We discuss the main challenges for the fabrication of emerging microLED displays. We shown that microtube technology is very well adapted to these new kind of displays, since it provides both mechanical and electrical connection of the microLEDs on the receiving substrate. Also, we present a new fabrication approach, where an elementary unit consists of all-in-one-RBG MicroLEDs on CMOS driving circuit.
Conspectus Conjugated polymers for application in organic solar cells (OSCs) have been developed from poly(phenylenevinylene) to poly(3-hexylthiophene) and then to “donor–acceptor” structures, providing power conversion efficiencies (PCEs) over 18% when blending with the electron acceptor as a two-component photoactive layer. Besides, graft-structural double-cable conjugated polymers that use an electron donor as conjugated backbones and an electron acceptor as pendant side units are one kind of conjugated polymer, in which charge carriers are generated in a single polymer. Therefore, double-cable conjugated polymers can be used as a single photoactive layer in single-component OSCs (SCOSCs). The covalently linked electron donor and acceptor enable double-cable polymers to maintain stable microstructures during long-term operation compared to two-component systems, which is very important for OSCs toward large-area applications. However, SCOSCs based on double-cable conjugated polymers provided PCEs below 3% in a long period, which is lagging far behind PCEs of two-component OSCs. The key reason for this is the limited number of chemical structures and the difficulty to tune the morphology in these polymers. In this Account, we provide an overview about our efforts on developing new double-cable conjugated polymers with rylene diimides as side units, and how to realize high PCEs in SCOSC devices. The studies start from developing a “functionalization–polymerization” method to synthesize the polymers containing rylene diimide acceptors, so that large amounts of double-cable conjugated polymers with distinct physical and electrochemical properties were obtained. Then, we will discuss how to control the nanophase separation in the crystalline region and optimize the miscibility in the amorphous region of double-cable polymers, simultaneously facilitating exciton dissociation and charge transport. With these efforts, a high PCE of 8.4% has been obtained, representing the record PCE in SCOSCs. In addition, the physical process and the stability of SCOSCs will be discussed. We hope that this account will inspire many innovative studies in this field and push the PCEs of SCOSCs to a new stage.
Double-cable conjugated polymers with near-infrared (NIR) electron acceptors are synthesized for use in single-component organic solar cells (SCOSCs). Through the development of a judicious synthetic pathway, the highly sensitive nature of the 2-(3-oxo-2,3-dihydroinden-1-ylidene)malononitrile (IC)-based electron acceptors in basic and protonic solvents is overcome. In addition, an asymmetric design motif is adopted to optimize the packing of donor and acceptor segments, enhancing charge separation efficiency. As such, the new double-cable polymers are successfully applied in SCOSCs, providing an efficiency of over 10 % with a broad photo response from 300 to 850 nm and exhibiting excellent thermal/light stability. These results demonstrate the powerful design of NIR-acceptor-based double-cable polymers and will enable SCOSCs to enter a new stage.
Excessive abdominal fat deposition is an issue with general concern in broiler production, especially for Chinese native chicken breeds. A high-fat diet (HFD) can induce body weight gained and excessive fat deposition, and genes and pathways participate in fat metabolism and adipogenesis would be influenced by HFD. In order to reveal the main genes and pathways involved in chicken abdominal fat deposition, we used HFD and normal diet (ND) to feed a Chinese native chicken breed, respectively. Results showed that HFD can increase abdominal fat deposition and induce adipocyte hypertrophy. Additionally, we used RNA-sequencing to identify the differentially expressed genes (DEGs) between HFD and ND chickens in liver and abdominal fat. By analyzed these DEGs, we found that the many DEGs were enriched in fat metabolism related pathways, such as peroxisome proliferator-activated receptor (PPAR) signaling, fat digestion and absorption, extracellular matrix (ECM)-receptor interaction, and steroid hormone biosynthesis. Notably, the expression of insulin-like growth factor II mRNA binding protein 1 (IGF2BP1), which is a binding protein of IGF2 mRNA, was found to be induced in liver and abdominal fat by HFD. Ectopic expression of IGF2BP1 in chicken liver-related cell line Leghorn strain M chicken hepatoma (LMH) cell revealed that IGF2BP1 can regulate the expression of genes associated with fatty acid metabolism. In chicken preadipocytes (ICP cell line), we found that IGF2BP1 can promote adipocyte proliferation and differentiation, and the lipid droplet content would be increased by overexpression of IGF2BP1. Taken together, this study provides new insights into understanding the genes and pathways involved in abdominal fat deposition of Chinese native broiler, and IGF2BP1 is an important candidate gene for the study of fat metabolism and adipogenesis in chicken.
Background Transmembrane proteins are vital for intercellular signalling and play important roles in the control of cell fate. However, their physiological functions and mechanisms of action in myogenesis and muscle disorders remain largely unexplored. It has been found that transmembrane protein 182 (TMEM182) is dramatically up‐regulated during myogenesis, but its detailed functions remain unclear. This study aimed to analyse the function of TMEM182 during myogenesis and muscle regeneration. Methods RNA sequencing, quantitative real‐time polymerase chain reaction, and immunofluorescence approaches were used to analyse TMEM182 expression during myoblast differentiation. A dual‐luciferase reporter assay was used to identify the promoter region of the TMEM182 gene, and a chromatin immunoprecipitation assay was used to investigate the regulation TMEM182 transcription by MyoD. We used chickens and TMEM182‐knockout mice as in vivo models to examine the function of TMEM182 in muscle growth and muscle regeneration. Chickens and mouse primary myoblasts were used to extend the findings to in vitro effects on myoblast differentiation and fusion. Co‐immunoprecipitation and mass spectrometry were used to identify the interaction between TMEM182 and integrin beta 1 (ITGB1). The molecular mechanism by which TMEM182 regulates myogenesis and muscle regeneration was examined by Transwell migration, cell wound healing, adhesion, glutathione‐S‐transferse pull down, protein purification, and RNA immunoprecipitation assays. Results TMEM182 was specifically expressed in skeletal muscle and adipose tissue and was regulated at the transcriptional level by the myogenic regulatory factor MyoD1. Functionally, TMEM182 inhibited myoblast differentiation and fusion. The in vivo studies indicated that TMEM182 induced muscle fibre atrophy and delayed muscle regeneration. TMEM182 knockout in mice led to significant increases in body weight, muscle mass, muscle fibre number, and muscle fibre diameter. Skeletal muscle regeneration was accelerated in TMEM182‐knockout mice. Furthermore, we revealed that the inhibitory roles of TMEM182 in skeletal muscle depend on ITGB1, an essential membrane receptor involved in cell adhesion and muscle formation. TMEM182 directly interacted with ITGB1, and this interaction required an extracellular hybrid domain of ITGB1 (aa 387–470) and a conserved region (aa 52–62) within the large extracellular loop of TMEM182. Mechanistically, TMEM182 modulated ITGB1 activation by coordinating the association between ITGB1 and laminin and regulating the intracellular signalling of ITGB1. Myogenic deletion of TMEM182 increased the binding activity of ITGB1 to laminin and induced the activation of the FAK‐ERK and FAK‐Akt signalling axes during myogenesis. Conclusions Our data reveal that TMEM182 is a novel negative regulator of myogenic differentiation and muscle regeneration.
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