Tuning the spontaneous light emission in phoxonic cavities

The modulation of spontaneous light emission of active centers through elastic waves in Si/SiO_2 multilayer phoxonic structures that support dual photonic-phononic localized modes, in the bulk or at the surface, is studied by means of rigorous full electrodynamic and elastodynamic calculations. Our results show that strong dynamic modulation of the spontaneous emission can be achieved through an enhanced acousto-optic interaction when light and elastic energy are simultaneously localized in the same region

A 1Gsample/s 6-bit flash A/D converter with a combined chopping and averaging technique for reduced distortion in 0.18(mu)m CMOS

Hard disk drive applications require a high Spurious Free Dynamic Range (SFDR), 6-bit Analog-to-Digital Converter (ADC) at conversion rates of 1GHz and beyond. This work proposes a robust, fault-tolerant scheme to achieve high SFDR in an av- eraging flash A/D converter using comparator chopping. Chopping of comparators in a flash A/D converter was never previously implemented due to lack of feasibility in implementing multiple, uncorrelated, high speed random number generators. This work proposes a novel array of uncorrelated truly binary random number generators working at 1GHz to chop all comparators. Chopping randomizes the residual offset left after averaging, further pushing the dynamic range of the converter. This enables higher accuracy and lower bit-error rate for high speed disk-drive read channels. Power consumption and area are reduced because of the relaxed design requirements for the same linearity. The technique has been verified in Matlab simulations for a 6-bit 1Gsamples/s flash ADC under case of process gradients with non-zero mean offsets as high as 60mV and potentially serious spot offset errors as high as 1V for a 2V peak to peak input signal. The proposed technique exhibits an improvement of over 15dB compared to pure averaging flash converters for all cases. The circuit-level simulation results, for a 1V peak to peak input signal, demon- strate superior performance. The reported ADC was fabricated in TSMC 0.18 ??mCMOS process. It occupies 8.79mm2 and consumes about 400mW from 1.8V power supply at 1GHz. The targeted SFDR performance for the fabricated chip is at least 45dB for a 256MHz input sine wave, sampled at 1GHz, about 10dB improvement on the 6-bit flash ADCs in the literature

Leptin as a critical regulator of hepatocellular carcinoma development through modulation of human telomerase reverse transcriptase

<p>Abstract</p> <p>Background</p> <p>Numerous epidemiological studies have documented that obesity is associated with hepatocellular carcinoma (HCC). The aim of this study was to investigate the biological actions regulated by leptin, the obesity biomarker molecule, and its receptors in HCC and the correlation between leptin and human telomerase reverse transcriptase (hTERT), a known mediator of cellular immortalization.</p> <p>Methods</p> <p>We investigated the relationship between leptin, leptin receptors and hTERT mRNA expression in HCC and healthy liver tissue samples. In HepG2 cells, chromatin immunoprecipitation assay was used to study signal transducer and activator of transcription-3 (STAT3) and myc/mad/max transcription factors downstream of leptin which could be responsible for hTERT regulation. Flow cytometry was used for evaluation of cell cycle modifications and MMP1, 9 and 13 expression after treatment of HepG2 cells with leptin. Blocking of leptin's expression was achieved using siRNA against leptin and transfection with liposomes.</p> <p>Results</p> <p>We showed, for the first time, that leptin's expression is highly correlated with hTERT expression levels in HCC liver tissues. We also demonstrated in HepG2 cells that leptin-induced up-regulation of hTERT and TA was mediated through binding of STAT3 and Myc/Max/Mad network proteins on <it>hTERT </it>promoter. We also found that leptin could affect hepatocellular carcinoma progression and invasion through its interaction with cytokines and matrix mettaloproteinases (MMPs) in the tumorigenic microenvironment. Furthermore, we showed that histone modification contributes to leptin's gene regulation in HCC.</p> <p>Conclusions</p> <p>We propose that leptin is a key regulator of the malignant properties of hepatocellular carcinoma cells through modulation of hTERT, a critical player of oncogenesis.</p

Calcul de la structure electronique d'alliages metalliques dilues par la methode L.M.T.O.-A.S.A

SIGLECNRS T 56494 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc