No abstract

Three amphiphilic block copolymers are employed to form polymeric micelles and function as nanocarriers to disperse hydrophobic aggregation‐induced emission (AIE) dyes, 1,1,2,3,4,5‐hexaphenylsilole (HPS) and/or bis(4‐(N‐(1‐naphthyl) phenylamino)‐phenyl)fumaronitrile (NPAFN), into aqueous solution for biological studies. Compared to their virtually non‐emissive properties in organic solutions, the fluorescence intensity of these AIE dyes has increased significantly due to the spatial confinement that restricts intramolecular rotation of these dyes and their better compatibility in the hydrophobic core of polymeric micelles. The effect of the chemical structure of micelle cores on the photophysical properties of AIE dyes are investigated, and the fluorescence resonance energy transfer (FRET) from the green‐emitting donor (HPS) to the red‐emitting acceptor (NPAFN) is explored by co‐encapsulating this FRET pair in the same micelle core. The highest fluorescence quantum yield (∼62%) could be achieved by encapsulating HPS aggregates in the micelles. Efficient energy transfer (>99%) and high amplification of emission (as high as 8 times) from the NPAFN acceptor could also be achieved by spatially confining the HPS/NPAFN FRET pair in the hydrophobic core of polymeric micelles. These micelles could be successfully internalized into the RAW 264.7 cells to demonstrate high‐quality fluorescent images and cell viability due to improved quantum yield and reduced cytotoxicity.

By simple modification of the functional groups on the boron–nitrogen‐containing skeleton, the energy level of the highest occupied molecular orbital (EHOMO) of emitters can be easily adjusted. Blue‐emission derivatives are developed, which are capable of showing small full width at half maximums and high photoluminescence quantum yields. Blue thermally activated delayed fluorescence (TADF)‐assisted fluorescence organic light‐emitting diodes (TAF‐OLEDs) based on two new emitters as the terminal emitter are fabricated, resulting in high external quantum efficiency (EQE) of up to 21.9%, high color purity, and high brightness (Lmax = 63 777 cd m−2). By analyzing the transient electroluminescence spectra of the TAF‐OLEDs, it is found that a smaller EHOMO difference between TADF‐assistant dopant (TADF‐AD) and terminal emitter efficiently helps to decrease hole trapping inside the emitting layer, hence resulting in a lower efficiency rolloff and a longer operational device lifetime. TAF‐OLEDs based on CzBNCz as a terminal emitter having the closest EHOMO to that of TADF‐AD show a maximum EQE of 21.9% together with a reduced efficiency rolloff (EQEs of 21.2% and 19.8% at 100 and 1000 cd m−2, respectively). This research provides a designing principle for a terminal emitter in TAF‐OLEDs with well‐matched energy levels towards reaching the requirements of commercial displays.

Hypoxia and serum depletion are common features of solid tumors that occur upon antiangiogenesis, irradiation and chemotherapy across a wide variety of malignancies. Here we show that tumor cells expressing CD133, a marker for colorectal cancer initiating or stem cells, are enriched and survive under hypoxia and serum depletion conditions, whereas CD133− cells undergo apoptosis. CD133+ tumor cells increase cancer stem cell and epithelial-mesenchymal transition properties. Moreover, via screening a panel of tyrosine and serine/threonine kinase pathways, we identified Hsp27 is constitutively activated in CD133+ cells rather than CD133− cell under hypoxia and serum depletion conditions. However, there was no difference in Hsp27 activation between CD133+ and CD133− cells under normal growth condition. Hsp27 activation, which was mediated by the p38MAPK-MAPKAPK2-Hsp27 pathway, is required for CD133+ cells to inhibit caspase 9 and 3 cleavage. In addition, inhibition of Hsp27 signaling sensitizes CD133+ cells to hypoxia and serum depletion -induced apoptosis. Moreover, the antiapoptotic pathway is also activated in spheroid culture-enriched CD133+ cancer stem cells from a variety of solid tumor cells including lung, brain and oral cancer, suggesting it is a common pathway activated in cancer stem cells from multiple tumor types. Thus, activation of PP2A or inactivation of the p38MAPK-MAPKAPK2-Hsp27 pathway may develop new strategies for cancer therapy by suppression of their TIC population.