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ABSTRACT: A wet-chemical method for increasing the number of quantum dots (QDs) per unit surface area of TiO2 was developed. High density QD surface coating was induced by a surface charge controlled SILAR method, which led to a sixfold increase in photocurrent density from 2.15 mA cm(-2) to 15.03 mA cm(-2) in a QD-sensitized solar cell based on a Hg-doped PbS sensitized 2.4 μm-thick TiO2 film.
Chemical Communications 06/2013; · 6.17 Impact Factor
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ABSTRACT: We report a novel method, nanoscale solvothermal reaction (NSR), to induce the quantum confinement effect of CdSe on nanostructured TiO(2) by solvothermal route. The time-dependent growth of CdSe is observed in solution at room temperature, which is found to be accomplished instantly by heat-treatment in the presence of solvent at 1 atm. However, no crystal growth occurs upon heat-treatment in the absence of solvent. The nanoscale solvothermal growth of CdSe quantum dot is realized on the nanocrystalline oxide surface, where Cd(NO(3))(2)·4H(2)O and Na(2)SeSO(3) solutions are sequentially spun on nanostructured TiO(2), followed by heat-treatment at temperatures ranging from 100 °C to 250 °C. Size of CdSe increases from 4.4 nm to 5.3 nm, 8.7 nm and 14.8 nm, which results in decrease in optical band gap from 2.19 eV to, 1.95 eV, 1.74 eV and 1.75 eV with increasing the NSR temperature from 100 °C to 150 °C, 200 °C and 250 °C, respectively, which is indicative of the quantum confinement effect. Thermodynamic studies reveal that increase in the size of CdSe is related to increase in enthalpy, for instance, from 3.77 J mg(-1) for 100 °C to 8.66 J mg(-1) for 200 °C. Quantum confinement effect is further confirmed from the CdSe-sensitized solar cell, where onset wavelength in external quantum efficiency spectra is progressively shifted from 600 nm to 800 nm as the NSR temperature increases, which leads to a significant improvement of power conversion efficiency by a factor of more than four. A high photocurrent density of 13.7 mA cm(-2) is obtained based on CdSe quantum dot grown by NSR at 200 °C.
Nanoscale 09/2012; 4(20):6642-8. · 5.91 Impact Factor
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ABSTRACT: The androgen receptor (AR) plays a central role in the development and progression of prostate cancer. AR expression is maintained throughout the progression of prostate cancer and is also associated with an aggressive, castration-resistant (CR) phenotype. Despite the critical roles of AR expression in prostate cancer progression, the exact signaling mechanism regulating AR expression remains unclear. In this study, we demonstrated that AR expression was increased by a low-affinity leukotriene B(4) receptor (BLT2)-linked pathway. We found that BLT2 was overexpressed in AR-positive prostate cancer cells, such as LNCaP cells, and BLT2 inhibition, using an inhibitor or siRNA knockdown, clearly attenuated AR expression and triggered apoptosis in these cells. These results suggest a role for BLT2 in AR expression and the survival of AR-positive prostate cancer cells. Moreover, we found that the NADPH oxidase family protein, Nox4, lay downstream of BLT2 and mediated the production of reactive oxygen species (ROS) and subsequent NF-κB stimulation, thereby inducing AR expression. Taken together, our results demonstrate that BLT2 plays a critical role in AR expression via a Nox4-ROS-NF-κB-linked pathway, thereby mediating the survival of AR-positive prostate cancer cells. Our findings point to BLT2 as a key regulator of AR expression and will contribute to the development of novel therapies for AR-positive prostate cancers, including androgen-responsive and CR prostate cancers.
Biochemical and Biophysical Research Communications 03/2012; 420(2):428-33. · 2.48 Impact Factor
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ABSTRACT: 12(S)-Hydroxyheptadeca-5Z,8E,10E-trienoic acid (12- HHT) is an enzymatic product of prostaglandin H(2) (PGH(2)) derived from cyclooxygenase (COX)-mediated arachidonic acid metabolism. Despite the high level of 12-HHT present in tissues and bodily fluids, its precise function remains largely unknown. In this study, we found that 12-HHT treatment in HaCaT cells remarkably down-regulated the ultraviolet B (UVB) irradiation-induced synthesis of interleukin-6 (IL-6), a pro-inflammatory cytokine associated with cutaneous inflammation. In an approach to identify the down-stream signaling mechanism by which 12-HHT down-regulates UVB-induced IL-6 synthesis in keratinocytes, we observed that 12-HHT inhibits the UVB-stimulated activation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB). In addition, we found that 12-HHT markedly up-regulates MAPK phosphatase-1 (MKP-1), a critical negative regulator of p38 MAPK. When MKP-1 was suppressed by siRNA knock-down, the 12-HHT-mediated inhibitory effects on the UVB-stimulated activation of p38 MAPK and NF-κB, as well as the production of IL-6, were attenuated in HaCaT cells. Taken together, our results suggest that 12-HHT exerts anti-inflammatory effect via up-regulation of MKP-1, which negatively regulates p38 MAPK and NF-κB, thus attenuating IL-6 production in UVB-irradiated HaCaT cells. Considering the critical role of IL-6 in cutaneous inflammation, our findings provide the basis for the application of 12-HHT as a potential anti-inflammatory therapeutic agent in UV-induced skin diseases.
Experimental and Molecular Medicine 03/2012; 44(6):378-86. · 2.48 Impact Factor
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ABSTRACT: Highly efficient quantum-dot-sensitized solar cell is fabricated using ca. 2-3 nm sized perovskite (CH(3)NH(3))PbI(3) nanocrystal. Spin-coating of the equimolar mixture of CH(3)NH(3)I and PbI(2) in γ-butyrolactone solution (perovskite precursor solution) leads to (CH(3)NH(3))PbI(3) quantum dots (QDs) on nanocrystalline TiO(2) surface. By electrochemical junction with iodide/iodine based redox electrolyte, perovskite QD-sensitized 3.6 μm-thick TiO(2) film shows maximum external quantum efficiency (EQE) of 78.6% at 530 nm and solar-to-electrical conversion efficiency of 6.54% at AM 1.5G 1 sun intensity (100 mW cm(-2)), which is by far the highest efficiency among the reported inorganic quantum dot sensitizers.
Nanoscale 09/2011; 3(10):4088-93. · 5.91 Impact Factor
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ABSTRACT: Recent studies have suggested that mast cells have critical roles in angiogenesis. However, the detailed mechanism by which mast cells contribute to angiogenesis is not yet clearly understood, especially in response to proinflammatory cytokines. In this study, we showed that the proinflammatory cytokine IL-1beta induces the synthesis of IL-8, a potent angiogenic factor, in human mast cells via the leukotriene B(4) receptor (BLT)2. We also characterized the BLT2 downstream signaling pathway and determined that BLT2-mediated IL-8 synthesis involves the upregulation of Nox1, a member of the NADPH oxidase family, Nox1-dependent reactive oxygen species generation and the subsequent activation of the redox-sensitive transcription factor NF-kappaB. For instance, knockdown of BLT2 and Nox1 with specific small interfering RNA, treatment with a specific BLT2 antagonist, LY255283, or treatment with a potential Nox inhibitor, diphenylene iodonium, suppressed IL-1beta-induced IL-8 synthesis. We found that the conditioned media collected from IL-1beta-treated human mast cell line HMC-1 had significantly enhanced angiogenic activity that could be dramatically attenuated by either small interfering RNA knockdown of BLT2 or treatment with neutralizing Ab to IL-8. Finally, the experiments were repeated using human primary cord blood-derived mast cells, and the results were clearly reproduced. Taken together, our results suggest that BLT2-Nox1-reactive oxygen species-dependent pathway plays a role in promoting the secretion of IL-8 from human mast cells in response to the proinflammatory cytokine IL-1beta, thus contributing to angiogenesis.
The Journal of Immunology 03/2010; 184(7):3946-54. · 5.79 Impact Factor
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ABSTRACT: Leukotriene B4 (LTB4) is an inflammatory mediator with potent biological activities in the pathogenesis of many inflammatory diseases. In the present study, we found that expression of BLT2, a low-affinity LTB4 receptor, is significantly upregulated in breast cancer cells. In addition, we observed that inhibition of BLT2 by a specific antagonist, LY255283, or by siBLT2 RNA interference caused dramatic apoptotic cell death in breast cancer cells, especially in the estrogen receptor (ER)-negative MDA-MB-468 and MDA-MB-453 cells, suggesting a role for BLT2 in survival of these breast cancer cells. In an approach to understand the downstream mechanism by which BLT2 mediates the potential pro-survival signaling, we found that the elevated reactive oxygen species (ROS) generation is associated with BLT2-mediated survival. Expression of Nox1, a member of the NADPH oxidase family, is also highly upregulated in a BLT2-dependent manner in these breast cancer cells, suggesting that 'Nox1-derived ROS' lie downstream of BLT2. Consistent with the proposed role of 'Nox1-ROS' in pro-survival signaling, knockdown of Nox1 with siNox1 or treatment with a ROS scavenging agent caused dramatic apoptotic death in these breast cancer cells. Taken together, our results demonstrate, for the first time, that the 'BLT2-Nox1-ROS'-linked cascade is involved in the pro-survival signaling, especially in ER-negative breast cancer cells.
Carcinogenesis 09/2009; 31(4):543-51. · 5.70 Impact Factor
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ABSTRACT: The leukotriene B(4) (LTB(4)) receptor BLT2 is expressed in endothelium, but no clear physiological function for it has yet been identified, especially in vascular angiogenesis. The purpose of this study is to characterize the potential function of BLT2 in vascular endothelial growth factor (VEGF)-induced angiogenesis.
VEGF significantly upregulates BLT2 expression in human umbilical vein endothelial cells (HUVECs), and BLT2 knockdown by siRNA or inhibition of BLT2 by a specific BLT2 antagonist LY255283 attenuates VEGF-induced angiogenesis, which was determined by its effect on the formation of tube-like structures and on transmigration. The role of BLT2 in VEGF-induced angiogenesis was more evident in vivo, where BLT2 inhibition by LY255283 almost completely blocked VEGF-induced vessel formation in Matrigel-plug assays. In addition, we found that VEGF upregulates synthesis of the BLT2 ligand, 12(S)-hydroxyeicosatetraenoic acid (HETE). siRNA knockdown of 12-lipoxygenase (12-LO) expression attenuates VEGF-induced angiogenesis in HUVECs, and the addition of 12(S)-HETE to the 12-LO knockdown-HUVECs restores VEGF-induced angiogenesis. The activation of BLT2 itself by either 12(S)-HETE or LTB(4) evoked significant angiogenic phenotypes, both in vitro and in vivo.
Our findings indicate that BLT2 plays an essential role in mediating VEGF-induced angiogenesis.
Arteriosclerosis Thrombosis and Vascular Biology 04/2009; 29(6):915-20. · 6.37 Impact Factor
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ABSTRACT: Papillary tumors of the bile duct are intraductal tumors with innumerable minute, frondlike papillary projections. These tumors may be either fixed to or detached from the bile duct wall. However, because the papillary projections on the surface of papillary tumors are long and slender, the tumors are friable and slough easily. The sloughed tumor fragments may float within the bile ducts, resulting in intermittent partial biliary obstruction and mimicking bile duct stones at clinical examination and at ultrasonography (US), computed tomography (CT), and cholangiography. A tumor manifests radiologically as thickening and irregularity of the bile duct wall or as a fixed or sloughed intraductal mass. A nonshadowing intraductal echogenic cast seen at US, an intraductal noncalcified soft-tissue mass with asymmetric wall thickening seen at CT, and an intraductal mass with a papillary surface and a serrated bile duct margin seen at cholangiography are all appearances that suggest a papillary tumor and may be helpful in differentiating a tumor from a bile duct stone.
Radiographics 23(2):447-55. · 2.85 Impact Factor
