| 1. |
- Illarionov, Y., et al.
(author)
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Interplay between hot carrier and bias stress components in single-layer double-gated graphene field-effect transistors
- 2015
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In: European Solid-State Device Research Conference. - : IEEE. - 9781467371339 ; , s. 172-175
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Conference paper (peer-reviewed)abstract
- We examine the interplay between the degradations associated with the bias-temperature instability (BTI) and hot carrier degradation (HCD) in single-layer double-gated graphene field-effect transistors (GFETs). Depending on the polarity of the applied BTI stress, the HCD component acting in conjuction can either accelerate or compensate the degradation. The related phenomena are studied in detail at different temperatures. Our results show that the variations of the charged trap density and carrier mobility induced by both contributions are correlated. Moreover, the electron/hole mobility behaviour agrees with the previously reported attractive/repulsive scattering asymmetry.
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| 2. |
- Illarionov, Y.Yu., et al.
(author)
-
Bias-temperature instability on the back gate of single-layer double-gated graphene field-effect transistors
- 2016
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In: Japanese Journal of Applied Physics. - : Institute of Physics (IOP). - 0021-4922 .- 1347-4065. ; 55:4
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Journal article (peer-reviewed)abstract
- We study the positive and negative bias-temperature instabilities (PBTI and NBTI) on the back gate of single-layer double-gated graphene fieldeffect transistors (GFETs). By analyzing the resulting degradation at different stress times and oxide fields we show that there is a significant asymmetry between PBTI and NBTI with respect to their dependences on these parameters. Finally, we compare the results obtained on the high-k top gate and SiO2 back gate of the same device and show that SiO2 gate is more stable with respect to BTI.
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| 3. |
- Illarionov, Yu.Yu., et al.
(author)
-
Hot-carrier degradation in single-layer double-gated graphene field-effect transistors
- 2015
-
In: IEEE International Reliability Physics Symposium Proceedings. - : IEEE conference proceedings. - 9781467373623 ; , s. XT21-XT26
-
Conference paper (peer-reviewed)abstract
- We report a first study of hot-carrier degradation (HCD) in graphene field-effect transistors (GFETs). Our results show that HCD in GFETs is recoverable, similarly to the bias-temperature instability (BTI). Depending on the top gate bias polarity, the presence of HCD may either accelerate or suppress BTI. Contrary to BTI, which mainly results in a change of the charged trap density in the oxide, HCD also leads to a mobility degradation which strongly correlates with the magnitude of the applied stress.
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| 4. |
- Illarionov, Yu.Yu., et al.
(author)
-
Impact of hot carrier stress on the defect density and mobility in double-gated graphene field-effect transistors
- 2015
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In: EUROSOI-ULIS 2015 - 2015 Joint International EUROSOI Workshop and International Conference on Ultimate Integration on Silicon. - 9781479969111 ; , s. 81-84
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Conference paper (peer-reviewed)abstract
- We study the impact of hot-carrier degradation (HCD) on the performance of graphene field-effect transistors (GFETs) for different polarities of HC and bias stress. Our results show that the impact of HCD consists in a change of both charged defect density and carrier mobility. At the same time, the mobility degradation agrees with an attractive/repulsive scattering asymmetry and can be understood based on the analysis of the defect density variation.
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| 5. |
- Passos, Vania, et al.
(author)
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Innate immune response to SARS-CoV-2 infection contributes to neuronal damage in human iPSC-derived peripheral neurons
- 2024
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In: Journal of Medical Virology. - : John Wiley & Sons. - 0146-6615 .- 1096-9071. ; 96:2
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Journal article (peer-reviewed)abstract
- Severe acute respiratory coronavirus 2 (SARS-CoV-2) causes neurological disease in the peripheral and central nervous system (PNS and CNS, respectively) of some patients. It is not clear whether SARS-CoV-2 infection or the subsequent immune response are the key factors that cause neurological disease. Here, we addressed this question by infecting human induced pluripotent stem cell-derived CNS and PNS neurons with SARS-CoV-2. SARS-CoV-2 infected a low number of CNS neurons and did not elicit a robust innate immune response. On the contrary, SARS-CoV-2 infected a higher number of PNS neurons. This resulted in expression of interferon (IFN) λ1, several IFN-stimulated genes and proinflammatory cytokines. The PNS neurons also displayed alterations characteristic of neuronal damage, as increased levels of sterile alpha and Toll/interleukin receptor motif-containing protein 1, amyloid precursor protein and α-synuclein, and lower levels of cytoskeletal proteins. Interestingly, blockade of the Janus kinase and signal transducer and activator of transcription pathway by Ruxolitinib did not increase SARS-CoV-2 infection, but reduced neuronal damage, suggesting that an exacerbated neuronal innate immune response contributes to pathogenesis in the PNS. Our results provide a basis to study coronavirus disease 2019 (COVID-19) related neuronal pathology and to test future preventive or therapeutic strategies.
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