Visualization of defect-induced excitonic properties of the edges and grain boundaries in synthesized monolayer molybdenum disulfide

Atomically thin two-dimensional (2D) transition metal dichalcogenides (TMDCs) are attractive materials for next generation nanoscale optoelectronic applications. Understanding nanoscale optical behavior of the edges and grain boundaries of synthetically grown TMDCs is vital for optimizing their optoelectronic properties. Elucidating the nanoscale optical properties of 2D materials through far-field optical microscopy requires a diffraction-limited optical beam diameter sub-micron in size. Here we present our experimental work on spatial photoluminescence (PL) scanning of large size ( $\geq 50$ microns) monolayer MoS$_2$ grown by chemical vapor deposition (CVD) using a diffraction limited blue laser beam spot (wavelength 405 nm) with a beam diameter as small as 200 nm allowing us to probe nanoscale excitonic phenomena which was not observed before. We have found several important features: (i) there exists a sub-micron width strip ($\sim 500$ nm) along the edges that fluoresces $\sim 1000 \%$ brighter than the region far inside; (ii) there is another brighter wide region consisting of parallel fluorescing lines ending at the corners of the zig-zag peripheral edges; (iii) there is a giant blue shifted A-excitonic peak, as large as $\sim 120$ meV, in the PL spectra from the edges. Using density functional theory calculations, we attribute this giant blue shift to the adsorption of oxygen dimers at the edges, which reduces the excitonic binding energy. Our results not only shed light on defect-induced excitonic properties, but also offer an attractive route to tailor optical properties at the TMDC edges through defect engineering.Comment: 10 pages, 4 figures in Journal of Physical Chemistry C, 201

Astronomers for planet Earth: engaging with the public to forge a sustainable future

Science Communication and Societ

Topical Peroxisome Proliferator Activated Receptor Activators Accelerate Postnatal Stratum Corneum Acidification

Previous studies have shown that pH declines from between 6 and 7 at birth to adult levels (pH 5.0–5.5) over 5–6 days in neonatal rat stratum corneum (SC). As a result, at birth, neonatal epidermis displays decreased permeability barrier homeostasis and SC integrity, improving days 5–6. We determined here whether peroxisome proliferator-activated receptor (PPAR) activators accelerate postnatal SC acidification. Topical treatment with two different PPARα activators, clofibrate and WY14643, accelerated the postnatal decline in SC surface pH, whereas treatment with PPARγ activators did not and a PPARβ/δ activator had only a modest effect. Treatment with clofibrate significantly accelerated normalization of barrier function. The morphological basis for the improvement in barrier function in PPARα-treated animals includes accelerated secretion of lamellar bodies and enhanced, postsecretory processing of secreted lamellar body contents into mature lamellar membranes. Activity of β-glucocerebrosidase increased after PPARα-activator treatment. PPARα activator also improved SC integrity, which correlated with an increase in corneodesmosome density and increased desmoglein-1 content, with a decline in serine protease activity. Topical treatment of newborn animals with a PPARα activator increased secretory phospholipase A2 activity, which likely accounts for accelerated SC acidification. Thus, PPARα activators accelerate neonatal SC acidification, in parallel with improved permeability homeostasis and SC integrity/cohesion. Hence, PPARα activators might be useful to prevent or treat certain common neonatal dermatoses

Defects in Stratum Corneum Desquamation Are the Predominant Effect of Impaired ABCA12 Function in a Novel Mouse Model of Harlequin Ichthyosis.

Harlequin Ichthyosis is a severe skin disease caused by mutations in the human gene encoding ABCA12. Here, we characterize a novel mutation in intron 29 of the mouse Abca12 gene that leads to the loss of a 5' splice donor site and truncation of the Abca12 RNA transcript. Homozygous mutants of this smooth skin or smsk allele die perinatally with shiny translucent skin, typical of animal models of Harlequin Ichthyosis. Characterization of smsk mutant skin showed that the delivery of glucosylceramides and CORNEODESMOSIN was defective, while ultrastructural analysis revealed abnormal lamellar bodies and the absence of lipid lamellae in smsk epidermis. Unexpectedly, mutant stratum corneum remained intact when subjected to harsh chemical dissociation procedures. Moreover, both KALLIKREIN 5 and -7 were drastically decreased, with retention of desmoplakin in mutant SC. In cultured wild type keratinocytes, both KALLIKREIN 5 and -7 colocalized with ceramide metabolites following calcium-induced differentiation. Reducing the intracellular levels of glucosylceramide with a glucosylceramide synthase inhibitor resulted in decreased secretion of KALLIKREIN proteases by wild type keratinocytes, but not by smsk mutant keratinocytes. Together, these findings suggest an essential role for ABCA12 in transferring not only lipids, which are required for the formation of multilamellar structures in the stratum corneum, but also proteolytic enzymes that are required for normal desquamation. Smsk mutant mice recapitulate many of the pathological features of HI and can be used to explore novel topical therapies against a potentially lethal and debilitating neonatal disease

The Fungicide Chlorothalonil Is Nonlinearly Associated with Corticosterone Levels, Immunity, and Mortality in Amphibians

Background: Contaminants have been implicated in declines of amphibians, a taxon with vital systems similar to those of humans. However, many chemicals have not been thoroughly tested on amphibians or do not directly kill them

BICEP Array cryostat and mount design

Bicep Array is a cosmic microwave background (CMB) polarization experiment that will begin observing at the South Pole in early 2019. This experiment replaces the five Bicep2 style receivers that compose the Keck Array with four larger Bicep3 style receivers observing at six frequencies from 30 to 270GHz. The 95GHz and 150GHz receivers will continue to push the already deep Bicep/Keck CMB maps while the 30/40GHz and 220/270GHz receivers will constrain the synchrotron and galactic dust foregrounds respectively. Here we report on the design and performance of the Bicep Array instruments focusing on the mount and cryostat systems

BICEP Array cryostat and mount design

Bicep Array is a cosmic microwave background (CMB) polarization experiment that will begin observing at the South Pole in early 2019. This experiment replaces the five Bicep2 style receivers that compose the Keck Array with four larger Bicep3 style receivers observing at six frequencies from 30 to 270GHz. The 95GHz and 150GHz receivers will continue to push the already deep Bicep/Keck CMB maps while the 30/40GHz and 220/270GHz receivers will constrain the synchrotron and galactic dust foregrounds respectively. Here we report on the design and performance of the Bicep Array instruments focusing on the mount and cryostat systems