Molybdenum disulfide (MoS2) is an extremely intriguing material because of its unique electrical and optical properties. The preparation of large-area and high-quality MoS2 nanosheets is an important step in a wide range of applications. This study demonstrates that monolayer and few-layer MoS2 nanosheets can be obtained from electrochemical exfoliation of bulk MoS2 crystals. The lateral size of the exfoliated MoS2 nanosheets is in the 5-50 μm range, which is much larger than that of chemically or liquid-phase exfoliated MoS2 nanosheets. The MoS2 nanosheets undergo low levels of oxidation during electrochemical exfoliation. In addition, microscopic and spectroscopic characterizations indicate that the exfoliated MoS2 nanosheets are of high quality and have an intrinsic structure. A back-gate field-effect transistor was fabricated using an exfoliated monolayer MoS2 nanosheet. The on/off current ratio is over 10(6), and the field-effect mobility is approximately 1.2 cm(2) V(-1) s(-1); these values are comparable to the results for micromechanically exfoliated MoS2 nanosheets. The electrochemical exfoliation method is simple and scalable, and it can be applied to exfoliate other transition metal dichalcogenides.
We investigated the dependence of electron mobility on the thickness of MoS2 nanosheets by fabricating bottom-gate single and few-layer MoS2 thin-film transistors with SiO2 gate dielectrics and Au electrodes. All the fabricated MoS2 transistors showed on/off-current ratio of ∼107 and saturated output characteristics without high-k capping layers. As the MoS2 thickness increased from 1 to 6 layers, the field-effect mobility of the fabricated MoS2 transistors increased from ∼10 to ∼18 cm2V−1s−1. The increased subthreshold swing of the fabricated transistors with MoS2 thickness suggests that the increase of MoS2 mobility with thickness may be related to the dependence of the contact resistance and the dielectric constant of MoS2 layer on its thickness.
Back-gated MoSe2 thin-film transistors (TFTs) with an Al2O3-capping layer were fabricated, and the device characteristics of the MoSe2 TFTs that are dependent on the Al2O3-capping-layer passivation were investigated. The output drain current was doubled, the fluctuation of the output current was suppressed, and the threshold voltage of the MoSe2 TFTs was negatively shifted with the Al2O3-capping layer. The on/off-current ratio of the MoSe2 TFTs is approximately six decades regardless of the Al2O3-capping layer, but the field-effect mobility was greatly increased from 2.86 cm2/Vs to 10.26 cm2/Vs after the deposition of the Al2O3-capping layer. According to the results of this study, the Al2O3-capping layer can enhance the device characteristics of MoSe2 TFTs.
Vocal fold scarring is a major cause of dysphonia. Vocal fold fibroblasts (VFFs) and the TGF-β signaling pathway play important roles in scar formation. Eupatilin, a chromone derivative of the Artemisia species, is a traditional folk remedy for wound healing. However, until recently, few studies investigated the therapeutic effects of eupatilin. We investigated the antifibrogenic effects of eupatilin on TGF-β1-treated human vocal fold fibroblasts (hVFFs). The optimal concentration of eupatilin was determined by a cell viability assay. Western blotting was used to measure the expression of alpha-smooth muscle actin during myofibroblast differentiation, fibronectin (FN), collagen type I (Col I), and collagen type III (Col III) extracellular matrix proteins, and Smad2, Smad3, and p38 in the fibrotic pathway. Measurements were made before and after eupatilin treatment. Eupatilin at 100 nM was shown to be safe for use in hVFFs. TGF-β1 induced hVFFs to proliferate and differentiate into myofibroblasts and increased Col III and FN synthesis in a time- and dose-dependent manner. Eupatilin suppressed TGF-β1-induced hVFF proliferation and differentiation into myofibroblasts through the Smad and p38 signaling pathways. Furthermore, eupatilin inhibited TGF-β1-induced FN, Col I, and Col III synthesis in hVFFs. Our in vitro findings show that eupatilin effectively suppressed TGF-β1-induced fibrotic changes in hVFFs via the Smad and p38 signaling pathways. Thus, eupatilin may be considered a novel therapeutic agent for the treatment of vocal fold fibrosis.
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