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      • Improved thin film morphology and bulk-heterojunction solar cell performance through systematic tuning of the surface energy of conjugated polymers

        Sun, Ying,Chien, Shang-Chieh,Yip, Hin-Lap,Chen, Kung-Shih,Zhang, Yong,Davies, Joshua A.,Chen, Fang-Chung,Lin, Baoping,Jen, Alex K.-Y. The Royal Society of Chemistry 2012 Journal of materials chemistry Vol.22 No.12

        <P>A detailed model study has shown that thin film morphology and bulk-heterojunction solar cell performance can be significantly improved by systematic tuning of the surface energy of the conjugated donor polymer through side-chain functionalization. Thiophene-flanked diketopyrrolopyrrole (DPP) moieties with different contents of cyanohexane side chains were incorporated into three low band-gap conjugated copolymers (<B>PIDTDPP1</B>, <B>PIDTDPP2</B> and <B>PIDTDPP3</B>) consisting of indacenodithiophene (IDT) donors and DPP acceptors. The resulting polymers possessed good solubility in common organic solvents and showed similar energy levels, bandgaps, and hole mobilities. However, the introduction of cyano groups onto the terminal of side-chains significantly changed their surface energy. Topographical images obtained from atomic force microscopy (AFM) proved that a better matched surface energy between polymer and PC<SUB>71</SUB>BM had led to enhanced miscibility, which resulted in better BHJ film morphology. Consistent with the surface energy enhancement, the performance of BHJ photovoltaic devices increased from 0.97% for <B>PIDTDPP1</B>, to 2.16% for <B>PIDTDPP2</B> then to 3.67% for <B>PIDTDPP3</B>. These results clearly reveal that tuning surface energy is an effective way to improve the morphology of the BHJ active layer and efficiency of the photovoltaic device.</P> <P>Graphic Abstract</P><P>We have shown that significantly improved thin film morphology and bulk-heterojunction solar cell performance can be achieved by systematically tuning the surface energy of conjugated polymer donors through side-chain functionalization. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c2jm15517f'> </P>

      • High-mobility low-bandgap conjugated copolymers based on indacenodithiophene and thiadiazolo[3,4-<i>c</i>]pyridine units for thin film transistor and photovoltaic applications

        Sun, Ying,Chien, Shang-Chieh,Yip, Hin-Lap,Zhang, Yong,Chen, Kung-Shih,Zeigler, David F.,Chen, Fang-Chung,Lin, Baoping,Jen, Alex K.-Y. Royal Society of Chemistry 2011 Journal of materials chemistry Vol.21 No.35

        <P>Two new semiconducting polymers based on indacenodithiophene and thiadiazolo[3,4-<I>c</I>]pyridine units were synthesized <I>via</I> Stille coupling polymerization. The polymers, PIDTPyT and PIDTDTPyT, exhibited main absorption bands in the range of 550–800 nm while their absorption maxima were located at around 700 nm in films. With two additional thiophene spacers, PIDTDTPyT showed a broader absorption band but a 20 nm blue-shifted maximum peak compared to that of PIDTPyT. Both of the polymers possess low bandgaps (∼1.6 eV) and deep energy levels for both the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO). Organic field-effect transistors (OFETs) device measurements indicate that PIDTPyT and PIDTDTPyT have high hole carrier mobilities of 0.066 and 0.045 cm<SUP>2</SUP> V<SUP>−1</SUP> s<SUP>−1</SUP>, respectively, with the on/off ratio on the order of 10<SUP>6</SUP>. Bulk heterojunction photovoltaic devices consisting of the copolymers and PC<SUB>71</SUB>BM gave power conversion efficiencies (PCE) as high as 3.91% with broadband photo-response in the range of 300–800 nm. The relationships between the photovoltaic performance and film morphology, energy levels, hole mobilities are discussed.</P> <P>Graphic Abstract</P><P>Low bandgap regiorandom polymers based on indacenodithiophene and thiadiazolo[3,4-<I>c</I>]pyridine units showed excellent OFET hole mobilities and promising photovoltaic device performance as high as 3.91%. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c1jm11564b'> </P>

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        Virtual Screening and Testing of GSK-3 Inhibitors Using Human SH-SY5Y Cells Expressing Tau Folding Reporter and Mouse Hippocampal Primary Culture under Tau Cytotoxicity

        Lin Chih-Hsin,Hsieh Yu-Shao,Sun Ying-Chieh,Huang Wun-Han,Chen Shu-Ling,Weng Zheng-Kui,Lin Te-Hsien,Wu Yih-Ru,Chang Kuo-Hsuan,Huang Hei-Jen,Lee Guan-Chiun,Hsieh-Li Hsiu Mei,Lee-Chen Guey-Jen 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.1

        Glycogen synthase kinase-3β (GSK-3β) is an important serine/threonine kinase that implicates in multiple cellular processes and links with the neurodegenerative diseases including Alzheimer’s disease (AD). In this study, structure-based virtual screening was performed to search database for compounds targeting GSK-3β from Enamine’s screening collection. Of the top-ranked compounds, 7 primary hits underwent a luminescent kinase assay and a cell assay using human neuroblastoma SH-SY5Y cells expressing Tau repeat domain (TauRD) with pro-aggregant mutation ΔK280. In the kinase assay for these 7 compounds, residual GSK-3β activities ranged from 36.1% to 90.0% were detected at the IC50 of SB-216763. In the cell assay, only compounds VB-030 and VB-037 reduced Tau aggregation in SH-SY5Y cells expressing ΔK280 TauRD-DsRed folding reporter. In SH-SY5Y cells expressing ΔK280 TauRD, neither VB-030 nor VB-037 increased expression of GSK-3α Ser21 or GSK-3β Ser9. Among extracellular signal-regulated kinase (ERK), AKT serine/threonine kinase 1 (AKT), mitogen-activated protein kinase 14 (P38) and mitogenactivated protein kinase 8 (JNK) which modulate Tau phosphorylation, VB-037 attenuated active phosphorylation of P38 Thr180/ Tyr182, whereas VB-030 had no effect on the phosphorylation status of ERK, AKT, P38 or JNK. However, both VB-030 and VB-037 reduced endogenous Tau phosphorylation at Ser202, Thr231, Ser396 and Ser404 in neuronally differentiated SH-SY5Y expressing ΔK280 TauRD. In addition, VB-030 and VB-037 further improved neuronal survival and/or neurite length and branch in mouse hippocampal primary culture under Tau cytotoxicity. Overall, through inhibiting GSK-3β kinase activity and/or p-P38 (Thr180/Tyr182), both compounds may serve as promising candidates to reduce Tau aggregation/cytotoxicity for AD treatment.

      • KCI등재

        A Neuroprotective Action of Quercetin and Apigenin through Inhibiting Aggregation of Aβ and Activation of TRKB Signaling in a Cellular Experiment

        Chiu Ya-Jen,Teng Yu-Shan,Chen Chiung-Mei,Sun Ying-Chieh,Hsieh-Li Hsiu Mei,Chang Kuo-Hsuan,Lee-Chen Guey-Jen 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.3

        Alzheimer’s disease (AD) is a neurodegenerative disease with progressive memory loss and the cognitive decline. AD is mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via a number of possible mechanisms such as down-regulation of brain-derived neurotrophic factor-tropomyosin-related kinase B (BDNF-TRKB) signaling pathway. 7,8-Dihydroxyflavone (7,8-DHF), a TRKB agonist, has demonstrated potential to enhance BDNF-TRKB pathway in various neurodegenerative diseases. To expand the capacity of flavones as TRKB agonists, two natural flavones quercetin and apigenin, were evaluated. With tryptophan fluorescence quenching assay, we illustrated the direct interaction between quercetin/ apigenin and TRKB extracellular domain. Employing Aβ folding reporter SH-SY5Y cells, we showed that quercetin and apigenin reduced Aβ-aggregation, oxidative stress, caspase-1 and acetylcholinesterase activities, as well as improved the neurite outgrowth. Treatments with quercetin and apigenin increased TRKB Tyr516 and Tyr817 and downstream cAMP-response-element binding protein (CREB) Ser133 to activate transcription of BDNF and BCL2 apoptosis regulator (BCL2), as well as reduced the expression of pro-apoptotic BCL2 associated X protein (BAX). Knockdown of TRKB counteracted the improvement of neurite outgrowth by quercetin and apigenin. Our results demonstrate that quercetin and apigenin are to work likely as a direct agonist on TRKB for their neuroprotective action, strengthening the therapeutic potential of quercetin and apigenin in treating AD.

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