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A very simple triple-band circularly polarised printed monopole antenna with bandwidth enhancement for 2.45/5.8 GHz wireless local area network (WLAN) and 3.5 GHz worldwide interoperability for microwave access (WiMAX) applications is presented. The circular polarisation characteristic at the WiMAX band was obtained by an inverted-U-shaped radiator rotated by 45°around the horizontal axis. To create the upper circular polarisation mode at the 5.8 GHz WLAN band, an I-shaped strip was added on the right side of the radiator. Finally, by attaching an inverted-Lshaped strip at the end of the I-shaped strip, the lower circular polarisation characteristic at the 2.45 GHz WLAN band was achieved. The proposed antenna is excited by a simple 50 Ω microstrip feed line using a transformer for impedance matching. The measured −10 dB impedance bandwidth is 450 MHz (2.35-2.8 GHz) and 4.1 GHz (3.3-7.4 GHz) and the measured 3 dB axial-ratio bandwidth reaches 12% (2.35-2.65 GHz), 10% (3.3-3.65 GHz) and 4.4% (5.6-5.85 GHz).

We report an efficient method for growing NiO nanostructures by oblique angle deposition (OAD) technique in an e-beam evaporator for supercapacitor applications. This facile physical vapor deposition technique combined with OAD presents a unique, direct, and economical route for obtaining high width-to-height ratio nanorods for supercapacitor electrodes. The NiO nanostructure essentially consists of nanorods with varying dimensions. The sample deposited at OAD 75° showed highest supercapacitance value of 344 F/g. NiO nanorod electrodes exhibits excellent electrochemical stability with no degradation in capacitance after 5000 charge-discharge cycles. The nanostructured film adhered well to the substrate and had 131% capacity retention. Peak energy density and power density of the NiO nanorods were 8.78 Wh/kg and 2.5 kW/kg, respectively. This technique has potential to be expanded for growing nanostructured films of other interesting metal/metal oxide candidates for supercapacitor applications.

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In breast cancer, the cytokine tumor necrosis factor-α (TNF-α) induces cell invasion, although the molecular basis of it has not been clearly elucidated. In this study, we investigated the role of daidzein in regulating TNF-α induced cell invasion and the underlying molecular mechanisms. Daidzein inhibited TNF-α induced cellular migration and invasion in estrogen receptor (ER) negative MCF10DCIS.com human breast cancer cells. TNF-α activated Hedgehog (Hh) signaling by enhancing Gli1 nuclear translocation and transcriptional activity, which resulted in increased invasiveness; these effects were blocked by daidzein and the Hh signaling inhibitors, cyclopamine and vismodegib. Moreover, these compounds suppressed TNF-α induced matrix metalloproteinase (MMP)-9 mRNA expression and activity. Taken together, mammary tumor cell invasiveness was stimulated by TNF-α induced activation of Hh signaling; these effects were abrogated by daidzein, which suppressed Gli1 activation, thereby inhibiting migration and invasion.