Defect Engineering for Enhanced Electrocatalytic Oxygen Reaction on Transition Metal Oxides: The Role of Metal Defects.

Metal defect engineering is a highly effective strategy for addressing the prevalent high overpotential issues associated with transition metal oxides functioning as dual-function commercial oxygen reduction reaction/oxygen evolution reaction catalysts for increasing their activity and stability. However, the high formation energy of metal defects poses a challenge to the development of strategies to precisely control the selectivity during metal defect formation. Here, density functional theory calculations are used to demonstrate that altering the pathway of metal defect formation releases metal atoms as metal chlorides, which effectively reduces the formation energy of defects. The metal defects on the monometallic metal oxide surface (Mn, Fe, Co, and Ni) are selectively produced using chlorine plasma. The characterization and density functional theory calculations reveal that catalytic activity is enhanced owing to electronic delocalization induced by metal defects, which reduces the theoretical overpotential. Notably, ab initio molecular dynamics calculations, ex situ XPS, and in situ ATR-SEIRAS suggest that metal defects effectively improve the adsorption of reactive species on active sites and enhance the efficiency of product desorption, thereby boosting catalytic performance.

SlMYC2 promotes SlLBD40-mediated cell expansion in tomato fruit development.

As a plant-specific transcription factor, lateral organ boundaries domain (LBD) protein was reported to regulate plant growth and stress response, but the functional research of subfamily II genes is limited. SlMYC2, a master regulator of Jasmonic acid response, has been found to exhibit high expression levels in fruit and has been implicated in the regulation of fruit ripening and resistance to Botrytis. However, its role in fruit expansion remains unknown. In this study, we present evidence that a subfamily II member of LBD, namely SlLBD40, collaborates with SlMYC2 in the regulation of fruit expansion. Overexpression of SlLBD40 significantly promoted fruit growth by promoting mesocarp cell expansion, while knockout of SlLBD40 showed the opposite result. Similarly, SlMYC2 knockout resulted in a significant decrease in cell expansion within the fruit. Genetic analysis indicated that SlLBD40-mediated cell expansion depends on the expression of SlMYC2. SlLBD40 bound to the promoter of SlEXPA5, an expansin gene, but did not activate its expression directly. While, the co-expression of SlMYC2 and SlLBD40 significantly stimulated the activation of SlEXPA5, leading to an increase in fruit size. SlLBD40 interacted with SlMYC2 and enhanced the stability and abundance of SlMYC2. Furthermore, SlMYC2 directly targeted and activated the expression of SlLBD40, which is essential for SlLBD40-mediated fruit expansion. In summary, our research elucidates the role of the interaction between SlLBD40 and SlMYC2 in promoting cell expansion in tomato fruits, thus providing novel insights into the molecular genetics underlying fruit growth.

Inhibition of miR-497 Attenuates Oral Submucous Fibrosis by Inhibiting Myofibroblast Transdifferentiation in Buccal Mucosal Fibroblasts.

PURPOSE: Oral submucous fibrosis (OSF) is a common chronic condition with poor prognosis, and existing therapies for OSF are limited in effectiveness. This study was designed to explore the role of miR-497 in arecoline (AR)-induced OSF. MATERIALS AND METHODS: After miR-497 was silenced or overexpressed in buccal mucosa fibroblasts (BMFs), different concentrations of AR (5-200 µg/ml) were applied to incubate BMFs, and 50 µg/ml of AR was chosen for subsequent experiments. Thereafter, collagen gel contraction assay was used to detect the contractile capacity of BMFs. Transwell assay and wound healing assay were applied to detect migration and invasiveness of the cells. In addition, immunofluorescence staining, qRT-PCR and western blot were conducted to measure the expression of miR-497, collagen I and α-SMA, as well as the phosphorylation of Smad2 and Smad3. RESULTS: After successful inhibition or overexpression of miR-497 in AR-induced BMFs, the results showed that miR- 497 inhibition suppressed the contractility, migration and invasiveness of AR-induced BMFs, whereas overexpression of miR-497 produced the opposite. In addition, miR-497 inhibition down-regulated the expression level of collagen I and α-SMA in AR-exposed BMFs. Furthermore, TGF-ß1 expression, Smad2 and Smad3 phosphorylation were also repressed in AR-induced BMFs after miR-497 inhibition. Correspondingly, overexpression of miR-497 reversed the expression of the aforementioned proteins. CONCLUSION: miR-497 inhibition may attenuate OSF by inhibiting myofibroblast transdifferentiation in BMFs via the TGF-ß1/Smads signaling pathway, indicating that miR-497 might represent an underlying target for treating OSF.