Organic semiconductors with variable charge carrier polarity are required for optoelectronic applications. Herein, we report the synthesis of three novel diketopyrrolopyrrole (DPP)-based D–A molecules having three different terminal groups (amide, ester, and dicyano) and study their electronic properties. An increase in electron acceptor strength from amide to dicyano leads to a bathochromic shift in absorption. Photoconductivity and field effect transistor (FET) measurements confirmed that a small increase in acceptor strength can result in a large change in the charge transport properties from p-type to n-type. The molecule with an amide group, DPP–amide, exhibited a moderate p-type mobility (1.3 × 10–2 cm2 V–1 s–1), whereas good n-type mobilities were observed for molecules with an ester moiety, DPP–ester (1.5 × 10–2 cm2 V–1 s–1), and with a dicyano group, DPP–DCV (1 × 10–2 cm2 V–1 s–1). The terminal functional group modification approach presented here is a simple and efficient method to alter the charge carrier polarity of organic semiconductors.

Poly(dimethylsiloxane) (PDMS) is a transparent and flexible elastomer which has a myriad of applications in various fields including organic electronics. However, the inherent hydrophobic nature and low surface energy of PDMS prevent its direct use in many applications. It is seldom utilized as a gate dielectric in solution-processed organic field effect transistors (OFETs). In this work, we demonstrate a simple method, extended ultraviolet–ozone (UVO) treatment, to modify the PDMS surface and effectively employ it in solution-processed OFETs as a gate dielectric material. The modified PDMS surface shows enhanced wettability and adherence to both polar and nonpolar liquids, which is contrary to the generally observed hydrophilic nature of UVO-treated PDMS surfaces because of the creation of polar functional groups. The morphological changes happening on the PDMS surface as a result of extended UVO treatment play a major role in making the surface suitable for all type of solvents discussed here. The contact angle measurements are used to give qualitative evidence for this observation. The modified PDMS is then used as a gate dielectric in solution-processed n- and p-channel OFETs using [6,6]-phenyl-C61-butyric acid methyl ester (PC 60 BM) and regioregular poly(3-hexylthiophene) (rr-P3HT) semiconductors, respectively.

This is a repository copy of High performance, transparent solution-processed organic field effect transistor with low-k elastomeric gate dielectric and liquid crystalline semiconductor: Promises and Challenges.

Although inflammatory pathways have been linked with various chronic diseases including cancer, identification of an agent that can suppress these pathways has therapeutic potential. Herein we describe the identification of a novel compound bharangin, a diterpenoid quinonemethide that can suppress pro-inflammatory pathways specifically. We found that bharangin suppresses nuclear factor (NF)-B activation induced by pro-inflammatory cytokine, tumor promoter, cigarette smoke, and endotoxin. Inhibition of NF-B activation was mediated through the suppression of phosphorylation and degradation of inhibitor of nuclear factor-B (IB␣); inhibition of IB␣ kinase activation; and suppression of p65 nuclear translocation, and phosphorylation. The diterpenoid inhibited binding of p65 to DNA. A reducing agent reversed the inhibitory effect, and mutation of the Cys 38 of p65 to serine abrogated the effect of bharangin on p65-DNA binding. Molecular docking revealed strong interaction of the ligand with the p65 via two hydrogen bonds one with Lys 37 (2.204 Å) and another with Cys 38 (2.023 Å). The inhibitory effect of bharangin on NF-B activation was specific, inasmuch as binding of activator protein-1 and octameric transcription factor 1 to DNA was not affected. Suppression of NF-B activation by this diterpenoid caused the downregulation of the expression of proteins involved in tumor cell survival, proliferation, invasion, and angiogenesis, leading to potentiation of apoptosis, suppression of proliferation, and invasion of tumor cells. Furthermore, the genetic deletion of p65 and mutation of p65Cys 38 residue to Ser abolished the affect of bharangin. Overall, our results demonstrate that bharangin specifically inhibits the NF-B activation pathway by modifying p65 and inhibiting IB␣ kinase activation and potentiates apoptosis in tumor cells.

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