Asymmetry of localised states in a single quantum ring: polarization dependence of excitons and biexcitons

We performed spectroscopic studies of a single GaAs quantum ring with an anisotropy in the rim height. The presence of an asymmetric localised state was suggested by the adiabatic potential. The asymmetry was investigated in terms of the polarization dependence of excitons and biexcitons, where a large energy di erence (0.8 meV) in the exciton emission energy for perpendicular polarizations was observed and the oscillator strengths were also compared using the photoluminescence decay rate. For perpendicular polarizations the biexciton exhibits twice the energy di erence seen for the exciton, a fact that may be attributed to a possible change in the selection rules for the lowered symmetry.Comment: accepted in Applied physics Letter

Excited exciton and biexciton localised states in a single quantum ring

We observe excited exciton and biexciton states of localised excitons in an anisotropic quantum ring, where large polarisation asymmetry supports the presence of a crescent-like localised structure. We also find that saturation of the localised ground state exciton with increasing excitation can be attributed to relatively fast dissociation of biexcitons (? 430 ps) compared to slow relaxation from the excited state to the ground state (? 1000 ps). As no significant excitonic Aharonov-Bohm oscillations occur up to 14 T, we conclude that phase coherence around the rim is inhibited as a consequence of height anisotropy in the quantum ring.Comment: 4 pages, 4 figure

QCD axion and quintessential axion

The axion solution of the strong CP problem is reviewed together with the other strong CP solutions. We also point out the quintessential axion(quintaxion) whose potential can be extremely flat due to the tiny ratio of the hidden sector quark mass and the intermediate hidden sector scale. The quintaxion candidates are supposed to be the string theory axions, the model independent or the model dependent axions.Comment: 15 pages. Talk presented at Castle Ringberg, June 9-14, 200

Mobile resistome of human gut and pathogen drives anthropogenic bloom of antibiotic resistance

BACKGROUND:The impact of human activities on the environmental resistome has been documented in many studies, but there remains the controversial question of whether the increased antibiotic resistance observed in anthropogenically impacted environments is just a result of contamination by resistant fecal microbes or is mediated by indigenous environmental organisms. Here, to determine exactly how anthropogenic influences shape the environmental resistome, we resolved the microbiome, resistome, and mobilome of the planktonic microbial communities along a single river, the Han, which spans a gradient of human activities. RESULTS:The bloom of antibiotic resistance genes (ARGs) was evident in the downstream regions and distinct successional dynamics of the river resistome occurred across the spatial continuum. We identified a number of widespread ARG sequences shared between the river, human gut, and pathogenic bacteria. These human-related ARGs were largely associated with mobile genetic elements rather than particular gut taxa and mainly responsible for anthropogenically driven bloom of the downstream river resistome. Furthermore, both sequence- and phenotype-based analyses revealed environmental relatives of clinically important proteobacteria as major carriers of these ARGs. CONCLUSIONS:Our results demonstrate a more nuanced view of the impact of anthropogenic activities on the river resistome: fecal contamination is present and allows the transmission of ARGs to the environmental resistome, but these mobile genes rather than resistant fecal bacteria proliferate in environmental relatives of their original hosts. Video abstract

Pontin functions as an essential coactivator for Oct4-dependent lincRNA expression in mouse embryonic stem cells

The actions of transcription factors, chromatin modifiers and noncoding RNAs are crucial for the programming of cell states. Although the importance of various epigenetic machineries for controlling pluripotency of embryonic stem (ES) cells has been previously studied, how chromatin modifiers cooperate with specific transcription factors still remains largely elusive. Here, we find that Pontin chromatin remodelling factor plays an essential role as a coactivator for Oct4 for maintenance of pluripotency in mouse ES cells. Genome-wide analyses reveal that Pontin and Oct4 share a substantial set of target genes involved in ES cell maintenance. Intriguingly, we find that the Oct4-dependent coactivator function of Pontin extends to the transcription of large intergenic noncoding RNAs (lincRNAs) and in particular linc1253, a lineage programme repressing lincRNA, is a Pontin-dependent Oct4 target lincRNA. Together, our findings demonstrate that the Oct4-Pontin module plays critical roles in the regulation of genes involved in ES cell fate determination.111311Ysciescopu

Consecutive junction-induced efficient charge separation mechanisms for high-performance MoS2/quantum dot phototransistors

Phototransistors that are based on a hybrid vertical heterojunction structure of two-dimensional (2D)/quantum dots (QDs) have recently attracted attention as a promising device architecture for enhancing the quantum efficiency of photodetectors. However, to optimize the device structure to allow for more efficient charge separation and transfer to the electrodes, a better understanding of the photophysical mechanisms that take place in these architectures is required. Here, we employ a novel concept involving the modulation of the built-in potential within the QD layers for creating a new hybrid MoS2/PbS QDs phototransistor with consecutive type II junctions. The effects of the built-in potential across the depletion region near the type II junction interface in the QD layers are found to improve the photoresponse as well as decrease the response times to 950 μs, which is the faster response time (by orders of magnitude) than that recorded for previously reported 2D/QD phototransistors. Also, by implementing an electric-field modulation of the MoS2 channel, our experimental results reveal that the detectivity can be as large as 1 × 1011 jones. This work demonstrates an important pathway toward designing hybrid phototransistors and mixed-dimensional van der Waals heterostructures

The anomalous U(1) global symmetry and flavors from an SU(5) x SU(5)′' GUT in Z12−IZ_{12-I} orbifold compactification

In string compactifications, frequently there appears the anomalous U(1) gauge symmetry which belonged to E8$\times$E8 of the heterotic string. This anomalous U(1) gauge boson obtains mass at the compactification scale, just below $10^{18\,}$GeV, by absorbing one pseudoscalar (corresponding to the model-independent axion) from the second rank anti-symmetric tensor field $B_{MN}$. Below the compactification scale, there results a global symmetry U(1)$_{\rm anom}$ whose charge $Q_{\rm anom}$ is the original gauge U(1) charge. This is the most natural global symmetry, realizing the "invisible" axion. This global symmetry U(1)$_{\rm anom}$ is suitable for a flavor symmetry. In the simplest compactification model with the flipped SU(5) grand unification, we calculate all the low energy parameters in terms of the vacuum expectation values of the standard model singlets.Comment: 18 pages, 4 figur

Sphingosine 1-phosphate receptor 4 promotes nonalcoholic steatohepatitis by activating NLRP3 inflammasome

BACKGROUND & AIMS: Sphingosine 1-phosphate receptors (S1PRs) are a group of G-protein-coupled receptors that confer a broad range of functional effects in chronic inflammatory and metabolic diseases. S1PRs also may mediate the development of nonalcoholic steatohepatitis (NASH), but the specific subtypes involved and the mechanism of action are unclear. METHODS: We investigated which type of S1PR isoforms is activated in various murine models of NASH. The mechanism of action of S1PR4 was examined in hepatic macrophages isolated from high-fat, high-cholesterol diet (HFHCD)-fed mice. We developed a selective S1PR4 functional antagonist by screening the fingolimod (2-amino-2-[2-(4- n-octylphenyl)ethyl]-1,3-propanediol hydrochloride)-like sphingolipid-focused library. RESULTS: The livers of various mouse models of NASH as well as hepatic macrophages showed high expression of S1pr4. Moreover, in a cohort of NASH patients, expression of S1PR4 was 6-fold higher than those of healthy controls. S1pr4(++/-) mice were protected from HFHCD-induced NASH and hepatic fibrosis without changes in steatosis. S1pr4 depletion in hepatic macrophages inhibited lipopolysaccharide-mediated Ca++ release and deactivated the Nod-like receptor pyrin domaincontainning protein 3 (NLRP3) inflammasome. S1P increased the expression of S1pr4 in hepatic macrophages and activated NLRP3 inflammasome through inositol trisphosphate/inositol trisphosphate-receptor-dependent [Ca++] signaling. To further clarify the biological function of S1PR4, we developed SLB736, a novel selective functional antagonist of SIPR4. Similar to S1pr4(+/-) mice, administration of SLB736 to HFHCD-fed mice prevented the development of NASH and hepatic fibrosis, but not steatosis, by deactivating the NLRP3 inflammasome. CONCLUSIONS: S1PR4 may be a new therapeutic target for NASH that mediates the activation of NLRP3 inflammasome in hepatic macrophages