Unconventional Enhancement of Photoluminescence in Multilayer MoS₂ within MoS₂/MoO₂ Heterostructures: Implication for Optoelectronic Devices

Monolayer two-dimensional (2D) transition-metal chalcogenides (TMDs) with a direct bandgap are promising in future optoelectronics due to the strong light–matter interaction. Comparatively speaking, their multilayer counterparts show a higher carrier mobility and current capacity over the monolayer. However, multilayer TMDs with an indirect bandgap exhibit weak photoluminescence (PL) emission, hindering their practical applications. In this work, we discovered an unconventional PL enhancement of multilayer MoS2 in chemical vapor-deposited MoS2/MoO2 heterostructures, whose intensity is an order of magnitude higher than that observed in multilayer MoS2 on SiO2/Si. The PL enhancement is mainly attributed to the surface plasmon resonance of MoO2, as evidenced by UV–vis absorption spectroscopy of the MoS2/MoO2 heterostructures and the laser wavelength selectivity of the PL enhancement. Meanwhile, a nanogap was observed at the interface of MoS2 and MoO2 by using high-resolution scanning transmission electron microscopy, which impedes the PL quenching induced by the charge transfer between multilayer MoS2 and metallic MoO2. To confirm the mechanism, MoS2/BN/MoO2 heterostructures were assembled by using insulating monolayer boron nitride (BN) to simulate the nanogap, and similar PL enhancement of multilayer MoS2 was observed. To the best of our knowledge, surface plasmon resonance-enhanced PL emission by a metal oxide substrate has been rarely reported until now. This work provides a platform for regulating the light–matter interaction of 2D materials, which will benefit their applications in optoelectronic devices

DataSheet_1_Physiological responses and transcriptomic analysis of StCPD gene overexpression in potato under salt stresses.pdf

IntroductionThe potato (Solanum tuberosum L.), one of the most vital food crops worldwide, is sensitive to salinity. Brassinosteroids (BRs) are crucial in tolerance to various abiotic stresses. The constitutive photomorphogenesis and dwarf (CPD) gene encodes C-3 oxidase, which is a rate-limiting enzyme that controls the synthesis of BRs.MethodsIn this study, we used StCPD gene overexpression (T) and un-transgenic (NT) plants obtained from our former research to illustrate adaptive resistance to salt stress at levels of phenotype; cell ultrastructure, physiology, and biochemistry; hormone; and transcription.ResultsResults showed the accumulation of 2,4-epibrassionolide (EBL) in T potatoes. We found that under high salt situations, the changed Na+/K+ transporter gene expression was linked with the prevalent ionic responses in T plants, which led to lower concentrations of K+ and higher concentrations of Na+ in leaves. Furthermore, RNA-sequencing (RNA-seq) data elucidated that gene expressions in NT and T plants were significantly changed with 200-mM NaCl treatment for 24 h and 48 h, compared with the 0-h treatment. Functional enrichment analysis suggested that most of the differentially expressed genes (DEGs) were related to the regulation of BR-related gene expression, pigment metabolism process, light and action, and plant hormone signal transduction.DiscussionThese findings suggested that StCPD gene overexpression can alleviate the damage caused by salt stress and enhance the salt resistance of potato plantlets. Our study provides an essential reference for further research on BR regulation of plant molecular mechanisms in potatoes with stress tolerance.</p

Image_3_Adiponectin Ameliorates GMH-Induced Brain Injury by Regulating Microglia M1/M2 Polarization Via AdipoR1/APPL1/AMPK/PPARγ Signaling Pathway in Neonatal Rats.tif

Adiponectin (APN), a fat-derived plasma hormone, is a classic anti-inflammatory agent. Multiple studies have demonstrated the beneficial role of APN in acute brain injury, but the effect of APN in germinal matrix hemorrhage (GMH) is unclear, and the underlying molecular mechanisms remain largely undefined. In the current study, we used a GMH rat model with rh-APN treatment, and we observed that APN demonstrated a protective effect on neurological function and an inhibitory effect on neuroinflammation after GMH. To further explore the underlying mechanisms of these effects, we found that the expression of Adiponectin receptor 1 (AdipoR1) primarily colocalized with microglia and neurons in the brain. Moreover, AdiopR1, but not AdipoR2, was largely increased in GMH rats. Meanwhile, further investigation showed that APN treatment promoted AdipoR1/APPL1-mediated AMPK phosphorylation, further increased peroxisome proliferator-activated receptor gamma (PPARγ) expression, and induced microglial M2 polarization to reduce the neuroinflammation and enhance hematoma resolution in GMH rats. Importantly, either knockdown of AdipoR1, APPL1, or LKB1, or specific inhibition of AMPK/PPARγ signaling in microglia abrogated the protective effect of APN after GMH in rats. In all, we propose that APN works as a potential therapeutic agent to ameliorate the inflammatory response following GMH by enhancing the M2 polarization of microglia via AdipoR1/APPL1/AMPK/PPARγ signaling pathway, ultimately attenuating inflammatory brain injury induced by hemorrhage.</p

Image_2_Adiponectin Ameliorates GMH-Induced Brain Injury by Regulating Microglia M1/M2 Polarization Via AdipoR1/APPL1/AMPK/PPARγ Signaling Pathway in Neonatal Rats.tif

Adiponectin (APN), a fat-derived plasma hormone, is a classic anti-inflammatory agent. Multiple studies have demonstrated the beneficial role of APN in acute brain injury, but the effect of APN in germinal matrix hemorrhage (GMH) is unclear, and the underlying molecular mechanisms remain largely undefined. In the current study, we used a GMH rat model with rh-APN treatment, and we observed that APN demonstrated a protective effect on neurological function and an inhibitory effect on neuroinflammation after GMH. To further explore the underlying mechanisms of these effects, we found that the expression of Adiponectin receptor 1 (AdipoR1) primarily colocalized with microglia and neurons in the brain. Moreover, AdiopR1, but not AdipoR2, was largely increased in GMH rats. Meanwhile, further investigation showed that APN treatment promoted AdipoR1/APPL1-mediated AMPK phosphorylation, further increased peroxisome proliferator-activated receptor gamma (PPARγ) expression, and induced microglial M2 polarization to reduce the neuroinflammation and enhance hematoma resolution in GMH rats. Importantly, either knockdown of AdipoR1, APPL1, or LKB1, or specific inhibition of AMPK/PPARγ signaling in microglia abrogated the protective effect of APN after GMH in rats. In all, we propose that APN works as a potential therapeutic agent to ameliorate the inflammatory response following GMH by enhancing the M2 polarization of microglia via AdipoR1/APPL1/AMPK/PPARγ signaling pathway, ultimately attenuating inflammatory brain injury induced by hemorrhage.</p

Image_4_Adiponectin Ameliorates GMH-Induced Brain Injury by Regulating Microglia M1/M2 Polarization Via AdipoR1/APPL1/AMPK/PPARγ Signaling Pathway in Neonatal Rats.tif

Adiponectin (APN), a fat-derived plasma hormone, is a classic anti-inflammatory agent. Multiple studies have demonstrated the beneficial role of APN in acute brain injury, but the effect of APN in germinal matrix hemorrhage (GMH) is unclear, and the underlying molecular mechanisms remain largely undefined. In the current study, we used a GMH rat model with rh-APN treatment, and we observed that APN demonstrated a protective effect on neurological function and an inhibitory effect on neuroinflammation after GMH. To further explore the underlying mechanisms of these effects, we found that the expression of Adiponectin receptor 1 (AdipoR1) primarily colocalized with microglia and neurons in the brain. Moreover, AdiopR1, but not AdipoR2, was largely increased in GMH rats. Meanwhile, further investigation showed that APN treatment promoted AdipoR1/APPL1-mediated AMPK phosphorylation, further increased peroxisome proliferator-activated receptor gamma (PPARγ) expression, and induced microglial M2 polarization to reduce the neuroinflammation and enhance hematoma resolution in GMH rats. Importantly, either knockdown of AdipoR1, APPL1, or LKB1, or specific inhibition of AMPK/PPARγ signaling in microglia abrogated the protective effect of APN after GMH in rats. In all, we propose that APN works as a potential therapeutic agent to ameliorate the inflammatory response following GMH by enhancing the M2 polarization of microglia via AdipoR1/APPL1/AMPK/PPARγ signaling pathway, ultimately attenuating inflammatory brain injury induced by hemorrhage.</p

Image_1_Adiponectin Ameliorates GMH-Induced Brain Injury by Regulating Microglia M1/M2 Polarization Via AdipoR1/APPL1/AMPK/PPARγ Signaling Pathway in Neonatal Rats.tif

Adiponectin (APN), a fat-derived plasma hormone, is a classic anti-inflammatory agent. Multiple studies have demonstrated the beneficial role of APN in acute brain injury, but the effect of APN in germinal matrix hemorrhage (GMH) is unclear, and the underlying molecular mechanisms remain largely undefined. In the current study, we used a GMH rat model with rh-APN treatment, and we observed that APN demonstrated a protective effect on neurological function and an inhibitory effect on neuroinflammation after GMH. To further explore the underlying mechanisms of these effects, we found that the expression of Adiponectin receptor 1 (AdipoR1) primarily colocalized with microglia and neurons in the brain. Moreover, AdiopR1, but not AdipoR2, was largely increased in GMH rats. Meanwhile, further investigation showed that APN treatment promoted AdipoR1/APPL1-mediated AMPK phosphorylation, further increased peroxisome proliferator-activated receptor gamma (PPARγ) expression, and induced microglial M2 polarization to reduce the neuroinflammation and enhance hematoma resolution in GMH rats. Importantly, either knockdown of AdipoR1, APPL1, or LKB1, or specific inhibition of AMPK/PPARγ signaling in microglia abrogated the protective effect of APN after GMH in rats. In all, we propose that APN works as a potential therapeutic agent to ameliorate the inflammatory response following GMH by enhancing the M2 polarization of microglia via AdipoR1/APPL1/AMPK/PPARγ signaling pathway, ultimately attenuating inflammatory brain injury induced by hemorrhage.</p