Velocity Saturation effect on Low Frequency Noise in short channel Single Layer Graphene FETs

Graphene devices for analog and RF applications are prone to Low Frequency Noise (LFN) due to its upconversion to undesired phase noise at higher frequencies. Such applications demand the use of short channel graphene transistors that operate at high electric fields in order to ensure a high speed. Electric field is inversely proportional to device length and proportional to channel potential so it gets maximized as the drain voltage increases and the transistor length shrinks. Under these conditions though, short channel effects like Velocity Saturation (VS) should be taken into account. Carrier number and mobility fluctuations have been proved to be the main sources that generate LFN in graphene devices. While their contribution to the bias dependence of LFN in long channels has been thoroughly investigated, the way in which VS phenomenon affects LFN in short channel devices under high drain voltage conditions has not been well understood. At low electric field operation, VS effect is negligible since carriers velocity is far away from being saturated. Under these conditions, LFN can be precicely predicted by a recently established physics-based analytical model. The present paper goes a step furher and proposes a new model which deals with the contribution of VS effect on LFN under high electric field conditions. The implemented model is validated with novel experimental data, published for the first time, from CVD grown back-gated single layer graphene transistors operating at gigahertz frequencies. The model accurately captures the reduction of LFN especially near charge neutrality point because of the effect of VS mechanism. Moreover, an analytical expression for the effect of contact resistance on LFN is derived. This contact resistance contribution is experimentally shown to be dominant at higher gate voltages and is accurately described by the proposed model.Comment: Main Manuscript:10 pages, 6 figure

Matériaux polymères pour la création de guides optiques

5 pagesNational audienceUn des objectifs de travail au laboratoire Foton est l'amélioration du confinement de la lumière dans les microstructures polymères, de par leurs propriétés optiques (indices de réfraction optimisés, transparence à la longueur d'onde choisie) et chimiques (compatibilité des matériaux de cœur et de gaine, stabilité dans le temps), ainsi que par la réduction des pertes intrinsèques et extrinsèques des guides. Pour cela, la détermination des propriétés physico-chimiques des polymères utilisés lors de la création d'un guide optique et l'optimisation des interfaces mises en jeu sont deux directions de travail privilégiées, sachant que les structures polymères sont réalisées en photolithographie conventionnelle par masquage dans l'UV à 365 nm sur un substrat de silicium, suivi d'une gravure RIE

Magneto-optical properties of InSb for terahertz applications

Magneto-optical permittivity tensor spectra of undoped InSb, n-doped and p-doped InSb crystals were determined using the terahertz time-domain spectroscopy (THz-TDS) and the Fourier transform far-infrared spectroscopy (far-FTIR). A Huge polar magneto-optical (MO) Kerr-effect (up to 20 degrees in rotation) and a simultaneous plasmonic behavior observed at low magnetic field (0.4 T) and room temperature are promising for terahertz nonreciprocal applications. We demonstrate the possibility of adjusting the the spectral rage with huge MO by increase in n-doping of InSb. Spectral response is modeled using generalized magneto-optical Drude-Lorentz theory, giving us precise values of free carrier mobility, density and effective mass consistent with electric Hall effect measurement.Web of Science611art. no. 11502

Low-frequency noise parameter extraction method for single layer graphene FETs

In this paper, a detailed parameter extraction methodology is proposed for low-frequency noise (LFN) in single layer (SL) graphene transistors (GFETs) based on a recently established compact LFN model. Drain current and LFN of two short channel back-gated GFETs (L=300, 100 nm) were measured at lower and higher drain voltages, for a wide range of gate voltages covering the region away from charge neutrality point (CNP) up to CNP at p-type operation region. Current-voltage (IV) and LFN data were also available from a long channel SL top solution-gated (SG) GFET (L=5 um), for both p- and n-type regions near and away CNP. At each of these regimes, the appropriate IV and LFN parameters can be accurately extracted. Regarding LFN, mobility fluctuation effect is dominant at CNP and from there the Hooge parameter aH can be extracted while the carrier number fluctuation contribution which is responsible for the well-known M-shape bias dependence of output noise divided by squared drain current, also observed in our data, makes possible the extraction of the NT parameter related to the number of traps. In the less possible case of a Lambda-shape trend, NT and aH can be extracted simultaneously from the region near CNP. Away from CNP, contact resistance can have a significant contribution to LFN and from there the relevant parameter SDR^2 is defined. The LFN parameters described above can be estimated from the low drain voltage region of operation where the effect of Velocity Saturation (VS) mechanism is negligible. VS effect results in the reduction of LFN at higher drain voltages and from there the IV parameter hOmega which represents the phonon energy and is related to VS effect can be derived both from drain current and LFN data

Focused Ion Beam Microfabrication

Contains an introduction, reports on x research projects and a list of publications.Defense Advanced Research Projects Agency/U.S. Army Research Office Grant DAAL-03-92-G-0217National Science Foundation Grant ECS 89-21728Defense Advanced Research Projects Agency/U.S. Army Research Office (ASSERT Program) Grant DAAL03-92-G-0305Semiconductor Research CorporationNational Science Foundation Grant DMR 92-02633U.S. Army Research Office Grant DAAL03-90-G-0223U.S. Navy - Naval Research Laboratory/Micrion Contract M0877

De 20 000 à 18 000 BP en Quercy : apports de la séquence du Cuzoul de Vers à la compréhension de l'évolution des comportements socio-économiques entre Solutréen récent et Badegoulien

Essai de synthèse des travaux menés autour du gisement du Cuzoul de Vers (Lot)

Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy

Mammalian target of rapamycin (mTOR) is a key regulator of cell growth that associates with raptor and rictor to form the mTOR complex 1 (mTORC1) and mTORC2, respectively. Raptor is required for oxidative muscle integrity, whereas rictor is dispensable. In this study, we show that muscle-specific inactivation of mTOR leads to severe myopathy, resulting in premature death. mTOR-deficient muscles display metabolic changes similar to those observed in muscles lacking raptor, including impaired oxidative metabolism, altered mitochondrial regulation, and glycogen accumulation associated with protein kinase B/Akt hyperactivation. In addition, mTOR-deficient muscles exhibit increased basal glucose uptake, whereas whole body glucose homeostasis is essentially maintained. Importantly, loss of mTOR exacerbates the myopathic features in both slow oxidative and fast glycolytic muscles. Moreover, mTOR but not raptor and rictor deficiency leads to reduced muscle dystrophin content. We provide evidence that mTOR controls dystrophin transcription in a cell-autonomous, rapamycin-resistant, and kinase-independent manner. Collectively, our results demonstrate that mTOR acts mainly via mTORC1, whereas regulation of dystrophin is raptor and rictor independent

Focused Ion Beam Microfabrication

Contains an introduction, reports on seven research projects and a list of publications.Defense Advanced Research Projects Agency/U.S. Army Research Office Contract DAAL03-88-K-0108National Science Foundation Grant ECS 89-21728U.S. Army Research Office Contract DAAL03-87-K-0126U.S. Navy - Naval Research Laboratory/Micrion Agreement M08774SEMATEC

Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy

mTor, acting mainly via mTORC1, controls dystrophin transcription in a raptor- and rictor-independent mechanism