Degradation of Two-Dimensional CH₃NH₃PbI₃ Perovskite and CH₃NH₃PbI₃/Graphene Heterostructure

Hybrid organic–inorganic metal halide perovskites have been considered as promising materials for boosting the performance of photovoltaics and optoelectronics. Reduced-dimensional condiments and tunable properties render two-dimensional (2D) perovskite as novel building blocks for constructing micro-/nanoscale devices in high-performance optoelectronic applications. However, the stability is still one major obstacle for long-term practical use. Herein, we provide microscale insights into the degradation kinetics of 2D CH₃NH₃PbI₃ (MAPbI₃) perovskite and CH₃NH₃PbI₃/graphene heterostructures. It is found that the degradation is mainly caused by cation evaporation, which consequently affects the microstructure, light–matter interaction, and the photoluminescence quantum yield efficiency of the 2D perovskite. Interestingly, the encapsulation of perovskite by monolayer graphene can largely preserve the structure of the perovskite nanosheet and maintain reasonable optical properties upon exposure to high temperature and humidity. The heterostructure consisting of perovskite and another 2D impermeable material affords new possibilities to construct high-performance and stable perovskite-based optoelectronic devices

Direct Observation of 2D Electrostatics and Ohmic Contacts in Template-Grown Graphene/WS₂ Heterostructures

Large-area two-dimensional (2D) heterojunctions are promising building blocks of 2D circuits. Understanding their intriguing electrostatics is pivotal but largely hindered by the lack of direct observations. Here graphene–WS₂ heterojunctions are prepared over large areas using a seedless ambient-pressure chemical vapor deposition technique. Kelvin probe force microscopy, photoluminescence spectroscopy, and scanning tunneling microscopy characterize the doping in graphene–WS₂ heterojunctions as-grown on sapphire and transferred to SiO₂ with and without thermal annealing. Both p–n and n–n junctions are observed, and a flat-band condition (zero Schottky barrier height) is found for lightly n-doped WS₂, promising low-resistance ohmic contacts. This indicates a more favorable band alignment for graphene–WS₂ than has been predicted, likely explaining the low barriers observed in transport experiments on similar heterojunctions. Electrostatic modeling demonstrates that the large depletion width of the graphene–WS₂ junction reflects the electrostatics of the one-dimensional junction between two-dimensional materials

Dual Function of RGD-Modified VEGI-192 for Breast Cancer Treatment

Identification of endogenous angiogenesis inhibitors has led to development of an increasingly attractive strategy for cancer therapy and other angiogenesis-driven diseases. Vascular endothelial growth inhibitor (VEGI), a potent and relatively nontoxic endogenous angiogenesis inhibitor, has been intensively studied, and this work shed new light on developing promising anti-angiogenic strategies. It is well-documented that the RGD (Arg-Gly-Asp) motif exhibits high binding affinity to integrin α_vβ₃, which is abundantly expressed in cancer cells and specifically associated with angiogenesis on tumors. Here, we designed a fusion protein containing the special RGD-4C motif sequence and VEGI-192, aimed at offering more effective multiple targeting to tumor cells and tumor vasculature, and higher anti-angiogenic and antitumor efficacy. Functional tests demonstrated that the purified recombinant human RGD-VEGI-192 protein (rhRGD-VEGI-192) potently inhibited endothelial growth in vitro and suppressed neovascularization in chicken chorioallantoic membrane in vivo, to a higher degree as compared with rhVEGI-192 protein. More importantly, rhRGD-VEGI-192, but not rhVEGI-192 protein, could potentially target MDA-MB-435 breast tumor cells, significantly inhibiting growth of MDA-MB-435 cells in vitro, triggered apoptosis in MDA-MB-435 cells by activation of caspase-8 as well as caspase-3, which was mediated by activating the JNK signaling associated with upregulation of pro-apoptotic protein Puma, and consequently led to the observed significant antitumor effect in vivo against a human breast cancer xenograft. Our study indicated that the RGD-VEGI-192 fusion protein might represent a novel anti-angiogenic and antitumor strategy

Expression of the CaMKIIβ throughout the brain by AAV-PHP.eB.

Volume-rendered and single-plane images of the brain expressing H2B-mCherry under hSyn1 promoter by the AAV (mCherry, green) counterstained with RD2 (red). A volume-rendered image is shown in the center. Single-plane and magnified images are shown for cerebral cortex, thalamus, hippocampus, midbrain, cerebellum, striatum, and olfactory bulb. Scale bar in the center image, 3 mm; other scale bars, 100 μm. AAV, adeno-associated virus; CaMKIIβ, calmodulin-dependent protein kinase IIβ; hSyn1, human synapsin-1. (TIFF)</p

Robust sleep induction by CaMKIIβ T287D mutant.

(A) Expression levels of endogenous CaMKIIβ and AAV-mediated transduced CaMKIIβ in the brain. Camk2bFLAG/FLAG represents homo knock-in mice in which the FLAG tag was inserted into the endogenous Camk2b locus. PBS: PBS-administrated mice. Immunoblotting against FLAG-tagged protein indicates that AAV-mediated expression of CaMKIIβ is lower than the expression level of endogenous CaMKIIβ. (B) Calculated transduction efficiency plotted against sleep duration. Transduction efficiency is an estimation of the number of AAV vector genomes present per cell in a mouse brain. After the SSS measurements, we purified the AAV vector genomes from the mice brains and then quantified them with a WPRE-specific primer set and normalized to mouse genomes. (C) Sleep transition profiles of mice expressing CaMKIIβ T287-related mutants shown in Fig 1F. The shaded areas represent SEM. (D) Sleep parameters during light or dark period of mice expressing CaMKIIβ T287-related mutants shown in Fig 1F. Multiple comparison tests were performed between all individual groups in each phase. (E, F) Sleep/wake parameters of mice expressing S114-related CaMKIIβ mutants (C) and S109-related CaMKIIβ mutants (D), averaged over 6 days. The shaded areas represent SEM. Multiple comparison tests were performed between all individual groups and resulted in no significant differences. The underlying numerical data can be found in S1 Data, and uncropped or raw image files for S3A Fig are provided in S2 and S3 Data files. Error bars: SEM, *p p p (PDF)</p

Time-of-day analyses for sleep parameters of mice with perturbed CaMKII activity.

(A) Sleep transition profiles of mice expressing the CaMKIIβ del mutant under hSyn1 promoter shown in Fig 2B and 2C. The shaded areas represent SEM. (B) Sleep parameters of mice expressing the CaMKIIβ del mutants shown in Fig 2B and 2C during light or dark period. Multiple comparison tests were performed between all individual groups in each phase. (C) Sleep transition profiles of mice expressing AIP2 or RARA mutant under hSyn1 promoter shown in Fig 2E and 2F. The shaded areas represent SEM. PBS: PBS-injected mice (n = 6). (D) Sleep parameters of mice expressing AIP2 or RARA mutant shown in Fig 2E and 2F during light or dark period. Multiple comparison tests were performed between all individual groups in each phase. The underlying data can be found in S1 Data. Error bars: SEM, *p p p hSyn1, human synapsin-1; (PDF)</p