RESUMEN
All-inorganic halide perovskite quantum dots (QDs) have recently received much attention due to their excellent optoelectronic properties. And their emission properties still need to be improved for further applications. Here, we demonstrated a remarkable emission enhancement of the CsPbBr3 QDs based on an Ag nanoparticle-Ag film plasmonic coupling structure. Through precise control of the gap distance between Ag nanoparticle and Ag film, the localized surface plasmon resonance (LSPR) peak was tuned to match the emission wavelength of the CsPbBr3 QDs. We achieved a 30-fold fluorescence intensity enhancement and a lower lasing threshold, which is 25% of that of the CsPbBr3 QDs without plasmonic coupling structure. It is attributed to that the plasmonic coupling structure exhibits an extremely strong local electric field owing to the coupling between LSPR of Ag nanoparticle and surface plasmon polariton of Ag film. This work provides an effective way to enhance the optical emission of perovskite QDs and promotes the further exploration of on-chip light source.
RESUMEN
All-inorganic halide perovskite CsPbX3(X = Br/Cl/I)quantum dots have gained a considerable attention in the optoelectronic fields. However, the high cost and poor stability of the prepared CsPbX3 quantum dots (QDs) are inevitable challenges for their future practical applications. And the high-performance CsPbX3 QDs are always needed. Herein, a facile and low-cost synthesis scheme was adopted to prepare the CsPbBr3 QDs modified by lead bromide (PbBr2) and tetraoctylammonium bromide (TOAB) ligands at room temperature in open air. The prepared CsPbBr3 QDs exhibited a high photoluminescence quantum yield (PLQY) of 96.6% and a low amplified spontaneous emission (ASE) threshold of 12.6 µJ/cm2. Stable ASE intensity with little degradation was also realized from the CsPbBr3 QDs doped with PMMA. Furthermore, the enhanced ASE properties of the CsPbBr3 QDs-doped PMMA based on distributed feedback (DFB) substrate was achieved with a lower threshold of 3.6 µJ/cm2, which is 28.6% of that of the (PbBr2 + TOAB)-treated CsPbBr3 QDs without PMMA. This work exhibits a promising potential in the on-chip light source.
RESUMEN
Magnetic-plasmonic nanoparticles (NPs) have attracted great interest in many fields because they can exhibit more physical and chemical properties than individual magnetic or plasmonic NPs. In this work, we synthesized Au- or Ag-decorated Fe3O4 nanoparticles coated with PEI (Fe3O4-PEI-M (M = Au or Ag) NPs) using a simple method. The influences of the plasmonic metal NPs' (Au or Ag) coating density on the magnetic and plasmonic properties of the Fe3O4-PEI-M (M = Au or Ag) NPs were investigated, and the density of the plasmonic metal NPs coated on the Fe3O4 NPs surfaces could be adjusted by controlling the polyethyleneimine (PEI) concentration. It showed that the Fe3O4-PEI-M (M = Au or Ag) NPs exhibited both magnetic and plasmonic properties. When the PEI concentration increased from 5 to 35 mg/mL, the coating density of the Au or Ag NPs on the Fe3O4 NPs surfaces increased, the corresponding magnetic intensity became weaker, and the plasmonic intensity was stronger. At the same time, the plasmonic resonance peak of the Fe3O4-PEI-M (M = Au or Ag) NPs was red shifted. Therefore, there was an optimal coverage of the plasmonic metal NPs on the Fe3O4 NPs surfaces to balance the magnetic and plasmonic properties when the PEI concentration was between 15 and 25 mg/mL. This result can guide the application of the Fe3O4-M (M = Au or Ag) NPs in the biomedical field.
RESUMEN
RhoB, a member of the Ras homolog gene family and GTPase, regulates intracellular signaling pathways by interfacing with epidermal growth factor receptor (EGFR), Ras, and phosphatidylinositol 3-kinase (PI3K)/Akt to modulate responses in cellular structure and function. Notably, the EGFR, Ras, and PI3K/Akt pathways can lead to downregulation of RhoB, while simultaneously being associated with an increased propensity for tumorigenesis. Functionally, RhoB, part of the Rho GTPase family, regulates intracellular signaling pathways by interfacing with EGFR, RAS, and PI3K/Akt/mammalian target of rapamycin (mTOR), and MYC pathways to modulate responses in cellular structure and function. Notably, the EGFR, Ras, and PI3K/Akt pathways can lead to downregulation of RhoB, while simultaneously being associated with an increased propensity for tumorigenesis. RHOB expression has a complex regulatory backdrop consisting of multiple histone deacetyltransferase (HDACs 1 and 6) and microRNA (miR-19a, -21, and -223)-mediated mechanisms of modifying expression. The interwoven nature of RhoB's regulatory impact and cellular roles in regulating intracellular vesicle trafficking, cell motion, and the cell cycle lays the foundation for analyzing the link between loss of RhoB and tumorigenesis within the context of age-related decline in RhoB. RhoB appears to play a tissue-specific role in tumorigenesis, as such, uncovering and appreciating the potential for restoration of RHOB expression as a mechanism for cancer prevention or therapeutics serves as a practical application. An in-depth assessment of RhoB will serve as a springboard for investigating and characterizing this key component of numerous intracellular messaging and regulatory pathways that may hold the connection between aging and tumorigenesis.