Assemblies of Colloidal CdSe Tetrapod Nanocrystals with Lengthy Arms for Flexible Thin-Film Transistors.

Herein, we report unique features of the assemblies of tetrapod-shaped colloidal nanocrystals (TpNCs) with lengthy arms applicable to flexible thin-film transistors. Due to the extended nature of tetrapod geometry, films made of the TpNC assemblies require reduced numbers of inter-NC hopping for the transport of charge carriers along a given channel length; thus, enhanced conductivity can be achieved compared to those made of typical spherical NCs without arms. Moreover, electrical conduction through the assemblies is tolerant against mechanical bending because interconnections between TpNCs can be well-preserved under bending. Interestingly, both the conductivity of the assemblies and their mechanical tolerance against bending are improved with an increase in the length of tetrapod arms. The arm length-dependency was demonstrated in a series of CdSe TpNC assemblies with different arm lengths (l = 0-90 nm), whose electrical conduction was modulated through electrolyte gating. From the TpNCs with the longest arm length included in the study (l = 90 nm), the film conductivity as high as 20 S/cm was attained at 3 V of gate voltage, corresponding to electron mobility of >10 cm2/(V s) even when evaluated conservatively. The high channel conductivity was retained (∼90% of the value obtained from the flat geometry) even under high bending (bending radius = 5 mm). The results of the present study provide new insights and guidelines for the use of colloidal nanocrystals in solution-processed flexible electronic device applications.

Influence of Dielectric Layers on Charge Transport through Diketopyrrolopyrrole-Containing Polymer Films: Dielectric Polarizability vs Capacitance.

Field-effect mobility of a polymer semiconductor film is known to be enhanced when the gate dielectric interfacing with the film is weakly polarizable. Accordingly, gate dielectrics with lower dielectric constant (k) are preferred for attaining polymer field-effect transistors (PFETs) with larger mobilities. At the same time, it is also known that inducing more charge carriers into the polymer semiconductor films helps in enhancing their field-effect mobility, because the large number of traps presented in such a disorder system can be compensated substantially. In this sense, it may seem that employing higher k dielectrics is rather beneficial because capacitance is proportional to the dielectric constant. This, however, contradicts with the statement above. In this study, we compare the impact of the two, i.e., the polarizability and the capacitance of the gate dielectric, on the transport properties of poly[(diketopyrrolopyrrole)-alt-(2,2'-(1,4-phenylene)bisthiophene)] (PDPPTPT) semiconductor layers in an FET architecture. For the study, three different dielectric layers were employed: fluorinated organic CYTOP (k = ∼2), poly(methyl methacrylate) (k = ∼4), and relaxor ferroelectric poly(vinylidene fluoride-trifluoroethylene-chlorotrifluoroethylene) (k = ∼60). The beneficial influence of attaining more carriers in the PDPPTPT films on their charge transport properties was consistently observed from all three systems. However, the more dominant factor determining the large carrier mobility was the low polarizability of the gate dielectric rather than its large capacitance; field-effect mobilities of PDPPTPT films were always larger when lower k dielectric was employed than when higher k dielectric was used. The higher mobilities obtained when using lower k dielectrics could be attributed to the suppressed distribution of the density of localized states (DOS) near the transport level and to the resulting enhanced electronic coupling between the macromolecules.

An Organic Vertical Field-Effect Transistor with Underside-Doped Graphene Electrodes.

High-performance vertical field-effect transistors are developed, which are based on graphene electrodes doped using the underside doping method. The underside doping method enables effective tuning of the graphene work function while maintaining the surface properties of the pristine graphene.

Apparent pH sensitivity of solution-gated graphene transistors.

Solution-gated graphene transistors were developed recently for use in pH sensor applications. The device operation is understood to rely on the capability of hydronium and hydroxide ions in solution to change the electrical properties of graphene. However, hydronium and hydroxide ions are accompanied by other ionic species in a typical acidic or basic solution and, therefore, the roles of these other ionic species must be also considered to fully understand the pH response of such devices. Using series of pH buffer solutions designed carefully, we verified that the magnitude and even the direction of pH-dependent Dirac voltage (VDirac) shift (the typical pH sensing indicator) depend strongly on the concentration and composition of the buffers used. The results indicate that the interpretation of the apparent pH-dependent VDirac response of a solution-gated graphene transistor must include the contributions of the additional ions in the solution.

pn-Heterojunction effects of perylene tetracarboxylic diimide derivatives on pentacene field-effect transistor.

We investigated the heterojunction effects of perylene tetracarboxylic diimide (PTCDI) derivatives on the pentacene-based field-effect transistors (FETs). Three PTCDI derivatives with different substituents were deposited onto pentacene layers and served as charge transfer dopants. The deposited PTCDI layer, which had a nominal thickness of a few layers, formed discontinuous patches on the pentacene layers and dramatically enhanced the hole mobility in the pentacene FET. Among the three PTCDI molecules tested, the octyl-substituted PTCDI, PTCDI-C8, provided the most efficient hole-doping characteristics (p-type) relative to the fluorophenyl-substituted PTCDIs, 4-FPEPTC and 2,4-FPEPTC. The organic heterojunction and doping characteristics were systematically investigated using atomic force microscopy, 2D grazing incidence X-ray diffraction studies, and ultraviolet photoelectron spectroscopy. PTCDI-C8, bearing octyl substituents, grew laterally on the pentacene layer (2D growth), whereas 2,4-FPEPTC, with fluorophenyl substituents, underwent 3D growth. The different growth modes resulted in different contact areas and relative orientations between the pentacene and PTCDI molecules, which significantly affected the doping efficiency of the deposited adlayer. The differences between the growth modes and the thin-film microstructures in the different PTCDI patches were attributed to a mismatch between the surface energies of the patches and the underlying pentacene layer. The film-morphology-dependent doping effects observed here offer practical guidelines for achieving more effective charge transfer doping in thin-film transistors.

The bacterial protein azurin enhances sensitivity of oral squamous carcinoma cells to anticancer drugs.

PURPOSE: Surgical therapy is the primary treatment for oral cancer, but it can cause facial distortion. Therefore, if anticancer drugs are effective against oral cancer, they may be used preferentially. However, oral squamous carcinoma cells (OSCCs) are resistant to these drugs, so finding a way to enhance the sensitivity of these cells to anticancer drugs is important. The bacterial protein azurin is known to selectively enter cancer cells and induce apoptosis. In this study, we show the anticancer effect of azurin in OSCC. MATERIALS AND METHODS: OSCC cell line (YD-9) was subjected to azurin treatment. Cell viability, morphology and protein expression levels were monitored after treatment of azurin. Cells were also subjected to combination treatment of azurin with either 5-fluorouracil or etopside. RESULTS: Azurin-treated cells showed decreased cell viability accompanied by apoptotic phenotypes including morphological change, DNA breakage, and increases in p53 and cyclin B1 protein levels. Combination treatment of azurin with other anti-tumor agents caused an increase in sensitivity to anticancer drugs in azurin-treated YD-9 cells. CONCLUSION: Azurin has a strong synergistic anticancer effect on oral cancer cells when it is used along with anticancer drugs.

Macrophage migration inhibitory factor homologs of anisakis simplex suppress Th2 response in allergic airway inflammation model via CD4+CD25+Foxp3+ T cell recruitment.

We have cloned the macrophage migration inhibitory factor (MIF)-like protein (Anisakis simplex (As)-MIF) from larvae of the whale worm (Anisakis simplex third-stage larvae). Asthma was induced in the mice using OVA/alum, with or without various concentrations of rAs-MIF treatment before OVA/alum challenge. Treatment with rAs-MIF coupled with OVA/alum during the challenge period induced a complete inhibition of eosinophilia and goblet cell hyperplasia within the lung and profoundly ameliorated the development of lung hyperreactivity. Also, rAs-MIF was shown to reduce profoundly the quantity of Th2-related cytokines (IL-4, IL-5, and IL-13) in the bronchial alveolar lavage fluid and allergen-specific IgG2a in sera. IL-10 and TGF-beta levels in the bronchoalveolar lavage fluid of the rAs-MIF-treated group were significantly higher than in the other groups. Additionally, CD4(+)CD25(+)Foxp3(+) T cells (regulatory T) were recruited to the spleen and lungs of the rAs-MIF-treated mice, but this recruitment was inhibited by anti-rAs-MIF Ab.

Toll-like receptor 4-mediated immunoregulation by the aqueous extract of Mori Fructus.

The aqueous extract of Mori Fructus (MF) exerts a change of phenotype and a cytoprotective effect in macrophages. The present study was carried out to investigate the immunomodulating activity of MF on the expression of nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), co-stimulatory molecules and also interferon-gamma (IFN-gamma) in macrophages and splenocytes. Toll-like receptor 4 (TLR4) is a promising molecular target for immune-modulating drugs. It was hypothesized that one possible upstream signaling pathway leading to immunoregulation of MF may be mediated by TLRs. Multiple signaling molecules (NF-kappaB, ERK1/2, p38 and JNK) of the TLR4 signaling pathway were also detected. It was found that MF increased NO production and TNF-alpha secretion in RAW 264.7 and peritoneal macrophages, co-stimulatory molecules expression in peritoneal macrophages and IFN-gamma expression in splenocytes. Further studies indicated that MF could significantly induce the phosphorylation of signal molecules of MAPKs and the degradation of IkappaBalpha which finally led to the activation and nuclear translocation of nuclear factor-kappaB (NF-kappaB) for the target gene expression. All those notions disclosed that the aqueous extract MF is a new TLR4 activator, which induces a Th1 immune response as a consequence of induction of cytokines secretion, especially TNF-alpha and IFN-gamma.

Increased expression of MIP-3alpha/CCL20 in peripheral blood mononuclear cells from patients with ulcerative colitis and its down-regulation by sulfasalazine and glucocorticoid treatment.

UNLABELLED: CCL20 expression is known to increase in the mucosal tissues of inflammatory bowel diseases (IBDs). Moreover, the discovery of Nod2 as the IBD1 susceptibility gene has underscored the significance of blood mononuclear cells in IBD pathogenesis. METHODS: This study addresses whether CCL20 expression is similarly altered in peripheral blood mononuclear cells (PBMCs) of patients with ulcerative colitis (UC), a major type of IBD in Korea. RESULTS: Expression of CCL20 was significantly up-regulated in the PBMCs of patients with UC compared with those of normal healthy controls. Interestingly, untreated UC groups expressed higher levels of CCL20 mRNA than either treated UC or normal control groups, suggesting that CCL20 could be modulated by anti-inflammatory drugs. Accordingly, a strong association between CCL20 levels and disease activity index was observed. Supporting these findings, results from a 3-month follow-up study revealed that the UC groups treated with 5-aminosalicylic acid and glucocorticoid exhibited dramatic decreases of CCL20 mRNA in PBMCs, accompanied by ameliorated disease states. Moreover, tumor necrosis factor-alpha- or interleukin-1beta-induced CCL20 secretion was greatly diminished by 5-aminosalicylic acid and/or glucocorticoid treatment of human intestinal epithelial HT-29 cells. Of note, CCR6 cell populations were significantly reduced in the blood of severe patients with UC compared with normal controls, whereas no significant changes in CCR6 cell populations were observed in the blood of patients with mild UC or acute colitis. CONCLUSIONS: Collectively, these findings suggest that CCL20 expression in blood mononuclear cells is associated with altered immune and inflammatory responses in patients with UC.

Iron chelator induces MIP-alpha/CCL20 in human intestinal epithelial cells: implication for triggering mucosal adaptive immunity.

A previous report by this laboratory demonstrated that bacterial iron chelator (siderophore) triggers inflammatory signals, including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs). Microarray-based gene expression profiling revealed that iron chelator also induces macrophage inflammatory protein 3 alpha (MIP-3alpha)/CC chemokine-ligand 20 (CCL20). As CCL20 is chemotactic for the cells involved in host adaptive immunity, this suggests that iron chelator may stimulate IECs to have the capacity to link mucosal innate and adaptive immunity. The basal medium from iron chelator deferoxamine (DFO)-treated HT-29 monolayers was as chemotactic as recombinant human CCL20 at equivalent concentrations to attract CCR6(+) cells. The increase of CCL20 protein secretion appeared to correspond to that of CCL20 mRNA levels, as determined by real-time quantitative RT-PCR. The efficacy of DFO at inducing CCL20 mRNA was also observed in human PBMCs and in THP-1 cells, but not in human umbilical vein endothelial cells. Interestingly, unlike other proinflammatory cytokines, such as TNF-alpha and IL-1beta, a time-dependent experiment revealed that DFO slowly induces CCL20, suggesting a novel mechanism of action. A pharmacologic study also revealed that multiple signaling pathways are differentially involved in CCL20 production by DFO, while some of those pathways are not involved in TNF-alpha-induced CCL20 production. Collectively, these results demonstrate that, in addition to some bacterial products known to induce host adaptive immune responses, direct chelation of host iron by infected bacteria may also contribute to the initiation of host adaptive immunity in the intestinal mucosa.

Catalposide, a compound isolated from catalpa ovata, attenuates induction of intestinal epithelial proinflammatory gene expression and reduces the severity of trinitrobenzene sulfonic Acid-induced colitis in mice.

Certain irinoid-producing plants have been used as herbal anti-inflammatory remedies. Here we evaluated whether catalposide (CATP), a single compound isolated from irinoid-producing plant Catalpa ovata, has a potential for preventing or ameliorating diseases characterized by mucosal inflammation. Preliminary microarray-based gene expression test revealed that CATP, which alone did not significantly affect expression of any of the >8,000 genes analyzed, attenuated the expression of tumor necrosis factor-alpha (TNF-alpha)-induced proinflammatory genes including interleukin-8 (IL-8) in human intestinal epithelial HT-29 cells. Down-regulation of IL-8 mRNA accumulation was also reflected by the decreased IL-8 secretion in CATP-treated HT-29 cells. The signal transduction study revealed that CATP significantly attenuates TNF-alpha-mediated p38 and extracellular signal-regulated kinase (ERK) phosphorylation. Further, CATP reduced NF-kappaB-mediated transcriptional activation as well as Ikappa-Balpha degradation. To establish the in vivo relevance of these findings, we examined whether CATP could affect intestinal inflammation in vivo using the mouse model of trinitrobenzene sulfonic acid (TNBS)-induced inflammatory colitis. Intrarectal administration of CATP dramatically reduced the weight loss, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, CATP suppressed the expression of TNF-alpha, interleukin-1beta, and intercellular adhesion molecule-1 along with the inhibition of NF-kappa B p65 translocation into nucleus in TNBS colitis. Collectively, current results demonstrate that CATP may be an effective agent for the treatment of diseases characterized by mucosal inflammation.

Soluble glucocorticoid-induced TNF receptor (sGITR) induces inflammation in mice.

Glucocorticoid-induced TNF receptor (GITR) was a new member of the TNF/nerve growth factor receptor (TNFR/ NGFR) family and induced in murine T cells by dexamathasone. Recombinant soluble GITR (sGITR) induced an inflammation in peritoneal membrane and changes in spleen after i.p. injection of 3 mg/kg in C57BL/6 mice. Spleen was enlarged and percentage of neutrophils and monocytes were increased. The area of red pulp in spleen was increased, while that of white pulp was decreased after GITR injection. The thickening of membrane and neutrophil infiltration was observed in peritoneal membrane with increased myeloperoxidase activity. At later time, neutrophil infiltration moved to inside the tissue with tissue damage. GITR ligand and GITR were expressed constitutively on the surface of spleen cells and cells from peritoneal fluid. In contrast, no significant change in the spleen and in peritoneal membrane was observed in mice treated with LPS. GITR may play a role in body's inflammatory processes.

Recombinant glucocorticoid induced tumor necrosis factor receptor (rGITR) induces NOS in murine macrophage.

Glucocorticoid induced tumor necrosis factor receptor (GITR) is a new member of the tumor necrosis factor-nerve growth factor receptor superfamily of which the function has not been well studied. The extracellular domain of GITR was produced in Escherichia coli and purified as a single band of predicted M(r) of 18.0 kDa. GITR and GITR ligand were expressed constitutively on the surface of Raw 264.7 macrophage cell line and murine peritoneal macrophages. An extracellular domain of GITR can activate murine macrophages to express inducible nitric oxide synthase and to generate nitric oxide in a dose- and time-dependent manner.