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Jinkwon Kim,Junsik Mun,Youngdo Kim,Bongju Kim,Jeong Rae Kim,Lingfei Wang,Miyoung Kim,Changyoung Kim,Jason W. A. Robinson,Yoshiteru Maeno,Tae Won Noh 한국자기학회 2021 한국자기학회 학술연구발표회 논문개요집 Vol.31 No.2
Ruddlesden-Popper (RP) phase oxides (An+1BnO3n+1, n = 1, 2, ...) have been spotlighted with versatile physical properties such as high-temperature superconductivity, colossal magnetoresistance. These emergent phenomena provide a platform for novel oxide-based electronic devices including spintronics application. However, high-quality RP-phase thin film growth has been disturbed by extended structural defects, such as out-of-phase boundaries (OPBs). OPB is a translational boundary between neighboring unit cells, shifted in a specific crystallographic direction. For instance, if RP-phase thin films grown on ABO₃ perovskite substrates, the structural mismatch between film and substrates induces a crystallographic shift in the c-axis direction, thus OPBs form at the film-substrate interface. Since OPB formation hampers the physical properties of RP-phase thin films, the suppression of the structural defects is highly required to carry out the high-performance RP-phase based functional devices. In this study, we suppressed OPB suppression in RP-phase oxide thin films by atomic-scale interface engineering. As model systems, the unconventional superconductor Sr₂RuO₄ (bulk Tc ~ 1.5 K) and La2-xSrxCuO₄ (bulk Tc ~ 39 K) thin films were employed. Despite the structural similarities between films and substrates, Sr2RuO4 and La2-xSrxCuO₄ films exhibited huge OPB formations. By controlling the atomic-scale interface engineering, the OPBs were significantly suppressed in the film structure. Notably, these OPB-free Sr₂RuO₄ and La2-xSrxCuO₄ thin films exhibited highly enhanced superconductivity than the film with huge OPB formation. Our study suggests a comprehensive method to suppress OPB formation in RP thin films, enabling superconducting spintronics devices based on the unconventional superconductivity.
Unconventional anomalous Hall effect from antiferromagnetic domain walls of Nd2Ir2O7 thin films
Kim, Woo Jin,Gruenewald, John H.,Oh, Taekoo,Cheon, Sangmo,Kim, Bongju,Korneta, Oleksandr B.,Cho, Hwanbeom,Lee, Daesu,Kim, Yoonkoo,Kim, Miyoung,Park, Je-Geun,Yang, Bohm-Jung,Seo, Ambrose,Noh, Tae Won American Physical Society 2018 Physical Review B Vol.98 No.12
( Bongju Kim ),( Youngcho Cho ),( Sunggil Kim ) 한국육종학회 2017 Plant Breeding and Biotechnology Vol.5 No.1
To introduce downy mildew resistance from a yellow-colored resistant cultivar, `Santero`, into a yellow breeding line, OT803, the F<sub>1</sub> hybrid was produced by crossing Santero and OT803. The bulb color of the F1 hybrids became light pink, suggesting involvement of complementation between the DFR-A and ANS genes in the onion anthocyanin biosynthesis pathway. Since Santero contained active DFR-A and inactive ANS alleles, OT803 was assumed to harbor active ANS and inactive DFR-A alleles. However, some yellow-colored individuals of OT803 were shown to contain the homozygous genotype of the active DFR-A<sup>R4</sup>-like allele. Sequencing of 4,830-bp full-length sequences of this DFR-A<sup>R4</sup>-like allele revealed that the nucleotide sequences of the DFR-A<sup>R4</sup> and DFR-A<sup>R4</sup>-like alleles were identical except for a single nucleotide deletion in the last exon. This single base-pair deletion resulted in creation of a premature stop codon at 2-bp downstream of the deletion mutation. This new DFR-A mutant allele was designated DFR-A<sup>PS2</sup>. The RT-PCR results showed that transcripts of the DFR-A<sup>PS2</sup> allele were significantly reduced, suggesting involvement of nonsense-mediated mRNA decay (NMD) mechanism. The systematic process consisting of PCR amplification and sequencing of the PCR products was modified to identify the DFR-A<sup>PS2</sup> allele among 16 different DFR-A alleles. No additional accession was found to contain the DFR-A<sup>PS2</sup> allele from 155 diverse onion germplasm, indicating very limited distribution of this new DFR-A<sup>PS2</sup> allele.