An intestinal zinc sensor regulates food intake and developmental growth.

In cells, organs and whole organisms, nutrient sensing is key to maintaining homeostasis and adapting to a fluctuating environment1. In many animals, nutrient sensors are found within the enteroendocrine cells of the digestive system; however, less is known about nutrient sensing in their cellular siblings, the absorptive enterocytes1. Here we use a genetic screen in Drosophila melanogaster to identify Hodor, an ionotropic receptor in enterocytes that sustains larval development, particularly in nutrient-scarce conditions. Experiments in Xenopus oocytes and flies indicate that Hodor is a pH-sensitive, zinc-gated chloride channel that mediates a previously unrecognized dietary preference for zinc. Hodor controls systemic growth from a subset of enterocytes-interstitial cells-by promoting food intake and insulin/IGF signalling. Although Hodor sustains gut luminal acidity and restrains microbial loads, its effect on systemic growth results from the modulation of Tor signalling and lysosomal homeostasis within interstitial cells. Hodor-like genes are insect-specific, and may represent targets for the control of disease vectors. Indeed, CRISPR-Cas9 genome editing revealed that the single hodor orthologue in Anopheles gambiae is an essential gene. Our findings highlight the need to consider the instructive contributions of metals-and, more generally, micronutrients-to energy homeostasis.

The EEG multiverse of schizophrenia.

Research on schizophrenia typically focuses on one paradigm for which clear-cut differences between patients and controls are established. Great efforts are made to understand the underlying genetical, neurophysiological, and cognitive mechanisms, which eventually may explain the clinical outcome. One tacit assumption of these "deep rooting" approaches is that paradigms tap into common and representative aspects of the disorder. Here, we analyzed the resting-state electroencephalogram (EEG) of 121 schizophrenia patients and 75 controls. Using multiple signal processing methods, we extracted 194 EEG features. Sixty-nine out of the 194 EEG features showed a significant difference between patients and controls, indicating that these features detect an important aspect of schizophrenia. Surprisingly, the correlations between these features were very low. We discuss several explanations to our results and propose that complementing "deep" with "shallow" rooting approaches might help in understanding the underlying mechanisms of the disorder.

Context effects on probability estimation.

Many decisions rely on how we evaluate potential outcomes and estimate their corresponding probabilities of occurrence. Outcome evaluation is subjective because it requires consulting internal preferences and is sensitive to context. In contrast, probability estimation requires extracting statistics from the environment and therefore imposes unique challenges to the decision maker. Here, we show that probability estimation, like outcome evaluation, is subject to context effects that bias probability estimates away from other events present in the same context. However, unlike valuation, these context effects appeared to be scaled by estimated uncertainty, which is largest at intermediate probabilities. Blood-oxygen-level-dependent (BOLD) imaging showed that patterns of multivoxel activity in the dorsal anterior cingulate cortex (dACC), ventromedial prefrontal cortex (VMPFC), and intraparietal sulcus (IPS) predicted individual differences in context effects on probability estimates. These results establish VMPFC as the neurocomputational substrate shared between valuation and probability estimation and highlight the additional involvement of dACC and IPS that can be uniquely attributed to probability estimation. Because probability estimation is a required component of computational accounts from sensory inference to higher cognition, the context effects found here may affect a wide array of cognitive computations.

Origin of exponential growth in nonlinear reaction networks.

Exponentially growing systems are prevalent in nature, spanning all scales from biochemical reaction networks in single cells to food webs of ecosystems. How exponential growth emerges in nonlinear systems is mathematically unclear. Here, we describe a general theoretical framework that reveals underlying principles of long-term growth: scalability of flux functions and ergodicity of the rescaled systems. Our theory shows that nonlinear fluxes can generate not only balanced growth but also oscillatory or chaotic growth modalities, explaining nonequilibrium dynamics observed in cell cycles and ecosystems. Our mathematical framework is broadly useful in predicting long-term growth rates from natural and synthetic networks, analyzing the effects of system noise and perturbations, validating empirical and phenomenological laws on growth rate, and studying autocatalysis and network evolution.

HBV X protein-based therapeutic vaccine accelerates viral antigen clearance by mobilizing monocyte infiltration into the liver in HBV carrier mice.

BACKGROUND: Hepatitis B virus (HBV) persistently infected about 250 million people worldwide, and a curative treatment remains an unmet medical need. Among many approaches to treat chronic hepatitis B (CHB), therapeutic vaccines have been developed for two decades, but none have yielded promising results in clinical trials. Therefore, dissection of HBV clearance mechanisms during therapeutic vaccination in appropriate models, which could give rise to new curative therapies, is urgently needed. Growing evidence indicates that prolonged and intensive exposure of antigen-specific T cells to viral antigens is a major cause of T cell exhaustion, and decreases anti-HBV immunity efficacy of therapeutic vaccination. HBV X protein (HBx) is expressed at low levels, and the understanding of its immunogenicity and potential in therapeutic CHB vaccines is limited. METHODS: HBV genome sequences from CHB patients were cloned into a pAAV plasmid backbone and transfected into immunocompetent mouse hepatocytes through hydrodynamic injection. Mice carrying > 500 IU/mL serum HBV surface antigen (HBs) for more than 4 weeks were considered HBV carriers mimicking human CHB and received 3 doses of weekly HBx vaccine by subcutaneous immunization. Serum HBV clearance was evaluated by monitoring serum HBs and HBV-DNA titers. Residual HBV in the liver was evaluated by western blotting for HBV core antigen. The splenic antigen-specific T cell response was quantified by a 15-mer overlapping peptide-stimulated interferon-γ enzyme-linked immunospot assay. Blood and hepatic immune cells were quantified by flow cytometric analysis. RESULTS: Our HBx-based vaccine induced systemic HBx-specific CD4+ and CD8+ T cell responses in HBV carrier mice and demonstrated significant HBs and HBV-DNA elimination. The protective effect persisted for at least 30 days without additional booster immunization. Different infiltrating myeloid cell subsets, each with distinctive roles during immune-mediated HBV clearance, were found in the liver of vaccinated mice. During vaccine therapy, inflammatory monocyte depletion resulted in sustained HBV clearance inhibition, whereas phagocytic monocyte-derived macrophage and Kupffer cell elimination resulted in only transient inhibition of vaccine-induced HBV clearance. CONCLUSIONS: We report the potential role of HBx as a major immunogen in an HBV therapeutic vaccine and the significance of a liver-infiltrating monocyte subset during hepatic viral clearance.

Interfacial States and Fano-Feshbach Resonance in Graphene-Silicon Vertical Junction.

Interfacial quantum states are drawing tremendous attention recently because of their importance in design of low-dimensional quantum heterostructures with desired charge, spin, or topological properties. Although most studies of the interfacial exchange interactions were mainly performed across the interface vertically, the lateral transport nowadays is still a major experimental method to probe these interactions indirectly. In this Letter, we fabricated a graphene and hydrogen passivated silicon interface to study the interfacial exchange processes. For the first time we found and confirmed a novel interfacial quantum state, which is specific to the 2D-3D interface. The vertically propagating electrons from silicon to graphene result in electron oscillation states at the 2D-3D interface. A harmonic oscillator model is used to explain this interfacial state. In addition, the interaction between this interfacial state (discrete energy spectrum) and the lateral band structure of graphene (continuous energy spectrum) results in Fano-Feshbach resonance. Our results show that the conventional description of the interfacial interaction in low-dimensional systems is valid only in considering the lateral band structure and its density-of-states and is incomplete for the ease of vertical transport. Our experimental observation and theoretical explanation provide more insightful understanding of various interfacial effects in low-dimensional materials, such as proximity effect, quantum tunneling, etc. More important, the Fano-Feshbach resonance may be used to realize all solid-state and scalable quantum interferometers.

Myocyte enhancer factor-2 and p300 interact to regulate the expression of homeostatic regulator Pumilio in Drosophila.

Pumilio (Pum), an RNA-binding protein, is a key component of neuron firing-rate homeostasis that likely maintains stability of neural circuit activity in all animals, from flies to mammals. While Pum is ubiquitously expressed, we understand little about how synaptic excitation regulates its expression in the CNS. Here, we characterized the Drosophila dpum promoter and identified multiple myocyte enhancer factor-2 (Mef2)-binding elements. We cloned 12 dmef2 splice variants and used a luciferase-based assay to monitor dpum promoter activity. While all 12 dMef2 splice variants enhance dpum promoter activity, exon 10-containing variants induce greater transactivation. Previous work shows dPum expression increases with synaptic excitation. However, we observe no change in dmef2 transcript in larval CNS, of both sexes, exposed to the proconvulsant picrotoxin. The lack of activity dependence is indicative of additional regulation. We identified p300 as a potential candidate. We show that by binding to dMef2, p300 represses dpum transactivation. Significantly, p300 transcript is downregulated by enhanced synaptic excitation (picrotoxin) which, in turn, increases transcription of dpum through derepression of dMef2. These results advance our understanding of dpum by showing the activity-dependent expression is regulated by an interaction between p300 and dMef2.

Specific diacylglycerols generated by hepatic lipogenesis stimulate the oncogenic androgen receptor activity in male hepatocytes.

BACKGROUND: Obesity-induced hepatocellular carcinoma (HCC) is more prevalent in males than in females, but the underlying mechanism remains unclear. The influence of hepatic androgen receptor (AR) pathway on the gender difference of HCC has been well documented. Here we investigated the role of hepatic lipogenesis, which is elevated in the livers of obese and nonalcoholic fatty liver disease (NAFLD) patients, in stimulating the AR pathway for the male preference of obesity induced HCC. METHODS: Male C57BL/6J mice were fed a fructose-rich high carbohydrate diet (HCD) to induce hepatic lipogenesis. The effect of hepatic lipogenesis on AR was examined by the expression of hydrodynamically injected AR reporter and the endogenous AR target gene; the mechanism was delineated in hepatoma cell lines and validated in male mice. RESULTS: The hepatic lipogenesis induced by a fructose-rich HCD enhanced the transcriptional activity of hepatic AR in male mice, which did not happen when fed a high fat diet. This AR activation was blocked by sh-RNAs or inhibitors targeting key enzymes in lipogenesis, either acetyl-CoA carboxylase subunit alpha (ACCα), or fatty acid synthase (FASN), in vivo and in vitro. Further mechanistic study identified that specific unsaturated fatty acid, the oleic acid (C18:1 n-9), incorporated DAGs produced by hepatic lipogenesis are the key molecules to enhance the AR activity, through activation of Akt kinase, and this novel mechanism is targeted by metformin. CONCLUSIONS: Our study elucidates a novel mechanism underlying the higher risk of HCC in obese/NAFLD males, through specific DAGs enriched by hepatic lipogenesis to increase the transcriptional activity of hepatic AR, a confirmed risk factor for male HCC.

Hypoxia-activated cytotoxic agent tirapazamine enhances hepatic artery ligation-induced killing of liver tumor in HBx transgenic mice.

Transarterial chemoembolization (TACE) is the main treatment for intermediate stage hepatocellular carcinoma (HCC) with Barcelona Clinic Liver Cancer classification because of its exclusive arterial blood supply. Although TACE achieves substantial necrosis of the tumor, complete tumor necrosis is uncommon, and the residual tumor generally rapidly recurs. We combined tirapazamine (TPZ), a hypoxia-activated cytotoxic agent, with hepatic artery ligation (HAL), which recapitulates transarterial embolization in mouse models, to enhance the efficacy of TACE. The effectiveness of this combination treatment was examined in HCC that spontaneously developed in hepatitis B virus X protein (HBx) transgenic mice. We proved that the tumor blood flow in this model was exclusively supplied by the hepatic artery, in contrast to conventional orthotopic HCC xenografts that receive both arterial and venous blood supplies. At levels below the threshold oxygen levels created by HAL, TPZ was activated and killed the hypoxic cells, but spared the normoxic cells. This combination treatment clearly limited the toxicity of TPZ to HCC, which caused the rapid and near-complete necrosis of HCC. In conclusion, the combination of TPZ and HAL showed a synergistic tumor killing activity that was specific for HCC in HBx transgenic mice. This preclinical study forms the basis for the ongoing clinical program for the TPZ-TACE regimen in HCC treatment.

An RNAi-mediated screen identifies novel targets for next-generation antiepileptic drugs based on increased expression of the homeostatic regulator pumilio.

Despite availability of a diverse range of anti-epileptic drugs (AEDs), only about two-thirds of epilepsy patients respond well to drug treatment. Thus, novel targets are required to catalyse the design of next-generation AEDs. Manipulation of neuron firing-rate homoeostasis, through enhancing Pumilio (Pum) activity, has been shown to be potently anticonvulsant in Drosophila. In this study, we performed a genome-wide RNAi screen in S2R + cells, using a luciferase-based dPum activity reporter and identified 1166 genes involved in dPum regulation. Of these genes, we focused on 699 genes that, on knock-down, potentiate dPum activity/expression. Of this subgroup, 101 genes are activity-dependent based on comparison with genes previously identified as activity-dependent by RNA-sequencing. Functional cluster analysis shows these genes are enriched in pathways involved in DNA damage, regulation of cell cycle and proteasomal protein catabolism. To test for anticonvulsant activity, we utilised an RNA-interference approach in vivo. RNAi-mediated knockdown showed that 57/101 genes (61%) are sufficient to significantly reduce seizure duration in the characterized seizure mutant, parabss. We further show that chemical inhibitors of protein products of some of the genes targeted are similarly anticonvulsant. Finally, to establish whether the anticonvulsant activity of identified compounds results from increased dpum transcription, we performed a luciferase-based assay to monitor dpum promoter activity. Third instar larvae exposed to sodium fluoride, gemcitabine, metformin, bestatin, WP1066 or valproic acid all showed increased dpum promoter activity. Thus, this study validates Pum as a favourable target for AED design and, moreover, identifies a number of lead compounds capable of increasing the expression of this homeostatic regulator.

Field Effect Optoelectronic Modulation of Quantum-Confined Carriers in Black Phosphorus.

We report measurements of the infrared optical response of thin black phosphorus under field-effect modulation. We interpret the observed spectral changes as a combination of an ambipolar Burstein-Moss (BM) shift of the absorption edge due to band-filling under gate control, and a quantum confined Franz-Keldysh (QCFK) effect, phenomena that have been proposed theoretically to occur for black phosphorus under an applied electric field. Distinct optical responses are observed depending on the flake thickness and starting carrier concentration. Transmission extinction modulation amplitudes of more than two percent are observed, suggesting the potential for use of black phosphorus as an active material in mid-infrared optoelectronic modulator applications.

Distal spike initiation zone location estimation by morphological simulation of ionic current filtering demonstrated in a novel model of an identified Drosophila motoneuron.

Studying ion channel currents generated distally from the recording site is difficult because of artifacts caused by poor space clamp and membrane filtering. A computational model can quantify artifact parameters for correction by simulating the currents only if their exact anatomical location is known. We propose that the same artifacts that confound current recordings can help pinpoint the source of those currents by providing a signature of the neuron's morphology. This method can improve the recording quality of currents initiated at the spike initiation zone (SIZ) that are often distal to the soma in invertebrate neurons. Drosophila being a valuable tool for characterizing ion currents, we estimated the SIZ location and quantified artifacts in an identified motoneuron, aCC/MN1-Ib, by constructing a novel multicompartmental model. Initial simulation of the measured biophysical channel properties in an isopotential Hodgkin-Huxley type neuron model partially replicated firing characteristics. Adding a second distal compartment, which contained spike-generating Na+ and K+ currents, was sufficient to simulate aCC's in vivo activity signature. Matching this signature using a reconstructed morphology predicted that the SIZ is on aCC's primary axon, 70 µm after the most distal dendritic branching point. From SIZ to soma, we observed and quantified selective morphological filtering of fast activating currents. Non-inactivating K+ currents are filtered ∼3 times less and despite their large magnitude at the soma they could be as distal as Na+ currents. The peak of transient component (NaT) of the voltage-activated Na+ current is also filtered more than the magnitude of slower persistent component (NaP), which can contribute to seizures. The corrected NaP/NaT ratio explains the previously observed discrepancy when the same channel is expressed in different cells. In summary, we used an in vivo signature to estimate ion channel location and recording artifacts, which can be applied to other neurons.

Seizure suppression through manipulating splicing of a voltage-gated sodium channel.

Seizure can result from increased voltage-gated persistent sodium current expression. Although many clinically-approved antiepileptic drugs target voltage-gated persistent sodium current, none exclusively repress this current without also adversely affecting the transient voltage-gated sodium current. Achieving a more selective block has significant potential for the treatment of epilepsy. Recent studies show that voltage-gated persistent sodium current amplitude is regulated by alternative splicing offering the possibility of a novel route for seizure control. In this study we identify 291 splicing regulators that, on knockdown, alter splicing of the Drosophila voltage-gated sodium channel to favour inclusion of exon K, rather than the mutually exclusive exon L. This change is associated with both a significant reduction in voltage-gated persistent sodium current, without change to transient voltage-gated sodium current, and to rescue of seizure in this model insect. RNA interference mediated knock-down, in two different seizure mutants, shows that 95 of these regulators are sufficient to significantly reduce seizure duration. Moreover, most suppress seizure activity in both mutants, indicative that they are part of well conserved pathways and likely, therefore, to be optimal candidates to take forward to mammalian studies. We provide proof-of-principle for such studies by showing that inhibition of a selection of regulators, using small molecule inhibitors, is similarly effective to reduce seizure. Splicing of the Drosophila sodium channel shows many similarities to its mammalian counterparts, including altering the amplitude of voltage-gated persistent sodium current. Our study provides the impetus to investigate whether manipulation of splicing of mammalian voltage-gated sodium channels may be exploitable to provide effective seizure control.

The Prognostic Role of QTc Interval in Acute Myocarditis.

BACKGROUND: Acute myocarditis is an inflammatory disease of the myocardium. Although a fulminant course of the disease is difficult to predict, it may lead to acute heart failure and death. Previous studies have demonstrated that reduced left ventricular systolic function and prolonged QRS duration can predict the fulminant course of acute myocarditis. This study aimed to identify whether prolonged QTc interval could also be predictive of fulminant disease in this population. METHODS: We retrospectively included 40 patients diagnosed with acute myocarditis who were admitted to our hospital between 2002 and 2013. They were divided into the fulminant group (n = 9) and the non-fulminant group (n = 31). Clinical symptoms, laboratory findings, electrocardiographic, and echocardiographic parameters were analyzed. Multivariate logistic regression analysis was used to identify the independent factors predictive of fulminant disease. RESULTS: Patients with fulminant myocarditis had a higher mortality rate than those with non-fulminant disease (55.6% vs. 0%, p < 0.001). Multivariate analysis revealed that wider QRS durations (133.22 ± 45.85 ms vs. 92.81 ± 15.56 ms, p = 0.030) and longer QTc intervals (482.78 ± 69.76 ms vs. 412.00 ± 33.31 ms, p = 0.016) were significant predictors associated with a fulminant course of myocarditis. CONCLUSIONS: Prolonged QRS duration and QTc interval, upon patient admission, may be associated with an increased risk of fulminant disease and increased in-hospital mortality. Therefore, early recognition of fulminant myocarditis and early mechanical support could provide improved patient outcomes. KEY WORDS: Fulminant myocarditis • Predictors • QRS complex • QTc interval.

Innexins Ogre and Inx2 are required in glial cells for normal postembryonic development of the Drosophila central nervous system.

Innexins are one of two gene families that have evolved to permit neighbouring cells in multicellular systems to communicate directly. Innexins are found in prechordates and persist in small numbers in chordates as divergent sequences termed pannexins. Connexins are functionally analogous proteins exclusive to chordates. Members of these two families of proteins form intercellular channels, assemblies of which constitute gap junctions. Each intercellular channel is a composite of two hemichannels, one from each of two apposed cells. Hemichannels dock in the extracellular space to form a complete channel with a central aqueous pore that regulates the cell-cell exchange of ions and small signalling molecules. Hemichannels can also act independently by releasing paracrine signalling molecules. optic ganglion reduced (ogre) is a member of the Drosophila innexin family, originally identified as a gene essential for postembryonic neurogenesis. Here we demonstrate, by heterologous expression in paired Xenopus oocytes, that Ogre alone does not form homotypic gap-junction channels; however, co-expression of Ogre with Innexin2 (Inx2) induces formation of functional channels with properties distinct from Inx2 homotypic channels. In the Drosophila larval central nervous system, we find that Inx2 partially colocalises with Ogre in proliferative neuroepithelia and in glial cells. Downregulation of either ogre or inx2 selectively in glia, by targeted expression of RNA interference transgenes, leads to a significant reduction in the size of the larval nervous system and behavioural defects in surviving adults. We conclude that these innexins are crucially required in glial cells for normal postembryonic development of the central nervous system.

Estimating Young's modulus of graphene with Raman scattering enhanced by micrometer tip.

We demonstrate that the Raman intensities of G and 2D bands of a suspended graphene can be enhanced using a gold tip with an apex size of 2.3 µm. The enhancement decays with the tip-graphene distance exponentially and remains detectable at a distance of 1.5 µm. Raman mappings show that the enhanced area is comparable to the apex size. Application of a bias voltage to the tip can attract the graphene so that Raman signals are intensified. The exponential enhancement-distance relationship enables the measurement of the graphene deformation, and the Young's modulus of graphene is estimated to be 1.48 TPa.

Evolutionary pressures on simple sequence repeats in prokaryotic coding regions.

Simple sequence repeats (SSRs) are indel mutational hotspots in genomes. In prokaryotes, SSR loci can cause phase variation, a microbial survival strategy that relies on stochastic, reversible on-off switching of gene activity. By analyzing multiple strains of 42 fully sequenced prokaryotic species, we measure the relative variability and density distribution of SSRs in coding regions. We demonstrate that repeat type strongly influences indel mutation rates, and that the most mutable types are most strongly avoided across genomes. We thoroughly characterize SSR density and variability as a function of N→C position along protein sequences. Using codon-shuffling algorithms that preserve amino acid sequence, we assess evolutionary pressures on SSRs. We find that coding sequences suppress repeats in the middle of proteins, and enrich repeats near termini, yielding U-shaped SSR density curves. We show that for many species this characteristic shape can be attributed to purely biophysical constraints of protein structure. In multiple cases, however, particularly in certain pathogenic bacteria, we observe over enrichment of SSRs near protein N-termini significantly beyond expectation based on structural constraints. This increases the probability that frameshifts result in non-functional proteins, revealing that these species may evolutionarily tune SSR positions in coding regions to facilitate phase variation.

Depletion of ß-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development.

Depletion of ß-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional ß-catenin knockout mice (Alb-Cre;Ctnnb1(flx/flx)) until 20 mo of age to determine the function of ß-catenin in the postnatal liver. ß-catenin was absent from the hepatocytes of ß-catenin knockout mice 4 wk after delivery. From 9 mo of age, hepatocytes were gradually replaced by newly formed ß-catenin-positive hepatocytes, which constituted about 90% of hepatocytes at 18-20 mo of age. This process was accompanied by active proliferation of bile duct/ductule cells. ß-catenin-positive hepatocytes exhibited elevated proliferation activity and expression of progenitor cell markers, but lower albumin and Cre. This might explain their intact ß-catenin protein, and suggest their origins from hepatic progenitor cells. Liver tumors arose spontaneously from ß-catenin-positive cells, and tumorigenesis was accelerated by hepatitis B X protein. These results indicate ß-catenin critical for the regeneration of mature hepatocytes. Failure to regenerate mature hepatocytes results in proliferation of hepatic progenitor cells that are able to maintain liver function but are predisposed to form liver tumors.

Design and implementation of a VoIP broadcasting service over embedded systems in a heterogeneous network environment.

As the digitization is integrated into daily life, media including video and audio are heavily transferred over the Internet nowadays. Voice-over-Internet Protocol (VoIP), the most popular and mature technology, becomes the focus attracting many researches and investments. However, most of the existing studies focused on a one-to-one communication model in a homogeneous network, instead of one-to-many broadcasting model among diverse embedded devices in a heterogeneous network. In this paper, we present the implementation of a VoIP broadcasting service on the open source-Linphone-in a heterogeneous network environment, including WiFi, 3G, and LAN networks. The proposed system featuring VoIP broadcasting over heterogeneous networks can be integrated with heterogeneous agile devices, such as embedded devices or mobile phones. VoIP broadcasting over heterogeneous networks can be integrated into modern smartphones or other embedded devices; thus when users run in a traditional AM/FM signal unreachable area, they still can receive the broadcast voice through the IP network. Also, comprehensive evaluations are conducted to verify the effectiveness of the proposed implementation.

Dramatically Enhanced Valley-Polarized Emission by Alloying and Electrical Tuning of Monolayer WTe2 x S2(1- x ) Alloys at Room Temperature with 1T'-WTe2 -Contact.

Monolayer ternary tellurides based on alloying different transition metal dichalcogenides (TMDs) can result in new two-dimensional (2D) materials ranging from semiconductors to metals and superconductors with tunable optical and electrical properties. Semiconducting WTe2 x S2(1- x ) monolayer possesses two inequivalent valleys in the Brillouin zone, each valley coupling selectively with circularly polarized light (CPL). The degree of valley polarization (DVP) under the excitation of CPL represents the purity of valley polarized photoluminescence (PL), a critical parameter for opto-valleytronic applications. Here, new strategies to efficiently tailor the valley-polarized PL from semiconducting monolayer WTe2 x S2(1- x ) at room temperature (RT) through alloying and back-gating are presented. The DVP at RT is found to increase drastically from < 5% in WS2 to 40% in WTe0.12 S1.88 by Te-alloying to enhance the spin-orbit coupling. Further enhancement and control of the DVP from 40% up to 75% is demonstrated by electrostatically doping the monolayer WTe0.12 S1.88 via metallic 1T'-WTe2 electrodes, where the use of 1T'-WTe2 substantially lowers the Schottky barrier height (SBH) and weakens the Fermi-level pinning of the electrical contacts. The demonstration of drastically enhanced DVP and electrical tunability in the valley-polarized emission from 1T'-WTe2 /WTe0.12 S1.88 heterostructures paves new pathways towards harnessing valley excitons in ultrathin valleytronic devices for RT applications.