Trion confinement in monolayer MoSe2 by carbon nanotube local gating

We have successfully confined trions into a one-dimensional restricted space of a MoSe2 device with CNT gate electrodes. The dry transfer process, including deterministic dry transfer of aligned CNTs, has led to an hBN-encapsulated MoSe2 device with CNT back gate electrodes. In contrast to a location without CNT gate electrodes, applying voltage via CNT gate electrodes significantly alters PL spectra at a location with CNT gate electrodes. PL imaging has revealed that image contrast from trions is linear along the CNT electrode underneath, consistent with 1D confinement of trions in response to the CNT local gating. The confinement width obtained from the PL image is 5.5 x 10^2 nm, consistent with nanoscale 1D confined trions with the diffraction limit broadening. This work has demonstrated electrical control of excitonic states at the nanoscale, leading to novel optoelectronic properties and exciton devices in the future

Two-dimensional atomic-scale ultrathin lateral heterostructures

Ultrathin lateral heterostructures of monolayer MoS2 and WS2 have successfully been realized with the metal-organic chemical vapor deposition method. Atomic-resolution HAADF-STEM observations have revealed that the junction widths of lateral heterostructures range from several nanometers to single-atom thickness, the thinnest heterojunction in theory. The interfaces are atomically flat with minimal mixing between MoS2 and WS2, originating from rapid and abrupt switching of the source supply. Due to one-dimensional interfaces and broken rotational symmetry, the resulting ultrathin lateral heterostructures, 1~2 mixed-dimensional structures, can show emergent optical/electronic properties. The MOCVD growth developed in this work allows us to access various ultrathin lateral heterostructures, leading to future exploration of their emergent properties absent in each component alone

Association of the rs738409 polymorphism in PNPLA3 with liver damage and the development of nonalcoholic fatty liver disease

<p>Abstract</p> <p>Background</p> <p>In a genome-wide association scan, the single-nucleotide polymorphism (SNP) rs738409 in the patatin-like phospholipase 3 gene (<it>PNPLA3</it>) was strongly associated with increased liver fat content. We investigated whether this SNP is associated with the occurrence and progression of nonalcoholic fatty liver disease (NAFLD) in the Japanese population.</p> <p>Methods</p> <p>SNP rs738409 was genotyped by the Taqman assay in 253 patients with NAFLD (189 with nonalcoholic steatohepatitis [NASH] and 64 with simple steatosis) and 578 control subjects. All patients with NAFLD underwent liver biopsy. Control subjects had no metabolic disorders. For a case-control study, the <it>χ</it>²-test (additive model) was performed. Odds ratios (ORs) were adjusted for age, gender, and body mass index (BMI) by using multiple logistic regression analysis with genotypes (additive model), age, gender, and BMI as the independent variables. Multiple linear regression analysis was performed to test the independent effect of risk allele on clinical parameters while considering the effects of other variables (age, gender, and BMI), which were assumed to be independent of the effect of the SNP.</p> <p>Results</p> <p>The risk allele (G-allele) frequency of rs738409 was 0.44 in the control subjects and 0.60 in patients with NAFLD; this shows a strong association with NAFLD (additive model, <it>P </it>= 9.4 × 10^-10). The OR (95% confidence interval) adjusted for age, gender, and BMI was 1.73 (1.25-2.38). Multiple linear regression analysis indicated that the G-allele of rs738409 was significantly associated with increases in aspartate transaminase (AST) (<it>P </it>= 0.00013), alanine transaminase (ALT) (<it>P </it>= 9.1 × 10^-6), and ferritin levels (<it>P </it>= 0.014), and the fibrosis stage (<it>P </it>= 0.011) in the patients with NAFLD, even after adjustment for age, gender, and BMI. The steatosis grade was not associated with rs738409.</p> <p>Conclusions</p> <p>We found that in the Japanese population, individuals harboring the G-allele of rs738409 were susceptible to NAFLD, and that rs738409 was associated with plasma levels of ALT, AST, and ferritin, and the histological fibrosis stage. Our study suggests that <it>PNPLA3 </it>may be involved in the progression of fibrosis in NAFLD.</p

Identification of mutations through dominant screening for obesity using C57BL/6 substrains

The discovery of leptin substantiated the usefulness of a forward genetic approach in elucidating the molecular network regulating energy metabolism. However, no successful dominant screening for obesity has been reported, which may be due to the influence of quantitative trait loci between the screening and counter strains and the low fertility of obese mice. Here, we performed a dominant screening for obesity using C57BL/6 substrains, C57BL/6J and C57BL/6N, with the routine use of in vitro fertilization. The screening of more than 5000 mutagenized mice established two obese pedigrees in which single nucleotide substitutions in Mc4r and Sim1 genes were identified through whole-exome sequencing. The mutation in the Mc4r gene produces a premature stop codon, and the mutant SIM1 protein lacks transcriptional activity, showing that the haploinsufficiency of SIM1 and MC4R results in obesity. We further examined the hypothalamic neuropeptide expressions in the mutant pedigrees and mice with diet-induced obesity, which showed that each obesity mouse model has distinct neuropeptide expression profiles. This forward genetic screening scheme is useful and applicable to any research field in which mouse models work

Formation of Sm(Co

Sm17(Co1–xNix)83 (at. %, x = 0, 0.2, 0.8, 1) alloy thin films are prepared on Cu(111) underlayers hetero-epitaxially grown on MgO(111) substrates by molecular beam epitaxy. The effects of substrate temperature and Ni/Co composition on the growth behavior and the detailed resulting film structure are investigated. Formation of RT5 ordered phase is enhanced with increasing the substrate temperature and the Ni composition. The long-range order degrees of Sm17Co83, Sm17(Co0.8Ni0.2)83, Sm17(Co0.2Ni0.8)83, and Sm17Ni83 films deposited at 500 °C are estimated to be 0.77, 0.82, 0.89, and 0.97, respectively. The Sm17(Co1–xNix)83 films with RT5 structure consist of two types of epitaxial (0001) variant whose orientations are rotated around the film normal by 30° each other. With increasing the Ni content ratio of x from 0 to 1, the volume ratio of two variants is varied from 53:47 to 94:6. The nucleation of only one-type variant with a smaller lattice mismatch with respect to Cu underlayer is promoted with increasing the Ni content ratio

Ordered phase formation in Sm-Ni thin film deposited on Cr(100) single-crystal underlayer

Sm17Ni83 (at. %) alloy thin films are prepared on Cr(100) underlayers hetero-epitaxially grown on MgO(100) single-crystal substrates by employing an ultra-high vacuum molecular beam epitaxy system. The effect of substrate temperature on the ordered phase formation is investigated. The films deposited below 300 °C consist of amorphous phase, whereas formation of SmNi5 ordered phase is recognized for the films deposited above 400 °C. The SmNi5 films with ordered phase consist of two types of (11$\bar 2$0) variant whose c-axes are lying in the film plane and rotated around the film normal by 90° each other. With increasing the temperature from 400 to 500 °C, the long-range order degree increases from 0.65 to 0.80. The ordered film formed at 500 °C shows an in-plane magnetic anisotropy reflecting the magnetocrystalline anisotropy of SmNi5 crystal

Genome-wide scan revealed that polymorphisms in the PNPLA3, SAMM50, and PARVB genes are associated with development and progression of nonalcoholic fatty liver disease in Japan.

We examined the genetic background of nonalcoholic fatty liver disease (NAFLD) in the Japanese population, by performing a genome-wide association study (GWAS). For GWAS, 392 Japanese NAFLD subjects and 934 control individuals were analyzed. For replication studies, 172 NAFLD and 1, 012 control subjects were monitored. After quality control, 261, 540 single-nucleotide polymorphisms (SNPs) in autosomal chromosomes were analyzed using a trend test. Association analysis was also performed using multiple logistic regression analysis using genotypes, age, gender and body mass index (BMI) as independent variables. Multiple linear regression analyses were performed to evaluate allelic effect of significant SNPs on biochemical traits and histological parameters adjusted by age, gender, and BMI. Rs738409 in the PNPLA3 gene was most strongly associated with NAFLD after adjustment (P = 6.8 × 10(-14), OR = 2.05). Rs2896019, and rs381062 in the PNPLA3 gene, rs738491, rs3761472, and rs2143571 in the SAMM50 gene, rs6006473, rs5764455, and rs6006611 in the PARVB gene had also significant P values (<2.0 × 10(-10)) and high odds ratios (1.84-2.02). These SNPs were found to be in the same linkage disequilibrium block and were associated with decreased serum triglycerides and increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in NAFLD patients. These SNPs were associated with steatosis grade and NAFLD activity score (NAS). Rs738409, rs2896019, rs738491, rs6006473, rs5764455, and rs6006611 were associated with fibrosis. Polymorphisms in the SAMM50 and PARVB genes in addition to those in the PNPLA3 gene were observed to be associated with the development and progression of NAFLD