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- Ferreira, Aires, et al.
(författare)
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Unified description of the dc conductivity of monolayer and bilayer graphene at finite densities based on resonant scatterers
- 2011
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Ingår i: Physical Review B. Condensed Matter and Materials Physics. - 1098-0121. ; 83:16
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Tidskriftsartikel (refereegranskat)abstract
- We show that a coherent picture of the dc conductivity of monolayer and bilayer graphene at finite electronic densities emerges upon considering that strong short-range potentials are the main source of scattering in these two systems. The origin of the strong short-range potentials may lie in adsorbed hydrocarbons at the surface of graphene. The equivalence among results based on the partial-wave description of scattering, the Lippmann-Schwinger equation, and the T-matrix approach is established. Scattering due to resonant impurities close to the neutrality point is investigated via a numerical computation of the Kubo formula using a kernel polynomial method. We find that relevant adsorbate species originate impurity bands in monolayer and bilayer graphene close to the Dirac point. In the midgap region, a plateau of minimum conductivity of about e2/h (per layer) is induced by the resonant disorder. In bilayer graphene, a large adsorbate concentration can develop an energy gap between midgap and high-energy states. As a consequence, the conductivity plateau is supressed near the edges and a “conductivity gap” takes place. Finally, a scattering formalism for electrons in biased bilayer graphene, taking into account the degeneracy of the spectrum, is developed and the dc conductivity of that system is studied.
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- McClenaghan, C, et al.
(författare)
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Sulfonylurea-Insensitive Permanent Neonatal Diabetes Caused by a Severe Gain-of-Function Tyr330His Substitution in Kir6.2
- 2022
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Ingår i: Hormone research in paediatrics. - : S. Karger AG. - 1663-2826 .- 1663-2818. ; 95:3, s. 215-223
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Tidskriftsartikel (refereegranskat)abstract
- <b><i>Background/Aims:</i></b> Mutations in <i>KCNJ11</i>, the gene encoding the Kir6.2 subunit of pancreatic and neuronal K<sub>ATP</sub> channels, are associated with a spectrum of neonatal diabetes diseases. <b><i>Methods:</i></b> Variant screening was used to identify the cause of neonatal diabetes, and continuous glucose monitoring was used to assess effectiveness of sulfonylurea treatment. Electrophysiological analysis of variant K<sub>ATP</sub> channel function was used to determine molecular basis. <b><i>Results:</i></b> We identified a previously uncharacterized <i>KCNJ11</i> mutation, c.988T>C [p.Tyr330His], in an Italian child diagnosed with sulfonylurea-resistant permanent neonatal diabetes and developmental delay (intermediate DEND). Functional analysis of recombinant K<sub>ATP</sub> channels reveals that this mutation causes a drastic gain-of-function, due to a reduction in ATP inhibition. Further, we demonstrate that the Tyr330His substitution causes a significant decrease in sensitivity to the sulfonylurea, glibenclamide. <b><i>Conclusions:</i></b> In this subject, the <i>KCNJ11</i> (c.988T>C) mutation provoked neonatal diabetes, with mild developmental delay, which was insensitive to correction by sulfonylurea therapy. This is explained by the molecular loss of sulfonylurea sensitivity conferred by the Tyr330His substitution and highlights the need for molecular analysis of such mutations.
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