Scalable CIGS Solar Cells Employing a New Device Design of Nontoxic Buffer Layer and Microgrid Electrode.

The efficiency of copper indium gallium selenide (CIGS) solar cells that use transparent conductive oxide (TCO) as the top electrode decreases significantly as the device area increases owing to the poor electrical properties of TCO. Therefore, high-efficiency, large-area CIGS solar cells require the development of a novel top electrode with high transmittance and conductivity. In this study, a microgrid/TCO hybrid electrode is designed to minimize the optical and resistive losses that may occur in the top electrode of a CIGS solar cell. In addition, the buffer layer of the CIGS solar cells is changed from the conventional CdS buffer to a dry-processed wide-band gap ZnMgO (ZMO) buffer, resulting in increased device efficiency by minimizing parasitic absorption in the short-wavelength region. By optimizing the combination of ZMO buffer and the microgrid/TCO hybrid electrode, a device efficiency of up to 20.5% (with antireflection layers) is achieved over a small device area of 5 mm × 5 mm (total area). Moreover, CIGS solar cells with an increased device area of up to 20 mm × 70 mm (total area) exhibit an efficiency of up to 19.7% (with antireflection layers) when a microgrid/TCO hybrid electrode is applied. Thus, this study demonstrates the potential for high-efficiency, large-area CIGS solar cells with novel microgrid electrodes.

Performance and Uniformity Improvement in Ultrathin Cu(In,Ga)Se2 Solar Cells with a WO x Nanointerlayer at the Absorber/Transparent Back-Contact Interface.

Thinning CIGSe absorber layer to less than 500 nm is desirable for reducing the cost per unit watt of photovoltaic-generated electricity, and also, the semitransparent solar cell based on such a thin absorber can be used in bifacial and superstrate configurations if the back electrode is transparent. In this study, a WO x layer is inserted between Cu(In,Ga)Se2 (CIGSe) absorber and tin-doped indium oxide back-contact to enhance the hole collection at the back electrode. A WO x interlayer with a thickness of 6 nm is found to be optimum because it causes a ∼38% relative increase in the fill factor of a ∼450 nm thick CIGSe-based device compared to the reference device without a WO x interlayer. While fixing the thickness of CIGSe, increasing the WO x interlayer thickness to ≥6 nm results in decreases of solar cell parameters primarily because of the emergence of a GaO x interfacial layer at the CIGSe/WO x junction.

Fabrication of metal-coated carbon nanowalls synthesized by microwave plasma enhanced chemical vapor deposition.

In this study, the coating of synthesized carbon nanowalls (CNWs) with various metal layers (Ni, Cu, and W) was investigated. CNWs were synthesized by microwave plasma enhanced chemical vapor deposition (PECVD) with a methane (CH4) and hydrogen (H2) gas mixture on a p-type Si wafer, and then coated with metal films (Ni, Cu, and W) using an RF magnetron sputtering system with four-inch targets. Different sputtering times (5, 10, 20, and 30 min) were established to obtain different thicknesses of the metal layers with which the CNWs were coated. Field emission scanning electron microscopy (FE-SEM) was used to examine the cross-sectional and planar conditions of the CNWs, and energy dispersive spectroscopy (EDS) was used to analyze the CNW elements. The FE-SEM analysis of the cross-sectional and planar images confirmed that the metal layers were synthesized to a depth of 0.5 µm from the surfaces of the CNWs, and to a greater depth at the ends of the CNWs, irrespective of the deposition time and the metal species. The resistivity of the as-deposited CNWs appeared as 4.18 x 10(-3) Ω cm; that of the metal-coated CNWs was slightly lower; and that of the Ni-coated CNWs was the lowest (1.74 x 10(-3) Ω cm). The mobility of the metal-coated CNWs was almost unchanged, and that of the as-deposited CNWs was 1.23 x 10(3) cm2 V(-1) s(-1).

Aqueous extract of Mosla chinensis inhibits mast cell-mediated allergic inflammation.

Allergic inflammatory diseases such as food allergy, asthma, sinusitis, and atopic dermatitis are increasing worldwide. In this study, we investigated the effects of aqueous extract of Mosla chinensis Max. (AMC) on mast cell-mediated allergic inflammation and studied the possible mechanism of this action. AMC inhibited compound 48/80-induced systemic and immunoglobulin E (IgE)-mediated local anaphylaxis. AMC reduced intracellular calcium levels and downstream histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. In addition, AMC decreased gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in human mast cells. The inhibitory effect of AMC on cytokine expression was nuclear factor (NF)-κB dependent. Our results indicate that AMC inhibits mast cell-mediated allergic inflammatory reaction by suppressing histamine release and expression of proinflammatory cytokines and the involvement of calcium and NF-κB in these effects. AMC might be a possible therapeutic candidate for allergic inflammatory disorders.

Ripe fruit of Rubus coreanus inhibits mast cell-mediated allergic inflammation.

In this study, we investigated the effect of a water extract of the ripe fruits of Rubus coreanus Miq. (Rosaceae) (RFRC) on mast cell-mediated allergic inflammation and studied the possible mechanism of action. Mast cell-mediated allergic disease is involved in many diseases such as anaphylaxis, rhinitis, asthma and atopic dermatitis. RFRC dose-dependently inhibited compound 48/80-induced systemic anaphylaxis and serum histamine release in mice. RFRC reduced the immunoglobulin E (IgE)-mediated local allergic reaction, passive cutaneous anaphylaxis. RFRC attenuated histamine release from rat peritoneal mast cells and human mast cells by the reduction of intracellular calcium. RFRC decreased the phorbol 12-myristate 13-acetate (PMA) and the calcium ionophore A23187 (PMACI)-stimulated expression and secretion of pro-inflammatory cytokines in human mast cells. The inhibitory effect of RFRC on cytokine production was nuclear factor (NF)-κB- and mitogen-activated protein kinase (MAPK)-dependent. In addition, RFRC suppressed the activation of caspase-1. Our findings provide evidence that RFRC inhibits mast cell-derived allergic inflammatory reactions, and for the involvement of calcium, NF-κB, MAPKs and caspase-1 in these effects. Furthermore, in vivo and in vitro anti-allergic inflammatory effects of RFRC provide affirmative proof of a possible therapeutic application of this agent in allergic inflammatory diseases.

Elsholtzia ciliata inhibits mast cell-mediated allergic inflammation: role of calcium, p38 mitogen-activated protein kinase and nuclear factor-{kappa}B.

Mast cell-mediated allergic reaction is involved in many diseases such as asthma and allergic rhinitis. Therefore, discovery of drugs for the prevention or treatment of allergic disease is an important topic in human health. In this study, we evaluated the effects of water extract of Elsholtzia ciliata (Thunb.) Hyland (Labiatae) (WEEC) on mast cell-mediated allergic inflammation and studied the possible mechanisms of action. WEEC inhibited compound 48/80-induced systemic and immunoglobulin E-mediated local anaphylaxis, and serum histamine release in mice. WEEC reduced intracellular calcium levels and downstream histamine release from human mast cells (HMC-1) activated with phorbol 12-myristate 13-acetate and calcium ionophore A23187. In addition, WEEC decreased gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-1ß and IL-6 in HMC-1. The inhibitory effect of WEEC on cytokine expression was nuclear factor (NF)-κB and p38 mitogen-activated protein kinase (MAPK) dependent. Our results indicate that WEEC inhibits mast cell-mediated allergic inflammatory reactions by suppressing histamine release and proinflammatory cytokine expression, and involvement of calcium, NF-κB and p38 MAPK in these effects.

Anti-allergic inflammatory activity of the fruit of Prunus persica: role of calcium and NF-kappaB.

Mast cell-mediated allergic symptoms are involved in many diseases, such as asthma and sinusitis. In this study, we investigated the effect of ethanol extract of fruits of Prunus persica (L) Batsch (FPP) on the mast cell-mediated allergic inflammation and studied the possible mechanism of action. FPP dose-dependently inhibited compound 48/80-induced systemic anaphylaxis and immunoglobulin E-mediated local allergic reactions. Histamine releasing from mast cells was reduced by FPP, which was mediated by modulation of intracellular calcium. In addition, FPP attenuated the phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-stimulated expression and secretion of pro-inflammatory cytokines in human mast cells. The inhibitory effect of FPP on pro-inflammatory cytokines was nuclear factor (NF)-kappaB dependent. Our findings provide evidence that FPP inhibits mast cell-derived allergic inflammation and involvement of calcium and NF-kappaB in these effects.