Semiconducting Divalent Metal Oxides as Blocking Layer Material for SnO₂-Based Dye-Sensitized Solar Cells

This study is to demonstrate that semiconducting materials can be used as the blocking layer material for the electrode of dye-sensitized solar cells (DSSCs) as well as insulating materials studied previously. We modified SnO₂ nanoparticles with various semiconductor divalent metal oxides (CdO, ZnO, NiO, CuO, and PbO) and fabricated DSSCs with the modified SnO₂ nanoparticles. The modifier metal oxides exist as very small nanoparticles, well dispersed on the surfaces of SnO₂ nanoparticles. Except for the case of PbO, all of the modifier materials improve the solar cell efficiency. The detailed mechanisms have been investigated. The basic properties of the modifiers increase the amount of dye adsorbed, increasing the current, and raise the flat-band potentials through deprotonation of the surface to increase the potentials. The coating materials block the recombination reactions between the electrons in the conduction band and the red–ox species in the electrolyte. Therefore, although the narrow band gaps and the d–d transitions of the coating materials may reduce the amount of photons to reach the sensitizer, such negative effects are reduced by the quantum size effects of the modifier metal oxides and are more than offset by the positive effects mentioned above. The case of PbO as the coating material appears to suffer from the high resistance arising from the highly anisotropic crystal structures of PbO. On the basis of the various observations depending on the nature of the modifier materials, a few suggestions are made in selecting good modifier materials

Sensitivity and false negative rate on skin test.

<p>*Five patients in whom causal contrast media could not be identified were excluded from this analysis among 51 patients with skin test results.</p><p>Iopromide, iopamidol, iomeprol, iohexol, and iobitridol are low-osmolar contrast media. Iodixanol is an iso-osmolar contrast media.</p

Anaphylactic reactions and total number of RCM use in every year of the study period.

<p>Anaphylactic reactions and total number of RCM use in every year of the study period.</p

Clinical characteristics according to the development of hypotension.

<p>Continuous variables are expressed as mean ± standard deviation.</p><p>*P<0.05, ^†P<0.01. ^‡Among the total 104 subjects, radiocontrast media involved in anaphylaxis could not be identified in seven patients who had experienced anaphylaxis prior to the introduction of electronic medical recording system.</p

Comparison of the number of contrast exposures according to the presence of hypotension.

<p>*p<0.05.</p

An Important Role of α-Hemolysin in Extracellular Vesicles on the Development of Atopic Dermatitis Induced by <i>Staphylococcus aureus</i>

<div><p>Skin barrier disruption and dermal inflammation are key phenotypes of atopic dermatitis (AD). <i>Staphylococcus aureus</i> secretes extracellular vesicles (EVs), which are involved in AD pathogenesis. Here, we evaluated the role of EVs-associated α-hemolysin derived from <i>S. aureus</i> in AD pathogenesis. α-hemolysin production from <i>S. aureus</i> was detected using western blot analyses. The cytotoxic activity of α-hemolysin on HaCaT keratinocytes was evaluated by measuring cell viability after treating cells with soluble and EVs-associated α-hemolysin. To determine the type of cell death, HaCaT keratinocytes were stained with annexin V and 7-AAD. The <i>in vivo</i> effects of α-hemolysin were evaluated by application of soluble and EV-associated α-hemolysin on the mouse skin. The present study showed that increased α-hemolysin was produced by <i>S. aureus</i> colonized on AD patients compared to healthy subjects. α-hemolysin production was also related to AD severity. In addition, EV-associated α-hemolysin was more cytotoxic to HaCaT keratinocytes than soluble α-hemolysin, and α-hemolysin-negative EVs did not induce keratinocyte death. EV-associated α-hemolysin induced necrosis, but soluble α-hemolysin induced apoptosis of keratinocytes. <i>In vivo,</i> skin barrier disruption and epidermal hyperplasia were induced by soluble and EV-associated α-hemolysin. However, AD-like dermal inflammation was only caused by EV-associated α-hemolysin. Moreover, neither skin barrier disruption nor AD-like skin inflammation was induced by α-hemolysin-negative EVs. Taken together, α-Hemolysin secreted from <i>S. aureus</i>, particularly the EV-associated form, induces both skin barrier disruption and AD-like skin inflammation, suggesting that EV-associated α-hemolysin is a novel diagnostic and therapeutic target for the control of AD.</p></div

EVs are more potent mediators of keratinocyte death compared to soluble α-hemolysin.

<p><b>A,</b> Confocal microscopy of human keratinocytes with DiI-labeled <i>S. aureus</i> EVs (red: <i>S. aureus</i> EVs, blue: nucleus). <i>S. aureus</i> EVs and nucleus are shown merged on DIC image (lower panel). Scale bar, 20 µm. <b>B,</b> α-Hemolysin in keratinocytes after treatment with identical amounts of soluble α-hemolysin and EVs. <b>C,</b> Viability of keratinocytes after treatment with each reagent. <b>D,</b> Time dependence of cell death. <b>E,</b> α-Hemolysin on intact and disrupted EVs after treatment with proteinase K. <b>F,</b> Keratinocyte viability after treatment with soluble α-hemolysin (3 µg/ml) and EVs (10 µg/ml) with the anti-α-hemolysin antibody (5% of culture media volume). * P<0.05; ** P<0.01 versus the PBS group; NS, not significant.</p

α-Hemolysin in <i>S. aureus</i> EVs is a key factor for EVs cytotoxicity.

<p><b>A,</b> The presence of α-hemolysin in culture media, EVs-removed culture media (media-EVs), and EVs from the <i>S. aureus</i> ATCC14458 strain. <b>B,</b> Hemolytic function of soluble α-hemolysin and EVs. <b>C,</b> Viability of human keratinocytes after treatment with soluble hemolysin (5 µg/ml), <i>S. aureus</i> culture media (10 µg/ml), and EVs (20 µg/ml). <b>D,</b> α-Hemolysin in EVs from the Newman strain, α-hemolysin-deficient mutant strain, and α-hemolysin complemented strain (pHla). Human keratinocyte viability after treatment with each EVs (40 µg/ml). <b>E,</b> α-Hemolysin in EVs from randomly selected <i>S. aureus</i> from healthy controls (HC) and atopic dermatitis (AD) patients. Viability of human keratinocytes after treatment with EVs (25 µg/ml). * P<0.05; ** P<0.01 versus the PBS group.</p

α-Hemolysin-positive <i>S. aureus</i> EVs induces atopic dermatitis-like skin inflammation.

<p><b>A</b> and <b>B,</b> Skin alterations after treatment with 5 µg of soluble α-hemolysin and EVs (A) and 10 µg of EVs from the Newman wild-type and α-hemolysin-deficient strains (B) (n = 5 mice per group). * P<0.05; ** P<0.01; *** P<0.001 versus the PBS group; NS, not significant.</p

Demographic and clinical characteristics of atopic dermatitis patients.

<p>Values shown are age in months (median), ratio of males versus females, percentage of methicillin-resistant <i>Staphylococcus aureus</i>, and percentage of patients colonized with α-hemolysin-producing <i>S. aureus</i>.</p>¶<p>The percentage was determined by the amount of α-hemolysin produced by <i>S. aureus</i> isolated from the patients. The amount of α-hemolysin was measured by band intensity using Multi Gauge V3.1. Scores are as follows: 0: zero; 1: up to 6000 arbitrary units (AU); 2: from 6001 to 15,000 AU; and 3: over 15,001 AU.</p