Monte Carlo study of coaxially gated CNTFETs: capacitive effects and dynamic performance

Carbon Nanotube (CNT) appears as a promising candidate to shrink field-effect transistors (FET) to the nanometer scale. Extensive experimental works have been performed recently to develop the appropriate technology and to explore DC characteristics of carbon nanotube field effect transistor (CNTFET). In this work, we present results of Monte Carlo simulation of a coaxially gated CNTFET including electron-phonon scattering. Our purpose is to present the intrinsic transport properties of such material through the evaluation of electron mean-free-path. To highlight the potential of high performance level of CNTFET, we then perform a study of DC characteristics and of the impact of capacitive effects. Finally, we compare the performance of CNTFET with that of Si nanowire MOSFET.Comment: 15 pages, 14 figures, final version to be published in C. R. Acad. Sci. Pari

Microwave Transport in Metallic Single-Walled Carbon Nanotubes

The dynamical conductance of electrically contacted single-walled carbon nanotubes is measured from dc to 10 GHz as a function of source-drain voltage in both the low-field and high-field limits. The ac conductance of the nanotube itself is found to be equal to the dc conductance over the frequency range studied for tubes in both the ballistic and diffusive limit. This clearly demonstrates that nanotubes can carry high-frequency currents at least as well as dc currents over a wide range of operating conditions. Although a detailed theoretical explanation is still lacking, we present a phenomenological model of the ac impedance of a carbon nanotube in the presence of scattering that is consistent with these results.Comment: Added reference

Regulation of caspase-3 processing by cIAP2 controls the switch between pro-inflammatory activation and cell death in microglia.

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International Licence. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons licence, users will need to obtain permission from the licence holder to reproduce the material.The activation of microglia, resident immune cells of the central nervous system, and inflammation-mediated neurotoxicity are typical features of neurodegenerative diseases, for example, Alzheimer's and Parkinson's diseases. An unexpected role of caspase-3, commonly known to have executioner role for apoptosis, was uncovered in the microglia activation process. A central question emerging from this finding is what prevents caspase-3 during the microglia activation from killing those cells? Caspase-3 activation occurs as a two-step process, where the zymogen is first cleaved by upstream caspases, such as caspase-8, to form intermediate, yet still active, p19/p12 complex; thereafter, autocatalytic processing generates the fully mature p17/p12 form of the enzyme. Here, we show that the induction of cellular inhibitor of apoptosis protein 2 (cIAP2) expression upon microglia activation prevents the conversion of caspase-3 p19 subunit to p17 subunit and is responsible for restraining caspase-3 in terms of activity and subcellular localization. We demonstrate that counteracting the repressive effect of cIAP2 on caspase-3 activation, using small interfering RNA targeting cIAP2 or a SMAC mimetic such as the BV6 compound, reduced the pro-inflammatory activation of microglia cells and promoted their death. We propose that the different caspase-3 functions in microglia, and potentially other cell types, reside in the active caspase-3 complexes formed. These results also could indicate cIAP2 as a possible therapeutic target to modulate microglia pro-inflammatory activation and associated neurotoxicity observed in neurodegenerative disorders

Low-frequency Current Fluctuations in Individual Semiconducting Single-Wall Carbon Nanotubes

We present a systematic study on low-frequency current fluctuations of nano-devices consisting of one single semiconducting nanotube, which exhibit significant 1/f-type noise. By examining devices with different switching mechanisms, carrier types (electrons vs. holes), and channel lengths, we show that the 1/f fluctuation level in semiconducting nanotubes is correlated to the total number of transport carriers present in the system. However, the 1/f noise level per carrier is not larger than that of most bulk conventional semiconductors, e.g. Si. The pronounced noise level observed in nanotube devices simply reflects on the small number of carriers involved in transport. These results not only provide the basis to quantify the noise behavior in a one-dimensional transport system, but also suggest a valuable way to characterize low-dimensional nanostructures based on the 1/f fluctuation phenomenon

Wide Contact Structures for Low-Noise Nanochannel Devices Based on a Carbon Nanotube Network

We have developed a wide contact structure for low-noise nanochannel devices based on a carbon nanotube (CNT) network. This low-noise CNT network-based device has a dumbbell-shaped channel, which has wide CNT/electrode contact regions and, in effect, reduces the contact noise. We also performed a systematic analysis of structured CNT networks and established an empirical formula that can explain the noise behavior of arbitrary-shaped CNT network-based devices including the effect of contact regions and CNT alignment. Interestingly, our analysis revealed that the noise amplitude of aligned CNT networks behaves quite differently compared with that of randomly oriented CNT networks. Our results should be an important guideline in designing low-noise nanoscale devices based on a CNT network for various applications such as a highly sensitive low-noise sensor

A Large-Scale Rheumatoid Arthritis Genetic Study Identifies Association at Chromosome 9q33.2

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease affecting both joints and extra-articular tissues. Although some genetic risk factors for RA are well-established, most notably HLA-DRB1 and PTPN22, these markers do not fully account for the observed heritability. To identify additional susceptibility loci, we carried out a multi-tiered, case-control association study, genotyping 25,966 putative functional SNPs in 475 white North American RA patients and 475 matched controls. Significant markers were genotyped in two additional, independent, white case-control sample sets (661 cases/1322 controls from North America and 596 cases/705 controls from The Netherlands) identifying a SNP, rs1953126, on chromosome 9q33.2 that was significantly associated with RA (ORcommon = 1.28, trend Pcomb = 1.45E-06). Through a comprehensive fine-scale-mapping SNP-selection procedure, 137 additional SNPs in a 668 kb region from MEGF9 to STOM on 9q33.2 were chosen for follow-up genotyping in a staged-approach. Significant single marker results (Pcomb<0.01) spanned a large 525 kb region from FBXW2 to GSN. However, a variety of analyses identified SNPs in a 70 kb region extending from the third intron of PHF19 across TRAF1 into the TRAF1-C5 intergenic region, but excluding the C5 coding region, as the most interesting (trend Pcomb: 1.45E-06 → 5.41E-09). The observed association patterns for these SNPs had heightened statistical significance and a higher degree of consistency across sample sets. In addition, the allele frequencies for these SNPs displayed reduced variability between control groups when compared to other SNPs. Lastly, in combination with the other two known genetic risk factors, HLA-DRB1 and PTPN22, the variants reported here generate more than a 45-fold RA-risk differential

Increased HIV-1 transcriptional activity and infectious burden in peripheral blood and gut-associated CD4+ T cells expressing CD30

HIV-1-infected cells persist indefinitely despite the use of combination antiretroviral therapy (ART), and novel therapeutic strategies to target and purge residual infected cells in individuals on ART are urgently needed. Here, we demonstrate that CD4+ T cell-associated HIV-1 RNA is often highly enriched in cells expressing CD30, and that cells expressing this marker considerably contribute to the total pool of transcriptionally active CD4+ lymphocytes in individuals on suppressive ART. Using in situ RNA hybridization studies, we show co-localization of CD30 with HIV-1 transcriptional activity in gut-associated lymphoid tissues. We also demonstrate that ex vivo treatment with brentuximab vedotin, an antibody-drug conjugate (ADC) that targets CD30, significantly reduces the total amount of HIV-1 DNA in peripheral blood mononuclear cells obtained from infected, ART-suppressed individuals. Finally, we observed that an HIV-1-infected individual, who received repeated brentuximab vedotin infusions for lymphoma, had no detectable virus in peripheral blood mononuclear cells. Overall, CD30 may be a marker of residual, transcriptionally active HIV-1 infected cells in the setting of suppressive ART. Given that CD30 is only expressed on a small number of total mononuclear cells, it is a potential therapeutic target of persistent HIV-1 infection