Enhanced Performance of PTB7:PC 71

The effects of gold nanoparticles (AuNPs) incorporated in the hole transporting layer (HTL) of poly[[4,8-bis[(2-ethylhexyl)oxy] benzo[1,2-b:4,5-b'] dithiophene-2, 6-diyl] [3-fluoro-2-[(2-ethylhexy)carbonyl]thieno[3,4-b]thiophened iyl]] (PTB7): [6,6]-phenyl C-71 butyric acid methyl ester (PC71BM) based solar cells are being systematically investigated in terms of the optical properties, electrical properties, and photovoltaic performance. The impacts of AuNPs on the optical response of the devices are modeled by finite-difference time-domain (FDTD) simulation. The size of the AuNPs used in this work is around 50-70 nm, so that 10-20 nm penetrated from the HTL into the active layer. We found that the power conversion efficiencies (PCEs) of the devices with AuNPs are significantly enhanced from 7.5%, for the control device, to 8.0%, 8.1%, and 8.2% for Au nanosphere-, nanorod-, and nanocube-incorporated devices, respectively. Among the photovoltaic parameters of the AuNP devices, the short circuit current density (JSC) exhibits the largest improvement, which can be attributed to the improved optical properties of the devices. On the basis of the calculation results, the scattering cross section for the samples in the presence of AuNPs can be enhanced by a factor of similar to 10(10)-10(13) and Au nanocubes exhibit superior scattering cross section compared to the Au nanospheres and nanorods with the same linear dimension. From the experimental impedance spectroscopy results, we found that the addition of AuNPs had little effect on the electrical properties of the device. The device performance is also found to be sensitive to the concentration and morphology of the AuNPs.Department of Electronic and Information Engineerin

HSF1 critically attunes proteotoxic stress sensing by mTORC1 to combat stress and promote growth.

To cope with proteotoxic stress, cells attenuate protein synthesis. However, the precise mechanisms underlying this fundamental adaptation remain poorly defined. Here we report that mTORC1 acts as an immediate cellular sensor of proteotoxic stress. Surprisingly, the multifaceted stress-responsive kinase JNK constitutively associates with mTORC1 under normal growth conditions. On activation by proteotoxic stress, JNK phosphorylates both RAPTOR at S863 and mTOR at S567, causing partial disintegration of mTORC1 and subsequent translation inhibition. Importantly, HSF1, the central player in the proteotoxic stress response (PSR), preserves mTORC1 integrity and function by inactivating JNK, independently of its canonical transcriptional action. Thereby, HSF1 translationally augments the PSR. Beyond promoting stress resistance, this intricate HSF1-JNK-mTORC1 interplay, strikingly, regulates cell, organ and body sizes. Thus, these results illuminate a unifying mechanism that controls stress adaptation and growth. Nat Cell Biol 2016 May; 18(5):527-3