Functionalized PFN-X (X = Cl, Br, or I) for Balanced Charge Carriers of Highly Efficient Blue Light-Emitting Diodes.

All-inorganic perovskite nanocrystals (PeNCs), CsPbX3 (X = Cl, Br, or I), have been considered as one of the prospective emissive materials for display applications, which showed superior photoluminescence quantum yield and high color purity with narrow spectral line width. Recently, high-performance green and red perovskite light-emitting diodes (PeLEDs) were introduced; however, the efficiency of blue PeLEDs still lagged owing to PeNCs' deep HOMO energy level (∼6.0 eV), which is in discord with the adjacent organic interlayer. In this work, we demonstrated an interfacial engineering strategy with conjugated polyelectrolytes, functionalized PFN (poly[(9,9-bis(3'-(N,N-dimethylamino)propyl)-2,7-fluorene)-alt-2,7-(9,9-dioctylfluorene)]) with halide anions, between the hole injection layer and PeNCs. By introducing PFN-X (X = Cl, Br, or I), they exhibit well-balanced charge carriers and resultant effective radiative recombination in the PeNC layer with reduced hole injection barrier and electron blocking behavior. Among them, in particular, the PFN-Cl-treated PeLEDs display a maximum external quantum efficiency of 1.34% at 470 nm electroluminescence emission with enhanced spectral operating stability.

Hyperbranched Copolymers Based on Glycidol and Amino Glycidyl Ether: Highly Biocompatible Polyamines Sheathed in Polyglycerols.

Functional hyperbranched polyglycerols (PGs) have recently garnered considerable interest due to their potential in biomedical applications. Here, we present a one-pot synthesis of hyperbranched PGs possessing amine functionality using a novel amino glycidyl ether monomer. A Boc-protected butanolamine glycidyl ether (BBAG) monomer was designed and polymerized with glycidol (G) through anionic ring-opening multibranching polymerization to yield a series of hyperbranched P(G-co-BBAG) with controlled molecular weights (4800-16700 g/mol) and relatively low molecular weight distributions (1.2-1.6). The copolymerization and subsequent deprotection chemistry allow the incorporation of an adjustable fraction of primary amine moieties (typically, 5-20% monomer ratio) within the hyperbranched PG backbones, thus providing potentials for varying charge densities and functionality in PGs. The copolymerization kinetics of G and BBAG was also evaluated using a quantitative in situ 13C NMR spectroscopic analysis, which revealed gradient copolymerization between the comonomers. The free amine groups within the deprotected P(G-co-BAG) copolymer were further utilized for a facile conjugation chemistry with a model molecule in a quantitative manner. Furthermore, the superior biocompatibility of the prepared P(G-co-BAG) polymers was demonstrated via cell viability assays, outperforming many existing polyamines possessing relatively high cytotoxicity. Taken together, the biocompatibility with facile conjugation chemistry of free amine groups sheathed within the framework of hyperbranched PGs holds the prospect of advancing biological and biomedical applications.

Long-term stable polymer solar cells with significantly reduced burn-in loss.

The inferior long-term stability of polymer-based solar cells needs to be overcome for their commercialization to be viable. In particular, an abrupt decrease in performance during initial device operation, the so-called 'burn-in' loss, has been a major contributor to the short lifetime of polymer solar cells, fundamentally impeding polymer-based photovoltaic technology. In this study, we demonstrate polymer solar cells with significantly improved lifetime, in which an initial burn-in loss is substantially reduced. By isolating trap-embedded components from pristine photoactive polymers based on the unimodality of molecular weight distributions, we are able to selectively extract a trap-free, high-molecular-weight component. The resulting polymer component exhibits enhanced power conversion efficiency and long-term stability without abrupt initial burn-in degradation. Our discovery suggests a promising possibility for commercial viability of polymer-based photovoltaics towards real solar cell applications.

HS-1793, a recently developed resveratrol analogue protects rat heart against hypoxia/reoxygenation injury via attenuating mitochondrial damage.

Resveratrol is known to exert a cardioprotective effect against hypoxia/reoxygenation (H/R) injury. HS-1793 is a novel, more stable resveratrol analog, but its cardioprotective effects were unknown. The present study aimed to test the cardioprotective effect of HS-1793 against H/R injury and investigate the role of mitochondria in Sprague Dawley rat heart damage using an ex vivo Langendorff system. HS-1793 ameliorated H/R-induced mitochondrial dysfunction by reducing mitochondrial reactive oxygen species production, improving mitochondrial oxygen consumption and suppressing mitochondrial calcium (Ca(2+)) overload during reperfusion. Moreover, HS-1793-treated rat heart showed reduced infarct size. Our data suggest that HS-1793 can protect cardiac against mitochondrial damage following H/R, thereby suppressing injury.

An analogue of resveratrol HS-1793 exhibits anticancer activity against MCF-7 cells via inhibition of mitochondrial biogenesis gene expression.

Resveratrol is a phytoalexin and polyphenol derived from grapes, berries, and peanuts. It has been shown to mediate death of a wide variety of cancer cells. Although resveratrol is considered an important potential chemotherapeutic agent, it is required at high doses to achieve a biologically or physiologically significant effect, which may be impractical for treating cancer. Thus, a more stable and potent derivative of resveratrol, with more effective tumoricidal activity, must be developed. A novel resveratrol analog, HS-1793, has recently been synthesized and was determined to exhibit a greater decrease in cancer cell viability than resveratrol. However, the underlying mechanism of HS-1793-induced cancer cell death remains unknown. We thus investigated the mechanism by which HS-1793 induces cell death and assessed whether this occurs through a mitochondrial-mediated mechanism. Using the MCF-7 breast cancer cell line, we determined that HS-1793 treatment significantly increased cell death at a relatively low dose compared with resveratrol. HS-1793 treatment more significantly decreased mitochondrial membrane potential, cellular ATP concentration, and cellular oxygen consumption rate than resveratrol treatment. At the molecular level, HS-1793 treatment down-regulated the expression of major mitochondrial biogenesis-regulating proteins, including mitochondrial transcriptional factor A (TFAM), Tu translation elongation factor (TUFM), and single-stranded DNA-binding protein. We conclude that HS- 1793 acts by regulating the expression of TFAM and TUFM, leading to a block in normal mitochondrial function, which sensitizes cancer cells to cell death. We therefore propose that HS-1793 can be a useful chemosensitization agent, which together with other such agents can efficiently target cancer cells.

The novel resveratrol analog HS-1793-induced polyploid LNCaP prostate cancer cells are vulnerable to downregulation of Bcl-xL.

Since resveratrol is not a potent cytotoxic compound when compared with other chemotherapeutic agents, several previous studies have been performed to obtain synthetic analogs of resveratrol with potent activity. Our previous study demonstrated that the resveratrol analog HS-1793 showed stronger antitumor activity than resveratrol in various cancer cells. We examined the antitumor activity exerted by HS-1793 in prostate cancer cells, and we observed that HS-1793 acts as a polyploidy inducer. Noticeably, multinucleation and polyploidization were induced in most LNCaP cells treated with HS-1793 at the dose causing a slight decline in cell viability. However, the induction of multinucleation and polyploidization was much lower in PC-3 prostate cancer cells treated with the same dose of HS-1793. Western blot and RT-PCR analyses showed that the expression of Aurora B was almost undetectable in LNCaP cells, but it was highly expressed in PC-3 cells. Further, silencing of Aurora B sensitized PC-3 cells to HS-1793-induced multi-nucleation. These results indicate that expression of Aurora B determines multinucleation in prostate cancer cells treated with HS-1793. Additional assays using multiple cancer cell lines show that the population of multinucleated cells induced by HS-1793 treatment is inversely proportional to Aurora B expression. We further elicited that the HS-1793-induced polyploid LNCaP cells are vulnerable to downregulation of Bcl-xL. Since the polyploidization in LNCaP induced by HS-1793 does not appear to cause definite commitment to apoptosis, the termination of polyploid cells by inhibition of Bcl-xL could provide an advantageous means to improve chemotherapeutic efficacy of HS-1793.

Enhanced open circuit voltage by hydrophilic ionic liquids as buffer layer in conjugated polymer-nanoporous titania hybrid solar cells.

We demonstrate the fabrication of a nanoporous titania (NP-TiO(2)) network structure by using a polystylene-block-poly(4-vinylpyridine) (PS-b-P4VP) diblock copolymer template and modifying the surface of NP-TiO(2) with ionic liquids (ILs), bmim-BF(4) and benmim-Cl. The effect of the molecular weight of PS-b-P4VP on the morphology of the NP-TiO(2) and IL-modified NP-TiO(2) are characterized by scanning electron microscopy and contact angle measurements. Subsequently, hybrid solar cells are fabricated using MEH-PPV and NP-TiO(2), and the effect of IL layers and IL concentrations on device performances are evaluated under AM 1.5 G illumination. The devices containing bmim-BF(4) and benmim-Cl show drastically enhanced open circuit voltages (V(oc)) of 1.05 V and 0.91 V, respectively, while the reference device without an IL layer exhibits a V(oc) of 0.60 V. Significantly improved V(oc) can be attributed to the change in interfacial energy levels by formation of ionic double layers at the TiO(2)/IL and at the IL/MEH-PPV interfaces. We also observed the trend that short circuit current decreased and V(oc) increased with increasing IL concentration, which is ascribed to interruption of charge transfer from MEH-PPV to TiO(2) and the change in interfacial energy level by shifting the vacuum level, respectively.

A newly synthesized, potent tyrosinase inhibitor: 5-(6-hydroxy-2-naphthyl)-1,2,3-benzenetriol.

In searching for new agents with a depigmenting effect, we synthesized a derivative of resveratrol, 5-(6-hydroxy-2-naphthyl)-1,2,3-benzenetriol (5HNB) with a potent tyrosinase inhibitory activity. 5HNB inhibited mushroom tyrosinase with an IC(50) value of 2.95 microM, which is more potent than the well-known anti-tyrosinase activity of kojic acid (IC(50)=38.24). The results of the enzymatic inhibition kinetics by Lineweaver-Burk analysis indicated 5HNB inhibits tyrosinase non-competitively when L-tyrosine was used as the substrate. Based on the strong inhibitory action of 5HNB, it is expected that 5HNB can suppress melanin production in which tyrosinase plays the essential role. Our expectation was confirmed by the experimentations with B16 melanoma cells in which 5HNB inhibited melanin production. We propose that 5HNB might have skin-whitening effects as well as therapeutic potential for treating skin pigmentation disorders.

A novel resveratrol analogue HS-1793 treatment overcomes the resistance conferred by Bcl-2 and is associated with the formation of mature PML nuclear bodies in renal clear cell carcinoma Caki-1 cells.

Bcl-2 protects cancer cells from the apoptotic effects of various chemotherapeutic agents. Inhibition or downregulation of Bcl-2 represents a new therapeutic approach to bypass chemoresistance in cancer cells. Previously we designed and synthesized the resveratrol analogue HS-1793 displaying stronger antitumor efficacy than resveratrol and further demonstrated the HS-1793 resistance conferred by Bcl-2 in human leukemic U937 cells. We undertook this study to determine if HS-1793 treatment can bypass the anti-apoptotic effects of Bcl-2 in human renal cancer cells, with a specific focus on the involvement of promyelocytic leukemia nuclear bodies (PML-NBs). Experiments were conducted with Bcl-2-overexpressing human renal clear cell carcinoma Caki-1 cells. Various apoptosis assessment assays demonstrated that HS-1793 overcomes the resistance conferred by Bcl-2 in Caki-1 cells by inducing apoptosis. We elucidated that HS-1793-induced formation of mature promyelocytic leukemia (PML) nuclear bodies (NBs) correlates with overcoming the anti-apoptotic effects of Bcl-2 in Caki-1 cells. Our findings show that the resveratrol analogue HS-1793 might provide a novel promising strategy for overcoming the resistance conferred by Bcl-2 via PML protein and the formation of mature PML-NBs.

A novel resveratrol derivative, HS1793, overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells.

The chemopreventive and chemotherapeutic properties associated with resveratrol offer promise for the design of new chemotherapeutic agents. However, resveratrol is not a potent cytotoxic compound when compared with other chemotherapeutic drugs. Thus, several studies were undertaken to obtain synthetic analogues of resveratrol with potent activity. The present study was undertaken to examine whether four resveratrol analogues (HS-1784, -1792, -1791 and -1793) that we had designed and synthesized show antitumor activity. Here, we observed that all of these resveratrol analogues displayed stronger antitumor effects than resveratrol in most cancer cells tested. We further examined whether HS-1793, showing potent antitumor effects in most cancer cells tested, overcomes the resistance conferred by Bcl-2, since overcoming the resistance conferred by Bcl-2 represents an attractive therapeutic strategy against cancer. Our viability assay showed that HS-1793 overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells. Various apoptosis assessment assays demonstrated that HS-1793 overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells by inducing apoptosis. Noticeably, we elucidated the marked downregulation of 14-3-3 protein by HS-1793, indicating that HS-1793 overcomes the resistance conferred by Bcl-2 in U937 cells via 14-3-3. We also observed that HS-1793 exerts its antitumor activity via Bad. However, overall data obtained from methylation specific PCR, RT-PCR and real-time PCR suggest that HS-1793 plays a role in the downregulation of 14-3-3 at a post-transcriptional level. Further understanding exactly how HS-1793 overcomes the resistance conferred by Bcl-2 via 14-3-3 may guide the development of future anticancer agents.

Inhibitory effects of 6-(3-hydroxyphenyl)-2-naphthol on tyrosinase activity and melanin synthesis.

As a part of an ongoing project searching for new skin-lightening agents, the inhibitory property of 6-(3-Hydroxyphenyl)-2-naphthol (HPN) on melanogenesis was investigated. The inhibitory action of HPN (IC(50)=15.2 muM) on mushroom tyrosinase was revealed. To further explore the action of HPN on melanogenesis, the inhibition of tyrosinase and melanin levels were measured in B16 melanoma cells (B16 cells). Results show that HPN inhibited tyrosinase activity and reduced melanin in B16 cells. Therefore, our data indicate HPN as a new candidate for depigmentation reagents.

4-(6-Hydroxy-2-naphthyl)-1,3-bezendiol: a potent, new tyrosinase inhibitor.

Tyrosinase is a key enzyme for melanin biosynthesis and known to be sensitive to ultraviolet light in the presence of oxygen. Therefore, finding effective tyrosinase inhibitors, either from synthetic or natural sources, can be beneficial in the treatment of melanin-related disorders. We synthesized 4-(6-hydroxy-2-naphthyl)-1,3-bezendiol (HNB), a new family of hydroxyl substituted phenyl naphthalenes, as the isosteres of oxyresveratrol. This study investigated inhibitory effects of HNB on tyrosinase activity. HNB inhibited mushroom tyrosinase with an IC(50) value of 0.07 microM, which is more potent than the anti-tyrosinase activity of kojic acid (IC(50)=38.24), a well-known tyrosinase inhibitor. The kinetic analysis of tyrosinase inhibition revealed that HNB is a competitive inhibitor (K(i) 4.78 x 10(-9) M at 0.125 microM and K(i) 6.21 x 10(-9) M at 0.25 microM). We further found that HNB also inhibited melanin production in B16F10 melanoma cells (B16 cells). In addition to tyrosinase inhibiting activity, melanin biosynthesis was inhibited by HNB in the B16F10 cells. These data strongly suggest that HNB can suppress the production of melanin via the modulation of tyrosinase activity.

Syntheses of hydroxy substituted 2-phenyl-naphthalenes as inhibitors of tyrosinase.

Oxyresveratrol and resveratrol, with hydroxy substituted trans-stilbene structure, exert potent inhibitory effects on cyclooxygenase, rat liver mitochondrial ATPase activity, and tyrosinase. As the isosteres of oxyresveratrol, a new family of hydroxyl substituted phenyl-naphthalenes were synthesized to show excellent inhibition of mushroom tyrosinase. Compound 10, which is isostere of resveratrol, showed IC50 value of 16.52 microM in mushroom tyrosinase activity. As compared to this, the reference compound, resveratrol, showed IC50 value of 55.61 microM. Compound 4, which is isostere of oxyresveratrol, showed IC50 value of 0.49 microM. Among the other three derivatives, compound 13 showed IC50 value of 0.034 microM.