Objective To investigate the effect of Rapamycin on proliferation and autophagy in human neuroblastoma (NB) cell lines and to elucidate the possible mechanism. Methods NB cells were treated with different concentrations of Rapamycin. Cell counting kit-8 (CCK-8) was used to measure proliferation, and flow cytometry (FCM) was used to analyze the cell cycle. EM was used to observe cell morphological changes. Western blotting (WB) was performed to detect the expression of Beclin-1, LC3-I/II, P62, mammalian target of Rapamycin (mTOR), and p-mTOR. Results Rapamycin inhibited the spread of NB cells in a dose- and time-dependent manner and arrested the cell cycle at the G0/G1 phase. EM showed autophagosomes in NB cells treated with Rapamycin. The WB results showed that the expression levels of Beclin-1 and LC3-II/LC3-I were significantly elevated in NB cells treated with Rapamycin, while the expression levels of P62, mTOR, and p-mTOR proteins were significantly reduced compared with the control cells (P<0.05). Conclusion Rapamycin inhibits cell proliferation and induces autophagy in human NB cell lines. The mechanism may be related to suppression of the mTOR signaling pathway.

For an organic-inorganic hybrid quantum dot light-emitting diode (QD-LED), enhancing hole injection into the emitter for charge balance is a priority to achieve efficient device performance. Aiming at this, we employ N,N'-bis(3-methylphenyl)-N,N'-bis(phenyl)benzidine (TPD) as the additional hole transport material which was mixed with poly(9-vinylcarbazole) (PVK) to form a composite hole transport layer (HTL) or was employed to construct a TPD/PVK bilayer structure. Enabled by this TPD modification, the green QD-LED (at a wavelength of 515 nm) exhibits a subband gap turn-on voltage of 2.3 V and a highest luminance up to 56 157 cd/m. Meanwhile, such TPD modification is also beneficial to acquire efficient blue and red QD-LEDs. In particular, the external quantum efficiencies (EQEs) for these optimized full-color QD-LEDs are 8.62, 9.22, and 13.40%, which are 3-4 times higher than those of their pure PVK-based counterparts. Revealed by the electrochemical impedance spectroscopy, the improved electroluminescent efficiency is ascribable to the reductions of recombination resistance and charge-transfer resistance. The prepared QD-LEDs surpass the EQE values achieved in previous reports, considering devices with small-molecule-modified HTLs. This work offers a general but simple and very effective approach to realize the low turn-on-voltage, bright, and efficient full-color QD-LEDs via this solution-processable HTL modification.

In conclusion, we found that several radiographic and sonographic parameters were associated with the prognosis of patients with NEC. The AUS model based on the logistic regression analysis was significant superior to the AR model in the prognostic prediction of NEC.

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In a typical light emitting diode (QD-LED), with ZnO nanoparticles (NPs) serving as the electron transport layer (ETL) material, excessive electron injection driven by the matching conduction band maximum (CBM) between the QD and this oxide layer usually causes charge imbalance and degrades the device performance. To address this issue, the electronic structure of ZnO NPs is modified by the yttrium (Y) doping method. We demonstrate that the CBM of ZnO NPs has a strong dependence on the Y-doping concentration, which can be tuned from 3.55 to 2.77 eV as the Y doping content increases from 0% to 9.6%. This CBM variation generates an enlarged barrier between the cathode and this ZnO ETL benefits from the modulation of electron injection. By optimizing electron injection with the use of a low Y-doped (2%) ZnO to achieve charge balance in the QD-LED, device performance is significantly improved with maximum luminance, peak current efficiency, and maximal external quantum efficiency increase from 4918 cd/m2, 11.3 cd/A, and 4.5% to 11,171 cd/m2, 18.3 cd/A, and 7.3%, respectively. This facile strategy based on the ETL modification enriches the methodology of promoting QD-LED performance.