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Jihyeon Jeon,Minsol Son,명노준 한국물리학회 2020 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.76 No.4
We investigate Dirac fermion transport through opposite quantum Hall edge channels in armchair graphene nanoribbons where a magnetic quantum dot (MQD) is placed between the edges. The resulting conductance shows distinguished resonant features according to the angle Φ between the valley isospins at the opposite edges. Particularly, for Φ = 0, the conductance exhibits a behavior characteristic of dissipative resonances when the edge--dot distance is sufficiently small {even though the unitarity of the whole system is conserved}. As the edge--dot distance increases, a crossover behavior emerges between two distinct regimes: largely perturbed and unperturbed MQD. Resonant energy converges to a specific energy corresponding to the eigenenergy of the localized states in the unperturbed MQD. For sufficiently weak couplings, a fine splitting of the conductance resonances is observed, of which splitting energy is several μeV. The finding of these finely split localized states in the MQD allows us to better elucidate related electronic and transport properties in graphene.
Dong Hyun Jo,Su Hyun Lee,Minsol Jeon,Chang Sik Cho,Da-Eun Kim,김현경,김정훈 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.11
Accumulation of pathogenic amyloid-β disrupts the tight junction of retinal pigment epithelium (RPE), one of its senescence-like structural alterations. In the clearance of amyloid-β, the autophagy-lysosome pathway plays the crucial role. In this context, mammalian target of rapamycin (mTOR) inhibits the process of autophagy and lysosomal degradation, acting as a potential therapeutic target for age-associated disorders. However, efficacy of targeting mTOR to treat age-related macular degeneration remains largely elusive. Here, we validated the therapeutic efficacy of the mTOR inhibitors, Torin and PP242, in clearing amyloid-β by inducing the autophagy-lysosome pathway in a mouse model with pathogenic amyloid-β with tight junction disruption of RPE, which is evident in dry age-related macular degeneration. High concentration of amyloid-β oligomers induced autophagy-lysosome pathway impairment accompanied by the accumulation of p62 and decreased lysosomal activity in RPE cells. However, Torin and PP242 treatment restored the lysosomal activity via activation of LAMP2 and facilitated the clearance of amyloid-β in vitro and in vivo. Furthermore, clearance of amyloid-β by Torin and PP242 ameliorated the tight junction disruption of RPE in vivo. Overall, our findings suggest mTOR inhibition as a new therapeutic strategy for the restoration of tight junctions in age-related macular degeneration.