Excitonic emission in van-der-Waals nanotubes of transition metal dichalcogenides

Nanotubes (NTs) of transition metal dichalcogenides (TMDs), such as MoS2 and WS2, were first synthesized more than a quarter of a century ago; nevertheless, many of their properties have so far remained basically unknown. This review presents the state of the art in the knowledge of the optical properties of TMD NTs. We first evaluate general properties of multilayered TMD crystals, and analyze available data on electronic band structure and optical properties of related NTs. Then, the technology for the formation and the structural characteristics of TMD NTs are represented, focusing on the structures synthesized by chemical transport reaction. The core of this work is the presentation of the ability of TMD NTs to emit bright photoluminescence (PL), which has been discovered recently. By means of micro-PL spectroscopy of individual tubes we show that excitonic transitions relevant to both direct and indirect band gaps contribute to the emission spectra of the NTs despite the presence of dozens of monolayers in their walls. We highlight the performance of the tubes as efficient optical resonators, whose confined optical modes strongly affect the emission bands. Finally, a brief conclusion is presented, along with an outlook of the future studies of this novel member of the family of radiative NTs, which have unique potential for different nanophotonics applications.Comment: 38 pages, 11 fugures, 106 reference

Stability analysis of a second-order difference scheme for the time-fractional mixed sub-diffusion and diffusion-wave equation

This study investigates a class of initial-boundary value problems pertaining to the time-fractional mixed sub-diffusion and diffusion-wave equation (SDDWE). To facilitate the development of a numerical method and analysis, the original problem is transformed into a new integro-differential model which includes the Caputo derivatives and the Riemann-Liouville fractional integrals with orders belonging to (0,1). By providing an a priori estimate of the solution, we have established the existence and uniqueness of a numerical solution for the problem. We propose a second-order method to approximate the fractional Riemann-Liouville integral and employ an L2 type formula to approximate the Caputo derivative. This results in a method with a temporal accuracy of second-order for approximating the considered model. The proof of the unconditional stability of the proposed difference scheme is established. Moreover, we demonstrate the proposed method's potential to construct and analyze a second-order L2-type numerical scheme for a broader class of the time-fractional mixed SDDWEs with multi-term time-fractional derivatives. Numerical results are presented to assess the accuracy of the method and validate the theoretical findings

Electrochemical determination of microRNAs based on isothermal strand-displacement polymerase reaction coupled with multienzyme functionalized magnetic micro-carriers

This study was supported by the National Natural Science Foundation of China (81371901), Doctoral Scientific Fund Project of the Ministry of Education of People's Republic of China (20134433110010), the Critical Point-of-Care Testing (CPOCT) Research grant of American Association for Clinical Chemistry (AACC) and 2015 Distinguished Academic Fellowships of Royal College of Engineering (DVF1415/2/79)

The role of Cx36 and Cx43 in 4‐aminopyridine‐induced rhythmic activity in the spinal nociceptive dorsal horn: an electrophysiological study in vitro

Connexin (Cx) proteins and gap junctions support the formation of neuronal and glial syncytia that are linked to different forms of rhythmic firing and oscillatory activity in the CNS. In this study, quantitative reverse transcription polymerase chain reaction (RT‐qPCR) was used to profile developmental expression of two specific Cx proteins, namely glial Cx43 and neuronal Cx36, in postnatal lumbar spinal cord aged 4, 7, and 14 days. Extracellular electrophysiology was used to determine the contribution of Cx36 and Cx43 to a previously described form of 4‐aminopyridine (4‐AP)‐induced 4–12 Hz rhythmic activity within substantia gelatinosa (SG) of rat neonatal dorsal horn (DH) in vitro. The involvement of Cx36 and Cx43 was probed pharmacologically using quinine, a specific uncoupler of Cx36 and the mimetic peptide blocker Gap 26 which targets Cx43. After establishment of 4–12 Hz rhythmic activity by 4‐AP (25 μmol/L), coapplication of quinine (250 μmol/L) reduced 4‐AP‐induced 4–12 Hz rhythmic activity (P < 0.05). Preincubation of spinal cord slices with Gap 26 (100 μmol/L), compromised the level of 4‐AP‐induced 4–12 Hz rhythmic activity in comparison with control slices preincubated in ACSF alone (P < 0.05). Conversely, the nonselective gap junction “opener” trimethylamine (TMA) enhanced 4–12 Hz rhythmic behavior (P < 0.05), further supporting a role for Cx proteins and gap junctions. These data have defined a physiological role for Cx36 and Cx43 in rhythmic firing in SG, a key nociceptive processing area of DH. The significance of these data in the context of pain and Cx proteins as a future analgesic drug target requires further study

Threatened reef corals of the world

10.1371/journal.pone.0034459PLoS ONE73

Electronic properties of single-layer and multilayer transition metal dichalcogenides MX2MX_2 (M=M= Mo, W and X=X= S, Se)

Single- and few-layer transition metal dichalcogenides have recently emerged as a new family of layered crystals with great interest, not only from the fundamental point of view, but also because of their potential application in ultrathin devices. Here we review the electronic properties of semiconducting $MX_2$, where $M=$Mo or W and $X=$ S or Se. Based on of density functional theory calculations, which include the effect of spin-orbit interaction, we discuss the band structure of single-layer, bilayer and bulk compounds. The band structure of these compounds is highly sensitive to elastic deformations, and we review how strain engineering can be used to manipulate and tune the electronic and optical properties of those materials. We further discuss the effect of disorder and imperfections in the lattice structure and their effect on the optical and transport properties of $MX_2$. The superconducting transition in these compounds, which has been observed experimentally, is analyzed, as well as the different mechanisms proposed so far to explain the pairing. Finally, we include a discussion on the excitonic effects which are present in these systems.Comment: 9 pages, 4 figures. Short review article for special issue of Ann. Phys. on "Two-dimensional materials

PhenoFam-gene set enrichment analysis through protein structural information

<p>Abstract</p> <p>Background</p> <p>With the current technological advances in high-throughput biology, the necessity to develop tools that help to analyse the massive amount of data being generated is evident. A powerful method of inspecting large-scale data sets is gene set enrichment analysis (GSEA) and investigation of protein structural features can guide determining the function of individual genes. However, a convenient tool that combines these two features to aid in high-throughput data analysis has not been developed yet. In order to fill this niche, we developed the user-friendly, web-based application, PhenoFam.</p> <p>Results</p> <p>PhenoFam performs gene set enrichment analysis by employing structural and functional information on families of protein domains as annotation terms. Our tool is designed to analyse complete sets of results from quantitative high-throughput studies (gene expression microarrays, functional RNAi screens, <it>etc</it>.) without prior pre-filtering or hits-selection steps. PhenoFam utilizes Ensembl databases to link a list of user-provided identifiers with protein features from the InterPro database, and assesses whether results associated with individual domains differ significantly from the overall population. To demonstrate the utility of PhenoFam we analysed a genome-wide RNA interference screen and discovered a novel function of plexins containing the cytoplasmic RasGAP domain. Furthermore, a PhenoFam analysis of breast cancer gene expression profiles revealed a link between breast carcinoma and altered expression of PX domain containing proteins.</p> <p>Conclusions</p> <p>PhenoFam provides a user-friendly, easily accessible web interface to perform GSEA based on high-throughput data sets and structural-functional protein information, and therefore aids in functional annotation of genes.</p

A TNF-JNK-Axl-ERK signaling axis mediates primary resistance to EGFR inhibition in glioblastoma.

Aberrant epidermal growth factor receptor (EGFR) signaling is widespread in cancer, making the EGFR an important target for therapy. EGFR gene amplification and mutation are common in glioblastoma (GBM), but EGFR inhibition has not been effective in treating this tumor. Here we propose that primary resistance to EGFR inhibition in glioma cells results from a rapid compensatory response to EGFR inhibition that mediates cell survival. We show that in glioma cells expressing either EGFR wild type or the mutant EGFRvIII, EGFR inhibition triggers a rapid adaptive response driven by increased tumor necrosis factor (TNF) secretion, which leads to activation in turn of c-Jun N-terminal kinase (JNK), the Axl receptor tyrosine kinase and extracellular signal-regulated kinases (ERK). Inhibition of this adaptive axis at multiple nodes rendered glioma cells with primary resistance sensitive to EGFR inhibition. Our findings provide a possible explanation for the failures of anti-EGFR therapy in GBM and suggest a new approach to the treatment of EGFR-expressing GBM using a combination of EGFR and TNF inhibition

On transmissible load formulations in topology optimization

Transmissible loads are external loads defined by their line of action, with actual points of load application chosen as part of the topology optimization process. Although for problems where the optimal structure is a funicular, transmissible loads can be viewed as surface loads, in other cases such loads are free to be applied to internal parts of the structure. There are two main transmissible load formulations described in the literature: a rigid bar (constrained displacement) formulation or, less commonly, a migrating load (equilibrium) formulation. Here, we employ a simple Mohr’s circle analysis to show that the rigid bar formulation will only produce correct structural forms in certain specific circumstances. Numerical examples are used to demonstrate (and explain) the incorrect topologies produced when the rigid bar formulation is applied in other situations. A new analytical solution is also presented for a uniformly loaded cantilever structure. Finally, we invoke duality principles to elucidate the source of the discrepancy between the two formulations, considering both discrete truss and continuum topology optimization formulations

Plasma Cholesterol-Induced Lesion Networks Activated before Regression of Early, Mature, and Advanced Atherosclerosis

Plasma cholesterol lowering (PCL) slows and sometimes prevents progression of atherosclerosis and may even lead to regression. Little is known about how molecular processes in the atherosclerotic arterial wall respond to PCL and modify responses to atherosclerosis regression. We studied atherosclerosis regression and global gene expression responses to PCL (&gt;= 80%) and to atherosclerosis regression itself in early, mature, and advanced lesions. In atherosclerotic aortic wall from Ldlr(-/-)Apob(100/100)Mttp(flox/flox)Mx1-Cre mice, atherosclerosis regressed after PCL regardless of lesion stage. However, near-complete regression was observed only in mice with early lesions; mice with mature and advanced lesions were left with regression-resistant, relatively unstable plaque remnants. Atherosclerosis genes responding to PCL before regression, unlike those responding to the regression itself, were enriched in inherited risk for coronary artery disease and myocardial infarction, indicating causality. Inference of transcription factor (TF) regulatory networks of these PCL-responsive gene sets revealed largely different networks in early, mature, and advanced lesions. In early lesions, PPARG was identified as a specific master regulator of the PCL-responsive atherosclerosis TF-regulatory network, whereas in mature and advanced lesions, the specific master regulators were MLL5 and SRSF10/XRN2, respectively. In a THP-1 foam cell model of atherosclerosis regression, siRNA targeting of these master regulators activated the time-point-specific TF-regulatory networks and altered the accumulation of cholesterol esters. We conclude that PCL leads to complete atherosclerosis regression only in mice with early lesions. Identified master regulators and related PCL-responsive TF-regulatory networks will be interesting targets to enhance PCL-mediated regression of mature and advanced atherosclerotic lesions. Author Summary The main underlying cause of heart attacks and strokes is atherosclerosis. One strategy to prevent these often deadly clinical events is therefore either to slow atherosclerosis progression or better, induce regression of atherosclerotic plaques making them more stable. Plasma cholesterol lowering (PCL) is the most efficient way to induce atherosclerosis regression but sometimes fails to do so. In our study, we used a mouse model with elevated LDL cholesterol levels, similar to humans who develop early atherosclerosis, and a genetic switch to lower plasma cholesterol at any time during atherosclerosis progression. In this model, we examined atherosclerosis gene expression and regression in response to PCL at three different stages of atherosclerosis progression. PCL led to complete regression in mice with early lesions but was incomplete in mice with mature and advanced lesions, indicating that early prevention with PCL in individuals with increased risk for heart attack or stroke would be particularly useful. In addition, by inferring PCL-responsive gene networks in early, mature and advanced atherosclerotic lesions, we identified key drivers specific for regression of early (PPARG), mature (MLL5) and advanced (SRSF10/XRN2) atherosclerosis. These key drivers should be interesting therapeutic targets to enhance PCL-mediated regression of atherosclerosis