Trifluoromethylation of 2D Transition Metal Dichalcogenides: A Mild Functionalization and Tunable p-Type Doping Method.

Chemical modification is a powerful strategy for tuning the electronic properties of 2D semiconductors. Here we report the electrophilic trifluoromethylation of 2D WSe2 and MoS2 under mild conditions using the reagent trifluoromethyl thianthrenium triflate (TTT). Chemical characterization and density functional theory calculations reveal that the trifluoromethyl groups bind covalently to surface chalcogen atoms as well as oxygen substitution sites. Trifluoromethylation induces p-type doping in the underlying 2D material, enabling the modulation of charge transport and optical emission properties in WSe2. This work introduces a versatile and efficient method for tailoring the optical and electronic properties of 2D transition metal dichalcogenides.

Electroluminescence from Megasonically Solution-Processed MoS2 Nanosheet Films.

Due to their superior optoelectronic properties, monolayer two-dimensional (2D) transition metal dichalcogenides (TMDs) have attracted significant attention for electroluminescent devices. However, challenges in isolating optoelectronically active TMD monolayers using scalable liquid phase exfoliation have precluded electroluminescence in large-area, solution-processed TMD films. Here, we overcome these limitations and demonstrate electroluminescence from molybdenum disulfide (MoS2) nanosheet films by employing a monolayer-rich MoS2 ink produced by electrochemical intercalation and megasonic exfoliation. Characteristic monolayer MoS2 photoluminescence and electroluminescence spectral peaks at 1.88-1.90 eV are observed in megasonicated MoS2 films, with the emission intensity increasing with film thickness over the range 10-70 nm. Furthermore, employing a vertical light-emitting capacitor architecture enables uniform electroluminescence in large-area devices. These results indicate that megasonically exfoliated MoS2 monolayers retain their direct bandgap character in electrically percolating thin films even following multistep solution processing. Overall, this work establishes megasonicated MoS2 inks as an additive manufacturing platform for flexible, patterned, and miniaturized light sources that can likely be expanded to other TMD semiconductors.

Chemomechanical modification of quantum emission in monolayer WSe2.

Two-dimensional (2D) materials have attracted attention for quantum information science due to their ability to host single-photon emitters (SPEs). Although the properties of atomically thin materials are highly sensitive to surface modification, chemical functionalization remains unexplored in the design and control of 2D material SPEs. Here, we report a chemomechanical approach to modify SPEs in monolayer WSe2 through the synergistic combination of localized mechanical strain and noncovalent surface functionalization with aryl diazonium chemistry. Following the deposition of an aryl oligomer adlayer, the spectrally complex defect-related emission of strained monolayer WSe2 is simplified into spectrally isolated SPEs with high single-photon purity. Density functional theory calculations reveal energetic alignment between WSe2 defect states and adsorbed aryl oligomer energy levels, thus providing insight into the observed chemomechanically modified quantum emission. By revealing conditions under which chemical functionalization tunes SPEs, this work broadens the parameter space for controlling quantum emission in 2D materials.

Room Temperature Lasing from Semiconducting Single-Walled Carbon Nanotubes.

Miniaturized near-infrared semiconductor lasers that are able to generate coherent light with low energy consumption have widespread applications in fields such as optical interconnects, neuromorphic computing, and deep-tissue optogenetics. With optical transitions at near-infrared wavelengths, diameter-tunable electronic structures, and superlative optoelectronic properties, semiconducting single-walled carbon nanotubes (SWCNTs) are promising candidates for nanolaser applications. However, despite significant efforts in this direction and recent progress toward enhancing spontaneous emission from SWCNTs through Purcell effects, SWCNT-based excitonic lasers have not yet been demonstrated. Leveraging an optimized cavity-emitter integration scheme enabled by a self-assembly process, here we couple SWCNT emission to the whispering gallery modes supported by polymer microspheres, resulting in room temperature excitonic lasing with an average lasing threshold of 4.5 kW/cm2. The high photostability of SWCNTs allows stable lasing for prolonged duration with minimal degradation. This experimental realization of excitonic lasing from SWCNTs, combined with their versatile electronic and optical properties that can be further controlled by chemical modification, offers far-reaching opportunities for tunable near-infrared nanolasers that are applicable for optical signal processing, in vivo biosensing, and optoelectronic devices.

Increased carbonylation, protein aggregation and apoptosis in the spinal cord of mice with experimental autoimmune encephalomyelitis.

Previous work from our laboratory implicated protein carbonylation in the pathophysiology of both MS (multiple sclerosis) and its animal model EAE (experimental autoimmune encephalomyelitis). Subsequent in vitro studies revealed that the accumulation of protein carbonyls, triggered by glutathione deficiency or proteasome inhibition, leads to protein aggregation and neuronal cell death. These findings prompted us to investigate whether their association can be also established in vivo. In the present study, we characterized protein carbonylation, protein aggregation and apoptosis along the spinal cord during the course of MOG (myelin-oligodendrocyte glycoprotein)(35-55) peptide-induced EAE in C57BL/6 mice. The results show that protein carbonyls accumulate throughout the course of the disease, albeit by different mechanisms: increased oxidative stress in acute EAE and decreased proteasomal activity in chronic EAE. We also show a temporal correlation between protein carbonylation (but not oxidative stress) and apoptosis. Furthermore, carbonyl levels are significantly higher in apoptotic cells than in live cells. A high number of juxta-nuclear and cytoplasmic protein aggregates containing the majority of the oxidized proteins are present during the course of EAE. The LC3 (microtubule-associated protein light chain 3)-II/LC3-I ratio is significantly reduced in both acute and chronic EAE indicating reduced autophagy and explaining why aggresomes accumulate in this disorder. Taken together, the results of the present study suggest a link between protein oxidation and neuronal/glial cell death in vivo, and also demonstrate impaired proteostasis in this widely used murine model of MS.

Protein carbonylation and aggregation precede neuronal apoptosis induced by partial glutathione depletion.

While the build-up of oxidized proteins within cells is believed to be toxic, there is currently no evidence linking protein carbonylation and cell death. In the present study, we show that incubation of nPC12 (neuron-like PC12) cells with 50 µM DEM (diethyl maleate) leads to a partial and transient depletion of glutathione (GSH). Concomitant with GSH disappearance there is increased accumulation of PCOs (protein carbonyls) and cell death (both by necrosis and apoptosis). Immunocytochemical studies also revealed a temporal/spatial relationship between carbonylation and cellular apoptosis. In addition, the extent of all three, PCO accumulation, protein aggregation and cell death, augments if oxidized proteins are not removed by proteasomal degradation. Furthermore, the effectiveness of the carbonyl scavengers hydralazine, histidine hydrazide and methoxylamine at preventing cell death identifies PCOs as the toxic species. Experiments using well-characterized apoptosis inhibitors place protein carbonylation downstream of the mitochondrial transition pore opening and upstream of caspase activation. While the study focused mostly on nPC12 cells, experiments in primary neuronal cultures yielded the same results. The findings are also not restricted to DEM-induced cell death, since a similar relationship between carbonylation and apoptosis was found in staurosporine- and buthionine sulfoximine-treated nPC12 cells. In sum, the above results show for the first time a causal relationship between carbonylation, protein aggregation and apoptosis of neurons undergoing oxidative damage. To the best of our knowledge, this is the first study to place direct (oxidative) protein carbonylation within the apoptotic pathway.

Changes in 20S subunit composition are largely responsible for altered proteasomal activities in experimental autoimmune encephalomyelitis.

We recently reported that the proteasomal peptidase activities are altered in the cerebellum of mice with myelin oligodendrocyte glycoprotein (MOG) peptide-induced experimental autoimmune encephalomyelitis (EAE). To determine whether these fluctuations are caused by proteasome activation/inactivation and/or changes in the levels of individual ß subunits, we characterized the proteasome subunit composition by western blotting. The results show that the rise in proteasomal peptidase activity in acute EAE correlates with an augmented expression of inducible ß subunits whereas the decline in activity in chronic EAE correlates with a reduction in the amount of standard ß subunits. Using pure standard (s) and immuno (i) 20S particles for calibration, we determined that the changes in the levels of catalytic subunits account for all of the fluctuations in peptidase activities in EAE. The i-20S and s-20S proteasome were found to degrade carbonylated ß-actin with similar efficiency, suggesting that the amount of protein carbonyls in EAE may be controlled by the activity of both core particles. We also found an increase in proteasome activator 11S regulatory particle and a decrease in inhibitor proteasome inhibitor with molecular mass of 31 kDa levels in acute EAE, reflecting a response to inflammation. Elevated levels of 19S regulatory particle and 11S regulatory particle in chronic EAE, however, may occur in response to diminished proteasomal activity in this phase. These findings are central towards understanding the altered proteasomal physiology in inflammatory demyelinating disorders.