We report a facile nonaqueous emulsion synthesis of colloidal halide perovskite quantum dots by controlled addition of a demulsifier into an emulsion of precursors. The size of resulting CH3NH3PbBr3 quantum dots can be tuned from 2 to 8 nm by varying the amount of demulsifier. Moreover, this emulsion synthesis also allows the purification of these quantum dots by precipitation from the colloidal solution and obtains solid-state powder which can be redissolved for thin film coating and device fabrication. The photoluminescence quantum yields of the quantum dots is generally in the range of 80-92%, and can be well-preserved after purification (∼80%). Green light-emitting diodes fabricated comprising a spin-cast layer of the colloidal CH3NH3PbBr3 quantum dots exhibited maximum current efficiency of 4.5 cd/A, power efficiency of 3.5 lm/W, and external quantum efficiency of 1.1%. This provides an alternative route toward high efficient solution-processed perovskite-based light-emitting diodes. In addition, the emulsion synthesis is versatile and can be extended for the fabrication of inorganic halide perovskite colloidal CsPbBr3 nanocrystals.
Because of the rich polymorphs and lower diffusion energy barriers of copper chalcogenide systems, the phase transformation of colloidal Cu2–x S (0 ≤ x ≤ 1) nanocrystals is critical for understanding their fundamental properties and designing convenient synthetic routes. In this work, high quality digenite Cu1.8S nanocrystals with rhombohedral structure were synthesized at gram-scale. The as-prepared colloidal nanocrystals undergo an in situ phase transformation from rhombohedral Cu1.8S nanocrystals to hexagonal CuS clusters upon keeping the resulting colloidal solution for a few days. The observed transformation was explored by a combination of structural and spectroscopic analyses, including powder X-ray diffraction, transmission electron microscopy, energy dispersive spectroscopy, and X-ray photoelectron spectroscopy characterizations. A possible mechanism is proposed and thoroughly discussed. We further determined the evolution of plasmonic absorption spectra during the transformation. The Cu1.8S nanocrystals and CuS clusters exhibit composition-dependent local surface plasmon resonance absorption (LSPR) in the near-infrared region, which are in good agreement with calculated extinction spectra based on Mie-Drude model. Combined experimental and theoretical analyses demonstrated that both the phase induced dielectric constant change and the composition induced carrier concentration variation account for the spectroscopic evolution.
We report a combined experimental and theoretical study of the synthesis of CH NH PbBr nanoplatelets through self-organization. Shape transformation from spherical nanodots to square or rectangular nanoplatelets can be achieved by keeping the preformed colloidal nanocrystals at a high concentration (3.5 mg mL ) for 3 days, or combining the synthesis of nanodots with self-organization. The average thickness of the resulting CH NH PbBr nanoplatelets is similar to the size of the original nanoparticles, and we also noticed several nanoplatelets with circular or square holes, suggesting that the shape transformation experienced a self-organization process through dipole-dipole interactions along with a realignment of dipolar vectors. Additionally, the CH NH PbBr nanoplatelets exhibit excellent polarized emissions for stretched CH NH PbBr nanoplatelets embedded in a polymer composite film, showing advantageous photoluminescence properties for display backlights.
Carbamazepine (CBZ) aggravates many generalized seizures types, particularly absence seizures, but the mechanisms underlying this are poorly understood. GABA signaling within the reticular nucleus (Rt) and the ventrobasal complex (VB) of the thalamus is critical to the neurophysiology of absence seizures. The hypothesis that CBZ aggravates absence seizures by acting at the VB thalamus via a GABA A receptor-mediated mechanism was investigated in a genetic rat model, generalized absence epilepsy rats from Strasbourg (GAERS). Seizure activity was quantified by a 90-min electroencephalogram recording postdrug injection. Intracerebroventricular injections of CBZ (15 g in 4 l) resulted in seizure aggravation versus vehicle treatment, with a mean increase in seizure time of 40%. This indicates that CBZ acts directly, rather than via a metabolite, on the brain to aggravate seizures. Seizure aggravation also occurred following bilateral microinjection of CBZ (0.75 g in 0.2 l) into the VB (53%) but not following injection into the Rt (Ϫ9%). However, seizure aggravation was blocked when the GABA A receptor antagonist, bicuculline (BIC, 0.04 g in 0.2 l), was coinjected with CBZ into the VB. Injection of BIC alone (versus vehicle) into the VB also blocked seizure aggravation following systemic administration of CBZ (15 mg/kg i.p.). In vitro studies in Xenopus oocytes expressing recombinant GABA A receptors demonstrated that CBZ produced a dose-dependent potentiation of the GABA current at a physiological relevant concentration range (1-100 M). These data demonstrate that CBZ acts at the VB thalamus to aggravate absence seizures in GAERS and that activation of GABA A receptors is critical to this effect.Aggravation of seizures by antiepileptic drugs (AEDs) is an important clinical problem that is often overlooked in practice (Lerman, 1986;Perucca et al., 1998). The neurobiological mechanisms underlying seizure aggravation are poorly understood. One of the drugs most implicated is carbamazepine (CBZ), a major first line AED for the treatment of focal seizures. In patients with generalized epilepsy syndromes, CBZ commonly causes an increase in a variety of seizure types, including typical and atypical absence seizures, myoclonic, atonic, and tonic seizures, and also on occasions generalized tonic-clonic seizures (Perucca et al., 1998). Of these, the aggravation of absence seizures is the most predictable and, with the availability of good animal models (Snead et al., 1999), the most amenable for mechanistic studies. In agreement with human studies, CBZ has also been demonstrated by our group and others to exacerbate spontaneous absence seizures in well validated rat models, i.e., low-dose pentylenetetrazole (McLean et al., 2004) and the generalized absence epilepsy rats from Strasbourg (GAERS) (Marescaux et al., 1984;Micheletti et al., 1985;Wallengren et al., 2005).The primary neuropathological correlate of absence seizures is bursts of highly synchronized rhythmic oscillatory glutamatergic firing between neurons in the...
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