][33][34][35] for reproducing quantities such as the resonance frequency, the quantum efficiency and the enhancement of field. The dipole antennas are also modelled as one-dimensional micro-cavities 34,36 , and the enhancement effect is attributed to the resonance of SPPs. In previous literatures, it is commonly believed that the enhancement effect of the antenna radiation or th...

As a common anticancer drug, cisplatin has been widely used for treating tumors in the clinic. However, its side effects, especially its nephrotoxicity, noticeably restrict the application of cisplatin. Therefore, it is imperative to investigate the mechanism of renal injury and explore the corresponding remedies. In this study, we showed the phenotypes of the renal tubules and epithelial cell death as well as elevated cleaved-caspase3- and TUNEL-positive cells in rats intraperitoneally injected with cisplatin. Similar cisplatin-induced cell apoptosis was found in HK-2 and NRK-52E cells exposed to cisplatin as well. In both models of cisplatin-induced apoptosis in vivo and in vitro, quantitative PCR data displayed reductions in miR-30a-e expression levels, indicating that miR-30 might be involved in regulating cisplatin-induced cell apoptosis. This was further confirmed when the effects of cisplatin-induced cell apoptosis were found to be closely correlated with alterations in miR-30c expression, which were manipulated by transfection of either the miR-30c mimic or miR-30c inhibitor in HK-2 and NRK-52E cells. Using bioinformatics tools, including TargetScan and a gene expression database (Gene Expression Omnibus), Adrb1, Bnip3L, Hspa5 and MAP3K12 were predicted to be putative target genes of miR-30c in cisplatin-induced apoptosis. Subsequently, Bnip3L and Hspa5 were confirmed to be the target genes after determining the expression of these putative genes following manipulation of miR-30c expression levels in HK-2 cells. Taken together, our current experiments reveal that miR-30c is certainly involved in regulating the renal tubular cell apoptosis induced by cisplatin, which might supply a new strategy to minimize cisplatin-induced nephrotoxicity.

Abstract. Transforming growth factor β1 (TGF-β1) has been associated with poor outcomes in patients with breast cancer. However, the functions and underlying molecular mechanisms of TGF-β1 in breast cancer remain unknown. Therefore, the present study aimed to identify the effects of components of the TGF-β/microRNA (miR-)21/phosphatase and tensin homolog (PTEN) signaling axis in breast cancer. TGF-β1 was identified to upregulate the expression of miR-21, and miR-21 was demonstrated to be significantly upregulated in breast cancer tissues compared with benign proliferative breast disease. In addition, the expression of miR-21 was significantly associated with increased TGF-β1 and clinical characteristics in patients, including tumor grade and lymph node metastasis (all P<0.05). Furthermore, in the breast cancer MCF-7 cell line, TGF-β1 was revealed to induce the expression of miR-21 in a doseand time-dependent manner. The results of the present study additionally demonstrated that increased miR-21, in response to TGF-β1 signaling, was associated with tumor invasion and chemoresistance in vitro. In addition, suppression of PTEN was mediated by TGF-β1-induced expression of miR-21 in breast cancer cells and using a miR-21 inhibitor revitalized the expression of PTEN. The results of the present study explored the functions of TGF-β1-stimulated expression of miR-21 to suppress the PTEN axis, which promotes breast cancer progression