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

Mechanical Characterization of Tungsten-Titanium-Lanthana alloy: Influence of Temperature and Atmosphere

The target is to evaluate the mechanical behavior of Ti and La2O3 dispersed W alloy, processed by HIP and compare it with a reference pure-W. Tests were performed in both oxidant (air) and inert (vacuum) atmosphere in a temperature range from -196 to 1200 °C

Understanding the Bias Dependence of Low Frequency Noise in Sin-gle Layer Graphene FETs

This letter investigates the bias-dependent low frequency noise of single layer graphene field-effect transistors. Noise measurements have been conducted with electrolyte-gated graphene transistors covering a wide range of gate and drain bias conditions for different channel lengths. A new analytical model that accounts for the propagation of the local noise sources in the channel to the terminal currents and voltages is proposed in this paper to investigate the noise bias dependence. Carrier number and mobility fluctuations are considered as the main causes of low frequency noise and the way these mechanisms contribute to the bias dependence of the noise is analyzed in this work. Typically, normalized low frequency noise in graphene devices has been usually shown to follow an M-shape dependence versus gate voltage with the minimum near the charge neutrality point (CNP). Our work reveals for the first time the strong correlation between this gate dependence and the residual charge which is relevant in the vicinity of this specific bias point. We discuss how charge inhomogeneity in the graphene channel at higher drain voltages can contribute to low frequency noise; thus, channel regions nearby the source and drain terminals are found to dominate the total noise for gate biases close to the CNP. The excellent agreement between the experimental data and the predictions of the analytical model at all bias conditions confirms that the two fundamental 1/f noise mechanisms, carrier number and mobility fluctuations, must be considered simultaneously to properly understand the low frequency noise in graphene FETs. The proposed analytical compact model can be easily implemented and integrated in circuit simulators, which can be of high importance for graphene based circuits design.Comment: 18 pages, 10 figure

Predicting hydration Gibbs energies of alkyl-aromatics using molecular simulation : a comparison of current force fields and the development of a new parameter set for accurate solvation data

The Gibbs energy of hydration is an important quantity to understand the molecular behavior in aqueous systems at constant temperature and pressure. In this work we review the performance of some popular force fields, namely TraPPE, OPLS-AA and Gromos, in reproducing the experimental Gibbs energies of hydration of several alkyl-aromatic compounds-benzene, mono-, di- and tri-substituted alkylbenzenes-using molecular simulation techniques. In the second part of the paper, we report a new model that is able to improve such hydration energy predictions, based on Lennard Jones parameters from the recent TraPPE-EH force field and atomic partial charges obtained from natural population analysis of density functional theory calculations. We apply a scaling factor determined by fitting the experimental hydration energy of only two solutes, and then present a simple rule to generate atomic partial charges for different substituted alkyl-aromatics. This rule has the added advantages of eliminating the unnecessary assumption of fixed charge on every substituted carbon atom and providing a simple guideline for extrapolating the charge assignment to any multi-substituted alkyl-aromatic molecule. The point charges derived here yield excellent predictions of experimental Gibbs energies of hydration, with an overall absolute average deviation of less than 0.6 kJ mol(-1). This new parameter set can also give good predictive performance for other thermodynamic properties and liquid structural information

Resistance gene pool to co-trimoxazole in non-susceptible Nocardia strains

The soil-borne pathogen Nocardia sp. causes severe cutaneous, pulmonary, and central nervous system infections. Against them, co-trimoxazole (SXT) constitutes the mainstay of antimicrobial therapy. However, some Nocardia strains show resistance to SXT, but the underlying genetic basis is unknown. We investigated the presence of genetic resistance determinants and class 1-3 integrons in 76 SXT-resistant Nocardia strains by PCR and sequencing. By E test, these clinical strains showed SXT minimum inhibitory concentrations of ≥32:608 mg/L (ratio of 1:19 for trimethoprim: sulfamethoxazole). They belonged to 12 species, being the main representatives Nocardia farcinica (32%), followed by N. flavorosea (6.5%), N. nova (11.8%), N. carnea (10.5%), N. transvalensis (10.5%), and Nocardia sp. (6.5%). The prevalence of resistance genes in the SXT-resistant strains was as follows: sul1 and sul2 93.4 and 78.9%, respectively, dfrA(S1) 14.7%, blaTEM-1 and blaZ 2.6 and 2.6%, respectively, VIM-2 1.3%, aph(3')-IIIa 40.8%, ermA, ermB, mefA, and msrD 2.6, 77.6, 14.4, and 5.2%, respectively, and tet(O), tet(M), and tet(L) 48.6, 25.0, and 3.9%, respectively. Detected amino acid changes in GyrA were not related to fluoroquinolone resistance, but probably linked to species polymorphism. Class 1 and 3 integrons were found in 93.42 and 56.57% strains, respectively. Class 2 integrons and sul3 genes were not detected. Other mechanisms, different than dfrA(S1), dfrD, dfrF, dfrG, and dfrK, could explain the strong trimethoprim resistance shown by the other 64 strains. For first time, resistance determinants commonly found in clinically important bacteria were detected in Nocardia sp. sul1, sul2, erm(B), and tet(O) were the most prevalent in the SXT-resistant strains. The similarity in their resistome could be due to a common genetic platform, in which these determinants are co-transferred.This study was presented at the 54th Interscience Conference on Antimicrobial Agents and Chemotherapy, ICAAC2014, Washington, DC, USA. We thank Adrian Burton for editing and language assistance (http://physicalevidence.es/english/welcome). We are very grateful to all persons who took part in this study, and to the sample providers.S

Angiotensin Type 1 Receptor Antagonists Protect Against Alpha-Synuclein-Induced Neuroinflammation and Dopaminergic Neuron Death

Altres ajuts: This study received funding from the Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas' intramural program (2014/01 and 2017/02), Galician Government (Xunta de Galicia, Consellería de Educación; GRC2014/002), Navarra Government (Departamento de Salud; 046-2017), and Fondo Europeo de Desarrollo Regional (Regional European Development Fund).The loss of dopaminergic neurons and α-synuclein accumulation are major hallmarks of Parkinson's disease (PD), and it has been suggested that a major mechanism of α-synuclein toxicity is microglial activation. The lack of animal models that properly reproduce PD, and particularly the underlying synucleinopathy, has hampered the clarification of PD mechanisms and the development of effective therapies. Here, we used neurospecific adeno-associated viral vectors serotype 9 coding for either the wild-type or mutated forms of human alpha-synuclein (WT and SynA53T, respectively) under the control of a synapsin promoter to further induce a marked dopaminergic neuron loss together with an important microglial neuroinflammatory response. Overexpression of neuronal alpha-synuclein led to increased expression of angiotensin type 1 receptors and NADPH oxidase activity, together with a marked increase in the number of OX-6-positive microglial cells and expression of markers of phagocytic activity (CD68) and classical pro-inflammatory/M1 microglial phenotype markers such as inducible nitric oxide synthase, tumor necrosis factor alpha, interleukin-1β, and IL-6. Moreover, a significant decrease in the expression of markers of immunoregulatory/M2 microglial phenotype such as the enzyme arginase-1 was constantly observed. Interestingly, alpha-synuclein-induced changes in microglial phenotype markers and dopaminergic neuron death were inhibited by simultaneous treatment with the angiotensin type 1 blockers candesartan or telmisartan. Our results suggest the repurposing of candesartan and telmisartan as a neuroprotective strategy for PD