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Perovskite quantum dots (PQDs) provide a robust solution-based approach to efficient solar cells, bright light emitting devices, and quantum sources of light. Quantifying heterogeneity and understanding coupling between dots is critical for these applications. We use double-nanohole optical trapping to size individual dots and correlate to emission energy shifts from quantum confinement. We were able to assemble a second dot in the trap, which allows us to observe the coupling between dots. We observe a systematic red-shift of 1.1 ± 0.6 meV in the emission wavelength. Theoretical analysis shows that the observed shift is consistent with resonant energy transfer and is unusually large due to moderate-to-large quantum confinement in PQDs. This demonstrates the promise of PQDs for entanglement in quantum information applications. This work enables future in situ control of PQD growth as well as studies of the coupling between small PQD assemblies with quantum information applications in mind.
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Although micelles derived from the solution self-assembly of amphiphilic molecules and polymers have been prepared with a wide variety of shapes, examples with well-defined branched structures have remained elusive. We describe a divergent, directed self-assembly approach to low dispersity dendritic micelles with a high degree of structural perfection and tailorable branch numbers and generations. We use block copolymer amphiphiles as precursors and a crystallization-driven seeded growth approach whereby the termini of fiber-like micelles function as branching sites. Different dendrimeric generations are accessible by adjusting the ratio of added unimers to pre-existing seed micelles where the branch positions are determined by the reduced coronal chain grafting density on the surface of the micelle crystalline core. We demonstrate the spatially defined decoration of the assemblies with emissive nanoparticles and utility of the resulting hybrids as fluorescent sensors for anions where the dendritic architecture enables ultrahigh sensitivity.
Assuntos
Dendrímeros/química , Micelas , Ânions/química , Cristalização , Compostos Ferrosos/química , Limite de Detecção , Microscopia de Força Atômica , Polivinil/química , Pontos Quânticos/química , Silanos/química , Espectrometria de Fluorescência , Sulfetos/análise , Propriedades de SuperfícieRESUMO
We have confirmed the presence of narrow, degenerately-doped axial silicon nanowire (SiNW) p-n junctions via off-axis electron holography (EH). SiNWs were grown via the vapor-solid-liquid (VLS) mechanism using gold (Au) as the catalyst, silane (SiH4), diborane (B2H6) and phosphine (PH3) as the precursors, and hydrochloric acid (HCl) to stabilize the growth. Two types of growth were carried out, and in each case we explored growth with both n/p and p/n sequences. In the first type, we abruptly switched the dopant precursors at the desired junction location, and in the second type we slowed the growth rate at the junction to allow the dopants to readily leave the Au catalyst. We demonstrate degenerately-doped p/n and n/p nanowire segments with abrupt potential profiles of 1.02 ± 0.02 and 0.86 ± 0.3 V, and depletion region widths as narrow as 10 ± 1 nm via EH. Low temperature current-voltage measurements show an asymmetric curvature in the forward direction that resemble planar gold-doped tunnel junctions, where the tunneling current is hidden by a large excess current. The results presented herein show that the direct VLS growth of degenerately-doped axial SiNW p-n junctions is feasible, an essential step in the fabrication of more complex SiNW-based devices for electronics and solar energy.
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Electron holographic tomography was used to obtain three-dimensional reconstructions of the morphology and electrostatic potential gradient of axial GaInP/InP nanowire tunnel diodes. Crystal growth was carried out in two opposite directions: GaInP-Zn/InP-S and InP-Sn/GaInP-Zn, using Zn as the p-type dopant in the GaInP but with changes to the n-type dopant (S or Sn) in the InP. Secondary electron and electron beam-induced current images obtained using scanning electron microscopy indicated the presence of p-n junctions in both cases and current-voltage characteristics measured via lithographic contacts showed the negative differential resistance, characteristic of band-to-band tunneling, for both diodes. Electron holographic tomography measurements confirmed a short depletion width in both cases (21 ± 3 nm) but different built-in potentials, Vbi, of 1.0 V for the p-type (Zn) to n-type (S) transition, and 0.4 V for both were lower than the expected 1.5 V for these junctions if degenerately doped. Charging induced by the electron beam was evident in phase images which showed nonlinearity in the surrounding vacuum, most severe in the case of the nanowire grounded at the p-type Au contact. We attribute their lower Vbi to asymmetric secondary electron emission, beam-induced current biasing, and poor grounding contacts.
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Background: A significant proportion of lupus nephritis patients develop chronic kidney disease (CKD) and progressive kidney fibrosis, for which there is no specific treatment. We previously reported that mycophenolate or rapamycin monotherapy showed comparable efficacy in suppressing kidney fibrosis in a murine model of lupus nephritis through their direct action on mesangial cells. We extended our study to investigate the effect of combined mycophenolate and rapamycin treatment (MR) on kidney fibrosis in NZBWF1/J mice. Methods: Female NZBWF1/J mice with active nephritis were randomized to receive vehicle or treatment with mycophenolate (50 mg/kg/day) and rapamycin (1.5 mg/kg/day) (MR) for up to 12 weeks, and the effect of treatment on clinical parameters, kidney histology, and fibrotic processes was investigated. Results: Progression of nephritis in untreated mice was accompanied by mesangial proliferation, glomerulosclerosis, tubular atrophy, protein cast formation, increased mTOR and ERK phosphorylation, and induction of TGF-ß1, IL-6, α-smooth muscle actin, fibronectin, and collagen expression. Combined MR treatment prolonged survival, improved kidney function, decreased anti-dsDNA antibody level, and ameliorated histopathological changes. The effect of combined MR treatment on kidney histology and function was comparable to that of mycophenolate or rapamycin monotherapy. In vitro studies in human mesangial cells showed that exogenous TGF-ß1 and IL-6 both induced mTOR and ERK phosphorylation and downstream fibrotic processes. Both mycophenolic acid and rapamycin inhibited inflammatory and fibrotic processes induced by TGF-ß1 or IL-6 by downregulating mTOR and ERK phosphorylation. Conclusions: Our findings indicate that combined mycophenolate and rapamycin, at reduced dose, improves kidney fibrosis in murine lupus nephritis through their distinct effect on mTOR and ERK signaling in mesangial cells.
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Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, imposing a great burden on the healthcare system. Regrettably, effective CKD therapeutic strategies are yet available due to their elusive pathogenic mechanisms. CKD is featured by progressive inflammation and fibrosis associated with immune cell dysfunction, leading to the formation of an inflammatory microenvironment, which ultimately exacerbating renal fibrosis. Transforming growth factor ß1 (TGF-ß1) is an indispensable immunoregulator promoting CKD progression by controlling the activation, proliferation, and apoptosis of immunocytes via both canonical and non-canonical pathways. More importantly, recent studies have uncovered a new mechanism of TGF-ß1 for de novo generation of myofibroblast via macrophage-myofibroblast transition (MMT). This review will update the versatile roles of TGF-ß signaling in the dynamics of renal immunity, a better understanding may facilitate the discovery of novel therapeutic strategies against CKD.
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Acute kidney injury (AKI) is one of the most common complications affecting hospitalized patients associated with an extremely high mortality rate. However, the underlying pathogenesis of AKI remains unclear that largely limits its effective management in clinic. Increasing evidence demonstrated the importance of long non-coding RNAs (lncRNAs) in the pathogenesis of AKI, because of their regulatory roles in transcription, translation, chromatin modification, and cellular organization. Here, we reported a new role of LRNA9884 in AKI. Using experimental cisplatin-induced AKI model, we found that LRNA9884 was markedly up-regulated in the nucleus of renal tubular epithelium in mice with AKI. We found that silencing of LRNA9884 effectively inhibited the production of inflammatory cytokines MCP-1, IL-6, and TNF-α in the mouse renal tubular epithelial cells (mTECs) under IL-1ß stimulation in vitro. Mechanistically, LRNA9884 was involved into NF-κB-mediated inflammatory cytokines production especially on macrophage migration inhibitory factor (MIF). Collectedly, our study suggested LRNA9884 promoted MIF-triggered the production of inflammatory cytokines via NF-κB pathway after AKI injury. This study uncovered LRNA9884 has an adverse impact in AKI, and targeting LRNA9884 might represent a potential therapeutic target for AKI.
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Transforming growth factor-ß (TGF-ß) was originally identified as an anti-tumour cytokine. However, there is increasing evidence that it has important roles in the tumour microenvironment (TME) in facilitating cancer progression. TGF-ß actively shapes the TME via modulating the host immunity. These actions are highly cell-type specific and complicated, involving both canonical and non-canonical pathways. In this review, we systemically update how TGF-ß signalling acts as a checkpoint regulator for cancer immunomodulation. A better appreciation of the underlying pathogenic mechanisms at the molecular level can lead to the discovery of novel and more effective therapeutic strategies for cancer.
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In the title compound, C(16)H(16)BrN, the benzene rings are inclined to each other with a dihedral angle between their mean planes of 50.5â (3)° and the C=C bond adopts a cis conformation.